“ ) 4) = aaeite @ atti bes > naeasaes eter ees) oiled > te ites wire “a ates a 3) : tod re ; piraccmts Ee rises 2 sen ard kept ext aes gin: ode ; 4 , a: Saag i . ‘ re aes me e0*<443 ‘ead fe bo rd fanmade | te ‘ Minne pan eaen ¢ ererartniry he: rah ate Beeler day hs hatte bate Ttsae tne i FO-S mek DT ede Bead bed bat Mare Pehl @rds be Lddie yt ¥ PerPt wat fate» ” ; aby abe v Bie f4¢ » Undebrthetig: + % fa) RESET bya-4sh onto’ adea? ‘ania Ghia. eae j iets pinta’ ans: “hopuseerseatsiias Sire ee vente ena eh Seam Paieie al * a 4 t St vas det inn 4 ene a 4 aise 4% 4 ’ ‘ t ? 43 eh : ti \oehe nag bony et, the™ #¥ +t of ‘ He an Pag tstho olen Weir 4 oe x - rats TONLE em mnatsat v tH ‘ . beh erat art id Pit ak: a aah e ar bay “ sgt sas8t ist ’ Ba at fae . th ie a J P\eteh\ ares * Weeaaihy er ieen} Veit pte Mttesy si ast Tee Heh tet inate yh a of: \bartpag Mag sini ante “7 ae oe sey rt t + *Feeange) bana ia T° faeraa phate ALTE LS Goat dete: ‘ a on rises N viet “ity iy pphiah tn Isat are . the iy 109 EG - are torenal pa see tia rT om on. ; 4 Ring te oy ex Wiss oe es +) lade 4 abt 4 , 4 : athe Hake he aay - ie > Pi] Oe! } oe iaeet hattoye gecaen ey oe) 4 tight sees gent genuhs i Veli ie Pret = Nc have Pe 4 (90 1 ePathensas “Tae cher ot ee W ts ik de) Libel ver nat + *hodine: gt tote ant Pipi fod bea tia petit . had & Bayi ialae Mar art . hes erat, a) hae ihe tS . qiestey Oh aes a ed i pith. . nraltaet +9 Ne te tes! as : yet Re ots gee Naty tgits> ey Palehet Po ipty™ heres Wee athe lta, 4 ; \ ivy b's ot betes em Hohn) fej atte ei nee * Cs * Ais Pia Spies einaeie Shetek: ) Say) kab igord er rdoge y “ GTI etree Pr rig nase ‘ ; W WV imei atone 194548 Boy iF ppd dl MN Pa ’ ites reds tle Haye ee faye talestt vay ; ahi ~~ ‘ “™/!, terete at: q yy hs ret py hover De : ry dept itiesty Perey eras Gilad ates ve tt Hints! BAgs Oeraere tary bode tasie Te suthegls i mehr ee phawgt sy 5 etwas aed ot imioet tiv ‘ye i ee a : erik tt rete Xi ty eh, we hes’ ae ee UE ieee Sites es trv Gard ib tea ett , eeytot onket eae eS hee tee ; eased polls (each a et SS Aesiy vite ae Peiiye + cane mae ' Wk ey Tort) peat oy in ie 23 . ies ets teeel oreey pauw aa west {a 4455 Sere Torey ELSE peer ae Uehara irre ee ‘ Ned wot mown fs eG od wo Gueh sie ty seieeeeen pee sae oe, daeasers segs gees tl] ~ a eprreepteepeatitie cet ena 1st tt SS eae oe ata eee eee aaah ede bese ie eTinlen pease ye bode pen ts ay os there 145854 inves mata rail 4 “ 3 » : s Vote eh hah ae eee Saat yeah | “ ’ : noaen : 4 a 3 ave oe stall ea titan Steere Sap in 3 oasis . ee eke * ’ RE, ve se, i ihe eee resort AS ae 8 4gt 4. ie ol + Titegieines me Chetan heer j rt vat nah? ay SS \ : nd - & S \ 3 : 4 yf Aa o ny re) Y : a) e = le > Jew ion ©. ie oy in ™ es aur { Ls yk ‘ en a er hy ih ; i's ; A Text Book of Veterinary Pathology 3. peas ne x ee it Fog a ' 7 Z anes f se Z Y ; i & rae n if 1 “ vi i Ges " 4 ue i ie ; i it a ia : “ 1 A ‘ Ae a4 , 4 4 ' “ M - ¢ Ai ’ , f ap ae t \ " : Ee 4 it q ’ { r : art moe : ya) : I 7 eee a n ; ; “a 4‘ ” *# j ing \ en i ' neato < ‘ : et tu) re , Piel, i oa ; i Lh ‘ , ? : i yo ; t vey x “ . / . i ' " 2 a 7 * k ! ; } *) Gy 4 ¥ f a i J n i . . ' k i i ie oe . A + ’ ¥ ‘ ci ~ Saal a . \ a - y . ar A \ ; : th ' : a 4 ’ i Tar 4 ’ ’ bi A j i 2% , . ¥ e! i m ’ i ‘ ou . 7 4 » ° - , , ' : 1 as: en tte ’ are : r i i =, rat ‘ f oto; N ; i » i ‘ . i ‘ . s ‘; | | Y . @ ay 2 . 74 1 *s § A TEXT BOOK VETERINARY PaltHOLOGY FOR STUDENTS AND PRACTITIONERS BY ol eKINSEEY. MSeD. Vv. S. Pathologist, Kansas City Veterinary College FULLY ILLUSTRATED CHICAGO ALEXANDER EGER 1910 Copyrighted at Washington, D. C., by ALEXANDER EGER 1910 Gc A271281 LINDEN BROS. PF.ESS, CHICAGO ee ee RD PREFACE. A knowledge of pathology is essential to practitioners and to students of medicine. The general considerations of pathol- ogy, whether in reference to diseases of the human or diseases of domestic animals, are practically identical. Many textbooks on this subject are available, but they are especially written for the practitioner and student of human medicine, and the illus- trations and examples are all in reference to diseases of the human. Such textbooks have been used by the author for sey- eral years in veterinary classes and it was thought that if the same general pathological principles could be exemplified by cases and illustrations in veterinary medicine, the subject mat- ter would be more readily understood by the veterinary student. This explains the issuance of the present volume. The writer has endeavored to place every phase of pathol- ogy from the veterinarian’s point of view. The entire subject matter has been expressed as far as possible in common every- day language, with the hope that all readers will have no trou- ble in grasping the pathologic facts. An extensive glossary has been appended and will be of considerable aid because practi- cally every technical term, with its analysis and definition, will be found therein. The author is greatly indebted to Dr. S. Stewart, Dean of the Kansas City Veterinary College; Dr. D. M. Campbell, edi- tor of The American Journal of Veterinary Medicine; Prof. W. FE. King, Bacteriologist of the Kansas State Agricultural College; Dr. F. J. Hall, Chief of the Food Inspection Department Kan- sas City, Mo., and formerly pathologist of the Medical Depart- ment University.of Kansas; Dr. L. Rosenwald, formerly patholo- gist of the Kansas City Veterinary College; Dr. Geo. F. Babb, Milk Inspector of the city of Topeka, Kansas; Dr. D. Cham- plain, editor of The Milk-Man, for suggestions made by them concerning the text matter. Also Dr. R. F. Bourne, physiologist of the Kansas City Veterinary College; Dr. C. D. Folse, City Milk and Meat Inspector of Marshali, Texas, and Mr. Chas. Sals- bery, microscopic laboratory assistant in the Kansas City Vet- erinary College, for their assistance in the preparation of the illustrations. The author consulted various text-books, journals and other publications while preparing the text for which acknowledge- ment is hereby made. If this book supplies the practitioner and the student of veterinary medicine with clear, concise statements of veterinary pathology, the purpose of the book has been fulfilled. Jae De CONTENTS. PCL ACC ee ane Seen rc Sh aie amu OR Ls Shara ke elle, Siosle Sop cos aE eee 5 CHAPTER PDeIMitiOQnGi er coe. Hoe cs See ei ee es CER WOe oe RSE 19 | ZT, 1s GEIS 8 Se ORS cr ers Grip ct hee ne ar a 20 GEbA Paha Revise | pencil Consideration of Disease 22°. fa22 oe ce es Se 34 siablexormwicectable Parasites so. ats aes ate neta as 48 SACCMATOMMCES ue ae eit aA aa me eee we a oe D1 SOM Z@MlVCSteS ings ast lak oy ie en te ie ey me eee ee 52 PUBIC AN Bale EAS MeO Steepe al ea athe a clea Porson a8 sek 62 IPE OEO AOE ae ese Be es ta Ne SG oe cere ai a ore 63 eke lraniintine prs ns Cone ne ele tle See ete estilo 4 63 PRIMO POC are slay cel eS ei conte fa San Coates Bs 69 CELA Iau | LYSATE NEA 2 Ss A ath ar mon me npr Geto ES rea Mag UA Owe ee aS mR 78 (Gia UNI B IR I MPAIROLMARONS wih ai. ya Seite 58 aS or, Sr ped eee aN ren 92 GiEEACARTO RAN: Circulatory Disturbances .......... sl RS eR Om MRCRS Ror 110 JeGVESA DUONG CIE Make: eden tant ee aii, NERSHE GAG ema Cae inch etre 112 JLA Aaa OOO Phra vO hes re Me a aay ach iar ce te Gl ake ar Peary pe ies Oedemas DWropsysOrtdy drops 22. ek Se 118 ANTE OO SISter csp ns tet ce os ayn, oa ae ok © Seat ee Fee ee as 122 Hmm QUIS TTI vac. oa eh adate ate ace CAR Ra Spit STEAM eae 128 SE eta is SS es Oa she Sei aie ae MRA ep PSN fs 132 \ Hyperemia (Passive) . SAR Resa ic Bear eras Reatard eas 133 IEP se SS an Oe ANC NAC) Nene et nt Ceo cr ahs Ce auneam Mark SRA 135 GEA RIDEIR: WAl rat MIE A@LO ese tay ee ey tetas secre Ws Sevag eR Cen we Uae aise e rane a BIO 138 CHAPTER Vil: IDO OLESSIVE MLISSUE CHANGES eh nt. cia saute Seas otal awe aid ane EA Ne Sena BIO My reat et arstnae, Ue wh see ge ward ata soak, at il CONTENTS. PAGE VWroumd-slealiine ties, (50s oo ere SS ea ta 183 Hypertrophy 75. ohn see ee 188 Hyperplasia... es.) 5.0 eo cee. ne ee ee oe Meétaplasia: 5. S52 4coiee’s eee eee are eee 193 Cir ACe ii ay see Retrogressive Tissue Changes ..... evi api wecaa tis tbace a ene 195 JEN OMO OM Ste Mees abrnncen ee eB a: Foe hea ee SS - 196 Cloudy, Siwrelllitie: 25 Uae ee fa a 200 atiys Changes: a. 4.0. oper ele ese eee 203 Amyloid: Changes :2 ia (nS oe eee eer 210 Hyaline “Changes 0.) cag eeeee te cloe pea a eee 212 Miutcotd Changes 77722. aia soiree tire crete eer eee 214 Colloid. Changes “ose nano ee 217 Serous.lniilt ratrony eee ee en ere 0 Glycosenie Infiltratione: 20.0 akc 221 Uratic infiltrations: 223 0 ee 223 Keeratociso arene ae ee eee hee 224. OSsificationy 22. heidi s tesa, cae ert een a 226 Caleareous Vimhlttation se. a oa. yee 227 Calotlic a2. aoe ia pets ace ee ca ee 230 CONGCKEMERES = peas Sor ees ok eee ee 238 Piginentaty Changes e5. soe te ee es ee 241 EXCESSIVE ship in CintatiOmye cue i so ee eee 243 Absence of, of Diminished: Etenventatt@ie = ae 249 | eve IDX. Neécrosis and Death). - 724252" .<%0 0 ee eee 251-262 Physiologice:Déath 2.2 po. oa eee ee 262 PathologicsDeath>. i. nee Seay arate oe 263 CIBUAIPTIDIR Ox, PUIMOLS 08 eth eee thnk Sigs 267 PaprOmiay yy... 2 2S Ue PS Mi eee ee ieee 278 IVETE ITE OG sia icin ae cSha teres at ona ie neem at ac tees 282 Chron droma ©. i5,5 50% ew ae nee ea ee 283 OSPE Gita a saihcele ce setk 6 0 Be aera ce 288 GVO: Facies hele oe 6c eae ee 289 Midomtoia, rculy, 2) Sukie Ae gee Bamana eee cetera 289 ThE hy ini: eee rade RRR, GGT Na Ur aap mR og 8 293 ARTO LOUIE a rye, ad mcrae Metre eke Noes et ote ceescans a 293 IY Icon ak: Waeape Meena tec areata pe “Man were Ci TRC Ce manana. ag 296 SST COLT ec sc SCI hls ec ee ee net noe oe ee ne ee 298 CONTENTS. 2 iil PAGE LEE Die OTTER Ae nn ee ee ee 318 Pinbrwenie te pithelial Mwmons .25 2.60.04 20s. ones ie ees 321 siete eMaMOIMEL Sytye. A Ca ae nehcee Sa yet oe ae had Glee eK Senge 331 SRL were. nets Soe ein Ne CRSA 2 y hie ee oe 32 Ry stome ts eset Vee ear io hee ts eee, CHAP BER Jek Ie ease Sad Weta nas ge eo aes SoS ase ahd ay pes Sect aare 39 CELA Pik. XEF: Renee Gives GreainilOmata, 2 625 foes ose hewadee ee dene oe | OAA PR CREMMOSisG th nee ee Ge ots 2 Se ey 8s +1 PE GMIOUNVeOSISn serie eek | xt cabiantee sas yee seem 345 [5 BYE ESS eeu ee one pe tena 3! DC ee aa ae ee 361 Psewelotma Coutasmcwy? =o) 260) F i es caf ei elea 3vA4 ReMieisctctingg ee See hos hs eats it CRS ome eed ORS octane Sila «Nass 373 LIST OF INSERTS. insert —— FB otanteal Names. 5 coe eee eee Next to page 45 Eetocher wel ACCA ie Ace ee Se es Bes ee eS Next to page 62 Risene ert bh rotentians wes eee eee Next to page 63 Reser eV —— Plelninmiies oe hele ope ci a efela ce ed 29 TS SpePmMatozOa sissies nce ace tue sieee omer aane, oaths Cac etencnens Pore eyeaee a mene a SO 16>-Red: Buckeye: en 5 ST cae ee ae ee esc ear rae 46 17— Astragalus: MOlissimus: Vinee corn ae ee ieee A7 16—- brichophyton Monsucansi aces cis oe eit rete ere ieee 49 LO As persilluss ui Satis secre emer iny kero oleae) cio.e ieee ee 50 207 Saccharoimy Ces MHATciimMinOStish Cine ee eee erat ie er 51 2i-— Group Bacteriar ciiac ew tes on also a erie elorcanle Seette she eet ea ee eee 53 22) 23>-Gr otip Bacteniay csr ivalth seiseae ce ele eee coe ohcu sneer okey rey eee 53 24+ Flagellate: sBacteria si ciicke otse «sists sate rete chee ala wepenet ees nner 54 Amon Oehneblehiteral” BACHE, cbogoobooeooben code dbogn gos e cone osogé cuore 54 20 Bacteriak Pission 57 6e: aaah. ae eis re opel aes nena oko Se cna hehe ne erorenle 56 27S por lation Las wcta averse oti elas els rete eptereasee te eee aero e as ee eee 57 28—Bacillus yAmbh racic es caakm caun cca ee Se sees tie) Ones Sree tee 50 207-Bacillus YF etainiic: oa oe ekepe vies lane sume aes ee NEE ecw tage ent aa eee ae 60 20-=Piroplasma> Bigemimuti cee scien weeks coker cdeustco oat esaa ees 62 3i>— Drypanosomasvansia(Mronty Katippbarasites ims. see irae 63 32—, Sancocystis) Miescher «(Eirom) ianppeleatasites))jo geri yenr ae 64. a= Taenia: Marotna tay ci: ats cbecie cr teue a ist aa ke ROR ee ee eee 65 a4—— Laeniia Camiiias 2 aicisc, sche ow eete atte sree Sie ene eRe des onde ee 66 35-—Taenta. -Echin0cOcets: : s/f. 0 s..:chae is cetera ee ee 66 30> Vaeniia’ Solivm. sci. ietie ce nck Wiis es opel alte ite ere reve a ee 67 37-—Stroney lis Air urs 9-6 uieta ce ew ls nen cen ral Meme perce tence 67 38-Strongylus: P aradOxus © -is:s.0re win sal atecabaheue fe eaten a eueketecenei ene at peer 68 20 ilaria: WPapillosa: (co. aise le te. cee Sraleysueren a seems Repel cl Oe Ry ara a eer eee ae 68 AG Oseyrgis: Ctivalat som ss etaae avavenetns 5 cathe ean tape ttt eae nen cere ten ey ett tentel ge penen EEE 69 AT Sy Aeamus Prachealis? scccs cov. ohetsieuguessukever nets ae eee CRO Rie eet ea 70 AZ—-SClETOSLOIMa) sll OSEOMIITD grea) wens a /assleeee ste rereterelaicmieus Cree eee eee ee 70 Ag UniChOCephalis DEpressitisctiltciuuar sterete ls rstettevene yie: sckers elders nee 70 A4——Melophar uss Oyvittis<. iene euste cies tae rdetete st tcire celcisa te ene meee te eee 7a FIGURE PAGE Pee CMM ID INDLTTSS CLS CHIN easels oy aeelacistayereeadepers so (0'< e)aciccdierchs ns selec aia a 72 WG-0 = iS OMNES (Stan Saeco db been to Coo Oo oda Gan Or er onipscr ross eicieie sors 72 Fir pare MMMM TIT STS oe sae Ss levaceteee MiG aes cle ole e\atela Sasa alee eierd Bis eam ts 78 48—As€aris Mystax ...... been eee e ete t ete e cece r eee e settee nesses eee 74 No BROT tele paviciii cise ee ia cate ees cae e ko 74 Fa meme orinyieliis) Gioas. 06.0. : a-st shee st STR ee oes 75 BRIT rf Sl ciliata ASV DUU RET She ests cee On ide me cco CO me 76 CemeenPETOMCELES Matis: h.0ciace wie ns seeiyy, een ek vie coie'S's 4 boos cece oe 76 Cee MMArOpInis = Phalanses ‘Owis. aoe fo+ ses vee cis Sees ones es beans 70 eet ICReM SCRE ACES et eco esac Onan acre tacks Wane dedechaeaeites 70 Nae trodrapisw Annimlatus: Bemale ic os ce h vais occis co ose cielse en oe a 5's 80 Seemtiatcarapus Anmulatus, Male =. 2. sccte nt. 2 esa Se eee oot ene ves 80 57—Margarapus Annulatus, Female laying eggs ..-..-..-...-.+-.-- 80 pee Mieka pis, AtnMtlattise Labyac s cece oie sso cies swisse ele 6a clots ole nln eee 80 = S== See RS GATISR A Rei oe I ROE, SR SRC Regier 0 fr coir chee ee eGR 81 Mien SOnOMtCS COMMIS. -OVIS a.o. slacn cele ate ctl checes sien ae alg O7—Fibtinotis: PICUrisy, (isis vi.0: cave ares ask a sees See ae ee 158 OS Myositis, “Acute a2. siucte soit cS be srolbe ele ahete: cpcaee eee eee ae 160 oo-—-Chremic™ P netmonian ied dienes aos lela eoenaa eee eee ee ee 162 100m Chitiomic tlepatatise si. ar A eR ay Orbe oe ey i hc 165 16£-—Pus, trom a ‘case of Strangles. .0. 20: See ee ee 168 102 —Suppurative” Nephritis: \.i.. 44.03. 5eo Re ee eee 170 10¢-—_Red- -Mepatization a s's.5 ci eid ee ee oe ee 172 104-—V asculan. Regeneration \.°.4 icc sie eke eiepetate easter 178 1O%-sHibrots, Wesenerations - 1.6. eee eer eee cree fy Sy culeverortanahcae aoe 179 Too W ound. Healings? 2.0... Preputialand@kenal: Relic Calculiir cs tie oe eee 234 124--Salivary: ‘Caleulli: si0o sac ae wie sre ace tite nee) es, ote See ee ee 225 1257; lntestinal --Galewlus; fs. 7s cys ees ase eee os ee 236 126=-Biltary “Cal e@ulies tare ec eee coh a eee 237 tag—Hair: “Balls. ics Ghai taleloiase ether sieok oe chico setae Carnet e 239 128—Inspissated Pais 2a t ce tierece ae ee eon as ace eh ee ee 240 126-Hemosiderm PigmentatiOn:, ses iiccsttela tate cis cue hse a costae eee 244, 130—Icteric Pigmentation 2655 e0 eee ek ee ee eee ee 246 TBE" NECLOSIS 8 sce ocsiejs S:0'elecereig oo «46 nts eee sede egeh eueene > ence CDM ee a 253. 132-—Bacillus~ Necrophorus. <..% i cine wteae atte ie eee ee ee ee 254 1, ag 2 0) Aer I Te eae we MEU RE Ey Ce 4 Gye gel ho Sage 8 255. 134—Ergot Poisonine’ Cattle: s.). vs.) scent oekene tae ee 256 LHS Fatty NGCHOSIS ie is sale oss Sic cca ea Goa Be Pete ae ec OAT SR ge ea 258 Ig6-—Necrotic “Center of -Tubercle: <). space eee he et eee 250 TAZe— DAT COMID, a's sis ae.sve sie ele. 40 weal = pelle rCaelOhene cnehes epaee eae Caer eta ee 270 1355 Metastatic: “Sar comatal - -.toterv vow nadetuenberc pare tete tk excuse ce peecien ts ane 273 13@—Epithelioma, Horse’ Head ac ccc scan ac eet tite od ieee ore ee ee 275 L4er— larg Frome 3. s 6... ewe ee ieiers sista phous Sen nie eee ne nn 279 Ph aot Rami alt O16) (0): NN ine RAR Si Ue rs Oh EA temo NSM ge Ca Se ee, 280 LIST OF ILLUSTRATIONS. Vii FIGUBE PAGE ee amma NR OEER A cet Steno ont Mey ac sai Shah ste stata aiel Grae ace iataeime's mine Se k's OG.a isles s 282 teres 0 HI GIENEE ROMERY cl ian eye one eS 3 cfs ttc crc eralete SacreietC eS c's ee ec cls 6 Cares ok se yale ok 284. Ht coda PERI APO NOLS a ~ kay (Pungus.-CActinomyces) “22. 2a iene oe ee cr ees ee 356 1o8—Actinomycone —Toneite eevee eseeonoe HIN}IA SIPI [Oy you01g UINj19}0B ot MC Wh tal Og de OS LAL Qader Fer tin pe ALICE Pera RL Tein Tee) ° uo0T}.10qQ8 SNOFJOOJUT ** sss ees eees eee oer ee eee we WINIBIIBA SNAT}IOQGB sn [Joe ‘SOSVISIP SUI cee ee ae eee MOT[O} 94} JO osnvo 94} aq ABUT vIIB}Neq BUTMOTIOJ on apa ESO uo;VBInddng*s***s*ssss** + (sayjortBA AUBUI) souUsSOAd 8N090000}d9.11g UOPPEINGANG* sess ess srre ceeeeeeee*s Sno soussoAd snod00000[ AYdeEeyS vseeeees SnoIne soauogoAd sno00000[AYydeyg oe eee oe eee ae eevee ere UOTJBINdCANG**ssseeseeee% Cece) oor eer eo ewe: oe =e ee ese ee eee oe . ° eer ee ese eee owe wee uojeinddng*:*: oeeere eee © ee ee wo we oe ow *snql[B sousZs0Ad 8nd00000 [AYU de1S ec eeee eee ee eee eo ae eee . Sntiess ee ee Ons .6) 8.88, Ole e608) See 6.028. 6-8 18-6 “eres ceue 8 LOL e.6—e)boN) 66: Bce) B: alee Buj19sue eBzJOBYyIOIIds » ° oeteeetorne oe oe oeeese ower e eevee ee BIS OSB ict: ethos. 29 sere oe et Berane . eer eee one snuly1dBo SNd000101 WW eeereeowr ees owe weet te@ewrr nee owveeeree UOTVeINddng'**sssseseee8 eee reer eee ese e ee ee eeseoaes syusBo XJ1IYOpPBiD ire db ea a) De he dee —a me et Mt ie " iy Rave: SB Z ae = aS Px. at + SEY | i ay ike i dae ae he Ee. aes Fae + pase Hecwaisss sell Lietied a tee, eae! AMEE ad Rene LINE ARR a Pao fF PARR eSB UE pal 4 ‘ ? ’ i ais i yA j { " ‘ LAN : ' * r . : h P { : } 7 * j ; ’ ¢ ‘Bho, ‘ hy al ‘ wnat ie, ma i GENERAL CONSIDERATION OF DISEASE. 63. Protozoa. Protozoa are microscopic single celled animals. They are very simple in structure, being composed of a mass of proto- plasm with or without a cell membrane. The cell membrane, when present, consists of concentrated protoplasm. The pro- tozoa having a cell membrane are constant in shape, as the Try- panosoma Evansi, and those not possessing a cell membrane vary in shape from a sphere to an irregular flat mass and are capable of changing their shape whenever occasion demands. Protozoa are larger than bacteria. Fis. ¢1.—Trypanosoma Evansi in a bloodsmear from a horse affected with surra. Protozoa require food similar to the foods of higher animals. Particles of food are inclosed or incorporated by them prepara- tory to digestion. Digestion is accomplished by means of fer- ments elaborated and secreted by the protozoa. The digested foods pass by osmosis into the protozoa, the undigested por- tion being extruded by rearrangement of the cell protoplasm. Respiration takes place by exchange of gases through the surface protoplasm of the protozoa. They reproduce by fission, budding, conjugation or sporulation. Protozoa are universally distributed. They all require con- siderable moisture. In fact most of them live either in fresh or salt water. A few only are parasitic. The specific action of pathogenic protozoa in the produc- tion of disease is not understood. Some may have a mechanical effect only put the evidence concerning others indicates that most of them produce an injurious chemic substance. Helminthes. This branch of the animal kingdom contains many species that are parasitic. Structural, animal parasites are much simpler 64 VETERINARY PATHOLOGY. bss hlard Rey CJ 9%) 32.—Sareoeystis Miescheri. Drawing made with Camera lucida. Fig. 1. Cross section sarecocyst, muscle cell enclosing sarcocyst ruptured. 5 3s Cross section of heart muscle cell. Fibrous connective tissue. than the closely related nonparasitic animals. The simplicity of parasites is a result of adaptation to environments in which es- sential structures of the nonparasitic type, useless to the para- sitic type, atrophy because of disuse. The parasitic helminthes are of the simplest structure, their nervous, digestive and respi- ratory systems being very rudimentary. Their food is obtained from their host. Some animal para- sites, as the tapeworm (Taenia) absorb digested food stuff from the intestine of their host, others subsist upon the host’s blood, (Uncinaria), and still others consume tissue juices and lymph, (Trichina spiralis). The reproduction of helminthes is accom- rae Eat vi EG es j San? vigt aor athe BRANCH PROTOZOA, Unicellular animal organ- isms, asexual, reproduce by fission, sporulation. or budding. ANNULATA, Specialized worlms com- posed of ring like sege- ments, simple head and eyes, usually eversible dentated pharynx, straight alimentary canal, well de- veloped nervous system. ORDER SPOROZOA, Reproduce by sporulation, no flagella, no cillia. INFUSORIA, Possess cilia. or flagella, reproduce by fission and budding. HIRUNDINEA, Slightly flattened on dor- sal and ventral surface, sucker at each end. CLASS COCCIDIA. SARCOSPORIDIA. FLAGELLATA. HYPOTRICHA. GNATHOBDELLA. INSERT III. AMILY GENUS SPECIES HOST PART INFESTED SOROSPERMIDAE. Coccidium oviforme Rabbits, G. pigs and manQLiver and intestine. Coccidium cuniculi Rabbit. Lieberkuhn’s glands and intestine. Coccidium avium Fowls. Liver and intestine | Sarcocystis Miescheri Pig. Muscles. Sarcocystis tenella Horse, ox, sheep, and pig. Muscles. 'RCOSPORIDAE. Balbiania gigantea Ox, sheep and dog. Connective tissue. | Lamblia intestinalis Sheep and dog. Intestine. Monocercomonas hepatica Pigeons. Liver, | Trypanosoma equiperdum. Horse. Blood. { Trypanosoma Evansi, Horse. Blood. “ Trypanosoma equinum. Horse. Blood. l\YPANOSOMATIDAE. Trypanosoma Brucei. Horse. Blood. if ( fATHOBDELLIDEA, Hirudo medicinalis.” Man and horse. Skin. Hirudo troctina. Man and horse. Skin, : Hirudo decora. Man and horse. Skin. | Hirudo Tagala. Man and animals. Haemopis sanguisuga. Horse. Anterior respiratory tract and intes- tine. a A tt GENERAL CONSIDERATION OF DISEASE. 65 Fig. 33.—Taenia Marginata. After Niles. a. Shows segments. b,c. Head latteral view. d. Head anterior view. plished by means of ova, or by the production of living larvae. The life history or cycle of helminthes is very interesting. In some cases the organism is parasitic in different animals during the different stages of its life cycle; for instance the Taenia cras- VETERINARY PATHOLOGY. Hiri Dts KAUNAS HA i Fig. 34.—Taenia Canina. After Railliet & Leuckart, a. Adult tapeworm. e. Cystic form. b. Head of same enlarged. phat setae Fig. 35.—Taenia Echinococeus. Niles & Neuman. a. Adult tapeworm. After Neuman, b. Part of hog’s liver showing cystic form. ma, a rudeinty nati nd i al eS ee Nem Ms rt A : x ate BRANCH CLASS ORDER CESTODA, Ribbon shaped, segment- have no fixation apparatus have no digestion apparatus FAMILY TAENIIDAE, Head always has _ four suckers between which is found a depression or a proboscis, Segments usu- ally have their gential op- enings on margin. INSERT IV. on head. Adult lives in in- testines. PLATYHELMINTHES, Flat worms, nearly ail hermaphodites, omy ( BOTHRIOCEPHALIDAE, ae TREMATODA, Found mostly in fishes. aoe F:at worms, nonsegment- Vek ed, have digestive canal, t= OD no anus, have one ar two Ses suckers on ventral surface. so DISTOMIDAE, i All have two suckers, an aq? anterior and ventral. 96 Se fe Mm Swe ACANTHOCEPHALA, = | = Slender worms, complete SENG ea aaa a3 digestive canal, are found Fac . ot : peyale Vids oe : = Hae in all, tissues’ ‘of domestic (0! (Y CH SREat-& 5 eae animals except bone. ASCARIDAE, 2 ap Large firm body, resemble bead ae & earth worms, mouth is es ere © surrounded by three lips. e 3 >, Usually found in small in- mS, testine, aS ao Da re 5 OXYURIDAE, Foy Cylindroid body, tail 2 = ay pointed, mouth nude, ln stomach large. EO pei a & © mi SD NEMATHELMINTHES, Round worms, nonseg- STRONGYLIDAE, mented, sexes separate. Body cylindroid, mouth either nude, armed or papillated, oseophagus large. NWHMATODA, Slender worms, complete | TRICHOTRACHELIDAB, digestive canal, are found} Body slender in anterior in all tissues of domestic] portion, eniarged poster- animals except bone. iorly for containing intes- tine, mouth nude, anus terminal, all live in intes- tine. FILARIDAE, Long thread like body, mouth or triangular ,oeso- phagus small. GNATHOSTOMIDAE, Head distinct, oviparous. ‘SPECIES HOST jaginatta Man fyst; Cysticercus cellulosae, of pig.) ‘solium Man yst; Cysticercus bovis, of ox.) “erfoliata Horse ‘aamiliana Horse “licata Horse ,enticulata Ox ‘xpansa Ox and sheep mbriata Sheep i) anata Dog Yysticercus tenuicollis of rumin ants.) ‘penurus ‘chinococcus Slcumerina rst; phalus latus Chepaticum (lanceolatum (Americanum Hma cervi “mus Westermanii MAynehus gigas egalocephalus ovis vis 4Ailla ‘marginata imystax ' deurvula (mastigodes { us Arnfeldi s micrurus us pulmonaris s filaria s rufescens paradoxus s Osteragi s contortus fjus filicollis s gigas s vasorum ama equinum ma tetracanthum ist hypostomum s trachealis firus dentatus ‘a trigonocephala la cernua ‘a radiatus jphalus affinis Sphalus crenatus jphalus depressiusculus ) spiralis papillosa tervina immitis ra megastoma fa microstoma a reticulata ke scutata ira sanguinolenta tomum cheiracanthus | : | ) st; (1) Cryptocystis trichodectis of (2) Cryptocystis pulecides of Dog, wolf and fox yst: Coenurus cerebralis in spinal cord and brain of sheep.) Dog and wolf "st; Echinococcus polymorphous, of herbivora and omnivora.) os Trichodectes latus.) Pulex serraticeps.) PART IN¥FESTED Intestine Intestine Intestine Intestine Intestine Intestine Intestine Duodenum and gall duct Intestine Small intestine Small intestine Small intestine Man, dog, cat Intestine Herbivora and omnivora Gall ducts vcore ox, goat, pig, ass,Gall ducts oF =¥ Sheep and ox Liver Ruminants Rumen Man, dog, pig and cat Lungs Pig Solipeds Ox Sheep Pig Dog Cat Horse Horse Solipeds Bovines goat, camel, deer goat and deer goat and goat ox, dog and man Dog Horse, ox, dog and man Solipeds Sheep and goat Birds and chickens Pig Dog and fox Sheep and goat Bovines Ox, sheep and goat Pig Dog Pig Horse Ox and deer Dog Horse Horse Horse Ox, sheep and goat Dog Pig, dog and cat Small intestine Small Intestine Intestine Intestine Intestine Intestine Intestine Posterior bowel Posterior bowel and lungs and lungs Bronchi Bronchi Bronchi Bronchi Bronchi Bronchi Abomasum Abomasum and duodenum Small intestine and abomasum Kidneys and arinary organs Heart Intestine Large intestine Large intestine Trachea 3 Region of kidney and liver Small intestine Small intestine Small intestine and lungs Caecum Large Caecum Muscles intestine Peritoneal and plural cavities Peritoneum Right heart and pulmonary arter- ies Right stomach Stomach Flexor tendons asd cervical liga~ ments Oesophageal wall Tumors of stomach, gullet aorta and Gastric mucosa a amen it pate eu i { Crean Tidy ‘ i i Ln pei vat Dey Mi vee fr i i " 5 Mi i ey GENERAL CONSIDERATION: OF DISEASE. wy, : my | ) Uy | Fiz. 36.—Taenia Solium. a. b. Adult worm. ec. Head of same enlarged. Fig. 37b. Fig. 37.—Strougylus Micrurus, after Railliet. a. Male and female. b. Caudal extremity of male. 6S VETERINARY PATHOLOGY. aX f ene Ol ne 29 B A f Fig. 38.—-Strongylus Paradoxus, after Railliet. a. Adult male and female. b. Caudal extremity of female. ce. Caudal extremity of male. J Sage \ ~ i UAL " ~/ | y i] Hi iil Mi | li I | ih Ww HAMA | | THT} | y Rie. 39a. andiiib: a. Adult male. ; b. Adult female. ec. Cephalic extremity enlarged. Fig. 39. Filaria Papillosa, after Neuman. GENERAL CONSIDERATION OF DISEASE. 69 ToS * | q ef ede Be one es ~e 1495 ee ae de = Uieese Pin, Serer BAbESES iN ha Soe iii | Beets 2 y, = = tt Ui i il asl Fig. 40.—Oxyuris Curvula, after Niles. a. Adult worm. >. Caudal. b. Cephalic extremity. sicollis inhabits the liver of the rat during its cystic stage and the intestine of the cat during the adult stage. Helminthes produce injury to their host by consuming food, by sucking blood and by liberating injurious chemic substances. Arthropoda. This branch includes many parasitic representatives, as flies and mosquitoes (diptera), fleas (siphonaptera) lice (hemip- tera), itch mites and ticks (acarina). The entire order, siphon- aptera and hemiptera, most of the order acarina, and many rep- resentatives of the order diptera are parasitic. Of the parasitic arthropoda some are temporary and some are permanent para- sites, and with one or two exceptions they are all external para- sites. The structural peculiarities that differentiate arthropoda from 70 VETERINARY PATHOLOGY. Ky i) ay i) Fig. 42.—Selerostoma Hypostomum, after Railliet. a. Cephalic extremity enlarged. b. Adult female. ec Adult male, ) es Sg ie fl i f : Fis. 41—Syngamus Trachealis, after Railliet. a Adult worm natural size. b. Male attached to female enlarged. Fig. 43.—Trichocephalus Depressiusculus c. Female enlarged. of a Dog, after Railliet. the other branches of the animal kingdom are their jointed ap- pendages, segmented body, and bilateral symmetry. The parasitic arthropoda obtain their food from their hosts. Some of them consume epidermal scales and hair, e. g, the 5° ’ eae in ee BY iar ‘ ng bul * : \ to - ay wt MA ee ny Re if a ei aco a y WOT yo Rade re, 5 SMA 9 8 i wah at. F mae are ata ae ABST Maes ; ¢ i Se ow ri a Shee ap PR es ce ey eR | 2 Sg eae Cotte A ate ra *- ae S ek area Te siiiaciaty cae teehee BRANCH INSERT V. ARTHROPODA Invertebrates with jointed appendages arranged in pairs. CLASS INSECTA (HEXAPODA), Air breathers, when adult have three pairs of. legs, and distinct head, thorax and abdomen. ARACHNIDA Air breathers with caphal- othorax and abdomen, have when adult four pairs of legs. Those here included are oviparous. ORDER DIPTERA Have two wings, two hal- teres, sucking mouth parts, and complete metamor- phosis, includes files and mosquitoes, HEMIPTERA Wings often absent, when present one pair thick and one pair thin., Sucking mouth parts, incomplete metamorphosis, and include the blood sucking lice. MALLOPHAGA Wingles lice with sucking mouth parts, and incom- plete metamorphosis, SIPHONAPTERA Wingless fleas with suck- ing mouth parts, and com- plete metamorphosis. ACARINA Usually short thick, non- articulated bodies, possess eamerostoma, larva usual- ly hexapodal, sexes sepa- rate. LINGUATULIDA. Internal parasite, elongat- ed, vermiform, annulated FAMILY MUSCIDAE Have soft probosis adapt- ed for suction, styJet of an- tennae plumose to the end. SS ee OELID Tie tN TABANIDAE Broad and slightly flat- tened body, large head, muscular wings, larva car nivarous, are oviparous. STOMOXIDAE losely resembles the mus- cidae. See ESSE SSS peered SIMULIIDAE d Thick body, bulging tho-]*~ rax, segs strong. | HIPPOBOSCIDAE | Flat body, head notched} 4% bri into thorax, legs strong, pupiparous, OESTRIADAE Body usually hairy, large wings, proboscis very small, oviparous. CULICIDAE Have tong slendor abdo- men, wings fringed with hairs, antennae plumose in males, oviparous. PEDICULIDAE Blood suckers, proboscis formed of upper and lower lips and armed with small spines, contains protrusile tube or sucker, oviparous. RISCINIDAE Not blood suckers, have long masticatory apparatus with which they eat epi- dermic wyroductions, ovi- parous. PULCIDAE Very agile, brown oval bodies, compressed latter- ly, biting mouth parts in larval stage. TQ b> OV. sb rt red et teed beet I IXODIDAE Large globular blood-suck- ers, oviparous, have undi- vided hypostome. GAMASIDAE Rostrum arranged for] | pricking or sucking, have] I no eyes. TROMBIDIIDAE | Soft, hairy, bright colored, rostrom a conical sucker. SARCOPTIDAE “ Smallest of the acarina, body soft, white or red- dish, eyes absent, ovipar- ous or ovoviviparous. TOD OT Te ek tent et TOTO TOTOTO bet DEMODECIDAE Very small, vermiform, hairless, cephalothorax and ee abdomen distinct, legs short, oviparous. LINGUATULIDAE Body segmented, com- pressed dorso-ventrally, crenelated. eee EE | EE eee SE 0 SE = aS a el IS SPECIES . domestica . vomitoria »bhaga carnaria xys calcitrans tobia serrata somyia macellaria us atratus us lineola i 1a morsitans um pecuarum f agus ovinus osca equina Pphilus equi hilus hemorrhoidalis rma lineata ovis equinus ‘pipiens bles punctipennis fla fasciata macrocephalus eurystermnus vituli piliferus s irritans stenopsis ectes pilosus ectes scalaris ectes spaerocephalus estes latus erraticeps : ritans errat f Ee annulatus us Australis ma Americanum entor electus ddoros Megnini ricinus e yssus gallinae ium holosericeum rritans — oe as scabei-var, equi. S scabei var. ovis. S scabei var. suis. scabei var. canis. 3s mutans S communis var. equi. €s scabei varfl bovis. es scabei var. equi. les scabei var, ovis. communis var. bovis. communis var. ovis. ses auricularum var. cani. es aureicularis var. felis. \& follicurlorum var. equi, x folliculorum var. bovis. * folliculorum var. cani., HOST Not generally parasitic Animals Animals Animals Animals Animals Animals Animals BPs ate Animals Animals Sheep Horse Horse Horse Ox Horse Sheep Animals Animals Animals Sporting dogs . ‘Horse, ox, sheep and dog Sporting dogs Fowls Fowls Animals ‘Man and animals eet PART INFESTED Wounds Wounds Skin Skin Skin Skin Skin f Skin around perinaeum M, M. of stomach M. M. of stomach and intestine Dorsal cutis and subcutis Sinuses of head Skin Skin Skin Skin Nasal cavities in ’ \ ay ‘ ti i » Ae ‘ ; j \ : j a } iv f \ , COMI OOS hth era Ria snk Win n he Pe edit, YS ij { k 4 - : \ \ i SFM be Z: A ¥) atte ) Ot Ny wake) | ER AC eatin ; yy pe iarhi es j sey Ta ATT ' Ab , ' un Ay i rf PARA Tea Cue) oe Jy al Voki) ’ GENERAL CONSIDERATION OF DISEASE. FA fp S ASS . ~— SS SN Fiz 44.— Melonhagus Ovinus, after Niles. a. Dorsal view of adult, d. Terminal segment of leg. b. Ventral view of adult. e. Shell of pupa. ec. Mouth parts enlarged. if tipas horse louse (Trichodectes Pilosus) and feathers, e. g., the chicken louse (Menopon Pallidum) others abstract blood, e. g., the hog louse (Hématopinus Suis), Itch mite (Sarcoptes scabe1 variety canis), and still others may consume tissue cells other than blood cells as epithelium. Reproduction of arthropoda is about the same as it is in helminthes. Disease resulting from infestation of arthropoda is due primarily to irritation induced mechanically or by chemic pro- ducts of the parasites, secondarily to loss of blood. He a. a7 (@ feb ere fi * SATAN (ae : SN ‘sil. a i =z “asi (iii Cc Bis, 45— Part - Gastrephilus Eoui, after Niles. Adult female. Adult female. Young larvae. Full grown larvae. Eggs cemented to hair. Egg shell showing lifting of operculum. Adult male, Terminal segments of male. Terminal segments of female. Vig. 45.—Fart II. Oecestrus Ovis. Adult female. ec. Dorsal view of larva. : b. Adult male, after Rily. d. Ventral view of larva, after Rily and Niles. OF DISEASE. CONSIDERATION GENERAL tL, i at Ee “Br rt? ya - » Sine 2 ' " U U x] get EB Be ey WA Kal iat {iy ai CW) UY EN Ge ATEN nO Larva. c. Male. Fig 47.—Culex Pungens, after Howard. Db. Female. a. 74 VETERINARY PATHCLOGY. NG S2emeere SSS Se Scenes lene ss Sizsresess 2 = == rr) os — = 5 = a cs os. - - = Cr —_—— === rie ee eee a 5 S35te toe : 48.—Asearis Mystax, after Niles. a. Cephalic extremity. dad. Caudal. Fig. Adult male. Adult female. cae Extension of Disease.—By extension of disease is meant the invasion and affection of adjacent structures and even remote tissues of the body. Some diseases are necessarily local, i. e., the cause is not capable of being transferred to adjacent or re- mote structures, e. g., ocular filariosis. Other diseases are in their earlier stages local, but later the cause may be transferred to some other part and produce secondary diseased foci or Fig. 49.—Distoma Hepaticum. Intestines. Oral sucker. Ventral sucker. Uterus. ao op metastases, e. g., tuberculosis. The extension of disease may be produced as follows: First, by the cause of tha disease passing along the natural channels and establishing secondary diseased foci, thus, Bray reports that calves become affected with necrotic gastritis and GENERAL CONSIDERATION OF DISEASE. aS enteritis when allowed to swallow the necrotic tissue during an attack of necrotic stomatitis. Second, by the spread of the cause into adjacent tissues, e. g Extension in like tissue, as in muscular tissue, is continuity as psorospermosis, while extension from one tissue to another of a different type, as from muscular to connective tissues, is con- tiguity as in actinomycosis. Third, by the lymph and lymphatic nodes, e. o. tuberculosis. Fig. 50.—Echinorynechus Gigas, after Niles. a. Cephalic extremity showing hooks. b. Worm with portion nf mucous membrane of intestine attached. Fourth, by the blood stream in which case the mestastases will be in the lungs, liver or kidney,—e. g. anthrax. Iifth,by passing along the nerve fibers as in rabies. Termination of Disease.—Termination is the ending or out- come of the condition or existing disease. Disease terminates as follows :— Recovery.—Disease terminates in recovery when the body tissues are effectually repaired and all structures have assumed their normal function. Diseases resulting from irritating or non-nutritious foods are corrected by expulsion or neutraliza- tion of the causative agent either by vomition, purgation or chemical union and by repair of the injured tissues, after which normal functioning continues. Tissue afflicted with mechanical 76 VETERINARY PATHOLOGY. injuries as wounds, recover when the destroyed portions have been replaced and the normal function has been resumed. Dis- locations terminate in recovery when the dislocations have been reduced and the parts assume their normal function. a & @) ~~ — 6.8 nO v =e rae a U4 a O r+ 45 — 3} ““N DN (ao) 2) — cB) S| a) Suppuration or liquefaction is the resulting change. lymph. 6 ars aaa raw) 3 nye ow X250 red cells and leucocytes. in, hrombus, showing the fibr 83.—Red T Fig. than 10US y be accomplished The outcome ducts ma = ative pro likely to be much more ser either by the blood stream or by the leucocytes. The removal of the degener of infective softening is ~ If the thrombus does not undergo degen- lly becomes or Very soon after a thrombus is formed the fibrin con- ing occurs. 10, sat eration 1t usua fied. le soften Organ simp when 3 zed, but it may become calci- gani . ~ f the 1ze€ O t does in the blood clot, thus reducing the s thrombus, and if it was a complete or occluding thrombus the reduction may be sufficient to allow the circulat tracts-as 4 on to be re- . « it CIRCULAR DISTURBANCES. 127 established. The endothelium and the vasa vasorum of the contacting vessel proliferate and extend into the thrombus soon after the fibrin contracts, the vasa vasorum usually being of sufficient extent to produce complete vascularization of the thrombus. The proliferated endothelial cells become fibrous connective tissue cells and produce fibrous connective tissue which later contracts and thus reduces the size of the throm- bus. The dead and disintegrated tissue in the thrombus is car- tied away by leucocytes, thus reducing the size of the throm: bus still more. The contraction of the fibers usually continues until there is a mere cicatrix where there once existed an oc- cluding thrombus. (This is a favorable termination.) The or- ganization may result in the formation of an excessive amount of fibrous tissue which may practically occlude the vessel, and the vessel itself become a fibrous cord. 4. Calcification of the thrembi in the human is quite com- mon, the calcified thrombi being called phleboliths and arteri- oliths, according to the vessel in which they occur. The same changes occur in thrombi of ‘lower animals. Effects -_The effects of thrombi depend upon the vessel imewmich it Oocciuis and the nature of the thrombus. If it eccurs in a terminal vessel the outcome will be different than if it occurs in a vessel having collateral branches. If the thrombus is occluding the outcome will be different than if it is parietal. A thrombus that is brittle or is easily detached will produce different results than one that is not easily broken and is adherent to the vessel wall. The general condition of the vessel wall is also a determining factor on the subsequent changes of a thrombus. The principle results are as follows: 1. Obstructed circulation, which may be either partial or complete, depending upon the nature of the thrombus and of the vessel and the rapidity with which collateral circulation is established. Continued partial obstruction in veins favors hyperemia with its consequent oedema. Degeneration in ar- teries favors anemia and atrophy. Complete obstruction re- sults in necrosis with or without formation of infarcts. 2. Production of embolism by fragments becoming de- tached and occluding smaller vessels. 3. Formation of new blood vessels. 128 VETERINARY PATHOLOGY. EMBOLISM. DEFINITION. SOURGE OF -EVBOET. Thrombic fragments. Cells, fat, leukemia, tumor, etc. Parasités. Ar, LOCATION, where vessels branch. EIEIO IES. Embolism is a condtion resulting from an obstruction of a blood vessel by a foreign body (embolus) that is suspended in the blood and is too large to pass through the vessel. An embo- lus is a foreign body in the blood such as air, sarcoma cells. Cre: Source of Emboli.— Thrombic fragments.— Fragments from disintegrating thrombi float in the blood until they arrive at vessels that are too small to allow them to pass and there becom- ing impacted produce embolism. An entire thrombus may also become detached and float in the blood stream as an embolus which, when impacted, would produce embolism. A thrombus in an artery usually extends back to, and ‘sometimes beyond the first branch, the projection frequently becoming loosened and carried into the branch as an embolus. Abnormal cells—Leukemia is frequently accompanied by leukemic infarcts, a result of plugging of vessels by the enlarged leucocytes or leukemic cells. Metastatic sarcomata are the result of sarcomatous cells floating in the blood and becoming impacted in small vessels where they multiply, thus producing secondary tumors. Fat cells are a frequent cause of embolism especially in the human, after a fracture of a long bone in which the blood vessels are lacerated and fat cells from the marrow enter the blood stream. ; Parasites —Embolism may be the result of animal parasites. The Strongylus armatus, in the larval stage is found in the blood vessels of the horse and frequently produces aneurisms of the anterior mesenteric artery. Here a thrombus forms, the fragments of which passing on as emboli thus produce obstruc- tions in the intestinal vessels which may result in thrombo- embolic colic. Vegetable microorganisms may cause embolism, thus bac- teria in the blood are emboli. Pyemia result from metastases of pyogenic organisms and pus. Apoplectic anthrax in sheep may be the result of emboli of Bacillus anthracis plugging the cerebral capillaries thus producing embolism. Air may act as an embolus and obstruct small vessels, or it CIRCULAR DISTURBANCES. 129 may become mixed with the blood and become entangled in the cardiac valves, thus interfering with heart action (a horse was destroyed in four minutes by injecting air into the jugular vein). Location.—Embolism occurs most frequently in arteries and in the portal circulatory system. Venous emboli as a rule pass to the right side of the heart and into the pulmonary arteries where they lodge. Fragments of thrombi from intestinal veins pass into the portal system and are lodged in the hepatic capil- laries thus producing embolism. Thrombic fragments from Fig. 84.—Embolism. The embolus lodged at the point of division of an artery. the pulmonary veins, bicuspid valve and semi-lunar valves pass into the arota and through its various branches and terminals as emboli and finally they occlude the containing vessel and thus produce embolism. Paradoxical embolism is the name applied to the condition resulting from obstruction of an artery with an embolus derived from the venous system and which has passed from the right side of the heart to the left through the foramen ovale. VETERINARY PATHOLOGY. — lars) © In some rare instances it appears that an embolus travels in the direction opposite to the flow of blood and produces obstruction; this is called retrograde embolism. Effect.—The results of embolism depend upon the composi- tion of the embolus, obstructed circulation and infarction. Fig. 85.—Anemic infarcts in the spleen. a. Infarcted areas due to emboli in capillaries supplying them. Composition of the embolus—Emboli composed of cells having the power to multiply, at the point of impaction (embol- ism) become secondary foci or metastases of the primary patho- logical condition, as metastatic sarcomata, leukemic infarctions, etc. Pathogenic bacterial emboli not only obstruct circulation, but also produce metastases of that disease as in necrobacillosis, anthrax, etc. Filarial emboli and emboli composed of fatty cells produce a mechanical effect only. Air emboli in small vessels are absorbed after a time. CIRCULAR DISTURBANCES. ol Obstructed circulation—Obstructed circulation when produced by non-infective emboli will have the same effects and terminations as the non-infective obstructive thrombi. Infarction.—Infarction is the process of obstructing a vessel with an embolus. The area supplied by the obstructed vessel is called an infarct. The area of infarction is determined by the region supplied by the occluded vessel and is usually wedge-shaped. An area supplied by an artery that has been in- farcted does not become bloodless at once because some of the blood remains in the vessels of the infarcted area and some may enter the periphery of the infarct through anastamosing capillaries and venules of adjacent regions. Infarcts may be anemic or hemorrhagic. An anemic infarct is one in which there is limited anasta- moses of venules and capillaries of contiguous areas. The blood remaining in the vessels of an anemic infarct soon becomes de- colorized and the area appears pale in color. Anemic iniarcts usually undergo necrosis early because of the lack of nutrition. The type of necrosis is largely dependent upon the nature of the embolus. Infarcts produced by infectious emboli usually suppurate or putrefy and infarcts produced by non-infective em- boli may become liquified, absorbed and replaced with fibrous tissue or it may become caseated or calcified and surrounded by a fibrous capsule and persist for a long time. A hemorrhagic infarct is one in which there are anastamoses of the vessels of the infarct and the venules and capillaries bf contiguous areas through which blood passes and becomes stagnated in the affected area. Hemorrhagic infarcts may be- come decolorized, there may be inflammation established around their periphery, or the blood and the involved tissue may be dis- integrated and absorbed. Infarcts may become cystic, caseous, calcareous, absorbed and substituted with fibrous tissue, or they may become infected and there may be abscess formation or gangrene. Infarction occurs most frequently in the kidney, spleen, brain, lung and less frequently in the heart, liver, retina, etc. Typical terminal arteries are common in the kidney and spleen and hence infarction frequently occurs in these organs. In the kidney anemic infarcts are most common, hemorrhagic and anemic infarcts occur in the spleen. Cardiac infarction is not common and is usually caused by thrombosis of the coronary vessels. Cerebral anemic infarction occurs occasionally and the infarct usually undergoes simple softening, hemorrhagic cere- bral infarction is rare. 132 VETERINARY PATHOLOGY. ISCHEMIA. DEFINITION. ETI OROG VE Diminished calibre of supplying arteries. Stimulation of vaso constrictor nerves. Inhibition of vaso dilator nerves. Tonic spasms of vessel musculature. Occulsion of supplying arteries. Mechanical. Tumors. Thrombi, etc. Collateral hyperemia. APPEARANCE. Macroscopic, pale, flabby, lower temperature. Microscopic, cell degeneration, atrophy or necrosis. EFFECTS—Depend upon extent and duration and may be atrophy or NeCrOSIS. ANEMIA, as usually considered, is a condition in which there is either a deficiency in the quality or in the quantity of blood. The discussion of this theme will be found in special pathol- ogy. ISCHEMIA is a condition in which there is insufficient or total absence of blood in a part of the body. Etiology.—Ischemia may be caused by influences that dimin- ish the calitre or occlude the vessels supplying blood to a part or by collateral hyperemia. The calibre of arteries may be diminished by contraction of the vessel musculature induced by low temperature, high temperature, drugs, etc., which stimulate the vaso-constrictor nerves, or inhibit the vaso-dilator nerves or cause tonic spasms of the vascular muscle. The supplying arteries may be occluded by mechanical pressure produced by bandages, ligatures, harness, collar, thronibi, emboli, neoplasms, tissue proliferations and tissue infiltrations. Ischemia in one part may be caused by hyperemiain a related part, because the blood of the entire body is easily contained in the vessels main- tained at the normal calibre, blood pressure causing an equal distribution of it; and if the vessels of one area are increased in calibre, followed by an increased inflow of blood, the quantity of blood will be diminished in some part, thus a marked hypere- mia of the spleen is usually accompanied by ischemia of the stomach. It is possible for sufficient blood to collect in the ves- sels of the liver to drain the system to a sufficient extent that the animal would die of ischemia of the brain. Appearance.—Macroscopic.—An ischemic tissue appears blood- less and is pale, flabby and of a lower temperature than the same tissue with a normal blood supply. If incised the tis- sue appears dry and there will be limited or no hemorrhage. CIRCULAR DISTURBANCES. eS Microscopic, the blood vessels are practically empty and the tissue cells are more or less shriveled as a result of insufficient moisture. Effects—The outcome of ischemia is determined by the length of time it exists and the degree of completeness of the condition. Temporary, partial ischemia usually terminates in complete recovery. Continued partial ischemia is a frequent cause of atrophy. Complete absence of blood for a considerable time results in necrosis. HY PEREMIA. DEFINITION. ETIOLOGY. Enfeebled circulation, Mechanical interference. APPEARANCE. Macroscopic, bluish, cold clammy. Microscopic, engorged veins, degeneration. EFFECTS—Depend upon cause, duration, degree and location and may be fibrosis, oedema, thrombosis, necrosis and recovery. Hyperemia is a condition in which there is an increased quantity of blood in a part. The condition is practically local for an increased total amount of blood could not be retained in the general circulation without increasing the general blood pressure which would result in an increased production of lymph and hence diminish the volume of blood. Physiologic hyperemia is evident whenever an organ or part is active. Local patho- logic hyperemia may be passive (venous) or active (arterial). PASSIVE OR VENOUS HYPEREMIA. Passive or venous hyperemia is a condition in which there is a normal quantity of blood constantly flowing into an organ or part, but a diminished quantity flowing out. An excess ci venous blood consequently accumulates in the part. Etiology.—Passive hyperemia is caused by enfeebled circu- lation due to weak heart, biscuspid and tricuspid insufficiency or stenosis, or diseased vessels and by pressure upon the outgoing vessels by ligatures, bandages, neoplasms, dislocations, fractures, ELE. Appearance.. Macroscopic—The affected tissues are bluish in color and usually feel spongy, cold and moist when palpated. Microscopic.—A tissue affected with venous hyperemia has distended capillaries and venules, the lymph spaces are engorged with lymph and the cells are swollen and their protoplasm cloudy. 134 VETERINARY PATHOLOGY. Effects.—The outcome of venous hyperemia depends upon the cause, degree, duration and organs affected. Thus venous hyperemia resulting from infective.phlebitis is more. serious than if caused by noninfective.agencies. A venous hyperemia caused by complete obstruction of a vein is more likely to be fatal than one resulting from partial obstruction. Venous hy- peremia of short duration is usually of little consequence but, if long continued, it results in necrosis or fibrosis depending upon the degree of obstruction. Venous hyperemia of vital organs, as the brain or lungs, 1s:more likely to have aetaral termination than if some less important structure as a muscle were involved. Therapeutic Venous Hyperemia propertly produced results in (a), diminution of pain, probably because of the dilution of the irritating substances (b), destruction of bacteria, the. accumulated blood serum possessing strong bactericidal properties (c), in- creased nutrition because of the increased amount of blood. Bier’s hyperemic treatment of open joints by producing venous hyperemia illustrates this type. Pathologic Venous Hyperemia may result in fibrosis, oedema, thrombosis, necrosis, or recovery. A long continued slight ven- ous hyperemia usually results in ‘fibrosis and is noted in the liver of animals affected with a slight tricuspid insuff- ciency or stenosis. A marked venous hyperemia, but not caused by complete venous obstruction usually results in oedema, and is noted in the peritoneal cavity (ascites), in animals in which the portal circulation is partially obstructed. Venous hyperemia caused by complete obstruction results in throm- bosis and is observed in intussusception of the intestines. If other venous channels are unable to convey the blood from a part in which there is a complete venous thrombus, necrosis occurs as in strangulated herniae. Venous hyperemia of short duration, even though it is quite extensive, results in complete recovery if the cause is removed and the tissues are repaired. CIRCULAR DISTURBANCES. HOD: ACTIVE OR ARTERIAL HYPEREMIA. ETIOLOGY. Increased calibre of arteries. Stimulation of vaso-dilator nerves. Inhibition of vaso-constrictor nerves, Paralysis of vessel musculature. Collateral ischemia. Diminished pressure. APPEARANCE. Macroscopic, red, hot, swollen. Microscopic, engorged arteries and capillaries. EPFECTS. Aypertrophy, hyperplasia, inflammation, recovery. Active or arterial hyperemia is a condition in which there is an increased inflow of blood to a part or organ without an equally increased outflow. Etiology.—Arterial hyperemia is caused by an _ increase in the calibre of the supplying arteries, by collateral ischemia and by diminished external pressure. The calibre of the supply- ing artery may be increased by stimulation of the vaso-dilator nerves, by heat, chemicals, etc., by inhibition of the vaso-con- strictor nerves, and by paralysis of the muscular tunic of the ABLCTY The calibre of the surface vessels is in part the result of ex- Fig. 86.—Hyperemia, hemorrhage and oedema of intestine of a horse. a. Surface exudate. c. Area of oedema. b. Engorged vessels. G. Subsurface hemorrhage. 136 VETERINARY PATITOLOGY. ternal pressure. If the external pressure is materially dimin- ished, there will be arterial hyperemia of the cutaneous arteries as is evidenced in hyperemia produced by cupping. Collateral ischemia may cause hyperemia of the related parts for the same reason that collateral hyperemia may cause ischemia. Appearance.— MJacroscopic—An arterial hyperemic part is scarlet red in color, usually feels dense, dry and has an increased temperature. If the tissues are incised, blood escapes freely. / 0 aA @ = < NISSS tees iNees Fig. 87.—Hyperemia of Kidney, showing engorged capillaries. Microscopic-—Tissues affected with arterial hyperemia con- tain dilated arteries and capillaries, the lymph spaces are en- gorged with lymph, the tissue cells may be considerably swollen and diapedesis may be noted. Effects.—The effects of arterial hyperemia depend upon the cause, degree, and duration and organs affected. Arterial hyperemia caused by infective agencies is more serious than if caused by other means. Arterial hyperemia of a_ sthenic type is usually succeeded by inflammation and asthenic hyper- emia may terminate in recovery. CIRCULAR DISTURBANCES. 16Y: Arterial hyperemia of short duration is 1ess serious than it would be if long continued, thus, active pulmonary hyper- aemia is occasionally aborted in the horse and such animals are usually ready for service in 24 to 48 hours, but if active pul- monary hyperemia continues for 24 hours it is succeeded by inflammation (pneumonia). Arterial hyperemia varies in different organs. Affections of the more highly organized structures are usually more seri- ous. : Physiologic arterial hyperenua is a condition in which there is an increased amount of blood flowing into a tissue be- cause of increased physiologic demand, thus during gastric di- zestion an excess of blood passes to the stomach through the gastric arteries. Therapeutic arterial hyperemia, when properly produced in a diseased part, results in (a), diminished pain, (b), resorp- tion of inflammatory exudate, hemorrhagic extravasate, and cedematous transudate, (c) increased nutrition, thus by the al- ternate use of cold and hot applications an arterial hyperemia is produced and is of value in strained tendons, bruises, etc. Pathologic arterial hyperemia, may produce hypertrophy, hyperplasia and permanent arterial dilatation. Excessive de- velopment of a part (hypertrophy or hyperplasia) may result from a long continued active hyperemia as in thickening of the skin as a result of continued application of blistering agents, but arterial hyperemia is as a rule of short duration for it usually terminates in recovery or is succeeded by inflammation. CHAPTER VI. INFLAMMATION. DEFINITION. GENERAL CONSIDERATION OF STIMULI AND REACTIONS. ETIOLOGY: Non-infective. Mechanic. Thermic. Electric. Chemic. Infective. Non-sup purative. Suppurative. FACTORS CONCERNED IN INFLAMMATION, (Phenomena.) Vascular, Constriction of vessels. Dilatation of vessels. Acceleration of rate of blood flow. Retardation of rate of blood flow and leucocytic margination, Oscillation of blood in the vessels and diapedesis. Stasis. Exudation. Exudate. Composition. Physic. Chemic. Histologic. Varieties. Serous. Fibrinous. Hemorrhagic. Factors determining quality and quantity. Cause of inflammation. Condition of animal. Location of process and of tissue affected. Signiticance of the exudate. Increased amount of nutrition to the affected part.— Dilutes, counteracts, neutralizes or destroys the irritant. Circumscribes the inflammatory process. Chemotaxis. Phagocytosis. THE SIGNS OF INFLAMMATION. Redness Swelling. Increased temperature. Pain. Impaired function. EPRPRECDS UPON THB, TiSSUE INVOLVED: Degeneration. Parenchymatous. Fatty. Mucoid. Serous. Amyloid. Hyaline. Necrosis. Regeneration or proliferation. 138 INFLAM MATION. 139 THE KINDS OF INFLAMMATION. Etiology. Simple. Infective. Non-sup purative. Suppurative. Surface. Sub-surface. Exudate. Serous. Fibrinous. Hemorrhagic. Tissue. Parenchymatous. Interstitial. Time, activity and results. Acute. Chronic. Miscellaneous. Catarrhal. Purulent. Ulcerative. Vesicular. Pustular, Proliferative. Specific. TERMINATION. Resolution. Tissue proliferation. Dissolution. CONGEUS LONS: Inflammation is a name applied to a group of pathologic processes including circulatory disturbances, retrogressive and progressive tissue changes. The term inflammation is difficult to define because of the several factors entering into the process dudeoer the variation o1 each iactor, lit may be defined as the reaction of a living animal tissue to an irritant. | A stimulus is anything that produces action in a living tis- sue. An irritant is anything that produces excessive stimulation in a responsive tissue. Stimuli and irritants differ only in degree. Mild friction of the skin is a stimulus to that structure. When the friction is intensified and the cutaneous function is overstimulated the friction becomes an irritant. All living tis- sues respond to stimuli and likewise to irritants. The response or reaction of a living tissue to an irritant, i. e. excessive tissue stimulation, accompanied by circulatory disturbances and by destructive or proliferative tissue changes, constitutes the pro- cess known as inflammation. The general phenomena of in- flammation will be better understood if some preliminary con- siderations of the reaction to stimuli are first discussed. General Consideration of Stimuli and Reactions.— It is a 146 VETERINARY PATHOLOGY. well known fact that all living things (organisms) respond to stimuli, A stimulus is that which excites or produces a tem- porary increased vital action, or it is any substance or agent capable of producing activity in a living tissue or producing an impression upon a sensory organ. We exqeie Or degree of response to a stimulus is directly proportional to the organi- zation and complexity of the tissue and especially those tissues which are: (a) capable of being stimulated; (b) capable of trans- mitting an impulse; and (c) capable of interpreting the impres- sions produced by the impulse. ‘The following discussion of response to stimuli is confined to animal tissues because inflam- mation affects animals only. Protozoa, although of the simpliest structure, consisting of a single cell, respond to the various stimuli. They respond to light. Thus, if a portion of a cover glass preparation of living amoebae be exposed to intense light, the amoebae in the lighted area will, in a short time, become restless and begin to move about and will finally move away from the area of light. By a specially arranged hot stage, so ‘that there are areas of different temperature, amoebae will be observed to ac- cumulate in the areas of favorable temperature and emigrate from those of unfavorable temperature. That is, they respond tO Of are responsive to thermic stimuli Ina, Similan amoebae respond to various chemical stimuli. If a drop of acid be so placed that it will slowly diffuse into the water or fluid in which the amoebae are being studied, they will move away from the acid. If an amoeba be divided by mechanical means so that one segment contains the entire nucleus and the other segment has no nucleus, it will be observed that the nucleated segment responds to the stimulus by regenerating tissus to re- place the nonnucleated segment which was removed. On the other hand, the nonnucleated segment of the amoeba may survive the shock of separation, but soon begins to degenerate and finally dies. Thus is shown the response of living struc- ture to photic, thermic, chemic and mechanic stimuli. If more complex animals be considered there will be ob- served a similar response to stimuli. Thus, the hydra responds to the various kinds of stimuli and has a remarkable power of regeneration of tissues. Vermes are very responsive to stimuli and all observers have noticed that when an angle-worm is cut in two both ends will crawl away. Vermes are among the lowest forms of animals that possess cells corresponding to white corpusctes or leucocytes of higher animals. These cells are observed to emigrate to the point of injury or to surround INFLAMMATION. 14] the foreign bodies or substances that are experimentally in- troduced into the bodies of vermes. This reaction is analogous to the reaction of the mammalian leucocytes. The discussion so far, has been with reference to animals that possess no blood or vascular systems, or at least only in a rudimentary form. Vertebrates are more highly organized and are consequently more responsive to stimuli than invertebrates. Mammalia are the most complex in structure of all animals and they are like- wise most responsive to stimul1. The mammalian cornea is a nonvascular structure being composed of fused layers of fibres arranged parallel to the sur- face. Between the layers of fibres connective tissue cells and lymph spaces are found but no nerves. The cornea is covered externally by the conjunctiva. If the cornea be irritated there will be a reaction, the extent of which depends upon the in- tensity of the irritant. A puncture of the cornea with a sterile needle produces the following reaction or tissue changes; (a) within a few hours after the injury the affected area appears swollen and the cells that were punctured begin to degenerate while the uninjured cells immediately surrounding the needle puncture become tumefied and vacuolated; (b) from twenty to thirty hours after the puncture, wandering cells appear in and around the injured area, and as the cornea is nonvascular they must be migratory connective tissue cells; (c) by the third or fourth day the punctured cells will have been removed, by solution or otherwise, from the affected areas. Those cells sur- rounding the injury will have divided by mitosis, the newly formed cells replacing those that were destroyed and _ the wandering cells will have migrated from the injured focus. (The destroyed epithelial cells of the conjunctiva are replaced by those next to the injury). If sterile iron dust, or other insoluble granular material is aseptically introduced into the cornea, a reaction, as described above, will take place, and, in addition, the migratory connec- tive tissue cells will ingest or incorporate the introduced par- ticles and carry them out of the injured focus. When the cornea is injured more severely, as by the ap- plication of a caustic solution (irritant), in addition to the above reaction, a migration of leucocytes from the marginal corneal vessels usually occurs within thirty hours. Some of the invading leucocytes become destroyed and some of them may multiply, but they usually all disappear from the point of injury within from forty to fifty hours. The length of time 142 VETERINARY PATHOLOGY. necessary for repair of such an injury is variable according to the extent of the injury and the readiness of response of the tissue. In vascular tissue the following reaction occurs. An asep- tic cutaneous incision unites almost immediately if the wound margins are placed and maintained in exact apposition. The tumefaction is slight because of the limited extravasate from the severed vessels. There is a slight exudate which coagu- lates and cements the margins or lips of the wound. In a microscopic section through such a wound some cells are found destroyed and others injured. The cells bordering such an in- jury sometimes increase in size to such an extent that they project into the cement between the two incised surfaces. Wan- dering cells and leucocytes in varying numbers appear through- out the entire injured area. The cement (exudate) and the de- generated and necrotic marginal cells are later absorbed. The cells bordering the incision multiply by direct cell division, the newly formed cells replacing those destroyed. New capillaries extend through the newly formed tissue. Finally the leucocytes emigrate and disappear from the injured area. In a more extensive injury, such as a gaping wound that later becomes infected, a more complex reaction is observed. The following changes take place during the first twenty-four hours after an injury of this nature is inflicted. There is hem- orrhage, the extent of which depends upon the size of the ves- sels severed and the gaping of the wound. The extravasated blood accumulates in the wound and also infiltrates the ad- jacent tissues. The injury (irritation) causes hyperemia, es- pecially of the arterioles, resulting in engorgement of the capil- laries. From the engorged and dilated capillaries there is marked exudation. The exudate escapes upon the wound sur- face and infiltrates the tissues of the injured area. The ac- cumulation of the hemorrhagic extravasate and the inflam- matory exudate plus the increased size of the vessels (hyper- emia) tumefies or swells the injured area. There is an ac- cumulation of mononuclear leucocytes or wandering connec- tive tissue cells in the injured tissue and an immigration of polymorphonuclear leucocytes. Many cells are destroyed out- right by the injury or by the action of infectious bacteria. Those cells bordering the destroyed cells are injured and be- come tumefied and may later undergo necrosis. The cells, es- pecially the connective tissue cells located peripherally to the injured cells, become enlarged and multiply by indirect cell di- vision. The injured cells are repaired and the newly formed INFLAMMATION. 143 cells are massed together and project outward thus replacing the destroyed cells. The discharge from such a wound after twenty hours con- sists of serum, shreds and fragments of necrotic tissue, dead cells (especially leucocytes) and a variety of microorganisms. The reaction in the above case consists of circulatory dis- turbances, degeneration, necrosis, and regeneration of tissues. Etiology—The exciting causes of inflammation may act from within the body, hematogenous or lymphogenous, or from without, i. e., extraneous as burning, etc. They may produce their action by direct contact upon surfaces of the body as from a blistering agent externally applied, or, by contact internaiiy, as from arsenic. They may produce their effect while being ex- creted, as in the production of nephritis by cantharides or tur- pentine. Some harmless agents may become irritants as the result of chemic change produced by some of the body juices or fluids (lysins). The causes of inflammation may be divided into two gen- eral classes, non-infectious and infectious. NON-INFEcTIOUS.—The non-infectious causative factors are not as active in producing inflammatory disturbances as the in- fectious agencies, but they are of some importance and should not be overlooked. Some have positively stated that “There is no inflammation without infection.’ Reasonable interpreta- tions of clinical and experimental observations supply suffi- cient evidence that there is inflammation without infection. The following are the principal non-infectious causes of in- flammation. | Mechanic or traumatic—Surgical wounds which heal _ by primary union are undisputed examples of. mechanically pro- duced inflammation. The reaction taking place in an aseptic incision consists in cell-destruction, slight circulatory disturb- ances, leucocytic immigration and regeneration of tissue. Such a reaction is typical of inflammation and the affected area is devoid of any infection. A sterile needle introduced into a tissue, the surface of which is aseptic, produces a reaction identical to the reaction observed in primary union of tissue. Mechanic or traumatic causes of inflammation may produce, or cause to be produced in the injured cells, chemic substances that are responsible for the reaction. Thermic—A temporary exposure to a high or low tem- perature is sufficiently irritating to produce a marked inflam- mation. Let those doubting this statement take the chimney from a lighted lamp and hold it in the hand for one minute and 144 VETERINARY PATHOLOGY. they will acknowledge that heat produces all the symptomatic evidences of inflammation and there is no infection. The prin- ciple object in the use of the thermo-cautery is to produce or estabiish inflammation. A thermo-cautery, or any severe burn, produces tissue necrosis, as well as the destruction of bacteria in that area (sterilization), and an inflammatory zone is im- mediately established around the necrotic tissue which is sterile and may remain free from infection. A short exposure to an extremely low temperature produces an inflammation. Ii the exposure is of long duration necrosis is likely to occur. “Chilblains” is an inflammation resulting from temporary exposure to a low temperature. Sloughing following freezing of calves’ ears, pigs’ tails and cocks’ combs are familiar examiples of necrosis resulting from long exposure to extremely low temperature. An inflammatory zone is es- tablished around necrotic areas produced by freezing similar to the inflammatory zone observed around necrotic areas pro- duced by burning. Thermic variations may produce chemic substances in injured tissues which are sufficiently irritating to establish inflammation. : Electric—It 1s common knowledge that electricity causes inflammation. Animals injured by hghtning usually show eyvi- dences of cutaneous inflammation. In cities animals as well as men frequently contact wires charged: with powerful electric currents and receive local injuries that are usually inflammatory in their nature. Chemic—There are matty chemicals that are irritants. A number of them are used as therapeutic agents when irritants are indicated. Mineral acids, caustic alkalies, mercury salts and arsenic are some examples of chemic agents that produce inflammation when applied in dilute solutions, and necrosis when applied in more concentrated form. A 10 per cent solu- tion of nitric acid applied to the skin for a very short time pro- duces inflammation. Inflammatory symptoms following the nitric acid application appear immediately; and, as the acid is a disinfectant, the inflammation cannot be the result of infec- tion. In animals poisoned by any of the mineral poisons there may always be observed an inflammation in the mucosa of the alimentary tract more extensive than could have been produced by infection in the limited time of action. Many reptiles, bees, wasps, and ants introduce chemic sub- stances into animal tissues that are extremely injurious and es- tablish inflammation of very rapid evolution. INFECTIOUS OR VITAL AGENCIES are the most important etiologic INFLAMMATION. 145 factors in the production of inflammation because they are the most frequent offenders. Infection usuaHy produce inflam- matory disturbances through the action of chemic substances elaborated by the infecting micro-organisms, as metabolic pro- ducts. The infection may be local and produce localized in- flammation as in a superficial abscess and in coccidiosis. The elaborated chemic substances may be absorbed from the local- ized infection and produce inflammation elsewhere in the body. Infection may be general and produce conditions similar to in- flammation in practically all the tissues of the body as in gen- eralized anthrax. However, the term inflammation is usually confined to local disturbances. The extent of irritation pro- duced by any infecting organism is dependent upon the virul- ency of the given organism and the resistance of the infected amimal. Thus, infection with Streptococcus pyogenes equi may produce pyemia in one animal and only a local abscess in an- other. Again, some bacteria, as the anthrax bacilli, may pro- duce septicaemia in one animal and localized inflammation in another. A concise etiological classification of inflammation produced by living organisms is impossible because of variations both in the virulency of the organisms and in the resistance of the tissues. Animal parasites are of considerable consequence in the production of inflammation. They may produce inflam- mation by mechanical interference, as the Echinorychus vigas which inserts its barbed proboscis into the intestinal mucosa thus injuring the tissue as well as opening an avenue for the entrance of various bacteria. The Trichina spiralis by perfor- ating the intestinal wall and by burrowing in the muscular tissue produces sufficient irritation to establish inflammation, the results of which are evidenced on microscopic examina- tion of a lesion. It has been suggested that the etiological factor of rabies is an animal parasite; the round-celled infil- tration of the ganglionic nerve cells and perivascular spaces having marked characteristics of the lesions of inflammation. Psorospermosis, a condition resulting from psorospermic in- festation, is inflammatory in its character. In a general way infective inflammations may be discussed as non-suppurative and suppurative. The non-suppurative infective inflammations are those in- flammatory disturbances in which there is no purulent fluid or pus produced. As examples the following may be cited—septic infection succeeding nail pricks in horses feet; blackleg in calves caused by the Bacillus anthracis symptomaticus, (Sar- 146 VETERINARY PATHOLOGY. cophysematous bovis); malignant oedema caused by the Bacil- lus of malignant oedema. Suppurative infective inflammation is characterized by the formation of pus. The causative bacterial agents of suppura- tion are designated as pyogenic bacteria or pyobacteria. The following are the most important bacteria of this class: Staphylococcus pyogenes aureus. Staphvlococcus pyogenes albus. Staphylococcus pyogenes citreus. Strepto-coccus pyogenes Baccillus pyocyaneus. Factors Concerned in Inflammation.—The animal body is an intricate mechanism composed of different tissues in various combinations. The phenomena of inflammation are the changes that take place in the tissues plus the conditions resulting from those tissue changes, thus including all the changes taking place in the inflammatory focus. The following are the most impor- atts VASCULAR DISTURBANCES.—These are universally present in animals possessing a vascular system, but inflammation, or a condition analagous to it, occurs in the tissues of animals that have no vascular system, and in nonvascular tissues of animals that have a vascular system. Hence vascular changes are not essential in the process. The vascular changes are dependent upon nervous influence, because the calibre of blood vessels, especially arteries, is controlled by vasomotor nerves, 1. e., vaso- dilators and yaso-constrictors; stimulation of the former produc- ing dilatation, of the latter constriction of the vessel. Inflam- matory areas become necrotic when dilatation of the supplying arteries and arterioles is inhibited. In experiments in which dilatation of the arterioles takes place the inflammatory pro- cess 1s limited and usually terminates in recovery in a short time. Necrosis usually succeeds inflammation in tissues in which communications of the vasomotor nerves have been de- stroyed. For example, the cubital nerve in the horse probably contains the vasomotor fibres that innervate the vessels of the foot and the median nerve the sensitive fibres that innervate the pedal structures. Median neurectomy is not succeeded by vascular disturbances, but cubital neurectomy is frequently succeeded by vascular disturbances and excessive exudation that terminates in necrosis followed by sloughing of the hoof. The following vascular changes occur in an inflammatory focus and in the order designated: Decreased calibre of the supplying arteries and arterioles. INFLAMMATION. WAZ Temporary contraction of arteries is the first result of the ap- plication of an irritant. . The cause of the constriction of the arteries is a spasmodic contraction of the musculature of the vessels. This is succeeded by a marked arterial dilatation. Dilatation of the arteries and arterioles. The response to stimuli on the arteries is rapid and always active, in veins slow and usually passive, in capillaries either rapid or slow but al- ways passive. Dilatation of vessels in an inflamed area is caused by stimulation of the vaso-dilators or inhibition of the Fig. 88.—Blood vessel, showing Corpuseles occupying central portion of stream, typical of normal circulation. vaso-constrictors. An increase in the calibre of the arteries results in an increased amount of blood flowing through them and into the capillaries. The increased amount of blood in the capillaries mechanically increases their calibre and also in- creases the amount of blood which enters the related veins and results in a dilatation of them. By increasing the lumen of a vessel the resistance to the flowing contents is correspondingly diminished and this results in a temporary acceleration of the rate of blood flow. Acceleration of the rate of flow of the blood. The cor- puscles occupy the axial, or central part of the stream as in the normal circulating blood. The arterial dilatation plus the acceleration of the blood flow constitute the essential factors in active hyperemia. 148 VETERINARY PATHOLOGY. Retardation of the rate of flow—A long continued dilata-> tion of a vessel results in injury especially to the endothelial lining. The injured endothelial cells become swollen, rough- ened and sticky. The leucocytes begin to appear in the peri- pheral portion of the stream, probably because of the libera- tion of some chemic substance by the endothelium that exerts a partial chemotactic action upon the leucocytes. They roll, a) ce) oO Fig. 89.—Dilated blood vessel showing corpuscles spread throughout the entire lumen typical of first stages of hyperemia. tumble, and creep along over the swollen endothelial cells and finally adhere to their roughened surfaces. The continued at- tachment of leucocytes to the endothelium diminishes the cali- bre of the vessel and increases the resistance thus retarding the rate of blood flow. Oscillation—The resistance of the flowing blood, due to the roughened endothelium of the vessels and accumulation of leucocytes becomes so increased that the propelling force is momentarily overcome. The blood in the engorged capillaries and arteries may temporarily cease flowing or it may flow toward the heart, i. e. in the reverse direction during the dias- tolic periods. This to and fro movement is termed ascillation. INFLAM MATION. 149 Stasis—The resistance may become greater than the pro- pelling force and the circulation cease for a varying period of time. This condition is denominated stasis. Exudation.—Varying quantities of the fluid and of the cell- ular constituents of the blood pass through the vessels nor- mally and an increased quantity escapes through during 1in:- flammation. The portion of the blood that escapes through the blood vessels is called exudate. The passing of the exudate rig. 90.—Blood vessel showing margination of leucocytes typical of the first stages ef inflammation. through the vessel wall is termed exudation. It is still unde- termined whether the normal tissue lymph is a secretory pro- duct of the capillary endothelium or is produced by such physi- cal processes as diffusion or filtration. The source of the in- flammatory exudate is no doubt, the same as the source cf nor- mal tissue lymph. Exudation is a result of the vascular dis- turbances. It has been previously stated that in normal circulatory blood the corpuscles occupy the axial stream and the plasma the 150 VETERINARY PATHOLOGY. peripheral stream. The corpuscles occupy the axial stream because they have a greater specific gravity than the plasma. Why the leucocytes enter the peripheral or plasmatic stream in inflammation has not been clearly determined, but it is probable that this margination is a result of chemotactic influences. After the leucocytes become marginated they pass through the vessel wall as follows: Small protoplasmic processes extend and project through the vessel wall. These processes gradually increase in size until the entire leucocyte has, by protoplasmic extension, passed through. The leucocytes usually pass be- tween the endothelial cells but they may pass directly through Kig, 91.—Blood vessel showing diapedesis of leucocytes typical of the exudative stage of inflammation. them. The exudation of erythrocytes is passive, the cells being forced through the vessel wall by pressure. To recapitulate: fluid exudation is either a physical process, such as filtration, or a physiologic process, a secretion; leucocytic exudation is a physiologic process depending largely upon the chemic influ- ences of the adjacent tissues, i. e., chemotaxis; exudation of erythrocytes is a physical process resulting from intravascular pressure plus diminished resistance of the vessel wall. Exudate. 1. Composition—Inflammatory exudate contains varying quantities of cells suspended in a fluid (plasma, tissue juice, etc). The fluid part of the exudate contains proteids (serum albumin and serum globulin) in excess of normal plasma. {t has a specific gravity of 1018 or more. The quantity of pro- teid is directly proportional to the severity of the process and INFLAM MATION. 152 is never less than 4 per cent and frequently as much as 6 per cent. It usually coagulates readily if withdrawn from the in- flammatory tissues. The coagulability of inflammatory exudate is so constant that it may be used in differentiating inflamma- tion from oedema. The exudate is usually acid in reaction. The fluid portion of the exudate is similar to the blood plasma with the exception of the varying percentage of proteids, and the presence of some other soluble substances. Leucocytes are the principal cellular elements found in the exudate, erythrocytes occurring only in certain inflammatory conditions, such as croupus pneumonia. The following types of leucocytes are especially concerned in inflammation; polymorphonuclear, lymphocytes small and large. Polymorphonuclear leucocytes with neutrophile gran- ules are the type most frequently found in an area affected with acute inflammation, providing the causative irritant was not too severe. About 70 per cent of the leucocytes present are of this type. These cells appear in the affected area in the be- gining of the process. They have the power of amoeboid movement and may emigrate from the blood and lymph vessels independently of the fluid exudate. These cells possess phago- cytic properties and probably produce and liberate antitoxic and bactericidal substances. They are the pus cells and constitute the bulk of the exudate in suppuration. These cells may be destroyed and disintegrated in the field of action or when the inflammatory process ceases they may migrate from the in- jured area and reenter the lymph or blood vessels. They do not become formative cells and never produce new tissue. Eosinophylic leucocytes, (polymorphonuclear leucocytes hav- Fig. 92.—Types of cells in inflammatory exudates. 1 Lymphocyte. 4—5. Polymorphonuclear leucocytes, 3. Transitional leucocyte. 6. Endothelial cells from lining of an artery. 2. Mononuclear leucocyte. 152 VETERINARY PATHOLOGY. ing acidophile granules), appear early in an inflamed area. They are usually quite limited in number except in localized inflammation induced by animal parasites. There are frequently observed in the liver, kidney, and other tissues, foci composed of a mass of eosinophiles and appearing as inflammatory cen- ters. These eosinophilic inflammatory foci are probably the re- sult of invasion of animal parasites. Eosinophiles are abundant in the lesions of bursattae and in epizootic lymphangitis. Their origin is, so far as has been determined, from the blood, the lymph and tissue spaces indirectly, and the bone marrow di- rectly.’ The specifre action of: these cells in intlammationg not known: They do not aid in the formation of new tissues. Mast cells or polymorphonuclear leucocytes with basophile granules are observed in subacute inflammation (Adami). Their origin is from bone marrow. Their nuclei apparently become disintegrated in inflamed tissue. The significance of these cells has not been determined. Lymphocytic invasion of the affected areas and an excess of them in the blood characterize some of the slow scoimeman chronic inflammatory processes such as tuberculosis and ac- tinomycosis. These cells also appear in affected tissues in the later stage of acute inflammation but are never very abundant. They may have their origin from the blood, the lymph and from adjacent lymphoid tissue. The large lymphocytes may have their origin from the small lymphocytes. Lymphocytes have a very limited power of amoeboid movement. They have never been observed to ingest bacteria although they may in- corporate fragments of destroyed tissue cells or other inert sub- stances. These cells may partake in the formation of new tis- sue but this has not yet been positively determined. Cells other than leucocytes are sometimes observed in in- flammatory foci. Endothelial cells, wandering connective tis- sue cells, giant cells, and red blood corpuscles may be present in inflamed areas. Endothelial cells are especially evident in serous membranes affected with inflammation. They appear later in the process than either polymorphonuclear leucocytes or lymphocytes. Their origin is probably from pre-existing, like cells. They usu- ally have a sluggish movement, are slightly phagocytic and also ingest fragments or particles of inert substances. These cells may be destroyed or they may emigrate from the affected area. Wandering connective tissue cells are usually present in inflamed tissues. These cells do not appear until some time INFLAMMATION. LS after the injury is inflicted because of their slow movement. Their source is from tissue spaces, and they are the preexist- ing wandering connective tissue cells that occur in practically cll tissues of the immature animal. They may be phagocytic but this property is not usually well developed. They are es- pecially active in the process of repair. Giant cells, so-called, are of common occurrence in some in- flammatory processes especially tuberculosis and actinomycosis. It is probable that endothelial cells are the progenitors of giant cells. Some investigators have intimated that wandering connective tissue cells may produce giant cells. The giant cells may be formed either by a multiplication of nuclei without divi- Fig. ¢3.—Castritis, hog, induced by a caustic, showing destruction of gastric mucosa. sion of the cell body or by a fusion of several independent cells (Syncytium). The latter view is the one most accepted at the present time. The function of the giant cell has not been specifically determined, but those in tubercular lesions fre- quently contain many tubercle bacilli indicating that they are phagocytic. Red blood corpuscles or erythrocytes occur in the inflam- matory exudate as a result of intense engorgement of the ves- sels. They begin passing through the vessel wall after the leucocytic migration. Increased intravascular pressure is the principal cause of their escape from the vessel, their passage through the vessel wall being entirely passive. 54 VETERINARY PATHOLOGY. 2. Varieties—Inflammatory exudates may be serous, fibrin- ous, or hemorrhagic. a. A serous exudate continues in the fluid state as long as it remains in the tissues or tissue spaces. It is composed almost entirely of fluid, having very few cells’ Whis variety orvex- udate is characteristic of mild inflammatory conditions. The constancy of the fluidity of the serous exudate is the result of the action of enzyms that continually convert the albuminous substances into soluble compounds as proteoses and peptones. b. Inflammatery fibrinous exudate contains two enzyms, one of which (leucoprotase) is active in an alkaline medium and the other in an acid medium. “These enzyms probably exert their greatest activity in a neutral medium, slight changes in reaction increasing digestion by the one, and suspending di- Fig. 94.—Acute Pleurisy. a. Engorged vessels. b. Exudate. gestion by the other.” In suppuration the acid digesting enzym probably disappears (Barker). A fibrinous exudate is one that coagulates within the tissues or tissue spaces. The coagu- lation of the exudate is identical with the coagulation of blood and is probably due to the liberation of fibrin forming enzyms from disintegrated leucocytes. Fibrinous exudate is the variety observed in inflammation resulting from severe irritation. The exudate usually contains many cells and a large amount of proteids. c. Hemorrhagic exudates are those in which the red blood cells as well as leucocytes and plasma have passed through the ves~ sel wall. This exudate coagulates the same as the fibrinous INFLAMMATION. Ls exudate. Intense irritants are usually the causative agents of hemorrhagic inflammation. Croupous pneumonia is character- ized by a hemorrhagic exudate. A so-called purulent exudate has been described but pus is not purely exudative for some of its constituents are not de- rived from the blood. Pus is composed of altered leucocytes, tissue shreds, and usually bacteria, suspended in a fluid. liquor- puris. Liquor puris is blood plasma and dissolved tissue. Pus contains no fibrin, the proteid constituents being converted into soluble compounds by cellular enzymes and bacterial ferments. 38. The following are probably the determining factors of the quality and quantity of inflammatory exudate. a. Cause of inflammation :---Generally speaking a mild irritant or injury produces a serous inflammation, and an intense ir- ritant produces fibrinous inflammation. Mechanical injuries, when there are no surface abrasions, produce an inflammation of a mild degree and the exudate is limited in quantity and is usually of a serous nature. Such injuries, however, usually produce abrasions which favor the invasion of micro organisms. Thermal disturbances of mild degree, produce a serous ex- udate, if more severe the exudate is extensive and of a fibrin- ous or hemorrhagic character. The use of a thermo-cautery is an excellent example of thermal production of inflammation and the severity of its use demonstrates the intensity of inflamma- tion and the variations of the exudate. An irritating chemical substance injected into a tissue produces inflammation char- acterized by excessive exudation especially of a serous fluid. The more irritating the chemical, the greater the quantity of exudate and the greater the percentage of proteids. External application of chemical irritants produces inflammation char- acterized by a serous or by a fibrinous exudate. This latter may be observed in the application of blistering agents. In- fective inflammation is usually accompanied by a marked exu- date from the beginning of the infection. The quantity and . quality of the exudate varies with the virulency of the organ- ism. There are some exceptions however, e. g., tetanus infec- tion causes a very limited exudate regardless of the virulency of the tetanus bacillus. In some infections, as malignant oedema, the exudate is largely fluid. In suppuration the ex- udate is almost entirely leucocytic. b. Condition of the animal effected. The exudate is usually limited in animals having normal vessels, heart action, and blood. In those animals in which the vessels are diseased and especially if the endothelium has been injured there is a ten- 156 VETERINARY PATHOLOGY. dency to excessive exudation. A weak heart is conducive to excessive exudation, e. g., inflammatory oedema. Animals pos- sessing dilute blood (hydremia) are predisposed to excessive fluid exudation. The leucocytic amoeboid movement may be tem- porarily suspended, or it may be increased during inflamma- tion, resulting in an absence or in an excessive number of leucocytes in the exudate. In animals having a clean close build the exudate is not so extensive as it is in those animals of a loose flabby make-up. c. The location and tissue affected. Exudation is in direct pro- portion to the vascularity and density of the tissue. Inflam- mation in compact bony tissue or beneath dense facia, liga- Lia eia3 Fig. 95.—Acute Meningitis. a. Exudate. b. Engorged vessels. ments or tendons is accompanied by a limited exudate. I[n- flammation of the cutaneous structure is usually associated with excessive exudation, which accumulates in the subcutane- ous areolar tissue. Inflammation of serous and mucous mem- branes is accompanied with exudation which may in part be discharged upon the surface but is usually accumulated in the substructures. 4. Significance of the exudate——The significance of the exu- date has had various interpretations. Virchow considered that the irritation producing the inflammation resulted in increased cellular activity in the injured area and that the exudate sup- plied increased nourishment to the area in which there was an excessive metabolism. Others have attributed to the exudate the ‘flushing out” of the injured area thus mechanically carrying INFLAMMATION. h57 away the irritant. The exudate dilutes the irritant, especially chemical irritants, thus reducing the activity of the causative agent and mitigating the inflammatory process. It has been determined that serum possesses some sub- stances, aS Opsonins, antitoxins, bacteriolysins and bactericides, that are detrimental to infectious agents either by their bacter- icidal action or by chemical union with bacterial products. Thus the exudate reduces the irritation of infection by render- ing bacteria inactive or by neutralizing their products. Phago- cytes are very important factors in the exudate as they ingest and destroy infectious micro-organisms. The opsonic index championed by Wright of London is based on the above. Fig. 96.—Inflammaticn. Gray Hepatization. a. Air cells engorged with leucocytes. b. Hyperemia of capillaries. In aseptic incised wounds the exudate is of value in cementing the incised surfaces together, although new tissue formation is retarded by an exudate. The exudate mechanically protects the injured surfaces in gaping wounds and possesses bactericidal properties for a short time after the injury has been inflicted. After the exudate becomes inactive in its protecting properties it is a favorable medium for infection and is then probably detrimental. Injurious chemic substances may result from the aseptic dissolution of an inflammatory exudate. Fibrinous exudates may be injurious or beneficial depending upon the location and the changes taking place in the exu- date. The fibrinous exudate in crotipous pneumonia is injuri- ous because it coagulates in the alveoli of the lung thus pre- venting the respiratory function of that area. The fibrinous 158 VETERINARY PATHOLOGY. exudate in serous cavities is beneficial, especially in tocalized inflammation, because it limits or circumscribes the inflamma- tory irritant or process by coagulating thus producing adhe- sions of the two serous membranes. Many horses upon which paracentesis abdominis or paracentesis thoracis is performed might succumb to generalized peritonitis or pleurisy 1 the inflammatory process established at the point of the puncture was not circumscribed by adhesions the result of organization Re ~. Ew Olg era “3 Cx Fig. 97.—Fibrinous Pleurisy, showing an extensive exudate upon surface, of fibrinous exudate. The immediate effect of a fibrinous exu- date in a serous cavity is beneficial but the adhesions are fre- quently permanent thus interfering with the normal function- ing of the part affected. The fibrinous exudate is also benefi- cial in croupous enteritis because of the protection of the dis- eased mucosa from mechanical injuries by food stuifs. Jt is on the other hand injurious in croupous enteritis for the exu- date is a favorable nidus for bacteria and they may produce substances that are irritating to the injured mucosa. The coagulated exudate may also hinder intestinal secretion. The INFLAM MATION. 159 fibrinous exudate of diphtheritic inflammation is very injurious because of its coagulation and pressure upon the tissues. CHEMOTAXIS.—It has been determined by experiment that chemic substances exert a definite influence upon motile cells. There is always a leucocytic migration into capiliary glass tubes previously charged with turpentine or croton oil and then insert- ed into living animal tissues. The same migration is ohserved when the capillary tubes are charged with bacteria or their products. Negative results are obtained when the tubes are charged with quinine or chloroform. This attraction of leuco- cytes toward chemic substances is positive chemotaxis. The repulsion of leucocytes from chemic substances is negative chem- otaxis. The term “Chemotaxis” unmodified includes positive and negative. Leucocytic migration into an inflammatory area is a result of chemic influence or chemotaxis. PuHacocytosis.—This is the incorporation and destruction of pathogenic bacteria and other foreign substances by phagocytes. Phagocytes are cells having the power of ingesting and destroy- ing microorganisms and other foreign particles. Polymorpho- nuclear leucocytes having neutrophile granules are the most ac- tive cells concerned in phagocytosis. Endothelial cells and wan- dering connective tissue cells may be under some conditions phagocytic. The phagocytic property of cells is variable depending upon the virulency of the micro-organisms or strength of the chemic substance and upon the resistance of the phagocyte. Bac- teria are enveloped by protoplasmic extensions from the cell body until they are entirely included in the aggressive phago- cyte. After the enveloping process there may be observed diges- tion vacuoles surrounding the bacteria. The included bacteria are destroyed by ferments produced by the phagocyte. It is an intracellular digestion. The length of time necessary for the phagocyte to destroy the bacteria is variable. The bacterial destruction may be instantaneous or the bacteria may possess sufficient vitality to destroy the phagocyte. There is consider- able evidence that infection is frequently generalized in the ani- mal body by leucocytes that have enveloped bacteria and wan- dered to another portion of the body. The included bacteria destroy the leucocyte and, thus liberated, establish a new cen- ter of infection. . Phagocytosis -is a very important factor in inflammation. No doubt many localized inflammatory conditions are aborted and the intensity of the attack of other infective inflamma- tory conditions reduced by the process of phagocytosis. There is a peculiar variation of phagocytosis occasionally observed, 160 VETERINARY PATHOLOGY. e. g., leucocytes becoming phagocytic toward other leucocytes. Fixed tissue cells may under some conditions become phago- cytic towards leucocytes; this perhaps is for the purpose of obtaining nutrition for the fixed tissue cells. The Signs of Inflammation.—Inflammation may be recognized in exposed tissues by the so-called “Cardinal signs:” redness, swelling, increased temperature, pain and impaired function. These signs are usually perceptible in the early stages of acute inflammation, but they may not be evident throughout the entire process. Mild, chronic inflammation may not be accompanied by any of the above signs. These signs are very variable in either acute or chronic inflammation of internal organs. Fig. 98.—Aecute Myositis. a. Leucocytis exudate. Muscle fibres disintegrated and vessels engorged. Redness (Rubor) is a constant sign in the early stages of acute inflammation. It is the result of an excessive amount of blood in the vessels of the affected area. Swelling (Tumor) is characteristic of acute inflammation. It is the result of the accumulation and retention of the inflam- matory exudate plus the increased amount of blood in the part. The extent of the swelling is in a direct ratio to the density of the tissue. Thus the swelling resulting from subperiosteal in- flammation may not be detected because of its limited extent. On the other hand, the swelling succeeding inflammation of loose areolar tissue may be very extensive, as in cellulitis. The swelling resulting from inflammation is usually firm, dense and quite resistant in contradistinction to swelling resulting from INFLAMMATION. 161 oedema, e. g., the tumefaction accompanying tendonitis is dense, while the swelling accompanying “stocking” is soft and doughy. The temperature (Calor) of tissue affected with active in- flammation is invariably increased. This is the result of the excessive cellular action in the inflamed area and the increased amount of blocd flowing into the part. Pain (Dolor) 1s a common symptom cf inflammation. This may be the result of pressure upon nerve endings by the accu- mulated exudate. However, oedema is accompanied by an ex- cessive accumulation of fluid in the tissues, and oedematous tissues are not hypersensitive. It seems more probable that in- flammatory pain is the result of the injurious action of the irritant or soluble products of the exudate upon the sensory nerve endings. The inflammatory pain is often referred to some other part of the body, e. g., in pleurisy the pain frequently appears abdominal. Impaired function (Functio laeso) is a constant feature ob- served in inflammation. In the beginning of the process the funciion of the affected tissues (especially secretory) is in ex- cess of the normal, but this is succeeded in the later stages by depression of the function. The increased function is a result of increased nourishment, increased stimulation, and probably increased pressure is also a factor; the depressed or diminished function is the result of the injurious action of katabolic prod- ucts, produced by excessive cellular action, and of the irritant producing the inflammatory process. Thus, in the beginning of acute nephritis there is an excessive amount of fluid (urine) excreted. this is succeeded by diminution or complete suppres- sion of the excretion (urine). Effects upon the Tissue Involved. — As a resuit of the inflammatory process the tissues involved may _ un- dergo various changes. These changes may be degenerative, necrotic, regenerative or proliferative in character. Degenera- tion usually precedes regeneration, but the two conditions may be independent of each other; thus in ulceration, degeneration and necrosis may alone be evident, and in the formation of a tubercle of tuberculosis proliferation is the principal process. Both conditions may exist at the same time in different parts of an affected area, degeneration taking place in the center of the diseased area and regeneration or proliferation in the peri- phery. Inflammation not accompanied by either degeneration or regeneration is rare. The injuries or irritants establishing inflammation may and frequently do produce death of some of the tissue cells; necrotic tissue is sufficiently irritating to pro- eZ VETERINARY PATHOLOGY. duce inflammation, and necrotic areas are usually surrounded by an inflammatory zone. Inflammation is confined to the reactive process of the injured cells and should not be confused with the death of the cells or necrosis. Degeneration and regeneration are distinctly opposite pro- cesses. The former is destructive, resulting in impairment and death, while the latter is constructive, resulting in overgrowth and proliferation. Degeneration is caused by insufficient food, inhibition of irritating products, or excessive and frequently perverted functional activity. Regeneration occurs when there is an adequate supply of nutrition, and depends upon the rever- WAS pe ~ar* ar DS , Va = // — Fig. 99.—Chronie Pneumonia. a. Alveolus. ec. Wandering leucocytes. b. Fibrous proliferation. sion of the cells to the embryonic type or stimulation of the reproductive properties of the cells, the latter usually at the expense of the normal functional activity. Both processes affect the cellular elements of the tissues, primarily and actively, and the intercellular substances secondarily and passively. Some exceptions will be mentioned later. The leucocytes and wander- ing cells may also undergo changes similar to those which the fixed tissue cells are subject. In general, degeneration character- izes acute inflammation and regeneration characterizes chronic inflammation. The importance of either of the above processes depends upon their extent The general consideration of the two processes has been combined for the sake of comparison; but they will now be considered separately. Degeneration.—Practically all degenerations, to which tis- INFLAM MATION. 163 sues in general are subject, are common in inflamed tissues. The following are the principal ones that have been described. 1. Parenchymatous degeneration (cloudy swelling), is the most common type in acute inflammatory tissues. It is indeed rare to examine sections of tissue affected with acute inflammation and not find this degeneration. The presence of parenchymatous degeneration is an additional factor frequently resorted to in diff- erential diagnosis of inflammation. This type of degeneration occurs in all tissues, but more especially in glandular structures. 2. Fatty degeneration does not occur as frequently as paren- chymatous degeneration. Like parenchymatous degeneration, it occurs in tissues affected with acute inflammation. It in- variably occurs in combination with parenchymatous degenera- tion and is usually a sequel of the latter. The presence of fatty degeneration in inflammatory tissue may cause confusion in microscopic diagnosis, especially if the degeneration is exten- sive. The degeneration is common in epithelium (glandular), muscular tissue and connective tissue. 3. Mucoid degeneration is quite common is inflamed tissues. It is characteristic of catarrhal inflammation. This degenera- tion affects the intercellular substance as well as the cells. Mucus is bactericidal, therefore it is protectant and beneficial, unless produced in sufficient quantity to induce mechanical in- jury. Epithelium and connective tissue are most frequently affected by this degeneration. 4. Serous degeneration, or more properly infiltration, is char- acteristic of tissues affected with inflammatory oedema or other inflammations in which there is excessive serous exudation. This condition results from the passage into the cells of extra- cellular serous fluid. The infiltrated fluid mechanically inter- feres with the activity of the cell. It occurs most frequently in muscular and connective tissue and occasionally in epi- thelium. 5. Hyaline degeneration is of common occurrence in tissues affected with chronic inflammation. It is the conversion of the tissue into a clear, waxy substance. It is common in the mus- cular tissue of blood vessels in chronic inflammatory foci as well as in fibrous tissue resulting from proliferative inflamma- tion. 6. Amyloid degeneration has been observed in chronic inflam- matory tissues (Adami), although this is not a common sequel of inflammation. An intercellular degeneration specifically affecting the ce- ment substances between the myocardial cells has frequently 164 7 VETERINARY PATHOLOGY. been observed in myocarditis. This causes a separation of the heart muscle cells, 1. e., fragmentation, which seriously inter- feres with their function. The striations of muscle cells fre- quently disappear as a result of inflammation. Necrosis (local death).—All degenerations produce impair- ment of function and frequently end in necrosis of the affected cells. Destruction of tissue is a common result of inflammation because of the various degenerations that accompany the in- flammatory process. Suppuration is a type of inflammation and is a liquifying necrosis. Necrosis of inflammatory tissue often occurs independently of suppuration, though both conditions result from the same cause. Diestroyed tissue constitutes a fac- tor im the future changes that occur in (the amected aiseue Superficial necrotic tissue is usually cast off. Ulceration is the condition resulting from a continuous and sometimes a pro- gressive cellular necrosis. An ulcer is a denuded surface result- ing from continuous and sometimes a progressive cellular necrosis. Subsurface necrotic tissue may be disintegrated or dissolved, and pass out of the affected area in the exudate or be jeammen out by phagocytes; necrotic tissue may become surrounded and permeated by large numbers of leucocytes which liberate dis- solving ferments, thus forming an abscess; this liquefied necro- tic mass may become inspissated, a condition termed caseation; the necrotic tissue may become impregnated with calcium salts, denominated calcification; finally, the necrotic tissue may be- come dissolved and encapsulated, thus forming a cyst. Regencration—This process usually begins when degenera- tion. ceases, although it may be evident from the first. (Gels concerned in regeneration undergo a reversionary change. be- coming similar to embryonic cells. Reproduction is an active, vital property of embryonic cells, and this is also the principal function of regenerating cells. The appearance of a tissue con- taining an exudate with the succeeding degeneration has been previously discussed. A concise comprehension of such tissue is essential to a clear conception of the appearance of regenera- tion in an inflammatory zone. Whether degenerated cells are capable of regeneration depends upon the kind of cells and the extent of the injury to them. Regeneration of tissues impaired or destroyed by acute inflammation consists in the enlargement and proliferation of the contiguous uninjured cells. The exu- date is usually diminished in quantity at this stage. Prolifera- tion in tissues affected with chronic inflammation is, in reality, a fibrous hyperplasia. Cirrhosis of any structure is usually the INFLAMMATION. 165 result of chronic inflammation. The lowest types of tissues. i. e., those passive in function, are most easily and most fre- quently regenerated, e. g., connective tissue. Surface epithe- lium is frequently regenerated—muscular and nervous tissues ee \ 4 = Sie, a a 2 ie, \ Ss Es i= Sh gs 2 a =a 4 ba 5S: 2 2, 3 3 Ss SS 5 3 >. =a a\ <-S ‘ awe L\ Ss Sa oS xe . ‘ ‘ - = ce = = oe 2 & Bou, / aif ENS ia Z oe Fe ‘ =e ' a ? 4 (i : a We \Wintas ) Pes. \ zig. 100.—Chronie Hepatitis, showing intralobural fibrous formation, which results in hypertrophic cirrhosis. are rarely regenerated. The age of the individual is an im- portant factor in the regeneration of injured tissues. ‘Tissties in young animals regenerate more readily than like tissues in old animals. The origin or source of the cells that regenerate connective 166 VETERINARY 2 PAE EIOLOG Ye tissue is still a disputed point. It is certain that fixed and wan- dering connective tissue cells are capable of this function. Endothelial cells are a type of fixed connective tissue cells which are active in regeneration of connective tissue. Mononuclear leucocytes as well as lymphocytes may be capable of ‘producing connective tissue. The regenerating connective tissue cells (fibroblasts) are either oval or spindle shaped, the: latter pre- dominating, especially during the active regeneration period. Endothelial cells are active in the productian:of new vessels. Inflammatory tissue is usually more vascular than normal tissue. In the vascularization of an inflammatory area the endothelial cells produce long protoplasmic projections. — Several of these projections of different adjacent cells may fuse, thus forming an anastomotic channel, or a single projection may separate in a longitudinal direction, thus producing an extension of the old channel. As the protoplasmic projections become larger and longer there is an activity in the cell nucleus indicative of mitosis, and cell division soon follows. This process of proto- plasmic projections and mitosis continues as long. as the in- flammatory process is active. The irregular blood channels (capillaries) so formed become saenomemdler by a layer of invol- untary muscle tissues and yellow elastic tissue as a result of extension of muscle fibres and connective tissue cells from the adjacent vessel, the whole structure being surrounded by a loosely arranged layer of white fibrous connective tissue. Thus the capillary becomes an arteriole. These cells that are active in vascularization are designated angioblasts. They are the progeny of endothelium. Inflammatory injuries to surface epithelium, as epidermis or mucous membrane, are usually repaired by multiplication of the cells bordering the injury. Irregular masses of nucleated protoplasm have been observed in myositis and may represent regenerating muscle cells. Kinds or Types or Inflammation.—It is difficult to classify inflammation because of the numerous variable factors that com- pose it. The following classification is based upon etiology, exudate, tissue involved, and time or severity of attack. Etiology.—FEtiologically, inflammation may be classified as simple and infective. 1. Simple inflammation is noninfective and results from me- chanic, thermic, electric or chemic interference. | Fractures, sprains, bruises and surgical-procedure wounds are types of mechanic inflammation. As types of thermic inflammation, burns and frozen tissues INFLAMMATION. 167 may be mentioned. Local inflammatory disturbances resulting from lightning or contact with electric currents are types of electrically established inflammation. The following may be mentioned as chemic inflammations; formalin dermatitis, ar- senical enteritis, chlorine pneumonitis, turpentine nephritis, and those induced by the bites of poisonous reptiles, scorpions, bees, wasps and ants; also those caused by the products of bacteria and animal parasites. The inflammatory processes established by mechanical interference may and usually do become infected either by external contamination or by the deposition of infec- tious agents from the blood or lymph. 2. Infective Inflammation is of more frequent occurrence than non-infective. It is the kind of inflammation that concerns the practitioner, veterinary inspector and sanitarian because of its tendency to become generalized in the infected animal, and is frequently transmissible to other animals. All tissues are sus- ceptible to infective inflammation except hair, wool, feathers, and the insensitive, nonvascular portions of the teeth, hoofs, claws and horns. Infective inflammation may be either non- suppurative or suppurative. (a) Nonsuppurative infective inflammation is typified in mal- ignant oedema, blackleg, localized anthrax and the earlier stages of tuberculosis and_actinomycosis,; and is characterized by the general phenomena of inflammation previously discussed. In- fective inflammation may be nonsuppurative in the earlier stages and in the later stages be complicated by typical suppuration, as in tuberculosis. More rarely nonsuppurative inflammation continues throughout the entire process, as in blackleg. (b) Suppurative infective inflammation or suppuration.— Suppuration is liquefying necrosis, and may be surface or subsur- face, circumscribed or diffuse. The liquefied necrotic tissue pro- duced by suppuration is pus. Pus is a fluid, varying from a thin watery substance to a thick, sticky, tenacious mass,:and is usu- ally alkaline in reaction. The color of pus is determined by the infective agent, and it may be white, lemon yellow, golden yellow, greenish yellow, green or black, and is frequently tinted red with blood. Pus obtained from horses, donkeys and mules is usually white or grayish white; from cattle, creamy yellow; from sheep, greenish yellow, and from hogs, green or greenish yellow. Pus is usually odorless, although it may undergo pu- trefaction with the evolution of ill-smelling gases. Actinomy- cotic pus has a nutty odor (Mayo). Pus may have a greasy, smooth, sticky or granular feel when rubbed between the fingers, depending upon its composition. 168 VETERINARY PATHOLOGY. Histologically, pus is composed of pus cells, i. e., leucocytes (the most of which are necrotic, though some of them may pos- sess vitality), shreds of necrotic tissue and tissue cells (the type of which depends upon the tissue affected), usually pyobacteria in varying numbers (many of them being included in the pus cells) and liquor puris (the plasma or fluid portion of the exu- date and the fluid resulting from the solvent action of the vari- ous ferments). Animal microparasites are found in the pus re- sulting from their activity. Practically all of the pus cells are derived from polymorphonuclear leucocytes, and are usually the neutrophile variety, there being only an occasional mononuclear leucocyte. Extensive nuclear fragmentation and parenchyma- tous and fatty degeneration of the cell protoplasm are evident in most pus cells, indicating that they have undergone necrosis. Degeneration or necrosis are also present in the fixed tissues of the suppurative areas. The pus found in acute abscesses or dis- charging from granulating wounds is usually a creamy fluid, yellowish in color. Sanious pus is a reddish fluid resulting from an admixture with blood. Ichorous pus is an acrid, corrosive fluid that excoriates the tissues it contacts. Muco-pus and serv- Fig. 101.—Drawing of a pus smear from a case of strangles, showing the organism arranged in chains— the Strevtococcus pyogenes equi. INFLAMMATION. 169 pus are mixtures of mucous and pus, and of serum and pus, respectively. Putrid pus is a thin, ill-smelling fluid, the result of putrefaction. Infection is the usual cause of suppuration. The following is a brief description of the process. Pyogenic micro-organisms gain entrance either by deposition upon or into a wound by passing through the tissue or are carried and deposited by the blood or lymph, and, finding conditions favorable, develop and multiply. In their development, pyobacteria produce chemic substances that are sufficiently irritating to establish an active hyperemia and also to exert a positive chemotactic influence, the latter attracting at first mononuclear leucocytes and later causing the migration of neutrophilic polymorphonuclear leuco- cytes to the focus of infection. Multiplication of the pyobac- teria and leucocytic immigration continue. Phagocytosis be- comes evident in leucocytes and some other cells, e. g., endo- thelial cells. Liberated ferments, produced by the pyobacteria, leucocytes and other cells, cause degeneration, necrosis and, finally, solution of the tissue involved. Continued pyobacterial multiplication stimulates an increased leucocytic immigration, and the tissues are thus densely packed with cells. There is a marked accumulation of leucocytes around the suppurative focus apparently attempting to circumscribe the affected area. Thus the process continues, there being a progressive liquefying cen- tral necrosis within and a marginal leucocytic accumulation without. The condition is repeated until the resistant influences of the animal body destroy the pyobacteria, or until the pyo- bacteria have destroyed the involved tissue, or the entire ani- mal. (Suppurative osteitis may occur subperiosteal or in the osseous tissue proper. I.eucocytes invade the lacunae and pro- duce solution of the mineral matter, and thus the bone becomes porous. If this process continues the bone ultimately liquefies ; this is termed caries.) Surface suppuration (purulent inflammation) is suppuration of a surface tissue. Pus produced in surface suppuration con- stitutes a purulent discharge, and a persistent purulent discharge is termed pyorrhoea. Inflammation of a mucous membrane ac- companied by a purulent discharge is purulent catarrh. In puru- lent catarrh the surface epithelium is infiltrated with leucocytes frequently to such an extent that the epithelial cells are disin- tegrated, become loosened and exfoliate. The surface cells of serous membranes and the skin are similarly affected in purulent inflammation. In any purulent inflammation there is always 170 VETERINARY PATHOLOGY. an engorgement of the subsurface vessels and the related areo- lar tissue is infiltrated with inflammatory exudate. Subsurface suppuration may be circumscribed or diffuse. Suppurative centers become circumscribed first by a dense wall of leucocytes and later by a fibrous capsule. The capsule is in nearly all cases denser on the side next to the more important tissue. Fibroblasts that form the circumscribing fibrous capsule are probably the wandering connective tissue cells or their progeny. The collection of pus in tissues, or lymph spaces, and as considered by some in body cavities, constitutes an abscess. The circumscribed pus may, by solvent action of its ferments, CN A / NAT 5 Saab arose We? CAL . oes ee tJ 7a y é Fig. 102.—Suppurative Nephritis. a. Normal kidney tubule. b. Suppurative focus surrounded by kidney tissue. dissolve or erode the limiting structure (cells or capsule), and be liberated; the erosive action being in the direction of the least resistance. In this way a surface discharge is effected. The channel of exit of the pus may persist and become circumscribed by a fibrous wall, thus forming a fistulous tract. If the pus cavity is completely evacuated by surgical interference or other- wise, and the cause removed, the surrounding tissue will, by proliferation, fill the space previously occupied by the pus. The pus in an abscess may be absorbed and the destroyed tissue be replaced by regeneration. If the capsule is exceedingly dense the contained pus may become caseated and calcified. Abscesses may be classified as superficial and deep; primary or metastatic (metastatic abscesses may or may not be embolic), simple or multiple, subfascial and intermuscular. A hot abscess INFLAM MATION. WA results from rapid, active suppuration, as submaxillary abscesses in strangles, while the so-called cold abscess results from a slow suppurative process, as in tuberculosis. Accumulations of pus in body cavities as the peritoneal, pleural, pericardial, synovial and the facial sinuses constitute empyema. Vesicles may be- come infiltrated with leucocytes, which become pus cells, and thus the vesicle becomes a pustule. Diffuse suppuration is not limited by any definite border line. It is the result of agencies possessing sufficient strength or virulency to continuously and progressively destroy and liquefy tissue or it occurs at a time when the resistance of the animal or its tissues is so greatly diminished that there is inability to successfully antagonize the causative agent. Purulent infiltra- tion is the permeation of tissues with pus. Phlegmonous in- flammation is the rapid and usually extensive infiltration of tissues with leucocytes (pus cells), and occurs most frequently in the subcutem and submucosa. Exudaic—According to the nature of the exudate inflammation tion may be classified as serous, fibrinous, and hemorrhagic. The physical properties, chemic and histologic composition of inflammatory exudate has been previously discussed. (a) Serous inflammation is characterized by a serous exudate. Inflammation of serous membranes and inflammatory disturb- ances of other tissues than serous membranes, caused by mild irritation, may be of this type. Occasionally serous:«inflamma- tion is the result of intense irritation as in malignant oedema. The terms serous inflammation and inflammation of serous membranes should not be used interchangeably, because in- flammation of serous membranes may be characterized by fibrinous or hemorrhagic exudate. A circumscribed accumula- tion of inflammatory serous fluid (exudate) in the deeper lay- ers of the epidermis or mucosa constitute a vesicle. Inflam- matory oedema, a serous inflammation, is the condition result- ing from the diffusion of an excessive amount of inflammatory serous exudate into tissues as in cellulitis (inflammation of sub-cutem). (b) Fibrinous inflammation designates that type of inflammatory disturbances in which there is produced a coagulable exudate. The exudate may coagulate within the tissues or upon the tis- sue surface. Croupous inflammation is the term applied to the condition resulting from the coagulation of the exudate upon a tissue surface. Piphtheritic inflammation is the condition pro- duced by coagulation of the exudate within the tissue and upon its surface. Croupous inflammation and diphtheritic in 12 VETERINARY PATHOLOGY. flammation are not distinctly separable although the former is usually milder than the latter. Typical croupous exudate may be detached without serious injury to the surface tissue but the diphtheritic exudate cannot be removed without detaching or extensively lacerating the surface tissue. Croupous pneu- monia and croupous enteritis are examples of croupous inflam- mation, the former being the most frequent type of pneumoania in horses and the latter occurring occasionally in cattle. Roup or avian diphtheria, and diphtheritic stomatitis and enteritis are examples of diphtheritic inflammation, the former being com- mon in fowls the latter in pigs. Fibrinous exudate may be present in inflammation of serous membranes, constituting fibrinous pleurisy, peritonitis, etc. (c) Hemorrhagic inflammation is significant of the action of an extreme irritant. Hemorrhagic exudate coagulates, especially upon surfaces, though it may coagulate within a tissue. Inflam- mation of tissues in which the blood vessels are of meager struc- trure (capillaries), and hence easily permeated or ruptured, is fre- quently of this type. Croupous pneumonia is a hemorrhagic in- flammation. Nephritis and hepatitis are frequently accom- panied by a hemorrhagic exudate. (Mucus and pus have been described as inflammatory exu- dates by some and as inflammatory products by others.) They Fig. 103.—Hemorrhagie Exudate (Red Hepatization.) INFLAMMATION. 173: are not inflammatory exudates. Inflammation of mucous mem- branes in which there is an excessive production of mucus is catarrh or catarrhal inflammation. (Suppuration is inflammation accompanied by the formation of pus and may be surface or sub- surface. Purulent inflammation is surface suppuration. ) Tissue.—Histologically a gland or organ is composed of parenchymatous and interstitial tissue. Pryaencsmmicce tissue is the essential or functioning portion of a structure, as hepatic cells. Interstitial tissue or stroma is the supporting framework of an organ or part as the stroma of a lymph node. The pro- cess of inflammation may occur in either the parenchyma or stroma. Classifying upon the basis of tissue affected then, there are the two forms, namely, pas cuciytnatous and eerie in- flammation. (a) Parenchymatous inflammation is usually the result of Severe, active irritation, the interstitial type results from the long, continued action of mild arritants. The two types may be present simultaneously in the same structure or they may occur independently. (b) Interstitial inflammation is often the sequence of paren- chymatous, although it may be the initial process. Inflammation of the hepatic cells is parenchymatous hepatitis, of the hepatic interlobular tissue, interstitial hepatitis, etc. Time, Activity and Results of the Process.—It is questionable if the length of time an inflammatory process continues should constitute a factor in its classification. By common usage, inflam- mation would be classified according to the time basis, as acute and chronic. Formerly this classification was based upon the time element alone, but the duration of inflammation is so vari- able that it is now recognized as an insignificant factor. The activity and results of the process are the basic essentials relied upon in differentiating acute and chronic inflammation. (a) Acute inflammation is characterized by a sudden onset, by a vigorous action and by production of retrogressive changes in or destruction to the tissue affected. (b) Chronic inflammation is characterized usually by an insiduous onset, by a mild action, and by resutling in prolifera- tion of tissue. The proliferated tissue may induce retrogressive changes, as atrophy, but this is only an indirect result of the pro- cess. Either acute or chronic inflammation may occur throughout the entire reaction or they may both prevail at the same time in different parts of the same structure. The causative agents may become less active as the process continues, thus acute inflam- 174 VETERINARY PATHOLOGY. mation is often succeeded by chronic inflammation. Injuries of tendons are usually accompanied by acute inflammation, but this usually subsides early and is succeeded by chronic inflam- mation. Chronic inflammation may be succeeded by acute in- flammation provided that the irritating factor be sufficiently in- creased or the resistance of the animal diminished. Miscellaneous.—a. Catarrhal inflammation is inflammation of a mucous membrane, accompanied by an excessive production and discharge of mucus. b. Purulent inflammation is characterized by the production of pus. This term is confined, by some, to surface suppuration. c. Ulcerative inflammation is one.in which there is erosion of surfaces, i. e., the production of ulcers. d. Vesicular inflammation is one characterized by the pres- ence of vesicles. e. Pustular inflammation is one characterized by the. pres- ence of pustules. f. Proliferative inflammation is practically the same as chronic inflammation. It signifies the production of new tissue. g. Specific inflammation is one resulting from a specific in- fection, as glanders. Termination.—The tendency of the reaction produced by an injury is always favorable, but the reaction may be so sud- den and extensive or continued so long that its results may be harmful. The termination of inflammation depends upon the extent, intensity, and duration of the irritant and the resistance of the tissues. Inflammation may terminate in resolution, tissue proliferation or dissolution. Resolution embraces the processes of repair and these may be summarized as follows: a. Remiloyvalor the cause: b. Re-establishment of circulation. This may be accom- plished in a few hours or perhaps not for several days depend- ing upon the extent of the injury and the kind of tissue injured. c. Restoration of vessels to their normal condition. The length of time required for restoration and the completeness of the process depends upon the severity of the injury and the re- establishment of the circulation. d. Removal. of the inflammatory exudate) The tintemne: quired to remove the exudate depends upon its nature. Serous exudates are usually removed by resorption, i. e., by the lymph channels. Fibrinous and hemorrhagic exudates are usually dis- solved and absorbed, or they may be carried away by phagocy- OL INFLAMMATION. 17 tes. Exudates may in part be consumed as nutrition by local cells. e. Disposal of necrotic tissue. Necrotic tissue is disposed of by sloughing, absorption, phagocytosis, or sequestration. Small areas of necrotic tissue are usually promptly absorbed or dis- pesed of by phagocytic action. Considerable time is usually re- quired in disposing of large areas or masses of necrotic tissue, unless it is superficially located and separates from the surround- ing tissue and sloughs. Subsurface necrotic tissue may be gradu- ally liquefied and absorbed, discharged through a fistulous tract (submaxillary abscess of Strangles), collected and carried out by phagocytes, encapsulated, or sequestrated, and remain per- manently in the tissue. Encapsulated necrotic tissue may be- come infiltrated with calcium salts. f. Regeneration of degenerated tissue and replacement of necrotic tissue. The regeneration of degenerated tissue consists in replacing the injured or destroyed cell protoplasm by normal protoplasm. If only a few cells are destroyed the adjacent cells reproduce and thus renewal is usually rapid. Connective tissue cells and surface epithelium are easily and efficiently regenerated, but cardiac muscle, ganglionic nerve and cartilage cells are rarely perfectly regenerated. Large areas of necrotic tissue are usually substituted by fibrous tissue. This proliferated tissue is termed granulation tissue in the beginning and cicatricial tissue after it has become dense and more or less contracted. Granu- lation tissue consists of capillary loops surrounded by masses of cells. These cells are largely fibroblasts and produce fibro- connective tissue. After the fibro-connective tissue has been formed it contracts, thus becoming cicatricial tissue. Cicatriza- tion is of value in closing gaping wounds, but is injurious when it occurs in internal organs as the liver, because the pressure produces atrophy and obstructs circulation. The capsule sur- rounding pus cavities, after the purulent fluid has been evacuated, becomes a granulating membrane which soon fills the gap with fibrous connective tissue. Exuberant granulation results from excessive multiplication of cells, undue extension of capillary loops, and failure of contraction of the fibrous tissue. Tissue Proliferation—tThe tissue proliferated in inflammatory resolution takes the place of tissues that pre-existed and had be- come necrotic, while that occurring in inflammation resulting from long continued mild irritation is not a substitution but an addition to the tissue already existing. In this latter phase tissue proliferation may begin in a very short time after the in- flammation is established or it may not appear for two, three, 176 VETERINARY PATHOLOGY. or several days. Fibro-connective tissue is invariably the pro- duct of tissue proliferation. Fibro-connective tissue prolifera- tion is closely associated with chronic inflammation, in fact it is almost inseparable from it. The proliferated tissue appears first in the frame-work of the tissue involved and may later extend into the parenchymatous tissue. If the proliferated tissue is excessive it may, by pressure, produce atrophy of the parenchy- matous tissue. Cuicatrization of the proliferated tissue causes an irregular lobulation and constriction of the involved organ, as in cirrhosis of the kidney. Strictures of hollow organs are pro- duced in the same way. Adhesions of serous membranes are produced by fibrous tissue formed during inflammation. Dissolution or destruction is a result of intense irritation. Necrosis of tissue is frequently a sequence of inflammation. A single cell or only a few cells may be destroyed or large areas of tissue may undergo necrosis. Ulceration results from con- stant cellular necrosis. Circulation may be obstructed by an inflammatory exudate and cause necrosis in large masses of tissue. It may terminate fatally, in partial recovery, or in reso- lution, depending upon the importance of the tissue involved in the affected animal. Conclusion.—Inflammation is the reaction of a living tissue to an irritant. Inflammation is a complex process, the result of many fac- tors. It is not always a result of infection. It is an adaptive, reparative and protective process. It may produce sufficient reaction to cause destruction of the portion involved and occasionally of the entire organism. CHAPTER Vif. PROGRESSIVE TISSUE CHANGES. REGENERATION. DEFINITION. EXTENT—Depends upon age and tissue involved. Blood. Connective tissue. Fibrous, White. Yellow. Cartilage—Rarely regenerated perfectly. Bone. Epithelium. Surface—Complete and perfect. Glandular—Irregular and incumplete. Muscle—Perfect regeneration rare. Nerve—Cells do not regenerate, fibres do, Regeneration is the process by means of which destroyed tissues are replaced. Tissue destruction is the result of necro- sis, primarily, and inflammation and degeneration, secondarily. Regeneration is accomplished by multiplication of pre-existing adjacent cells or by invasion and multiplication of wandering connective tissue cells. The proliferating cells assume the charac- teristics of embryonal cells, that is, their reproductive property is over-developed and their other vital functions depressed. The power of regeneration of a tissue is inversely proportional to its specialization. Regeneration of the tissues of the less complex animals is more nearly perfect than that of the tissues of highly organized animals; thus invertebrates regenerate entire organs or parts. Spallanzani cut off the legs and tail of a salamander and observed in the course of three months six crops of these members. In the entire three months 687 perfect bones were re- produced and the regeneration was perfect regardless of the point of amputation. The tissues of young growing animals are more easily regenerated than those of mature animals. Single cells or small areas of tissue are more perfectly regenerated than large areas. In some cases destroyed tissues are not regenerated but are replaced by fibrous tissue. The functions of some de- stroyed tissues and organs may be performed by other struc- tures. Thus, if the tibia of a dog is destroyed, the fibula in- creases in size and assumes its function. Destruction of one kidney is succeeded by a compensatory hypertrophy of the other 177 178 VETERINARY PATHOLOGY. kidney... The law of specificity, 1. e., cells beget like cells, is the same in regeneration and in physiologic processes. Regen- eration is the outcome of the unhindered multiplication of cells. Blood is continually regenerated during the natural life of an animal. The normal maintenance of blood is a physiologic pro- cess, but regeneration of blood or some of its constituents may, under certain conditions, be abnormal, as in leukemia. Leuco- cytes are produced in lymphoid tissue of the lymph nodes, spleen and bone marrow, and it is possible that they may multiply in the tissue spaces. Erythrocytes probably have their origin in the red marrow of bones in adult animals. The red blood corpuscles are nucleated in the beginning but the nucleus vanishes by so- lution or extrusion before the cells reach the general circulation except in case of severe hemorrhage or other conditions in which there has been rapid, extensive loss or destruction of blood. Blood vessels are usually the first tissue regenerated in the repair of wounds. Blood vessels are formed in the embryo by canalization of large mesodermal cells, many of which fuse, thus forming continuous canals that later become blood vessels. This er Fi eg ANT TRON RO eT Te RE Fig. 104.—Vasecular Regeneration, showing vascular buds. type of vascular formation is not common in repair of injured vessels or regeneration of destroyed vessels. The usual manner of vascular regeneration is by the growth and development of endothelial buds from adjacent vessels. These buds are solid, conical processes which extend outward from the capillary en- dothelium. The buds or processes increase in size and become hollow at their base, the cavity being thus continuous with the ‘umen of the pre-existing vessel. As the buds increase in size PROGRESSIVE TISSUE CHANGES. 179 there is an increase in the number of cells composing them. Union or fusion of buds or processes from different vessels re- sults in anastomosis or inosculation. These processes are thus the forerunners of capillaries and by a dilatation and an increase in the thickness of their walls due to formation of fibrous and muscular tissue, arteries and veins are formed. The new vessels produced in the repair of an injury are invariably in excess of the normal vascular requirements of the part. The excess ves- sels in an injured area are obliterated by cicatrization. Connective tissue is usually completely regenerated. Con- nective tissue is regenerated from pre-existing connective tissue cells, wandering cells and endothelial cells. Mucoid connective tissue is not normally found in the adult animal except in a modified form in the vitreous chamber of the eye. Mucoid tissue is not regenerated, although it is possible that other types of regenerated connective tissue are mucoid in the beginning. Fibrous connective tissue is rapidly and completely regen- erated. White fibrous connective tissue is frequently substi- tuted for other tissues. ‘The fibres in regenerated fibrous con- 4 Es 3s Ceti im. Sina ne : Se ae rt ie EW AS Se RES = * Fig. 105.—Fibrous Regeneraticn, nective tissue have the same origin as those in normal fibrous tissue. Regeneration of white fibrous tissue may be studied in the union of the ends of a tendon after tenotomy. The space between the ends of the tendon is filled with blood and lymph which escaped from the severed vessels. The pre-existing con- nective tissue cells bordering the wound in the tendon, together with wandering cells, begin proliferating within forty-eight hours, their progeny being fibroblasts. The fibroblasts produce a tangled mass of fibrous connective tissue, and at the same time there is vascularization of the extravasate which occupies the space between the severed ends of the tendon. After the ends 180 VETERINARY PATHOLOGY. of the tendon are firmly united by the mass of newly formed fibrous tissue the extravasate and the fibres, excepting those ex- tending in a longitudinal direction, are absorbed. Finally the repair is so complete that the defect is not visible to the unaided eye and is difficult to detect microscopically. Scars are bands, sheets or masses of white fibrous tissue and indicate imperfect regeneration, the fibrous tissue in scars being largely a substitu- tion tissue. Yellow elastic tissue is not as perfectly regenerated as white fibrous tissue. White fibrous tissue usually is substituted for yellow elastic tissue when the latter has been destroyed. Regeneration of cartilage is very imperfect probably because of its irregular supply of nourishment. Destroyed cartilage is usually replaced by fibrous tissue. In some instances injuries to cartilage are succeeded by excessive cartilaginous prolifera- tion. A case was observed in which the arytenoid cartilage was severed in an operation to relieve roaring; six months later there had developed at the point of operation a cartilaginous mass as large as a goose egg. Perfect regeneration of cartilage does occur, although it is rare. Regenerating cartilage cells are de- rived from the inner portion of the perichondrium. Fibrous tissue formation usually precedes the regeneration of cartilage, althe1gh it may be formed from the beginning. Osseous tissue is usually perfectly regenerated . The cells that produce osseous tissue are called osteoblasts. Osteoblasts are usually derived from the osteogenetic layer of the perios- teum, although they may have their origin from undifferentiated connective tissue cells. The formation of osseous tissue is usu- ally preceded by mucoid, fibrous or cartilaginous tissue. The various stages of osseous regeneration are very similar to those of normal bone formation. QOsseous regeneration may be illus- trated by the union of a fracture as follows: Blood and lymph vessels are ruptured when the fracture is produced. Blood and lymph escapes into the surrounding tissues and the interstice between the two ends of the fractured bone. The injury pro- duces necrosis and establishes inflammation. Vascularization of the injured area initiates the process, after which there is solu- tion of the extravasate, exudate and necrotic tissue. Osteo- blasts accompany the newly formed vessels and produce irregu- lar masses of fibrous tissue which later calcify. The calcareous tissue is infiltrated with osteoclasts derived from the blood which dissolve out regular canals in the regeneration of long bones, and irregular cavities in the regeneration of flat or irregular bones. Osteoblasts appear in the canals and cavities, formed PROGRESSIVE TISSUE CHANGES. 81 by the osteoclasts, and produce fibrous lamellae which are later calcified. This process continues until the canals or cavities are filled with lamellae excepting a small central cavity which. con- tains blood vessels, thus Haversian systems are frequently com- pletely regenerated. Excess of osseous tissue formed over and around bones at the line of fracture (provisional callous), is usually later reabsorbed. Adipose tissue is not a typical primary tissue. It is derived from the undifferentiated connective tissue cells by the conver- sion of their protoplasm into fat. Adipose tissue is consumed when the food supply is deficient, and the cells become typical connective tissue cells or are destroyed. Adipose tissue is also formed when the food supply exceeds the demand as a result of production and accumulation of fat in the connective tissue cells. Dentine is not replaced except in some of the lower animais. Epithelium of surfaces is constantly destroved and regen- erated. The outgrowth and shedding of the superficial epi- dermal cells is a physiologic process. Epithelization of small abrasions of the epidermis and mucous membranes is rapid and complete, the regenerating cells having their origin from the epithelium bordering the injury. If the denuded surface is large regeneration may proceed from the cells of the sweat glands of the skin, or mucous glands of mucous membranes as well as the epithelium bordering the injury. Squamous epithelium is more completely regenerated than columnar. Constant destruction of columnar cells may cause the production of short columnar cells and finally squamous cells. This, however, is rare, as the law of specificity is practti- cally without exception. Glandular epithelium is not regenerated as perfectly as surface epithelium (excepting the sweat glands, oil glands, mucous glands, gastric glands, Brunner’s glands, crypts of Lieberkihn and uterine glands). Any of the foregoing will regenerate from small islands of cells either in the duct or body of the gland. The epithelium of the mammary gland in- creases in amount during lactation and diminishes when lacta- tion ceases. By observation it has been determined that mam- mary epithelium regenerates after it has been destroyed by ab- scess formation or other destructive processes, provided newly formed fibrous tissue is not substituted. By analogy it might be supposed that the destroyed epithelium of salivary glands and of the pancreas may be regenerated, but this has not been clinically or experimentally demonstrated. The liver is a tubu- lar gland and regeneration of a single cell or a few cells is not 182 VETERINARY PATHOLOGY. uncommon, but large areas of liver tissue are probably never regenerated, although some pathologists claim that they have observed the regeneration of the major portion of a liver lobe in the dog, cat and rabbit. Kidney cells, especially of the tubules, are constantly regenerated, although the regeneration of an entire tubule has never been observed. The testicular and ovar- ian tissues are probably never regenerated except in the physio- logic maintainance of spermatogenesis and oogenesis. Muscular tissue is imperfectly regenerated. Injuries of invol- untary muscular tissue are usually repaired by the substitutiou of fibrous tissue which may later be replaced by involuntary mus- cular tissue, the latter being derived from the adjacent muscle cells. Two or three days after an injury to a voluntary muscle fibre, the nuclei near the injury divide and a multinucleated protoplasmic mass is formed on the damaged fibre. These pro: toplasmic masses extend into the substituted fibrous tissue and may split longtitudinally into regular fibres but more frequently they die and disintegrate. Destroyed heart muscle cells are invariably replaced by fibrous tissue. Nerve cells are not regenerated, at least in adult animals, although their processes, axones and dendrites, are regenerated in peripheral nerves. After a nerve fibre is injured the axone degenerates to the distal end and to the first or second node of Ranvier proximally. A few days after the injury the axone, if its continuity has not been destroyed, begins to elongate, ex- tending peripherally, in the direction of least resistance, which is in the old sheath. If the axone extends in the original sheath the tissue deprived of its nerve supply may become perfectly innervated. The rate of growth of an axone has been variously estimated at from .1 mm. to 1mm. in twenty-four hours. Foot lameness in horses that has been completely relieved by meta- carpal and metatarsal neurectomies, sometimes reappear, in from eighteen months to three years after the operation, thus indicating that there has been reinnervation. If the proliferating axone does not continue in the original nerve sheath it may become entangled and coiled up in the scar tissue, of the wound, thus producing sensitive scars and amputation neuromata. PROGRESSIVE TISSUE CHANGES. 183 WOUND HEALING. DEFINITION. CLASSIFICATION. Etiology. Traumatic. Thermiic. : Chemuc. = Location. : Surface. Subsurface, (Cephalic, cervical, thoracic, etc.) Character. Incised. Punctured. Lacerated. Contused. Stab. Gun shot. Bites. Condition. Aseptic. Septic. HEALING. Primary union, (First Intention.) Hemorrhage arrested. Approximation of wound margins. Adhesion of wound lips with exudate. Multiplication of related cells. Vascularization., Epithelization, Secondary union, (Second Intention.) Hemorrhage arrested. Immigration of leucocytes to wound margins. Infection. Sup puration. Granulation. Cicatrization. Epithelization, The regeneration of the individual tissues has been discussed. The simultaneous regeneration of the tissue-complex of an area in which there has been previous tissue destruction constitutes wound healing. A wound is the result of sudden interruption of the continuity of tissue or tissues. Some have restricted the term ‘wound’ to those conditions resulting from traumatisms ; others confine it to injuries of soft tissue, and again some main- tain that wounds occur only upon a surface. There is no good reason for restricting the term, because both thermic and chemic influences produce tissue destruction not distinguish- able from wounds mechanically inflicted. A fracture is a break in the continuity of osseous tissue and is repaired in the same way as wounds of soft tissue. Rupture of the liver or spleen is characterized by tissue destruction and regeneration, the entire process being identical with that in surface wounds. Wounds ‘result from sudden and violent action. Thus ulcers or necrotic 184 VETERINARY PATHOLOGY. tubercular centers are not wounds. A bruise may of May not be a wound, depending upon the nature of the lesion, i. e, whether or not the interruption of tissue has been mete Wounds may be classified as te cause, location, character, and condition. 1. Etiologically wounds may be traumatic, thermic or chemic. 7 2. According to location wounds may be, surface or subsur- face, aih lorena Cemvicaly thoracie ene By 2S Te) alee character, wounds may be incised, punctured, lacerated, contused, stab, shot, or bullet and from bites. 4. Wounds may be aomimmecnions amd amicenens| Traumatic wounds usually heal more readily than wounds re- sulting from thermic or chemic causes because traumatisms are caused by mechanical force only and the destructive influence ceases immediately upon removal of the cause; whereas the in- fluence of thermic and especially chemic causes are more lasting as their action continues after the wound has been produced. Wound healing may be of one of two types, healing by pri- mary union (first intention), and healing by granulation (sec- ond intention or secondary union). These two modes of heal- ing differ only in extent. Other methods of healing have been described as immediate union, healing by third intention, and healing under a scab. Immediate union, signifies union of parts of a cell or the cut ends of fibres, etc., and is now thought to be impossible; healing under a scab and healing by third intention are properly discussed under the caption of primary union or eranuation. , | Healing by Primary Umnon.-—-This is the most desirable method of wound healing and is usually obtained in veterinary practice only in surgical wounds and recently inflicted, clean cut wounds. This mode of healing is of short duration and is ac- companied by little if any infection and limited inflammation. Healing by primary union takes place only in clean cut wounds, i. e., when the tissues are smoothly and evenly divided and in which hemorrhage is limited and easily controlled. After hem- orrhage ceases or has been arrested the extravasate coagulates thus agglutinating and drawing the wound margins together. If the incised surfaces or severed tissues be approximated by surgical procedure the coagulated extravasate and exudate as- sists in maintaining them in that position. In surface wounds varying quantities of serum and lymph discharge and coagulate upon the surface thus forming a scab. The injury producing the wound and the extravasate are sufficiently irritating to es- PROGRESSIVE TISSUE CHANGES. 185 tablish hyperemia and in some cases slight inflammation ac- companied by a serous exudation and a leucocytic immigration. The hemorrhagic extravasate is gradually disintegrated and re- moved by phagocytes and at the same time, there is enlarge- ment and extension by multiplication of the marginal tissue cells of the wound into the coagulum which serves as a support for the regenerating tissue. Vascularization accompanied by fibrous formation initiates the process of regeneration in the healing of a wound by primary union. Vascularization is usually limited because of the small size of the wounds. The newly formed vessels are capillaries and supply the regenerating tissue. Fibrous tissue 1s produced in sufficient quantities to replace all tissues destroyed. Disintegration of the coagulum and regeneration of new tis- sue thus proceed until the newly formed tissue has entirely re- placed the extravasate. The scab is firmly held upon the wound SS ——————— ae Wess SSS ate > < - SS j x lx bans NS c) ~ \ @\ y j py 8G ‘f ] | aa y a SSS 6. 48, nS SS OT 517) = eo LESS é a ol ies 5 Se / See OS: \ e168 2S ee a SS es ; Fig. 106.—Wound Healing by first intention. a. Fibrinous exudate with proliferation of vessels. ec. Bottom of wound. b. Regeneration of epithelium. da. Leucocyies. 186 VETERINARY PATHOLOGY. by fibrils continuous with the coagulated extravasate and as the latter is absorbed the scab gradually becomes loosened and finally drops off leaving a shining surface. The regenerated tissue formed in the extravasate is embryonic fibrous tissue the amount of which depends upon the quantity of coagulum. Upon the embryonic tissue thus formed, in surface wounds, epithelization is usually rapid and complete. The scar appears. pale pink and is tender until cicatrization takes place and then appears white, dense, firm and hard. Whether the fibrous tis- sue produced in wound healing is substituted later by the nor- mal tissues of the part involved depends upon the generative power of the tissues destroyed. To recapitulate, healing by primary union embraces, coagula- tion of the hemorrhagic extravasate, agglutination of the wound margins, hyperemia, inflammation, vascularization, fibrous form- ation, disintegration of the hemorrhagic extravasate and in- flammatory exudate, cicatrization, epithelization and substitu- tion. Healing by granulation—This is the usual mode of wound healing in domestic animals. It differs from the healing by primary union in that there is invariably infection and suppur- ative inflammation, degeneration and necrosis preceding regen- eration. This mode of healing takes place in irregular wounds having lacerated margins and in which there is considerable de- struction of tissue and extensive hemorrhage and in wounds the margins of which are not approximated. The extravasated blood may coagulate in the wound, especially in subsurface wounds, and also in surface wounds in which the margins are approximated and retained by mechanical means, such as su- tures, adhesive tape, etc. Im lacerated on gaping “cutee wounds, as wire cuts, the coagulum becomes detached and drops out leaving the wound margins covered by a thin layer of coagulated serum. Within a short time after the injury is inflicted there is extensive leucocytic immigration into the tis- sues bordering the wound. The infective micro-organisms cause destruction and solution of the marginal cells until the tissue re- sistance or local immunity checks their activity. Upon the ex- posed wound surfaces there appears velvet like projections (granulations), which are capillary loops regenerated from ad-. jacent vessels. Between and intermingled with the granulaticns, regenera- tion of connective tissue takes place. Constant exposure of the: wound insures continued infection which retards the granula- tiou more or less, depending upon the extent of the infection,, PROGRESSIVE TISSUE CHANGES. 187 the degree of activity of the micro-organisnis and the resistance of the tissue. The destroyed tissue in the wound is ultimately replaced with granulation tissue and, if the wound is upon tre surface, epithelization proceeds as in healing by primary union. The embryonic granulating connective tissue contracts i. e., Fig. 107.—Exuberant Granulation, resulting from wire cut. cicatrizes about the time that epithelization occurs. Cicatriza- tion constricts and obstructs the capillary vessels, that are in excess of the normal, thus diminishing the blood supply. If ci- catrization does not occur new capillary loops (granulations) are rapidly extended producing a fungoid bloody growth, called excessive or exuberant granuation (proud flesh). The efficient regeneration and substitution of the destroyed 188 VETERINARY PATHOLOGY. tissues in wounds that heal by granulation is possible only in very young animals and in tissues not highly organized. To recapitulate, healing by second intention embraces sup- puration, granulation, cicatrization, epithelization and_ substi- tution. In some individuals the formation of fibrous connective tis- sue 1s continuous and there is formed large masses of cicatrical tissue known as keloids. Keloids are classified with neoplasms by some authors. lala IN Ohetah ye EMIOLOEGYE Antenatal. Unequal pressure. Amniotic adhesions. Post-natal. Increased nutrition. Increased function, Internal secretion. Diminished pressure. APPEARANCE. Macroscopic. Microscopie, LASSE. AUER C IED). (EPULIBE JES. Hypertrophy literally means excessive nutrition. By usage the term.has come to mean, an abnormal increase in the size of | an Organ, Or parte In a imore restricted and edenmite senses aye pertrophy is a term applied to that condition resulting from an abnormal increase in the size of the essential cells of the part. Thus an increase in the size of the liver as a result of an in- creased amount of the interstitial tissue or an increase in the size of a kidney due to an accumulation of an inflammatory ex- udate or oedematous transudate is not an hypertrophy, al- though such conditions have been called false or pseudo-hyper- trophy. Tumors produce an increase in the size of the struc- ture affected, but this should not be confused with hypertrophy. Hyperplasia is a condition resulting from abnormal increase in the number of the cells though it is difficult to differentiate from hypertrophy. COMPENSATORY TFYPERTROPHY is the name applied to that type of hypertrophy caused by increased functional activity. Thus an increased blood pressure maintained for some time induces compensatory hypertrophy of the heart. CONCENTRIC HYPERTROPHY is a term denoting an hypertrophy of PROGRESSIVE TISSUE CHANGES. 189 the tissues of a hollow organ, accompanied by a diminution in the lumen of the hollow organ, e. g., hypertrophy of the heart, oesophagus, intestine, or any other hollow organ in which the hypertrophied tissues occupy a portion and thus diminish the lumen of the organ. In some instances hypertrophy represents a normal, physio- logic process. The increased size of the pregnant uterus, and the enlargement of the mammae during the gestation period are examples of physiologic hypertrophy. Increased size of the heart and voluntary muscles in horses trained for racing rep- resents a physiologic hypertrophy. After the destruction of one kidney by disease or the removal of one by operation, the re- maining ‘kidney increases in size and ultimately performs the HAGEL of both, this is functional or physiologic hypertrophy and also compensatory hypertrophy. In fact practically all hy- pertrophies are physiologic, however, the hypertrophied struc- tures are abnormal, therefore the condition is pathologic. Excessive development of an entire animal 1. e., giantism is designated by some as general hypertrophy. Excessive development of a part as one foot is designated local hypertrophy. Local hypertrophy is much more common than general hypertrophy. Hypertrophy may be inherited, (natural) or acquired. Ac- quired hypertrophy may be antenatal or postnatal. : Etiology. INHERITED HYPERTROPHY.—The cause of inherited hypertrophy is unknown except that there is an inherited impulse to grow large. This type of hypertrophy is noted in giants. ANTENATAL HYPERTROPHY is ttsually the result of unequal pres- sure and amniotic adhesions. THE CAUSATIVE FACTORS OF POSTNATAL HYPERTROPHY are, Ist, in- creased nutrition, 2nd, increased function, 3d, a stimulus, prob- ably an internal secretion, that causes the affected tissue to con- sume excessive quantities of food. Two or more of these etio- logic factors are usually evident in all cases of hypertrophy. Increased nutrition—A long continued, mild arterial hypere- mia in a tissue insures increase of the nutritive supply to the affected part and such parts usually become hypertrophic. Increased function is the prime causative factor of physiologic or functional hypertrophy. Increased function is intimately associated with increased nutrition, in fact long continued in- creased function without increased nutrition is not possible. In the production of functional hypertrophy the part must be 190 VETERINARY PATHOLOGY. accustomed to the extra work gradually. An excessive amount of work, assumed at once, by any structure will produce atrophy or degeneration. Cardiac hypertrophy is invariably functional as it usually is the result of valvular defects. Hypertrophy of the involuntary muscle anterior to a stricture is also functional as it results from increased muscular action to force the contents of the intestine past the stricture. Voluntary muscular hyper- trophy is also functional. Some unknown cause is active in the production of certain hypertrophie conditions. This unknown cause is probably an internal secretion, at least this would appear to be the cause of hypertrophy of the mammae and uterus in pregnant animals. That certain internal secretions are required to sustain the nor- mal balance in the growth of tissues is evident in disease of the pituitary body which frequently results in excessive develop- ment of certain parts (acromegaly). By diminishing the external pressure, experimentally, some parts have been noted to become hypertrophic. This is because of arterial hyperemia produced by diminished pressure. Appearance. Macroscopically, hypertrophied organs or parts are larger and heavier than normal and may be regular or irregular in shape. The general appearance of hypertrophied parts otter than size is not usually sufficiently distinct to differentiate them from normal. Microscopic——Renal compensatory hypertrophy is_ charac- terized by increased length and size of the uriniferous tubules. Hypertrophy of muscular tissue is characterized by increase in the size of muscle cells. In general hypertrophied organs or parts contain an excess of parenchymatous tissue. Effects.—The effect of hypertrophy varies according to the tissue affected. There is usually an increased functional capac- ity in an hypertrophied structure. The heart musculature may become hypertrophied to such an extent that its force ruptures some important blood vessel and causes death. Increased func- fiom of hypertrophied suprarenal “bodies |= tends sto=sineresse blood pressure by the production and elimination of large quan- tities of adrenaline which causes constriction of arteries and cardiac dilation or rupture. PROGRESSIVE TISSUE CHANGES. 191 HY PERPLASIAS DEFINITION. VARIETIES. Parenchymatous. Interstitial. ETIOLOGY. APPEARANCE. Macroscopic. Microscopic. GESSUBLAPFEC LED. EFFECTS. Hyperplasia, according to the derivation of the word, is ex- cessive formation. Hyperplasia and hypertrophy are incorrectly used interchangeably by some. Hyperplasia should be used to designate the condition resulting from an abnormal increased size of a part due to an increase in the number of cells of the part. Accepting the last definition, hyperplasia may be due to an increased number of parenchymatous cells, or an increased number of interstitial cells the two types being called parenchy- matous hyperplasia and interstitial hyperplasia respectively. Parenchymatous hyperplasia and numerical hypertrophy are sometimes used synonymously. Interstitial hyperplasia is prac- tically the same as fibrous hyperplasia. Parenchymatous hyperplasia is not of common occurrence It is usually either inherited or congenital. The descended or scrotal testicle of single cryptorchids is usually enlarged because of an increased amount of parenchyma and hence is an example of parenchymatous hyperplasia. ‘e Fig. 108.—Hyperplasia Interstitial Testicular Cells. a. Interstitial hyperplastic tissue. b. Seminiferous tubules not fully developed. 192 VETERINARY PATHOLOGY. Interstitial hyperplasia is quite common as it is usually evi- dent in chronic inflammatory tissues and it is also occasionally observed in structures affected with functional fibrosis as is evi- dent in the liver of animals afflicted with disturbances of the cardiac valves. Etiology. The cause of parenchymatous hyperplasia is. unknown. Inter- stitial hyperplasia is produced by the long continued action of mild irritants or other substances that produce over stimulation. Appearance. Macroscopic—Parenchymatous hyperplastic structures are regularly or irregularly enlarged and are heavier than normal. Fig. 109.—Pen drawing of an Hyperplastic Ureter, ox, natural size. Interstitial hyperplastic parts vary in appearance according to the amount of hyperplastic fibrous tissue. The part may vary from normal to dense, hard, pale irregularly lobulated masses of fibrous tissue. Microscopic—Parenchymatous hyperplastic structures have the same appearance microscopically as sections of normal tissue. Sections of tissue affected with interstitial hyperplasia con- tain an increased quantity of fibrous tissue which may be readily PROGRESSIVE. TISSUE CHANGES, 193 recognized microscopically especially if the section is stained with hematoxylin and picro-fuchsin. Effects. A part affected skin puneadkoeiees hyperplasia will have an increased functional capacity. The effects of an increased functional capacity of a structure depends upon the part in- volved, and may or may not be injurious to the animal in which it occurs. Interstitial hyperplastic structures have an increased quantity of fibrous tissue and usually a diminished amount of parenchy- matous tissue and a diminished function. Interstitial hyper- plasia of the walls of hollow organs may cause irregularity of the lumen (intestine) and hinder passage of the organ’s con- tents. METAPLASIA. Metaplasia is the name applied to the conversion of a devel- oped or matured tissue into another closely related. Under normal conditions a matured tissue has specific cells and a char- acteristic structure. The character of a tissue may be changed by certain pathologic conditions. Metaplasia should not be con- ee fesse. a eee ee Comes Fig. 110.—¥Fibrous Tissue Ossification. a. Fibrous tissue. b. Osteoblasts. 194 VETERINARY PATHOLOGY. fused with degenerative or infective tissue changes which are observed in functional or inflammatory fibrous formation. Meta- plasia is usually concerned in the conversion of one variety of a primary tissue into another variety of the same tissue as fibrous tissue into bone and occurs in physiologic processes as well as in disease. Metaplasia occurs in scars, the conditions consisting of the replacement of fibrous tissue by osseous tissue. This type of metaplasia is also evident in bone spavin, ringbone, sidebone, as well as in scars resulting from fistulous withers, poll evil, etc. Metaplastic osseous formation was recently noted in the omen- tum of a sheep. The conversion cf lymphoid tissue into adi- pose tissue is metaplasia. The replacement or substitution oi sqnamus epithelium for cubic or columnar epithelium repre- sents a type of metaplasia. Metaplasia is of little significance except as a pathologic con- dition. CHAPTER VIII. RETROGRESSIVE TISSUE CHANGES. DEFINITION. ; ETIOLOGY. Variations in nutrition, Chemic poisons. Chemic reaction of tissue. Variations of temperature. Variations of function. VARIETIES. Atrophy. Degeneration. Infiltration. Pigmentation. Physiologic cell growth and function are dependent upon nor- mal metabolism. Retrogressive processes are those conditions in which normal cell growth and function are diminished or sus- pended. Retrogressive tissue changes are caused primarily by abnormal cell metabolism or abnormal functioning, and are accompanied by structural or chemic alteration of the cell proto- plasm or diminution in the size of the cells. Metabolic disturbances may be caused by the following: Diminished nutritive supply caused by (a) occlusion or di- minution of the calibre of nutrient vessels; (b) insufficient supply of food to the animal; (c) incomplete or lack of digestion of the ingested food; (d) failure of absorption of digested food; (e) inability of the cells to utilize digested food that has been carried to them. Nutrition may be supplied in excess of the normal requirements, thus disturbing the metabolic equilibrium. Excess nutrients may be stored within the cells or they may be converted into energy by oxidation. In the former the stored food is a mechanical hindrance to cell action and in the latter the cell is overworked in converting the food into energy. With- holding of nutrient substances from cells produces destructive metabolism and ultimately cell death. Chemical substances, 1. e., poisons exert their action on cells by combining with some of the protoplasmic constituents or by accelerating, inhibiting or suspending the action of the cell enzyms, thus interfering with metabolism. Chemtc reaction of a tissue influences the action of cel! 195 196 VETERINARY PATHOLOGY. enzyms, and hence is a factor in metabolism and in bringing about retrogressive tissue changes. Variations in temperaturs-—The various albumens of protop- lasm are coagulated at different temperatures. An increase of 3.6° F. is sufficient to coagulate one group of albumins and an increase of 9° F. is usually fatal because of the coagulation of other impor- tant albumin constituents of the cell protoplasm. Fever is invariably accompanied by coagulation of some albuminous constituents of protoplasm although it is possible that chemic substances as well as the high temperature may have some influence in this coagulation. Diminished temperature retards metabolic process- es and if tissues are exposed for a sufficient time to a low tem- perature the protoplasm dies and metabolism ceases. Diminished or increased cell functioning are factors in the causation of retrogressive changes. Diminished functioning for a considerable length of time results in atrophy and 1f function- ing of a specific part is decreased progressively through several generations there will be failure of development of that part (aplasia). Excessive functioning, to a limited extent, in a part supplied with an excess of food, produces hypertrophy. Functioning beyond the nutritive supply produces degeneration and finally destruction of the cells. Retrogressive tissue changes include atrophy, degeneration, infiltration and pigmentation. MINOLTA DEFINITION. DIFFERENTIATION. KINDS. Physiologic. Pathologic. ETIOLOGY. Physiologic. Senility. Pathologic. Disturbed nutrition. Disturbed function. Undue pressure. APPEARANCE. Macroscopic. Microscopic. WAS SOT AUB IEUBIC IL IBID, JBJRIBIEC IES), Atrophy is that condition in which there is a decrease in the size of an organ or tissue caused by a decreased size or a dimin- ished number of the composing cells. In some instance the interstitial tissue increases and replaces the atrophied cells and the affected organ does not diminish in size. The term atrophy RETROGRESSIVE TISSUE CHANGES. 197 is usually restricted to a local diminution in size, as, of an organ or part, although it has been applied to the condition resulting from a general wasting away of all the tissues of the body, i. e., emaciation. - Atrophy is differentiated from degeneration by the fact that the former is purely a diminution in the size of the part, (a result of decreased size or diminished number of the cells and without any alterations in the cell protoplasm) while the latter consists of chemical changes of the cell protoplasm and may result in in- creased or diminished size of the cells. Atrophy and degenera- tion may occur simultaneously in the same structure, the result- ing condition being known as atrophic-degeneration or degenera- tive-atrophy. Hypoplasia is an underdevelopment in contradis- tinction to atrophy, which is diminution in the size after the part has been developed. Atrophy may be physiologic or pathologic. PHYSIOLOGIC ATROPHY is a term used to designate the normal diminution in the size of an organ or part. This occurs in the thymus gland which is well developed at the time of birth. Soon after this it begins to diminish in size and is practically extinct by the time the animal matures. The mammary gland atrophies after lactation ceases. Testicles and ovaries atrophy after the period of reproduction or sexual activity. Senile atrophy is a term employed to designate all atrophic conditions occurring in the tissues of old or aged animals. Senile atrophy is a physio- logic process. PATHOLOGIC ATROPHY is a term used to designate abnormal diminution in the size of an organ or part. Pathologic atrophic disturbances involve muscular, glandular and nervous tissue although no tissue is exempt. This type of atrophy is of fre- quent occurrence, viz., diminution of muscle cells in lameness, sweeney, etc., diminution in the size of the liver in hepatic atrophy, renal, cardiac, splenic and gastric atrophy. Etiology.—Pathologic atrophy may be the result of either disturbed nutrition or disturbed function. Disturbed Nuirition.—Atrophic disturbances resulting from mal-nutrition are most frequently the result of insufficient food. Cells receiving insufficient food gradually shrink in size, possi- bly because of auto-digestion. Insufficient nutritive supply may be due to a diminished quantity of blood or an impoverished blood. Diminished quantity of blood, i. e., a local anemia, is a result of diminishing the calibre or obstructing the supplying vessels. Thrombic formation, aneurisms, etc., may cause partial or even 198 VETERINARY PATHOLOGY. complete obstruction of nutritive vessels and thus be a causative factor in atrophy. Starvation, or failure, of assimilation of food is a cause of atrophy (general). However, in such cases atro- phic degeneration of the cells is usually evident by the time the body weight has diminished */,, of the total weight | @enmius chemic substances may indirectly be of significance in the pro- duction of atrophy, but they influence either the cell nutrition or function. . Excess nutrition may induce metabolic disturbances of suffi- cient gravity to cause the cells to become sluggish and more or less inactive to such an extent that they will become atrophied. However, excess food is a much less frequent cause of atrophy. than insufficient food. | 3 Disturbed function.—Diminished or excessive functioning are causative factors in producing atrophy, the former being the most frequent cause. Tissues deprived of function usually be- come more or less atrophied. When an afferent nerve fibre is disconnected from its end organ, (the mechanism by which it picks up impressions), it begins to atrophy at once, probably because of its failure to function. Muscles not functioning atrophy. Thus there is muscular atrophy during most cases of lameness. Diminished cardiac function resulting from dimin- ished blood pressure, is succeeded by atrophy of the heart muscle. Glandular structures become atrephied because of disuse. Excessive functioning, long continued, causes fatigue and in some instances paralysis, the latter usually being succeeded by atrophy. Atrophy from excess function is sometimes observed in race horses, show animals and is not uncommon in musicians, acrobats, trapeze operators, etc. _ Pressure—Aside from the influence of the vaso-motor mech- anism there may be sufficient pressure from tumors, hyperplas- tic formations, mechanical contrivances, as harness, etc., to dim- inish or obstruct vessels and cause atrophy. Pressure may also exert influence other than diminishing the blood supply, for con- stant pressure alone causes atrophy, e. g. pressure atrophy of osseous tissue. Pressure atrophy, accompanying cirrhosis of glandular structures as the liver or kidney, is usually caused by pressure of the newly formed fibrous tissue which partially ob- structs the nutrient vessels. However, the compression of the parenchymatous cells disturbes their metabolic equilibrium and is also aeiactOr OlesOmie iniportance: Appearance. Macroscopic. Atrophied organs are usually di- minished in size, are irregular or regular in shape, have a dry shrunken anemic appearance and are usually pigmented. The RETROGRESSIVE TISSUE CHANGES. 1s parenchymatous tissue is most frequently involved, interstitial tissue rarely becoming atrophied. The diminution in size may be uniform throughout, the atrophied part thus retaining its nor- mal shape, or the diminution may be unequal in different parts, thus producing a lobulation of the affected portion. Atrophied bone usually maintains its normal external shape, as the process is-essentially a rarefication in which the Haversian and medul- lary canals are increased in size. Pulmonary atrophy may con- sist of diminution of the alveolar membranes to such an extent that they rupture, thus produciing large cavities. Atrophic mus- cular tissue is usually more intensely pigmented than normal muscle. The source of the excess pigment in atrophic muscles may be from the atrophied muscle cells or it may have its origin _ from the blood. Microscopic—TVhe cell body and nucleus shrink in size in simple atrophy without previous alteration in the cell structure. In numerical atrophy the cells first diminish in size and then dis- integrate and die. Thus atrophy, disintegration and necrosis are evident in numerical atrophy. The appearance of atrophic tis- sues vary according to the structures involved. Atrophic kidney tissue is characterized by the diminution in the size or in the number of the glomerular and tubular cells. The tubules and _glomeruli may collapse the supplying capillaries becoming oblit- erated by pressure of the hyperplastic fibrous tissue. In muscu- lar atrophy, the muscle cells diminish in size probably because some of the fibrillae disappear. Effects.— The effect of atrophy depends upon the structure involved the extent of the condition and the age of the animal. If the involved structure is not vital and the atrophy is of only slight extent and in a young animal, in which the regenerative power is good, the part will recover if the cause is removed. Extensive atrophy of vital structures in old animals is usually fatal or at least predisposes to other conditions that are fatal. Again, a part may partially recover after atrophic disturbances. 200 VETERINARY PATHOLOGY. CLOUDY SWELLING. DEFINITION. OCCURRENCE. PATOL OGE Chemic. Bacterial products. Phosphorous, Arsenic, etc. Thermic. APPEARANCE. Macroscopic. Microscopic. TES SOI, AUREUS 1185). Epithelium. Muscle. Nerve. IM HEG ILS. Cloudy swelling, albuminous, granular or parenchymatous degeneration is a retrograde metamorphosis in which the proto- plasm of the cell becomes granular. The granules in cells affected with cloudy swelling are albuminous, at any rate they are solu- ble in an excess of a 2% solution of acetic acid or a 1% solution of potassium hydroxide, and give the typical albumin reaction to the xanthoprotein test. Active glandular cells, especially those that produce ferments, are normally granular; but the granules in these cells do not respond to the foregoing tests and hence are not albuminous. Cells in the earlier stage of fatty degeneration are granular but the granules are not dissolved by solution of acetic acid or potassium hydroxide, and they are dissolved by ether or chloroform and are stained red with Sudan III. There- fore they are fat granules. Cloudy swelling probably occurs more frequently than any other retrogressive change. It invariably affects parenchymatous cells in areas afflicted with acute inflammation and is usually associated with infective diseases. Etiology.—The causes of cloudy swelling may be divided in- to two groups, Chemic and Thermic. Chenuic substances produce cloudy swelling either by influ- encing the action of cell enzyms, thus causing the separation (coagulation) of the cell albumins, or by combination with the albumins of the cell protoplasm thus forming new compounds - (albuminate of mercury, etc.) that are of no value to the cell. Excessive quantities of albuminous substances may be assimi- lated by the cells, the unused portion becoming coagulated or rendered insoluble as it accummulates, thus producing cloudy swelling. The chemic substances that produce cloudy swelling are usually soluble and are in solution in the blood or lymph from which they readily diffuse into the cell body where they exert their action. RETROGRESSIVE TISSUE CHANGES. =01 Of the chemic substances capable of producing cloudy swell- ing bacterial products are the most important. The diphtheria toxin is probably the most active of all bacterial products in the production of cloudy swelling. Other organic substances as leu- comains and phenol are capable of producing this degeneration as well as many inorganic substances as arsenic, mercury, phos- phorous and the mineral acids. Thermuic disturbances, especially high temperature, is prob- ably a cause of cloudy swelling. Halliburton has demonstrated that certain high temperatures produce turbidity or granular degeneration of cells. From experimental evidence it is appar- ent that different groups of the albumins of the cell protoplasm are separated (coagulated) at different temperatures. The high- er the temperature the more fixed the coagula and the more dificult they are of solution. From the present known facts, although the chemistry is not determined, it is evident that high Fig. 111.—Cloudy Swelling, showing granular degeneration of kidney cells. 202 VETERINARY PATHOLOGY. temperature is at least a predisposing if not an exciae cause of cloudy swelling. Appearance.—Macroscopic.—An organ or part affected with cloudy swelling, has a parboiled appearance, it is lusterless and lighter in color, softer in consistency, and is slightly enlarged. Microscopic-—An organ or part affected with cloudy swelling appear cloudy, because of the presence of many small albuminous granules, and the cells are slightly enlarged, hence the name cloudy swelling. The increased size of the cell results from co- agulation, the coagula occupying more space than the non-coag- ulated protoplasm. If the tissues of an organ are examined with the high power microscope the cell may appear slightly swollen and its limiting membrane quite distinct ; it may be considerably swollen and have an indistinct membrane; or, finally, it may have ruptured and the space it previously occupied may contain a mass of granular debris. The protoplasm of the cell body may con- tain small, irregular granules, the nucleus may be almost normal, slightly degenerated, or it may even be entirely disintegrated. Tissues Affected.—Epithelium, muscular, nervous, and con- nective tissue are affected with cloudy swelling, the frequency being in the order mentioned. Cells of excretory organs are especially affected because of their eliminative function. Effects.—The effects of cloudy swelling depend upon the structure involved, the extent of the involvment, and the age of the affected animal. Affected muscular tissue has a diminished contractile power. Renal tubules may be occluded because of the swollen tubular cells and the affected cells may also have a diminished functional capacity. The function of any structure is decreased and in extreme cases inhibited by cloudy swelling of its component cells. Cloudy swelling is usually a repairable process, providing the cause is removed before the cells are destroyed. RETROGRESSIVE TISSUE CHANGES. 203 PAL DY CE ANGES: PHYSIOLOGIC (Fatty Infiltration). DEFINITION. ETIOLOGY. Excess food. Insufficient exercise. Heredity. Influence of disease. Unsexing. Lactation. V enesection. APPEARANCE. Macroscopic—Greasy, pale color. Microscopic—Droplets of fat between cells. RES SOE: Ar EECELED: Normal depositions. Epithelium, muscle. EFFECTS. PATHOLOGIC (Fatty Degeneration). DEFINITION. ELTOLOGY: Insufficient food. Inability of cells to utilize food. Excessive activity. APPEARANCE. Macroscopic—Greasy, pale, light. Microscopic—Droplets of fat in cells. ISSUE SAP PECTED: Epithelium. Muscle. Nerve. EPRECTS. Adipose tissue is not a specific tissue, but represents a modi- fied connective tissue. The cells that later become fat cells, are originally flat or spindle shaped and usually occur in clusters or eroups. There are certain locations, called fat depositories. where fat usually occurs. Normally the principal fat depositories are located in relation to the kidney capsule, subserosa (parietal, visceral and omental peritoneum), subcutem, intermuscular areo- lar tissue, and in the orbital fossa. A well fattened animal has accumulations of fat in all the fat depositories. In an emaciated animal limited quantities of fat occur only around the kidney in the omentum, and orbital fossa. Normal adipose tissue varies in color and consistency in the different animals. In general it is white or yellow and appears lobulated when cut across. The consistency depends upon the melting point of the fat. Olein is the principal kind of fat in the hog, stearin and pal- mitin in the ox, and stearin in the sheep. It has been demon- 204 VETERINARY PATHOLOGY. strated, however, by Prof. Hopkins, of the University of Illi- nois, that the body fat is the same as the ingested fat. (Hogs were fed on cotton seed oil and the presence of the same kind of fat was demonstrated in the hog tissue.) It has also been found that butter fat in cow’s milk is the same as ingested fat. Opinions are at variance in reference to the digestion and assim- ilation of fat. The fat splitting enzyms convert the fats into fatty acids and glycerine. ‘The alkali present in the intestines unites with a part of the fatty acid, forming soap, the latter and the glycerine pass by osmosis into the intestinal epithelium or through the mucous membrane where the glycerine is substituted for the alkali, the alkali passing back into the intestinal lumen to form more soap (Hammersten). Some of the fat may be so finely emulsified that it passes directly into and through the in- testinal epithelium, and some of it may be incorporated by leu- cocytes, and thus carried from the lumen of the intestine to the lacteals (Howell). Fat droplets are present in the circulating blood. The exact manner of the production of fat cells in normal . adipose tissue has not been determined. All normal animal tissues contain varying quantities of neu- tral fat. As much as 23 per cent of fat has been extracted irom kidney tissue (Adami). The proportion of neutral fat in the same kind of tissue varies in the same animal under different conditions and in animals of different species under the same conditions. Thus the quantity of fat in the muscular tissue of an emaciated animal is less than in an animal in good flesh. The muscular tissue of the hog contains more fat than the muscular tissue of the ox, sheep, horse or dog. In fact the presence of fat droplets betwen the muscle cells is a distinguishing characteris- tic of porcine muscular tissue. There is no definite limit to the quantity of fat normally contained in the tissues of any animal. Certain abnormal fatty changes occurring in the various tis- sues have been described as fatty infiltration and fatty degen- eration. These changes, although originally thought to be en- tirely distinct, are closely related and may represent different stages of the same process. These fatty changes may be dis- cussed as phvsiologic fatty changes (fatty infiltration), and path- ologic fatty changes (fatty degeneration), although there is na good reason for the division of the subject other than to recog- nize the previous classification and prevent undue confusion. RETROGRESSIVE TISSUE CHANGES. Z03 Physiologic Fatty Changes. (Fatty Infiltration.) Physiologic fatty changes is a condition in which there is an excessive accumulation of fat, but the function of the affected part is not materially changed. Etiology. E«cess Food.—House dogs and cats and many family horses are usually fed to excess, resulting in the deposition of exces- sive quantities of fat in practically all tissues, thus producing general obesity. The “Strassburg goose” is force-fed with dough balls in excessive quantities until excessive obesity is produced, the liver especially becoming the seat of marked fatty accumulations. In fact all prime “butcher stuff” is affected with physiologic fatty changes or dietary obesity. Insufficient Exercise—Animals kept in tie stalls or in close quarters have a tendency to become excessively fat, especially if they are fed a full ration, because there is diminished oxidation on account of lack of exercise and the bulk of the consumed food is stored as fat. | V cnesection.—Frequent bleeding diminishes the percentage of red blood corpuscles and thus indirectiy diminished oxidation and favors fat accumulation. Disease-—Some diseases appear to influence the physiologic deposition of fat. The early stages of tuberculosis in cattle and hogs and distomatosis in sheep is accompanied by physiologic fatty deposition. During convalescence from some diseases there is an increased deposition of fat. Lactation.—The early period of lactation is accompanied by fatty accumulation especially in the liver. (Possibly the liver may act as a distributing center of fat.) The fatty accumulation in the liver is evident regardless of any variations in the composi- tion of food stuff. Heredity —Some animals, especially hogs, except the Tamworths and Yorkshires, appear to have an inherent tendency to become excessively fat. Castration.—Removal of the genital glands favors fat accumula- tion in the tissues. Castrated dogs and cats, especially if cas- trated when mature, become obese. In general the exciting causes of physiologic fatty changes are excess of food or diminished oxidation, heredity being a pre- disposing factor. VETERINARY PATHOLOGY: IQ © Or Appearance.—Macroscopic.—Vissues affected with fatty infil- tration are greasy or oily, more friable than normal, and paler in color, the color being uniform throughout or mottled. The quan- tity of blood in the fat varies, there being more, in general, in the fat of young animals. Muscular tissue in which there is a fatty accumulation contains areas or strata of fat and strata_of muscular tissue. The deposition cf fat may be so extensive in muscular tissue of hogs that there is little evidence of muscle. Subserous accumulations of fat may be localized, giving the ap- pearance of masses of fat, or it may be accumulated diffusely as thick lavers of fat. In dogs and cats the excess fat is usually deposited around the kidneys. Microscopic.—In the early stages of physiologic fatty changes, small droplets of fat are observed between and within the cells. The intracellular fat gradually increases and assumes the space within the cell, the nucleus being crowded to the margin of the cell and may ultimately disappeer. wy ) “it eile ry aN o lem Fig. 112.—¥Fatty Infiltration, liver, hog, showing infiltration of globules from periphery of lobule toward its center. Tissue Affected.—All tissues are subject to fatty accumula- tions, excepting the normal depositories, the liver being most prone to the affection. Effects.—The influence of physiologic fatty changes is de- pendent upon the extent of the condition and the duration of RETROGRESSIVE V©ISSUE CHANGES. 207, ime process. li the nuclei of the cells, are not injured and the process is discontinued the infiltrated fat is disposed of and the part recovers. If non-regenerative cells, such as heart muscle, are destroyed, they will not be regenerated, even though the fat is reabsorbed. The destroyed heart muscle cells may be replaced with fibrous tissue. Pathologic Fatty Changes. (Fatty Degeneration.) Pathologic fatty change, or fatty degeneration, is a condition in which the protoplasm of the affected cells diminishes because of an increase of the intracellular fat. Fat or some of its cleav- age constituents is probably constantly present in varying quan- tities in all active cells. Pathologic fatty changes are of frequent occurrence, being associated with diseases of malnutrition, and occurring in acute febrile diseases and many of the infective diseases. [t is espe- cially evident in chronic phosphorous poisoning and some other chemically induced diseases. — Pathologic fatty change is differentiated from cloudy swelling as follows: The droplets of fat are soluble in ether and chloro- form and are not dissolved with dilute acetic acid or potassium hydroxide ; while the granules in cloudy swelling are insoluble in ether and chloroform, but are soluble in dilute acetic acid or po- tassium hydroxide. Again the fat droplets are stained red by Sudan III, while the granules of cloudy swelling are not. Fatty degeneration is difficult to differentiate from fatty infil- tration, and in some instances it is impossible to differentiate them; in fact, future investigation may confirm the identity of the two processes. In the early stages the fat droplets are usu- ally intracellular in fatty degeneration, and intercellular in fatty infiltration. Etiology.—In general, fatty degeneration is the result of the disturbance of cell metabolism. The production of energy, be- ing intimately associated with the metabolism of fat, becomes a factor in the causation of fatty degeneration. Specifically, disturbed nutrition is the principal cause of fatty degeneration. Disturbed nutrition may be the result of, Ist, variation in the composition of the blood, 2nd, diminished quantity of blood, 3rd. diminished oxygen supply, and 4th, changed environments of the cells. Insufficient supply of cell nutriment is the principal in- 208 VETERINARY PATHOLOGY. fluence resulting from circulatory disturbances or altered com- position of blood. Diminished oxygen supply results in incom- plete oxidation of the available intracellular fat which is then accumulated within the cell. Changed environments include the variation of the chemic reaction of a tissue, the tissue tempera- ture, amount of fluid, etc. Disturbance of the environments in- fluences the cell metabolism and may cause the union of cleav- age products of fat that exist within the cell, or the infiltration and intracellular accumulation of fat may be favored. Changed environments may also render the cells unable to utilize the food brought to them. The causes of cloudy swelling are also etiological factors in the production of fatty degeneration, in fact, fatty degeneration is frequently associated with cloudy swelling and the fatty de- generation is the result of disturbed metabolism. Disturbed metabolism is produced by insufficient or improper food, dimin- ished supply of oxygen, or inability of the cells to utilize the food or oxygen supplied, the inability of utilization being a re- sult of the damaging influence of chemic or thermic variation of the environments of the cells. Appearance.—Vacroscopic.—A tissue affected with fatty de- generation varies in appearance according to the extent of the process. In general, affected tissues are paler in color (change in color is frequently in patches which appear yellowish), lighter in weight (in extreme case, liver tissue affected with fatty de- generation, floats in water), greasy or oily in appearance, (a knife blade that had been used in sectioning a fatty tissue 1s usually smeared with drops of oil or fat), and usually swollen or enlarged in the early stages, succeeded by diminution in size as the fat is resorbed. Tissues affected with fatty degeneration are less elastic, and more friable. Microscopic.—In the very early stages the cells contain small granules that are differentiated from the granules of cloudy swelling only by the chemic test referred to above or by special stains,as Sudan III. As the degeneration progresses, the minute fat droplets coalesce, forming drops sufficiently large to be rec- ognized microscopically, as small, clear spots or holes in the cell protoplasm in sections of tissue fixed in fluids that are sol- vents for fats and as fat drops in fresh tissues. The affected cells are swollen to an extent which is proportional to the degree of the degeneration. Ultimately the cell membrane ruptures and the enclosed fat is liberated, thus producing a condition not RETROGRESSIVE TISSUE CHANGES. 209 differentiable from fatty infiltration. The nucleus is usually not involved in the beginning, but as the degeneration progresses in the cytoplasm, the chromatin network disappears and the entire nuclear structure finally becomes disintegrated, producing the so-called granule cell. The degeneration may be continuous throughout a tissue or it may be more or less patchy. The ex- tent of involvement of the cells in an affected area is usually unequal, some cells being only slightly affected, others contain- ing considerable fat, and still others being entirely converted into fat. Fig. 113.—Fatty Degeneration of the Liver, showing the early stage of the process around the central vein. Tissue Affected—Glandular tissue, particularly the liver, is probably most prone to become affected with pathologic fatty changes, or fatty degeneration. Muscular tissue is quite subject to fatty degeneration, especially heart muscle. Epithelium other than glandular, nervous and connective tissues, are not exempt from this process. Tumors are occasionally observed to be affected with pathologic fatty changes. Necrotic tissue fre- quently becomes a fatty mass or an entire cadaver may be con- eZ) VEPERINARY, PADRE OEROG YS. verted into a fatty mass termed adipocere, which is no doubt the result of ferments liberated from the dead tissue. Effects.—The conversion of the cell protoplasm into fat im- pairs the cell function. At least diminished cell action, as well as disturbed cell metabolism is evident in cells affected with pathologic fatty change. In cells slightly affected, the droplets are either oxidized or are extruded from the cell (absorbed when the cause is removed). Cells more extensively affected may be destroyed, leaving a meshwork of vessels and fibrous tissue. The area may later be filled with the new parenchymatous cells arising from the surrounding less affected zones, and, like those destroyed, it may persist as a mass of fibrous tissue, 1. e., a scar. If regeneration occurs there must be an adequate blood supply. The degenerated cells may become caseated as a result of the conversion of the fatty material into a cheese ike mass. The usual cause of caseation of fatty debris is diminished or obstructed blood supply resulting in gradual absorption of the fluids, saponification of the fats and in some instances the forma- tion of cholesterin. Caseated material derived from the fatty debris may later be liquified or calcified. ANY EOD CHANGES: DENTON EMOTO GY APPEARANCE. Macroscopic. Microscopic. TISSUE AFFECTED—Subendothelium, IBIBO IPS. Some masses may be found in the acini of the prostate gland, especially in old dogs and aged humans, that respond to the iodine test and are considered by some authorities as amyloid bodies. Physiologic amyloid formations have not been observed other than in the prostate gland and they probably have a pathologic origin. Thus a physiologic prototype of amyloid formation 1s unknown. : Amyloid substance (amylin) is an albuminoid, insoluble in water, alcohol, ether, chloroform, xylol, dilute acids or alkalies and is not acted upon by pepsin. When tissue containing amy- loid substances is immersed in Lugol’s solution the amyloid areas assume a mahogany brown color and the normal tissue is stained a yellowish brown. (To make this test wash the affected tissue thoroughly until all blood has been removed, apply a lib- RETROGRESSIVE TISSUE CHANGES. CA | eral quantity of Lugol’s solution for one or two minutes, wash the excess of the reagent off and the above color reaction will be observed). The test is equally applicable to macroscopic and microscopic sections. If the sections, macroscopic or micro- scopic, are immersed in dilute sulphuric acid, after the application of Lugol’s solution, the amyloid area will assume a blue color, the normal tissue a brown color. The analine dyes usually stain amyloid substances some shade of red. The source of amylin is not definitely known. It may be derived from the blood or from tissue cells. The formation of amylin may depend upon variations in the percentage of some chemic substance in the blood or tissue juices. Amyloid formation is not common in the domestic animals. Occasionally a dog is observed that is affected with amyloid ac- cumulations in the prostate gland. One case has been observed in a hog in which the liver was affected, and, excepting this, the carcass showed evidence of no other lesions. Etiology.— The cause of amyloid change is not known, al- though it has been assumed by some pathologists to be associ- ated with chronic suppurative conditions, as, tuberculosis, and other chronic debilitating diseases, as carcinomatosis. The tissues from several animals affected with chronic suppurative processes, as fistulous withers, poll evil, quittor, tuberculosis, glanders, casecus-ivmphadenitis, as well as tissue from animals affected with tumors have been examined, but amyloid changes have not been found. Increased or diminished quantity of some of the salts of the blood may be found to be an etiologic factor in amyloid changes. Appearance.— Macroscopic— Affected tissues or organs are larger, paler, and firmer than normal. The amyloid areas are homogeneous and translucent in appearance. The entire organ or tissue appears homogeneous when the amylaceous material is diffuse. Microscopic—Amyloid substance is deposited in the frame- work beneath the endothelial cells lining the blood vessels. It appears as an annular homogeneous mass encircling the vessel. The amyloid substance may accumulate to such an extent that the vessel is obstructed. After the capillaries have been gorged beyond their resistance they rupture, thus allowing the amyloid substance to permeate the interstitial spaces where it appears microscopically as irregular homogeneous masses. Tissue Affected.—The blood-vascular subendothelial con- nective tissue is the principal location of amyloid formation, although it may occur in lymph vessels and even the perimysium Zee VETERINARY PATHOLOGY. and endomysium may be affected as well as the stroma of the mucous membranes. The liver, spleen, and kidney are the most frequent locations of the process, probably because of the large number of capillaries in those organs. _ Fig. 114.—Amyloid Denegeration, Liver. a. Liver cells. b. Amyloid material. Effects——The condition is so rare that it is not possible to generalize upon the effects of the process. The amylaceous ma- terial is insoluble in the body fluids and it is quite probable that if a part becomes affected, it remains so permanently. HY ALINE CHANGES. DEFINITION. ERIOLOGY: APPEARANCE. Macroscopic. Microscopic. TISSUE AFFECTED. Vessels, Muscles. PPE CIS: This is a pathologic condition characterized by the conversion of the cell substance into a homogeneous material called hyaline. In the phenomena accompanying the physiologic changes of the corpus luteum of pregnancy, a hyaline substance is produced. The physiologic formation of hyalin, aside from that produced in the corpus luteum of pregnancy, has not been recorded. The formation of hyalin is quite common in the muscular RETROGRESSIVE TISSUE CHANGES. 213 portion of the blood vessels of tissues affected with chronic in- flammation and in the blood vessels of sarcomata. It has also been observed in voluntary and heart muscle in certain diseased processes. Hyalin, an albuminous substance very similar to amylin, does not respond to the iodine test, and is not acted upon by alcohol, ether, chloroform, acids, ammonia, or water. Acid stains, as eosin and acid fuchsin, have an affinity for hyalin and stain it quite intensely. Etiology.—The specific cause of hyaline formation is not definitely known. Certain predisposing factors, however, are of interest. Wells found that lactic acid injected into voluntary muscle was succeeded by hyaline formation, and it may be as- sumed that the cause of hyaline changes in voluntary muscle is excess of sarcolatic acid. Some diseased processes, as chronic inflammation, tuberculosis, and sarcomatosis are accompanied by conditions that tavor hyaline formation. Fig. 115.—Hyaline Denegration, Vessels. a. Hyaline around arteries-in maxilla of colt. Appearance.— Macroscopic.—Rarely does this condition be- come sufficiently marked to be recognized with the unaided eye. The hyaline substance appears as a translucent, homogen- eous, firm mass, intermingled with the normal tissue. Microscopic.—The hyaline substance appears as glassy areas, and the adjacent tissue frequently becomes less distinct. Except for the affinity of hyaline substances for acid stains and its fail- 214 VETERINARY PATHOLOGY. ure to react to iodine it is difficult to differentiate from amyloid change. Tissues Affected.—Muscular tissue, involuntary muscle, especially of the blood vessels, voluntary muscle and heart mus- cle are subject to hyaline,changes. Connective tissue is less fre- quently involved and epithelium rarely, if ever. Effects—When hyaline has been formed in small quanti- ties and the cause is removed the hyaline substance is resorbed and the affected cells repaired. If the production of hyalin has replaced the protoplasm of large cell masses, especially of mus- cular cells, the area will probably not be repaired with muscular tissue, though it may be with fibrous tissue, provided the cause is removed, MUCOED CHANGES: Physiologic. DEFINITION. ETIOLOGY—Physiologic, pathologic. AIP IE 1B AUR AUN C12, Macroscopic. Microscopic. TISSUE AFFECTED—Connective, epithelium. IBJNRAEIE ICS. The transformation of cell protoplasm into mucus is evident in the physiologic production of mucus in the surface epithelium of mucous membranes as well as in mucous glands. The physi- ologic conversion of protoplasm into mucus is the result of in- tracellular enzyms, or at least depends upon protoplasmic activy- ity. As the mucus is produced the cell becomes enlarged and ultimately ruptures, discharging the mucus. The mucus may be formed only in the distal end of the cell or it may entirely re- place the protoplasm of the cell. In the former the remaining protoplasm of the cell regenerates the portion destroyed. In the latter the adjacent cell multiplies, thus filling the gap. Mucus is a viscid, glairy stringy nitrogenous fluid. The principal ingredient of mucus is mucin, a glucoproteid, although there may also be present pseudomucins. Mucin imbibes water. thus becoming swollen, and from this swollen mass there is pre- cipitated a stringy material by addition of alcohol or dilute acetic acid. Pseudomucin forms a gelatinous mass when dissolved in water, but by the addition of alcohol to this gelatinous mass a stringy precipitate is formed which is redissolved in excess of water, differing in this respect from mucin. 1 RETROGRESSIVE TISSUE CHANGES. ZA Pathologic. Pathologic mucoid formation affects cells and intercellular substance. Cellular pathologic mucoid change is identical to normal mucus formation except that it is in abnormal locations or is in excess in those locations in which mucus is normally produced. Intercellular mucoid formation is a condition result- ing from the conversion of intercellular substances—fibres, matrix of cartilage and bone—into mucus. Pathologic mucoid changes occur rather frequently. It is evident in catarrhal in- flammation, in cyst formations and as a retrogressive process in many tumors. Etiology.—The cause of pathologic mucoid changes is not known. Excessive cellular mucoid formation accompanies mild inflammatory disturbances of mucous membranes—so calied catatrh. The increased producticn of mucus in catarrhal inflam- mation may be the expression resulting from the exaggerated function of the mucous membrane induced by the excessive quantity of blood supplied. Intercellular mucus formation may result from improper nutrition or injurious influences induced by chemic substances. It has long been thought, although it has never been proven, that some product is evolved when the thyroid gland is dis- eased that causes a mucus degeneration of all fibrous tissue in the body (myxoedema). Some sarcomata and carcinomata are affected with mucoid changes, probably the result of chemic sub- stances elaborated by the tumor cells. Appearance.—Macroscopic.—Mucus of pathologic origin is not differentiable from physiologic mucus. In pathologic conditions accompanied by mucus formation the mucus is frequently mixed with other substances, as blood, pus and food stuff. Thus the mixture assumes various appearances. A discharge composed of mucus and pus (muco-purulent) 1s common in practically all catarrhal inflammation, being the characteristic discharge of catarrhal pneumonia and is the usual discharge from the respira- tory tract and conjunctiva, in dogs affected with distemper, in horses afflicted with “stock yard fever,” etc. The appearance of a tissue affected with pathologic mucus changes, regardless of whether the cells or intercellular sub- stance is involved, depends upon the quantity of mucus pro- duced. If there is a limited quantity of mucus and it is equally distributed throughout, the affected tissue will appear swollen and soft. If more extensive and diffuse the affected tissue will be soft, spongy, and slimy. If the entire structure has practically been converted into a mass of mucus, it will appear as a slimy, Zi6 VETERINARY PATHOLOGY. stringy, pulpy substance from which varying quantities of mucus may be expressed. The mucoid changes may affect circumscribed local areas that appear moist and soft, spongy, or even cystic in contradistinction to the surrounding normal tissue. - Microscopic-—Mucus appears as a stringy substance containing varying quantities of detritus. Fixing agents coagulate mucin in which case it appears as a more or less homogeneous mass containing many fibrillae or threads of coagulated material. Fig. 116.—Mucoid Degeneration. a. Fibrous tissue. e. Mucoid cells. b. Mucous substance. Microscopic appearance of a tissue affected with pathologic mucoid changes is variable according to the extent of the pro- cess but in general the picture observed is the same as that of the normal tissue plus the mucus. Tissue Affected.—Epithelium and the cells and intercellular substance of connective tissue as well as some tumors are sub- ject to mucoid changes. Effects.—The effects depend upon the extent, duration, and regenerative ability of the affected tissue. RETROGRESSIVE TISSUE CHANGES. 217 COLLOID-CHANGES: DEFINITION. ETIOLOGY—Unknown. APPEARANCE. Macroscopic. Microscopic. DISSUE APFEGCTED. Thyroid, prostate, tumors. EFFECTS. The term “Colloid” has rather an indefinite meaning and by present day writers is used to indicate a variety of substances. “The word colloid is merely morphologically and macroscop- ically descriptive of certain prcducts of cell activity or disinte- gration, which have nothing in common except the fact that they form a thick glue like or gelatinous, often brownish or yellow- ish substance” (Wells). One type of colloid substance is a physiologic product of the thyroid gland, it is in part a secre- tion of the thyroid cells and in part a conversion of those cells into colloid material. This product is normally absorbed as it is produced though it may accummulate in small quantities in the gland acini, especially in aged animals. Chemically the physiologic thyroid colloid is composed of iodo-thvreoglobulin (a compound of globulin and thyroidin). Thyroid colloid is glue like in consistency and varies in color trom brown to yellow. Colloid and mucous are closely related. Colloid does not increase in bulk when it is suspended in water, neither is it precipitated by alcohol or acetic acid—two tests that are usually sufficient for differentiation of mucus and colloid. Pseudo-mucin is more difficult to differentiate from colloid. The latter, however, contains iodine and the former does not. Pathologic colloid changes are conditions resulting from the excessive production and retention of collagenous material. The disturbance induced by excessive colloid accummulation is usu- ally not serious although it may cause fatal termination. This condition occurs more frequently in old dogs than in other ani- mals. Sheep occasionally show lesions of this condition, in some instances the entire flock becoming affected. Pathologic colloid accummulation is a constant lesion in the thyroid gland of animals suffering from exophthalmic goitre. Colloid changes have been observed in cattle, sheep, horses, mules and one case has been recently noted in a calf. Etiology.—The specific exciting cause of pathologic colloid changes is not known but undue exposure to inclement weather is a predisposing cause of considerable moment. Exposure, in some instances, appears to become an exciting cause of thyroid 218 VETERINARY PATHOLOGY. colloid accummulation. A flock of 128 healthy, yearling sheep shipped from south central New Mexico to the Kausas City stock yards, were all found to have enlarged thyroid giands at the time of slaughter, which was about 24 hours after their arrival at the stock yards. The thyroid glands were found on micro- scropic examination to be affected with pathologic colloid accum- ulation. This occurred in April, the sheep, having been sheared just previous to shipment, and the weather having been very inclement during the entire time that they were in transit. Other entire flocks of sheep that have been unduly exposed have been affected in a like manner: Fig. 117.—EFhotograph of a thyroid gland affected with Colloid Degeneration, Endemic goitre in the human is indicative of an infectious: cause though the individual cases in non-affected areas ae the infection theory. The absence or diminished quantity of iodine in the ieee water or air, may be a causative factor in the production of goitre and other colloid accummulations in the thyroid glands. Appearance.— Macroscopic.—Colloid most frequently oc- curs in masses, varying in size from mere microscopic points. to bodies as large as a lead pencil rubber or even cyst like bod-- RETROGRESSIVE TISSUE CHANGES. 219 ies as large as a black walnut. More rarely the colloid material may have infiltrated the tissue spaces and become diffuse. Col- loid varies in consistency from a watery to a jelly like mass, is usually of a clear amber color, although it may be translucent or of a deep mahogany tint. | An affected tissue contains variable sized areas oj hyaline, rather firm, amber or mahogany colored masses deposited ir- regularly throughout the entire structure. Microscopic—tThe cells are noted to contain small droplets of colloid material which is constantly produced and passed out of the cells and accumulated in the acini, tubules, or intercellu- lanyspaces. Other entire cells are -converted’-into- a colloid Fig. 118.—Colloid Degeneration, Thyroid Gland. a. Colloid material completely filling the acini of gland. mass. ‘The conversion of a large number of cells into colloid material in one vicinity produces colloid masses or the so-called colloid cysts. Colloid substance is homogeneous or slightly gran- ular and is stained, by acid stains. It assumes an orange color when stained according to Van Giesen’s method. Tissue Affected.—Epithelium is probably the only tissue in which colloid formation occurs. The thyroid gland is most commonly affected. There is a degenerative change occurring in carcinomata that is similar to the colloid formation although it may be pseudomucin formation. McFarland states that col- loid casts occur in the uriniferous tubules, in kidneys affected with chronic inflammation. Ziegler regards the prostatic con- cretions, of the human, that do not react to iodine, as colloid. 220 VETERINARY PATHOLOGY. Effects.—The effects of colloid accumulation depend upon the extent of it. The exact function of the thyroid gland has not been determined but it is quite certain that the iodine compound, iodothyrein or thyroiodin is the active principle of the thyroid secretion. It is not known whether the thyroid secretion has some action pon cell metabolism or neutralizes various poison- ous substances that result from metabolism or poisons intro- duced into the body from without. The colloid accummulations in goitre contain less iodine per given volume than the normal secretion, but the total quantity of iodine is materially increased resulting in circulatory disturbances, as rapid weak pulse, in- creased metabolic activity especially of proteids, ancreased secre- tions, irritability, etc. Diminished iodine production, as ob- served in myxoedema, is not common in colloid accummulation. SEROUS INFILTRATION. DEFINITION. ETIOLOGY—(Oedema). APPEARANCE. Macroscopic. Microscopic. IES S (OIE AUB C IBID), I HB OTE. _Serous infiltration is a condition in which excessive quantities of lymph or serous fluid infiltrates the cells. In the anatomo-physiologic discussion of the cell, the nutri- ents were said to be obtained by specific selective action of the cells and by osmosis. Osmosis is probably the most important mode of passage of extracellular substances into the cell. In hydremia or other conditions in which cells are bathed by excessive quantities of fluid, there is a tendency for them to become hydropic. Serous fluid that enters the cells in serous infiltration is thin, watery and contains small quantities of proteids and salts. Etiology.—The cause of serous infiltration is an excess of serous fluids in the tissues. Serous infiltration is, therefore, an accompanying condition of oedema and the causes of oedema would likewise be the primary cause of serous infiltration. year-old” colt by Dr: Eo Ss). iiyesses Fig. 123.—Urinary Caleuli 1. Preputial calculus. 2. Renal pelvic calculi. Naperville, Ill. Cystic calculi may cause no inconvenience or they may produce sufficient irritation to establish a severe cys- titis. They may obstruct the urethral opening resulting in reten- tion of urine and rupture of the bladder. Frequently they become imbedded in the walls of the bladder, and may cause dilatation or pouching of its walls. Sometimes the calculi pass out of the bladder and become lodged in the urethra, resulting in retention of urine, difficult micturition, and usually urethritis. 5. Urethral calculi are common in old dogs. also in the bull and ram, and have been observed in the horse. They occur in the urethra, in the beginning of the gutter of the os penis in the dog, usually in the first curve of the penis in the bull, just pos- terior to the meatus urinaris in the ram and at the ischial arch RETROGRESSIVE TISSUE CHANGES. 235 in the horse. They usually cause difficulty in micturating and may completely obstruct the urethra with the same results that are produced by occluding the urethral opening of the bladder. Urethral calculi may produce erosions of the urethra and sur- rounding tissues and thus, produce an artificial urinary canal through which the urine will be discharged, this is probably more common in male bovines, than in other animals. About 200 urethral calculi were observed in the urethra of one steer by Dr Bo F. Kaupp: 6. Preputial calculi sometimes occur in geldings, although these are more frequently accumulations of the secretion from the ad- jacent sebaceous glands. W. Williams reported cases in which there was formation of stalactite bodies in the prepuce of oxen and sheep that had been fed food material containing a large per cent of phosphates. A preputial calculus weighing 11 grams (*/, oz.) and another weighing 10 grams were obtained from a hog by a veterinary inspector. Salivary calculi occur most frequently in the horse, although they do occur in the ass, ox and sheep. Their formation depends upon the ingested water containing a large quantity of car- bonates of potassium, sodium and magnesium and the presence of calcium salts in the saliva. (Dr. J. M. Lawrence, Veterinarian U. S. Army, Fort Wingate, N. M., operated upon two horses, removing from Steno’s duct in each a salivary calculus. In the center of one of these calculi an oat grain (nucleus) was Fig. 124.—Photograph of a Salivary Caleulus removed from Steno’s Duct, horse. found upon which the deposit had taken place. This calculus weighed 19 grams (*/, oz.) The result of salivary calculi is to obstruct the outflow of saliva, the retention of which in the smaller ducts may cause inflammatory, degenerative or atrophic changes in the gland, and if the calculi are not removed the des- truction of the gland or the rupture of the duct and a salivary fistula. Tartar on dogs’ teeth has an origin similar to that of salivary calculi. 236 VETERINARY PATHOLOGY. Gastric Calculs (gastroliths) occur in the paunches or reticula of cattle, sheep and goats. They are exceptionally rare in the horse and hog, and probably never occur in dogs and cats. Intestinal Calculi or enteroliths are found in the large intes- tine of the horse, especially those fed upon bran. These cal- culi are composed primarily of ammonio-magnesium phosphate, the magnesium phosphate being dissolved out of the bran by the acid of the gastric juice and uniting with nascent ammonia form- ing an almost insoluble phosphate. Enteroliths may be of enor- mous size, in some cases, weighing as much as ten kilograms (22 Ibs.). These calculi are likely to cause erosions of the mucous Fig. 125.—Photograph of an Intestinal Caleulus haying a circumference of 12 inches and weighing 3 pounds. membrane as well as obstruction of the lumen of the intestine. Linch, of Albany, N. Y., reported a case in the Review, 1906, in which a calculus weighing 3.4 kilograms (74 lbs.) was found. Gage reported a case in which a calculus weighing .9 kilo- grams produced fatal results. Hodgkins and Son of Hanley, Eng- land, recently obtained three enteroliths, each weighing 1.6 kilo- grams (3% lbs.) from the intestine of a horse. Biliary Calculi (Choleliths) are not rare in the domestic ani- mals. They vary from the size of a pea to a baseball, are tinted yellow, brown, red, green, or may be chalk white in color. Fre- quently they occur in large numbers, are variable in shape, and structure. They are usually composed of biliary pigments in RETROGRESSIVE TISSUE CHANGES. ear combination with calcium, although carbonates and phosphates are common ingredients. Biliary calculi may form in the biliary collecting tubules of the liver in the bile duct or in the gall blad- der. The results of their presence depend upon their location and size. Ii they are small and cause no obstruction there will be no inconvenience from them. Ii they are of a size that they can be forced through the bile ducts they will produce severe colicky pains at the time of passage. They may-be sufficiently large to obstruct the bile duct of some principal collecting tubule and produce a stagnation and resorption of bile, resulting in Fig. 126.—Biliary Caleuli, Ox. 1. Showing Facets. 3. Showing Crevice. 2. Showing Facets and Lamination. various disturbances because of the presence of the bile in the blood. Lacteal Calculi (galactoliths} may be formed in the galacto- phorus sinuses, particularly of the ox. They are usually com- posed of calcium phosphate. Phleboliths or calculi in veins have been observed by Spoon- er in abdominal veins and by Simmonds in the jugular vein. They are probably the result of calcification of thrombi which have later become detached from the vessel walls and are true calculi. They produce an obstruction in the vessels in which 238 VETERINARY PATHOLOGY. they occur. They may be of slight significance or may cause a fatal termination, depending upon the importance of the vessel and extent of the collateral circulation or anastomoses. These calculi are usually composed of calcium compounds. Arteriolths are calculi formed in arteries. Their cause, for- mation, composition and termination being practically the same as that of phleboliths. Lithopedia are calcified foetuses. In extra-uterine foetation the foetus occasionally lives only for a short time. Dead extrauter- ine foetuses frequently become impregnated with lime salts, producing the so-called lithopedia. Lithopedia may also occur within the uterus. This class of calculi is quite common in swine and some cases have been observed in cattle and sheep. CONCREMENTS. DEFINITION. ETIOLOGY. EU RIUEINUB.S,. Hair balls. Fecal matter. Bile. Pus. Milk. Cerumen. Concrements are accumulations of organic material in the cavities of hollow organs. Their effects are practically the same as the effects of calculi. Their formation depends upon the collection and massing together of organic substances derived either from the body in which the concrements occur or from — some extraneous source. They may be homogeneous or hetero- geneous in structure; oval, spherical, or angular and faceted in shape, variable in size, color and number, (873 oat hair concre- ments were found in the great colon of a horse by C. Roberts, M. R. ©. V.-S:)- They may be composed of hair, mucus, fecal matter, casein, inspissated pus or bile, ingesta of various kinds, SIUC Hair Balls (Egagaropiles) are accumulations of hair into masses. They occur most frequently in animals that lick them- selves as the ox and deer. Other animals are affected as the hog, dog and cat, also man, especially barbers, hair-sorters, hair-dress- ers, etc. Dr Ay Trickett observed a Persian cat that wonmece a mass of hair 34-inch in diameter and 3 inches long. Egagaro- piles vary in size from a pigeon’s ege to a basket ball. They are in some cases simply masses of hair in others they are im- pregnated and incrusted with mineral substances, giving them RETROGRESSIVE TISSUE CHANGES. 239 the appearance of calculi. Hair balls incrusted with mineral salts taken from the deer by someone’s grandfather or great- grandfather is the ordinary ‘‘mad-stone” in use at the present time. Recently a hair ball (bristles) completely filling the stom- ach was obtained from a hog slaughtered in a packing house. Hair bails are usually found in the abomasum or large intestines of the ox and in the stomach or large intestine of the hog. The presence of a hair ball produces the same effects that would be produced by any other indigestible body of the same size in the same location. Fecal Concrements.—The intestinal contents may accumulate into compact masses. These concrements interfere with the Fig. 127.—Hair Batts. (Egagaropiles. ) 240 VETERINARY PATHOLOGY. movement of food-stuff through the canal and may completely obstruct it. Appendicitis in the human is frequently a result ofa fecal concrement in the vermiform appendix. These concrements occur most frequently in the horse, dog and cat. They are usu- ally composed of cellulose in the horse, of bones and bone frag- ments in the dog and cat. The large intestine is the usual loca- tion of them in the horse and the small intestine in the dog or cat. Maxwell reported a case in which alfalfa accumulated in the large intestine of a horse, the concrements being trom 17% to 2244 cm. (7 to 9 inches) -in diameter. The fine -hawigen clover or oats frequently accumulates and forms concrements. The results of fecal concrements depend upon either mechanical interference in the passage of intestinal contents, erosion of the intestinal mucous membrane or perforation of the intestinal wall, or a combination of two or more of the above. Inspissated Bile.—If the outflow of bile is obstructed it will become condensed or inspissated to a degree depending upon the length of time of obstruction. Inspissation of bile frequently occurs. The animals most frequently affected are the ox and hog. An ox liver, containing several concrements composed of inspissated bile in the interlobular ducts, was recently presented to the Kansas City Veterinary College museum. Bile in this condition may form masses which in general appearance resem- ble biliary calculi. It is sometimes impossible to differentiate biliary calculi from inspissated bile, and, in fact calculi are Figs. 128. 2 1. Imspissated pus from long abscess. Inspissated pus, guttural pouch, horse. RETROGRESSIVE TISSUE CHANGES. 241 frequently of secondary origin, the thickened bile forming the nucleus. The results of inspissated bile depend first upon the resorption of bile into the system and, second, upon the absence of bile in the intestine. Inspissated Pus.—Empyema sometimes terminates, when there is no surgical interference, in resorption of the liquor puris. after which the solid constituents frequently mass together, forming concrements. These concrements may form in any cav- ity in which the suppuration is slow going or chronic, provided the movement of the part is limited. Their formation has been noted in the guttural pouch. After formation they may become calcified. They are of little importance except as pathologic phenomena. Lacteal concrements result from the coagulation of the casein of milk and its accumulation in the galactophorous sinuses. These concrements occur in the cow and can usually be expelled through the lacteal duct by manipulation. Ceruminous concrements occur in animals in which the hair or wool extends far into the external auditory meatus. They are composed of cerumen and are the result of an excessive pro- duction or limited excretion of it. They may form into sufficient masses to completely occlude the external auditory canal and thus interfere with hearing. Concrements have been found m the bronchial tubes. Their formation depends upon the accu- mulation and condensation of mucus or purulent fluid. They may obstruct bronchioles and produce atalectasis. Prostatic concrements frequently occur in old dogs. They are present in many of the enlarged prostate glands. They con- sist of masses of accumulated colloid-like material. The results depend upon the pressure that they may exert. Thus there may be an obstruction to the outflow of urine. PIGMENTARY CHANGES. Physiologic pigmentation is variable. The color and extent of pigment varies in different animals and in the same animal under different conditions. All physiologic pigmentation is the result of deposition of hemoglobin or some of its derivatives. The skin of animals is usually extensively pigmented, with the exception of albinos and some white skinned animals not albinos. The production of the cutaneous pigment is not well understood but probably results from metabolic activity of the deeper layers of epidermal cells. Because of the intense cutan- 242 VETERINARY PATHOLOGY. eous pigmentation of animals, erythema, hemangiomata and other pathologic processes are not as evident as like conditions in the human. The excessive cutaneous pigmentation protects the skin from the injurious influences of sunlight. Hair, wool, fleece, fur and feathers are variously colored, the color depending upon the soluble pigment in the cortical portion of the cutaneous appendages. ‘The color of the skin is usually an index to the color of the hair or similar epidermal appendages. The color of hoofs, horns, and claws is probably dependent upon cutaneous pigment. Voluntary muscle tissue is pigmented with varying quanti- ties of hemoglobin, excepting the so-called white meat of fowls (the sternal muscles and muscles of the pectoral arch). The pigmentation of the voluntary muscles varies in the different animals. The equine muscles are the most intensely red, the intensity of pigmentation in the muscles of other animals being in the following order: bovines, ovines, porcines, canines, felines. The flesh of duck and quail and the dark meat of other fowls is darker even than equine muscle. Heart muscle is very dark in color because of the excessive quantities of pigment. Gizzard muscle is intensely pigmented. Involuntary muscle of all ani- mals is very light in color, because of the limited quantity of pigment contained. ‘The significance of the pigmentation of muscle is not known, possibly the hemoglobin of the muscle cell has some important metabolic function. The mucous membrane, particularly of the mouth, is fre- quently pigmented. The buccal mucous membrane of the sheep and dog is often black. The uterine mucous membrance of the bitch is occasionally quite black as a result of pigmentation derived from the uterine glands, and no doubt is indirectly a derivative of hemoglobin. Bones, especially the internal portion of the articular extremi- ties, are frequently pigmented from the red marrow that occupies the spaces in the cancellous bone. The liver and spleen are naturally deeply pigmented because of the excess of free hemoglobin in those organs. The kidney also appears pigmented, probably because of the excess quantity of blood contained in it. The choroid tunic of the eye is deeply pigmented with a substance not unlike melanin, the purpose of which is to absorb rays of light. RETROGRESSIVE TISSUE CHANGES. 243 EXCESSIVE PIGMENTATION. (Hyperchromatosis.) DEFINITION. ETIOLOGY OR SOURCE. Fematogenous. Hemoglobin. Hemosiderin. Hematoidin. Hepatogenous. Bilirubin. - Biliveridin. Cellular. Suprarenal—Addison's disease. Tumor—M elanin. Pregnancy. Freckles. Extraneous. Pneumonokoniosis. Anthracosis—Carbon. Siderosis—Iron. Chalicosis—Lime. Kalinosis—Clay. Argyriasis—Silver. EAT LOO: EFFECTS. Excessive pigmentation, also known as pigmentary infiltra- tion, is a pathologic condition characterized by the presence of an excess of pigment in the tissues. Pathologic pigmentation is quite common. Icterus, melanosis, and anthracosis are types of pathologic pigmentation. This condition may be congenital as melanosis maculosa of calves, or it may be acquired as in icterus. Etiology.—In pathologic pigmentation the coloring matter may be derived from internal sources, as blood, bile and ceils, or from external sources as coal dust, silver, lead and various pig- ments. Bioop.—-Pigmentation as a result of deposition of hemoglobin of the blood is designated hematogenous pigmentation. Hemo- globin is the principal hematogenous pigment, although hemo- siderin and hematoidin, both derivatives of hemoglobin, are of some importance. Hemoglobin is the normal coloring matter of the red blood cells and muscle. It constitutes about 90 per cent of the solids of red blood cells. It is a compound proteid and exists only in combination with lechithin. Hemoglobin splits up readily into 244 VETERINARY PATHOLOGY. globin and hemochromogen, the latter combines with oxygen to form hematin. Hemoglobin is liberated from the red blood cells in all condi- tions in which there is rapid destruction of these cells, as in tick fever, anthrax. hemorrhagic septicemia, toxic doses of chlorate of potassium, lead poisoning, etc. A portion of the liberated pig- ment is eliminated by the liver and kidneys, thus excessive quan- tities of bile and bloody urine (kemaglobinuria) are a feature of tick fever, lead poisoning, etc. The liberated hemoglobin not eliminated from the body is deposited, especially in the vessel walls, but ultimately diffuses intc the lymph and infiltrates prac- tically all tissues. Post-mortem staining is the result of hemo- globin deposition into the dependent tissues. Hemoglobin is also liberated from muscle tissue in azoturia and other diseased conditions of muscle. The hemoglobin liberated from muscular tissue is disposed of in the same way as that derived from red Fig. 129.—Haermosiderin Pigmentation. Tubules containing deposits of haercosiderin in the cells. Normal kidney tubules. oe RETROGRESSIVE, “TISSUE ‘CHANGES. 245 blood cells. Hemoglobin pigmentation, the results of bruising, is common in the superficial tissues of animals slaughtered im- mediately after shipping. Hemosiderin is a derivative of hemoglobin. It is yellowish brown in color, is insoluble in water, alcohol, ether, chloroform, dilute acids and alkalies. It contains iron and gives the typical iron reaction with potassium ferrocyanid. Hemosiderin is the common pigment observed in tissues that have been previously stained with hemoglobin. Extravasated blood observed in pete- chiae and hematomata appear as typical hemoglobin pigmenta- tion for a few days, after which the hemoglobin is converted into hemosiderin and the affected parts become a yellowish brown. Hemosiderin pigmentation is observed in tissues of animals that have been bruised three or four days prior to slaughter. It 1s also observed in post-mortem examinations of animals that have been affected with diseases accompanied by hemorrhages for a period of three to five days, as purpura hemorrhagica, acute tick fever, anthrax, etc. Hemosiderin pigmentation is of common occurrence in tumors. Hematoidin is an iron free pigment, probably derived from hemosiderin. It is soluble in chloroform, but is insoluble in water, alcohol and ether. It occurs in rhombic crystals and is occasionally observed in old hemorrhagic foci. Blood pigments, hemoglobin, hemosiderin, and hematoidin are deposited in the cells and intercellular substances. The pig- ments are removed by solution and resorption of the dissolved pigment or by leucocytes which incorporate the ineoluble pig- ment granules and carry them out. Blood pigmentation has little effect upon the tissue in which deposition occurs, but the flesh of food producing animals is usually condemned when pigmented because of its unsightly appearance. The deposition of a brownish or blackish pigment in bones (ochronosis) is occasionally observed in the carcasses of cattle which were apparently in good health. The cause of this pig- mentation is unknown. It probably does not injure the tissues or the meat for food, but such meats are usually condemned be- cause of their unsightly appearance. Another brownish pig- mentation of muscular tissue (xanthosis) is associated with mus- cular atrophy or disease of the suprarenal bodies. This condi- tion is of no consequence except public sentiment prevents the sale of such meat. BILE pigmentation results from the resorption of bile and its 246 VETERINARY PATHOLOGY- deposition in the tissue. Bile pigmentation is designated hepa- togenous pigmentation and the condition produced is commonly known as icterus or jaundice. Obstruction of the bile duct or any of its radicles by pressure, duodenitis, calculi, etc., will result in retention of the generated bile which is later resorbed into the blood. Destruction of considerable numbers of liver cells or diminution of their function may possibly result in the retenticn in the blood of those products that are normally converted into bile, and thus produce a hematogenous icterus. Excessive pro- duction of bile, as in acute tick fever, is frequently accompanied by resorption of some of the bile and its deposition throughout the body, thus producing a generalized icterus. Bile staining is most evident in the conjunctiva and ocular sclera of the living animal where it produces a lemon or greenish yellow discolorization. Jf resorption of bile is very extensive it may appear in the urine. In carcasses, biliary pigmentation is most evident in the adipose tissue, especially the subcutaneous fat, although it is usually well marked in the subserous fat and may be detected in the lymph nodes, spleen, kidney and muscu- lar structures. The bile may be deposited in the cells or between the cells as greenish-yellow amorphous granules. The granules are read- ily soluble ia alcohol, hence they are best detected in frozen sec- tions. De 10 -@ \ a Ooo! wee DOES 6 Ay re 5s QOn £208 aba? MWOEX— Ve PAIgG OO. @, @) S AG EY Z wren Gj, OY SOS 6-8 Cro Ox@ oes Hin & ye 7 Ee ACD» & @ 2K. DS SOHO OCS GG AOG ake © WG A > ty A SA z (2G, “3 x : : ; C DREAES 7 19,0: 3! FO” > O\sbery Fig. 130.—Iecterus affecting lymphatic tissue. a. Normal tissue. b. Deposit of bile pigment. OS @ 5 \ Atel RETROGRESSIVE TISSUE CHANGES. aay The effects of resorption of bile are variable. The tissues are discolored; there may be pruritus, as the bile appears to act as an irritant cn nerve endings; putrefactive changes may occur in the intestine, and the heart may be depressed. Other inconstant symptoms may appear, especially if the quantity of resorbed bile is large. CELLS.—Aside from hematogenous and hepatogenous pigmenta- tion the products of certain body cells become a factor in hyper- chromatosis. The principal pigment produced by cellular activity is mel- anin. Melanosis maculosa is a congenital, cutaneous, pathologic pigmentation of calves resulting from the excessive production of melanin by cutaneous cells in certain areas. Melanotic deposits are of common occurrence in the various glandular tissues, especially the liver, kidney, and suprarenal glands. The deposits in the glandular tissue may occur in the cells or intercellular spaces, and may appear as irregular yellow- ish-brown or black masses. Melanin may occur in the form of fine granules or be flocculent. Black kidneys are occasionally observed, in abattoirs, especially in hogs. These usually result from deposition of delicate, flocculent masses of melanin in the kidney cells. Melanesis is of most frequent occurrence in white animals, although it has been observed in Aberdeen angus cattle, red short horns, black and bay horses, and black and red hogs. Melanotic tumors are pigmented with melanin. The melanin may be a product of the tumor cells or of the adjacent tissue cells. The principal melanotic tumors are the melano-sarcomata, although there may be a benign melanotic tumor called a mel- anoma. In a disease of the suprarenal capsule in the human (Addi- son’s disease) there is a peculiar bronzing of the skin. This con- dition has not been noted in the domestic animal, probably be- cause of the dense pigmentation of the skin. It is thought to be a form of melanosis. -A pigmentation has been noted in atrophic tissues, especially atrophied muscles. The pigment of atrophic muscles may be the result of disturbed cell metabolism or it may result from con- centration of the pigment, because of the diminution in the size of. the cells. Brown atrophy of the heart is a condition in which pigmentation is prominent. Freckles are pigmented areas of the skin in the human, the result of cutaneous cellular action. Because of the intense pig- 248 VETERINARY PATHOLOGY. mentation of the skin in domestic animals, freckles are not easily observed, except in white animals. Pregnancy in the human is frequently accompanied by local- ized pigmented cutaneous areas.’ Such areas have not been re- corded in domestic animals. Aside from the blood, bile and cellular activities, pigments may be introduced into the body from without. The most common external substance that produces pigmen- tation is carbon. The most extensive pigmentation by carbon is in the lung, producing the condition known as anthracosis. Anthracosis 1s a common condition in the lungs of animals used in and around coal mines, in cities in which there is large quan- tities of coal smoke, in cats and other pet animals confined in coal bins, engine houses, etc. The inhaled carbon is largely ex- creted in the mucus discharged from the respiratory tract, al- though some of it is deposited in the epithelium of the air cells, and ultimately may be found in the interstitial tissue of the lung. Anthracosis apparently produces little harm unless it is exces- sive, when it predisposes to inflammatory disturbances. When examined in gross the lungs vary in color from a gray to a deep black. Microscopically small particles of carbon may be observed in the cells and intercellular substances of the lung tissue. Arg\riasis 1s a condition 1n which silver is deposited in a tissue. After the silver is deposited it is combined with sulphur, thus forming silver sulphid, which is brownish black and imparts a similar color to the tissue. Argyriasis is not common in animals except those used in and around silver smelters or as a result of the application of some silver preparation to the tissues. Siderosis is a condition in which iron is deposited in a tissue. Iron, like silver, usually combines with sulphur, forming the sulphid, which is brown or black in color. Siderosis is not common in domestic animals, except in the intestinal epithelium of animals that have been medicated with iron preparations. Hydrargirosis is a condition resulting from the deposition of mercury in a tissue. This condition is present in the intestinal mucosa after medication with calomel or other mercury prepara- tions. The mercury sulphid, which is brown or black in color, is the usual pigment in hydrargirosis. Plumbosis is a term applied to pigmentation with lead. This form of pigmentation may be evident in the intestine in chronic lead poisoning. It appears as a bluish black pigment. Tattooing is the introduction of insoluble pigments into tissues. In tattooing, the tissues are first punctured or injured, after which some insoluble pigment is introduced into the wounds. RETROGRESSIVE TISSUE CHANGES. 249 Some of the pigment is carried out by leucocytes and some of it is entangled in the cicatrix of the healing wound, where it re- mains permanently. Tattooing is a very valuable means of marking stock, as it gives a positive means of identification. Registered cattle, horses, sheep, hogs, dogs, etc., are tattooed in the ear, and fowls on the legs. The wound is made with an instru- ment similar to a hog ringer, in which slugs containing needle points arranged in the form of figures or letters are used. This instrument is used to punch holes into the inner surface of the external ear, immediately after which carbon is rubbed into the wound. When the wounds are healed, the tattoo may be easily observed. Effects.—Excessive pigmentation of a tissue or tissues is of little pathologic significance. Pigmented tissues are probably not hindered in their physiologic activities, excepting in so far as the cause of the pigmentation is an etiologic factor in the dis- turbance of the functioning of a part. Icteric pigmentation is of consequence because of the action of the bile upon nerve cells. Pigmentation, especially when excessive, is a basis for the condemnation of meat and meat products because of public sen- timent. ABSENCE OF, OR DIMINISHED PIGMENTATION. (Hypochromatosis. ) Visible pigmentation may be less than normal, and in some instances there is a complete absence of pigment. Areas con- taining less pigment than normal. and depigmented areas are permanently white in color, as they are not affected with sun- light or any other conditions that tend to produce pigmentation. This condition may be of antenatal or postnatal origin. Etiology.—Antenatal absence of, or diminished pigmentation: may be inherited or it may be caused by disturbances of the embryonic cells that produce normal pigmentation. Postnatal absence of, or diminished pigmentation is usually the result of disease in which areas of tissue have been destroyed and later substituted by cicatricial tissue. The total absence of pigment (achromatosis) is not of com- mon occurrence, being most frequent in rabbits, birds and rats (albinos). An albino is an animal devoid of cutaneous and chor- oid pigment, the condition being inherited or congenital. The animals thus have white skin and usually white hair and their eyes are pink or red because of the absence of choroid pigment, 250 VETERINARY PATHOLOGY. the blood being observed through the transparent ocular struc- ture. The so-called “Wall-eyed” horses have little if any pig- ment in the choroid tunic, and frequently they have depigmented localized cutaneous areas. Depigmentation is probably never generalized. Permanent localized depigmentation, leucoderma or vitiligo, is a character- istic symptom affecting the external genitals of horses afflicted with dourine. ‘It is also observed in cicatrices resulting from burns or extensive operative procedure. Surgeons usually make incisions in an oblique direction in order that the hair in the ad- jacent skin may cover the scar. Scars are usually devoid of hair, and when hair is present it may lack pigment. The application of some medicaments on the skin of some animals causes the hair to lose its pigment. | Temporary depigmentation is evident after an attack of coi- tal exanthema, vaginitis accompanied by an ichorous discharge, and by many other conditions characterized by erosion or necro- sis of cutaneous tissue. Effects.—The absence of pigment is of no Serious conse- quence except in some animals. Hogs that are white skinned cannot be raised in some localities because of the effects of the sunlight. Depigmentation of the choroid is also of some conse- quence, because the eye is exposed to the effects of excessive light, CHAPTER: 1X. NECROSIS AND DEATH. NECROSIS. DEFINITION. ETIOLOGY. Suspended nutrition. Thermic. Burning. Freezing. Chemic. VARIETIES, According to cause. Inanition. Thermic. Chemic. According to character of necrotic tissue. Coagulation, Colliquation. Caseation. Gangrene. Mummification. Miscellaneous. Senile. Fatty. Focal. Jack-sores. TISSUES AFFECTED. DISPOSERION- OF NECROTIC TISSUE. Absorption. Exfoliation. Encapsulation. Sequestration. BERPBCTS.- Necrosis is local death. It is death of a part of the living body. The term necrosis is applicable to the death of any kind of tissue, glandular, muscular, osseous, etc. Necrosis is usually a rapid process, that is, it is sudden death of a part. Death of a cell or a group of cells that have been previously affected with degen- eration, 1. e., a slow or lingering death, is termed necrobiosis. Caries is a term used to designate necrosis of dentinal or osseus tissue. Cells are constantly worn out and destroyed in physiologic active tissues. The physiologic destruction of cells is not usu- ally thought of as necrosis although the cause and manner of death may be similar, and there may be no difference in the ap- pearance of cells destroyed by physiologic and pathologic pro- cesses, 251 252 VETERINARY PATHOLOGY, The term necrosis is applicable to the pathologic death of a single cell, although such a limited necrosis is rarely recognized. Clinically necrosis is usually not noted except when the area is sufficiently large to observe with the unaided eve. All tissues of all animals are subject to necrosis, and it may occur upon a surface or in subsurface structures. Bursattae is a disease characterized by necrosis of the skin. Necrotic stoma- titis, a disease in puppies, calves and pigs, is accompanied by necrosis of the buccal mucous membrane. Tuberculosis, glan- ders, actinomycosis, and caseous-lymph-adenitis are diseases in which there is surface or subsurface tissue necrosis. Etiology.—Necrosis may be primary but it is more _fre- quently secondary. Secondary necrosis is a sequel or result of some other pathologic process, as hemorrhage, oedema, throm- bosis, anemia, hyperemia, inflammation, degeneration, infiltra- tion and infection. Primary necrosis is the result of; (1) obstructed nutrition; (2) chemic substances; (38) temperature variations. Obstructed nutrition—A tissue or part, from which nutri- tion is entirely obstructed, will die after all the available nutri- ents have been consumed. Nutrition may be obstructed from a part by some mechanical means. An occasional result of mechanically obstructed nutri- tion is observed in dogs in which a rubber band has been placed upen a leg, an ear, the tongue, or the tail; the circtiatiom bemme thus obstructed the part distal to the rubber band soon becomes necrotic. The improper adjustment of bandages, especially when used to support fractures, is frequently a cause of necrosis. Tumors, cysts, abscesses and other pathologic enlargements may exert sufficient pressure to obstruct circulation and produce necrosis. Fractures and herniae may mechanically occlude blood vessels and result in necrosis. The seriousness of omental hernia or, in fact, any hernia, is due,to the fact that the vessels supplying the hernied structures are occluded, resulting in ne- crosis and the absorption of the products of the necrotic tissue. The plugging of a terminal vessel by a thrombus or an em- bolus (infarction) produces necrosis if collateral circulation is not established. Thrombo-embolic colic is a condition usually caused primarily by the larvae of the Strongylus armatus enter- ing and producing a parietal thrombus in the anterior mesen- teric artery, fragments of the thrombus become detached, pass down to and occlude the terminal mesenteric arteries, resulting in ischemia of the walls of the intestine, and if the circulation is not soon established the ischemic area becomes necrotic. NECROSIS AND DEATH. 253 A part or organ separated from the remainder of the body undergoes necrosis sooner or later, the time depending upon the condition of the tissue and the temperature in which the sep- arated portion is kept. Maceration and bruising produces ne- crosis to a varying degree, depending upon the extent of the in- jury. Fig. 131.—Photograph showing Necrosis 2bove the foot of a horse. Chemic substances.—Certain ‘chemic substances as_ phenol, arsenic, mercury bichloride, strong solutions of the caustic alka- lies and mineral acids, as well as the products of a large number of bacteria, are tissue destroyers. Phenol abstracts water from all cells to a sufficient extent *o destroy their vitality, and it pro- duces a rapid disintegration of red blood cells. Arsenious tri- oxide is frequently applied on tumors because of its erosive action. Bichloride of mercury combines with the cell albumins, forming albuminate of mercury, thus inhibiting the cell action. and when all of the cell albumin is combined the cell is de- stroyed. The caustic alkalies and mineral acids coagulate the cell albumin or abstract the cell water, thus destroying them. The Bacillus necrophorous produces chemic substances that cause coagulation of the cell protoplasm (coagulation necrosis). se VETERINARY PATHOLOGY. De Schweinitz has described a chemic substance produced by the Tubercle bacillus, as necrotic acid, which is thought to pro- duce necrosis in tubercular lesions. The toxin of the diphtheria bacillus produces focal necrosis in practically all tissue in an individual afflicted with diphtheria. The products of pyogenic bacteria produce marked tissue destruction. Chemic substances produce necrosis by coagulation of the Fig. 132.—Bacillus Necrophorus—Pleomorphiec form. albumin by dehydration or by the formation of new cell com- pounds, thus inducing metabolic disturbance and cell death. lemperature variations—All active cells have a maximum and a minimum temperature. Thermic variations beyond these means are injurious and destructive if the variation is extensive. The high temperature causes coagulation of the cell protoplasm (cloudy swelling), which, if extensive, destroys the cells. Necrosis resulting from burning is of common occurrence. Low temperature is not as rapidly destructive as high temperature. Freezing produces necrosis of the tissues of warm blooded ani- mals, probably because of cell disintegration induced by the for mation of ice in the cells. Types or Varieties of Necrosis.—Several factors may be used as the basis for the classification of necrosis. Etiology.—According to the cause, necrosis may be: a. In- anition necrosis, b. Thermic necrosis, c. Chemic necrosis. - NECROSIS AND DEATH. Inanition necrosis is that type resulting from obstructed nutrition. As an example of this type may be mentioned the necrosis of the scrotum and its contents in rams induced by placing a rubber band moderately taut around its upper portion. = Ce : ie ~ ed in the This is a method frequent] structures in ani- superficial mals afflicted with diseases that cause them to constantly assume Bed sores observ Tams. duced by pressure upon the nutrient vessels or thrombic forma- tion secon the decubital position, are the result of obstructed nutrition in- g . Cc dary to bruisin Thermic necrosis results from exposure to extreme tempera- Thus necrosis of cutaneous tissues is of Common occur- tures. ls as a result of conflagrations or undue exposure rence in anima 256 VETERINARY PATHOLOGY, to the solar heat rays or thermo-cautery. Necrosis induced by freezing is very common in calves, pigs, and chickens, in the temperate and frigid zones. Chemic necrosis is represented by the extensive destruction of the buccal, oesophageal, gastric, and intestinal tissues induced by the ingestion of lye. Corrosive sublimate and arsenious tri- oxide destroy the mucous membrane and frequently the deeper tissues of the alimentary tract in animals poisoned with these agents. Location.—Necrosis may be surface or subsurface. Surface Fig. 134.—Ergot Poisoning in Cattle. Photograph by Dr. W. T. Spencer. 1. Sloughing above the feet. 2. Sloughing of the ends of the tails. necrosis may be of the skin, mucous or serous membranes. Sub- surface necrosis may be of any tissue, muscle, bone, glandular, SIUC. Nature or condition of the necrotic tissue. 1. Coagulation necrosis.—This type of necrosis is character- ized by the coagulation of the necrotic tissue. It is the result of the presence of some enzym that produces the formation of fibrin or some allied substance. Coagulation necrosis is evident in the coagulation of blood and inflammatory exudates. The exudate in fibrinous inflammation (croupous and diphtheritic) usually becomes firmly coagulated. On the other hand, coagulation is rarely observed in collections of lymph, as in ascites, etc. The necrotic tissue in anemic infarcts, especially in the kidney, is sometimes coagulated. 2. Colliquation necrosis.—The condition resulting from solu- NECROSIS AND DEATH. 257, tion of a substance or surface area of necrotic tissue is colliqua- tion. Solution of the necrotic tissue is the result of enzyms that dissolve or digest the dead tissue. Suppurative processes (as abscess formation, etc.), are examples of this type of necro- sis. Liquefication of anemic infarcts, inflammatory exudates and thrombi, with or without the formation of cysts, is colliqua- tion necrosis. In the brain of horses that have died of the so- called blind staggers areas are found containing liquefied nerve tissue. 3. Caseation necrosis.—When the fluid is absorbed from h- quefied necrotic tissue, the remaining solids may become cheese- like, thus producing the condition known as caseation. Caseation may be primary, but it is more frequently secondary to liquefying necrosis. Caseous material is granular, soft or crumbly in con- sistency. Caseation is characteristic of the typical lesion of cas- eous-lymph-adenitis in sheep and goats. Liquefaction precedes caseation in this disease. Tubercular lesions, especially in the bovine, is characterized by caseation, although they later become calcified. Necrotic centers of a caseous nature are observed in the lesions of bursattae. 4. Mummifying necrosis (mummification, dry gangrene).— Necrotic tissues superficially located may become dessicated, thus producing the condition known as mummifying necrosis. This type of necrosis occurs upon a surface that is freely exposed to air and of tissues in which there is little moisture. The ear, tail and hoof lesions, characteristic of ergotism, are the most typical examples of mummifying necrosis. In ergotism, the lesions are produced by constriction of tle’ varterioles. -Vhis. in turn. in- creases blood pressure, and, consequently, the work of the heart. This ultimately results in the diminution or complete absence of blood from the extremities, and the latter sooner or later become necrotic. The necrotic tissue, as ears, tails, etc., in animals affected with ergotism become mummified because blood is prac- tically shut off from the affected parts and the contained moist- ure soon evaporates, for they are freely exposed to the air on two or more surfaces. Frozen tissues may become mummified. The umbilical cord in new born animals undergoes mummifica- tion. 5. Gangrene.—By the laity, the term “gangrene” is used to designate any type of necrosis, and by some medical men it is used to signify death of soft tissue en masse. Gangrene is that type of necrosis characterized by putrefaction of the necrotic tis- sue. Gangrene invariably occurs in tissues in which there is a good supply of moisture, as in a tissue affected with venous con- 258 VETERINARY PATHOLOGY. gestion, and usually occurs upon a surface because infection is more likely to occur there. Parenchymatous mammitis of the bovine is frequently succeeded by necrosis and putrefaction of the necrotic tissue (gangrene). Gangrenous pneumonia is not uncommon and may be the result of embolic metastasis of organ- isms from septic metritis, etc., or it may be induced by medica- ments introduced into the lung. Miscellaneous. 1. Senile Necrosis.—This is a type of necrosis occurring in old age. It is not uncommon in old dogs and aged horses, and is usually the result of inelasticity of the arteries and an insuff- cient supply of nutrition. 2. Fatty Necrosis.——This is a condition characterized by the y AK Vy Fig. 135.—Multiple Fatty Necrosis. Fat cells undergoing disintegration, because of Saponification. conversion of fat into fatty acid and glycerine, that is, saponifica- tion of fat. The name fatty necrosis is a misnomer, as the condi- tion is not necrosis. It should be called saponification of fat. In fact, a fully developed fat cell represents that amount of stored, available food, and there is in reality no vitality in the cell, and necrosis in dead tissue is not conceivable. Again, the real exist- ing condition is saponification of the fat, not necrosis. The prob- able cause of fatty necrosis is resorption of steapsin induced by pancreatic disturbances, although steapsin may be absorbed from the intestine. Some four or five cases have been observed in the dog, several cases in the sheep, and one horse was examined that was affected with fatty necrosis. In each of the above cases ~ of a yellow- , or the cell ; but later be- > come more or less calcareous as a result of combination of lime salts with the free fatty acid. Recently it has though all fatty y oO co) > - - -like crvstals arenchymatous tissues un- In microscopic section the cells NECROSIS AND DEATH. If the lesions are advanced, calcareous granules Focal necrosis.—In certain infective diseases it has been In gross appearance the involved portions are dull, lusterless, noted that small foci of the various p opaque, slightly raised, usually circumscribed areas, Fatty necrosis usually involves the omental fat, and espe- ish white color. cially that in close proximity to the pancreas The areas affected are at first soft and spon tissue is subject to this condition. oO. been suggested that this condition is caused by disturbances of there was evidence of pancreatic lesions, as inflammation, hem- the islands of Langerhan. orrhage and atrophy was noted in one case. of the affected areas may contain needle substance may appear as a granular mass. may be observed by palpation. 3 oO @ @ © re) Visa 6 S e @ e&° Oe €,e 6 e & & EXG Be @ ge e ‘J i) Cs ® @ & eo @ ry eg ~S@ /@ @B 6 ae a) 3S ee S ee 2 © Ss @s "é oa e- 6 e@ © ak fee e 9 Oo he AS Sh, i Qs gS an “2 seb tee St adign Toca eres eee ee Te 8, © Be® 9 mo & @,59 wl? @ ® S) SO 8 Oe. EO “el BS Gy MQ, 8 COS? Oo tH 8 wg @ G2 0 of @99 S “4,0 aa ed xo @ @ S98 »® ar aa Qe ‘) “oo 66299 ® Ces g.2 8 oY oo ween Og o6 9% eos oP ees surrounded Showing necrotic center and leucocytes. x250. epitheloid cells, lung. by small round cells, 136.—A necrotic tubercle; Fig. 260 VETERINARY PATHOLOGY. dergo necrosis. In many instances, this occurs in the absence of any circulatory disturbance, indicating that the exciting cause, chemic substance, is carried by the blood and appears to have a selective action for certain tissue. This type of necrosis is com- mon in diphtheria and typhoid fever in the human and in hog cholera, glanders, generalized tuberculosis and probably some other infective and chemically induced diseases of the lower ani- mals. The areas affected are frequently not sufficiently large to observe with the unaided eye. Microscopic sections show the cells in various stages of necrosis. The nucleus may be appar- ently normal or entirely disintegrated, the cell body may be granular or hyaline, it may be intact or appear fragmented. Leu- - cocytic invasion of the necrotic area is of frequent occurrence, and may at first give the impression of an infected focus. Necro- tic tissue in focal necrosis may be absorbed and the destroyed tissue regenerated ; it may become liquefied, thus forming a cyst; it may become infected and be succeeded by abscess formation, or it may be substituted with scar tissue. 4. Jack-Sores.—This is a name applied to a very prevalent condition in jacks in which there is necrosis of the skin and sub- cutaneous tissue. Perhaps jack-sores should not be classed as a separate or distinct type of necrosis, but it is so common that it merits a special mention. The skin and subcutaneous struc- tures of the legs, venter surface of the abdomen and thorax, and maxillary region are most frequently affected. The necrotic areas may be very extensive, in some instances involving the entire metatarsal or metacarpal region. The etiology of “Jack-Sores” is not known, but no doubt it is the result of malnutrition and probably an irregular, indefinite lymphatic circulation is the primary cause. Tissue Affected.—No tissue is exempt from necrosis. The tissue affected depends upon the cause, the animal and geog- raphical location. Disposition of Necrotic Tissue.—Necrotic tissue or products derived from it are more or less irritating and may produce an inflammation in the living tissue around the necrotic mass. The perinecrotic inflammation insures an increased number of leucocytes around and in the necrotic area. The necrotic tissue, leucocytes and other living ceils may produce enzyms that will ultimately dissolve the necrotic tissue. There may be a contraction of the necrotic tissue and later it may separate from the surrounding normal tissue. The reaction of the adja- cent living tissue may be limited and cause the production NECROSIS AND DEATH. 261 around the necrotic area of a fibrous or osseous capsule, or even cause a fibrous formation throughout the entire necrotic mass. From the foregoing it is apparent that necrotic tissue may be disposed of as follows: 1. Abscrption. 2. Exfoliation. 3. En- capsulation. 4. Sequestration. Absorption—The necrotic mass is more readily absorbed when it is in a liquid state (colliquation), although leucocytes, and various other cells may produce enzyms that are capable of dissolving coagulated necrotic tissue. Absorption of fluid ne- crotic tissue is in part accomplished by means of the lymphatic tissues, and in part by means of leucocytes that incorporate and convey fragments of necrotic cells to the various organs that dispose of waste materials. Necrotic infarcts are occasionally entirely absorbed. Exfoliationn—Necrotic surface tissue is frequently disposed of by separation of the dead from the living tissue as a result ot inflammation or contraction of the necrotic mass. The separated necrotic mass is the sphacelus. The process of separation and sloughing is exfoliation. Exfoliation is the usual disposition of necrotic extremities induced by freezing and by ergot poisoning. Encapsulation—rThe irritation produced by subsurface ne- crotic tissue may be insufficient to cause an acute inflammation, but it may stimulate fibrous hyperplasia. Thus a fibrous capsule or wall is built around the necrotic mass, 1. e., it becomes encap- sulated. In some instances the encapsulated necrotic tissue later becomes calcified, or it may become liquefied, the capsule retain- ing the liquid, thus a cyst is formed. Fibroblasts may extend into the necrotic area and form fibrous tissue throughout the entire mass, thus there would be a mass of cicatrizing fibrous tissue permeating the necrotic mass. Sequestration.—This is a term applied to the separation of subsurface necrotic tissue, more especially necrotic bone, from the surrounding healthy tissue. The separate necrotic portion is termed the sequestrum, and the process of its separation sequestration. Af osseous sequestrum may be encapsulated, the capsule later becoming osseous, thus forming an involucre. Effects.—Necrosis is the condition resulting from tissue des- truction. The effects of tissue destruction depend upon the variety of tissue, the extent and locaticn of the condition, and the age and condition of the animal in which it occurs. Ii the tissue destroved is capable of regeneration, or if it is limited in extent, and the animal is otherwise in good condition, the effects will be insignificant. If the tissue destroved cannot he regener- 262 VETERINARY PATHOLOGY. ated and is extensive, the animal will be deprived of that quan- tity of tissue and if the function of the destroyed tissue is of prime importance, the animal will die. Necrosis is invariably associated with inflammation, which is especially active around the necrotic area, and the results of this inflammatory reaction must also be considered in estimat- ing the sum total of the effects of necrosis. DEATH. DEFINITION. ETIOLOGY. Suspended heart action. Respiratory arrest. Suspended brain action. SIGNS. Post Mortem Staining. Temperature change. Muscular rigidity. Decomposition. IMIS IES. Mirror. Blister. Incision. Relaxation of sphincter muscles. Death is the condition resulting from the permanent arrest of all functions. Death should not be confused with necrosis. The former refers to somatic death and the latter to the death of a part. It is difficult and in fact impossible to determine the exact time when life ceases in a body. The various body tis- sues do not all become lifeless when the individual as a whole dies. The length of time that vitality is retained in the tissues of a dead animal depends upon the variety of tissue, the age of the animal and the cause of death. The less highly organized, the tissue, the longer its vitality is retained. The tissue of young animals possess their vitality for a longer time than the same tissues of an aged animal. Death results from disturbance of certain vital centers and these tissues, as well as all others speci- fically acted upon by the agency that causes death, lose their vitality earlier than tissues not acted upon. Death may be physiologic or pathologic. Physiologic Death. This is that type of death observed in old animals. During em- bryonic life the principal function of all tissue cells is reproduc- tion. As the tissue becomes more matured, the reproductive prop- erty of its cells gradually diminishes and has practically disap- NECROSIS AND DEATH. 263 peared in old age. Cell repair is complete in early life, but gradu- ally diminishes as the animal becomes aged. The activity of cells and their life cycle is limited as is that of all active structures either animate or inanimate. Therefore, if new cells are not pro- duced and the old cells are not repaired their energy or vital forces are finally exhausted and they degenerate and die. If large numbers of cells of all tissues die the animal involved is incapaci- tated and ultimately sufficient cells die to diminish the function of the vital organs to such an extent that there is collapse and som- atic death. Physiologic death is initiated by a gradual decline which may continue until the individual dies. Or after a long per- iod of slow decline, death may be sudden as a result of a sudden- lv diminished function of a vital organ. Physiologic death is sim- ilar in a way to the collapse of the one horse chaise which, as the story runs, was used until it literally fell to pieces. Very few domestic animals die a physiologic death. Those animals whose flesh is used for food are butchered long before physiologic death would intervene, and those animals used as beasts of burden are usually destroyed when their earning capacity is monetarily less than the food they consume. Pathologic Death. Pathologic death signifies the ending of life prior to the time that the vital forces have been exhausted. Etiology.—Pathologic death is that type caused by accident or disease process. Death primarily is the result of permanent suspension of heart action, respiration or brain functioning. Suspended heart action may be caused by influences acting upon the cardiac nerve centers ia the medulla or upon the heart mus- culature direct. The significance of suspended heart action is self evident. There being no blood circulating the tissue would soon consume all available nutriment and then succumb. Tem- porary arrest of heart action is called syncope. Respiratory arrest is usually the result of nervous influences though clonic spams of the respiratory muscles would produce a similar effect. The absence of respiration implies the absence cf oxygen to oxidize the blood and the tissues and the absence of oxygen for a considerable length of time results in carbon- dioxide poisoning and death. Apnoea is a condition in which respiration is arrested. Permanent arrest of all brain functioning even for a brief period results in cessation of all the principal functions and death. ~64 VETERINARY PATHOLOGY. Thus, suspended brain function results in arrest of heart action and respiration either of which results in somatic death. Coma is a term used to designate a condition in which all conscious- ness or recognition of environments is suspended but the con- trol of vital functions is still maintained. Signs of death.—The changes that occur in dead tissue are of considerable importance especially to inspectors of carcasses of animals, the flesh of which is intended for human consump- tion. The most important post mortem changes in tissues are as follows; post mortem staining (livores mortis) ; death stiffen- ing (rigor mortis) ; and decomposition or putrefaction. Post Mortem Staining—TVhe blood usually undergoes changes immediately after death. The disintegration of red blood cells allows of the liberation of hemoglobin which is deposited more or less extensively upon the inner lining of the blood vessels and heart and also filters through the vessels and stains the peri- vascular tissues. The length of time after death that post mor- tem staining becomes evident depends upon the cause of death. In fact the purplish staining along the cutaneous vessels evident in dead bodies may be evident in the living body of animals. Thus liberation of hemoglobin takes place during life in the blood of animals affected with septicemic diseases. Temperature changes.—The carcasses of all dead animals assume the temperature of the environment sooner or later. The length of time necessary for the body heat to pass out of a dead body depends largely upon the cause of death. In some diseases, those in which tissue change is limited, the temperature is sub- normal at the time of death and rapidly assumes the environmen- tal temperature after death. In other diseases, those in which tissue changes are extensive, the temperature may vary from normal to considerably above normal at the time of death and may increase for several hours after death. Temperature changes may be extremely variable in a carcass. Also a remarkably low subnormal temperature has been observed in many living ani- mals, especially those in a comatose state and yet the animals recover. The thermic variations should never be relied upon in determining whether or not life is extinct, at least not within 48 hours after the animal is supposed to be dead. Rigor Mortis—That the body of an animal becomes rigid after death is common knowledge to all observers. Rigor mortis re- presents a condition of the muscle fibre in which it becomes rigid as if in a tonic contraction. The length of time after death that rigor mortis appears and'the length of time that it persists de- pends upon the condition of the animal at the time of death. NECROSIS AND DEATH. 265 Thus muscular rigor appears usually in a few minutes after death and is of brief duration in animals, that have died as a result of a long continued exhaustive disease, as chronic tuber- culosis. On the other hand rigor mortis may not become evi- dent until 24 hours after death in animals that have been killed while in a perfect state of health and it may continue for from two to four-days. In catalepsy, muscular rigidity is a charac- teristic symptom. Other conditions, however are sufficient to differentiate this from rigor mortis. Decomposition or putrefaction is caused by the action of putre- fying bacteria. The decomposition of a tissue is sufficient evidence of the fact that it is lifeless. Decomposition or putrefaction is not easily detected in the early stages. The evolved odor is usually the accepted sign of decomposition and during some seasons of the year, decomposition may not become evident for several days after death. The carcasses of animals dead of septic infections usually decompose immediately after death, e. g. carcasses dead of anthrax, hog cholera, etc. Tests.—Because of the uncertainty of the above signs espe- cially, during the first 24 or 48 hours after death, certain tests are recommended to determine the presence or absence of life in a certain body. They, like the above signs, are not absolute. The mirror test—Respired air contains more or less water vapor. Respiration is not always perceptible. Water vapor is condensed upon a cold surface. The procedure of this test con- sists in holding a mirror over the nostril and if any air is ex- pired the watery vapor from the expired air will be condensed and rendered visible upon the surface of a mirror. This test is not infallible for the respiratory functions may be so diminished that the moisture (watery vapor) of the expired air is insufficient for condensation upon the mirror. Blister Test.—Blisters or vesicles can usually be produced by heat or chemic vesicants applied to the skin of a body in which life still exists. The formation of vesicles is not possible in dead tissue because the production of a blister represents the response of a living tissue to an irritant and only living tissues are cap- able of reacting. Vesicle productions varies in living animals and in some cases they are not produced. Incision.—Because of the elasticity of living tissues, all incised wounds gap in the living body. Tissue elasticity disappears when the tissue dies, consequently incised wounds in dead tis- sues do not gap. 266 VETERINARY PATHOLOGY. Certain post mortem changes are rather constant in the eye. These changes consist of a cloudiness of the lens and the aque- ous humor, the condition gradually becoming more intense. The surface of the eye, i. e., the conjunctiva, becomes dry and scaly in appearance. All sphincter muscles are usually relaxed at the time of death and remain so permanently. CHAPTER. X: TUMORS. (Neoplasms.) DEFINITION. FREQUENCY. STRUCTURE. Cells. Intercellular. Vessels. Nerve tissue. SUZAE: SHAPE. GOEOK: CONSISTENCY. NUMBER. GROWTH. EXTENSION. NATURAL RESISTANCE. RETROGRESSIVE CHANGES. CLINICAL CONSIDERATION. ETILOLOGY. VARIETIES. Occurrence. Primary. Secondary. Recurrent. Structure. Histoid. Organoid. Teratoid. . Clinically. Benign. Malign. Tissue. Adult. Epithelial and connective—Papilloma. Connective, Fibrous—Fibroma. Mucous—M yxoma. Cartilage—Chondroma. Osseous—Osteoma. Dentine—Odontoma. Adipose—Lipoma. Glia—Glioma. Muscular. Involuntary—Leiomyoma, V oluntary—Rhabdomyoma. Vascular. Blood vessel—Hemangioma. Lymph vessel— Lymphangioma. Nervous. Neuroma., 267 268 VETERINARY PATHOLOGY. Embryonic. Connective. Sarcoma. Endothelioma. Hypernephroma. Placentoma. Epithelial. Carcinoma. Epithelioma. Adenoma. Aypernephroma. Plancentoma. Adult and Embryonic. Any and all tissues. Teratoma. The term “tumor” was formerly used to indicate any swelling in animal tissues. They, more than any other pathologic entity, have been studied and investigated by scientists, and yet little is known of their pathology. With the present limited knowledge it is impossible by definition to clearly differentiate them from some other pathologic conditions. They have been defined as new growths of tissue developing independently in any tissue of the animal body and atypical in structure and function. Also they are non-inflammatory growths of new tissue, persistent, independent of the surrounding structures, atypical in structure and function. A more concise idea can be formulated by think- ing of them as parasites, that is, they are new growths of tissue that develop in or upon the animal body at the expense of the animal, and are subject to the same pathologic conditions that the normal tissues are, as degeneration, necrosis, etc. Frequency.—Tumors are of frequent occurrence. They are more common in dogs particularly aged ones thar in other animals. Of 12% animals presented in the daily clinic at the Kansas City Veterinary college during one college session, 12 were affected with tumors. The frequency of tumors in animals treated in the Berlin, Dresden, and Munich veterinary colleges for an average period of seven years is shown by the following: Of 86,613 diseased horses, 1,113 suffered from tumors, or 1.3 per cent. Of 85,537 diseased dogs, 4,020 suffered from tumors, or 4.7 per cent. f 4,972 diseased cattle, 102 suffered from tumors, or 2 per cent. Structure.—Tumors are composed of cells and usually, an intercellular substance. The cells may be similar to normal em- bryonic cells or to adult cells. The embryonic tumor cells differ from normal embryonic cells in that the former have no ten- dency to become matured while the latter have. The accom- panying cut shows a section of a sarcoma composed of embrvy- TUMORS. 269 onic cells that are similar to embryonic connective-tissue cells. Papillomata are composed of cells that are very similar, if not identical, to adult epithelial cells, and are supported by an adult connective-tissue framework. Tumor cells are very similar to the cells of normal animal tissues. They have practically the same structure and require the same kind of nutriment. However, they do differ from the normal tissue cells in their power of growth and reproduction. Tumor cells are usually more susceptible to changed environ- ments than normal tissue cells. The nuclei of the cells of a rap- idly growing tumor are usually larger probably because of in- creased functional activity. The intercellular substance of tumors is as variable as the intercellular substance of normal tissues. Tuniors having a mesodermal origin usually have an intercellular substance closely reseinbling that of normal connective tissue and hence may be mucus, fibrous, cartilaginous, or osseous. Tumors of an ectoder- mal or an entodermal origin may appropriate the pre-existing tissue framework for their stroma. Some tumors, like some normal tissues, are practically devoid of intercellular substance. Again, in some tumors the blood-vessels are the only intercellular substance. Anatomically the intercellular substance or stroma is an integral part of a tumor and its function corresponds to the function of intercellular substance of normal tissue. The cells and intercellular substance of tumors may be so arranged that the resulting structure approximates that of normal tissue (histoid tumors), but is never identical to a normal tissue. The different parts of a tumor may be assembled so that the resulting organization appears as an atypical gland or organ (organoid tumor), or tumors may be composed of structures derived from all three germ layers grouped indiscriminately but having some resemblance to an embryo (teratoid tumors.) Like normal tissue, tumors are usually nourished, by blood and lymph. The blood and lymph vessels may be structurally the same as normal vessels, or they may be composed entirely of tumor cells. The vessels have their origin from pre-existing ves- sels in the tissue from which the tumors are developed. They may be telangiectatic, cavernous, or plexiform, and _ their course is usually along the tumor stroma. Blood and lymph may also permeate the tumor through intercellular spaces, frequently resulting in hemorrhage or lymphorrhage. Some tumors have no blood or lymph supply, their nourishment probably being derived from consumption of normal tissue. Nerve cells and axones have been demonstrated in some 270 VETERINARY PATHOLOGY. tumors. They are, in some cases at least, a result of peripheral extension and development of the tumor tissue around normal nerve tissue, thus entangling it in the tumor. It is an open question whether nerve tissue exists in tumors except in those derived from normal nerve tissue or those in which normal nerve tissue 1s entangled. 3 Leucocytes are common in tumors. Lymphocytes and poly- morphonuclear leucocytes have been demonstrated in the blood and lymph channels, perivascular and intercellular spaces, and within the tumor cells. The cells and the manner in which they are assembled, the structure and arrangement of the intercellu- lar substance, and the presence of the blood and lymph vessels indicate a common origin of tumor tissue and normal tissue. Fig. 137.—Section of Sarcoma, showing sarcomatous cells and blood vessels. Size.—Tumors are quite variable in size. They may become so large that they mechanically destroy life. An abdominal sub- serous lipoma, about the size of a wash-tub and weighing thirty- eight kilograms, (831% lbs.) was observed in an ox. A Six- kilogram (13 1/, lbs.) fibroma was removed from the inferior cervical region of an eighteen kilogram (40 lbs.) dog. A twelve TUMORS. ZEt kilogram (26 2/5 Ibs.) chondroma was obtained from the ster- num of a fifty kilogram (110 lbs.) sheep. All of the above tum- ors were of sufficient size to mechanically inconvenience the animals afflicted, and in one case resulted fatally. From the enormously large tumors there are all gradations to those miscroscopic in size, miliary tumors. The size of tumors is determined to some extent by the amount of nourishment sup- plied, the kind of tissue of which they are composed, and their location. Shape.—The form of tumors is largely determined by the loca- tion and the kind of tissue in which they occur. They may be spherical, ovoid, elliptoid, nodular, miliary, tubercular fungoid, polypoid, tabular, elongated cylindrical etc. Where there is no resistance or only a slight resistance there is a tendency to sphericity. In outline they may be regular or irregular, smooth, nodular or even granular and in some cases the exact outline cannot be determined. Large tumors that in shape approach a sphere are designated as spherical, ovoid, elliptoid, etc. Those that vary in size from a pigeon egg to a small pea are spoken of as nodular tumors. Miliary tumors are small spherical growths varying from a small pea to those microscopic in size. Spherical or oval tumors causing an elevation in the tissue in which they grow are known as tubercular tumors. Fungoid or projecting tumors are those that develop from the surface or sub-surface tissue, being attached to the normal tissue by a wide base. Polypoid tumors or polypi have the same origin and project as fungoid tumors, but are attached by means of a small pedicle. Tabular tumors are flat and usually develop be- neath the surface and especially beneath fasciae, tendons or liga- ments. Color—The color of tumors is dependent upon; first, the kind of tissue composing them; second, pigmentation; third, degeneration; and fourth, the amount of blood they contain. A rhabdomyoma is more intensely colored than a fibroma, provided that the blood supply is the same in both, because of the hemo- globin in the muscular tissue. Melanomata and chloromata are so classified because of the deposition of pigment in them. Tum- ors, like normal tissues, become changed in color as a result of the various degenerations. Those having a limited blood supply are pale in color, while those having a large blood supply are highly colored. Hemorrhages may result in a deposition of hemoglobin or some of its derivatives, thus giving the tumor a mottled appearance. Mottling may also result from an un- equal blood supply. iw) NI NS) VETERINARY PATHOLOGY. Consistency.—Some tumors are soft and spongy, jelly-like, and from this type there are all variations up to those that are hard and resistant, bone-like. Their consistency is determined largely by the kind of tissue composing them and the secondary changes (degenerations) that affect them. Myxomata being largely composed of mucus are soft, fibromata are more resistant and osteomata are bone-like. Chondromata are usually quite firm and resistant, but they may undergo mucoid degeneration and: become soft and spongy. Colloid degeneration is rather common in carcinomata, rendering them glue-like in consistency. Otcca- sionally a tumor becomes calcified as a feat of Ce ReOuls infil- tration. Number.—Tumors may be single, that is, a single one only occurring in the animal body. Single tumors are usually benign although they may be malign. An animal may be afflicted with a great many tumors at the same time (multiple tumors). Tum- ors may become multiple by metastasis. Tumors resulting from metastasis are designated secondary and the original tumor pri- mary. Multiple tumors may be malign, as sarcomata, carcino- mata, etc., or they may be benign, as multiple fibromata. Tum- ors that recur after they have been removed are designated recur- rent tumors. Growth.—-The growth of tumors is the result of the inherent proliferative property of the tumor cells. Some tumors grow like an onion, there being a multiplication and accumulation of the central or internal cells, resulting in an interstitial expansion and an increase in the size of the tumor. Practically all benign tum- ors grow by interstitial expansion. Malign tumors grow by mul- tiplication of the peripheral cells and their ie fration as well as by interstitial expansion. The extent of growth of all tumors is proportional to the amount of nourishment they receive and to the adjacent tissue resistance. The relative amount of nourish- ment to tumor tissue and to normal tissue in the same body may be very unequal. Thus a tumor frequently receives an excessive amount of nourishment and grows rapidly, while the normal tis- sue in the same body is deprived of nourishment, resulting in its atrophy or degeneration and emaciation. As a rule, the rate of growth is indefinite. Malign tumors grow more rapidly than be- nign. A tumor that is growing rapidly may cease growth, dim- inish in size, grow again and diminish again. Diminution in size may be succeeded by absorption and disappearance. Extension.—The manner of extension of the various tumors depends upon the migratory properties of the tumor cells and the relation and structure of the blood and lymph vessels. Tum- TU MORS. 27S ors composed of embryonic cells extend more repidly than those composed of adult cells because embryonic cells are plastic and are to some extent capable of amoeboid movement. Adult cells are fixed in their form and none of them, excepting leucocytes and endothelial cells are migratory. The nutrient vessels of tumors are sometimes formed of tumor cells that are easily de- tachable, a structural peculiarity predisposing to tumor metas- tasis. Fig. 138.—Photograph of a section of a horse’s lung, showing Metastatic Sarcemata. Benign tumors usually extend only by growth in continuity or contiguity. In fact, practically all tumors composed of adult tissues extend by pushing aside the normal tissue. Malign tum- ors are extended by blood, as sarcoma; by lymph, as carcin- oma; or they pass from one point to another through natural channels as the digestive and respiratory tracts. Summary.—Tumors may be extended (1) by growth in con- tinuity, (2) by growth in contiguity, (3) by blood, (4) by lymph, (5) by natural channels other than the blood and lymph vessels. Natural Resistance.—Normal tissues have a natural resist- ance to any injurious influence as the formation of tumors, in- 274 VETERINARY PATHOLOGY. flammation, degeneration, etc. Tissue resistance to the devel- opment of neoplasms varies in different animals, in the same animal at different times, and possibly also in the different tis- sues of the same animal. The resistance of the surrounding tissue is made evident in some cases by the formation of a fibrous wall or capsule that limits and separates the tumor and the nor- mal tissue. Degeneration and necrosis may also be interpreted to be a result of opposed action by the invaded tissue. Retrogressive Changes.—Tumors are subject to the same degenerative processes that normal tissues are. Hemorrhages, necrosis and degenerations are frequent in tumors because of the imperfectly formed and irregular distribution of the supplying vessels. The results of hemorrhage into tumors depend upon the amount of extravasted blood and the secondary changes therein. A tumor the size of a cocoanut would likely become necrotic if a vessel ruptured and a half a liter of blood escaped into the tumor tissue. A small quantity of extravasate when infected with putrefactive microorganisms as a rule results in necrosis of the tumor tissue. Necrosis is a sequel of ob- structed circulation or results from the solvent action of meta- bolic products. Thus, necrosis may be the result of thrombosis or embolism. Thrombic formation is especially prevalent be- cause of the irregularities of the lining of the tumor vessels. Emboli are common, as they are frequently detached tumor cells. Circulation may also be interfered with by pressure of the tumor tissues, thus obstructing the efferent or afferent blood vessels. Some metabolic products of tumors constantly dissolve the sur- face cells, resulting in ulceration, a common necrotic condition observed in tumors. Tumors may be invaded with pyogenic bacteria, resulting in suppuration. Of the degenerations, mucoid and colloid are the most com- mon. Fatty degeneration and calcareous infiltration occur less frequently. Mucoid degeneration affects connective tissue and epithelial tissue tumors, occurring more frequently in the former. Colloid degeneration is found in epithelial tissue tumors. A four-kilogram (9-lb.) renal hypernephroma undergoing colloid degeneration was obtained on post-mortem examination of a three-year-old steer. Fatty degeneration usually succeeds necrosis in tumor tissue. Calcification of tumors is quite com- mon. Pigmentation is more common in tumors than in normal tissue. Melanomata are tumors containing melanin that has been deposited in the tumor cells. Chloromata are tumors con- taining a green pigment. Hemoglobin, hematoidin and hemo- TUMORS. WAS siderin are frequently found in tumors after hemorrhage into the tumor tissue. Clinical Considerationm—Tumors are benign or malign. Benign tumors are usually encapsulated, i. e., they grow only by interstitial expansion; are composed of adult or matured tissue; have no tendency to recur when removed, and have only a mechanical effect upon the body in which they occur. Malign tumors are usually not encapsulated; they grow by peripheral infiltration; are usually composed of embryonic tissue; fre- quently recur when removed, and have a tendency to kill by absorption of the metabolic products which are deleterious to the body. Malign tumors of domestic animals are not as fatal as they are in the human. Many horses affected with sarcomata have been permanently relieved by operation. Etiology.—There are some predisposing factors as heredity and breed peculiarities that are frequently involved in the devel- opment of tumors. Cadiot refers to a family of dogs in which the females were affected with carcinomata of the mammae for Fig. 139.—Photograph of a horse affected with an ocular Epithelioma. This was a sequel of a wire cut 276 VETERINARY PATHOLOGY. two successive generations. Hereford cattle are more frequently affected with ocular tumors than any other breed. Injuries in which there is a destruction of the tissue surfaces predisposes to tumor formation, and, in many instances, in the human, sub- surface wounds are a causative factor in the production of epithelial embryonic tumors. A few cases of epitheliomata have been studied in the horse and ox that were secondary to injuries. The exciting causes of tumor formation have not been defin- itely determined, and this accounts for their undetermined char- acteristics. Many theories have been advanced. Cohnheim ad- vanced the idea that tumors were developed from misplaced embryonic cells (cell rests). This theory has received the sup- port of many pathologists. It is in accord with the general biologic law that every cell produces a cell like itself or “like begets like.’ The supporters of this theory have not proved it. but the opponents have not disproved it. All biologists recog- nize the complexity of embryonic development and are aware of the possibility of cells becoming entangled or misplaced dur- ing the formation period. Experiments have demonstrated the possibility of successfully transplanting tissue, both embryonic and adult, into a foreign location in the body. Transplanted em- bryonic tissue, however, does not remain as such, but soon be- comes mature tissue, whereas malignant tumor cells have no tendency to become matured. Transplanted tissue cells do not infiltrate the surrounding tissue nor form metastases, but remain as distinct islands of cells. The parasitic theory has been supported by a large number of scientists. No doubt malignant tumors resemble infectious diseases in that they extend by metastasis and produce similar effects. However, the uncertain transmission of tumors from one animal to another is certainly antagonistic to the parasitic theory. 3 Bashford, superintendent of the Imperial Cancer Research Fund, London, England, successfully transplanted 66 per cent of sporadic tumors. On the other hand, Ehrlich has successfully transplanted only about 14 per cent of sporadic tumors. No one has produced a satisfactory proof of the isolation of any causa- tive parasite. By some authorities bacteria were thought to be the active agent in tumor production, and by others protozoa were claimed as the causative factor, and, more recently, many radical observers have proclaimed that yeast were the cause. Some have even claimed that the tumor cells are parasites. Chemic disturbances, particularly changed chemic reaction in a tissue, is responsible for tumor formation according to some. TU MORS:.: DIR, An alkaline secretion at points where exposure and irritation occurs produces carcinomata (Hertzler). Following this thought an acid reaction in a normally alkaline tissue would tend to pro- duce sarcomatous tissue. The specific causative factor of tumor formation is not known, but it is something that excessively stimulates the reproductive power of cells. In fact, all other functions practically cease, the entire cell energy being expended in reproduction. That is, tumors are the result of a disturbance in the cell nietabolism in which reproduction is far in excess of the physiologic limit and is exercised at the expense of all other functions. Varieties.—There is no satisfactory method of classifying tumors. Some authors have attempted methods of classifying, but until more is known concerning them a classification is un- wise. The following is an attempt at grouping them, but is in no way complete. They may be grouped as to: OCCURRENCE. - Primary—The original or first tumor. ~ Secondary—Metastatic tumor. Recurrent—A newly developed tumor at the point Fv out which one has been recently removed. ETE GI MONI EE Histoid—Simple tissue tumor. Organoid—Organ-like tumor. Teratoid—Mixture of various tissues resulting in a Structure re- sembling an embryo. GEENI CALEY. si = Benign—No tendency to kill. Malign—Having a tendency to kill. The following scheme shows the general structure and rela- tion of the various tumors: Wiyscomlas CC nondnroma: gs cies. acie ae sly el)e6 Connective ..-3 Osteoma, odontoma, ..-..-----.----+---.. etnoniay Gili@niame rere es ech, sieeve Fibroma : Epihoiam 10 eee Papillomawe yen ose ieee etts f Adult Tissue . 4 ipsonin aoa etOtiny Omit tater, cons are crseag eat k hat Se : ; Winald@myoimiay se ees see sheet wa Sto ce: . Lymphangioma ...-- WN Hee Neha eect SO ES Sa lemma deorOimasant% hase ed ome eS Tumors , Nervous-neuroma ( Round Cell .4 Connective-sercoma spindle Cell Myeloid Cell Endothelioma } Placentoma Garcimomia wast. vaso Hypernephoroma | Epithelium 1 INGER OMIAM : eas Sees 3 | lL Epithelioma ........- J j L Embryonie Tissue 4 BULOLB19 278 VETERINARY PATHOLOGY. FIBROMA. Fibromata are tumors composed of adult fibrous connective tissue. They occur in all animals. The skin and subcutaneous areolar tissue is their most frequent location, but no tissue is exempt. They are frequently found in the region of the sternum of the horse and ox, in the ovary and uterus of the cow, and in the perineal and elbow regions of the dog. In the skin and sub- cutaneous tissue they usually appear as loose, circumscribed, nodular growths. Some fibromata have no well defined border. or line of demarcation but are apparently diffused through the tissue. This type, however, is somewhat rare, and possibly they are not fibromata. They may become so large that their pres- sure produces atrophy, degeneration or necrosis of the skin covy- ering them, or the surface epithelium may produce sufficient new tissue to compensate for the increased surface. These tu- mors are usually single, that is, only one tumor occuring in the individual; but they may be multiple. Multiple fibromatosis is occasionally observed in the subcutaneous tissue of horses. They are variable in size, being so small in many instances that they are not observed in an ordinary examination. A fibroma may be so large that the diagnostician would mistake it for a malignant tumor, a hernia, cold abscess, etc. Their shape is as variable as their size. They may be oval, tabular, tubercular, nodular, and, in fact, they may have any conceivable shape and contour. If the skin or covering tissue is incised or dissected away the tumor is usually found to be surrounded by a fibrous capsule or, in rare instances, it may blend imperceptibly with the surround- ing normal tissue. They are not difficult to remove in their entirety because of their encapsulation. When they are excised their blood supply is found to be disproportionate to their size. With the small or limited blood supply there is a tendency to a slow growth and degeneration and necrosis. With an exces- sive blood supply there may be rapid growth and perhaps fre- quent hemorrhages into the tumor tissue. If the excised tumor is sectioned and the cut surface examined with the unaided eve, it appears to be composed of compact bundles of fibrous connec- tive tissue atypically arranged (hard fibroma) or of loosely ar- ranged bands of fibrous connective tissue inclosing areolar spaces (soft fibroma). In color the section appears pearly white with grayish-white, yellowish-white or dull pink areas, depending upon the compactness of the tissue, whether the fibre bundles are cut longitudinally or transversely, and the amount of blood contained. A fibroma is firm, dense and resistant, and when cut TUMORS. 279 into there may be a creaking sound similar to that produced in cutting a tendon. They have little or no tendency to peripheral infiltration but grow by central or interstitial expansion, mechan- ically pushing the contacting tissue aside. If the tumor has degenerated or become necrotic quite a dif- ferent picture than the above will be seen. It may be a mass of mucus as a result of mucoid degeneration. It may contain necrotic areas or the entire tumor may undergo necrosis, the necrotic tissue becoming liquified, coagulated, caseated or calci- fied. Hemorrhage into the tumor tissue may give it a mottled appearance. The hemorrhagic spots may be red, yellowish-red or greenish-red, depending upon the changes in the hemoglobin. Microscopically, the tumor tissue appears as white fibrous connective tissue, being composed of cells and a white fibrous intercellular substance. ee SO Re , FS a pei A ‘ BLO N\ ~ Ns \ AN | vn) Rear Se Se ak TIAN Ne MN) b SASS SEEN ( \N CLE iY lg Zee’, % Y Ay “fgg Za, ES SS —", Rees Fig. 140.—Section of a hard Fibroma showing: 1. Transverse section of bundles of Fibres; 2. Longitudinal section of bundles. The cells are usually few in number, are flat and have a flat, oval nucleus. Cells are more prevalent in the rapidly growing tumors. The arrangement of the fibres varies and is the deter- mining factor of the denseness of the tumor. A hard fibroma is made up of bundles of fibres extending in 280 VETERINARY PATHOLOGY. various directions and occupying practically the-entire space, _there being no interfunicular spaces. The bundles are compact masses of parallel, wavy fibres, with here and there a cell. The fibres are of two varieties, viz.: glia fibres and collagen fibres. Glia fibres are found along the surface of the cell and are parallel to its long axis. They are straight or slightly curved and prob- ably extend from one cell to another. Collagen fibres are out- side but lie close to the cell and appear slightly wavy. Collagen fibres predominate in fibromata. Blood vessels are few in num- ber and may be absent. : A soft fibroma is composed of smaJl bundles or bands of fibrous tissue loosely arranged. Ceils and blood vessels are more numerous than in hard fibromata. The general appearance of a loose fibroma magnified one hundred diameters is very similar Fig 141.—Soft Fibroma, showing wavy loosely arranged fibres, to areolar tissue, except that in the former yellow elastic tissue is absent, while in the latter it is present. All variations in the compactness of the fibrous tissue is found from the soft to the hard fibroma. In fact some sections indicate that a soft fibroma becomes a hard fibroma by an increase in the intercellular fibres. Clinically, fibromata are innccent or benign tumors. Their rate of growth is relatively slow. ‘They may cause a fatal termin- ation by mechanically obstructing the lumen of a hollow organ, as the intestine, by pressure upon vital organs, as the brain, or they may become so large that the affected animal is unable to move about in search of its food. Thus Kitt mentions a fibroma TUMORS. . 281 that weighed 178 kilograms (391 */, lbs.) They do not extend by metastasis, neither do they recur when removed. Fibromata can usually be differentiated from inflammatory new growths by the history of the case, fibromata having nu defined cause and inflammatory new growths resulting from irri- tation. Microscopically, inflammatory new growths contain mi- totic plasma cells and fixed connective tissue cells, while mitosis is rarely observed in fibromata. There is also an extensive blood supply in inflammatory growths, but a limited supply in fbroma- tous tissue. Actinomycotic and botryomycotic tissues are recog- nized by the presence of the causative fungi. Spindle-cell sar- comata may be confounded with fibromata and are sometimes difficult to differentiate. Sarcoma cells usually contain more protoplasm than fibroma cells, and this may be used as a basis for differentiation. By a gross examination a leiomyoma may be mistaken for a fibroma, but the microscopic appearance of the nuclei is characteristic. The nuclei of fibroma cells are oval while those of leiomyoma cells are rod-shaped. Ii the fibroma contains degenerated or necrotic centers the differentiation may be more difficult in gross section but microscopic examination of the unchanged tumor tissue will be sufficient. When the en- tire tumor has degenerated or become necrotic diagnosis may be impossible. Fibromatous tissue may be found in other tu- mors or fibromata may become contaminated by permeation or infiltration of other tumor tissue as mucoid, sarcomatous, etc.. resulting in a fibro-myxoma, fibro-sarcoma, etc. The first por- tion of the compound word denoting that the mixed tumor con- tains more of that tumor tissue. Thus a fibro-myxoma is a tumor composed of fibroma tissue (fibrous connective) and myx- oma tissue (mucoid connective), the former predominating. Mixed tumors will be discussed after consideration of the simple tumors. A keloid is a dense overgrowth of white fibrous connective tissues in a cicatrix. These growths are quite common in the negro, especially at the point of an injury, as a razor cut or ear puncture for an ear-ring, etc. Because of their frequency and extent they have been considered as tumors by some authors. They are not true tumors but rather an inflammatory new growth resulting frem improper cicatrization in wounds. They are not common in the lower animals. 282 VETERINARY PATHOLOGY. MYXOMA. Myxomata are tumors composed of mucoid connective tissue. These tumors may be a subvariety of fibroma. Purely myxo- matous tumors are not very common, occurring more frequently in combination with other tumor tissue. They are usually found in connective tissue, but in no special location. They have been found in the heart, along nerve trunks, in the nostril, and a case has been reported of a pure myxoma involving the entire orbital structures in a horse. These tumors are usually about the size of a hen’s egg, rarely becoming very large, probably because of their destruction by degeneration. They are invariably single. They appear as semi-solid masses, surrounded by fibrous cap- sules and are usually dirty-white or gray in color. After they are removed and an incision made into them a mucus or gela- tinous, ropy fluid escapes. The cut section appears as a glassy, semi-transparent, semi-solid mass and is very similar to Whar- ton’s jelly. The escaped fluid will be found by chemical test to contain considerable mucin. Their blood supply is usually very meager, in fact some authors regard myxomata as a mucoid degeneration because of their limited blood supply. Microscopically, a myxoma is composed of stellate cells, in Fig. 142.—Section of Myxoma from the orbital fossa of a horse, showing stellate cells. TUMORS. 283 which the cell processes are apparently continuous with the pro- cesses of adjacent cells. Myxoma cells have an oval nucleus and the spaces between the cells and cell processes are filled with mucus, which appears as a stringy, gray substances that stains red with eosin. Myxomatous cells produce both kinds of fibres, | i. e., glia and collagen fibres. The collagen fibres are more or less separated from each other by a varying quantity of fluid containing mucin. Myxomata are prone to degeneration, result- ing in the formation of a cyst, or the fibrous capsule may become eroded, allowing the degenerated contents to escape into the sur- rounding tissue or upon a surface. In the latter case the degen- erated contents is usually absorbed. Cicatricial tissue is usually produced in the cavity or space occupied by the myxoma. Sub- surface, myxomatous, degenerated areas may become infected, resulting in abscess formation. Clinically, myxomata are benign tumors. They grow slowly by interstitial expansion, do not recur when removed, and ex- tend only by continuity or contiguity. These tumors are differentiated from muccid degeneration, as the latter contains no stellate cells, and there are usually some of the cells present in mucoid degeneration that are normally present in that area. Clinically, it may at times be difficult to distinguish between mucus retention cysts and myxoma, but by the exploring needle the contents of the cyst may be evacuated and thus the nature of the mass will be determined. CHONDROMA A chondroma is a cartilaginous tumor. They occur in cattle, sheep, dogs, horses and fowls. They are found most frequently in the location in which cartilage is normally found. The ster- num seems to be a favorite location for their development, prob- ably because of the frequent injuries of the sternal! cartilage due to the fracture of ribs and other injuries. They not infrequently occur in other bones, possibly developing from islands of cartil- age that have not ossified, or from marrow or periosteum. They also occur in glandular tissue as the thyroid, parotid, ovary and testicle, and a few cases of chondromata of the lung have been reported. These tumors appear as hard, nodular, well-defined growths, unless they are undergoing degeneration. In this case they may be of the nature of cysts, or if their capsule is ruptured, they may be soft, spongy, diffuse masses. They are variable in size. A chondroma weighing 12 kilograms (26 1/5 lbs.) was obtained 284 VETERINARY PATHOLOGY. from the sternum of a sheep killed in a Kansas City abattoir. Another about the size of a pigeon’s egg and attached to the sternum of a small hen was found by a city meat inspector. Their shape is very irregular, but they are most frequently oval. As a rule they have a regular surface, though they may be lobulated. They are usually separated from the surrounding tissue by a fibrous capsule, but they may be firmly adherent to the adjacent tissue. In cutting, the tumor gives a resistance sim- ilar to cartilage and they may be gritty because of calcification or ossification. The ablated tumor is bluish-white if it is a pure chondroma. Degenerated areas will vary in color according to the kind and degree of the degeneration. Necrotic centres appear dull gray or yellowish-white and white if calcified. If the tumor is mixed the color will vary according to the contaminating tumor tissue. : Chondromatous tissue is composed of cartilage cells and an intercellular substance. The cells are irregular in size and shape and the number found in each lacuna is more variable than that in normal cartilage. The size, shape and arrangement of cells in different areas in the same tumor is variable. The cells are fre- quently degenerated, the nucleus fragmented and the cell mem- brane ruptured, allowing the cells to fuse as a homogeneous Fig. 143.—Section of Chondroma from sternum of a sheep, showing lacunae with inelosed cartilage cells. TUMORS. 285 mass. The lacunae are not so distinct as those in normal cartil- age, and their capsule may be absent. The intercellular substance is usually homogeneous, as in normal hyaline cartilage, or it may be fibrous, as in normal fibro-cartilage or elastic cartilage. The in- tercellular substance becomes fibrous towards the margin of the growth and finally forms a perichondrium. The cells may be arranged in rows near the perichondrium, but they are more likely to be irregularly distributed. The microscopic appearance of a degenerating, necrotic or mixed chondroma depends upon the kind and extent of the condition existing. Clinically, chondromata are usually benign, but they may be- come malignant because of their extent. Some surgeons have recorded csses of metastatic chondromata. These tumors are frequently lobulated and may be multiple. They have little ten- dency to recur when removed. LIPOMA. Lipomata are tumors composed of adipose tissue with a con- nective tissue framework supporting the vascular supply. They occur quite commonly in the horse, ox, and dog, but none of the domestic animals are exempt. They usually develop where adi- pose tissue normally exists, as the subcutaneous tissue, submu- cosa and subserosa, omentum, ete. They may also occur in tissue that contains no fat, as the liver, kidney and even the brain. They occur most frequently in the subcutaneous tissue in the horse; in the intestinal and omental subserosa of the ox and hog; in the subcutaneous and conjunctival submucosa in the dog, and in the uterine submucosa of the sheep and the cow. Lipomata are usually circumscribed, but they may be diffuse. The accompanying cut is from a photograph of a two-year-old colt in which there is shown a diffuse subcutaneous lipoma of the left hind leg. These tumors may become enormous in size in the horse and ox, some cases having been reported of lipomata as large as a wash-tub and weighing 30 to 70 kilograms (66 to 154 lbs.). In consistency, these tumors may be firm and dense or soft and flabby. They are usually surrounded by a fibrous capsule and in section those from the peritoneum and omentum ere yellowish or white in color. Peritoneal, omental, submucous and subcutaneous lipomata have a smooth surface; intestinal lipomata are usually lobulated. Bands of connective tissue may divide the tumors into lobes or lobules or the connective tissue may be diffuse throughout the entire structure. In cutting a lipoma the resistance varies accerding to the quantity of fibrous connective tissue it contains. If osmic acid is applied to the free 286 VETERINARY PATHOLOGY. surface of the gross specimen it stains the adipose areas black but has no effect upon other tissue. Occasionally groups of adi- pose cells become necrotic and calcify, thus forming gritty areas. Complete necrosis with sloughing or calcification is not rare in the larger lipomata. Fig. 144.—Trom photograph taken 6-20-’7 of a colt affected with a Subcutaneous Lipoma. Photograph presented by J. IT. MeNeil. TUMORS. 287 Microscopic sections of lipomatous tissue closely resemble normal adipose tissue, except that the cells may be larger and perhaps more irregular in shape. As in normal adipose tissue the adipose cells are supported by connective tissue cells and fibres. The application of Sudan III and osmic acid gives further proof of the composition of the cells. Lipomata may be multiple but they are typical benign tumors, though death may result from the mechanical effects produced Fig. 145.—Section of a Lipoma from omentum of an ox, showing framework. of adipose cells, by them. They do not form metastases. Subserous lipomata pro- duce volvuli which terminate fatally in horses. Large periton- eal or omental lipomata of the ox and dog frequently cause suffi- cient displacement of the abdomina! organs to materially de- range their function. Subcutaneous carpal lipomata in the horse may become so large that they mechanically interfere with loco- motion. Lipomata may have a fibrinous infiltration and organ- ization resulting in lipomatous elephantiasis. 288 VETERINARY PATHOLOGY. OSTEOMA. An osteoma is a tumor composed ef osseous tissue. Pure osteomata are not common. They occur most frequently in re- lation to bones and usually at the union of osseous tissue devel- oped from different ossifying centres. These tumors are quite common in mules, appearing as projecting pedunculated masses attached to the inferior maxilla. More rarely they are found in other organs, as the lung, parotid gland, mammary gland, etc. Fig. 146.—Perdunculated Osseous Tumor Maxilla. Horse. These tumors are usually small, rarely becoming as large as a cocoanut. They are hard, nodular masses that are frequently lobulated and usually firmly attached to the surrounding tissue. It is possible that they are developed from osseous cells which have been misplaced in bone formation or from the osteogenetic layer of the periosteum. When they develop adjacent to pre- existing bone the periosteum or endosteum surrounds them. Those osteomata developing in other structure than bone are surrounded by a distinct membrane which is usually very sim- ilar to periosteum. Osteomata may be classified as: (1) hard, ivory or eburnated, and (2) soft, spongy or cancellated. Either of the foregoing classes may be homologous or heterologous. Homologous osteomata occur in bony structures and may be an exostosis or an enostosis. Heterologous osteomata occur in other tissue than bone. Hard, ivory or eburnated osteomata are structurally very similar to the compact osseous tissue of a long bone. Haversian systems may be present or they may be absent. If the Haversian systems are present they are irregularly arranged and are ap- proximately perpendicular to the surface of the related bone. If TUMORS. 7 289 the Haversian systems are absent the tumor is composed of superimposed lamellae like the outer circumferential lamellae of the shaft of a long bone. Soft, spongy or cancellous osteomata are surrounded by a periostoid membrane. In structure they are similar to cancellous osseous tissue. The marrow spaces may be occupied by tissue that is structurally identical to red marrow or they may be filled with sarcomatous tissue, fibrous connective tisssue, etc. The blood vessels are usually normal in structure and their distribu- tion is through Haversian canals in the hard osteoma or the spaces in the soft osteoma. Ostecmata are invariably single; do not recur when removed ; have no tendency to form metastases ; and hence are benign. They should be differentiated from (1) ossification of inflam- matory new growths as ringbone, spavin, myositis ossificans, etc.; (2) hyperplasia of osseous tissue; (3) ossification of tumor tissue as fibromata, chondromata, etc.; (4) metaplasia in which osseous tissue is the end product; (5) calcification. GLIOMA. A glioma is a tumor composed of supporting cells (neuroglia cells) of the tissue of the central nervous system. Neuroglia tissue occurs in two forms, as ependymal cells lining the neural canal and the ventricles and as glia cells which are derived from the ependymal cells and act as a supporting framework of the central nervous system. Gliomata are of two types, depending upon the type of cells composing them, viz., spider cell glioma and mossy cell glioma. Gliomata have been observed only two or | three times in the domestic animals. They usually have their origin in the gray matter near the central canal of the spinal , cord or in the gray matter of the cerebrum. They do not become ' large and they are usually not encapsulated. They are composed of cells that are very similar to normal neuroglia cells. The glioma ceils mav be slightly larger than neuroglia cells but they | have the fibre-like processes characteristic of them. These tumors do not form metastases but are likely to produce a fatal termination by pressure upon nerve centers. ODONTOMA. Odontomata are tumors composed of dental tissue and usu- ally occur:in connection with teeth, particularly the superior molars. QOdontomata are of frequent occurrence, the majority of dental diseases in two f9 five-year-old horses being due to 290 VETERINARY PATHOLOGY, - them (Williams). Facial bulging is a common symptom of them and there may be an excessive mucus discharge from the nostrils. Cystic odontomata may produce super-resonance, which is useful in differentiating them from empyema of the facial sinuses. These tumors are derived from the enamel organ, dentine papilla, or the tooth follicle. Their derivation to some extent determines their structure. Those derived from the enamel organ are composed of an enamel covering and in some cases the entire odontoma is enamel. Dentine is usually the pre- dominating tissue in those derived from the dentine papilla. From the tooth follicle there are usually formed cystic odonto- mata, although they may be fibrous or may contain ossified cen- tres and cementum. Their structure varies considerably and it is not rare that all of the above structures are represented in one odontoma. In size, odontomata vary from microscopic masses to irregu- re ~ WSs NS Fig. 147.—Photograph of an Odontoma of the interior maxilla of a horse, TUMORS. 291 lar bodies. Theift shape and color are as variable as their size. Epithelial or enamel odontomata are the highest in the scale of hardness of all tumors. Other types of odontomata are soit. Cystic odontomata may be single or multiple, as many as three hundred having been observed in a single follicular tumor of this type. They may grow very rapidly but more frequently they develop slowly. They have no tendency to form metastases. Degeneration is common in those developing from the tooth follicle. Clinically they are benign but may cause fatal termina- tion mechanically or from infection. According to the derivation Sutton describes four classes of odontomata as follows: 1. Those derived from the enamel organ or epithelial odonto- mata. They usually appear as irregular masses covered with enamel. They may contain cystic cavities separated by enamel partitions. Epithelial odontomata are usually surrounded by a firm capsule, and in some instances appear to have had their origin from a mucous membrane. Miscroscopically they are found to be composed of ename! cells and irregular columns of epithe- lial cells forming alveoli. The epithelial cells vary in shape from columnar to the stellate or typical progenitors of enamel. These tumors occur in most of the domestic animals and usually in early life. Two epithelial odontomata were obtained from the left maxillary sinus of an aged horse used for dissecting pur- poses. These odontomata were completely enclosed in an osse- ous mass, the maxillary sinus being completely filled by the new growth. The facial bones were slightly bulged. The osseous formation surrounding the odontomata and the thickening of the facial bones indicated that considerable time had elapsed since their formation. 2. Those derived from the tooth follicle. Depending upon the nature of the neoplasm this group may be further subdivided into follicular and fibrous odontomata, cementomata and com- pound follicular odontomata. Follicular odontomata result from hyperplasia of the tooth follicle tissues which thus prevents the normal eruption of the tooth. They may appear as simple or multiple cysts. Their walls may be calcareous or osseous but they are more frequently membranous. The cysts are usually subdivided into many com- partments, the cavities of which are lined with epithelium. This lining epithelium secretes a viscid fluid, the accumulation of which is responsible for the enlargement of the cysts. They occur in sheep, hogs and horses. Fibrous odontomata are produced by a marked increase of 292 VETERINARY PATHOLOGY. the enveloping fibrous. capsule of the follicle. The hyperplastic fibrous tissue usually fuses with the cementum, and the entire mass may later become calcified or ossified. These odontomata are most common in ruminants, goats especially being affected. ‘They are prone to occur in animals afflicted with rickets. Cementomata (Osteocystoma capsulare dentiferum) are formed by ossification cf excess tissue developed around the tooth follicle. The hyperplastic cementum may include several tooth germs. They appear as masses of cancellous or spongy bone and are structurally very similar to cementum, being com- posed of irregular spaces surrounded by osseous tissue contain- ing branched lacunae. They are most common in horses, occur- ing most frequently in connection with the incisor teeth. Fig. 148.—Enithelial Odontoma. Compound follicular odontomata result from the ossification of irregularly located areas of the tooth follicle tissues, thus leaving intervening areas of fibrous tissue. The ossified masses are designated denticles and they may be very numerous, as many as three hundred having been observed in a single tumor. The intervening tissue usually degenerates and becomes of a liquid consistency. Thus the tumor appears as a cyst containing many cavities. The denticles vary in size and consistency. These tumors have been observed in the goat, sheep, ox, and horse. TUMORS. 293 3. Radicular odontomata are those derived from the dental papilla, developing from the roots of a tooth after the crown has formed. They appear as bony masses and are frequently enclosed within the maxilla. Structurally, they consist of den- tine and cementum, the dentine usually being surrounded by a cemental capsule. They are occasionally observed in domestic animals, being most common in boars. 4. Composite odontomata are composed of varying amounts of irregularly arranged enamel, dentine and cementum. A single tumor may contain several teeth fused into one mass. Their structure varies with the amount of each of the above named constituents they contain. Thus they may be almost entirely enamel or contain a very little enamel. They may be solid and massive or cystic. They are very likely to cause suppuration and necrosis of the adjacent tissues. This type of odontomes occurs more frequently in the horse. Dentigerous cysts are more properly classified as a type of teratomata and will be discussed with that group of tumors. NEUROMA. Neuromata are tumors composed of nerve tissue. They are exceedingly rare. They occur in connection with ganglionic cells and most frequently those of the sympathetic ganglia, al- though they may occur in the brain. They appear as nodular growths varying from the size of a pin head to that of an apple They are gray or white in color, rather firm, and usually sur- rounded by a capsule. Irregularly shaped ganglionic cells inter- posed with some nerve fibres constitute their minute structure. These tumors should be differentiated first from the so-called “amputation neuromata,’ which are simply an entangled mass of regenerated axones and are not tumors; second from fibromata that develop from the perineurium or endoneurium of a nerve trunk. . Neuromata may be multiple but they are benign. ANGIOMA. ‘These are vessel tumors that are developed independently of pre-existing vessels. But it is frequently impossible to deter- mine whether the mass of vessels is a result of excessive growth of the pre-existing vessels (hyperplasia) or whether they are newly-formed vessels. Possibly angiomata should be discussed under the caption of 294 VETERINARY PATHOLOGY. endotheliomata as it has been thought by some that the endothe- lium is the only neoplastic portion of an angioma. This group is composed of (1) hemangiomata. (2) lymphan- giomata. Heuele Hemangiomata are blood-vessel tumors. In the human they are found most frequently in the skin and may occur in the skin in domestic animals, but are not often observed there because of the pigmentation of the skin. They are found most frequently in the liver and the spleen of the ox, dog, horse and sheep. An occasional case is observed in the subcutaneous tissue of the horse. Hemangiomata may be subdivided into four varieties. Hemangioma simplex (Capillary telangiectases, nevus, birth mark) is a tumor in which there is an excess of capillary vessels are considerably enlarged or dilated. The vessel wall is usu- ally altered in structure, the endothelial cells being larger and the perivascular tissue more dense. These are quite common in the liver of the ox where they appear as irregular blood spots, red or purplish 1n color. Fig. 149.—Haemangioma Simplex. a. Large capillaries engorged with blood. b. Liver cells. Cavernous hemangioma (hemangioma cavernosum) is a tumor composed of spongy tissue similar to erectile tissue. The caver- nous spaces are filled with blood, thus coloring the tumor red or bluish-red. These tumors are found most frequently in the liver and spleen. An ox liver containing cavernous spaces, each as large as a hen’s egg and containing parietal thrombi, has been DD observed. A lobulated enlargement in the spleen of a dog was TUMORS. 295 found to be a cavernous hemangioma. The spaces in cavernous hemangiomata are lined by endothelium that is supported by a very limited amount of white fibrous connective tissue, yellow elastic tissue being practically absent. Fis. 150.—Photograph of spleen of dog affected with an Hemangioma Carvernosum, Hemangioma hypertrophicum is a blood-vessel tumor composed of masses of relatively small vessels, in which the vessel walls are hypertrophied. One of these tumors occurring in the subcu- taneous tissue of the metacarpal region of a horse has been observed. It appeared as a mass beneath the skin and was about the size of a hen’s egg. Pulsations could be observed and by palpation they were quite distinct. The tumor when removed was a tangled mass of blood-vessels with comparatively small openings. Microscopically, the vessel walls were found to be hypertrophied. The vessels were held together by fibrous con- nective tissue. Cirsoid aneurisms are tumors composed of dilated and enlarged 296 VETERINARY PATHOLOGY. tortuous arteries. This variety of hemangiomata is not comnion in the domestic animals. Lymphangiomata are tumors composed of newly-formed lym- phatic vessels. These tumors are not common; in fact, only one Fig. 151.—Section of Hemangioma Hypertrophicum, showing an increase in the number of the vessels and an hypertrophy of their walls. or two cases have been reported by veterinarians. The tumors may be conveniently divided into capillary and cavernous. Angiomata are usually benign tumors, although by rupture they may produce fatal hemorrhage or lymphorrhage. MYOMA. Myomata are muscle tumors. They are divided into two classes:» 1:-Le1omyomata) or the /smooth) amuscle tumionsauee: Rhabdomyomata or the striated voluntary muscle tumors. My- omata, found occasionally in the human, are rare in the lower animals. TUMORS. 297 Leiomyomata are found most frequently in those locations in which involuntary muscle tissue normally exists, as the uterus, bladder, intestine, etc. They are nodular or diffuse, dense, pale pink masses appearing very similar to fibromata. Microscopic- ally they are composed of miscellaneously arranged involuntary muscle cells. They differ from fibromata in that the muscle cells are thicker and usually not as long as the fibres of fibromata. Frequently they are combined with fibromata forming a leiomyo- fibroma, making the diagnosis more difficult. Leiomyoma cells may be very similar to the cells of a spindle-celled sarcoma, but Fig. 152.—Leiomyoma, small intestine, mule. the nuclei of the former are long and rod-shaped while those of the latter are oval in shape, a characteristic usually sufficient for diagnosis. The cytoplasm of the leiomyoma cells stains densely with acid stains. Rhabodomyomata have been found in the kidney, ovary and testicle. They are probably the result of the development of misplaced embryonic myoblasts. These tumors are usually pale in color. In microscopic section the cells are irregularly striated, 298 . VETERINARY PATHOLOGY. and are variable in shape and arrangement. These tumors are Fig. 153.—Leiomyoma., a. Smooth nucleus cell, showing nucleus. Sauk COE A sarcoma is a tumor composed of embryonic connective tis- sue cells. Ihe cells have no tendency to’ become matute iam constantly appear as undifferentiated embryonic cells. Sarcomata are of frequent occurrence in all domestic animals. They have no predilection for tissue or location, and are variable in size and shape. They may be circumscribed but ‘are more frequently dif- TUMORS. 299 fuse. Metastases are frequent in the lungs, liver and kidney. Metastatic sarcomata are usually circumscribed. Sub-surface sarcomata may produce necrosis of the surface tissue, the tumor projecting as a red, granular mass, which ap- pears very similar to exuberant granulation. The surface tissue may not be destroyed, the tumor appearing as a sub-surface nodule or diffuse mass. Some sarcomata are encapsulated and are easily enucleated, but the malignant varieties have no cap- sule and it is impossible to differentiate the surrounding tissue from that of the tumor. Sarcomatous tissue may be soft and spongy or hard and dense, depending upon the extent of the intercellular substance and the kind of cells composing it. In color they vary from gray or white to pink and they may be mottled, depending upon hemorrhage, pigmentation, or necrosis. the microscopic appearance varies with the different varie- ties, but in general they are composed of embryonic cells having Fig. 154.—Photograph of a horse affected with Sarcoma of the Mediastinum result- ing in obstructed circulation. (a) Oedeima inferior thoracic region. (c) Subcutaneous veins. (ov) Jug lar vein engorged with blood. ; 300 VETERINARY PATHOLOGY. a limited amount of intercellular substance. The cells may be round, spindle, or myeloid, and the intercellular substance may be mucoid, fibrous, cartilaginous or osseous. The cells contain a large centrally located ovoid nucleus, occupying practically the entire cell body. Mitotic figures are common in rapidly growing sarcomata. Frequently there are multipolar mitotic figures indicating the possible division of a cell into three or more daughter cells. Karyolysis or nuclear fragmentation is well marked in those cells that are centrally located in the tumor, that, is, in degenerating centres, and in cells of sarcomata that Fig. 155.—Section of tumor, showing mottled appearance, a result of Necrotic centres TUMORS. OH are not growing rapidly. The portion of the cell body not occu- pied by the nucleus is composed of undifferentiated protoplasm. In appearance the intercellular substance varies according to its composition. An abundance of capillaries and small blood vessels are found in sarcomata. These may be normal in struc- ture or they may be infiltrated with sarcomatous tissue, and, in some cases, the blood flows through channels formed by sar- coma cells. Hemorrhage is of frequent occurrence in sarcomata. The blood vessels have no regularity in their distribution, a structural peculiarity frequently resulting in degeneration and necrosis. Lymphatic spaces and vessels are absent in sarcomata, excepting lympho-sarcomata, unless they are entangled during the development of the tumor. Nervous tissue has not been demonstrated as a distinct entity in sarcomata. ‘There are usu- ally many leucocytes and frequently some plasma cells in sar- comatous tissue. The plasma cells may produce the intercellular structures of sarcomata or they may become adult connective cells and produce fibrous connective tissue. Fig. 156.—Round cell Sarcoma. The rapid development and the irregular distribution of blood vessels predispose sarcomata to destructive processes. Mucoid degeneration frequently occurs and may result in the complete destruction of the tumor. Necrosis is also quite common, and suppurative conditions are not rare. If the normal tissues are eroded, exposing the tumor tissue, septic infection is common and sometimes results fatally. This group of tumors may be classified, according to their S02 VETERINARY PATHOLOGY. cellular elements, as (1) round-celled sarcomata, (2) ‘spinidites celled sarcomata, and (3) myeloid-celled sarcomata. Round-cell sarcoma. This tumor is composed primarily of round cells (spherical cells) and is rather common. ‘They de- velop in any tissue and are, as a rule, the most malignant tu- mors of this entire group. They are soft, spongy, and usually quite vascular, and, as a rule, are not encapsulated. Structurally the cells of this variety approximate the embry- onic epithelial cells more closely than do those of any of the other types. According to the size of the cells two classes may be recognized, viz.: small and large. There is, however, no dis- tinct line between the two classes. The small, round cells are about the size of lymphocytes while the large, round cells are as large and sometimes much larger than mononuclear leuco- cytes. The nuclei of this type of sarcoma cells are) relates much larger than the nuclei of lymphocytes or leucocytes. In fact, the nucleus occupies practically the entire. cell bodya= Wine intercellular substance is very limited and is usually mucoid or reticular. Blood vessels are usually numerous, and their walls are frequently formed by sarcomatous cells. Metastatic growths are frequently in this type. The cut on page 273 is from a pho- tograph of the lung of a horse, showing metastatic round-celled Fig. 158.—Photograph of sheep’s heart, showing a lympho sarcoma of the pericardium. TUMORS. 303 me eae —~ ® /(@(@/ee! CS e/@) ‘eo Fig. 158.—Section of a Lympho Sarcoma of a dog’s omentum, showing the lymph vessels and sarcomatous tissue. sarcomata. The primary tumor involved the eye-ball and finally destroyed the sott structures ot the entire orbit... In this: case two or three metastatic tumors were observed in the liver also. ines cut on page 299 1s a photograph of a horse in which there was an extensive sarcomatous formation in the thoracic cavity involving the mediastinum, pericardium, pleura and some smaller nodules in the lung. (The lung nodules were, no doubt, metastatic formations.) Because of their tendency to form metastases and the rapid peripheral infiltration these tu- mors usually cause a fatal termination. Lympho-sarcomata are a variety of round-celled sarcoma, and are called lymphomata by some authors. They are quite com- mon in all domestic animals. These tumors have their origin in lymphoid tissue and are extended by the lymph. Two cases have been studied in the ox in which the primary lesion was in the wall of the abomasum. One case of generalized lymphosar- comatosis has been observed in a chicken. A pericardial lym- 304 VETERINARY PATHOLOGY. phosarcoma was found in a post-mortem examination of a sheep. An omental lymphosarcoma in a dog was reported in the Ameri- can Veterinary Review, December, 1905. The color, consistency and size of lymphosarcomata is quite variable. Microscopically these tumors are found to be composed of lymphoid cells, the tumor cells being supported by stellate cells. Lymph vessels are usually quite numerous and their structure is similar, if not identical, to that of normal lymph vessels. The stellate supporting cells and the presence of lymph vessels are the distinguishing characteristics of lymphosarcomata. There is no leucocytosis in animals affected with lymphosarcomata, while in those affected with leukemia leucocytosis is well marked. These tumors are malignant. They form metastases through the lymph and blood channels. They are usually surrounded by a very thin capsule. Fig. 159.—Photograph of a mule affected with a spindle cell Sarcoma of the eyelids, 1. Granular denuded tumorous surface. 2. Granular fungoid tumorous mass. TUMORS. 305 Spindle-Cell Sarcoma.—Tumors of this variety are composed of spindle-shaped cells. They are more firm and dense than the round-cell sarcomata. These tumors are not rare, occurring most frequently in connection with the skin or subcutaneous tissue. Some of the resistant and incurable cases of fistulous withers are spindle-celled sarcomata. A collar boil that did not respond to treatment was found to be a spindle-cell sarcoma. These tumors are common in the eyelids of horses and mules and are sometimes quite resistant to surgical interference. The Fig. 160.—Section from spindle cell Sarcoma of a mule’s eyelid. cells vary from short, thick fusiform cells to elongated fibre-like cells. Spindle cells are more matured than the cells of round- cell sarcoma. Round cells have no tendency to become spindle cells, neither do spindle cells become either round cells or ma- tured connective tissue cells. The cells in spindle-cell sarcomata have no definite arrangement but extend in all directions. In microscopic section some cells are cut transversely, others ob- liquely, and still others longitudinally. Hence we find the nucleus is centrally located, is usually spherical or oval in shape, and is not as large in proportion to the size of the cell as that of the round cells. Some have suggested a classification of this 306 VETERINARY PATHOLOGY. group into large and small-celled varieties. The cells are usu- ally held together by reticular connective tissue. This may be demonstrated in sections in which the sarcoma cells have been dissolved out by acetic acid. The density of the tumor depends upon the relative quantity of protoplasm the cells contain and the amount of intercellular material. A tumor composed of short, thick spindles is less dense than one composed of fibre- like cells. Blood vessels usually have normal vessel walls and are not as numerous as they are in round-cell sarcomata. Fig. 161.—Myelcid or Giant cell Sarcoma of the Humerus. a. Giant cells. b. Sarcoma eGells. These tumors are usually encapsulated, rarely form metas- tases and are, in general, not as malignant as the round-cell variety. They may be mistaken for fibromata, but a careful study of a microscopic section is usually sufficient for differen- tiation. Fibromata contain no elements that appear like trans- verse sections of spindle cells. Leiomyoma may be differen- tiated by the shape or-the nucleus and therseleetive achHonsas stain as picrofuchsin. Myeloid-Cell Sarcoma (Giant-Cell Sarcoma)—This is a variety of sarcoma characterized by the presence of myeloid or large multinucleated giant cells (mvyeloplaxes). Surgeons and pathologists frequently find myeloid sarcomata in man, but they are rare in domestic animals. They are invariably found in relation to, or in connection with, bone-marrow, or more rarely TUMORS. 307 in relation with periosteum. They frequently contain cartilag- inous, osseous or calcareous centres. Microscopically, they are composed of myeloid cells and round or spindle cells. The myeloid cells are the distinguishing elements of this variety of sarcoma. The size of the myeloid cells is variable, frequently being 80 to 100 microns in diameter and with an irregular outline, varying in shape from a sphere to an elongated mass. Their protoplasm may be quite granular or almost clear, They have many nuclei—150 being observed in one cell. These nuclei have no definite arrangement but occur miscellaneously throughout the entire cell body. The round and spindle cells are like those occurring in round and spindle-cell Fig. 162.—Photograph of horse’s head affected with mixed cell Sarcoma. sarcoma. There may be an excess of one or the other or they may be equal in number. The intercellular substance varies from mucoid to calcareous in nature. There is usually an exces- sive blood supply, the blood vessel walls being usually normal | VETERINARY PATHOLOGY. in structure. Degeneration as well as necrosis and calcification are of frequent occurrence in myeloid sarcomata. These tumors may not be completely encapsulated, though there is always a tendency for them to be circumscribed. They are the least malignant of all sarcomata. They rarely form me- tastases. Mixed-Cell Sarcoma.—This is a variety of sarcoma charac- terized by the presence of variously shaped cells, as round, spin- dle and even stellate cells. This variety is not as common as either the round-cell or spindle-cell varieties. They have been observed in the horse, hog and ox, but they doubtless occur in all domestic animals. They affect bone, glandular tissue, and meninges of the brain, in fact, no tissue is exempt. An inter- esting case of mixed-cell sarcoma of the inferior maxilla of a horse was described in the December Veterinary Review, 1905. The tumors frequently degenerate and become necrotic. Mi- croscopically they are composed of round cells and_ spindle cells that are identical in structure with those described in the discussion of round-cell and spindle-cell sarcomata. Stellate cells may be present, and are very similar in structure to mucoid connective tissue cells. The cellular elements are supported by reticular tissue or by fibrous connective tissue. The number of blood vessels is variable. There is an excess of vessels in those Fig. 163.—Photograph of Maxilla of horse shown in Fig. 162, showing 3 bony points; the remainder of the maxilla being completely destroyed by the sarcomatous tissue, TUMORS. 309 made up principally of round cells and in those that have a lim- ited amount of intercellular substance. The vessel walls may be normal or they may be composed of sarcomatous tissue. De- generate or necrotic changes in the tissue necessarily alter the microscopic appearance. Fig. 164.—Section of a mixed cell Sarcoma of the inferior maxilla of a horse. These tumors are usually diffuse; that is, they are not encap- sulated. They form metastases, and hence are malignant. Alveolar Sarcoma.—This is a sarcoma characterized by the arrangement of the sarcoma cells into groups or nests, and is occasionally found on domestic animals, especially in the ox and hog. The reproductive glands, ovary and testicle, are the struc- tures most frequently invaded by them. They may become quite large. An alveolar sarcoma obtained from the ovary of a heifer weighed 15 kilograms (33 lbs.) and was about 20 cm. (8 in.) in diameter. Microscopically the cells are usually round, although they may be spindle-shaped. The stroma of the tumor is made up oi 310 VETERINARY PATHOLOGY. ‘two portions. One portion is usually composed of spindle cells which are connected into dense bands extending in various direc- tions and forming alveoli; hence the name alveolar: The other portion of the stroma is intercellular and corresponds to that of the round-cell sarcoma. The arrangement of the cells into nests is suggestive of a carcinoma, but the differentiation is not diffi- cult and depends upon; first, the presence of intercellular sub- stance between the cells which is present in sarcomata but is absent in carcinomata; second, sarcomatous cells are embryonic connective tissue cells and hence contain nuclei relatively large in proportion to the size of the cell, while carcinomatous cells are embryonic epithelial cells and contain nuclei relatively small in proportion to the size of the cell. \ ey) be © “Ys ao 4 @ ox By) N\ iN \ ©2 60 ase eae PLP 5) 0 Ly 29, ne Q\g 8 oe See > as ‘) $6. 90 Pee Dee VW oa glee eee Coe AN en) (SPRIT Sa aie < cog Soa oo W\ 4 7 oer Oe oO @ \\ “eblabied 0G DeLee i Fig. 165.—Section of Alveolar Sarcoma from ovary of heifer showing alveoli filled With sarcomatous cells. These tumors grow slowly. They are usually encapsulated and have no tendency to form metastases. They are very mildly malignant. Enthothelioma is a tumor composed of endothelium. This is a tumor that is not specifically a sarcoma, but may be so classed. Endothelium has the same origin as connective tissue, 1..e., the TUMORS. Said! mesoderm. Embryonic endothelial cells are structurally iden- tical with embryonic connective tissue cells. These tumors are not very common in domestic animals. An endothelioma was observed in the lung of a dog, another in the testicle of a bill. These tumors may have their origin from the endothelium lining blood or lymph channels, peritoneum, pleura, pericardium, arach- noid membrane, any organs developed from mesothelium, or deflections from any of them. They are variable in shape, size, color and consistency. Microscopically they are composed of cells that most fre- Fig. 166.—Section of Endothelioma from a bull’s testicle. Note the bands of connective tissue and arrangement of Cells. quently resemble sarcoma cells, although they may approximate the structure of carcinoma cells. The cells may be arranged in tubules, transverse or oblique sections appearing as sections of gland tubules or acini. If arranged in columns transverse or oblique sections appear as cell nests. The cells are usually cubical or spherical in shape, although they may be spindle or even squamous. The stroma varies according to the tissue in- vaded and may be dense fibrous or mucoid. Blood vessels are usually quite numerous, and if the endothelium is derived from B12 VETERINARY PATHOLCGY. the endothelium of a vessel, the vessel may be very irregular i calibre and structure. If the cells occur in columns or nests 1 will be necessary to differentiate them from carcinomata. Thi differentiation involves the comparison of cells derived fror mesoderm and those derived from entoderm or ectoderm, Th only essential difference, and that is not constant, is the size c the nucleus, The differentiation may also be governed to som extent by the distribution of the blood vessels. If the cells occu. in tubules, their differentiation from the adenoma will be neces: sary. Adenomata may be differentiated by observing the sam< Fig. 167.—From drawing of a Nodule of a Mediastinal endothelioma. 1. Column of endothelial cells. 2. Diffuse mass of endothelial cells. factors that are used in differentiating endotheliomata from car- cinomata. Alveolar sarcomata are very difficult to differentiate from endotheliomata, in fact it is sometimes impossible. These tumors are not encapsulated and usually form meta- stases. They usually occur in internal organs and hence surgical relief is impossible. Fatal termination is the usual outcome. Fibrosarcoma.—This is a tumor composed of both adult and embryonic connective tissue. They are quite common, espe- cially in the eyelids and in labial commissures of horses and TUMORS. 33 mules. Several cases of dense tissue growths in the withers of horses have been observed. These animals when presented ap- peared to be affected with chronic inflammation of the subcutan- eous tissue or deeper structures. Most of the above cases were clinically diagnosed as fistulous withers and an operation recom- mended. The operation usually consisted of dissecting away the dense masses of tissue. The cases were usually returned in Fig. 168.—A so called grape sarcoma from uterus of a cow. oles VETERINARY PATHOLOGY. from four to six weeks after the operation with growths larger than those present before the operation. The operation was usually repeated two or three times with the same results. On microscopic examination these growths were found to be fibrosarcomata, being composed principally of fibrous connective tissue in which there were some spindle cells and occasionally a few round cells. The presence of both fibrous and sarcomatous tissue is the principal characteristic of these tumors. The num- ber, size and distribution of blood vessels are very irregular. These tumors are not distinctly encapsulated, but they do not form metastases. They are prone to recur after ablation. They may destroy life after a considerable time, as their growth is TU MORS. ) 315 relatively slow. Operation usually stimulates them to grow more rapidly. Melanosarcoma.—A melanosarcoma is any variety of sarcoma in which melanin is deposited in the tumor cells. These tumors are quite prevalent. Gray horses seem to have a special predis- position to them, but they are also found in bay and black horses, black or red cattle, black hogs, and, in fact, all varieties of do- Fig. 170.—Melano Sarcoma of hog skin. mestic animals regardless of color. On microscopic examination, melanin is found deposited in the tumor cells. The melanin may be in masses or granular and occasionally it may be found out- side of the cells. Excepting the deposit of melanin, these tumors have the same microscopical appearance as the round or spindle- cell sarcomata described before. 316 VETERINARY PATHOLOGY. Melanotic sarcomata are frequently malignant. In an autopsy of a gray mare metastases of melanosarcomata were found in the liver, lung, spleen and kidney, the primary growth being located in the subcutaneous tissue on the right superior portion of the anus. Another case was observed in which there was general- ized melanosarcomatosis in a short-horn cow. Myxosarcoma.— This is a tumor composed of myxomatous and sarcomatous tissue. The existence of this group of tumors oe ; a rz) Senet Ae, a EC VE Fig. 171.—Section of Melano Sarcoma of a horse’s liver, showing the deposit of melanin in the tumor cells. is doubted by some pathologists because sarcomata are prone to undergo mucoid degeneration, and, because if the mucoid degen- eration is of limited extent and generalized throughout the en- tire tumor, differentiation would be practically impossible. If the mucoid degeneration affects localized areas the differentia- tion is not difficult. One myxosarcoma has been studied. It in- volved the right lobe of the liver of a cow but was not the cause of death. The tumor, about the size of a goose egg, was encap- sulated, soft and pale pink in color. Microscopically it was composed of stellate cells, the pro- cesses of which were apparently united, thus forming alveoli. TUMORS. 317 There were also round cells, some areas being composed almost entirely of round cells and others of stellate cells. The round cells were like the round cells found in sarcomata. The alveoli formed by the stellate cells were filled with a stringy mucus ma- terial. A few blood vessels were observed but they were not as numerous as in pure sarcomata. These tumors may be malignant. When they occur upon or near available surfaces they usually become necrotic, slough and produce no further trouble. wy eG ogee: \ DPS is . = a ASS Fig. 172.—Section of a Myxo-Sarcoma, from a cow’s liver, showing: 1. Spaces formed by the union of the processes of the stellate cells. 2. Sarcoma cells. Chondrosarcoma and tumors composed of chondromatous and sarcomatous tissues are not common. They usually occur in the location most favorable for chondromata. A chicken affected with a chondrosarcoma of the sternum was obtained at a butch- _er’s stall at the city market in Kansas City recently. Microscopically, these tumors are found to be composed of a mixture of chondromatous and sarcomatous tissues in varying proportions. Sometimes the chondromatous tissue is apparently stroma for the sarcoma tissue proper. In other cases the stroma is apparently formed of sarcomatous tissue and the chondro- matous tissue is the essential portion of the tumor. 318 VETERINARY PATHOLOGY. These tumors may grow to an enormous size. They are not as malignant as pure sarcomata and metastatic tumors are rare. They should be differentiated from chondrofying sarcomata and from sarcomata involving cartilage. ~Osteosarcoma.—This variety of tumors is composed of osseous and sarcomatous tissues. They are rather common, occurring in the horse, dog and ox. Microscopically, osteomatous and sarcomatous tissues are arranged in various proportions and in various relations, but the combining tissue in any case must be new growth tissue. Ossifying sarcomata are not osteosarcomata, neither are sarco- mata of osseous tissue osteosarcomata. These tumors are, usually malignant, but they do not form metastases. Hemangiosarcoma.—These tumors are composed of heman- giomatous and sarcomatous tissues. They are relatively com- mon, occurring in the location common for haemangiomata and may affect any of the domestic animals. These tumors are essen- tially very vascular and are highly colored. In microscopic examination variations are observed in differ- ent hemangiosarcomata. The sarcomatous tissue in some cases appear to have had its origin from the tunica adventitia of the vessel wall; in other cases the sarcomatous tissue appears to have had its origin independent of the vessels. Again, the ves- sels may act as the supporting stroma for the sarcomatous tissue. The vessels may be capillary or cavernous, sinusoid or plexiform. The vessel wall may be practically normal, but more frequently it is either hypertrophied, as a result of increased number of the cellular elements or increase in the size of the cells, or it may be thin, scale-like and atrophied. Sometimes the endothe- lial cells lining the vessels are cubic or columnar in shape, thus diminishing the lumen of the vessel. The sarcomatous cells may be either spindle-shaped or round. These tumors are quite malignant, and they usually grow rapidly. The metastatic tumors are most frequently pure sarco- mata. eve lel US O(OuUIL A (Warts.) Papillomata are fibro-epithelial tumors. These are perhaps the most common of all tumors. They occur upon the surface of the skin, and upon mucous, serous, and synovial membranes. They are very common upon the skin of calves, especially around the eyes, ears and poll. They occur most frequently on the lips, TUMORS. : 319 buccal mucous membrane, and arms of dogs. The skin of the legs and lips are the common locations in the horse. The lumen of the oesophagus of the ox may be almost occluded by the pres- sence of masses of papillomata. In a horse used for dissecting the cardio-pyloric junction was found to be a mass of these tumors. ‘lhe mucous membrane of the bladder of the ox, sheep Fig. 173.—From photograph showing Papillomatosis of mucous membrane of lips of a horse. and hog is sometimes studded with papillomata. These tumors have also been observed upon the combs and wattles of fowls. They sometimes occur in horses’ feet but are usually necrotic and do not have the appearance of papillomata. These tumors may be hard, i. e., covered over by stratified Squamous epithelium that has become cornified. This variety is 320 VETERINARY PATHOLOGY. invariably found upon the skin and constitutes the growths ordi- narily known as warts. Vhey may also be soft, and are then found upon mucous, serous or synovial membranes, in which case the covering epithelium is not cornified. Hard papillomata or warts may appear as tabulated masses, as fungoid growths or as a mass of villi. Any of the above forms may have a smooth surface or be fissured with a very irregular surface. They vary in size from a millet seed to an apple. They may be single but are more frequently multiple. Microscopically, they are composed of adult epithelium and of fibrous connective tissue in varying proportions. They sug- gest the structure of cutaneous papillae. In fact, they have been (ees 7° SWE) es ra é 8 (bocgeer rae afi §, 16 OB pf Fev B2aA Soe? SSas 9 cet renee ee 2 r: 2 o Oa ae oe ee 3 s x) Oo 6 8 ae. Oe. —— Be Sark ‘Bw "ae pe eek Of". 2 (aa . RAV: Qaees em. pee eS Ye © Z a8 Q OY \ 7, \ 7 Ae: ROS \ ; oA ‘ : SSS i a Ais é 5 2) ees oe 9} } iS 5 : y : ri Ges aw yy es / == S a, fy KK 1655 Fig. 180.—Section of an Adenoma from the frontal sinus of a mule, showing the arrangement of tumor tissue into acini and tubules. Clinically these tumors, as a class, are malignant, but do not produce fatal results as rapidly as carcinomata. Many individ- ual adenomata are benign. A horse’s tail was recently ampu- tated that for three years had been affected with an adenoma of the sebaceous glands. A bitch affected with an adenoma of the mammary gland has been under observation for two years and is normal except for the presence of the tumor. These tumors rarely. recur when removed. From experience it has been found that mammary adenomata of the bitch usually result fatally im- mediately after operation. (The operation appears to produce 328 VETERINARY PATHOLOGY. sufficient shock to destroy hfe.) Adenomata are extended by means of the lymph. Various combinations of adenomata are common. | 3 Adeno-Sarcoma.— This is a tumor composed of adenomatous and sarcomatous tissue. These tumors are seldom observed dur- ing life because they cccur in the kidney, and it is not an easy matter to palpate the kidney in the domestic animal unless there is extreme emaciation. They usually affect only one kidney. They occur in young animals and are most common in the hog although one has been observed in a horse. These tumors grow Tapidly and, may hecome very lange. “Day reported omenenae weighed 27.2 kilograms (60 lbs.) foumd in the kidney of a ioe Renal adenosarcomata usually have their origin near the kid- ney pelvis. The renal tissue is gradually displaced by the tumor, and in some instances the kidney tissue is entirely destroyed as a result of pressure atrophy. The tumors are usually confined to the kidney, but they form metastases, in the lung (through the blood, or in the sublumbar lymph nodes (through the lymph.) In gross appearance, these tumors are irregular in outline. They are usually surrounded by a thin fibrous capsule from which fibrous bands project into the tumor dividing it into VP Oe Te Sea ve go e 68 : SRA Baek. ae ; 88S Pao HS PA EMOE MM ~ Pa oye” ee pe Fig 181.—Section of an Adeno-Sarcoma of the kidney of a hog, showing the sarcomatous tissue between the acini and tubules. TUMORS. 329 irregular lobes. ‘These tumors are usually mottled, though they may be uniform and of a white or light gray color. Microscopically, adenosarcomata are composed of epithelium and connective tissue. The amount and arrangement of the two types of tissue are variable. Some areas may be entirely epi- thelium (adenomatous) and other areas connective tissue (sarca- matous). The epithelium is arranged as grandular tissue, the tubes and acini of which are irregular in shape and size and may contain disintegrating, epithelial cells or their products. The epithelium is usually arranged in a single layer in the tubes and acini though they may be grouped in some instances and Fig. 182 —Section of a Cystadenoma of the mammary gland of a sheep, showing: 1. Coagulated cvstic contents surrounded by an atrophied acinous wall. thus appear similar to carcinomatous nests of cells. The epithe- lial cells are small and usually contain finely granular chromatin. The connective tissue cells are usually fusiform although they may be nearly spherical in shape. They contain relatively large nuclei in which granules may be observed. Cystadenoma is also common, especially in those adenomata that produce secretion. They are found in the adenomata of the mammary and sebaceous glands. Hypernephroma are tumors which may be classed either with SW) VETERINARY PATHOLOGY. sarcomata or carcinomata and is composed of tissue similar to ad- renal tissue. They occur most frequently in the kidney, ovary, or adrenal body itself. Hypernephromata are rarely diagnosed as such in living domestic animals. They are variable in size, fre- quently weighing as much as five kilograms (11 lbs.) Usually gray in color and invariably containing hemorrhagic areas they thus appear mottled. There is usually an encapsulating mem- brane present. Blood-vessels are numerous, especially in the stroma. Degeneration and necrosis is of common occurrence. X 250 Fig. 183.—Hypernephroma of the kidney of an ox, showing large» typical hyperne- phromatous cells containing fat droplets. Microscopically, these tumors are found to be made up oi large cells similar to epithelial cells and usually containing fat droplets. These cells are arranged in rows or columns, the columns being separated from each other by a small amount of stroma. The columns of cells may be quite variable in their diameter, appearing at times as long, slender columns and again as rather long nests of cells. The stroma is composed of fibrous connective tissue and contains many blood-vessels. Clinically, these tumors are very malignant, and, although TUMORS. Soll they are encapsulated, they form metastases through the blood. They usually result fatally in the human, even after operation, probably because of the liberation of considerable of the adrena- lin substance which increases blood pressure to such an extent that heart failure supervenes. PLACENTOMA. (Syncytioma. ) A placentoma is a tumor composed of tissue similar to the chorionic villi. These tumors have been described under a variety of names as syncytioma malignum, deciduoma malignum, chorio-epithei- ioma, epithelioma seritonale, chorio-carcinoma. Only recently have placentomata been recognized as distinct tumors. . A placentoma is essentially a tumor of the uterus. They are not common in domestic animals but this may be because of iail- ure to recognize them. The uterus or fallopian tube is their most frequent location. They occur more frequently after spur- ious or mole-pregnancy and usually appear a short time after parturition. Abortion is a predisposing cause. The primary tumor almost invariably occurs in the uterus though a few cases have been reported in women in which the primary tumor was in the kidney. They are very malignant. These tumors appear as soft, spongy, villous, bleeding masses and are variable in size. They have the general appearance of placenta or foetal membranes in both the primary and the metas- tatic tumors. They begin to develop at the cotyledons or zone of placental attachment and rapidly extend into the uterine mus- cular tissue and invade blood vessels, thus metastases occur in a short time after the tumor appears. Because of their struct- ure (embryonic cells and rich vascular supply) they grow rap- idly. The presence of a placentoma is indicated by uterine hem- orrhage occurring a few days after normal parturition or abor- tion. The uterus is enlarged and the affected individual rapidly Decomes anemic and emaciated. The uterine discharge usually contains shreds of the tumor and the cavity of the uterus is occupied with a soft bleeding mass. Microscopically, these tumors are composed of a protoplasmic ground-substance, which is arranged in an irregular network forming alveoli. The protoplasmic mass is usually continuous, there being no evidence of cell partitions, and it contains many nuclei thus forming a syncytium. Within the alveoli of the pro- SZ VETERINARY PATHOLOGY. toplasmic mass occur many small variously shaped cells. Blood cavities and canals are abundant and hemorrhagic areas are not uncommon. TERATOMA. These tumors are composed of the different kinds of tissues that approximate the structure and arrangement of normal tissue so closely that it is difficult to differentiate them macrosopically or microscopically from normal tissues and organs. Teratomata are so closely related pathologically to malformation, that in some cases it is impossible to determine which condition exists. Structurally they are found to be composed of either embryonic or adult tissues. Cutaneous structures are the most frequent tis- sues observed in this class of tumors, although tissues of bone, muscle, intestine, rudimentary eyes, brain, etc., have been found in them as well as sarcomatous and carcinomatous tissue. Fig. 184.—Dermoid Cyst from the withers of a horse. These tumors are quite variable in size, shape and color. In consistency, they vary from a viscid mass to dentine and enamel. They are usually single, grow slowly and rarely form metasta- ses, although a few have been observed that grew rapidly, metas- tasized and recurred when removed. They frequently undergo degeneration tending to cystic formation. Clinically, teratomata are benign, only rarely terminating fatally. Etiologically, they are as mysterious as the other types of tumors. They may have their origin from tissue inclusions. Some teratomata may succeed imperfect tissue union. The the- Tumors TABLE I. ( Myxoma, chondror « Osteoma, odontoma. f Connective. 4 Lipoma, glioma. | | r Papilloma. ( Adult tissue. 4 Epithelsm we Se J M uscular—Myoma......... | rien ste Pie Vascular—angioma...... Hemang toma. i ay Lymphangioma. | Nervous—neuroma. _.f Round cell. Spindle cell. | ( Connective—Sarcoma J Myeloid cell. | Endothelioma. Hypernephroma. | | Embryonic tissue. | Placentoma. [ Carcinoma. | Epithelium. 4 Adenoma. _ Epithelioma, Ss = ‘DUOIDAI T. TUMORS. 355 ory of parthenogenesis may be applicable in the explanation of some of them, but the specific cause or causes of teratomata has not yet been determined. Teratomata are of frequent occurrence in all domestic ani- mals but are more prevalent in equines. They are found in any tissue and in all parts of the body although they are more fre- quent in the skin, ovaries, testicles, kidneys and parotid glands. Fig. 185.—Dermoid Cyst from eye of a steer, showing tuft of hair growing uvon cornea. Because of the heterogenous structure of teratomata they are difficult to classify. | Dermoid cysts are teratomata composed primarily of skin and its appendages (hair, sebaceous glands, horn, teeth, etc.) They may be solid, but are more frequently cystic. In size they vary from a pea to a basket ball. There is usually surrounding them a dense capsule from which a villous mass may be ob- 334 VETERINARY PATHOLOGY. served projecting into the cyst cavity. Extending from the vill- ous projection are tufts of hair or teeth. The villus is, in struct- ure, very similar to skin. In some teratomata hair and teeth are produced directly from the inner portion of the cyst wall. Cys- tic dermoids usually contain hair and a pultaceous material de- rived from the sebaceous glands or they contain teeth and a vis- cid fluid. Dermoid cysts without any capsule are occasionally observed. The accompanying cut illustrates hair extending from the anterior surface of the eye. Those found in the ovaries Fig. 186.—Dentigerous Cyst on left inferior maxillary of 3 years old colt containing 431 teeth. Removed Dec. 11, 1905, by H. M. Stevenson, Perry, Iowa. usually contain elements of all three germ layers. Those of the testicles may contain vestiges of all the germ layers, but are usually cystadenomatous or cystocarcinomatous in type although they may contain cartilage, teeth, osseous tissue, etc. Solid der- moid cysts are a heterologous mass, of embryonic or adult tissue. Dentigerous cyst is the name applied to those dermoid cysts containing teeth. These are the most important to the veterin- arian because they are of the most frequent occurrence. They are invariably encapsulated and may or may not contain a villus TUMORS. 335 projection. The teeth vary from an irregular conglomerated mass of dental tissue to those perfect in form and structure. The con- ‘stant production and accumulation of the containing viscid fluid results in enlargement of the cyst and frequently rupture of the capsule and the production of a fistula. The most frequent lo- cation of dentigerous cysts is near the base of the ear in the region of the parotid gland although they may occur in any other place especially in the ovary and testicle. They are most common in horses. Cholesteatoma is a teratoma composed of pearl like masses of epithelium in which there is more or less cholesterin. They are not common but have been observed in the brain, (choroid plexus and tuber cinereum) and urinary organs. There was recently obtained from near the kidney of an ox, a mass of substance of a waxy consistency, that gave the typical reaction of cholesterin and was probably a cholesteatoma. CYSES. DEFINITION. ETIOLOGY. Retained secretion. Obstructed outflow. Excessive production in ductless glands. Retention of hemorrhagic extravasate. Colliquation necrosis. False bursae. Parasites. STRUCTURE. VARIETIES, Retention; Atheroma. Exudation; Hygroma, Shoe boil, Capped hock, Meningocele. Extravasation; Hematocele, Hematoma. Degeneration; Colliquation necrosis, Hydatiform Parasitic; Echinoccosis, Measley pork, Dermoid; Cutaneous, Dentigerous SECONDARY CHANGES. EFFECTS. A cyst is a bladder like growth surrounded by a capsule and containing a liquid, semiliquid or gelatinous material. Cysts are not true tumors. However, a tumor may become cystic, (Cystoma,) and the capsule surrounding a cyst may proliferate and become a true tumor. Collections of inflammatory and oede- matous fluids, are not usually considered as cysts. Cysts may be single or multiple. The latter are designated multilocular cysts. Cause._-Cys‘s may be caused by, 1. obstruction of gland ducts, thus favoriny ercvmulaticn erd retention of a normal secretion 336 VETERINARY PATHOLOGY. or excretion, e. g., renal cysts; 2. By excessive secretion into duct- less structures, e. g., distension of bursae; 3. By extravasation into the tunica vaginalis sac, e. g., hematocele; 4. Liquefying necrosis, e. g., formulation of cysts in the cerebrum of horses affected with “blind staggers!’ "5. Pdrasites, ee, Cysticereas cellulosae. : Structure.—The cystic wall varies according to the age cf the cyst. In the beginning it may represent the original gland structure or a condensation of the normal tissue of the part. Later the cystic walls may. be lined with epithelium or endothel- ium, which actively secretes as long as the cyst grows. The cys- tic capsule may be composed entirely of fibrous connective tissue. In some instances the primary capsule is fibrous and later an endothelial lining develops. The cyst wall or capsule may be Ie 187 —Retention Cyst in cervical region of dog. ay TUMORS. S07; firmly adherent to the adjacent tissue or it may be loosely at- tached. The cystic content varies according to the nature of the cyst. Urine, milk, saliva, mucus, semen, liquor folliculi and other secre- tions and excretions are represented in cystic contents. Blood i. e., hemorrhagic extravasates and various tissues that have undergone colliquation necrosis may represent the contents of cysts. The various secretions, excretions, extravasates, exudates and necrotic tissue usually undergo some modification when re- tained within a cyst. Varieties.—Kctention cysts, those resulting from the accumu- lation and retention of normal secretions, e. g., ovarian cysts. renal cysts, mammary cysts, testicular cysts, ranulae, mucus cysts, sebaceous cysts (Atheromata). Fig. 188.—Uterine Cyst the capsule of which had become osseous. Exudation cysts, those resulting from excessive secretion into ductless glands or cavities, e.g., hygroma, capped hock, meningo- cele: Extravasation cysts, those resulting from hemorrhage into tis- sues or closed body cavities, e. g., hematocele, hematoma. Degeneration cysts, those resulting from liquefaction of ne- crotic tissue ,e. g. colliquation cerebral cysts. Parasitic cysts, those resulting from the development of para- sites in the tissue, e. g., cysticercus cellulosae, cysticercus bovis, cvsticercus echinococcus, etc. 338 VETERINARY PATHOLOGY. Dermoid cysts, those resulting from inclusion of cutaneous tissue. These have been discussed under the head of teratomata. Secondary Changes.—The cystic wall may become the seat of inflammatory disturbances, neoplastic formation or necrosis. In some instances cysts are destroyed because of the disintegration of their capsule, by disease. : The cystic contents may undergo degeneration, become in- spissated or calcified. Effects.—The effects of cyst formation depend upon the tissue involved and the size and nature of the cyst. "The cysts frequently become so large that the entire organ is destroyed, e. &., Ovattan and renal-cysts. In some cases: the cysts: may destroy life, especially if a vital organ, e. g., the brain ts in- volved. Cysts may persist for years and be of no serious con- sequence, on the other hand they may seriously inconvenience the functional activity of the part involved and impair the health of the animal from the beginning. CHAPTER X1. FEVER (Pyrexia): DEFINITION. ETIOLOGY.—Toxins; ptomains; katabolic tissue products; drugs. PERIODS OR STAGES (Course). Onset (Stadium Incrementi). Acme (Stadium Fastigium). Decline (Stadium Decrementt). Convalescence. VARIETIES, according to Course. Regular. Irregular, Duration and temperature variation. Ephemeral. Continuous. Remittent. Intermittent. Severity. Sthenic. ,~Anmna Asthenic. * SYMPTOMS. Chill, diminished secretious, increased heart ection and respircticn, nervousness and restlessness. LESIONS. ; Parenchymatous degeneration, hemolysis, hyaline degeneration, loss of fat. Body heat is a product of metabolism. The body heat or temperature of warm blooded animals is practically constant, although changed environment, diet and use or occupation pro- duce some variations. Thus a horse confined in a barn has a temperature .5 to 1° F. higher than when not so confined, pro- vided the diet is the same in both conditions. A narrow ration is conducive to increased oxidation and consequently a higher temperature. Animals in action have a higher temperature than when at rest. Thus a dog’s temperature is from 1 to + F. higher immediately after than it is before a chase. The accurate regulation of body temperature 1s accomplished by the action of the thermo-regulating center or centers. Tissue action is always accompanied by increased heat production, and frequently different parts of the same animal may vary 1 to 6° F. in temperature. The equalization of body heat and the distribu- tion of heat to the different parts of the body is accomplished by means of the circulating blood. Heat is continually produced in the animal body and is constantly eliminated from the bodv 239 340 VETERINARY PATHOLOGY. in the excretions (air, perspiration, urine and feces), as well as by direct radiation. The relative amount of heat dissipation by the excrements and by radiation varies in different animals. Normal temperature is the balance of equilibrium maintained between thermogenesis (generation of heat) and thermolysis (dissipation of heat). The normal temperature of an animal used during the day is about 1° F. higher in the evening than in the morning. Fever is a condition in which the equilibrium between ther- mogenesis and thermolysis has been overthrown, 1. e., there is a disturbance of metabolism accompanied by increased tempera- ture. It is not a disease but a symptom complex, common to several different pathologic conditions. Fever should be dif- ferentiated from heat stroke and sunstroke. In heat stroke there is no disturbance of thermogenesis or thermolysis, but the ther- molytic centers are unable to cope with the existing external conditions, and there is accumulation of heat in the body, whereas fever is a result of disturbed equilibrium between thermogene- sis and thermolysis. Sunstroke is a condition produced by the action of actinic or chemic rays of the sun upon the nerve cen- ters, temperature variations being only a predisposing factor. Etiology.—Fever is usually caused by bacterial products as toxins, endotoxins and bacterial proteids. Tissue products as leucomains, peptones and various albumins are also capable of producing fever. Certain therapeutic agents are causative fac- tors Of fever, | Course.—The course of a fever may be divided into four per- iods or stages, as follows: Onset (stadium incrementi) is the period of increase between the time of normal temperature and the time that the tempera- Fig. 189.—Charts showing two fever curves. On the left is given the temperature and on the top each number signifies one day or 24 hours. From 1 to 13 is the onset; from 13 to 17 and 20 respectively the Acme; from 17 to 32 is a gradual decline (lysis); and on 20 is shown a rapid declined (crisis). FEVER. 341 ture reaches its average height. The length of the onset and the temperature during this period is variable. Acme (stadium fastigium) is that period of time that the temperature remains high. It is the time from the termination of the onset to the beginning of the decline. Decline (stadium decrementi) is the time extending from the termination of the acme until the temperature reaches the nor- mal level. A sudden decline, i. e.. when the temperature sud- denly changes from acme to normal, is called crisis. In a iarge percentage of the cases of fatal equine pneumonia the tempera- ture suddenly drops from the acme to normai, or even subnor- mal, the sudden change (crisis) causing death. Excessive varia- tions, as a sudden rise of temperature of a sudden fall of tem- perature (may be to subnormal) are of rather frequent occur- rence a short time before death and is called the moribund or premortal stage, A gradual decline from acme to normal is called lysis. Convalescence is that period extending from the time that the temperature becomes normal until the animal has recovered. This period varies in length, a long continued fever essentially requiring a long period for convalescence. The temperature variation during this period is inconstant, but usually there is only slight fluctuation from the normal. Varieties.— Fevers may be classified according to course, to duration, and to temperature variation as follows: According to the course fevers are regular and irregular, typi-_ cal or atypical. A regular fever is characterized by the appear- ance of the various stages or periods of fever as described above. An irregular fever is one in which the stages are not distinct or are not regular in their appearance and duration. : According to duration and temperature variations, fever may be ephemeral, continuous, remittent or intermittent. Ephemeral fever is of brief duration, usually lasting not longer than 24 hours. It is the type of fever observed in nervous, ex- citable animals. This variety of fever may be produced at will by some nervous women. Continuous fever is that type in which there is a continuous high temperature. In continuous fever there are usually morn- ing and evening variations the same as in the normal tempera- ture. Croupous pneumonia without complications is an example of disease in which there is a continuous fever. Remuittent fever is characteristic of pyemia and is recognized by the irregularly periodic variations of temperature in which the temperature is always above normal. Ry, VETERINARY PATHOLOGY. Intermittent fever is the name applied to that type in which there are periodic variations, the temperature becoming normal between the fever periods. Intermittent fever is observed in equine pernicious anemia. Fever may also be classified as: 1st. Sthenic. 2nd. As- thenic. Sthenic fever is active, vigorous and destructive. As- thenic fever has an insidious onset and is slow in action. CECH OW ets 19 20 2) g& 23 24 2S 26 2&7 29 2% 50 3h 22 bi Seer x Ada alt ila Pinte: Pisin Se eel ail ae se ok| waza eS ie RRS Sia eee le a Le oleae ela Saale ea hs (00 4 i is 7M PR ed (ea aa ne Re Se eo Mawee eike eee ee aD. Fig. 190.—Continuous fever chart showing morning and evening variations, but a continuous high temperature. Symptoms.—Fever is usually ushered in by a chill because of the constriction of cutaneous vessels which thus diminishes the temperature of the skin and produces the sensation of chill- ing. ‘There are diminished secretions, as perspiration, saliva and urine. In long continued fever there is constipation because of - absorption of fluid from the intestines. The pulse rate is usually BG MO 7, 18, V9 20.2 2k PB Rt AS AC RTS CA SOS ee 6' ee a ee Pete emanc “CULLEN Io SS ee ea nee osc eee eeNeseco Mat oa hat (ean eb Dd Ne Tedd [ed clo Veco os se Lc etd eA Mote ec ake dea a fe es es oo) an Ae a PEE tei a othe ald celia Eales re ‘ 4 Fic. 191.—Remittent fever chart, showing variations in which the temperature is always above normal. & increased and its character is changed because of the action of katabolic products on the nerve centers. Respiration is increased probably because of an effort to eliminate large quantities of air and waste material, and thus there is a tendency for the tem- perature to be diminished. The affected animal is more or less nervous and restless. FEVER. 343 3 8 IS 16 17 19 49 Ro RI 8% 23 Be 2S ZL 27 28 29 30 Br 32 See 1 ENE Ss oo Bimmer Seer eer ae eee ne Ao Bese eee eS aga ae _ 224 SSN Baw ee eee Ss eae eee eee ee oP pet Bar sei ie pol le Seles eee | Fig. 192.—Intermittent fever chart in which there are periods of normal tempera- ture. Lesions.—All parenchymatous structures are affected with cloudy swelling, the extent of which depends upon the degree of temperature and its duration. Hemolysis is more or less ex- tensive. Chronic or long continued fever usually causes hyaline degeneration, especially of the vessel walls. The affected animal rapidly diminishes in weight because of the consumption of fat. CHAPTER XII. INFECTIVE GRANULOMATA. Intective granulomata embraces a group of specific inflam- matory conditions characterized by the proliferation of endothe- lial cells, fibroblasts and other cells. Though the consideration of the following diseases belongs more properly to a discussion of infective diseases, their description will be of value to the stu- dent of general pathology. LUBE NEUIEOSES: Tuberculosis is a specific, infective disease, caused by the bacterium of tuberculosis affecting practically all of the higher animals and also some of the lower forms of animal kind. Extent.—McFarland states that 14% of the deaths in the hu- man family are from tuberculosis. It is probable that 25% of all humans have or have had tuberculosis. The prevalence of animal tuberculosis is variable in different communities, the percentage depending upon methods employed for control and eradication under different sanitary laws, upon transportation rules and regulations and upon the conditions un- der which the animals are maintained. The exact percentage of tubercular animals in any country is not known, but the relative number has been determined by tuberculin testing and by post- mortem examination at abattoirs. In the United States) the percentage, generally speaking, is low in comparison with other countries. According to the post-mortem findings of 7,621,717 cattle slaughtered in United States establishments having official inspection during the fiscal year beginning July 1st, 1906, and ending June 30th, 1907, 29,8350, 1 e5 -4%* weres tuberoutar This percentage is probably below the actual percentage, as dairy cattle are more extensively affected than beef cattle. The Secretary of Agriculture in his report for 1908 holds that 1% of beef cattle and 10% of dairy cattle are tuberculous. According to the above report 2% is the estimated prevalence in the United States of tuberculosis among swine. Porcine tuberculosis is apparently on the increase in the United States. In Germany it varies from 1-7%. Equine tuber- 344 INFECTIVE GRANULOMATA. 345 culosis is not common in the United States, or at least only a few cases have been reported. Tuberculosis is usually found in those horses and mules that have been fed on tubercular cows’ milk. ie Tuberculosis cf sheep is very rare and the disease is still less common in goats. Dog and cat tuberculosis is not uncommon and is usually observed in pets of tubercular humans, although barn cats, espe- cially those fed milk from tubercular cows, frequently become tubercular. (A dairy was recently inspected in which 68% of the cows were tubercular and on autopsy three barn cats also were found to be affected in a like manner.) Tuberculosis of fowls is more prevalent in the United States Fig. 193.—Bacterium Tuberculosis Bovine. Pus showing leucocytes and tissue shreds. than is ordinarily suspected, although the percentage of affected birds is difficult of determination because there is at present no official inspection of fowls. Etiology— Tuberculosis is caused by the Bacterium tuberculo- sis. This bacterium has rounded ends and is frequently slightly Hen lttvariess item 2 to 5 microns. im length and. trom’.3 toms in width. (These bacteria may appear as long, delicate, mycelial threads, branching forms, or even as a ray lke fungoid growth, the form depending upon the environment. The pleomorphism of this micro-organism has caused some doubt as to its classifica- tion as a bacterium.) The Bacterium tuberculosis may occur singly or in pairs, and it is not uncommon to find several lying 346 VETERINARY PATHOLOGY. side by side. They do not form spores, but they may contain granules and vacuoles, and they may have a beaded appearance because of fragmentation of their cytoplasm. The Bacterium tuberculosis is extremely resistant to external injurious influences, probably because of a wax-like substance that constitutes about one-third of the body weight and forms the principal part of the external covering or capsule. (These bacteria are stained with difficulty but when once stained retain their stain even though subjected to the action of alcohol and acids.) The staining peculiarities are probably due to a fatty substance they contain. Source of infection.—The bacterium tuberculosis may be transmitted direct from tubercular to healthy animals, but infec- tion is more frequently obtained from foodstuffs, or barns, feed racks, watering troughs, posts, soil, etc. Tubercular animals are almost constantly. eliminating the bacterium which contam- inates everything that the tubercular discharges contact. The cadavers of tuberculous animals are usually deposited in the soil, and, in many instances, the proper precautions are not taken to destroy the infecting micro-organism. Infected manure is spread upon the soil and thus it becomes infected. The various crops, including hay, grown upon a tubercular infected soil, may be contaminated with the Bacterium tuberculosis and infect sus- ceptible animals that consume such food. Sometimes the car- casses of animals dead of tuberculosis are thrown into rivers or creeks, thus infecting the water. The waste products of many small slaughter houses are fed to hogs and this affords oppor- tunity for them to become infected. Skimmed milk and whey from creameries and cheese factories are also sources of tuber-' cular infection. Channel or avenue of entrance of the infection—The Bacter- ium tuberculosis may gain entrance into the tissues of a healthy, susceptible animal through the mucous membranes or through abrasions of the skin, though the latter mode of infection is not of common occurrence in domestic animals. Cutaneous infec- tion is occasionally observed in the mammae of sows and in the castration wounds of barrows. From clinical and experimental evidence and autopsy lesions observed in abattoirs, it seems evident that the digestive tract is the principal channel of entrance of the Bacterium tubercu- losis in hogs, cattle and fowls. It was originally erroneously concluded that the presence of pulmonary tubercular lesions was positive evidence that the infection had gained entrance through the respiratory tract. Tubercular free experimental animals fed INFECTIVE GRANULOMATA. 347 foodstuff contaminated with the Bacterium tuberculosis have frequently become affected with primary pulmonary tubercular lesions. (The possibility of inhalation of the infection was care- fully guarded against in these experiments.) It is presumed that the Bacterium tuberculosis is incorporated by leucocytes in the digestive tube and that the leucocytes then pass through the intestinal wall into the lacteals and thence to the thoracic duct to the right heart and on to the lung, the first capillary system encountered, where they may lodge and establish tubercular foct. No doubt the respiratory tract is the channel of entrance in some cases of tuberculosis, but the number of animals infected through this channel is very small. An occasional case of tuberculosis may be the result of infec- tion through the genito-urinary organs. Thus the penis of a bull may become infected by serving a cow afflicted with uterine or vaginal tuberculosis, and this same bull by copulation may infect other cows. Tubercular lesions are occasionally observed in the superficial inguinal glands of steers, and this may be the result of infection in the castration wounds. Conjunctival infection may occur as a result of forcible dis- charge of infection from the respiratory tube of an affected animal, In summarizing, the digestive, respiratory, cutaneous abra- sions, and genito-urinary organs are the principal channels of entrance of the Bacterium tuberculosis, the frequency being in the order mentioned. Lesions.—The characteristic lesion of tuberculosis is the tubercle. A tubercle is a nonvascular nodule, composed of leu- cocytes, endothelial, giant and connective tissue cells, with a tendency for the central part of the nodule to undergo necrosis. The lesion may vary in animals of different genera and in differ- ent animals of the same genus. Thus tubercular lesions in hogs may differ in some particular from those in cattle because of variations in the resistance of the hog and ox. Variations of the tubercular lesions in different individuals of the same genus occur because of variation of individual resistance of the infected ani- mal and variation of the virulency of the infecting organisms. Tubercular lesions may be modified or obscured by lesions re- sulting from secondary infections. The initial or primary lesion may occur in any tissue or organ. Lymphoid tissue, however, is more frequently affected than any other. The Bacterium tuberculosis and its products are the etiologic factors in the formation of a tubercle. The bacterium having lodged in a tissue favorable for its growth and development, be- 348 VETERINARY PATHOLOGY. gins to multiply and to eliminate those products that stimulate the surrounding connective tissue and endothelial cells to in- crease in number, and, at the same time, exerts a positive chemo- tactic action upon leucocytes. If the influence of the bacterial products is exerted upon the connective tissue and’ endothelium, the resulting tubercle will be composed of connective tissue cells and endothelial cells, and if the influence of the bacterial pro- ducts is of a chemotactic nature, the tubercle will contain leu- cocytes. Structurally, a young tubercle consists of a cellular focus in- fected with varying numbers of the Bacterium tuberculosis. As G oT ee We Tete aes Fig. 194.—Small cellular tuberele; liver, x500. Showing small round cells with tu- bercle bacilli scattered here and there, also a few partially destroyed hepatic cels. INFECTIVE GRANULOMATA. 349 the bacteria multiply the quantity of their products is increased, and these stimulate cellular multiplication and accumulation, and thus the tubercle grows. The formation of a tubercle constitutes a tissue reaction, but there is no vascularization; that is, no new blood vessels are formed, and the existing capillaries in the invaded tissues are finally obliterated. A tubercle is, therefore, strictly non-vascular, although in the very beginning the affected zone may be hyperemic. Cells constituting a tubercle obtain nutriment from adjacent tissues by absorption. Tubercles grow by multiplication of the peripheral cells, the central cells becom- ing degenerated after they have consumed all available nutrition. The structure and appearance of a tubercle varies according to its age, thus: a tubercle in the very early stages is a cellular mass, a little later the central portion of the cellular mass becomes necrotic, and at about the same time a median zone, consist- ing of bacteria, endothelial, and, in some cases, giant cells, becomes evident; the outer zone is the active zone and is com- posed of bacteria, connective tissue cells and leucocytes. As the tubercle becomes larger the necrotic zone extends to the ‘median and outer zones toward the periphery. Necrosis is usually evident in tubercles that have attained the size of a pea. The central necrosis is primarily of the coagulation type, but the coagulated necrotic tissue may become liquefied, always be- comes caseous and usually calcified according to the quantity of fluid contained. The calcification may be limited in extent, the necrotic tissue containing small calcareous particles that cause tHe MECLOtic tissife to have a) eritty feel; or it may be so ex- tensive that the tubercle cannot be dissociated except by the use of a sledge. Liquefied tubercular necrotic tissue (pus) is yellow- ish in color in the ox, dirty white in hogs and yellowish in fowls. It is not sticky, although it becomes quite thick and is finally caseated.. Tubercles may vary in size from a microscopic point to large masses. All tubercles are small in the beginning and are usually entirely cellular. Small cellular tubercles in which there is no necrosis are designated miliary tubercles. Miliary tubercles ap- pear as minute, grayish, translucent, pearl-like specks or nodules. If all the lesions in an affected animal are miliary in character, the disease is termed miliary tuberculosis. Miliary tuberculosis is most common in hogs. The appearance of a tubercle changes when central necrosis begins. The color of caseous and calcareous tubercles varies from a dirty white to a yellow color. The tubercles may or may not be encapsulated. The capsule of a tubercular lesion is rela- 350 VETERINARY PATHOLOGY, tively thin, though it is tough. Secondary tubercles may develop from a primary tubercle, and daughter tubercles may develop from a secondary tubercle, thus are produced the irregular nodu- lar tubercular masses. The tissues contiguous to a tubercle are ischemic, probably because of the enfringement of the affected areas with lymphoid cells. Little difference is noted in tubercular lesions in the various NS JOSOG APL TA e V vee a Bo DOORS — > S So 2) ©. d S = +s Be eS Nee, e $52 6,00\ = Ae Boe Peas (82a EA TEa$4 ae ge Cece ceieeeee 2 G0 wee. \eeaasecess? i <9) ; ae @ ‘a a 7a ROG Ge! \ a Q Gig Boom Se tiase ‘on Ga ie Oe, FB @EDD APO WW As eee 6 LEO ESLER =O AN S: WSNG ONO Bog coats ae KS 9g ee Wc MOSSES & WS 6 WS / VP re os 6 a g OO On. & O-o0, ee Wagon SR cok s Ce} oe Oo 9040 COO DO@ 0 bese @o2 oe} 690@ 6gGa0@ eLESPE gee OH ES) CGO? =e oe 1 =o = Bee = Fig. 195.—A Lesion of Tuberculosis from the Post-pharyngeal Lymph Gland of an Ox. A—giant-cells; b—caseous center within the tubercle; c-—fibrous capsule. tissues except possibly osseous tissue and serous membranes. Tubercular lesions of osseous tissue are usually associated with extensive suppuration of the osseous structures, while tubercular lesions of serous membranes are frequently entirely cellular in’ structure and do not undergo central necrosis. Bovine tubercular lesions ate usually encapsulated and become quite extensively calcified. The age of the lesions is sometimes important in medico-legal cases. Calcification usually begins INFECTIVE GRANULOMATA. Soul when the tubercle is from six to eight months of age and is ex- tensive by the time the lesion is one year old. Tubercular masses are occasionally observed in the lung, bronchial or mediastinal glands, and in the liver. These masses may contain all stages of tubercular formation or the entire mass may all be in the same stage of development, as liquefying necrosis, caseation or calcifi- cation. Tuberculosis of serous membranes of bovines should receive special mention because of the characteristic appearance of the lesions. Bovine serous membrane lesions vary in size from a millet seed to a walnut, but are usually about the size of a pea. These lesions are frequently thickly studded over large areas of a serous membrane.. The nodules are surrounded by a firm cap- sule which causes them to appear as pearl-like bodies, and hence Fig. 196.—Photograph of a tubercular mammary gland, Ox. the name, “pearly disease.” Sometimes serous membrane tuber- cular lesions are very extensive; this type may be called “mass tuberculosis.” Porcine Tubercular lesions are characterized by enlargement of lymphatic glands, the formation of tubercles of variable sizes in Or upon serous membranes and within the substance of glandular organs, bones and other connective tissues. The tubercles pro- duce increased density of invaded soft tissues and are, therefore, easily detected except in very recent infection. The tubercular nodules in the early stages present about the same color as the surface of the tissue invaded. In sectioning the tubercle the cen- tral portion is caseous and slightly yellow or fibrous and white. S52 VETERINARY PATHOLOGY. Sometimes there is a combination of both conditions and occa- sionally the tubercles contain calcareous granules. The central portion of porcine tubercles rarely contains liquefied necrotic tissue.’ Microscopically porcine tubercular lesions are always cellular in the beginning. The cellular tubercles are fairly constant in structure regardless of the tissue in which they occur) Wie center 1s at first represented by a mass of lymphoid cells, the other cellular elements occurring as the tubercle develops. Necrosis, or fibrosis, succeeds the cellular stage in the por- cine tubercular lesion. Necrosis of tubercles is probably the result of the activity of very virulent bacteria or the low resis- tance, of the infected animal. The necrotic center may be sur- rounded by a cellular zone (lymphoid and endothelial cells), or it may be surrounded by fibroblasts. ‘The necrotic material is invariably caseated and later becomes calcified. Fibrous lesions vary from the formation of small quantities of fibrous tissue to dense fibrous centers. Fibrous lesions are probably produced by bacteria of low virulence, or occur in ani- mals having a marked resistance. The central portion of the fibrous lesion may become calcified. The so-called arbor vitae gland is a fibrous center in which the fibrous tissue is arranged similar to the trunk and branches of a tree, hence the name. This lesion is observed im thewmes in the cervical lymph nodes: The bacterium tuberculosis fas been demonstrated in about 30 per cent of arbor vitae glands. The lesions of porcine tuberculosis are in brief either cellu- lar, necrotic and calcified tubercles, or cellular, fibrous and calci- fied tubercles. The lesion is always non-vascular as in other animals. Avian tubercular lesions are very similar to mammalian tubercles, and may occur in practically any tissue. Microscopically, avian tubercules are found to contain giant cells, endothelioid cells, small round cells and connective tissue cells, the arrangement of which is the same as described in mammalian tubercles. Avian tubercular lesions have been found in the liver, spleen, intestine, mesentery, kidney, lung, skin, and bones, the frequency being in the order mentioned. Avian tubercles in glandular tissue, i. e., in the liver, kidney, spleen, etc., begin as small, dirty, white cellular foci. They usu- ally occur singly, though they may occasionally become conflu- ent, thus producing nodules a quarter of an inch in diameter. As the tubercles in glandular tissue undergo necrosis, they as- sume a yellowish color. Intestinal tubercles are about the same INFECTIVE GRANULOMATA. 35D size as those in glandular tissue. The intestinal lesions are usu- ally quite hard and dense and present a glistening appearance. Necrosis frequently destroys the intestinal wall iad thus a tuber- cular intestinal ulcer is produced. Mesenteric tubercles are fre- quently pedunculated and they invariably present a pearf like appearance. Extension.—Tuberculosis, except in some cases of the acute form, essentially a localized disease. However, the disease, even in the chronic form, has a tendency to extend and involve new tissue. The extension may be accomplished by means of, first, the lymphatic system, second, the digestive, respiratory and genito-urinary tubes, third, the blood vascular system and fourth, by continuity and contiguity. Tuberculosis is usually extended by the lymphatic circulation. Thus the first group of lymph nodes through which the lymph passes from a tubercular lesion is almost invariably involved. In fact this is a characteristic of the disease. The large per cent of lymphatic lesions is also evidence of extension by means of the lymph. It has been previously stated that hogs are invariably infected by ingestion of tubercular material and in 93 per cent of . tubercular hogs the submaxillary lymph nodes are affected, which is further evidence of lymphatic extension. The fact that infec- tion may extend along the digestive, respiratory or genito-urin- ary tracts, has been demonstrated. Thus the discharges, con- taining the Bacterium tuberculosis from a pharyngeal tubercle may pass through the oesophagus and stomach and find a nidus favorable for its development in the intestine. In a like manner the lung tissue may become affected by extension from laryngeal, tracheal or bronchial tuberculosis and prostatic tuberculosis may result from extension of renal tubercular lesions. In extensive or generalized tuberculosis the tubercles not infrequently in- volve and produce necrosis of the blood: vessel walls and the virulently contaminated necrotic material being discharged into the blood resulting in tubercular metastasis. Thus tuberculosis is extended by means of the bleed. Extension by the blood in- variably results in generalized tuberculosis which is _ usually acute. In the discussion of tubercular lesions, the formation of sec- ondary and daughter tubercles was mentioned. The production of secondary and daughter tubercles is a means of extension. lf the new ly formed tubercles are in the same kind of tissue as the primary tubercle then the extension is by continuity. If the secondary or daughter tubercles are in tissues dissimilar to that 354 VETERINARY PATHOLOGY. in which the primary tubercle occurs the extension is by con- tiguity. In the majority of the cases of lymphatic extension and in some of the cases of blood extension the Bacterium tuberculosis is incorporated in and transported by leucocytes. The leucocytes usually have sufficient vitality to destroy the incorporated bac- teria but occasionally the leucocytes may be destroyed after having transported the bacteria a considerable distance. Thus a Bacterium tuberculosis from a pulmonary tubercle may be incor- porated by a leucocyte and carried to the kidney and the leuco- cyte being destroyed the liberated bacterium may establish a tub- ercular focus in the renal tissue. The occurrence of Bacterium tub- erculosis in the milk of cows having no mammary tubercular lesions as well as the fact that ingestion of tubercular material frequently causes pulmonary tuberculosis, may be due to leuco- cytic incorporation and transportation of the infecting micro- organism. Elimination.—From the sanitary point of view it is always of considerable importance to know the channels or avenues through which infectious agents are discharged in order that they may be destroyed. Tuberculosis affects all tissues and the Bac- terium tuberculosis may not be eliminated from the affected ani- mal or it may be discharged in one or more of the secretions or excretions. It has been determined by the Department of Agri- culture that about 40 per cent of tubercular cattle eliminate the Bacterium tuberculosis in their feces. The same investigators also found, in a limited number of dairies, that about 25 per cent of tubercular cows, regardless of location of the lesions, eliminated the Bacterium tuberculosis in their milk. These are facts of prime importance in adopting means for checking the progress or for suppression of the disease. The discharges from the respiratory tract of tubercular animals frequently contain the Bacterium tuberculosis, especially if they have pulmonary lesions of the disease. The urine and discharges from the female genital organs may be contaminated with the infection. Renal tuber- culosis, however, is not of frequent occurrence and it is not probable that the Bacterium tuberculosis is eliminated in the urine of tubercular animals in which there are no renal lesions. In general the channel of elimination of the bacterium tuber- culosis depends largely upon the location of the lesion. Tuberculin and Tuberculin Test—Tuberculin is a bio-chemic material containing the products and the disintegrated bodies of the Bacterium tuberculosis. It is prepared by growing the Bacterium tuberculosis in glycerine bouillon for a certain length INFECTIVE GRANULOMATA. 355 of time. The glycerine bouillon culture is filtered and the fil- trate sterilized by heat and concentrated to the desired strength by evaporation over a water-bath. The active principle of tuber- culin is probably a nucleo-proteid or its chemic derivatives. Tuberculin is a very reliable diagnostic agent. Its chief use in veterinary medicine has been in the diagnosis of tuberculosis in cattle. It is practically as reliable in the detection of human, porcine and probably avian tuberculosis as in the detection of bovine tuberculosis. The principal method of application has been by subcutaneous injections and noting the temperature changes in the suspected animal. The normal temperature of the animal is ascertained previous to the injection and the tempera- ture is taken every two hours, beginning eight hours after tuber- culination. On the day succeeding the injection a rise of from two to three degrees Fahrenheit is considered a reaction and this sig- nifies that the patient is tuberculous. This reaction is probably due to the specific irritating action of the injected tuberculin upon the tubercular foci producing intense hyperemia around and disintegration of the tubercle. Thus there is a sudden dis- charge of tubercular products into the system and the intense re- action, thermic and constitutional follows. A purified tuberculin used directly in the conjunctival sac is now on the market. The ophthalmic reaction consists of the production of a marked hyperemia of the conjunctive in from six to ten hours after tuberculination. At the present time the technique is at fault or the tuberculin is of inferior quality and the ophthalmic tuberculin test cannot be relied upon. ACTINOMYCOSIS. Actinomycosis is a specific, inflammatory granuloma, caused by the Cladothrix actinomyces and characterized by the forma- tion of tumorous masses of fibrous tissue that usually develop suppurating centers and fistulous tracts. Distribution and extent.—Actinomycosis is prevalent in Eu- rope, Australia, Africa, North and South America. The extent of the disease varies in different countries. According to the 24th Annual Report of the Bureau of Animal Industry there were slaughtered in establishments having federal inspection 7,621,717 cattle, of which 22,742 were found to be affected with actinomy- cosis, or one in about each 340. The actual per cent is even larger, for many animals afflicted with actinomycosis are slaugh- tered where there is no official inspection maintained. Susceptible Animals.—Cattle are more frequently affected 356 VETERINARY PATHOLOGY. with this disease than other animals, though actinomycosis of sheep, goats and hogs is occasionally reported. A few cases have also been observed in the horse, mule, dog and wild ani- mals. - Etiology.—A fungus, the Cladothrix actinomyces or actino- myces bovis, is the specific cause of actinomycosis. The life his- tory of this organism is not known, but it is thought that it passes a part of its life cycle upon some of the grasses. Each matured fungus is composed of a central body 10 to 40 microns in diameter, from which the radiating filaments (mycelia) extend outward for a distance of from 5 to 20 microns, then becoming enlarged, terminate in club-shaped bodies from 10 to 50 microns in length. Thus the matured fungus has the appearance of a rosette and is commonly called the “ray fungus.” Detached clubs are capable of reproducing the entire rosettes as described. The fungus can be cultivated in artificial media where it develops a tangled mass of mycelia. Source.—The Cladothrix actinomyces is probably most fre- Fig. 197.—Drawing of Actinomyces (Ray fungus) in section of tongue, INFECTIVE GRANULOMATA. 357 quently cbtained from vegetation, especially wild rye (Hor- dium murinum) consumed by the animal. Infection occurs most frequently in animals fed on dry feed as fodder, stover, straw or hay. During January and February, 1908 .86% or 376 cattle of 41,405 slaughtered had actinomycosis of the tongue or submax- illary lymph nodes, and of 12,484 cattle slaughtered in July, 1908, 44 or .84% were affected with actinomycosis. Some rather exten- sive outbreaks have been investigated in which it seems highly probable that infection has been direct from one animal to an- other, or indirect by means of the discharge of actinomycotic ani- mals that had been smeared on rubbing posts, feed racks and feed troughs. (Of 98 head of cattle, three of which were actinomycotic when placed in the feed lot in November, 42 head were affected with actinomycosis when inspected 2% months later.) Channel of Entrance.—The causative fungus may gain en- trance into the system by way of the digestive tract, the respira- tory tract or through the skin. Abraded surfaces appear to be essential for infection, though it has not been proven that the fungus cannot penetrate uninjured surfaces. The digestive tract is the most frequent channel of entrance in cattle. The tongue, especially the dorsal surface at the junction of the base and apex, is subject to injury by the rough, harsh food consumed by cattle. Tongue injuries may also be inflicted by licking boards, posts, etc., containing nails and splinters. Awns of wheat, barley and rye, chaff, splinters and hair accumulate in the erosions or wounds of the tongue, producing the so-called “hair sores.” More than 12% of 48,000 cattle slaughtered during the winter months in one of the Kansas City packing houses had “hair sores” upon their tongues. The “hair sore’ is intimately associated with lingual actinomycosis; indeed it is rare to find actinomycosis of the tongue or submaxillary lymph glands when there is no “hair sore.” Diseased teeth, especially if the gingival mucous mem- brane is involved, also provide an entry for the ray fungus. The possibility of the infection passing through the intestinal or gastric wall explains the cases of peritoneal actinomycosis that are occasionally observed Respiratory infection is not of common occurrence. This type of infection probably occurs by inhalation of chaff or awns con- taminated with the Cladothrix actinomyces. The skin is probably the most frequent channel of entrance in hogs. Actinomycotic scirrhus cords are quite common, the in- fection taking place in the castration wound. Mammary acti- nomycosis is sometimes observed in sows, especially those run- ning in stubble fields, the infection taking place through abra- 358 VETERINARY PATHOLOGY. sions produced by the stubble. Abrasions resulting from rub- bing on stanchions and feed boxes may be a source of infection in dairy cattle. - ae Lesions.—Macroscopic.—Actinomycotic lesions may be sur- face or subsurface. The fungus may invade and produce the lesion in any tissue. Surface lesions begin as small inflammatory centers which usually thicken and become elevated above the general surface. The lesion gradually increases in size, and in some cases assumes a fungoid appearance. At this stage the lesions vary in size from a small pea to a walnut. The surface tissue may become eroded as a result of the extension of necrosis from the lesion and the typical actinomycotic pus discharged or more frequently the lesion becomes encapsulated by the formation of a dense fibrous capsule. The capsule usually limits the development of the lesion and it may be diminished in size by the contraction of the fibrous tissue constituting the capsule. Subsurface lesions, though beginning as inflammatory centers, are invariably lcircumscribed by, a dense, fibrous wall. As the disease progresses the center of the lesion undergoes lique- fying necrosis. The necrosis extends, producing irregular, tor- tuous sinuses that may extend through the capsule and into the surrounding normal tissue. Ultimately the liquified necrotic tissue (pus) would ordinarily be discharged upon a surface, or the fungus contained in the necrotic tissue (pus) would perfor- ate the primary capsule and cause the production of a secondary fibrous capsule. Thus the lesion is frequently composed of sev- eral communicating cavities (multilocular) containing actinomy- cotic pus. If such a lesion is incised and pressure applied the typical beads of actinomycotic pus will appear in various places upon the cut surface. Actinomycotic pus is creamy, sticky, tenacious, yellowish-white and contains small, yellow, gritty granules. The pus has a greasy feel and may have a slight odor. If the pus is permanently maintained within the capsule, its fluid content is absorbed and becomes caseous. Osseous actinomycosis is of common occurrence. The fungus having gained entrance produces inflammation, which is suc- ceeded by disintegration of the osseous tissue and the formation of cavities or pockets. By growth and extension of the infect- ing fungus, inflammation and disintegration is favored, and thus communicating cavities are formed in the affected bone. As the process of rarefaction continues within there is new osseous tis- sue deposited without. Thus bone affected with actinomycosis INFECTIVE GRANULOMATA. 359 becomes enlarged and cancellous and has a honeycombed ap- pearance. Microscopic—The presence of the Cladothrix actinomyces in a tissue produces an irritation resulting in an accumulation of dules on the dorsum of an Ox tongue, j cotic no Imomy: 198.— From photograph, showing act 360 VETERINARY PATHOLOGY. small round cells, the production of endotheloid and giant cells by the invaded tissue, and finally the development of a fibrous cap- sule around the entire mass. The fungus may appear in the be- ginning as mycelial elements, but later it has the typical rayed appearance. In old lesions the central portion or body of the fungus becomes calcified. | Surrounding the clubs or mycelium in the early stages are varying numbers of small, round cells (lymphocytes). As the disease progresses, the matured fungus is more or less surrounded by giant cells that actually contact the fungus. The actinomycotic giant cell is very irregular in shape and size and has varying numbers of nuclei scattered indiscriminately throughout the cell body. Endotheloid cells appear marginally to the giant cells. These cells are similar in appearance to the endotheloid cell of tuber- culosis, having a relatively large cell body and a small, single nucleus. The small, round cells are first noticed immediately around the fungus, but later they infiltrate the surrounding tissue also, and are in excess of all other cells in the lesion. Fibroblasts appear in the margin of the early lesion, and through their activity a thick fibrous capsule is produced. Actinomycotic pus is found to be composed of tissue shreds and fragments, lymphoid cells and some polymorphonuclear leucocytes, an occasional endotheloid cell and the Cladothrix actinomyces. Extension.—The extension of actinomycosis has usually been described as taking place only by growth in continuity or contig- uity, or by passing along the respiratory, digestive or genito- urinary tubes. By a careful observation of over 72,000 cattle slaughtered, it has been found that many cases, in which there were “hair sores” but no actinomycotic tongue lesions, showed actinomycosis of the submaxillary lymph nodes. The majority of cases of lingual actinomycosis are accompanied by involve- ment of the submaxillary lymph nodes. That practically all cases of actinomycosis of the submaxillary lymph nodes occurred in animals having “hair sores” is indicative of lymphatic exten- sion. It is therefore quite probable that actinomycosis may be extended in the animal body by means of the lymph. Differential Diagnosis——Bovine actinomycosis may be con- founded with tuberculosis, nodular disease, abscess formation and various tumors. Tubercular lesions calcify, actinomycotic lesions rarely be- come calcified. Tubercular. pus is usually quite different from INFECTIVE GRANULOMATA. 361 actinomycotic pus. The former is not sticky or tenacious, and does not contain the small, yellow, gritty granules found in the latter. The capsule of an actinomycotic growth is thicker and denser than the capsule of a tubercular growth. The two diseases can be differentiated positively by microscopic ex- amination of the pus and the lesion. The Bacterium of tuber- culosis would be found in tubercular pus and the Cladothrix actinomyces in the actinomycotic pus. Tubercular lesions are characterized by the presence of the horse shoe giant cell, the actinomycotic giant cell is irregular in outline and size, is poly- nuclear, the nuclei being scattered indiscriminately through the the cell body. Nodular disease, though not very prevalent in cattle may be mistaken for actinomycosis. The nodules of nodular disease are in the intestinal wall. The pus in the nodule is greenish yel- low in color, and though fluid in the early stages, it later be- comes caseous but never contains the calcareous granules. Microscopically the finding of the Cladothrix actinomyces in actinomycotic lesions or pus and the absence of this fungus in the lesions of nodular disease is sufficient for differentiation. From abscesses the differentiation may be made by the pecul- larity of the pus, and the capsule, which is usually much more dense in actinomycotic lesions than in abscesses. Osteosarcomata may produce lesions in bone similar to actin- omycotic lesions. A microscopic examination is always suffi- cient for differentiation of these diseases. Ovine actinomycosis may be confounded with ovine caseous lymphadenitis and nodular disease. Ovine caseous lymphaden- itis is essentially a disease of lymphoid tissue characterized by the formation of greenish yellow pus that later caseates in con- centric layers, but never contains gritty granules. The color of the pus and the arrangement of the caseated necrotic tissue is usually sufficient for differentiation of ovine caseous lymphaden- itis from actinomycosis. | The remarks on the differentiation of nodular disease in bovines is equally applicable to ovines. GLANDERS. Glanders is a specific, infective disease, especially affecting equines, caused by the bacterium mallei. Glanders is prevalent in all countries with the possible ex- ception of Iceland, Australia, and some isolated islands. The disease is found in practically all parts of the United States. It is 362 VETERINARY PATHOLOGY, more prevalent in those portions of a country in which there is extensive horse traffic. The invasion of a province or a country by an army is usually succeeded by the appearance of glanders. Etiology.—Glanders is caused by the Bacterium mallei. This organism was described by several different investigators in 1882. It is similar in appearance to the Bacterium tuberculosis, has rounded ends, is from 2 to 3.5 microns in length and .3 to .5 microns in width. This bacterium occurs singly except that when grown upon potato medium, pairs or even long filaments are not rare. Like, the Bacterium tuberculosis, it produces ple- omorphic forms when cultivated in different media or under varying conditions. In old cultures it frequently becomes short and is sometime coccoid in appearance. Branching forms are not uncommon. It does not form spores. The Bacterium mallei is stained by aqueous solutions of ana- Fig. 199.—Bacterium Mallie, x1000. line dyes that are slightly alkaline in reaction, such as Loef- fler’s methylene blue. It is so-called “Gram negative,” 1. e€., it is decolorized by Gram’s solution. Source of Infection—Infection probably occurs most fre- fluently in an indirect manner, i. e., the infection is obtained from some surrounding object or thing that has been contamin- ated with the infected discharges of a glandered animal. The Bacterium mallei is strictly parasitic and the source of the micro-organism is either the discharges from an infected animal or the carcasses of animals that have died of glanders. Fortunately this bacterium possesses little re- INFECTIVE GRANULOMATA. 363 sistance to light, dessication and other external influ- ences and consequently the infection in discharges is as a rule, promptly destroyed. The length cf time that the Bacterium mallei may exist outside of the animal body and retain its viru- lency has never been absolutely determined. Authentic cases of glanders have appeared in horses that had been placed in stalls that had been vacant for one year, but prior to that time occupied by glanderous horses. A few reports are indicative of the fact that the Bacterium mallet may retain its virulence in infected buildings for two or even three years, but these re- ports need further substantiation. It seems probable from clin- ical and experimental evidence that, except in the animal body, the virulence of Bacterium mallei is rarely retained longer than one year. In cities, public drinking fountains, hitching posts and feeding troughs are probably the greatest sources of infection. The purchase of second hand harness, wagons, and other equipment should be regulated by ordinances or laws to prevent the spread of such infections as glanders. The Channels of Entrance of the Infection.—All exposed surfaces and natural openings of the body may permit the Bac- terium mallei to gain entrance to the tissues. In glanders, as in tuberculosis it has been quite conclusively demonstrated experimentally that the majority of the cases of glanders results from the ingestion of the Bacterium mallei. No doubt infection may occur by inhalation of the infectious agent and an occa- sional case may be the result of cutaneous inoculation. It is possible for the discharges containing the Bacterium mallei to become pulverized: and carried’ by air currents and in- haled. Farcy may or may not result from cutaneous infec- tion. Such inoculations are easily accomplished by bridles, harness, saddles, curry combs, etc. More rarely the conjunc- tival membrane may be the channel of entrance. For example a horse, affected with nasal glariders may sneeze or cough and thus infection be forcibly introduced onto the mucous mem- Dratie of tiesevye Or anotier horse: Lesions.—Macroscopic—The lesions of glanders are found especially in the mucous membrane of the anterior respiratory passages, lymph nodes, lung and skin, the frequency being in the order mentioned. It is probable that the Bacterium mallei primarily affects lymphoid tissue. The gross lesions may be diffuse or circumscribed, depending upon the virulency of the infecting organisms and the resistance of the affected animal. Diffuse glander lesions are usually found in animals having 364 VETERINARY PATHOLOGY. little resistance and in which the disease assumes an acute form. In the nasal mucous membrane, diffuse, glanderous les- ions appear as severe inflammation in which the submucosa is extensively infiltrated. The engorgement of the tissue may be sufficient to obstruct circulation and result in necrosis of the mucous membrane thus producing ulcers variable in size and ir- regular in contour. The submaxillary lymph nodes are invari- ably hard and enlarged and may or may not be adherent to the maxilla. Pulmonary, diffuse glander lesions vary in size from a hazel nut to a basket ball and are irregular in shape. These lesions are grayish or dirty white in color. The lesions may undergo a central necrosis or they may become fibrous in nature. The necrotic material may be of a semi-solid or caseous consis- tency and in the smaller foci there may be calcificationsgeim practically all cases of pulmonary glanders the bronchial and mediastinal lymph nodes are enlarged and contain cellular necro- tic or fibrous centers. : Diffuse cutaneous lesions are not of common occurrence. They may be present in acute general glanders, the manifesta- tion in the skin being of the nature of a diffuse gangrenous der- matitis. Cutaneous nodular lesions may become diffuse as a result of rapid and extensive necrosis. Diffuse lesions occur in lymphoid tissue. Splenic lesions are usually nodular though a few cases have been reported in which there were diffuse lesions of the spleen. Osseous lesions are usually diffuse and appear as a suppurative osteitis. Nodular lesions are common in animals that have a marked resistance or in those cases infected with mildly virulent bac- teria. In chronic glanders the lesions are usually nodular. The appearance of nodular lesions in the nasal, pharyngeal and tracheal mucous membranes as well as in the mucous lin- ing of the facial sinus varies according to the age of the lesion. In the beginning the lymphoid tissue of the mucosa or submu- cosa becomes swollen and the tumefaction is surrounded by a hyperemic zone. As the disease progresses there is necrosis which not only involves the lesion but also the surface tissue, thus producing an ulcer. The size depth and contour of the ulcer necessarily depend upon the extent of the necrosis. In some instances the nasal septum and facial bones may be per- forated. The ulcers vary in size from mere points to areas as large as a silver dollar. The large ulcers are usually the result of two or more necrotic centers becoming confluent. The de- nuded surface is usually limited or surrounded by a raised oy) INFECTIVE GRANULOMATA. 36 border, the latter being the result of cellular infiltration. The tissue adjacent to the denuded surface may finally produce sufficient new tissue or granulation tissue to repair the injury. If the necrosis involves only the superficial epithelium the re- pair will be complete and there will be no scar, but if the necrosis has involved the mucosa and portions of the submucosa. Fig. 200.—Nasal septa, showing glanderous ulcers. A nasal septum from glandered horse. A crateriform ulcer having a thick raised border with a depressed granulating center. Shows characteristic outline of an ulcer, also fusion of two Or more primary ulcers. Thumb tacks. A nasal septum from a second glandered horse. Typical crateriform ulcers and large necrotic area the result of fusion of several ulcers. Cicatrices shown as irregular white spots. Thumb tacks. le N Leplea lk) eo to 365 VETERINARY PATHOLOGY, there will be large quantities of cicatricial tissue produced and consequently a scar. In nodular glanders of the anterior air passages, the submaxillary lymph nodes are invariably enlarged and contain fibrous, caseous or calcified necrotic foci. Pulmonary nodular lesions are usually dirty white in culcr and vary in size from pin point centers to masses as large as a man’s head. These nodules in the beginning are entirely cellu- lar and are surrounded by an hyperemic zone. As they become larger the central portion usually becomes necrotic and the hyperemic zone becomes infiltrated with fibroblasts that pro- duce a fibrous capsule. The small nodular lesions may be small and thickly distributed throughout the entire lung. The large : Fig. 201—Cutaneous Glanders—Farcy. i. A large erosion or ulcer (farey bud) on the internal surface of fetlock,. 2, 3 and 4, Other ulcers appearing along the course of the lymphatics, INFECTIVE GRANULOMATA. 367 lesions are usually few in number and they may be forined Ly two or more nodules becoming confluent. The central casecus necrotic tissue in the small foci frequently becomes calcified. Calcification is usually not evident in the large pulmonary tes- ions. The bronchial and mediastinal glands are invariably in- volved and they may be caseous, calcified or indurated. Nodular lesions of the skin are found in the superficial por- tion of the dermis or in the subcutaneous tissue. The nodules in the skin rarely become larger than a pea but those of the subcutaneous tissue may become as large as a hen’s ege. The central portion of the cutaneous and subcutaneous nodules and SS & lod ,7, -> ES Fig. 202—Microsecopic Section through a glanderous ulcer. Margin of ulcer-necrotic tissue. Normal nasal mucous membrane. Showing depth of erosion. Small round cells. Epitheloid cells. Fibrous tissue. ay ed ho Nae the superficial tissue covering them become necrotic and a sticky, tenacious, semi-fluid material is discharged onto the surface. The related lymphatic vessels are all engorged and the lymph nodes are enlarged and later become indurated. The tissue destroyed in the lesions of cutaneous glanders may be partially regenerated, but are more frequently repaired by the substitution of fibrous tissue thus producing a thickened fibrous skin. | Small nodular lesions have been noted in the spleen, liver and kidney. The splenic lesions may be caseous or calcified. Hepatic lesions are usually caseous. The portal lymph nodes are usually involved when lesions are present in the liver and 368 VETERINARY PATHOLOGY. the lymph nodes along the hiltis of the spleen are invaded in splenic lesions. Microscopic.—A small lesion is the result of a diffuse prolif- eration of lymphoid and endotheloid cells and migration of polymorph leucocytes. The proliferated cells may accumulate in groups, thus producing nodules. In the beginning there is usu- ally a well marked hyperemic zone around the cellular center The cells constituting the central portion of the lesion later un- dergo necrosis and about the same time the hyperemic zone becomes less evident. A fibrous capsule may or may not en- close the lesion, depending upon whether it is diffuse or nodular. In the nodular form of the disease there is a proliferation of fibroblasts in the tissue that was previously hyperemic. The fibroblasts produce the capsule that characterizes nodular gland- ers. In the older subsurface centers there is formed caseous material and in the small centers calcareous particles. In sur- face lesions, necrosis or fibrosis is evident. Diagnosis. —Mallein is a filtrate obtained from a glycerinated bouillon culture of the Bacterium mallei. Mallein is of diagnostic value only. The cause of the reaction of glandered horses to mallein is due to increased tissue action. The reaction noted in glanders con- sists in a thermic disturbance, a swelling at the point of inocu- lation, stiffness in gait, general depression and there is usually frequent urination. The temperature variations in glanders range from 2° F. to 5° F. The maximum rise of temperature usually occurs in from ten to twelve hours after malleination, though it may not appear until the eighteenth hour after injection of the mallein. The high temperature evidenced in a mallein reaction is maintained for a period of from 24 to 60 hours. The swelling is usually quite large and is very sensitive. The lymphatic ves- sels that are related to the swollen area become engorged and present a knotted appearancee. The swelling characterizing a mallein reaction persists for several days. Stiffness of gait may be due largely to the disturbance induced by the swelling at the point of injection, but at least in some cases it is evident that the stiffness of gait is not proportional to the size of the swell- ing. Aside from stiffness the reacting animal has a dejected appearance. The cause of frequent urination is not known. Agglutination.—The bacterium mallei produces an agglutinogen which causes the animal body to produce an agglutinin. A spe- cific agglutinin is found in small quantities in the blood serum of normal horses and in larger quantities in horses with gland- ers. The agglutination test for glanders depends upon the same principle, as that upon which the typhoid agglutination INFECTIVE GRANULOMATA. 369 depends. The agglutinin appears to cause the bacterial cell membrane to become sticky and thus the bacteria acted upou adhere to each other when they are brought into contact and clumps or clumping of the bacteria results; this constitutes the agglutination reaction. Blood serum is obtained from the suspected animal and placed in a normal salt solution in which are suspended dead Bacteria mallei. A series of four tubes is usually used in order that different dilutions may be made. In the 1st tube the dilution is made 1 to 200, 1. e. one part of serum is taken to 200 parts of salt solution in which the Bacterium mallei is suspended. In the 2nd tube, the dilution is made 1 to 500, the 3rd tube 1 to 800 and in the 4th tube, 1 to 12C0. These tubes are placed in an incubator. The reaction consists in a deposit of clumped or agglutinated Bacteria mailei in the bot- tom of the tube. Normal horse serum usually contains suff- cient agglutinin to produce a reaction in tube number one, that is in a dilution of 1 to 200. A deposition in tube number two is considered suspicious and deposits in tubes three and four is positive evidence of glanders. The reaction time is from 24 to 60 hours. The agglutination test is an accurate means of diagnosis it the test fluid is properly prepared and has been properly pre- served and if the operator uses care in making the test. The time required is much less than the time necessary in making the mallein test. Another advantage is that the blood serum of an animal dead of suspected glanders can be as readily tested as the serum from a living animal—hence it is useful in medico- legal cases. EPITHELIOMA CONTAGIOSUM. Epithelioma Contagiosum is a specific infective disease of fowls and it may be transmissible to pigeons. The disease is widespread in the United States. It is, according to Cary the most serious drawback to the poultry industry of the south. It is quite prevalent in Hawaii, and has been described in many different localities in Europe. Etiology.—The cause of contagious epithelioma is unknown. The evidence obtainable at the present time indicates that the eiologic factor is either a protozoon, (coccidium), or an ultra microscopic or filterable virus. Lesions.—Macroscopic——The disease is initiated by a catarrhal inflammation of the mucous membrane of the head and neck. The disturbance may be localized in the eye, nose or mouth, or 370 VETERINARY PATHOLOGY, may involve all those parts. The inflammatory disturbance stim- ulates or is accompanied by a proliferation of epithelial cells in the eye, nose, mouth or even on the wattles and comb. These epithelial new growths are at first grayish, have a smooth, glis- tening appearance and are surrounded by a hyperaemic zone. Later the growths, which become nodular, undergo degenera- tion, especially upon the surface. The necrotic tissue may re- main and form a scab or it may slough leaving a ragged, brown- Fig. 203. Left side of head, showing eye with extensive accumulation of caseous necrotic material. ish or grayish indurated surface. These nodules may become as large as a pigeon’s egg. They frequently entirely obstruct vision and in some cases destroy the eye; those appearing in the nostril may seriously interfere with respiration or even obstruct the air passages; and nodules in the buccal cavity may prevent eating or the prehension of food; while those that occur in or upon the wattles and comb may be so extensive that these structures are practically destroyed. These nodules may entirely undergo necrosis, the necrotic tissue becoming dry and scaly or necrosis may begin an the? centeruqmmme nodule and be of a liquefying character and when the entire nodule has undergone necrosis the mass is discharged as a thick, watery fluid containing flakes of coagulated necrotic tis- sue. Again the discharge may be thick and creamy or it may even be of a caseous nature. INFECTIVE GRANULOMATA. 7a Microscopic——These nodules are found to be composed largely of epithelial cells supported by irregular bands of connective tissue in which there is a limited blood supply. The majority of cells are very large. Some of these cells contain oval re- fractile bodies that have been considered as protozoa by some. Fig. 204. Right side, showing growth from eye, nasal cleft, and mouth. These bodies are also observed between the cells. The epithelial cells, especially those in the center of the nodule, usually show more or less of a nuclear disintegration. The marginal cells in the nodules are usually more or less flattened. The cell nests 3/2 VETERINARY PATHOLOGY. may develop from glandular or surface epithelium, which, in the attempt to repair the eroded surface, becomes entangled in the ragged edges of the ulcers and develop as an epithelioma. The cell nests increase in size by a multiplication of the peri- pheral epithelial cells. The rapidly multiplying marginal cells ra; { g Mie PS EKy Fig. 205.—Microscopie section of Epithelioma contagiosum. Surface of growth from nasal mucous membrane. Area of epithelial cells, cells large in center, becoming smaller and finally blending with the connective tissue. 8. Apparently connective tissue undergoing mucoid degeneration. Probably blood vessels, but the cells are smaller than normal red blood cells of the chicken. The cells are also quite irregular in shape. 5. Degeneration of central cells. The nucleus of the cell first degenerates and finally the cell body. WS) consume practically all of the central cells and there is central necrosis of the cell nests. The nests are irregular in size and outline and they are grouped to form the nodules. The nodules may or may not have bands of clear, hyaline substance that represents fibrous tissue undergoing hyaline or mucoid degeneration. GLOSSARY. Ablated (L.Ab, from and Ferre, to bear). Removal of a part as by cutting off. Abnormalities (L.Ab, from and Norma, rule). Conditions not in accord with the usual. Aborted (L.Ab, from and Oriri, to arise). Prevented from full development. Abraded (L.Ab, from and Radere, to rub). Having the surface tissue rubbed off. Abseess (l.Ab. from and Ceder, to de- part). A circumscribed, molecular disintegration of sub-surface tisSue-. Absorption (L.Ab, from and Sorbere, to suck in). The process of taking up substances into the tissues. additional). Accessory (lL. Accessorius, In addition to. Achromatosis (Gr.A, without, Chroma, color and osis, a condition of). A eondition of absence of color. Acidophile (l.Acere, to be sour and Gr. Phileein, to love). Readily stain- able with acid dyes. Acini (l.Acinus, a grape). The small- cst lobules or parts of a compound structure. Acromegaly (Gr.Okros, end and Megalos, large). A condition characterized by overgrowth of the extremities and face. Actinomycosis (Gr.Aktis, a ray, Mukes, fungus and osis, a condition 08g). A disease caused by the ‘ray fungus.” Cladothrix actinomyces. Adenoma (Gr.Aden, gland and Oma, tumor). An epithelial tumor re- sembling a gland in structure. Adipocere (L.Adeps, fat and Cera, Wax). A wax-like substance formed by exposure of tissue of a cadaver to moisture with air excluded. Aerobie (Gr.Aer, air and Bios, Requiring free oxygen (air) der to live and multiply. Agglutinin (L.Agglutinare, to stick to- life). in or- gether). An adaptation product or the body cells produced by immu- nization with corresponding cells which causes a clumping or coales- cing of the kinds of cells used in immunization. Agglutinogen (L.Agglutinare, to stick together). A substance present in 3 3 bacterial immunization which gives rise to the prodxction of agglutin- ins by the body cells. Alveolar (L.Alveolus, a small lobe)- Pertaining to an alveolus, (A small cavity for a tooth or histologic di- vision in a lung, gland, etc.) Amboceptor (Gr.Ambo, both and L. Ca- pere, to take). One of the types of receptors or intermediary bodies im Ehrlich’s lateral side-chain theory. Amitosis (Gr.A, without and Mitos, thread.) Direct division of cells without formation of thread-like structures. Amniotic (Gr.Amnion, a foetal mem- brane.) Pertaining to the amnion, one of the foetal membranes. Amoeba (Gr.Amoibe, a change.) A co- lorless, single-celled, animal organ- ism that constantly undergoes changes of form. Amylaceous (Gr.Amulon, _ starch.) or the nature of, or containing starch. Amylin (Gr.Amulos, starch.) The in- soluble wall of a _ starch grain. Starch cellulose. Amyloid (Gr.Amulos, starch and Eidos, form.) Like starch. Anabolism (Gr.Ana, up and Ballein, to throw.) The transformation of food- stuffs into complex tissue-elements. Anaerobie (Gr.A, without, Aer, air and Bios, life.) Able to live in the ab- sence of free oxygen or air. Anaphase (Gr.Ana, up and Phasis, phase.) The third stage in mitotic cell division. Anasarea (Gr.Ana, up and Sarx, flesh., An accumulation of non-inflamma- tory serum in the _ sub-cutaneous areolar tissue. Anastomosis (Gr.Ana up and Stomoein, to bring to a mouth.) The establish- ment of a communication between two distinct portions of the same organ (Usually vessels). Anemia (Gr.A, without and Haima, blood.) A deficiency of blood or of any of its constituents. Angioblast (Gr.Aggeion, a vessel and Blastos, germ.) One of the cells of angioblastic origin concerned in the formation of vessels 374 Angioma (Gr.Aggeion, vessel and Oma, tumor.) A tumor composed of ves- sels independently of pre-existing blood or lymph vessels. Anhydremia (Gr.A, without, Hudor, wa- ter and Haima, blood.) A diminu- tion of the watery constituents of the blood. Ankylosis (Gr.Agkulos, stiffened, and osis, a condition of.) A union of bones in an articulation. Anlagen (Ger.Anlagen.) The founda- tion or design of a structure, the beginning. Anomaly (Gr.A, without and Homalos, average.) A marked deviation from the normal. Antenatal (L.Ante, before and Natus, born.) Existing before birth. Anthracosis (Gr. Anthrax, black and osis, a condition of.) A lung disease characterized by deposition of coal dust. Antitoxin (Gr.Anti, against and Toxi- kon, poison.) A substance elabo- rated by the body-cells to counter- act the toxins of other cells. Aplasia (Gr.A, without and Plasis, for- : A condition of failure of mation. ) development. Apnoea (Gr.A, without and Pheein, to breathe. ) A translent cessation of respiration. Argyriasis (L.Argentum, silver and osis, a condition of.) A cordition of pig- mentation by deposition of silver. Arteriolith (Gr.Arteria, to keep air, trachea and Lithos, stone.) A cal- culus or stone in an artery. 4rteriosclerosis (Gr. Arteria, trachea, Skleros, hard and osis, a condition of.) A chronic inflammation of ar- teries with hardening of the walls, especially of the intima. Arthropoda (Gr.Arthron, a joint and Pous, foot.) A class of animals hav- ing jointed legs. Ascites (Gr.Askos, a bag.) An abnor- mal collection of non-inflammatory fluid in the peritoneal cavity. Assimilation (l.Ad. to and Similare, to make likes) The process of taking up food-stuffs by the tissues and mak- ing them a part of themselves. Asthenic (Gr.A, without and Sthenos, strength.) Characterized by absence of strength or violence. Asymmetrical (Gr.A, without, Sun, to- gether and Metron, measure.) Be- ing unlike in corresponding organs or parts of opposite sides of a body that are normally of the same size. Atavismal (Gr.Atavus, grandfather.) A condition of reappearance in an in- GLOSSARY. dividual of a peculiarity possessed by a more or less remote progeni- tor. Atelectasis (Gr.A, without, Telos, form and Ektasis, expansion.) Imperfect expansion or collapse of the air ves- icles of the lung. Atheromatous (Gr.Athere, gruel, Oma, tumor and ous. of the nature of.) Of the nature of an aethroma. (A sebaceous cyst containing a grumous material. ) " Atresia (Gr.A, without and Tretos, per- forated.) Failure of a normal open- ing or canal to develop. Atrophy (Gr.A, without and Trophe, nourishment.) A condition in which there is a decrease in size or num- ber of the composing cells of an organ or tissue. Atypical (Gr.A, without and Tupos, type.) Not conforming to type, ir- regular. Autosite (Gr.Autos, self and Sitos, food.) A monster capable of independent existence after birth. Avidae (L.Avis, bird.) A family of ver- tebrates. Bactericidal (Gr.Bakterion, a little stick and L.Coedere, to kill.) Destructive to bacteria. Basophile (Gr.Basis, foundation and Pheleein, to love.) A substance that readily combines with basic dyes. Benign (L.Benignus, kind.) Not danger- ous to health or life. Bifida (L.Bis, twice and Findere, te cleave.) Divided into two parts.j Biologic (Gr.Bios, life and Logos, stu- dy.) Pertaining to Biology. (The study of the structure, function and organization of living forms.) Buccal (L.Bucca, cheek.) Pertaining to the cheeks. Bursattae (L.Bursa, purse.) Small bur- sae or vessels. A disease of the skin characterized by necrosis. Calcified (1..Calx, lime and Fiere, to be- come.) A condition of deposition of calcareous matter in tissues. Canalization (L.Canalis, a canal.) process of formation of canals. Caries (l.Caries, rotten.) The molecular necrosis of bone, enamel, dentine. ete. corresponding to soft tissue. Carcinoma (Gr.Karkinos, tumor. ) A newegrowth. Catarrh (Gr.Katarrhein, to flow down.) An inflammatory condition of a mucous membrane in which there is an excessive production of mucus. Caustie (Gr.Kaiein, to burn.) or anemic) in an organ produced by obstruction of a terminal vessel. Infection (L.In, in and _ Facere, to make.) The invasion of the body by pathogenic micro-parasites and the sum-total of the disturbances pro- duced by their presence therein. Infectious (L. In, into and Facere, to make.) Capable of communicating a disease. inflammation (l..In, and Flamma, flame.) The reaction of a living animal] tls- sue to an irritant accompanied by circulatory disturbances and by de- | structive or proliferative tissue changes. and Durus, hard.) GLOSSARY. Ingested (L.In, in and Gerere, to bring.) Taken into the stomach or alimen- tary tract. Inherited (L.In, to and MHaerere, to cleave.) Born to or belonging to by birth. Inhibiting (L.In, in and MHabere, to hold.) Holding in check or hinder- ing from doing a thing. Inimical (L.In, not and Amicus, friend.) Having a hostile tendency. Liable to injure. Inoculating (L.In, into and Oculus, a bud.) The introduction of a virus of a disease into a wound or abra- sion of the skin. Inosculation (L.In, into, and Os, mouth.) The joining of blood vessels by di- rect communication. Insidious (L.Insidioe, ambush.) Coming on stealthily or imperceptibly. Inspissated (L.In, intensive term and Spissare, to thicken.) Thickens by removal of fluid. ; Insusceptibility (L.In, not and Susci- pere, to receive.) Not having a lia- bility to acquire a disease. Intercellular (L.Inter, between and Cel- la, cell.) Existing between the cells of a tissue. Interfunicular (L.Inter, Funiculus, cord.) Existing the bundles of tissue. Intermittent (L.Inter, between and Mittere, to send.) Characterized by intervals between. Interstice (L.Inter, between and Stare, to stand.) Spaces between or to stand between. Interstitial (L.Inter, between and Sis- tere, to place.) Pertaining to struc- tures between the cells of a part. (Stroma. ) Intracellular (L.Intra, within and Cella, between and between cell.) Existing within the cells of a tissue. Intrinsie (L.Intra, within and Secus, otherwise.) Situated entirely within or pertaining exclusively to a part. Intussusception (L.Intus, within and Suscipere, to receive.) A slipping of one part of an organ (usually in- testine.) into the parts beyond. Invagination (L.In, within and Vagina, a sheath.) The unsheathing of a tis- sue. Involuere (L.In, in and Volvere, to wrap.) The covering or sheath con- taining the sequestrum of necrosed bone. Irritant (L.Irritare, to excite.) Anything that produces an excessive action Or functioning in a responsive tissue. GLOSSARY. Ischemia (Gr. Ischein, to check and Hai- ma, blood.) A local anemia. [schiopagus (Gr.Ischion, hip and Pa- gos, union.) A monster with two heads and with bodies united at the hips. Karyokinesis (Gr.Karuon, nucleus and Kinesis, motion.) Indirect cell-divi- sion with formation of thread-like structures. (Mitosis. ) Karyolysis (Gr.Karuon, nucleus and Luein, to loose.) The morbid de- struction of the cell nucleus. Katabolism (Gr.Katam, down and Ball- ein, to throw.) The transformation of complex tissue-elements into simp- ler ones in the production of energy. Keratitis (Gr.Keras, horn or cornea and Itis, inflammation. ) Inflammation of the cornea, Keratosis (Gr.Keras, horn or cornea and osis, a condition of.) A disease of the skin characterized by an over- growth of horny tissue. Kinetic (Gr.Kineein, to move.) Pertain- ing to motion. ; Keloid (Gr.Kele, a claw and _ HBidos, like.) A raised, cutaneous dense Overgrowth of white fibrous con- nective tissue in a cCicatrix, very common in the negro. Lacerated (L.Lacerare, to tear.) Condi- tion of being torn apart leaving ragged edges. Lacunae (L.Lacuna, a small lake.) Small pits or depressions: Hollow spaces. Laminated (L.Lamina, a plate or scale.) Made up of laminae, of thin flat plates: Lecithin (Gr.Lekithos, the yolk of an A complex nitrogenous sub- distributed in egg.) stance found wideiy the body tissues. Leiomyoma (Gr.Leios, smooth Mus, muscle and Oma, tumor.) A tumor composed of unstriped muscle tis- sue. Lesion (L.Laesio, to hurt.) bid structural change. Leucoderma (Gr.Leukos, white and Der- ma, skin.) A condition of abnormal whiteness of the skin—Albinism in patches. A mor- Leucomain (Gr.Leukos. white of egg and Oma.) A product of metabolism of the tissues of the body and nor- mally present in them. Leucocytosis (Gr.Leukos, white, Kutos, cell and osis, a condition of.) An increase in the relative number of leucocytes in the blood. 381 Leucoprotase (Gr.Leukos, white and Protos, first.) A ferment. Leukemia (Gr.Leukos, white and Hai- ma, blood.) A condition in which there is a vroportional increase of leucocytes in the blood. Lobulate (Gr.Lobus, a lobe and diminu- tive term.) Containing smal] lobes. Lumen (L.Lumen, light.) The cavity surrounded by walls of a tubular vessel. Lymph (L.Lympha, water.) That por- tion of the blood which passes through the capillary walls into the perivascular spaces and consists of diluted plasma, leucocytes and usually waste materizl. Lymphogenous (L.Lympha, water and Gr. Gennaein, to produce.) Pro- ducing lymph, Lymphocyte (lL.Lympha, water and Gr.- Kutos, cell.) A variety of leucocyte found in lymph glands. They are small, with very large nucleus. Lymphorrhagia (L.Lympha, water and Gr.Hragnunai, to burst forth.) The flow of lymph from a _ ruptured lymph-vessel. Lysin (Gr.Luein, to loose.) A cell pro- duct with power of cleavage of other cells or substances. Lysis (Gr.Luein, to loose.) A gradual decline. Generally used in combina- tion to signify destruction or break- ing up. Maceration (L.Macerere, to make soft.) The softening of a solid by soaking in 2 liquid. Macroseopiec (Gr. Makros, long and SKo- pein, to view.) Visible with the un- aided eye or without the use of a miscroscope. Malformation (L.Malus, ma, form.) An abnormal ment of an organ or part. Malign (L.Malus, bad.) Likely to kill. Mammalia (L.Mamma, breast.) A class of vertebrates that suckle their young. bad and For- develop- Margination (L.Marginase, to furnish with a border.) The act of furnish- ing with a district border. (The accumulation of leucocytes on the interior of a vessel wall.) Mast-cell (Ger. A large type of with basophilic stainable. Melanin (Gr.Melas, black.) A black pig- ment, natural in some tissues, often pathologic. Melanosis (Gr.Melas, black, osis, a con- Mast-zellen, food-cell.) leucocytes filled granules, highly 382 dition of.) A condition of abnor- mal pigmentation with melanin. Metabolism (Gr.Meta, after and Baliein, to throw.) The phenomena by which foodstuffs are transformed into com- plex tissue-elements or complex tis- sue-elements are converted into simpler ones in the production of energy. Metamorphosis (Gr. Meta, after and Morphoein, to change, and osis, 2 condition of.) A change of shape or structure, usually a degeneration. Metaphase (Gr. Meta, after and Phasis, phase.) The second period in in- direct cell-division. (Mitosis.) Metaplasia (Gr. Meta, after and Plasis, formation.) The conversion of a developed or matured tissue into another closely related tissue. Metastatic (Gr.Meta, after and Stasis, halt.) Pertaining to Metastasis, The transfer of a diseaSe process from one organ to another by means of blood or lymph. Metrorrhagia (Gr.Metra, uterus and Hregnunai, to burst forth.) Hemorr- hage from the uterine mucosa, the extravasate being almost wholly re- tained in the uterus. Micron (Gr.Mikros, small.) One one- thousandth of a millimeter (1- 25,000 of an inch). Represented by the greek letter mu. Microparasite (Gr.Mikros, small, Para, beside and Sitos food.) A parasite requiring high magnification for ob- servation. Microphyte (Gr.Mikros, small and Phu- ton, plant.) A microscopic plant. Microscopic (Gr.Mikros, small and Sko- peein, to view.) Not visible with the unaided eye. Microzoa (Gr.Mikros, small and Zoon animal.) A microscopic anima] or- ganism. Micturition (L.Micturire, to urinate.) The passage of urine. Staling. Miliary (l.Milium, millet.) Consisting of small tubercles or nodules of the size of millet seed. Mitosis (Gr.Mitos, thread and osis, @ condition of.) Indirect cell-division with formation of thread-like struc- tures. Karyokinesis. Mole (l.Moles, a mass.) A mass formed in the uterus by arrested develop- ment or degeneration of a foetus. Also a Nevus. Monaster (Gr.Monos, single and Aster, star.) The single star or wreath in indirect cell-division (mitosis). Monochorionic (Gr.Monos, single and GLOSSARY. Chorion, a foetal membrane.) Hav- ing a single chorion. Mononuclear (Gr.Monos, single and L.- Nucleus, nucleus.) Having but one nucleus. Morbid (L.Morbus, to disease. Moribund (L.Moriri, to die.) In a dying condition. Morphology (Gr.Morphe, form and lLo- gos, study.) The study of the form and structure of organized beings. Mucus (L.Mucus.) The viscid fluid se- ereted by special glands of mucous disease.) Pertaining membranes. Multiparous (L.Multus, many and Pare- re, to produce.) Bringing forth more than one offspring at a birth. Mycelial (Gr.Mukes, a fungus and He- los, an overgrowth.) Pertaining to a mycelium. Mycelium (Gr.Mukes, a fungus and He- los, an overgrowth.) The vegetative filaments of a fungus. Mycosis (Gr. Mukes, fungus and osis, a condition of.) A growth of fungus in the tissue. Myeloid (Gr.Muelos, marrow and Hidos, like.) Resembling marrow. Myoblast (Gr.Mus, muscle and Blastos, germ.) . Schistosis, 95. Schizomycetes, 52. Scirrhous carcinoma, 321. Regeneration osseous tissue, 180. Regeneration white fibrous, 179. Regeneration yellow elastic, 180. Regenerative inflammation, 175. Regenerative power, 177. Remittent fever, 342. Reinnervation, 182. Renal adeno-sarcoma, 328. Renal tubular calculi, 233. Renal pelvic, 233. Resistance to tumors, 273. Retention cyst, 337. Siderosis, 248. Retention theory of immunity, 87. Significance of inflammatory exu- Retrogressive tissue changes, 195-6. date, 156. Retrogressive tissue in tumors 274. Signs of death, 264. Rhabdomyoma, 297. Signs of inflammation, 160. Rhexis, 113. Situs Viscerum inversus, 102. Rigor mortis, 264. Sodium urate, 223. | Ringworm, 40. Specific inflammation, 174. Round cell sarcoma, 302. Specificity law of, 178. Rupture, 40-183. Spina bifida, 96. Spindle cell sarcoma, 325. Ss Sporotrichium audouini, 49. Sporulation, 56. Stadium decrementi, 341. Stadium incrementi, 340. Staining, post mortem, 264. Stearin, 203. Sternopagus, 107. Sthenic fever, 342. Streptococcus, 53. Stimulus, 130. Stocking, 121. Substitution, 185. Sub-surface necrosis, 256. Suppuration, 167. ‘Suppuration subsurface, 170. Suppuration surface, 167. Sebaceous cyst, 337. Secondary tumors, 272. Senile atrophy, 197. Senile necrosis, 258. Sequestration, 261. Sequestrum, 261. Serous exudate, 154. Serous inflammation, 220. Serous inflammation appearance, 220. Serous inflammation cause, 220. Serous inflammation effects, 220, Saccharomyces, 51. Saccharomyces cerevisiae, 51. Saccharomyces farciminosus, 52. Salivary caleuli, 235 Saponification, 258. Sarcinae, 53. Sarcoma, 208. Sarcoma alveolar, 300. Sarcoma cells, 300. Sarcoma mixed cell, 308. Sarcoma myeloid cell, 306. Sarcoma round cell, 306. Sarcoma structure, 301. Sarco-chondroma, 317. Sarco-endothelioma, 312. Sarco-fibroma, 312. Sarco-hemangioma, 318. Sarco-lymphoma, 303. Sarco melanoma, 315. Sarco-myxoma, 316. Sarco-osteoma, 318. Suppurative osteitis, 160. Surface necrosis, 156. Symmetrical duplicates, 106. Synactosis, 95-8. Syncope, 77. Svneytium, 153. INDEX. Syncytioma malignum, 331. Syndactylus, 08. Synmelus apts, 69. Synmelus dipus, 98. Synmelus monopus, 99. Synorchism, 99. Synophthalmia, 908. T Tattooing, 248. Temperature, cause of cloudy swell- ing, 201. Temperature, cause of degenerations, 196. Telophase, 28. Teratoid tumors, 269. Teratoma, 332. Termination of disease, 75. Tests for death, 265. Thermic causes of disease, 42. Thermic necrosis, 254. Thkermogenesis, 340. Thermolysis, 340. Thoracopagus, 107. Thoracoschisis, 97. Thrombosis, 122. Thrombosis cause, 123. Thrombosis, effects, 127, Thrombus, 122. Thrombus annular, 124. Thrombus appearance, 124. Thrombus calcification, 127. Thrombus complete, 124. Thrombus decolorization. 125. Thrombus, extension, 124. Tkrombus infective softening, 126. Thrombus location, 123. Thrombus organization, 126, Thrombus parietal, 124. Thrombus red, 124. “rrombus simple softening, 125. “'rombus. white, 124. “ime tonsurans, 49. Tophi, 223. Toxic immunity, 84. Toxophore, 89-90-91. Transportation 102. Traumatic wounds, 184. Tricephalus, 109, Tricophyton tonsurans, 49. Tubercle, 340. Tuberculin, 354. Tuberculin test, 354. Tuberculosis, 344. Tuberculosis Tuberculosis Cuberculosis Tuberculosis Cuberculosis Cuberculosis Tuberculosis Tumors, 267. Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors Tumors primary, 272. Tumors Tumors secondary, 272. Tumors shape, 271. Tumors size, 270. Tumors structure, 268. Tumors teratois,, 277. Tumors varieties, 277. Twins, 106. benign, 277. body resistance, 273. cause, 275, cells, 260. clinically, 275. color,:271- consistency, 272. extension, 272. frequency, 268. growth, 272. histoid, 277. intercellular substance, 269. malign, 277. metastasis, 272. mottled, 271. number, 272. nutritive supply, 260. organoid, 277. of extent, 344. etiology, 345. avenue of infection, 346. source of infection, 346. lesions, 347. extension, 353. elimination, 354. 399 organs, retrogressive changes, 274. 400 U Ulcer, 164. Ulceration, 164. Ulcerative inflammation, 174. Union dorsal, 106. Union posterior, 106. Union ventral, 106. Wrates.: 223% Uratic infiltration, 223. Uratic infiltration appearance, 223. Uratic infiltration cause, 223. Uratic infiltration effects, 224. Ureter calculi, 234. Uretheral calculi, 234. Uric acid, 223. V Valvular insufficiency, Ito. Valvular stenosis, IIo. Varieties of tumors, 277. Vascular buds, 178. Vascular constriction, inflammation, 146. Vascular dilation, 147. Vascular permeability, 111. Vascular regeneration, 178. Vascular variations, III. Vascularization, 178-185. Venesection in fatty changes, 205. INDEX. Venom, 48. Vesicle, 42. Vesicular inflammation, 174. Viper, 48. Vitiligo, 250. w Wandering cells, 152. White. fibrous regeneration, 179. Wound, 4o. Wound cause, 184. Wound healing, 184-5. Wound subsurface, 184. Wound surface, 184. Wound traumatic, 184. X Xanthosis, 245. Xiphopagi, 107- Y Yellow elastic regeneration, 184. y 4 Zooparasites, 63. Zootoxins, 78. e 4 Gh