Se — __—lCc cell Mea ae Seb y8 MEY My wy $3 ney La teens Y he. ayn ES arate Rae Bk, A has ‘it ~ SS a ONY, “f y * eau "9 TRS ARTS r, EME NE Evin WL Faq Class S Book 4. A Uae 0 Copyright N° COPYRIGHT DEPOSIT: W? JB AP TED IR2 IP IN] AY IR. NZ Paes Ou ledhalnO MN trae ses See Rei S INS Ore So INE APR Ae LICE 1B} Aer KIN Ss bine M: Ses, DIVES: Author of Veterinary Pathology, Swine Diseases, Ete. Illustrated CHICAGO AMERICAN VETERINARY PUBLISHING COMPANY 1921 fax! S : A v4 5 rae > Copyright American Veterinary Publishing Co. 1921 ©t.a605699 Diseases OF ResPrrRATORY ORGANS TABLE, Or. CONTENTS CHAPTER I. GENERAL SWINE MANAGEMENT. ......-.----------:--c--ceece-seeseeceeneecneee coer e erence seen nes nesncnn en enencnnneas 11 Choice of Breed; Age for Mating; Selection of Herd Boar; The Brood Sow; Farrowing; Care of Stock Hogs—Success Depends on Feeding; Breeds of Swine—Poland-China, Duroc-Jersey, Berkshire, Chester White, Mule-Foot, Bacon Hogs, Hampshire, Tamworth, The Large Yorkshire; Feeds and Feed- ing—Feeding Requires Care and Judgment; Garbage Feeding; Sanitation— The Hog House Ventilation Necessary, Proper Drainage Essential, Value of Quarantine; General Diagnosis—History of Paramount Importance, Attitude of Animal, Diseases of the Skin, Congestion, Eczema, Temperature Variations, Examination of Heart and Pulse Rate, Diseases of Respiratory Organs, Nasal Discharge, Cough, Nature of Feed and Water Should Be Determined; Diges- tive Disturbances, Uro-genital Disturbances; Nervous Disorders; Autopsy— Obtain Permission and Authority, The Subject for Autopsy, Equipment, Rec- ords, Technic; Restraint; Medication—The Hypodermic Syringe; Anesthesia —Indications, Anesthetics and Administration. CHAPTER II. FD EG ESS TIVES GIVES TTS IVs Pee a ee eR, ey cere hak a ead aaa cede a i Ree 63 Anatomic Consideration—Mouth, Tongue, Salivary Glands, Teeth, Pharynx, Esophagus, Stomach, Intestine, Liver, Pancreas; Physiologic Consideration-— Digestion; Mouth and Associated Parts; Lips—Malformations, Cheilitis, Tu- mors; Tongue—Glossitis, Tumors, Parasites; Mouth—Stomatitis, Epizootic Aphthae, Scurvy; Teeth; Parotid Glands; Tonsillitis; Pharynx—Pharyngitis, Paralysis, Tumors; Esophagus—Malformations, Stenosis, Dilatation, Perfora- tion, Esophagitis, Tumors; Aberration of Appetite; Stomach—Malformations, Foreign Bodies, Emesis, Anemia, Hematemesis, Peptic Ulcers, Hyperemia, Gastritis, Dilatation, Tumors, Parasites; Intestines—Malformations, Enter- orrhagia, Obstruction, Dilatation, Emphysema, Enteritis, Poisoning, Parasites, Tumors, Diarrhea, Constipation; Prolapse of the Anus and Rectum; Liver-- Malformations, Foreign Bodies, Rupture, Icterus, Cloudy Swelling, Fatty Changes, Amyloid Changes, Glycogenic Infiltration, Gall Stones (Cholethiasis), Hyperemia, Hepatitis, Tumors, Parasites, Pancreas; Peritoneum Injuries, Ascites, Peritonitis, Tumors, Parasites. CHAPTER TIT. Ee en Nad eR 8 en nas Acre eee eel AG Anatomical Consideration—Respiration; Nose—Epistaxis, Catarrhal Rhinitis, Infectious Nasal Catarrh (Malignant Catarrh), Tumors; Larynx—Laryngitis, Tumors; Trachea—Malformations, Stenosis, Tracheitis, Tumors; Bronchial Tubes—Stenosis, Bronchitis, Bronchial and Pulmonary Strongylosis; Lungs —Atelectasis, Emphysema, Edema, Hemorrhage, Pneumonia, Tumors, Para- sites; Pleura—Hydrothorax, Hemothorax, Pneumothorax, Pleurisy, Tumors; Spasms of the Diaphragm (Thumps). CHAPTER IV. HUUiTe = Garb NGETUAGT W109 808 DEVI eee sce cme, eee eres ieee EN Non? DA eimatss a tk Be 172 Genital Organs—Boar, Sow, Mammary Secretions; Kidneys—Malformations, Hydronephrosis, Hemorrhage, Fatty Changes, Calculi, Congestion, Nephritis, Albuminuria, Uremia, Hematuria, Parasites, Tumors; Ureters—Malforma- mations; Bladder—Malformations, Hemorrhage, Dilatation, Calculi, Cystitis, Tumors, Urethra, Stricture Urethritis; Male Generative Organs—Prostate Gland, Bulbo-Urethral or Cowper’s Glands; Testicles—Orchitis and Epi- didymitis, Tumors, Parasites, Penis; Female Reproductive Organs; Ovary— Malformations, Hemorrhage, Oophoritis, Cysts, Dermoid and Dentigerous Cysts, Tumors; Fallopian Tubes—Malformations; Uterus—Malformations, Injuries, Hemorrhage, Tumors; Vagina; Vulva; Mammary Glands—-Mam- mitis, Tumors. CHAPTER V. EE ORITTO NGM cs Senter Se a eee Pe pe Re RE. eee Seek oe 209 Prevalence; Susceptibility; Types of Abortion; Cause; Dissemination; Symp- toms; Treatment. CHAPTER VI. SETS RIAD Vigo oe once ee Ue oe Micra ACN 7 Pokal eae ee oma, Pe a es Ne Occurrence; Cause and Symptoms; Treatment; Retained Placenta and Me- tritis. CHAPTER VII. UNO MAEIESVAND DISEASES On) YVOUNGSPIGS#.0.2 oc ae ede ak ae ee ee 214 Persistent Urachus; Atresia Ani; Omphalophlebitis, Pyemie Arthritis (Navel Ill); Rickets; Scour in Pigs; Pulmonary Ascaridiasis; Infectious Ihinitis (Bull-Nose or Sniffles) ; Stomatitis in Sucklings (Sore Mouth in Pigs). CHAPTER, VIII. Orcas: On! TocomonION Hos eto Ps ae Rn or 2 Sore Feet; Fatty Changes in Muscle—Muscular Rheumatism, Articular Rheu- matism; Polyarthritis; Osteomalacia—Purulent Osteomyelitis; Trichinosis; Cysticercosis (Measles) ; Sarcosporidiosis; Tumors. CHAPTER IX. BUSSEIVES eed N= Ss tees se cee ct EO ee Ee St oe it Ae ee ee Erythema; Sunburn; Freezing; Hemorrhage; Urticaria; Impetigo (Measles) ; Kezema; Dermatitis Granulosa; Necrobacillosis, Actinomycosis; Tumozs; Pigmented Mole; Parasites; Flea Infestation; Lousiness (Phthiriasis) ; Mange; Tick Infestation; Thread Worm Infestation; Ringworm Infestation. CHA PAVERS. CPRCOUUATORY ORGANS Sooo sea seach oc echo awww tcc nne oe nae cee eee Heart—Hemorrhage, Fatty Changes, Dilatation, Pericarditis, Tumors, Para- sites, Chronic Endocarditis ; Blood-Vessels; Blood—Anemia, Leukemia; Spleen —Necrosis, Hypertrophy, Tumors. CHAPTER XI. CER RIN ERY OUSHO NSTE MG sce eee eee ote ee eee Seu atte 3 Sunstroke and Heat Stroke; Lightning Stroke; Epilepsy; Eclampsia; Parai- ysis in Pigs; Chorea; Cerebral Hyperemia; Parasites. CHAPTER XII. TENE CTIOUWS SIDTSHASES | (ccs 5 gs Sore ee es oe ac oa nn Sa eee sect ane oe seca enee Sao e eRe 27 Hog Cholera; Serum Production—Location of Buildings, Construction of Buildings, Arrangement of Plant, Operation; Swine Plague, Hemorrhagic Septicemia; Infectious Necrotic Enteritis; Necrobacillosis—Necrotic Stoma- titis, Necrotic Enteritis, Necrotic Rhinitis, Necrotic Pneumonia, Necrotic Hepatitis, Necrotic Splenitis, Vaginal, Vulvar and Preputial Necrosis, Necrotic Dermatitis, Unusual Forms of Necro-Bacillosis; Paratyphoid Infection; Sal- monellosis; Malignant Edema; Anthrax (Charbon) ; Tuberculosis; Swine Ery- sipelas; Rabies; Foot and Mouth Disease (Aphthae Epizooticae) ; Tetanus. CEUNRAE Reel SITING ER a fe ee cee ee ac Ze eg ae a A en Nhe SS Reed re Een ae Castration—Age for Castration, Instruments, Restraint, Technic, Care After Castration; Sequelae of Castration—Hemorrhage, Scirrhous Cord, Actinemy- cosis, Parasites, Botryomyces, Scrotal Hernia; Spaying of Sows; Ablation of the Mammary Glands; Operation to Remove Swirls; Obstetrics—Age of Puberty and KEstrum, Gestation Period, Anatomy of the Female Genital Organs; Parturition—Difficult Parturition Dystocia; Cesarean Section—Anes- thesia, Restraint, Instruments, Technic; Hysterotomy; Hysterectomy; Acci- dents of Pregnancy. EISt- OF ILLUSTRATIONS AES UTA NVI Og ER OUIS Cece sees se een meee cee eee EN Ne eA eee ee ee ES ROE AN EE 14 inten OTeOlee Darr Own pt. TOUS Cie: tase ne ee wre pene epee nese ence eee Bere ae UD 15 MOD TNS Os Wepeet aeRO; WA TN O's ed CO ULS GS ee ieee ee se A a ee ats See ease ee Ree reer Ie (COESEREPETIOU IS X10 0 10) 0 Va ee es en PoE ee a one ee 18 SSrricyl la ONE =W AVcr SC IH COC TS tee oa aa ee orcas eae sores ce och ct cack ag Secs est Senna 31 SI GIUP =] ECG SSR EE ae Ase ce ee RN eA ey Dep, es ec cee 32 Siellital (CSCS ee reenter Raia Mah eet hos RSs cose ea hte A epee ieee RS eae Ec ea eR E Re reC 33 LSU” Dek NONI) Sa eee ee eo eae ea Dee Sah eh catn aR een aoe ee Sales te gaat gt 38 ETO CME OUS Cl: QING VAT AS 5 9s 2 oe ES Sy eee Bae gies 2a raga ea eee sadn enn sane der une ea meeeoaoenad-beece 39 LAYS LTISSSIASISITY Oy OMG ls (ofa al es C0) WV Se sce eee Pe EP oe dec Ss Mivages es Siete 40 SO VSI Comes ex AS LUIIT Gee tetsaca eterna ee Sen omens Eee Geih ee BOO gd cates errs cee cake saat AS cena ee Oe 43 Wei ut OW Ot, WO WEST ila W escent een sere ace eee eee neat antec e Soe eee eee eee 66 Dy mbt ONE: O fies lp OC Tyee AW et eee eee tee a a a dae ce eee noes yas eee Br hee Gates 66 Denbiiioneot mls —oritihs—O)l cial eee ee eee eee ee ree A FES he CE a Ee fee 67 Weniiiionwote lowers dawnt 18 —Vlomths- Ol Ge oeseeses see erect seer eees Cee eee eee 67 By eptaned Glatme etm lems GES ENG area eae ee eee cee ees oe Aeacs Aae res MOR Owe) Sele rte 69 \SHE@RGIVEG) OY UCL TIPS EDO eae a eee eS nee 70 BxentenaceGmotOnmachss Mmtestine mdse me esses ee ene eens a eee accreted 71 WLANEEIE OE Ts ROE ca a a ha ee ie eR eae eee 72 JOnveteshowin em leObUleg aes eer eee, Lee ecw LE ce en Do pee eee) 73 (COUSIN nee re ree Foe ES DG Sete he eae ates een eS Cotes 77 EN }UUNUE SG RS ELT IS in ae er ae Mee 95 AATEINGS UNG! Le yaamyolny (Cae wakes Thay TM oi essiteih OSS) Se ee ete ie eee ee ee eee a eee eee 8 102 INNTTRD RYOTE Sa em a oS Re Pne, aS e eT A 106 NG RBI TETISS SG YUTT0 o r eE Sae aE NE PO PSE oe) eae ee 118 Gneamborhyam Chts) eel Ge CEOS) ees eee eee nae oe eee eee eee oe eae pense 122 (CUM PORUIC es EW OEM A) eae ec Cin SREB iA PE aes Saga een 136 DTG treo ran caso el PO GY CUI eas a cee ae ee secon ce nee eer ey eee cece ah rcs eae a ee 139 Pe sreCO TN Ea AMAR AMC} x Ope EO Sa WW) is knee ME nN eV TST S ee eee eee ees 155 TC a OUT Gs ges Sten ere ae eye RY SE eae ee oe ee ee 160 Ove lreaerse cdl bent UUIND OTNNG cle ee ek ele ane eee Ee Se SS cece eee ten eee ...-162 Grate mOf lero os W ar tla Teri Ore WV TMS See eee ere CAR Bee Renate aaah 2e, per eee eae 167 WG SITCUGS Cire) BCE ea an eee BE ee APR eh a ee ae ee a ee 175 External and Internal Generative Organs of Sow...................-..-.... CFs eee oer a ete ea 176 LESTIGINEN ILE SN eo, Oa IR A Pa ee Shee A Se PN ee er Oe Weft Fed TAROT In VET CNY Cin Vga eee cen eee ee eee ee Bieter Le cope care Wc hhc Mae 179 TELE YOST SATO a SI WAYS ee ke ees ae eh GP ope ee Pee NOE aR mt nN Pea 182 VEC TKG HAVEN See is PE ae ee a SI el Begg Mann Bile Eg Peek a BUS eaene Neen Pacer ae SE 183 ANGISTIRT ASE SOEY Ca ey 18 OVEN od AGG WAC Dy ee ene see Pe Oe ee Nene ne Ae neat cate eee 190 iNesticlemoOke kui doling Oats eek ws shes nae ft akc cu see tects seteae coer e Mean eis steeiy eae SEL Se a eee 196 nie Choma lie ViammM ar yn Glam dass. jen. fale ele pel ete cee ee oe et ee eee et 203 PE RVEUCG FT Ln ane Se ee tae Ee oe eee eas REBEL Ca Be eae Settee Se tA RE Pe 215 VER EU CUMTL ETSY Sea AE aR he See ANE ne eee Eee a erie 217 T Rasy CARTTIES) =k oe as 2S ar 9 dy Re ORS 0s a a ee Be Oe ee ae 218 TE SMCS) cS ie Si er tN et Puce SOUR es Tah eie ys C87 ep TOR TN OR Cone se Sr OR Ree One er See oe 219 NSLS > YAO RIA Me ee fa ee A Saree ance ee ee. EE eal oS dO 235 Mirseulatnmmenony tLooe Writlon iVleas ley Wists esses cee, no ance ees ee ere 235 HRaCoNe camel VE AAS © VV ETIN ec cce eae erode capes e ee eee cence cee oncd den ccanevusesoere seen a tere hehe aoe 235 ( COWSI STEIN x AoE ORE, eer ail Bee RL Ni haat ee re WE ye ee TORE SUSU. STS a a oe Eee ee ee 236 SURAT HONA, IR YE INT USN 9d RG a a eS ene EEE 237 IGG Olm Oia lev UGAS es td Cai bee sr nee at er Cee Shee ee AD SOR See uns ae er, eee 238 Feduneulated) Pibroma 22.2222... UE Bea lee Se BEC od NY RL Set Arrears Wee er ae che ene, 239 Pere NINE GCL Ce VN ihn lame t Meeeaten snare ace eo ee eso see ac eb tan aa dicn ea eaede scabs Nee ntnosatt cence een aot 243 TERE ON a GE OUCESTISY ae ee ese ae ge ee ee Ne er 246 TP Tita evnthea ls LUNES seat eee eae BO rk a ee oR ee Se ae 247 NTE Me LSU ypae ALD DUIS, So ee ee era ee tle a ee to are 249 Bemale iho ge svouse: 2 2. osc oir eee tees oa se erg ey open eee ee ee ee 249 Sarcoptie Mange SMitie jc. 2022 c ees ei ee eee ee Le es ge ree ee eee eee hee see 250 PaO oh Mane Pasa RoE se ae Oe renee Re i a ee Ak ee 251 ose Mane em Showin ousl edi clea 10sec celly seas eee eee a en eee 252 Convenient Trough for Vaccinating... as eae PR ET re, SE ee 253 PigwAtfected With HollicularsMange.0.) ie. ee ee ee 254 hoe Wrallowaote Concrete ss eee poli et AON I Ie tains Sek Ree 255 loeb eart. With EB ChinoCoCCii 2 sfes 2 aks AUR 2 EN (ees ea ee Cae 258 Hearts Wath tuberculous cProliferations: =. 0. e nreeiee oe ee ee ee 259 Spleen With) Part of Gastrosplenie Ligament... ne ee Monte a nF 261 Floe-Choleragt i256 te ae Ge echt ae eee gh ce te ke 271 Menleighlio eMC holerag: ee i ben eM VER oie La - cea ee ae nee ee) Cae mee" Freark, Showing, -Pissue; Femorrhagesa:. 22) ee hs We eee eke we phe 273 Imiflam ed: SATs elecce: aie ee OR el ole ee CANN Bh Nie. © ce x ea eR 274 Mucous; Membraneyot the, dintestine." Gara 2 we oe) gee ee be een ee 275 Lag 011] 0} ght a0. 6 Voce eee eee a ee ARTI O Lg PEE Melee Mee ME Re ect Ss ok 277 Barge) glintestine sok blomtos..352 5 220 ol rie So ee eh oe a ee 279 large “Intestine vot (om: 2k ont oe oS i Se tae ee ee 279 Lungs Showing Attached Lymph Glands............. abaste eeage scien sevse) Vacs Oo) oe nr 281 Head Showing Wymph Glands=- 022 en goieei in dnt gece 282 TeyamphiiGlamels wesc oe anna ae A) Ales coe es ee a be eict ise panto 287 Mucous) Membranevok Bladdertss 5 32h h Ue A ee eo en eee 288 Fog sGholeras@arcasses. sto het on Sake ee We Aa ee as mad alan 0 ede ee 289 Vanusy bleedinoe ht oonisci) 9). have iv te ee ae PS are ed a 294. Phy perimmmn nizing, ROO me sce coe eee a en ce 0 ie ee ee 296 Serum Cen trp hurg tra poet h Co wins ee eee ee aa =e te Oe 298 Sterilizin a SIUOOUN A ic oes here IR NY OOP I Deiae he We Rs te 299 Gholenasilmimapne CO gs 22825 ek Fo eae Yt aa eee ae Pee 301 Hog. Lungs With Chronic Swine Plague-<...20.2 300 2 303 LUM ONAL yas Viixed ss lnrechon-Satarsniiale emer OMe eee eee 305 Group Of Rigs s oiet sc soe oh | ee lee cis ances ee a eee koe, 306 Rigs Showing .\Various “Symptoms: 29.2.3. \ oe a Se 307 SICK ET GO gn 24 ost ee a OS eee ee ee 307 Insanitanye (Conditions) 2: fos 0 sts ka Sad ae UE ee ee 309 Necrobic-tHmbenitigt:. 0s ee ks eee ee Mi eed aie ee ee 310 Diphtheriheesh mtenitismie a= ener ooo astendent deca Seacds Sed olesdetesehs cree ee oer ee 311 INeGchobacilOsis p74 e354 tone en eee eee ORE De eT Ae 318 IGEN CROSIS3 Aorta ie ee NO eee eee ee ae nee oes Boat Le ae Se ee 323 BB aeills) 7 AME ACs meee eee ee Ae oot eine ore ee ten eo et EF A eee ae ess eee 328 Vertebral tnberculosis, in the. Hogs Soe ee ee ee 331 Tuberculosiszot tthewlonp ue: es 2 aes ee ee ed ee ee 333 ‘Tuberculosis}of, thers kins. 25's eee et ee ee ee 334. ‘Tuberculosis of the 4Pleuna.- abe ee ee ee ee 336 Prolitera tions: OMmbleamtv Vial Ves set scree reset Sa ele a ee eee en ee 338 Bi aeull hrs Se esti ep nee ee sae ee, Oe we en ate eg eS ee ee ee 343 Hestraintzotearcers odretons Cas tr altel om eee weee eaten nee reese ne eee eee 345 Restraint for “Castratvo me. s2s: xsi cs. cesec te ieee ee ee ee ees ce ot ess ee ee eee 345 SSS V ENT ec ATL CH gS bnve yee PS AS Coa at Te mae a een ee ee 346 ELoldin oye lowtor@ astra tion: se:5 5 eee a toes noare ee ee wens Se eee ie ee 347 PN CUIMOMViCOSIS, op sete ck trees take Wet Swe eee ae Si! EPMA 2 Ord ee So eee ee 351 Selmmhouss Condiges = wane ee ete see gee Staaee eas oes Be see oad eee eS erence Pace na ne ee 352 Niultiple eAbscesses bin) BOate = sea Seer ee Le, SON ee ee B54 DSRS] Ore LO Gey (0 amo) OY. AA 0 eae peer eet ee Oa Ae ol 5 fk Se oeral trey ere peer eater eg 355 IinternalsGenitalaOroans ote 0 wees eens SI Sync sessed ectan cess settee ee 356 PASO eT xO fe MM carvan ry, 1G ea ee ae cer nee ee a ee B57 PREFACE The increasing importance of the swine industry demands in- creased efficiency in swine practice, and this is briefly the reason for the publication of this book at this time. The original edition of ‘‘Swine Diseases’’ has been materially in- creased by the addition of chapters on the general care and manage- ment of swine, breeds of swine, surgical operations and obstetrics; in fact, the author has attempted to briefly and clearly desecibe all phases of the management and diseases of swine in such a way that the student of veterinary medicine, municipal, state and Bureau of Animal Industry veterinarians, and the veterinary practitioner will find it a valuable ready reference. Because of the detailed descrip- tion of methods of treatment it has been deemed advisable to change the title of the revised edition to ‘‘Swine Practice’’. The author has freely consulted the various textbooks, periodicals and experiment station publications, bearing upon the subject of management and diseases of swine. To his publisher, D. M. Camp- bell, the author desires to express his appreciation. Awl Kinsley: Kansas City, Mo. CHAPTER I GENERAL SWINE MANAGEMENT Care of Stock Hogs. Autopsy. Breeds of Swine. Restraint. Feeds and Feeding. Medication. Sanitation. Anesthesia. General Diagnosis. Importance of Swine Industry WINE raising has for many decades been a very important occu- pation in practically all civilized countries. The essential food that caused so much concern, because of its scarcity, during the recent world war was fat; and pork is the chief source of that valuable product. The most intensive swine raising and feeding in the United States, have been largely confined to the great corn belt, but this may be changed in the future because of the splendid packing and _ trans- portation facilities and efficiently developed methods of immuniza- tion of swine against hog cholera and other swine diseases. Thus it is now possible to produce pigs in large numbers in sections of the country where insufficient graii is raised to finish the fattening, because these pigs can be sold at market centers, for a good profit to the producer, immunized and sent to the corn belt to farmers where they are full fed and marketed as fat hogs. Swine are sold for pork, feeders or breeding stock. The largest number of swine are sold for pork and this naturally includes those swine that were purchased as feeders. The number of breeding hogs has increased by leaps and bounds in recent years and the veterinary practitioner should familiarize himself with the problems concerned in the general management of swine. The advice a veterinarian gives to his client relative to problems in swine husbandry will necessarily vary according to location and will probably depend to some extent upon the local crop conditions. Many farmers and ranchmen in the semi-arid sections of the country could produce feeder pigs at a profit and it should be the business of veterinarians to give information and even demonstrate the feasi- bility of such a plan. Veterinarians in the corn belt, on the other i SWINE PRACTICE hand, will find the problems concerned in fattening of hogs and the production of breeding hogs of paramount importance. CHOICE OF BREED The breed of hog to be selected is a matter of personal choice with the breeder. In the middle west, the Poland China and Duroc-Jer- sey are the most popular breeds, although practically all breeds have their admirers. In recent years the demand for lighter hogs instead of the very fat animals that formerly topped the market has given great impetus to the raising of Hampshires and other semi-bacon types. Many breeders do not consider it necessary to use pure-bred sows in the production of market hogs. However, there seems to be no question among breeders but that pure-bred boars should be used. The grade sow and the pure-bred boar for the production of market hogs are especially favored by the breeders who are limited as to capital. It is also the usual procedure with beginners in the industry. The selection of the breeds is largely a matter of choice with the individual, although we find a great many that favor the pure-bred Poland China boar with the grade Duroc sow, but further investi- gation may show an equal number favoring the pure-bred Duroe boar and the grade Poland China sow. The desideratum is—good feeding qualities, early maturity and prolific females. Inbreeding is a question on which the veterinarian is frequently consulted. Inbreeding once removed is permissible, but continuous inbreeding is usually hazardous as weakly, deformed pigs are likely to result. Line-breeding is the mating of related animals that have descended from the same common ancestry. Thus, the defect of inbreeding may also appear in line breeding but by careful selection of the indi- vidual, line breeding has been found to be of value in emphasizing the good points of a particular strain of any breed of hogs. Cross-breeding is the mating of pure-bred animals of different breeds. This breeding produces a thrifty and usually hardy type with the first cross but when continued further the progeny degen- erates to uncertain types, a large number being scrubs. Grade breeding is the mating of a pure-bred boar with grade sows. If grade breeding is continued sufficiently long, practically a pure- GENERAL SWINE MANAGEMENT 13 bred herd can be established. However, this method of creating a pure-bred herd is objectionable because of the length of time required. AGE FOR MATING The age for mating animals is a question of considerable interest and importance, but from general observation it would appear that mature animals of about the same age generally produce best results. Frequent difficulties arise, particularly in farrowing, when young sows are mated with aged boars, and this should be avoided so far as possible. The mating of aged sows with young boars is attended with fair success, although a mature boar usually produces stronger pigs and a larger litter. The length of time to keep breeding animals is also an important question with breeders. Up to four or five years of age is usually the most profitable length of time for the breeding period of both male and female. The best age at which a boar should be put into service varies somewhat, according to the breed of hogs. Generally speak- ing, such animals should not be used under nine or ten months of age. Some sows will not take the boar during the period of estrum and others are bred with considerable difficulty. Such sows are of no value as breeding animals unless they produce pigs. This type of sow diminishes the vitality of the boar. It is sometimes desirable to breed a small sow to a large boar or a large sow to a small boar. These various breeding difficulties are largely overcome by the use of a breeding crate. Many different types of breeding crates have been devised. The type selected should be so constructed that it will be convenient and fulfill the requirements. In constructing a breed- ing crate, the one important feature that should be provided is that the sow will be in a natural position when confined in the crate. SELECTION OF HERD BOAR ' The quality of a herd boar should be carefully recognized and generally the points sought by the successful breeder are: big bone, large for his age, a long, wide, deep body, properly developed back, short neck and head, wide deep chest, low hams, short legs, and good feet. He should stand well on his toes, have small ears and a wide space between the eyes, have the proper color, fine hair, good action, gentle disposition and show distinct masculinity. Care of the boar is also of prime importance for success to the 14 SWINE PRACTICE breeder. In fact, the length of time of usefulness of such an animal is determined largely by the care in maintenance. The frequency of service of the boar varies with individuals and particularly accord- ing to their age. A young boar may be put to service every second or third day; whereas a mature boar may be put to service once or twice daily. Boars should be kept separate and in the summer time should be provided with a small pasture, and supplied plenty of fresh water. Winter care should include warm housing, with plenty of bedding and a maintenance ration. A common mistake of breeders is that. of keeping their herd boar too fat. Another very important consideration for health and prolonging the period of productivity of boars is in requiring them to take ample exercise. Boars should Fig. 1. Farrowing House at Longview Farms. not be kept in small pens. Most breeders provide a small pasture for their breeding boars. If a large lot or a pasture is not available, feeding should be done in one end of the pen and the water supply kept in the opposite end which will necessitate the taking of some exercise to obtain feed and water. In the selection of a herd boar, the appearance and development of the testicles should not be overlooked. Cryptorchids or boars in which either or both testicles have not descended into the scrotum should be rejected. Cryptorchidism, although usually of congenital origin, is a malformation that is frequently transmitted to the male progeny. ‘About 5 per cent of the male progeny of one of Missouri’s most famous boars, Chief Tecumseh II, were eryptorehids. Liberty GENERAL SWINE MANAGEMENT ils Chief and Chief I Know, two boars sired by Chief Tecumseh II, were noted boars and from 3 to 5 per cent of their male get were cryp- torehids. Chief Perfection II, sired by Chief Tecumseh Il, was the sire of Cherokee Perfection, which in turn sired about 3 per cent of eryptorchids. Thus this structural defect appeared in at least three generations. ’’ THE BROOD SOW The quality required in the sow is, of course, practically analogous to that required for the boar. The general contour and appearance should be strongly feminine, otherwise marks of identification should be as indicated in the male. The udder should be well formed and Fig. 2. Interior of farrowing house—more expensive than practical. provided with ten or twelve teats, distinctly defined, and these shouid extend well forward and backward and be wide apart. Most breeders claim that sows from mature animals are the best breeders. The most prolific age in sows is from two to four years. Many breeders breed gilts once and then fatten them for market, believing it to be profitable. It would be better and more profitable if these breeders would select from such gilts those that are prolific and good breeders and keep them for breeding until they are at least four years of age, rather than to trust to the single breeding as some have done in the past. Guilts should not be bred until they are nine or ten months of age. Whether or not the breeder should produce two litters of pigs a 16 SWINE PRACTICE year depends entirely upon circumstances. A large percentage of the breeders so arrange their schedule that two litters can be pro- duced each year and thus apparently make the breeding business much more profitable. The care of the brood sow is practically the same as that of the boar, except that several sows may be main- tained in the same enclosure during both winter and summer months, or during the entire year, excepting the farrowing season and for three or four weeks thereafter. The dates for farrowing should be carefully considered and will necessarily vary according to whether the breeder is desirous of pro- ducing two litters per year or one, and will depend on climate and the housing facilities on the farm. In the middle west, where two litters are produced annually, the majority of breeders favor the dates between the middle of March and the middle of April for the first litter and the middle of September to the middle of October for the second litter. When different dates than the above are selected, particularly for the spring litter and especially in the northern countries, the breeder must be certain that he has the facili- ties for keeping the small pigs properly sheltered from inelement weather. A few breeders will naturally select other dates than those indicated and perhaps have goods reasons for so doing. When breeders have several sows, they usually prefer to have them all farrow about the same time, to economize labor in the care of the pigs. This, of course, is ordinarily advisable. The provision for farrowing, particularly as to housing, is very important. Most sue- cessful breeders now favor the individual hog house, and this is cer- tainly profitable where surroundings and climatic conditions will permit. As to the type of house, there is a variety of opinions but if the house is so constructed that it will protect against inclement weather and be so arranged that there is good drainage and that the pigs can be protected from the sow crushing them, it will meet all of the usual requirements. For early spring farrowing, some pure-bred breeders have provided heated hog houses, containing several indi- vidual pens without outside runs, which is of course a desirable method but relatively expensive. The single farrowing house is most desirable for grade breeding and particularly where a large number of hogs are kept on the same farm every year. The period of estrum occurs in the sow every twenty-one days until she conceives. The absence of the period of estrum is the first indication of pregnancy. Sows usually begin to fill in the flank and GENERAL SWINE MANAGEMENT 17 show piggy in about six weeks after conception. The period of gesta- tion is from 112 to 120 days. FARROWING The breeder who does not isolate the sows from the general herd for farrowing and who does not provide clean and relatively sanitary quarters, will not be successful in raising pigs. For the best results, sows should have a change of diet about two weeks before farrowing, by reducing the fat forming foods and increasing the muscle and bone forming elements. The ration should be rather limited and should be of a laxative nature. Where feasi- ble, alfalfa hay or meal will be found to be a splendid diet, particu- larly when combined with skim milk. Needless to say, a change of diet should be rather gradual and not sudden. Fig. 3. One-sow farrowing houses. The farrowing house should contain a good quality of bedding, but this should not be used extravagantly, as a limited amount of bedding is more desirable than heavy bedding. The bedding mate- rail should be clean and not contain fibers or straws that are long and in which the little pigs might become entangled. Sometimes, sows, particularly young ones, may have difficulty in delivery, and in such eases provision must be made in order that the life of the dam and pigs both will be saved. The veterinarian should advise his client that such cases should be seen immediately when it is determined whether or not it will be necessary to perform a cesarean section. Some veterinarians have provided a special room in their hospital in which this operation is conducted, the farmers delivering patients direct to them. In this way, the veterinarian can perform the operation for a reasonable fee and he has the surround- 18 SWINE PRACTICE ings in which the best possible service can be given. The use of for- ceps may be indicated, but each case is distinct within itself and it is not possible to give positive directions for such operations. Good breeders see that each pig begins breathing, and when neces- sary artificial respiraton is resorted to. Also each pig is required to suckle, and chilling of the recently farrowed pig is prevented. Pig eating sows are sometimes observed. This habit is usually the result of improper diet. It can usually be prevented by providing proper feed, although when a sow has formed the habit it is difficult to cure it and it may be necessary to fatten the sow for slaughter. Fig. 4. CESAREAN SECTION. Photcgraph taken seven days after the sow was delivered of seven pigs by laparotomy. Proper care of the suckling pig is necessary. They usually require considerable attention for about the first ten days. In recent years it seems probable that as much as 30 per cent of the spring crop of pigs has been lost. These extensive losses were due to a variety of conditions, the most important of which were abortion, scour, parasitism, pneumonia, swine plague and_ goiter. Abortion is becoming a serious menace to the swine industry. A detailed description of this disease appears elsewhere. Suffice is to say at this time that it appears to be of an infectious nature. Abort- ing sows should be isolated and this is one important factor that favors the individual farrowing house and separate pens for each sow and her litter. Breeders should be urged to divide their brood sows into small lots. Pig scour may be intimately associated with abortion disease in the sow. It has also been found that digestive derangement result- GENERAL SWINE MANAGEMENT 1e8) ing in diarrhea may be caused by Bb. suisepticus, B. suipestifer, B. paratyphoid, B. enterititis and colon bacillus, and probably also some other microbian agents. In some isolated cases, scour in pigs has been found to be due to digestive derangement of the sow. This disease will also be discussed elsewhere in detail. Scour due to various infecting microbian organisms may be largely prevented by providing sanitary surroundings for the brood sow and her litter. If the infection gains a foothold, the various indicated biologics combined with proper feeding and sanitary measures will be found to be of considerable value. Parasitic pneumonia has been found to be a very potent factor in the loss of pigs. Losses incidental to this disease occur in pigs ten days of age and from that up to two or three months of age. The majority of cases of parasitic pneumonia in suckling pigs are due to the larval form of the ascarid. The life history of this parasite will be found detailed in the chapter on Intestinal Parasites. This loss in pigs can be prevented by elimination of parasites from the intestines of the brood sow prior to farrowing. It seems prob- able that these parasites may exist in a latent form for a consider- able time in the soil. Hence, the successful breeder provides for a frequent change of lots. Defective development of the thyroid gland has been found to be an important factor in some of the losses of the annual pig crop, particularly in some of the northern states. The exact cause of this condition has not yet been determined but it seems probable that the food of the brood sow is deficient in some necessary nutritive or erowth element. This condition can be prevented by the adminis- tration of iodin or some of its salts to the brood sow, during the period of pregnancy. Because of the recurrence of this condition in succeeding years on the same farm, it seems justifiable to recom- mend iodin salts to the pregnant animals on that farm. Brood sows while suckling pigs should be given a good ration, containing the elements that stimulate the flow of milk and provide sufficient bone and muscle-forming ingredients. A breeder can not expect a sow to produce a good litter of pigs on a ration insufficient to maintain her in good living condition. The age for weaning pigs depends somewhat on the development and condition of the pigs. Generally speaking, pigs should be weaned at from ten to thirteen weeks of age. Most breeders diminish the milk-producing foods for the sow a few days prior to the time 20 SWINE PRACTICE of weaning, although a few breeders advocate the weaning of a few of the pigs at a time. This method is not, generally speaking, advis- able. The sow and pigs usually do better if all of the pigs are weaned at the same time, and the pigs should be sufficiently sep- arated from the sow, so that neither can hear nor see the other. On the best regulated breeding and feeding farms the pigs are classified as soon as they are weaned, separating those desired for breeding purposes from those to be used for feeding. Some feeders prefer to even re-classify their feeding lots, claiming that they have found it profitable to market pigs that are all practically the same size and color. The feeding of the different classes of pigs will be essentially different. The fattening hogs will be given a fattening ration, whereas, the breeding hogs will be given a growing ration. It is always advisable to properly identify pure-bred pigs that are to be kept for breeding. Different tags are available for this pur- pose, the choice of which will depend entirely on the breeder. Care of Stock Hogs The suecessful handling of stock hogs is one of the most importaut problems of the live stock industry in the United States. There are many sections in which insufficient grain is raised to fatten hogs, but the climate and surroundings are such that pigs can be produced and transported to those areas in which grain is raised in sufficient quantity to fatten more hogs than are normally produced in those areas. It does not seem possible to change this state of affairs and conse- quently the extent of the production of feeder pigs will be largely determined by the success that feeders have with pigs delivered to their farms for feeding purposes. Many points must be considered in purchasing stock hogs. buccal mucous membrane. Injuries to this membrane are predis: posed to infection that may produce pathologic conditions, varying from simple inflammation to suppuration or even necrosis. Lips MALFORMATIONS Malformations of the lips of swine are not rare, the most frequent malformation being the condition popularly termed harelip (schistosis labia). This condition is rarely observed in mature swine, because the defect renders nursing extremely difficult and frequently impossible; such pigs, therefore, die before they have passed the nursing stage. Schistosis labia, when not associated with other developmental errors, can usually be sufficiently relieved by surgical interference that the pig can suckle and develop to maturity. In operating to relieve harelip the fibrous tissue on either side of the fissure should be dissected away and the skin surfaces freshened, after which the fissure is closed by suturing with silk. It may be necessary to feed the pigs for two or three days after the operation. CHEILITIS The lps are also subject to injuries inflicted by rough foods or by foreign bodies in the food. Wounds, too, may be inflicted by dogs. Because of their location, lip wounds are predisposed to infection. Inflammatory processes of the lips are usually confined to the mucous surface. Catarrhal cheilitis is of rather common occurrence, particularly in small pigs, and may be either acute or chronic. This condition is usually caused by improper food or by undue exposure to very 76 SWINE PRACTICE dry atmosphere. ‘The lesions of the acute type consist of small erevices which in extreme cases may bleed freely. In the chronic type the cracks and crevices become more extensive and the su- rounding tissues are infiltrated with varying quantities of newly formed fibrous tissue. Catarrhal cheilitis, either acute or chronic, is not a serious condition and is usually corrected when the cause is removed. The irritated infected areas of the lips should be thor- oughly cleaned with a lukewarm 1 per cent solution of salt, after which it is advisable to apply some antiseptic. Suppurative cheilitis is occasionally observed. It is usually the result of infection of the subsurface labial tissues with pyogenic bacteria. The usual form of this type of cheilitis is circumscribed. and the lesions are similar to the lesions observed in the usual abscess formation. This condition is relieved by operation. The small ab- scesses should be opened freely with a sharp-pointed bistoury and the pus removed, after which the wound should be painted with tincture of iodin. Necrotic cheilitis is very prevalent in some sections of the United States, particularly in young pigs. The usual causative agent is the Bacillus necrophorus. This microorganism produces a variety of lesions and is of so great economic importance that all of the dis- ease processes resulting from it will be discussed under the topic, ‘** Necrobacillosis. ’’ Vesicular cheilitis has been reported as occurring in suckling pigs. This condition is probably caused by a yeast, the oidium albicans. The lesions of vesicular cheilitis are practically confined to the mucous surfaces of the lips. The’ mucous membrane is tumefied and searlet red in color, and in the beginning and later small, sharply cireumseribed vesicles appear and the mucosa becomes white, due to the accumulated desquamated epithelium and mucus. The vesicles rupture and the vesicular membrane may slough, leaving a denuded surface, or the vesicular membrane may collapse after the discharge of its contents and appear as a small, white mass upon the mucous membrane. This condition is usually not serious, although it may cause considerable inconvenience in sucking. It is usually relieved by the topical application of properly selected antiseptics. TUMORS Labial tumors are not of common occurrence in swine, although (‘broma, myxema, and epithelioma have been observed. DIGESTIVE SYSTEM id Tongue The tongue is subject to injuries of various types. Tongue injuries may be inflicted by improper food, by foreign bodies in the food, or by sharp, irregular teeth. The symptoms of injuries or foreign bodies in the tongue consist of persistent champing of the teeth, moving the head from side to side while prehending or chewing food and more or less ptyalism. When such symptoms are evidenced a thorough examination should be made after the animal has been properly restrained. The pro- cedure for relief will depend upon the causative factor. Nails, splinters, or other foreign bodies should be removed and the wound Fig. 21. GLossitis. This tongue taken from an apparently normal hog, contained twenty-four polished nails lodged in one place. swabbed with tincture of iodin. Ragged edges of lacerated wounds should be removed before antiseptics are applied. GLOSSITIS Inflammatory disturbances of the tongue may involve the mucous membrane only or the submucous muscular portion of the tongue. The inflammations of the lingual mucous membrane are practically identical with those of the lips and will not be given further con- sideration. Inflammation of the lingual musculature is usually the ‘sequel of an injury which had provided an avenue of entrance for_ infection. Inflammation of the substructures of the tongue may be 78 SWINE PRACTICE acute or chronic, diffuse or circumscribed, nonsuppurative or sup- purative. Diffuse nonsuppurative subsurface glossitis is usually acute and is the result of infection with streptococci or some septic microorganism. The lesions in this type of glossitis consist of a diffuse, extensive tumefaction of the tongue, which on section evidences enlargement of the blood vessels and abundant accumulations of pus, or other inflammatory products, between the muscle bundles, while the mus- cle tissue presents a parboiled appearance. Acute circumscribed subsurface suppurative glossitis partakes of the nature of an abscess. Chronic glossitis is most frequently diffuse and is exemplified in cases of diffuse lingual actinomyecosis. The lesions consist primarily of an excessive quantity of fibrous tissue which may contract un- equally in different portions of the tongue, thus producing an irregu- larity of the surface of the organ. Portions of the tongue in which excessive quantities of fibrous tissues are developed become dense and hard, and cut with considerable resistance. The symptoms evidenced in acute glossitis are difficulty of pre- hension and mastication, irregular movements of the head, champ- ing of the teeth, and in extreme cases refusal of food and drink and the dribbling of saliva or saliva mixed with pus and in some instances there will be more or less blood mixed with the saliva. Diffuse suppurative glossitis is not common. It should be treated by mild antisepties, using agents that are not injurious should they be swallowed. Abscesses of the tongue when so located that it is possible to operate, can be relieved by making a good free incision (lengthwise of the tongue) and permitting the pus to escape, after which the wound should be swabbed with tincture of iodin. as Stenosis ae thorax Tracheitis Teese 'f Hemothorax umors Pneumothorax Da, Bete ml xa Bronchial Tubes Pleuri acute ‘ . eurisy 5 Stenosis ~ ) ehronie .._ f Catarrhal Tumors Bronchitis J |, e a : | Parasitic Spasms of Diaphragm Se Anatomical Consideration Snout.—The snout is formed by a fusion of the upper lip and the structure that corresponds to the nose in other animals. It is short and eylindrical. The skin of the snout is thin and quite sensitive. The nostrils are open on the flat surface of the snout. ‘They are round and rather small and separated by the os rostri which is a prolongation of the septum nasi. Nasal Cavity—The nasal cavity varies in different breeds of swine, but in general it is long and narrow. It is divided behind a trans- verse plate into an upper part that communicates with the meatus of the ethmoid and a lower or respiratory portion. The nasolachrimal duct is in the posterior portion of the ventral portion of the cavity. ee DISEASES OF RESPIRATORY ORGANS 147 Larynz.—The larynx is long and has considerable mobility, due to the relatively loose attachments of the laryngeal cartilages. The vocal cords extend obliquely downward and backward. ‘They are close together. and hence the rima gilottidis is narrow. Each vocal cord has an opening communicating with the laryngeal saccules. Trachea and Bronchi.—The trachea extends from the larynx down- ward along the inferior portion of the cervical region into the thoracic cavity where it bifureates, forming the bronchial tubes. The trachea is six to eight inches in length and contains about thirty-five incomplete cartilaginous rings. There are two principal bronchial tubes, one being distributed to the right and the other to the left lung. ecb a hee ee ee or eee p ee 260 JN AKETAME, ORF AVN SUMO TRO Mee scoetee ee ccna 92 TANTO HSU OV SAS CT eet eee ete e e a ae 61, 363 Anesthetics, Administration of_..... 61 JANA EUU RS) 00 ile ae et ee eee eee eee 260 JANN OUEST earn nas Sie ee 328 PNAS open OLATNS Cl Ol esees a ec eee ee 125 ATOM PENS CPOWAD ONG ce rseserere nae akee oss rece 81 ANOLON, CVOWAT OCS snes oe eee eee 341 JAN OHOLEUATLETE HAN) OVEN ERIKO VOLO) een eoe cee cece: 89 PATS GLITETIG) Same ony GNI Cl eeceeernes oes BA eee 214 ANTEC WUE TY ETNTTEN SON oe eee 230 PNG CAN: CHUAGIS pment eae tee Se 138 NSCaridiasis,— © WHMtOMATy, 22> ces- so 222 BANS GallelSy MSULUIIND) eco so2e nde ences eye 117, 145 BNS CMC Sw We rie aes ace ess eae eet lite eee ear 142 PNUCLECUASI GI pene ctant oie cee eu ee ee 158 JAN BYTES WS G2) een ne en Ne ee Ter 214 Attitude significant in diagnosis... 46 Autopsy, Equipment for ................. 53 Autopsy, Method of holding ......... 52 Autopsy, Permission necessary .... ....... 52 PNUD OS Ay TRACOUCIS “Geo eece eee eee 54. JNTOOE IG SAO YGCS WO Lee chee eee 53 ANTUOUS\ 7 LES UOMO Cit sees eee eee 55 BseLeMnes:, HME NT ACIS) 2: cece ete 8 ans ee estes 328 Ba cillnsmoteeICOChy gee ee ee 330 Bacwias pyogenes. 24 0.0 so age ne! 206 Jajevoililns Sinaia, Gy 274, 325 Bacillus swisepticus~ 22.622 6ot 302 aC Me NOLS kee anes cts ele es 28 Belladonna, poisoning \2).222 0 113 CR athe e gee een ee a Re, et ted, oy 4 26 bladders Calculigumethesse se 193 Bladder, Dilatations-of the. 22. 25. 192 Bladder, Hemorrhage into the... 192 Bladder, Inflammation of .................... 194 Bladder, Malformations of —................. 191 Biladderwlumorceoteticee ssa 195 Bileedino strom thes nosess se 148 Blood Ging tive ulin ekene seen ee een 185 Boar Caresoipherdss == Sie: ae See 14 Oates Genitalaoneains motes =e 174 BOATS elec hone Ole hicrde == eee 13 Botryomyces ascoformans ...................... 352 IB OLY OMNYCOSISuee eee 207, 852 Brainy Elyse emi a0 fees ee eee 268 Brain. Vialiformea bon Salote eee ene 263 Brain, searasites = Ol bie ee ees 269 Breeds ChoicenO ieee eee 12 IB LONE ise Au LOU yam O tees 147 EEOC Males hen S1Gimeeeseeee sees eee eee A Bronchial strong ylosise = 156 Bronchial tubes, Malformations of-_... 153 SOM ChibiSeen Cartantsys hey tepeee =e eee nee eee 154 Brood! Sows he hese eee es oes ee ee 15 Buccal membranes, Injuries of-...... 79 Bullbo-ure tlaiallige Veil Sees ee 196 IBullEnoses ee eee eee eee 223 Calculieinsthes lad erie ee 193 Caleculifingthes prepuce = 199 Calewlif Renal si ees eee eee 180 Campsomyia macellaria.......... 198, 247, 351 Carbohydrate concentrates, Fat and... 35 Carbolic acid poisoning: .....-...-42.- 111 Cars Overloading #2 =e ee 21 GaGtratio inte tt eo re eeee etees ees 344 CERIO, AVQe OR Sa ee eee 344 Castration. a Gare saiite tees eee 348 Castration, Parasites following —....... 351 @astrabion;sectiel acm otege ss eee 348 Castrationy ech nicy Ol esse 346 Caustic potash poisoning ...................-..-. 110 Caustic soda’ poisoning 26225732 110 Cerebral enema yes ee ee 268 Cesarean Sections 2 ee eee 362 Ghar Oris pete ee re ee 328 (Chen TS ee ee ree 75 @hre inte @ atari all eee eee 75 (GEMS ee INE CROLL C ye ee escent ere 76 he witiSss Supp pt arty seen 76 ChreilitisHeViesicuil aie eases cee eee Bp 1G Chester” White) -=------=-— Wieser ete Oe 2226 (© ba coyeall nsy pen se eee 62 @holelithiasish 222s see ete es 130 Cholera, Annual loss 368 INDEX Cholera, Diagnosis of 222 = 286, ~Diticult, parturition... 40 ee 361 Cholera, Entrance of infection... 280 Digestion. <3 .0%. at Rae 74 CholenasWitiolo gyi. $i. nee pare eter 272 Digestive disturbances ........_. 50 Cholera, Geographical distribution. 270 Dilatationsotebladdenis.s aaa 192 Cholera, tae is 5.c ies es ee See 270 ~=—- Dilatation of esophagus _.................. 87 Cholera esion sie eee eee! 281 Dilatation ots heart ieee) eae 258 Cholera, Mode of infection... 280 — Dilatation’ of intestine 2. - ae 104. Cholera, Period of incubation... 280 Dilatationwof stomach see 98 Cholera, Predisposing causes of... 219 ~Distoma Americanum | =...32 eee 140 Cholera, Preventive treatment —............ 292 Distoma hepaticum Cholera,cRropnosis; tite. stesso see 288. Distoma lanceolatum 2.) eee 140 Cholera, Rules and regulations... 290 Distomatosis. (222. 139 Cholera serum, Clarified anti-hog 295 Distomiasis, Pulmonary.............._. 168 Cholera serum production, anti-heg 293 Drainage: essential... 3. 0) eee 43 Cholera, Source of infection................. 276 Dropsy,, Abdominal 4...) eee 142 Cholera Susceptibility, to. 2.0 280. Dropsy.of the thorax... eee 168 Cinollema, Shymnyowonns Cie ee 284°. Diysentery -..0- icy ee 123 Cholenasireabment so tes ae 289. Dystocia. 2.0 361 Cholera virus, Persistence of... 274. : CON OCORREE eon Be sag SE RU ee a eae eA gece 268 Kiehinococepsis’ ===. = eee 140 ih OSS ihc eee ave eee eee ee 135 Echinococcosis of the heart................... 258 Clean: GENIN eee wees ben eee 295 Kehinococcosis pulmonum = _...--.-- 168 Cloudy. swellno ot livers. = 85 = 129). Eiclamipsiayes. 2-2 a ee 266 Coccidiosis te eas Seis he eee 137 NCZEOUNA, « (eeze. ck Wiehe enh as ae 47, 244: Cockleburs poisoningie= =) ss 112 Edema, Mai omen ee 325 Concentrates, Fat and carbohydrate. 35 Edema,y bullmonainy. ye 159 Concentrates; sproteinese se 35 Elephantiasis):.22. 2 2 eee 246 Cons bipabionm's eens ats ee ee A ee 124. Bim eSiSh eee es ae swohustcns ee 91 Corrosive sublimate poisoning 111 Emphysema of the intestine...................... 105 Cotton-seed meal poisoning... NG Emphysema, Pulmonary 2.222222 158 Gough at ee eS ee es ee eee 49 Endocarditis 208.20 e eee 260 Cowper ses land see ee 196 Enteritis, Acute catarrhal -................ 105 @ross-breedin pee se sees ee ee iZ Enteritis, Chronic catarrhal .................. 107 Cryptogami es peisominic iene 115 smtenitis, CrowpoOus 2 eee 108 Cryo tonchiGisniee ese eeres eenn eee ee ees 14 Enteritis, Infectious necrotic —... 108, 308 @ystictealculli AS e Te 193 Eimtenitisy Necroticr. sane eae 320 Cys tiGELCOSIS paces ale eee ee 141, 237 Enteritis: (Loxie’ 2.5... 109 Gysticercus: cellmlosaena ees 259, 269 BNtGROGE Naas =e ee ge 101 CyShiGencusetenniGo! Senn 144 Epididymitis: 22222 2202 = 197 Gy SUILIS’ 0 eee ee a So Eee ee 194 Epilepsy 32 dpe g sree peSe Bev See dnae tons aaa eee 265 Cystitis, Catarnhalk 25 ee es ee 194 Epistaxisn- 928 =e) 148 Cystitis, Purulent=\.2> = ee 194, Epizootic aphthae a atiped Soees sonnet cobs ate tol (CayyGuss MOET 1S OMEN oe ee ee ee 200 Eirysipelas;. Swine 7.2) see 338 Hiny themida) ts ee ee 241 Demodetic wmang esac ee 252 Msophagitis. 28..0-22e2 225 eee ee 88 Demodex folliculorum, 2.) eee 252 Esophagostoma dentatum ...................... 119 Dentitionseclampsia =... ee 266 Esophagus, Anatomy of ............-....-- 69 Dermatitis oranulosa 220. ot ee 245 Esophagus, Dilatation of ~.................... 87 Dernmatitis,. Necrotie- 22) ee tae 322 Esophagus, Constriction of -.................. 86 Diagnosis, Differential .2...62....0...... 45 Esophagus, Inflammation of —............ 88 DidenosisssGeneralles se. ee 44. Jsophagus, Malformations of —........ 86 Diaphragm, Spasms: Of...) 171 Ksophagus, Perforation of —...........-.. 87 | VEEN aT ef hes Mes to me ele eae cee wae NEE A eC 12% Jsophagus, Tumors of... Bases 89 INDEX 369 IBIS UIT See) Os genet Sera ee eed 3D eidleanta@licarasiies Otte: ee een ene 259 SEEM OCCURGENCG) Of setae eee 16 les l@e cia SU rUMVeN RS woh) esas eee se ee 258 1 ENR Oth ae aN lt ati Rane ee Oe A ee a Se Gi > GLE AUS LOG: saeh ee eee cas ee ened, ee 264 IBIGTTMENIEMVSSG: Soo Beer tcescceeees pecans peace 92 Fallopian tubes, Malformation of... 201 Ellematopinus fee eo ene ee ane 248 EEO Win ber, 2.4 0h Ce Den te Up eae Merin AUT Nea a sane oe cos kee ee ae Se toe 188 HarrowimovGates!, 22. see eee 16 Hemorrhage into the bladder................. 192 Farrowing, Difficulties in...................... fg} Jelean@ieid meyenS “To Wave lave ieee 257 Marrow OUSES! © 22:c ee ee ee Gs ale emonrrhaee sone mies WiNCS meee 101 Fat and carbohydrate concentrates... 35) dlemornhare ol the kidme ys) eee 178 Hatty, changes) in’ the heart 22-2. OF ieee ElemOmrha reson sOvelisye nese Se Ee 200 Fatty changes in the kidney .................. 190) sem Orrhareror stomach nese anes 92 Hativechangess ime thes liver js = 129 ee emornrhia cero teibecuisnn = eee meee 202 Fatty changes in muscles. ..........-....-...--- op) Jeleimormogyete, lembbanoneny sc ee 159 Feed and water in diagnosis.................... HOW slemorrhae cese pice nn deren eee nea 301 LPNS SOUN MEE SEE ONS sees cee ce rete Siem wlLVenl0-thoraxs ates ewe mee ete eee 169 Reedine; Lvequirentents tor ess SAG mew alle ality] Gm Iniyiyo CT NUN cl ere eee ee ee 132 Feeding, Success depends upon.............. apy MBI FOLENS ON OW RE NSH ECSRSS Sar eee 137 JOVI BIOGEN NING occas ee By JEIGOR VE TANTO NAS ese ea oe ee eee 137 iHemale genital organs, Anatomys ot. 360 .; bepatitis ic. 222 Bet cecte eerste 132 Hil eames tation cee ee ee eee GAS) eile patibis, eNCULe mmLeTStitial yee eee 135 Foot and mouth disease... 341 Hepatitis, Acute parenchymatous —.... 133 LO OLAS ON Ohms teense tee ts, nt Seng A 228 Hepatitis, Chronic interstitial —............ 135 NOTE] 2770) O CUES eve Te ese ee 128 TRIG ORNTNUIE SS INIG CROC Re ee 321 Foreign bodies in stomach. .................... 90M Hepatitisy supp umabivel ye ee 13: Foreign bodies in tongue ...........-._._. (Ges eter des Oats CALC eO eer eee ee 14. BSE ZU OW pe eee ake ne ne een ese A ae UE PW JelereGl Joyaeehe, ISKCON Wit» te 13 Jelena SSVOTRO EN Sense om nh ce eee 352 oilestanese ee ates ee pet -\hee 139 History, Importance in diagnosis.......... 46 Garbase feeding: I 1 A eC eee G2 Gatbage: poisoning 2. 522k 114 Hog bacon nent oa 28 Gastritis, Catarrhal eee a Gactritiss Chronic 2.0.5. g7 Hog house, Mississippi -.........-..-.--.-..-....- 40 Gastritis, Croupous. q.80 26-2 96 Hog house, The 022-0 3o Gastritis, Phieemonous — 2.20.52... 2-222: 9g Hog, Lard 24 CaSbnO-ChtelitiGheee eee ee e109 Hogs, INGUIN YS dle Ws eles seeetee ees coy See 23 Generative organs, Male. 196 Hogs, Number of pure-bred -................. 2; Genital organs, Anatomy of female_....360 Hydronephrosis 2... AT Genitalgorneanseote boat es es = 174 Hydrothorax _......... soistesaas snes 168 Genital organs Of SOW o.-.::::sescsec2-s00e0---- 175. 0 clyperemilar or they diver ye 22-2 eee 132 Gestation, Period of...........-0.-..-.. 17, 360 Hyperemia of stomach —.......... 94 Gigantorhynchus hirudinaceus.. j21 Hypodermic syringe, Administration QT OSCURI See eee ae ont en ee "7 WUD Go se sedee st ace sae aces a siae oe ee 60 Glycogenic infiltration of the liver... 130 Hysterectomy ~.---..--------.---2e -------BO4 (Grade-breeding. 2.2.6.0 TOW A YVSTEROLOMy (see eee B04 ~ ELLENTON) 201 SIS ec ee aa DOM Matter cited Wn kee ee LIP ea aimed 128 LealFyaqt ofstnihte}: aeeae wee mae Me Seri ue ae ere eet a 28 : ; Fea, nl aeationwote, ee. seeee 258 Tmnpetigo mi SCY tena ce fo os Cat eehiore ots Heart. Examination of 222-02. 4g Imbreeding ~------------------eeee I2 Heart, Fatty changes in................... OR Ue ChHOUS MMe COM CNet enilise geese 308 Gani, emornEh aces lines es PSr/ [NORE ONNIS) jOMOKSTUN AMONG) © ee ee cee ee 22 370 INDEX Imtestinal mnecrobacillosis. 22-2 315 umes; Llemornhace ots ee 159 MnbeS tinal OAVASULGS. 2:eeee ese ere 116 Lungs, Inflammation’ of —-- eee 161 [Irate oe wD NNO AS — ee cece cece 122) lungs; “Parasiteswof' 2. 168 Intestine, Emphysema of -......-..------------ 105. Lungs, Tumors in 2222222222 167 Intestine, Hemorrhage of —.....-..-.--.--- 101 Intestine, Inflammation of -—-..............-- 105 Male generative organs, Diseases of......196 Intestine, Malformation of -..-......... LO Malionant? catarr hye ss. ee 150 Intestines Obstructions Of je 103) sMalionantedennays2 22 eee 325 HimbeStimess: Aula tOuaiyanO fegee een eee 71 Mammary abscesses) ===. 206 Intestines, Dilatation’ (Ol 104 Mammary glands, Ablation of —_.......... B57 Mammary glands, Inflammation of -..205 TA Taan CLC won ora ie teu a ae ae 128 Mammary glands, Injuries to —.......... 205 Milam arya WU ONS ease eee eee 208 Kade y.ssn COMP ESULOM Ope meen 181 Cun i iui os aoc an SGV CH ID Gyo ID) 1G 9 S Vigne Oa ee ee 177 Le Ganehea ts FO Co a p Kidneys, Fatty changes in...................... 180 a ri a Bats bes: Sane Bed ee oe Kidneys, Hemorrhage of =. 17 ATMOS; ESN matous 2 205 enor ein larnatienn et 181 Mammitis, ‘Luberculous) ee 208 a) , a QGAUIUIL Ul .-..-..-.---------------- J r Kidneys, Malformation of ——__............... 177 Mange ........-------- ETE DFAT EE eee a = * IKGlomnveyey, IP anRISES Chr eee actos ce 190 Mange, Demodetic ~~ Bs: EGG ha veNraSS MM Mh naVov ech One ees ee ee oe 190 Mange, Red iS ey I 52 : MWiamig ery Sait CO) tC ee ee 249 eardeiony. a Sit) renee wee O14 Mating; Alive forse ee 13 : Meéasles: 23-2222 ee 243 LE eA eT eV Le UAT TS eee eee 153 Ee ee Measly “pork: 2... 322. ee 237 IDenanimeitons, (eienea nll 2st eee aceecesenees 151 Keene MS oe ne hey @ Medication. 523.22 59 DyeANTs VAIO ts S yp © OULD OUTS see eee 152 : 5 mete ; Mien Gunyep O1S OMIM Gy eee Be 111 JUeyaabeso VANTIN ONT (0) te we ees eT : Per 2 ibraviesath : 261 Metastroneylusapiiness.= ea 156, 168 hs EEO REN ees 3 Metritis 25.4.5 22 202 Weulkkorrhearge SE See eae 204. rep ARE Li eae Syn Metritis and Retained Placenta... 213 SAGEM HO UUTNES SOROS pared Seance cote 264 : 5 a SANs . - : Milk, Composition of sow’s................- 176 JTW OS ONE UIE sec oee erento iaeeeeseoe 12 : 3 Tans : . o Mixed. bacterin’ ......-22 316 ApS; Luntlamomabiom Of feese ere 15 : eae A ; = Mole; Pismented) =e 246 ZL Soy MU cULiE OMA LLO Ws Ol) eee eee 15 3 eae aie Mouth Anatomy ot 9 Lae 65 ZN) Spee NUL OTS ik O ieee eee eee SSG cp aes a : ‘ ; : Mouth; Injuries of 2222 75 liver; sumaloids-chan@esm ine. 130 2 ‘ aad = Mule=fo0ot ¢.2..25..2.2 2 27 livers] Anatomiyee Ol eee 13 Z se j ney BURR é Muscles, Fatty changes in............. ae 229 ILanvere, (Clomoly SNC bia er acento 129 peop a noe thy 8 999 iver. Patty changes in 2.1 120 ee ey ee as ee ac ILakyeies Stoner Voxoxeless Mn ot cee oeee ext 126 Liver, Glycogenic infiltration of the_.1380 Nasal catarrh -.--..---2----. ete 150 Liver, Hyperemia of ..-.------cc--ccece-- 132 Nasal cavity, Anatomy Of ==) ee 146 (eigen. Unt ammauion Oke ee 132 Nasal discharge — ----:--.-------2--= eee 49 iverse vial fom dtlOl si. O lene e eae 126 Nasal, tumors==..2 ee 151 MeIVeESe aras hleSm Oke aes ee eee ees 137 Navel ill ~....-. 214 Inver ehnpbune (ot se eee eens. 197. Necrobacillosis!~— 2) = ee 317 iver: Lumorse0f oc es 137 Necrobacillosis, Intestinal] -...--...2 315 [OG AW ot tee ee ee ee 343 Necrobacillosis of the skin_.2=-2-2== 245 WsOUSITICSS) on ee ly eee oc eee at ee 248 Necrobacillosis, Unusual forms of... 323 Lungs, Anatomy of .......... SRA ne REET S TS 147 - Necrosis of the Spleen! = eas 261 ferumorssn Colla Se: Olimar 158), -Necrotic denn atts 522 AGAIN Se Ce Tn ca geese eee eee 159. . Necrotic enteritis eee 320 JLowayers, Lo paay OVaNsreeO es) COME se ee ce eee 158 Necrotic enteritis, Infectious... 308 Necrotic hepatitis Necrotic pneumonia Necrotic rhinitis Necrotic splenitis Necrotic stomatitis Necrotic vaginitis Necrotic vulvitis Nephritis Nephritis, Acute interstitial Nephritis, Acute parenchymatous Nephritis, Chronic Nephritis, Chronic interstitial Nephritis, Purulent Nervous disorders Niehi, shade “poisoning 2:0. 2... Nose bleed Obstetricseceee ate ee eee ee Obstruction of intestines.............0....... OmiphatopneDitis® = |.5.2.25 2.22 et ee STOTT HSE epee eee ne ne OTC hb Siege tere ee NG Es Od Organs of locomotion, Injuries to Organs of locomotion, Malformations ULE Se ee eee sce eae ne Pan eee Ornithodorus megnini — 00.0... Osteomalacia Osteomyelitis, Purulent Ovarian cysts Ovarian tumors vames mUiiilrless tOs se ek wt Ovaritis Ovary, Hemorrhage of Ovary, Inflammation of Ovary, Malformation of Pancreas, Anatomy of Fail@hed ssl dubyje MeCLOSIS: Of = Pancreas, Tumors of Papilloma Ent nIS esl eile <0 ee 8 OS Parasites following castration... Parasites, Intestinal Parasites of the brain Parasites of the heart Parasites of the kidney Parasites of the liver Parasites of the peritoneum Parasites of the skin Parasites of the Parasites of the INDEX 371 201 199 200 200 200 Parasites of ‘themtongue? 2.2.2.5 .2.. 79 Parasites, “Pulmonary 222)...022.....45. 168 arasiticy pnetmionia, <..206 0 3.8 19 Paratyphoid infection —.............. 315, 324 Parotid glands, Injuries of-............ 82 PRU OUILIS 9 ces eee ee ek ee oe eee Ses 82 AYU TELM 3 ee 3) eee Sc Ce Se pe 361 leeirremneses, ID MO WINE soe ee 361 EMIS, SINURES s LG he ot ee See 199 RenisssVMallitonmeanionsmo tenes ee 199 BE DUIG OCEn Ss eee eee eee A be Ul eo 93 Perforation of the esophagus... 87 Pericardial stamens. 2-2-8) = ek eee 258 IPEricarcinig: ss oo reat Se ee ee 258 Peritoneum, Inflammation of 143 Peritoneum, Injuries of the. eet 142 ETILOne nM ma arasivesmO ni seer 144 PerHLOnenum.) LUMOls Oh) 8 ee 144 eR iCOMELIS: tee le nce cera recess re 143 PRAY MOUS] tet 6. hee sO ee ee oe eh 84. PAT yi eAN ATOM yee Olsens ee ae 68 Rhanynsx Inyuries sO£- fess ee 83 Pharynx,vParalysise ofss2-) ate 85 Jelnenanmb<, Abimbemoins (Or ol 86 hEnol poIsOMiN er. eee a ee 111 Feil Dut Spies.) at ee eee ohn Ae ok 260 Phosphorous poisoning SetG) POINTE IA SIS). 2a 2 oe ee ee ee es 248 Eig ac are > Ot Suckling: sa, <2 = ene: 18 ES Calin G-SOWS ane ae ee 18, 89 E08 7S CO Uniti eee es eee ee 18, 220 Pigs,.Classifieatiom of. = ee 20 Pigs, Identification of pure-bred__. 20 Bec a RAlyS1s Sipe se ete ee he Roa 266 LPMISS SOI SOMONE TMs cot eco ee ae ee P15) Pigs,s Weaninp. time 2s. 2e el ae 20 Rilemraselinitlanimnadtiommot een ee 170 FA euiiclape Un OL Sir Olaaee se e ee ital LEUIISWAA CULesi eae eae ce 170 EJeunisves Chronic. 72 = tA eo oe 170 Plewro“pmeumonla a... ae 168 ERneumoniass Catarthal ee 161, 307 eNeUMOnIane GhnTOnice aes 166 Eneumonias roupous © ...22 le 162 PNeMMOIa. Ganonenousy yee eee 165 Pneumonia, Infectious Pneumonia, Interstitial Pneumonia, Necrotic Pneumonia, Parasitic Pneumonia, Purulent Pneumonia, Septic Pneumonia, Verminous € Oe INDEX Pew O= thoi axqueess eee 168, 169 Poisoning, Belladonna (Deadly night SS eG) eee 113 Poisoning, Caustic potash, soda... 110 Roisonminess Cocke ui ene 112 Poisoning, Cotton-seed meal -........ 116 Poisoning) Crypto rani see eee 115 Hoisoniniess Gana meee eee 114 Poisoning, Phenol (Carbolic acid)... 111 Poisoning, Mercury (Corrosive Sullolinmate:) iy. basse testes eee eng ee 111 Poisoning, Os MOTOUS tes. en eee 110 Poisoning, Sodium chloride -......__.. 10S Poland China, Characteristics of............ 24 Pro ypeanr Ula tel Si ee ect eee eee eee ee 231 UO Kean GAS LCS Nae eee ee wee eee 237 ne omaieygey \ CCl Emits) Ogee ee eer 365 2G] PTA CYss 1 SUS HO ha ae eee 17 Re puilalle COM CHEM ENIGS geen seeeeee eee 199 Breputial Sint amma tions see eee 199 ere joutblall ome CROSS Meese eee eee 322 IPOH OTE Ort WAY LVONS) ee eens eet escecteces 125 Brolapsesot sthe sme chimnhee eee 125 Riroteimteconcentrates sss a 35 SUN Ty Teed) le @ Lea SL aes eee 266 Pulmonary ascaridiasis ................---...-- 222 PmlmonaryastronigylOsiss eas asses 156 Qiks, LE SeeemlMeNAOVN | Ole se ere eee CAS JET OVERELE ope 74 GONE) NCO FSB AE ea msc 359 Pure-pred hogs; Number oie 23 Fz Viel OTE | MW Sense ease ee ena eee 187 Py emilee arth nbig2: coe eae haere eee 214 PyOsalpinxe ssh oe oe ee ee ee 201 QirarantineeaVialue Olas 44. ] R21 0 Vetere seco ire Aeon Peer aca nee 339 Rvalchitiss 5 oo. 2 ee ee ees 216 Rec tn e.0 lays ClO eee eee ee ee 125 Vemealescall ull. 22s eo sae eg ere eee 180 ) ACERS ONE (0) Che eee ire Ree eae eae eee 147 Respiratory disease, How recognized... 49 IVES tala Of, pS © eee eae ee eee 56 Fe Eee lito) elite aes eee ene ees 213 Euine Uninet GS tne ACT CU aise me eee eee 230 Runeumnaitisms. Mis ctrl eee eee 229 IRI mbar, (Caieiedme il 8 oe 149 IMO UME OIG ee ee eee 150, 223 FURIES SINC CrO ULC wee eee eee 320 RICKGuS secre. pete eA ot SEP AR OMe REM ee 216 Ringworm ............ sida Baa cess Beane ees ee 255 FUP EU CEtOTh eiMlivi Gye sesece ee neers sh eeepc eeeeee 127 Salivary glands, Anatomy of.................. 65 Salmonellosis. s2. = ee B25 anitation( «22-21-22 37 Sarcocystis: miescheria saa 240 Sarcomatosis «24.2.1... 85 262 Sarcoptes: Scabiel s= == =e 249 Sarcoptic mange! ee eee 249 SA COSPOLIGIOSIS see ees eee 24.0 Sclerosis - -.1.-5:6 3 135 Scour SCOUr MNs Pigs... oe 220 SCrEW= WOT My cis eee erie ene 198, 351 Serew-worms in the prepuce................... 199 Scrotall *iernla® = ee 352 DCUPVY i eee te Se a ee 81 Self=feedersic. 5442 eee S2a ee Septicemia,, Elemorrhacic 2.22 = see 301 Serum; ‘Clear.2.25.220- 4 ee 295 Serum production, Anti-hog cholera....293 Siphonaptera -3..5 ee 248 Skin. Convestion) Of AT Skins Hireezing- sof =22= se eae 242 Skin, Hemorrhage from: theses 242 Skin; Inflammation: of eee 245 Skin Imijunies to) ee 241 Skin. Parasites 1.5.4.2 246 Skane dumors! (of theses. nee 245 Sniffles 2.22.42 223 Snout, Anatomy Of == 146 Sodium chloride poisoning... 109 pore; feet... ee 228 Sore Mo wWth Ins Pls S— ee 225 SOWsn So odessa een ee. 15 Sow, Genital! (organs) 0f-= === 175 Sow’s milk, Composition of... 176 SOW Soul ume c ll Oye ee eee. 18, 89 Sows, Unsexing. =. 356 Spasm of the diaphragm: 171 Spaying: 222.2) 5. ee a 356 Spinal cord, Malformation of............. 263 Spirocheta: (SUIS) G2... = ee 275 Spleens rlypertrophiyas 0 tase 261 Spleen, Necrosis of Spleen, Tumors of Splenitis, Necrotic Stenosis of tke brenchis == een 154 Stenosis of the esophagus -........._.__- 86 Stenosis) of the tracheaz === =seaeen 153 SLephanumOsis) eee 138 Stephanurosis, Pulmonary -..........---.-- 168 Stephanurus) demitertuy eee 145 Sterility. (Causes) otis sa eee 212 INDEX Bic Su@milliay, Iker, Ol ose eee 212 Senility OCCURRENCE Of meee eee 212 Shige Sygaay oO ONE ste 212 SLecoilhy, Dreatment -Of- <2 aes 212 Su@@ls Inomcy (CAS Nike eee ees 20 Stock hogs, Immunization of... roll Shock shoes. OCleChion) Ofte seen 21 Diockshoess Slime nite Ole gee eee 20 SlomlachyeAmeatowniys Oh je ee a (LY SHOMMACH A MMETINTAN Oilew eeccee oreo eee 92 Sfomachss Dilatation vols ese ane 98 Stomach, Foreign bodies in... 90 Stomach, Hemorrhage of - 2. 92 Sii@anedn, lealyoenene) Ol eee 94 Stomach Inflammation of = 94 Stomach, Malformations of --................. 90 Stomach. earasites, Of 22.2. 100 SOMME Chee OT: Sie Oke eee eee eee 99 SMO TUE EI OSS ee ee eee 79 Stomeatibiss @atarmlals 2 eo eee 80 Stomatitis im Sucklings =.202.2.2- pereacahs 225 SOMA bLSy UNECROLIC= 2.8 tee 81, 319 SOMA uUulSsn kM OMROWOUS eons en eee 80 Syeoramancnmersy LOM Cera a Ne see eee ee 81 SOM AUbIUIGsmVReESTC@ IAI eee see ee ene 81 Sirickiuneroh tine juiretinital: nee ee 195 Strongylosis of the bronchi —................ 156 Sironewlosiswonathe umes, =e 156 SUG MIM ce SO LOUIAbILIS ieee eee 225 (SULIT ONT eae ie ee eee 241 SHOUTS” see ee eee a ee 264 WINE ME SIP elas esters fae ete tae meee 338 SHINS ]OUGTUES oe Beene eee eae 22, 301 Swine plague, Symptoms of_—._...-..-..-..- 23 Swine estrella. ee eee eee 56 SWIRLS aeeEMEDMO Valle (Ole es eee 357 Taenia Echinococcus -.... 140, 144, 168, 190 TP AGVMM) TONE EAT ETEEY seeeeee eeemeer es cooerenrrs eee are 141 MaeiiamsOliumy feet en ee eee 190 “JUPAS COE = Sa ee ner eee 30 ANSSW ok, LOPE WOMB LOT OSE | eee seeree eetoreereemeeeres 67 TNE Oy Dn TOWNES Oe ee comer 82 Mecth ye lnneoularities| Of ese 82 Temperature, Variations of_............... 48 Mesticless Inflammation of -22-2--.--+--—-—- 197 Testicles, Malformations of ......-----..--.- 196 hesticless seanasites! vom tne 198 BES tL Cuil ents UUUNNN OS) ee eee eee eee 197 UVENEENINTG) a oe ee se cee ce Re 343 INGUIN CH ae ene ea eos basic: eee eee er ec ane ea eo 171 Thread worm infestation of the skin_..255 Thymus gland, Anatomy of...........-.---.-- 147 Thyroid gland, Anatomy of .-.....-....-..---- 147 Thyroid gland, Defective development OES eat ie eee arenes: (A ar 19 Mick= ames tarblomy 2scceseee ete eee seme 255 Mongues Anatomy (Ole sees tee ees 65 Mongue, Horeign bodies inte 17 Mongue) Inflammation: of 222. = o> 77 ALORS; MOONE) OE beaten eee cece ia Monpue, Parasthes Ob ses cence eee 19 BOTH GAUL 12S ak © nee ene 78 MonSillittis eee ee ee eS 83 Ronsils., Imiflamammnrtionm (Of =e 83 Mracheake Aum ait OmniyasOteeess eee 147 Trachea, Malformations of -..--.........--.- 153 Mrachedse SueMmOS 1S. fesse ects eee ee eee 153 itera Ine alls tna ONS) eeeeseee eens ene 153 STACH ew Spe eee bento ea ee VORA Centers ts 153 Miracheitiss 1. @roupouss ne 152 Giichinellae soit lis tees renee 121, 234 GMB Tei @ EMINO SUS tie soe eee se eee eee 233 ATIC O WELZ O ATS. ese ase eee ee eee ere 90 Trichocephalus crenatus —-...... era 7-10) Timmmnores Git Ware lowe Vel -25..2- ee eet 195 Mumerscok the esophapusyges se 89 (ummorseote bliee Ine alts tenes eee 258 ARwTTV OTE, ina ers ere eee ee ce cacteceoeneece see 122 AD pORTOIES, GE TOE RCIA eee eee eects 190 PRIM OTS 20 fast hie wil eats vill Koes eee 153 AUiWaYOTES Cat Wve Whos et cree 76 abruiianvonns. Ge wove: WNW Se eee oe ree teas 137 AMP imams; Thm Wave) WbeMerS teen eeeneeccee sss 167 AETVOMSs Nia allie see ieee Bete eee cenee 151 (OTTUENOTES Oil WEY OBI eae o oa eee eee 201 TES TUIVOS spe ky OTs Gay Clee ee 258 Tumors of the peritoneum —--....-.....--- 144. TMMMMIKOVES, OE Woe PON AT | Sea see cee cere 86 WDiwUeRONESS Gi TH ove [ONS WIRRY eee eee eee 171 SDS TONGS tO eee LS cl Meee ee eee 245 TMUMORS Oi Wie SOMES soe eee 262 Tumorsvot tne stomach) lee s-cee se -- 99 eM UMNO Ss Oleeble mbes (iC @S)y ee eeeen ee seeere ee 197 AM UOT OTS OH THOS, WOM ee cee eee 78 SUMTOTSs Ofeiiies bach ease se see ee 153 (bina ONES OE WO) CMC eee 208 AMOR OIF NE TAKEN) a ooo 204 ANU OESRGWICETS cece edeectenerecetere rend teceeceenoetceee 329 Tuberculosis, Prevalence among swine_3s0 Dui oyerecerull GSES Che Ove Wee (olor ee eee 208 Od ders etlumia Ons inohe eee ne et nee 208 UW Cees ren es arts Teer eee 312 a4 INDEX Wil eros iG tice eae eee 93° Vagina, Inflammation» of 225s 204 Urachus, Persistent 27 ee OVA” Vagina, Injuries, toy 22202 eee 204 Deine ran ete reece ed Peer ee 188 Vagina, Malformations of the... 204. Ureters, Malformation of ...............----- 191) | Waginal necrosis 222). 822 Urethra, Inflammation of ...............--— TOS, — Walginttis” 224s ee 204 Wrethra, Injuries sof ‘thes. -= 2 195°. Valvular insufficiency, eee 260 Urethra, Malformations of the ........... 195) Ventilation: 22 22 = eee 41 Wirethray ourichume sof etinesesee 195 WierMINOUS) PMEUNTO Na yee 307 Witethritise ee ee ee ee RQ = WACIQUSNESS | . Mick Bie waulvia.) Necrobacillosisi oi ees =e 204 Wirkicaring =e re ee en naka, D4) OVaw VET ATCCKOSIS ese en eo ee 322 Witerimes hemorrhage yy esse eee 202 Wiberin Ge bUNDOGS) eee ee eee ee D0dr Watt): 2225.2 Ace eee eee 245 Witerusss UntlanamMationl Ot eee PADRE AVIS ewMIN ME, NPE) TOPs ances tree tcnecec osteo 19 iter See lmyjunse Sa bomb ie ee een ee eee 201 Witeruss. VMaltormablons mot eens PANT NEO avis Aor Maneater ences 30 A seater teem BNW or ee Te sh f ) in * i i f ae, 7 ga a EA