fLIffiA SS I s©2H 1 IV If 1 /Mft^fr November, 1970, Montana Fish and Game Department Official Publication Information-Education Division Digitized by the Internet Archive in 2010 with funding from Montana State Library http://www.archive.org/details/montanawildlifenov1970mont Montana Wildlife STATE OF MONTANA Governor Forrest Anderson Fish and Game Commission CHAIRMAN— Hugh G. King VICE CHAIRMAN— Joseph J. McCaffery MEMBERS— Raymond E. Clausen Joseph J. Klabunde Patrick J. McDonough Department Director Frank H. Dunkle Edited by VERNON CRAIG k&mim /■-• j*& 8 ^V k^™s '**''wh&attek■*■x Featuring Tularemia In Montana by — Doctor William L. Jellison Turtles of Montana by — Jeffrey H. Black Series 2 of Montana Animals INDEX TULAREMIA Tularemia in Montana 6 History in Montana 7 Epidemiology in Relationship to Certain Animals 8 Epidemiology in Relationship to Certain Montana Animals 10 Epidemiology in Montana 12 Probable Number of Cases 14 Tularemia in Sheep 15 Two Kinds of Tularemia 17 Tularemia in Semi-Aquatic Mammals and the Presence of F. Tularensis in Water.... 19 Tularemia in Other Animals _ 22 The Human Disease 22 Tularemia and Plague 22 Bibliography 24 i ■ 0 r jTg^v 1 y^RHS '"--. "' \H JB 35 1_ ■ -^ j * i * , '% * L *x?^l ^frr - ^k M TURTLES Turtles of Montana 26 Common Snapping Turtle 27 Western Box Turtle 28 Painted Turtle 29 Western Spiny Softshell 30 About the Authors William L. Jellison is a native of Flathead County where he attended rural school and high school. He is a graduate of Montana State University. From 1929 to 1962 he was a member of die staff at the Rocky Moun- tain Laboratory and engaged in laboratory and field studies of many diseases including spotted fever and tularemia. His work at Hamilton has been interrupted many times for graduate study, military assignments and expeditions to Burma, China, Alaska, Korea, Europe and Argentina. He retired from the U. S. Public Health Service in 1962 but has remained active in scientific work, civic affairs, teaching at die University, and maintains the Ricketts Memorial Museum at Hamilton. Doctor Jellison had tularemia in 1930 and spent die 4th of July and 16 more days in die Hamilton hospital. Besides contributing almost daily blood samples for lab- oratory tests, he was set upon several evenings by cages of hungry mosquitoes in order to determine if they could pick up infection from a human case. Jeffrey Black, now completing Doctorate work at the University of Oklahoma, received his Bachelor of Science from Oregon State Uni- versity. He worked two years on his Master of Science Degree at the University of Montana, Missoula. While in Montana, Jeffrey Black traveled more than 40,000 miles to collect information and specimens. He autiiored "Amphibians of Montana," a MONTANA WILDLIFE issue which featured the first in a series of Montana animals. Martin Nolan, Rocky Mountain Laboratory technician who died of tularemia in 1931. - *A TULAREMIA IN MONTANA The Rocky Mountain Laboratory (RML) of the U. S. Pubhc Health Service at Hamil- ton, Montana, has been a center of tularemia research for about 45 years. Montana with its diversified avian and mammalian faunae has been an excellent area for field and epi- demiological observations and these have been supported by intensive laboratory studies. Case finding has probably been more thorough in Montana than in any other state. As a result of these studies both the incidence (rate per 10,000 population), 8.5, and actual number of cases, 576 recorded for Montana, are high in comparison with those of other western states. This combination of circum- stances has resulted in considerable advance- ment of our knowledge of an interesting and highly infectious bacterial disease of man, domestic animals, wild birds and wild mam- mals. The first few papers on tularemia were concerned with its presence in ground squir- rels in California. Ticks were in no way associated with the disease; however, in the RML, which specializes in the study of ticks and tick-borne diseases, it was inevitable that we became involved in tularemia research. ,'i ■■<%: ■**b*v^ / About 90% of all cases of tularemia in the United States probably comes from direct con- tact with rabbits of some kind. We now know that ticks of several species are frequently infected with the causative organ- ism, Francisella tularensis, and in fact are probably the most important vectors among the many arthropods known to carry the or- ganism in nature. Dr. H. E. Lamb of Gooding, Idaho, gave a talk in 1923 on what he called "Glandular type of tick fever" and which he supposed was an unusual manifestation of spotted fever. His patients had been bitten by ticks and lesions developed at the site of tick attach- ment. The symptoms and lesions he described were recognized by Dr. R. R. Parker and his associates at Hamilton, as suggestive of tula- remia, a disease described and named by Dr. Francis in 1921. By serological tests it was soon demonstrated that Dr. Lamb's patients had been ill with tularemia. This gave a clue for the identification of one of the undiag- nosed infections observed in the laboratory animals used for testing ticks. By cultural studies it was soon proved that some of die test guinea pigs and rabbits were dying of tularemia (Parker, Spencer and Francis, 1924). From here on tularemia research was an im- portant part of the RML activities. HISTORY IN MONTANA Outstanding episodes of tularemia in Mon- tana because of their historical significance, economic loss or scientific interest are many. Some of these will be discussed in greater detail later. In the early days of study, many labora- tory workers became infected. During 1924 and 1925, six members of professional and technical staff, including the Director, at the Canyon Creek Laboratory, Hamilton, con- tracted the disease and were seriously ill. Three were ill at one time. Presumably these three became infected when ticks were being removed from an experimental rabbit. One man was only an observer at the operation. This pattern of infection has occurred at nearly every laboratory that engaged in tula- remia research in England, Russia and the United States. Before the development of an effective vaccine, practically everyone ac- tively engaged in tularemia research became infected and there was at least one death. Sixty-five laboratory cases were recorded by 1951 (Sulkin and Pike). An epizootic in sage grouse at Roy, Mon- tana, in 1931, was associated with heavy infestations of bird ticks, Haemaphysalis cin- nabarina. An epizootic is an outbreak of dis- ease in animals. Tularemia was present in the grouse and ticks and may have been a major cause of fatalities. H. cinnabarina is not usually an abundant tick in Montana. In 1931, Martin Nolan, a laboratory tech- nician at Rocky Mountain Laboratory, died of tularemia contracted in the laboratory. In April and May, 1934, an epizootic occurred in sheep at Ringling, associated with heavy infestations of wood ticks, Dermacentor andersoni. Over 400 sheep were affected and 200 died. Tularemia was also diagnosed in jack rabbits in the area. There were no human cases involved in this episode, at though men were employed in picking ticks from sheep, dipping and even skinning dead sheep. Blood tests indicated none of these men were immune or had experienced previ- ous infection. A widespread epizootic in beaver and muskrats throughout most of Montana and several other states lasted from 1939 through 1943. Many human cases resulted from con- tact with these fur-bearing animals. A study of this outbreak resulted in the first isolations of F. tularensis from water samples in North America. The first isolates came from ponds along the stream bed on the Musselshell River near Roundup. A case of intense and persistent septic sore throat with systemic illness near Bozeman was diagnosed as anginal form of tularemia and was attributed to contaminated food or water. A study revealed three other similar cases associated with the same rural, domestic water supply. F. tularensis was isolated re- peatedly from the kitchen tap. These were among the first and the most definite cases in North America attributed directly to water, although hundreds of cases in Europe and the U.S.S.R. have been attributed to water- borne organisms. In May, 1964, a dramatic outbreak of dis- ease in mature cattle and calves associat- ed with heavy infestations of wood ticks, D. andersoni, occurred at Big Sandy. Tick pa- ralysis affected most of the animals but a diagnosis of tularemia was established in two sick calves and in three lots of ticks from three calves. At least 30 mature animals were affected and we were informed 12 cows and four calves died. Losses were accentuated by severe storms which further weakened the animals and handicapped rescue and care of animals out on the range. We had studied severe outbreaks of tick paralysis in cattle and of tularemia in sheep but both diseases appeared in this epizootic. Concurrently with the epizootic in cattle at Big Sandy, May, 1964, and during the same storm, severe losses and illness in young lambs and ewes and many abortions were experi- enced on numerous ranches near Jordan. The sheep were heavily infested with wood ticks, D. andersoni. F. tularensis was isolated from one dead ewe and tularemia was diagnosed in many convalescent sheep by the agglutina- tion test. Some sheep were apparently affect- ed by tick paralysis only. Ranchers in the area later provided the following estimate of losses: lambs — 991, ewes — 824, yearlings — 108, and bucks — 4. —7— Male Female Rocky Mountain wood tick, Dermacenlor andersoni, an important carrier of tularemia in nature. Since the first studies on tularemia in sheep in nature by Parker and Dade (1929) there has been confusion between tick paralysis and tularemia in these animals. In all sheep epi- zootic studies where I have participated, tula- remia appeared to be the main cause of dis- ease but in the Jordan outbreak there were certainly some cases of tick paralysis. Tularemia was demonstrated in one mare and five foals near Belgrade by Claus, New- hall and Mee (1959) of the Veterinary Re- search Laboratory at Bozeman and the Veteri- nary Hospital at Belgrade. All animals were heavily infested with D. andersoni. Two foals died and F. tularensis was isolated from their tissues. The mare and three surviving foals had received antibiotic treatment. This appears to be the first and only report of tularemia in horses in North America. EPIDEMIOLOGY IN RELATION TO CERTAm ANIMALS In 1945, Jellison and Parker published a paper which attempted to clarify some of the concepts about epidemiology of tularemia. Until that time and in many instances since 1945, practically every general paper on tula- remia defined it as "a disease of wild rodents transmissible to man." Technically this is only partially correct. For a long time zoolo- gists classified all the rabbits with the rodents but in a separate suborder. Zoologists are now in general agreement that the rabbits deserve a separate order, Lagomorpha. Rab- bits are as distinct from true rodents, such as rats, mice, porcupines and squirrels, as they are from sheep and cattle. They differ from the true rodents in arrangement of teeth, bony structure, internal anatomy and biology. They also differ markedly in their parasites, diseases and reactions to diseases. Available statistics (1945) showed that about 90% of all cases of tularemia in the United States came from direct contact with rabbits of some kind. Therefore, it would be more accurate to state "tularemia in North America is primarily a disease of wild rabbits and to a lesser extent of wild rodents and is transmissible to man." Quite a few cases do come from contact with muskrats, beaver, ground squirrels and tree squirrels which are true rodents. Parker further emphasized rabbits it is the cottontails, that are the principal source of infection. By a series of maps it was clearly demonstrated that there is a close relationship Jellison and that among the Sylvilagus spp.. between the geographical distribution of cot- tontails and that of tularemia in all of North America. No comparable geographical rela- tionship is recognized for any other kind of wild rabbits. Domestic rabbits are unimpor- tant as a source of human infection in nature. In 1945 records were available for over 14,000 cases in the United States and only 38 or 39 for all of Canada. The northern limit of cottontail distribution closely follows the Canadian border from Washington to New York. Tularemia was conspicuously ab- sent from New England and the Pacific Northwest, west of the Cascade Mountains. Cottontails are rare or absent in these areas. In central states where there is the greatest concentration of cases, no other kind of wild rabbit is present. ® m I \S •Vj Among Ihe rabbits, il is the cottontails that are the principal sources of tularemia infection. Map below shows distribution of certain cot- tontails in North America — from Hall, 1951. Fie. 39. Distribution of Sylvilagus nuttalM, S. floridanus and S. ins onus. Guide to kinds: ■ 9. S. /. hitchensi 18. S. f. orizabae 1. S.n.nuttallU 10. S. f. floridanus 19. S. f. connectent 2. S. n. grangeri 11. S. f. ammophlltu 20. S. f. russatus 3. S. n. pinetis 12. S. f. coenatus S. f. robustus 21. S. f. aztecua 4. S.f.similis 13. 22. S. /. chiapensi* 5. S. f. mcamsi 14. S. /. chapmani 23. S. f. uucatanicus S. f. hondurensU 6. S.f.Uanentit 15. S. f. holzneri 24. 7. S.f.alacer 16. S. f. restricttu 25. S. f. costaricensit 8. S. /. mallunu 17. S. f. subcinctus 26. S. insonut The periodic, dramatic die-offs of snowshoe hares are well known, but it has never been proven that tularemia is an important factor in their "cycles." There is a group of rabbits present in southern and eastern United States known as swamp rabbits, subgenus Tcrpeti of the genus Sylvilagus, whose role in the epidemiology of tularemia has not been determined or record- ed in the literature. By 1945, about 50 of the 14,000 cases had been attributed specifically to contact with jack rabbits. The organism has been isolated from sick and dead jack rabbits which prob- ably are an important source of infection for ticks and deerflies which carry die disease to man. Tularemia may be a very important fac- tor in the ecology of jack rabbits, especially at times of widespread epizootics, but we have yet to study such a die-off in which tularemia appeared to be a significant cause of mor- tality. Aldiough intensive studies have been made on snowshoe hares in the United States and Canada, it has never been proven that tula- remia is an important factor in their periodic die-offs and snowshoes are unimportant as a source of human infection. Clinical cases from rabbit contacts are still uncommon in New England, Canada, and Alaska where snowshoes are abundant and are shot and trapped by the millions for human food. EPIDEMIOLOGY IN RELATION TO CERTAIN MONTANA ANIMALS The distribution patterns for rabbits re- ferred to previously have some application to Montana, since we have all three types, cot- tontails, snowshoes, and jacks, within the state. Snowshoes are present in the western half of the state, mainly in the mountains, and in the northeastern corner; cottontails appear to be present in every county widi the possible exception of those in the northwest corner of the state; jack rabbits are widely distributed in Montana but also seem to have been absent from the northwest corner, al- though there are recent records for Fladiead County by Hoffman, Wright and Newby (1969). As a native of the upper Flathead Valley, I would say cottontails and jack rabbits were not indigenous to Flathead and Lincoln Coun- ties or to the western part of Glacier Park. The northern limit to their distribution west of the Continental Divide appears to have been about St. Ignatius, Post Creek, Charlo, Moiese and Hot Springs. A field party from RML collected a specimen about two miles north of Moiese, October 16, 1944, and they are present around buildings on the Bison Range at Moiese. Tularemia cases are conspicuously rare in Flathead and Lincoln Counties and Glacier Park, west of the divide. Laboratory records show the five cases recorded for Flathead were in 1924, 1; 1945, 2; 1950, 1; and 1951, 1. The three for Lincoln County were 1952, 1; 1955, 2. It is possible some of diese were contracted elsewhere. About 1945, cottontails appeared in the upper Flathead and were frequently seen on our ranch at LaSalle. An adult specimen was collected there by Charles Jellison in Febru- ary, 1945. It was rumored that a shipment of cottontails had been brought into the valley and liberated by sportsmen but this is not documented. Cottontails are now common on Angel Point, near Lakeside, and possibly, other places in the valley. This population may represent an extension of their range northward from Lake County or, possibly, intentional introduction. I do not know of any record for Lincoln County although I have made inquiries on this subject. I found a freshly dead young rabbit near the Flathead River on the home ranch at LaSalle, September 9, 1937. It exhibited le- sions on the spleen and liver suggestive of tularemia and tissues taken to the RML yielded cultures of F. tularensis. I was never —10— (N) = TOTAL CASES _N. - CASE RATES PER 100,000 PER YEAR Tularemia cases and case rates by Fish and Game Administrative Districts, 1925-1964. (From Philip, Casper and Lackman, Journal of Infectious Diseases, 19G7.) certain whether this was a young cottontail or a snowshoe, as it was in summer pelage. As far as I know, this is the only isolate of F. tularensis from any source in this northwest corner of Montana. Muskrats and beaver are abundant in Flat- head and Lincoln Counties. I can see no reason why tularemia should not be as prev- alent in beaver and muskrats in Flathead and Lincoln Counties as it is in Lake, Missoula, and Ravalli, since this form appears to be entirely independent of cottontails and ticks. An outbreak of tularemia in beaver and musk- rats was reported in Waterton Lakes National Park, Canada, just north of Glacier Park, by Langford (1954). We did study one outbreak of disease in beaver in the Whitefish area, Flathead Coun- ty in 1961. Many fresh carcasses and fresh hides were examined and tissues were tested in laboratory animals. Skin abscesses and damage to pelts were more prominent than fatalities. We found no lesions characteristic of tularemia, failed to establish tularemia or any other infection in laboratory animals, and we did not arrive at any satisfactory diag- nosis. The winter weather had been exceed- ingly mild in the area and may have had some relationship to the outbreak. (Reported in Daily Interlake, Kalispell, April 4, 1961.) The belief persisted that this was an outbreak of tularemia regardless of our studies and re- ports. Several of us engaged in the study had just participated in field and laboratory work on an epizootic in field mice in Oregon, where 187 separate isolates of F. tularensis were established, so we were not unfamiliar with the disease and organism. Hunters, trappers, ranchers, county agents and game wardens are valuable sources of information when one is investigating animal diseases. They are often keen observers and in close contact with nature. However, their interpretation of what they observe is some- times erroneous. In this respect they do not differ from "scientists and experts." If one is interviewing hunters and trappers regarding diseases in animals, one standard reply is, "Oh yes, I recognize tularemia in a rabbit when I see it. It produces large water blis- ters under the skin." This just is not so. The large water blisters under the skin, in the flesh or among the visceral organs of rabbits are larval stages of tapeworms of seveial species. These develop into typical tapeworms in the intestines of coyotes, bobcats or other wild and domestic carnivores. They are not usually harmful to the rabbit host. The characteristic lesions of tularemia are small to medium greyish-white foci on the spleen and liver and sometimes on the lungs of infected animals. There are several bac- terial diseases that produce lesions so similar to these that they cannot be distinguished —11- Characteristic lesions of tularemia on liver (above) and spleen of laboratory animal. with certainty even by a laboratory worker with much experience. Demonstration of the organism in microscope slides aids in diag- nosis but is not definite. Confirmation can be established only by isolation of die organism in culture, eidier direct or after animal pas- sage. In many animals, including wild mice, birds, carnivores and sheep, the lesions are in- distinct and even presumptive diagnosis is difficult. Animals found dead in nature or those obviously sick should be regarded with great suspicion and contact should be avoid- ed except to dispose of the animal as safely as practical or else saved for laboratory ex- amination. EPIDEMIOLOGY IN MONTANA The best summary of tularemia cases in Montana was presented by Philip, Casper and Lackman (1967) from records of the Rocky Mountain Laboratory and the Montana State Board of Health. Data were avadable for 576 cases that occurred from 1925 through 1964. Most of them (87%) occurred in the southern half of die state. About 50% of the cases were in 11 southeastern counties of the 56. These cases were separated into two groups on the basis of source of infection: Ticks, rabbits or sheep were responsible for 326 or about 82% of the 400 cases where source of infection was known. Muskrats, beaver or water were responsible for the re- maining 18%. In Western, Middle, and Eastern Montana there is a decline in cases from south to north with the conspicuous exception of Garfield County, which is about in the center of the state. This decline is less marked in the west, where infection is often attributed to muskrats and beaver, than in the east, where infections are caused by contact with ticks, rabbits, or sheep. In a map prepared by Philip and Casper (1969) 14 counties have an annual case inci- dence of over 0.5 per 10,000 in the years 1925- 1964. Twelve of these counties are in the southern half of Montana, the exceptions being Petroleum and Garfield in central Mon- tana. Not a single county in the northern tier of states has such an incidence of 0.5 or over. I would associate this case distribution to the abundance or scarcity of cottontails, whose nortiiem limit of distribution approximates die Montana-Canadian border. Cottontails cer- tainly decrease in abundance and in territory occupied as they approach tiieir northern limit of distribution in Montana, but this is not documented with reliable statistics. Such a relationship between cases and cottontail dis- tribution was indicated in a series of maps by Morgan (1949) for Wisconsin and by Yeatter and Thompson (1952) for Illinois. DECLINE IN CASES FROM SOUTH TO NORTH BY COUNTIES SOUTH Ravalli— 13 Carbon— 14 Carter— 12 INTERMEDIATE NORTH Lake — 5 Flathead— 5 Lincoln — 3 Wheatland— 3 Judith Basin — 1 Hill— 3 Fallon— 15 Wibaux — 0 Richland — 1 Sheridan — 0 —12— 40 -i 30 - UJ 20 o or UJ 0_ 10 - o -J TICK- BORNE TULAREMIA WATER-BORNE TULAREMIA uliu r>cn 2 UJ < 5 Tularemia, Montana, 1925-1964. Percentage distribution of cases by probable source of infection. | ] LESS THAN 0.5 Average annual tularemia case rate per 10,000 population, Montana, 1925-1964. (From Casper and Philip, Public Health Reports, 1969). —13— PROBABLE NUMBER OF CASES We assume that there are many cases of tularemia that are not reported to health of- ficials and do not get into the records. There are certain ways of projecting sound statistical data to support this assumption. Whenever a few cases are reported in a limited area by physicians, an epidemiological study and interviews with physicians and patients usually identifies additional current cases and others that occurred many years previously. In early years it was obvious that more cases were reported in states or around cen- ters where there were active research projects on tularemia such as Ohio, Montana and Washington, D.C. Although epidemiological reporting has greatly improved, this still may be true not only of tularemia but other dis- eases. In a distribution map prepared by the U. S. Public Health Service and published by Simpson (1929) recording 806 cases the lead- ing communities were: STATE CASES 1 Ohio 92 2 Montana 66 3 Tennessee 51 4 Washington, D. C. 45 5 Missouri 39 6 Mississippi 39 7 Illinois 38 This was greatly changed by 1948 when a map published by Jellison, Owen, Bell and Kohls showed the eight leading states were: STATE CASI 1 Illinois 2905 2 Ohio 1478 3 Arkansas 1407 4 Missouri 1396 5 Virginia 1363 6 Kentucky 1315 7 Georgia 1189 8 Tennessee 1101 Montana ranked number 22 with 354 cases. By 1955 there were records, based on physicians' and State Health Department re- ports, of 64 cases in sheep-shearers. Extensive surveys of sheep-shearing crews accompanied by interviews and blood samples identified 31 cases. Not one of these had been reported through regular channels. Had three or four of these been included in both records, it would have given a basis for calculation (Lincoln Index) of the probable total cases in shearers. As another example, Casper and Philip (1969) made a special study in Garfield Coun- ty, a large area of sparse population, about 1,981 people, which has reported 58 cases of tularemia. This is more than any other county except Rosebud (62 cases) which is immedi- ately south of Garfield. Third in number is Powder River (30 cases) in southeastern Mon- tana. Most of the cases in Garfield County have been reported by Dr. Ferrand, County Health Officer, a long-time resident of the County Seat, Jordan, the only physician in the county and one who has been familiar with the disease for many years. Following the 1964 epizootic in sheep and concurrent cases in sheep industry workers, Casper and Philip presented the following statistics: four of the 12 patients did not seek medical care and would have been missed ex- cept for the intensive survey. In a skin-test survey, 24 persons were found to react to F. tularensis antigen and only four of those had been diagnosed previously. These authors concluded, "If the population tested was rep- resentative of the total population, the true incidence of tularemia infection in Garfield County was five times higher than reported." With the advent of effective antibiotics for treatment of tularemia it is reasonable to as- sume that case reporting is even more neglect- ed by physicians. A recent report (Anon., 1970) from the Public Health Service, received while this manuscript was in preparation, gives the fol- lowing information. For the nine-year period, 1960-1968, a total of 2,594 cases of tularemia were reported in the United States. During the eight-year period, 1960-1967, 23 deaths attributable to tularemia were re- ported for a case fatality rate of 0.96 per cent. In the decade prior to 1946, the case fatality rate had been 9.5 per cent. The decline in mortality probably reflects both the decline in morbidity and the avail- ability of streptomycin after September. 1946 —14— TULAREMIA IN SHEEP Among the more spectacular manifesta- tions of tularemia are the occasional devastat- ing epizootics in domestic sheep that have been observed in Montana, Idaho, and at least once in Alberta. Practically every outbreak has been studied at the RML, and all of these have several features in common. The sheep are out on range land in early spring, they graze through an area where wood ticks are abundant and pick up a heavy infestation of ticks. Presumably, an epizootic of tularemia has been present here in rabbits the previous summer and left behind a large number of ticks infected with very virulent strains. Within a few days sheep start dropping out of the band, sicken and die. By this time the band may be miles from the real tick-infested area. Within a few days, half the band may be sick and 10% will die. Prompt attention with manual removal of ticks, dipping, spraying and dusting along with supportive care will save many sheep. In one instance antibiotics were administered with apparent beneficial effect. Adverse weather conditions which are frequent at this time of year complicate the situation and lead to losses of hundreds of animals. According to the few laboratory tests that have been made, sheep are quite resistant to tularemia infection but a combination of heavy infestation with ticks, many of which are infected, reduced vitality after a long winter, shortage of feed and early spring storms seem to overcome this natural resist- ance. Very sick sheep may respond to tick removal, food and shelter and eventually re- cover. Loss of a few range sheep in the spring of the year, especially at lambing time, out of bands numbering in the hundreds or thou- sands does not attract particular attention. Possibly many of these sporadic losses are due to tularemia, but we have little information on this point. When a real epizootic strikes, the loss is too serious to be overlooked but in some instances information on such outbreaks has been weeks or months in reaching our laboratory. Whenever practical, an immedi- ate on-the-spot-study has been made. We Sick animals left behind from a band of sheep near Ringling, 1934. About 200 sheep died of tularemia. —15— have been aided in these studies by the fact that die agglutination reaction is very persis- tent in sheep and a reasonably certain diag- nosis can be established in surviving animals months after the epizootic. Serological tests were used to study several epizootics in Idaho and in the 1964 outbreak in Jordan. Before shearing, convalescent animals may also be conspicuous by severe damage to their fleece. Severe illness of any kind causes a "break" in the wool and part or the entire fleece may be shed. A broken fleece is only an indication of illness, which may or may not have been tularemia. It is understandable that sheep owners who have had experience with quarantine and enforced dipping are reluctant to report disease to health or veterinary authorities, but in the case of suspected tularemia prompt re- porting and diagnosis could help to avert serious losses. We have also experienced some reluctance among biologists, game managers and wild life administrators to report animal disease in their jurisdiction. Up until 1955, we had records of 189 cases of tularemia in people associated with the sheep industry. At least seven of these were fatal. This included herders, owners, and shearers. It was quite conspicuous diat none of these cases in the United States and only one in Canada were associated with acute outbreaks in sheep. At such times men are working picking ticks by hand, dusting, dip- ping, or spraying the flock, treating sick animals and even skinning the dead ones and so are grossly exposed to infection. We have no explanation for this apparent lack of trans- mission. However, in the 1964 epizootic at Jordan, Garfield County, there were at least 12 acute cases among those employed in the sheep industry. Some of the sick owners and herders were trying to treat and care for their flocks during the storm when they should have been in the hospital. A summary of our studies on tularemia in sheep was published as a Public Health Monograph in 1955 (17 pages) and copies arc still available. TWO KINDS OF TULAREMIA The epidemiology of tularemia was greatly clarified when research workers at Hamilton •••< Pelts, carcasses and sick sheep at Ringling epizootic, 1934. —16— v>JIHflHII^HI Lamb with badly broken fleece after recovery from tularemia. and in Russia reached the conclusion that there are at least two distinct kinds of tula- remia. These two differ in mode of transmis- sion and virulence and the respective causa- tive organisms have minor cultural differences. One kind is associated with rabbits, is fre- quently transmitted by ticks, is more virulent, is the common type for human infection in the United States and insofar as we know is limit- ed in distribution to North America. This type in man was 5% to 7% fatal before- effective antibiotics became available for treatment. The second type is mainly associated with true rodents (order Rodentia), i.e., muskrats. field mice and beaver in the United States and Canada and with water rats (a small muskrat like mammal) and mice of many lands in Russia and Siberia. It is also associated with hares and rabbits in Scandinavian coun- tries, continental Europe, Russia, and Japan. This kind is of lesser virulence, is rarely or never fatal to man, and is highly fatal for rodents, oft^n appearing in devastating epi- zootics in muskrats, voles, beaver, and water rats. It is sometimes transmitted by ticks and * *£ ** ft* z ^V **A -^ ' 1 Km. Tularemia organisms, small dark bodies, and red blood cells, large white discs, in blood smear from a vole, Microtus montanus. —17— is frequently associated with water where it appears to be independent of arthropod trans- mission. During epizootic periods and fre- quently in the absence of any observed mortality in animals, the organisms can be isolated from water of streams, ponds and rivers by injection of samples into laboratory animals. We assume wild animals become infected from the water and also by canni- balism. The Russian scientists have proposed sepa- rate subspecific names for the organisms causing the two types, Francisella tularensis tularensis, the North American type; and Francisella tularensis palearctica, the more widespread type. Both types of tularemia are widely distributed in Montana. The main laboratory criterion for identifi- cation of cultures of the two varieties is that minimal doses of the first type will cause fatal infection in domestic rabbits, whereas with the other type moderate doses of the organ- ism will infect but not kill domestic rabbits. The animals often do not show visible signs of illness. Most of our cultures are readily classified in one or the other of these two types. However, Russian workers have pro- posed names for several additional varieties of the organism and other workers in the United States have suggested there are vari- ous intergrades between the two fairly well- defined subspecies. Intensive study on tularemia in semi- aquatic mammals and in the water habitat has necessitated modification of some of the epidemiological concepts expressed by Jelli- son and Parker (1945), but has greatly ex- panded our knowledge of the disease. This type appears to be entirely independent of ticks and cottontails in North America. Hun- dreds of cases have been reported in trappers in Canada (Wood, 1951); also skin and sero- logical tests indicate prevalence in Alaska (Philip et al, 1962) where recognized clinical cases are extremely rare. We have isolated and described a new organism from a Utah water sample which is very similar to F. tularensis but can be dis- tinguished by cultural and serological tests. This has been called Francisella novicida. It is pathogenic for mice, hamsters, and guinea pigs in the laboratory but has not been defi- nitely associated with disease in man or ani- mals in nature (Larson, Wicht, and Jellison, 1955). The American muskrat, an important source of tularemia infection for man. U. S. Bureau of Sport Fisheries and Wildlife photo. -18— TULAREMIA IN SEMI-AQUATIC MAMMALS AND THE PRESENCE OF F. TULTRENSIS IN WATER Prior to 1939, a few cases of tularemia in the United States had been attributed to con- tact with muskrats and first among these were two cases reported by Dr. Harold Schwartz of Butte (1929). He treated two Japanese section workers who skinned a muskrat and both became infected. These cases were not considered unusual because the muskrat is a typical rodent, even though it prefers a semi- aquatic habitat. The muskrat, however, is ex- ceptionally free of ticks, fleas and lice which we usually think of as being carriers or trans- mitters of tularemia. In the U.S.S.R. and in many European countries, there is an animal called the water- rat or vole-rat, Arvicola terrestris, also known as Arvicola amphibius, that is a counterpart of our muskrat but is smaller. It is extremely abundant at times and is hunted and trapped by thousands for its fur. The muskrat has also been introduced into Europe and U.S.S.R. and now occupies the same habitat as the water-rat. Russian investigators had reported at least two major epidemics involving 200 and 800 cases respectively in water-rat hunters prior to 1929. In 1935 two Russian scientists observed and reported (1936) an epidemic of at least 43 cases in communal farm workers and at- tributed infection to drinking water from a small stream. Portal of entry appeared to be mouth and throat. The organism was isolated from the stream by animal inoculation. In 1939, four or five dead beaver were reported in the vicinity of Roundup by local game wardens. We were already aware of the Russian experiences. Autopsies, animal inocu- lations and cultures soon proved the beaver had died of tularemia. This was the first of many beaver that were to be found dead within the next few years. The first water samples taken from ponds where beaver were found dead along the stream bed of the Mus- selshell River produced tularemia in labora- tory animals. This was the first isolation of F. tularensis from water in North America. Reports of beaver fatalities and human cases from beaver and muskrat contacts were quite numerous through 1943 and have been spo- radic since that time. Locations of epizootics in muskrats and beaver, 1938-1842. —19— Swamp near Florence, Ravalli County, where epizootic in muskrats occurred in 1949. Intensive studies on this phase of tularemia epidemiology in Montana, Idaho, Oregon, and Utah were continued for several years and led to many interesting observations, which were published in a National Institute of Health Bulletin, No. 193. In one drainage area east of Hamilton, 1,198 water samples were taken during a 16-month period. These were tested for presence of F. tularensis by injection into guinea pigs. 703 of the 1,198 samples, or 58%, infected one or more test animals. Several water samples were taken each month from another small stream in the same general area, and at least one sample was positive each month for 16 consecutive months, winter and summer. Infection has resulted from water samples taken in mid-stream of flood-swollen creeks and rivers; it has been demonstrated in samples from clear mountain streams, spring- fed streams (a few hundred yards below the spring), marshes, stagnant ponds, ponds along river channels at low water, from kitch- en faucets of domestic, rural water supplies and from the historically famous Frog Pond on die campus at Montana State University, Bozeman. If field mice, muskrats or beaver dead of tularemia are found adjacent to or in streams, it is good assurance that the water will prove to be infectious; however, many streams carry the organism where we can find no evidence of animal mortality. Dead beaver, because of their large size, were the most common indicators of epi- zootic areas and, where these animals were obtained fresh, they almost always yielded F. tularensis cultures. Muskrats found dead by trappers were also a reliable source of in- fection. Close examination of stream banks and adjacent meadows sometimes resulted in finding freshly dead and infected field mice, Microtus spp. Illness in trappers was also an indication of epizootic areas. At this time we have no logical explanation for the presence of such a fastidious organism as F. tularensis in ponds, streams and rivers throughout northwestern United States. We do not believe the contamination comes from decomposing animal carcasses. —20— Tularemia had been conspicuously scarce or absent in the New England states, exclusive of New York, prior to 1968 and New York had reported only 66 cases up to 1944. How- ever, in 1968, the largest outbreak of tularemia in man associated with aquatic mammals in North America occurred suddenly in Vermont, a state that had no previous record of tula- remia (Young et al, 1969). Forty-seven cases appeared within a few weeks in persons who were trapping and skinning muskrats. There were no fatalities but 14 patients had severe prostrating illness, a few had extremely mild infections. F. tularensis was isolated from one human case, from four of 78 trapped muskrats and from an unspecified number of mud and water samples. No isolations were made from rabbits. In contrast to some epizootics and epidem- ics which we have studied in the west, evi- dence of die-off in the muskrat population was "conspicuous!}' absent." Both trappers and dealers agreed muskrats were more abundant in 1968 than in the previous five years. The report available (Young et al, 1969) does not mention finding a single dead animal in the infected area. For example, McDermid (1946) reporting on die epizootic in muskrats in Horicon Marsh, Wisconsin, stated, "State clean-up crews picked up 1,114 dead muskrats from the Horicon Marsh area and burned the car- casses." Dozens of dead beaver and hundreds of dead muskrats were observed in some previ- ous epizootics in Oregon, Utah, Montana, Wis- consin and Canada (Parker et al, 1951). We have referred several times to the con- clusion that isolates of F. tularensis from wa- ter, muskrats, and beaver are of somewhat lower virulence than isolates from sheep, ticks, and rabbits in the United States. By 1951, we had reports of over 100 cases in beaver and muskrat trappers. We had no record of a fatal case from these sources, whereas a case fatal- ity rate of 5% to 7% (mainly rabbit contact cases) was expected prior to use of antibiotics in treatment. Many cases (1938-1951) were very mild and ambulatory. Some trappers con- tinued on their regular daily trap rounds and Emery Buker collecting water samples for laboratory tests. This stream near Hamilton carries tularemia organisms al all seasons of the year. -21— would not have been diagnosed, except for intensive case finding and questioning of trap- pers in epizootic areas. On the other hand it would be difficult to convince some trappers that they had a "mild case of tularemia." This would especially apply to an elderly trapper who survived a severe infection by himself in winter in an isolated cabin near Klamath Falls, Oregon. He had little recollection of the terrible ordeal when he finally made his way back to civilization. TULAREMIA IN OTHER ANIMALS In 1945, Burroughs and his associates com- piled a list of the vertebrates known to be naturally infected from all continents. This included 48 species and 27 genera. Some of these had been reported as infected in a single instance only. Some were known to be im- portant reservoirs and to have experienced widespread epizootics. Sheep, cattle, horses, rabbits, muskrats, beaver, field mice, and sage grouse have been discussed in this paper. There are reports in die literature of infec- tion in dogs and cats usually from eating in- fected animals. Information on cats up to 1929 was summarized by Dr. Simpson who stated, "Francis places die cat among mildly suscept- ible animals." Individual reports, mostly based on laboratory tests, were very conflicting. Some cats apparently died from natural in- fection but die proof was not conclusive. In laboratory tests, a few kittens and even adults died after eating infected tissue, but odier cats remained well. It would seem diat some retesting of cats would be desirable using isolates of known virulence, measured doses of inoculum and more standardized groups of experimental animals. About the same could be stated in regard to dogs and tulare- mia. One of the important roles assumed by both dogs and cats is catching or retrieving sick or dead animals and bringing diem home and exposing people. About 1930, I obtained a tame cub bear from the Fish and Game Department for ex- perimental work. It was kept at the laboratory for several weeks and then fed a dish of ice cream garnished with chopped spleen and liver from a tularemic guinea pig. The bear became very sick but recovered and showed a strong agglutination titer for F. tularensis. Epizootics in ranch mink being fed wild jack rabbit meat have been experienced in southern Idaho; many mink died. THE HUMAN DISEASE In human tularemia the first sign of dis- ease is usually marked inflammation at the point of infection, a wound, tick bite or deer- fly bite. This lesion rapidly develops into a prominent ulcer or "boil" and is accompanied by swelling and tenderness of the regional lymph nodes. Systemic symptoms, high fever, headache, chills and prostration appear early — at times suddenly. Widiout antibiotic treat- ment the course of illness may last several weeks or even months. Involved lymph nodes may become very large and painful and are often surgically treated for drainage or com- plete removal. Spontaneous rupture and per- sistent drainage is not unusual. Complete re- covery may take months. The initial lesion heals slowly and often a center of dead tis- sue sloughs away leaving a characteristic "punched-out ulcer" and a permanent scar. Many variations in clinical manifestations have been recognized, including multiple ini- tial lesions, septic sore throat at onset, and systemic illness without obvious indication of portal of infection. The latter is referred to as typhoidal type and includes a few rapidly fatal family outbreaks from eating poorly cooked rabbit. Eye infection with prominent involvement of local lymph nodes is well rec- ognized and results from rubbing infective material into the eyes. Degrees of illness range from slight inconvenience to rapidly fatal disease. Before antibiotics were developed, no spe- cific treatment was available and cases in the United States were frequently fatal. Now, sev- eral antibiotics have proved to be extremely effective and immediate dramatic cures are observed even in very severe cases. Strepto- mycin and tetracycline preparations are rec- ommended and may be administered by mouth or injection. Penicillin is not effective. TULAREMIA AND PLAGUE It is very difficult or impossible for even an experienced laboratory worker to distin- guish between tularemia and plague in the autopsy of a wild or laboratory animal. Tu- laremia was first described as a plague-like —22- Mnii Guinea pigs that survived tularemia infection because of streptomycin treatment, 1945. disease of rodents in California where it was encountered in ground squirrels that were being examined for plague. It could be dis- tinguished from plague only by culture and by microscopic examinations. There is a story that a culture and infected laboratory animals were used in a West Coast medical school as demonstrations for tulare- mia, until one skeptical student identified the culture as the plague bacillus. In man the initial illness and presence of buboes or enlarged lymphatic nodes are very similar in plague and in tularemia. Without antibiotic treatment, plague would be about 50% fatal, tularemia 5%. Plague can appear in a pneumonic form that is highly contagi- ous and 90% fatal; tularemia may also be pneumonic but is not known to be contagious in humans. This distinction is not just academic or applicable to California. In 1934, 1935, and 1936 plague was found to be widespread in ground squirrels in Beaverhead and Madison Counties, Montana. Great die-offs of ground squirrels were observed in Beaverhead Coun- ty and plague was found in many squirrels. In November, 196S, a fatal case of plague occurred near Salmon, Idaho, and infection was attributed to a snowshoe hare which the hunter shot and tied to his saddle horn. This was the first time in North America that the snowshoe hare had been incriminated in plague although cottontails are a recognized source of human infection in Arizona and New Mexico in recent years. A fatal case of plague was reported near Boise, Idaho, in 1939, but the source of infection was more obscure. Plague was also present in ground squir- rels in Alberta, Canada, north of Montana. LITERATURE For the benefit of anyone who may be- come especially interested in tularemia, I would like to state that there are 15 bound volumes of reprints on tularemia in the Rocky Mountain Laboratory Library. There are also several books on the subject. Numerous pub- lications on the disease are still available for distribution from the Laboratory and from my personal library. In my personal collec- ts— tion, designated as the Parker-Davis Memori- manuscripts, pictures and lantern slides, al Library, I have the library of the late Dr. A bibliography on tularemia prepared and Edward Francis who described and named published in mimeographed form by the Tech- tularemia in 1921. This collection contains his nical Library, Camp Derrick, Fredrick, Mary- laboratory and field notes, correspondence, land, in 1952, contains 81 pages of references. BIBLIOGRAPHY 1970. Anonymous. Tularemia-United States 1960-1968. Morbidity and Mortality Week- ly Report, U. S. Public Health Service. 19 (9):94-100. 1955. Bell, J. F., Owen, C. R., and Larson, C. L. Virulence of Bacterium tularense. I. A study of virulence of Bacterium tularense in mice, guinea pigs and rabbits. Jour. Inf. Dis. 97:162-166. 1955. Burrows, A. L., Holdenried, R. Longanecker, D. S., and Meyer, K. F. A field study of latent tularemia in rodents with a list of all known naturally infected vertebrates. Jour. Inf. Dis. 76:115-119. "1969. Casper, E. A., and Philip, R. N. A skin test survey of tularemia in a Montana sheep-raising county. Publ. Hlth. Reports 84:611-615. 1959. Claus, K. D., Newhall, J. H., and Mee. D. Isolation of Pasteurella tularensis from foals. Jour. Bact. 78:294-295. 1942. Gwatkin, R., Painter, R. H., and Moynihan, I. W. Tularemia in sheep. Can. Jour. Comp. Med. June 1942: 163-168. 1951. Hall, E. R. A synopsis of the North American Lagomorpha. Univ. of Kansas Publications, Museum of Natural History 5: 119-202. 1969. Hoffman, R. S., Wright, P. L. and Newby, F. E. The distribution of some mammals in Montana. I. Mammals other than bats. J. Mamm. 50: 579-604. "1964. Jellison, W. L., Jacobson, H., and Flora, S. Tick-borne tularemia and tick paralysis in cattle and sheep. Proc. 68th Ann. Meeting of U. S. Livestock Sanitary Association, Memphis, 1964. °1961. Jellison, W. L., Owen, C, Bell, J. F., and Kohls, G. M. Tularemia and animal populations. Wildlife Disease 17: 22 pages. °1950. Jellison, W. L. Tularemia: Geographical distribution of "deerfly fever" and biting fly. Chrysops discalis Williston. Publ. Hlth. Re- ports 65: 1321-1329. 1959. Jellison, W. L., Bell, J. F., and Owen, C. R. The Oregon meadow mouse irruption of 1957-1958: Mouse disease studies. Bulletin Ore- gon State College, pp. 71-80. "1950. Jellison, W. L., Epler, D. C, Kuhns, E., and Kohls, G. M. Tulare- mia in man from a domestic rural water supply. Publ. Hlth. Reports 65: 1219-1226. "1955. Jellison, W. L., and Kohls, G. M. Tularemia in sheep and sheep industry workers in western United States. Publ. Health Monograph No. 28, pp. 1-17. 1951. Jellison, W. L., Kohls, G. M., and Philip, C. B. Tularemia: Muskrats as a source of human infection in Utah. Rocky Mt. Med. Jour. 48: 594-597. 1945. Jellison, W. L., and Parker, R. R. Rodents, rabbits and tularemia in North America: Some zoological and epidemiological considera- tions. Am. Jour. Trop. Med. 25: 349-362. 1953. Kuhns, E., Houtz, C. S., and Axley, A. Tularemia from a porcu- pine. Rocky Mt. Med. Jour. Sept., 1953, p. 736. 1954. Langford, E. V. An outbreak of tularemia in beaver and muskrats in Waterton Lakes National Park, Alberta. Can. Jour. Comp. Med. 18: 28-30. 1955. Larson, C. L., Wicht, W., and Jellison, W. L. A new organism resembling P. tularensis isolated from water. Publ. Hlth. Reports 70: 253-258. * Indicates reprints are still available from the Rocky Mountain Laboratory at Hamilton or from Doctor Jellison. 1946. McDermid, A. M. Report on muskrat disease outbreak. Wisconsin Conservation Bulletin 9: 21-22. 1949. Morgan, B. B. Tularemia in Wisconsin. Trans. Wisconsin Acad. Sci. Arts and Letters 39: 1-19. 1959. Olsufiev, N. G., Emelyanova, O. S., and Dunayeva, T. N. Compara- tive study of strains of B. tularense in the old and new world and their taxonomy. Jour. Hyg., Epid., Microbiol., and Immun. 3: 138- 149. 1955. Owen, C. R, Bell, J. F., Larson, C. L., and Ormsbee, R. A. Viru- lence of Bacterium tularense. II. Evaluation of criteria of virulence of Bacterium tularense. Jour. Inf. Dis. 97: 167-176. 1929. Parker, R. R., and Dade, J. S. Tularemia: Its transmission to sheep by the wood tick, Dermacentor andersoni Stiles. J. Am. Vet. M. A. 75: 173-191. 1932. Parker, R. R., Philip, C. B., and Davis, G. E. Tularemia: Occurrence in the sage hen, Centrocercus urophasianus, also report of addi- tional cases following contacts with quail, Colinas virginianus. Publ. Hlth. Reports 47: 479-487. 1926. Parker, R. R., and Spencer, R. R. Six additional cases of laboratory infection of tularemia in man. Publ. Hlth. Reports 41: 1341-1355. 1924. Parker, R. R., Spencer, R. R., and Francis, E. Tularemia. XI. Tu- laremia infection in ticks of the species Dermacentor andersoni Stiles in the Bitter Root Valley, Montana. Publ. Hlth. Reports 39- 1057-1073. 1951. Parker, R. R., Steinhaus, E. A., Kohls, G. M., and Jellison, W. L. Contamination of natural waters and mud with Pasteurella tular- ensis and tularemia in beavers and muskrats in the northwestern United States. Nat. Inst. Health Bull. No. 193, pp. 1-61. 1935. Philip, C. B., Jellison, W. L., and Wilkins, H. F. Epizootic tick- borne tularemia in sheep in Montana. J. Am. Vet. M. A. 86; 726-744. 1961. Philip, C. B., and Owen, C. Comments on the nomenclature of the causative agent of tularemia. International Bull. Bact. Nomencla- ture and Taxonomy 11: 67-72. 1967. Philip, R. N., Casper, E. A., and Lackman, D. B. The skin test in an epidemiological study of tularemia in Montana trappers. J. Inf. Dis. 117: 393-402. 1929. Simpson, W. M. Tularemia. Paul B. Hoeber Inc., Publishers New York, pp. 1-162. 1951. Sulkins, S. E., and Pike, R. M. Survey of laboratory-acquired in- fections. Am. J. Publ. Hlth. 41: 769-787. 1952. Yeatter, R. E., and Thompson, D. H. Tularemia, weather and rab- bit populations. Bull. Illinois Nat. Hist. Survey 25(6): 351-382. 1969. Young, L. S., Bicknell, D. S., Archer, B. C, Clinton, J. M., Leavens. L. J., Feeley, J. C, and Brachman, P. S. Tularemia epidemic: Ver- mont, 1968. Forty-seven cases linked to contact with muskrats. New Eng. J. of Med. 280: 1253-1260. ACKNOWLEDGMENTS The tularemia manuscript was prepared with much help from the present staff at the Rocky Mountain Labora- tory. Published and unpublished data were supplied by Dr. Robert Philip and Miss Elizabeth Casper, R.N. Most of the photographs came from the Graphic Arts Department and were prepared by Mr. Nick Kramis or his successor, Mr. Charles Taijlor. Several animal portraits were obtained from the U. S. Bureau of Sports Fisheries and Wildlife. Dr. Cora Owen has edited the manuscript and made many corrections and improvements. TURTLES OF MONTANA By JEFFREY H. BLACK, University of Oklahoma . . . Photos by Author Most children have had pet turtles, but lit- tle do they realize that their pets are members of an ancient and long-lived group of reptiles. Fossil relatives of turtles are found in rocks at least 175 million years old. Turtles today are found on every continent and in almost every area where winter is not perpetual. There is considerable folklore associated with turtles. Many Asian people believed that the earth rested upon the back of one of these reptiles. Numerous stories are told of the strength and longevity of turtles and most everyone has heard the story of the race between the tortoise and the hare. Ceremonial rattles made of dried turtle shells filled with pebbles figure in the rain dances of the south- western Indians. One might wonder if a "turtle," "tortoise" and "terrapin" are the same thing. All can properly be called turtles, but the edible fresh water kinds sold in markets are known as terrapins, while the land turtles with stump- shaped hind legs may be called tortoises. Turtles belong to the Class Reptilia which also includes snakes and lizards. The major difference between turtles and other living reptiles is the shell covering the body. The shell is of two parts, an upper rounded cara- pace and a flatter ventral plastron. The cara- pace and plastron are connected on each side by a bridge. The shell is of bony plates, cov- CARAPACE ered by horny plates and provides protection against predators, dessication, and other dan- gers. Turdes see well, their sense of smell is adequate, and their hearing is well-developed. They lack teeth, but have jaws covered with sharp horny beaks. They are the only vertebrates in which the limb attachments are inside the ribs. All have two pairs of legs with five fingers and toes bearing claws. The tails of the males are usually longer than those of females and the anal openings are often situated farther out on the tails of males than on the females. These external characteristics will usually separate the sexes. The eggs of turtles are adapted for devel- opment on land and will not develop in water. Their eggs have membranes homologous with those of bird eggs and fetal membranes of mammals. The ability to produce eggs has allowed turtles to become independent of wa- ter for breeding and to be the first large group of vertebrate animals to occupy the land. Turtles are beneficial to man because of their scavenging habits. They also consume large numbers of mosquito larvae and other insect pests, and have potential food value to humans. PLASTRON -^26— COMMON SNAPPING TURTLE (Chelydra serpentina serpentina) Distribution: The common snapping turtles are closely restricted to water in the eastern half of Montana. They may inhabit lakes, rivers, slow streams, ponds and marshes. Description: The large head with powerful jaws, the serrated rear margin of the carapace, a long tail with a saw-tooth crest, and a neck covered with many warty tubercles are distinguishing characters. The plastron is cross-shaped and covers only part of the underside. The com- mon name "moss-backs" refers to a mat of firmly attached algae that flourishes on the backs and on the upper parts of the tails of many individuals. Breeding: Mating occurs in the spring or early sum- mer and eggs are laid from May to October. The nests are dug by the females some dis- tance from water; 8 to 80 eggs are laid bv an individual in the earth 2-5 inches deep. Hatching occurs in about 4 months. Habitat: The preferred habitat of the common snap- ping turtles is almost any kind of aquatic habi- tat. They inhabit water where aquatic plants are abundant and where there is a soft bank or bottom for hibernation and hiding. Feeding: These turtles are adept at catching any- thing that swims, but there need be little con- cern as to the adverse effect of snapping turtles on game fish in wild waters of Mon- tana. It is a conservative estimate that not more than one game or pan fish is eaten per day by an individual snapping turtle. They also feed on frogs, crayfish, other reptiles, birds and aquatic plants. Behavior: The common snapping turtles probably hibernate in Montana from October to May. Hibernation occurs under water and beneath bottom mud or debris. Individuals may sun themselves on land or may float at the water's surface. The temperment of snapping turtles is well known. They can strike with the speed of a rattlesnake and are often ill-tempered and very apt to bite. The snapping turtles not only defend themselves with their jaws, but also keep predators at a distance by secreting a powerful musk. They can be carried safely by the tail, but be careful! —2.7- WESTERN BOX TURTLE (Terrapene ornata) Distribution: The occurrence of western box turtles in Montana needs confirmation. The only record of their occurrence is that of Dr. F. V. Hayden who reported them near the Yellowstone River in Montana, 1871. If present, they probably inhabit the southwestern counties. Description: These are the only strictly land-going turtles in Montana and are distinguished by their rather high carapaces and stubby feet which are adapted for walking on land. They have shells with yellow striping on dark back- grounds and the plastrons are hinged in front allowing the turtles to completely enclose themselves within their shells. The plastrons are yellowish, with or without dark bars. Males have the first toenails of hind feet turned inward, reddish irises of the eyes and reddish spots on the forelegs which usually distinguishes them from the females. Breeding: These turtles breed during the spring and fall and eggs are laid in nests from May through July. Around 3 to 5 eggs are laid by each female. During courtship the males tap the carapaces of the females with their plas- trons and may bite at their shell margins. Habitat: The western box turtles are primarily in- habitants of the plains regions where there is rolling country, grass, low bushes, and sandy soil. They are rarely found in wooded areas. Feeding: Western box turtles primarily feed upon plant materials and also beetles and other insects. They have great value as destroyers of insects. Behavior: During warmer weather, most activity oc- curs during the morning and late afternoon. During die heat of the day, diese turtles seek shelter under objects, bushes, or in self-made burrows. Hibernation occurs during the win- ter when turtles can burrow up to two feet beneath the soil. —28— PAINTED TURTLE (Chrysemys picta) Distribution: Painted turtles are the most commonly seen turtles in Montana and occur throughout the state excepting at very high elevations in the western mountains. Description: These are our most brighdy colored turtles. Yellow stripes adorn the heads and legs and a red spot or bar is situated behind each eye. The carapaces are low and their margins may be marked with yellow. The plastrons are red or orange in young turtles with the dark markings well-developed. Males have longer nails on their front feet than do die females. Breeding: Males have long claws on the forefeet which are vibrated rapidly besides die cheeks of the females during courtship. Eggs are laid during May or June in nests on the shore. Eggs, numbering from 6 to 20 are buried in the earth 2-5 inches deep and hatch in about 4 mondis. Habitat: The preferred habitat of painted turtles in Montana seems to be practically any body of water. They are found in large bodies of water such as Fort Peck Reservoir to water- filled roadside ditches. These turtles are as- sociated with lakes, ponds, rivers and streams in Montana. Painted turtles are frequently on land moving between adjacent bodies of wa- ter. Home ranges may include parts or all of several water bodies. Feeding: Painted turtles probably use smell and sight as die primary methods of locating food. Food is eaten whole or is torn with the aid of the front feet. The painted turtles are more or less neutral in their food habits, consuming large quantities of plant food, crayfish, snails, clams, tadpoles, and small fish. Behavior: These turtles are often seen in groups sunning on muddy banks, on logs or other ob- jects. They are quite wary and immediately enter the water and swim to the bottom when disturbed. They hibernate during the winter in the mud or debris on streams, lake, or pond bottoms. —29- WESTERN SPINY SOFTSHELL (Trionyx spiniferus hartwegi) Distribution: In Montana, the range of western spiny softshell turtles lies in the southeastern part of the state. The northern boundary appears to be in Roosevelt, Valley, Phillips, Blaine, Chouteau, and Cascade Counties. Their range extends west to Canyon Ferry Reservoir and then south to the Wyoming border. Description: The western spiny softshells are very dif- ferent from other Montana turtles. These are the "pancake" turtles which have very flat, flexible shells. The shells are covered with leathery skin and have flexible edges. The carapaces are marked with numerous dark spots; their necks are long and the snouts are proboscis-like with nostrils opening at the ends. The feet of these reptiles are broadly webbed and well adapted for pushing these very aquatic turtles at high speed through the water. Breeding: Softshell turtles seldom leave the water except to lay eggs — March to July. Sandy soil is preferred for the nests. Eggs number about 10 to 30. Habitat: These are highly aquatic turtles and are found primarily in rivers and streams, but also in ponds, lakes and ditches. They appear to prefer waters with a bottom of gravel, sand, silt or mud. Feeding: These are primarily carnivorous turtles. They feed upon insects, frogs, tadpoles, snails, —30— crayfish, fish and earthworms, and occasion- ally aquatic plants. Behavior: Hibernation occurs in the sand or muddy bottoms of their aquatic habitats. They often He in shallow water buried in mud or sand with their heads extended to the water sur- face. They should be handled with care as they can inflict painful bites. -31- -32— RETURN REQUESTED Return to INFORMATION-EDUCATION DIVISION MONTANA FISH & GAME DEPARTMENT Helena, Montana ZIP 59601 Sec. 34.66, P. L. & R. U. S. POSTAGE PAID Permit No. 50 Helena, Montana