Hand-reared mule deer fawns (Odocoileus hemionus), white-tailed deer fawns (Odocoileus virginianus), pronghorn fawns (Antilocapra americana) and wapiti calves (Cervus elaphus nelsoni) were exposed to contagious ecthyma lesion material obtained from Rocky Mountain bighorn sheep (Ovis canadensis canadensis) to determine the susceptibility and pathogenesis in these species. All four species developed mucocutaneous proliferative lesions of the oral cavity, grossly and histologically compatible with contagious ecthyma. The limited clinical responses to the virus indicated that contagious ecthyma would not seriously impact free-ranging individuals.

Serologic evidence of contagious ecthyma (CE) was found in domestic sheep (Ovis aries), domestic goats (Capra hircus), Dall sheep (Ovis dalli), and muskox (Ovibos moschatus) in Alaska. A moose (Alces alces) calf and a caribou (Rangifer tarandus) fawn were susceptible to experimental infection and both developed antibody titers as a result. CE virus was isolated from lesions of Dall sheep which were involved in a natural outbreak of the disease.

Blood samples were collected from humans and several species of free-ranging wild animals in Alaska. Sera were tested for antibody to Jamestown Canyon (JC). snow shoe hare (SSH), North way (NOR). Klamath (KLA), Sakhalin (SAK), Great Island (GI), and Silverwater (SIL) virus. JC antibody was found in 54% of 121 human, 89% of 97 bison (Bison bison), 51% of 84 Dall sheep (Ovis dalli), 43% of 68 snow-shoe hare (Lepus americanus), and 3% of 33 arctic fox (Alopex lagopus) sera. SSH antibody was found in 42% of 121 human, 89% of 97 bison, 41% of 84 Dall sheep, and 65% of 68 snow shoe hare sera. NOR antibody was found in 14% of 121 human, 94% of 97 bison, 84% of 84 Dall sheep, 43% of 69 caribou (Rangifer tarandus), 3% of 68 snowshoe hare, 48% of 64 grizzly bear (Ursus arctos), 3% of 33 arctic fox, and 78% of 27 moose (Alces alces) sera. KLA antibody was found in 5% of 121 human and 40% of 97 bison sera. SAK antibody was found in 2% of 97 bison and 3% of 33 arctic fox sera. GI antibody was found in 1% of 97 bison sera. No SIL antibody was found in any sera tested. Thus the natural host ranges of JC, SSH, NOR. and KLA viruses have been extended by inference from the occurrence of antibody.

A systemic streptococcal infection in cultured bullfrogs in Brazil was characterized by necrotizing splenitis and hepatitis with hepatic and renal hemorrhage. A non-hemolytic Group B Streptococcus appeared to be the cause of the lesions, and the stimulus for the splenic reticuloendothelial hyperplasia observed in the animals. Stress may have been a factor in the development of the pathological condition.

Mycobacterium paratuberculosis originally isolated from bighorn sheep (Oris canadensis) with spontaneous paratuberculosis was used to orally inoculate Rocky Mountain elk (Cervus elaphus nelsoni) calves, mule deer (Odocoileus hemionus) fawns, white-tailed deer (Odocoileus virginianus) fauns, bighorn × mouflon (Ovis musimon) hybrid lambs, and domestic lambs. All experimentally exposed animals became infected. During the first year of infection, hybrid and domestic sheep were able to control the infection but infection was progressive in elk and deer. Clinical paratuberculosis occurred only in mule deer.

Serum samples from 89-4 wild animals (representing 31 species) from Trinidad and Grenada were examined by the microscopic agglutination test for leptospiral antibodies; 198 were positive. These included 39 bats, 88 mongooses, six opossums, 10 peridomestic rodents, 15 forest rodents, 10 lizards, and 30 toads. Thirteen pathogenic serogroups were involved. Thirty-nine Leptospira isolates were reported from mongooses, opossums, rodents and toads.

Four littermate 6-wk-old red foxes (Nos. 1–4) were fed Toxoplasma gondii, Sarcocystis cruzi, S. tenella and S. capracanis. One littermate fox (No. 5) served as the control. Two foxes (Nos. 1,2) were fed tissue cysts of T. gondii and two foxes (Nos. 3. 4) were fed oocysts of T. gondii. Twenty-one to 42 days later, the same five foxes were used to test the infectivity of meat of goat, sheep, and ox experimentally inoculated with Sarcocystis. Fox 2 was fed goat meat and shed S. capracanis-like sporocysts 10 days later. Foxes 3 and 4 were fed beef, and they shed S. cruzi-like sporocysts 9 days later. Fox 5 was fed sheep meat and shed S. tenella-like sporocysts 8 days later. Foxes were killed between 36 and 55 days of the experiment and their tissues were inoculated into mice to recover T. gondii. All foxes remained clinically normal and T. gondii was recovered from all inoculated foxes and not from the control. Sarcocystis sporocysts from foxes induced lethal infections in goats, sheep, and ox. The sporocysts. meronts, merozoites, and sarcocysts of fox-derived parasites were similar to those derived from coyotes or dogs. It was concluded that the red fox can act as a final host for the three pathogenic species of Sarcocystis in cattle, sheep, and goats.

Vertebrate host specificity, experimental laboratory vectors, and a description of Plasmodium (Novyella) kempi sp. n. from eastern wild turkeys (Meleagris gallopavo silvestris Vieillot) in Iowa are presented. Plasmodium kempi is infective for domestic turkeys, bobwhites (Colinus virginianus), chukars (Alectoris graeca), guinea fowl (Numida meleagris). peacocks (Pavo cristatus), and canaries (Serinus canaria), produces a transient infection in mallards (Anas platyrhynchos) and domestic geese (Anser anser), but will not infect ring-necked pheasants (Phasianus colchicus), pigeons (Columba livia), Japanese quail (Coturnix coturnix), leghorn white chickens (Gallus gallus), or starlings (Sturnus vulgaris). Oocysts and (or) sporozoites were recovered from 68% (84/124) and 98% (60/61) of the Culex pipiens pipiens and C. tarsalis examined, respectively. Oocysts developed faster and sporozoites invaded the salivary glands sooner in C. tarsalis (6 days) than in C. p. pipiens (7 days). Culex tarsalis transmitted P. kempi more effectively than C. p. pipiens, although both species were capable of transmitting the parasite by natural feeding. Oocysts developed and sporozoites also were produced in C. restuans, but its ability to transmit the parasite was not determined. Aedes aegypti (Rockefeller strain) and A. triseriatus were refractive to P. kempi. Plasmodium kempi produces trophozoites with large refractile globules and fine cytoplasmic extensions, mature schizonts in the form of a condensed fan containing four to eight nuclei (usually 5), and elongate gametocytes with irregular borders. All stages are confined almost exclusively to mature erythrocytes, with no effect on host cell size or position of host cell nucleus. Plasmodium kempi is most similar morphologically to P. (Novyella) hexamerium and P. (Sovyella) vaughani. It differs from P. hexamerium in having large refractile globules in trophozoites and immature schizonts, an inability to infect starlings, an absence of phanerozoites in capillary endothelium of the brain, and the ability to develop in C. pipiens mosquitoes. Plasmodium kempi is more like P. vaughani morphologically, but differs by infecting turkeys and ducks (transient), by its inability to infect starlings, its lack of morphological variation even when in different hosts, and its ability to develop in C. pipiens and C. tarsalis.

Cuterebra lepusculi Townsend parasitize cottontail rabbits (Sylvilagus nuttallii) in southern Idaho. Peak parasitism was 69% in mid-September. Mean development time in the host was 27 days. The species is univoltine in Idaho. Partially developed larvae were transferred from freshly killed to living hosts and the resulting larvae matured normally. Developing pupae were cooled or warmed to retard or speed development and synchronize adult emergence.

Wild lagomorphs and woodchucks collected predominantly in southern Ontario, Canada were examined for subspecies of Obeliscoides cuniculi (Graybill). Obeliscoides cuniculi multistriatus was found in snowshoe hares (Lepus americanus). Obeliscoides cuniculi cuniculi was found in cottontail rabbits (Sylvilagus floridanus), European hares (Lepus capensis) and woodchucks (Marmota monax). Prevalence of Obeliscoides cuniculi multistriatus in snowshoe hares was 100% and mean intensity (and range of intensity) was 760 (9–4,198) in Lindsay, Ontario in 1980. Mean intensity in hares varied trimonthly. The highest mean intensity of worms occurred in spring when most worms were adult. Transmission occurred mainly in spring. Most worms present in fall (70%) and winter (54%) were fourth stage. Immature fifth-stage and gravid females were present in hares during fall and winter. Prevalence and mean intensity of O. c. cuniculi in cottontails was 15% and 29 (1–118). Prevalence and mean intensity of O. c. cuniculi in woodchucks was 6% and 56 (16–118). European hares were infected with O. c. cuniculi, prevalence was 10% and mean intensity was 60 (36–83). In Ontario woodchucks and European hares were common in areas frequented by cottontail rabbits and probably acquired sporadic infections of O. c. cuniculi from infected cottontails.

The parasitic development of Obeliscoides cuniculi multistriatus Measures and Anderson, 1983 was studied in New Zealand white rabbits (Oryctolagtis cuniculns). Third-stage larvae exsheathed within 24 hr. The third molt occurred 3 days and the fourth 8–11 days post-infection. All worms were fifth stage 14 days post-infection. Males were mature at 16 days and copulation occurred in 15–16 days. Females were gravid at 18 days. The prepatent period was 16–22 days. The patent period was 61–118 days and males lived longer than females. All stages were found in the mucosa except the fifth which was found lying on the mucosal surface within a layer of mucus. Petechiae were the only lesions seen in experimentallv infected rabbits. Patent infections of O. c. multistriatus were established experimentally in infected woodchucks (Marmota monax), snowshoe hares (Lepus americanus) and cottontail rabbits (Sylvilagus floridanus). Patent infections of O. c. cuniculi were established experimentally in snowshoe hares. Patent infections of O. c. multistriatus did not appear in experimentally infected HPB white (Swiss Webster) mice (Mus musculus), Wistar rats (Rattus norvegicus), H.O.R. F₁ Syrian hamsters (Mesocricetus auratus), H.O.R. F₁ smooth-haired guinea pigs (Cavia porcellus) and H.O.R. F₁ gerbils (Meriones unguiculatus).

Congenital ocular and related anomalies were studied in two unrelated young raccoons. One animal was anophthalmic and had severe anomalies of the central nervous system, consisting of meningoen-cephalocele, pachygyria, hydraneneephaly, cerebellar cavitation, syringomyelia, and other defects. A second animal was microphthalmic with congenital defects of the nose, maxilla and teeth. Ocular lesions were severe and included chorioretinal colohoma, retinal folds, disorganized neuroectodermal cell layers, spherophakia, cataract and other defects. The nose had unilateral abnormal epithelium, hair follicles, sweat glands and sebaceous glands, and a lack of parietal cartilage on the affected side.

Hemorrhagic enteritis and hepatitis of suspected adenovirus etiology were the apparent cause of death of nine captive American kestrels. Cloaeal hemorrhage was the only prominent gross lesion; disseminated hepatocellular necrosis, and intranuclear inclusion bodies were evident microscopically. Electron microscopy revealed numerous adenovirus-like particles associated with the hepatic lesions. Attempts to serologically identify the agent were unsuccessful.

A disease resembling thiamine-responsive polioencephalomalacia of domestic ruminants is described in four wild pronghorn from Saskatchewan. One animal was found dead, two were recumbent and unable to rise and the fourth was staggering and ataxic. Lesions were confined to the brain and consisted of brain swelling with herniation, symmetrical hemorrhagic foci in the thalamus and brainstem, and laminar necrosis of cortical neurons. All animals had been eating grain prior to their death. Possible pathogenetic mechanisms including changes in rumen microflora resulting in thiamine deficiency, plant and salt intoxication are discussed.

To assess the effect of crude oil on selected gastrointestinal parasites of fish, winter flounder (Pseudopleuronectes americanus) naturally infected with a digenetic trematode (Steringophorus furciger), were exposed to contaminated sediment or water soluble fractions of Venezuelan crude oil for 34 and 160 days respectively. Similarly, Atlantic cod (Gadus morhua) harboring an acanthocephalan (Echinorhynchus gadi), were treated with extracts of Hibernia and Venezuelan oils for periods of 81 to 140 days. In all cases prevalence and intensity of parasitic infections were lower in oil-treated fish. The effect appeared to be more pronounced within fish exposed to water soluble extracts than to oil-contaminated sediment. Fewer parasites present in fish exposed to oil might be attributed to direct toxicity induced by drinking water soluble fractions of crude oil and/or modification of the gut environment brought about by changes in host physiologv.

Clinical hematology and blood chemistry values are reported for the killer whale. These represent a panel of 13 hematological and 21 serum chemistry measurements determined on killer whales maintained for display at Sea World facilities. The values have been collected over a 10-yr period from 14 active, clinically normal individuals, six males and eight females. The cumulative normal values for each of these animals fall into well-defined clusters from which central tendencies and the range of values can be established. No significant male–female differences were observed for any measurement. There were consistent differences among the killer whales in hemoglobin, hematocrit and red blood cell count. A decrease in total white blood cell counts was associated with age and/or changes in parasite loads. Younger animals exhibited higher glucose levels and lower total protein levels. Serum urea nitrogen (BUN) and creatinine were elevated in older and larger males. Lactic dehydrogenase activity was lower in all animals of Pacific origin, as compared to animals from the Atlantic, regardless of age or sex. These “normal” differences emphasize the importance of establishing an animal's individual hematologic and blood chemistry profile by routine sampling.

Twenty-three (9 male, 14 female) wild horses (Equus caballus) in the Great Basin Desert were immobilized by ground techniques with succinylcholine chloride during 1,950 person-hr. Induction (x̄ = 2.09 ± 0.59 min) and recovery (x̄ = 12.4 ± 5.0 min) were rapid and most animals were returned in less than 10 min to original bands. Dosages ranged from 0.66–0.77 mg/kg body weight and neither abortions nor band changes in group membership resulted. However, a few concerted efforts up to 24 hr were needed to return some animals to original bands and three non-drug related mortalities occurred. The responses of bands to darted members and the overall influence of the operation on reproduction, movements, and social structure are presented.