Charles P. Hibler

PREVALENCE OF GIARDIA SP. IN A BEAVER COLONY AND THE RESULTING ENVIRONMENTAL CONTAMINATION

The prevalence of Giardia sp. in a beaver (Castor canadensis) colony in Colorado was determined by the collection and analysis of fecal samples over a period of 14 mo. Environmental contamination was monitored through the use and analysis of water filter samples. Beaver shed cysts of Giardia sp. in their feces throughout the year with temporal variations in the prevalence, and became infected as kits and remained infected as juveniles and adults. Beaver served as amplification hosts for Giardia sp. and contaminated surface waters downstream from their dams in late spring and early fall. In slow moving waters the cysts of Giardia sp. settled rapidly. Muskrats (Ondatra zibethicus) were the only other species of wildlife shedding cysts of Giardia sp. on the study area.

Experimental infection of mule deer with Parelaphostrongylus tenuis.

Six adult and three fawn mule deer (Odocoileus hemionus) were experimentally infected with a range of 75-100 infective larvae of Parelaphostrongylus tenuis. Five of the six adult deer developed clinical signs of neurologic disease that terminated in paralysis between 35 and 80 days. The sixth deer developed slight signs of neurologic disease for 10 days, but recovered. All three mule deer fawns developed neurologic disease. Adult meningeal worms were recovered from the subdural space of the spinal cord of two fawns. Eggs were observed on the cranial dura mater of one of these fawns, indicating that P. tenuis can complete its life cycle provided mule deer can survive the damage resulting from the infection. Neither eggs nor larvae of P. tenuis were recovered from the feces or lungs of infected mule deer. Clinical signs and histologic lesions observed in experimentally infected mule deer resembled those reported in infected moose (Alces alces americana). Two critical periods were apparent in mule deer infected with P. tenuis: nematode migration through the spinal neural parenchyma, and penetration of the adult nematodes into the cranial neural parenchyma. While most adult deer were unable to survive the first critical period, fawns survived the first but succumbed to infection during the second critical period.

TRANSPLACENTAL TRANSMISSION OF Protostrongylus SPP. IN BIGHORN SHEEP

Third-stage larvae of Protostrongylus spp. were recovered from the liver and lungs of a bighorn sheep foetus and from the placenta of the ewe.

FURTHER OBSERVATIONS ON Protostrongylus sp. INFECTION BY TRANSPLACENTAL TRANSMISSION IN BIGHORN SHEEP

Tissues from two bighorn sheep fetuses and four neonatal bighorn sheep lambs were examined for evidence of natural Protostongylus infection occurring by the transplacental route. Forty-three third-stage larvae (L3) were recovered from the fetal liver of case 1; one L3 from the cotyledons of case 2; 189 L3 from the liver and 46 L3 from the lungs of case 3; 146 La from the liver and 43 L3 from the lungs of case 4; and 133 L3 from the liver and 33 L3 from the lungs of case 5. Fifty-two L3 and fourth-stage larvae (L4) were recovered from the lungs and five L3 from the liver of case 6. Digestion with Pepsin-HCL was a more effective method for recovery of L3 than baermannization, but L4 larvae were digested.

EXPERIMENTAL CONTAGIOUS ECTHYMA IN MULE DEER, WHITE-TAILED DEER, PRONGHORN AND WAPITI1

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.

Morphology of the larval stages of Elaeophora schneideri in the intermediate and definitive hosts with some observations on their pathogenesis in abnormal definitive hosts.

Morphology of the larval stages of Elaeophora schneideri from the horse fly and the normal definitive host (Odocoileus hemionus) are described. Development of larvae in the horsefly begins in the fat bodies, but larvae enter the haemocoele early in the first-stage of development and remain in the haemocoele until they are third-stage (infective) and then migrate to the head and mouth parts. Infective larvae in the definitive host begin development in the leptomeningeal arteries and are immature adults in 2 weeks. At 3.5-4 weeks they migrate into the carotid arteries and grow to sexual maturity about 4.5 months later. In abnormal definitive hosts (Cervus canadensis or Ovis aries) larvae remain in the leptomeningeal arteries for 5 weeks or longer initiating the clinical manifestations of elaeophorosis.

HORSE FLIES AND Elaeophora schneideri IN THE GILA NATIONAL FOREST, NEW MEXICO*

During June and July, 1970 and 1971, 3697 of 15,223 horse flies (Diptera: Tabanidae) belonging to seven species were dissected and examined for larval Elaeophora schneideri Wehr and Dikmans, 1935, in the Gila National Forest, New Mexico. Hybomitra laticornis (Hine) comprised 90 percent of the six infected species. Almost 13,300 larvae were recovered with an average of 25 larvae per infected fly. Infective larvae were found in four species. Based on occurrence in collections, prevalence of infection and larval recovery, H. laticornis is considered to be the most important horse fly vector of this filarial parasite in southwest New Mexico. H. tetrica rubrilata (Philip) and Tabanus eurycerus Philip may be important vectors in other areas.

EXPERIMENTAL INFECTION OF IMMATURE MULE DEER WITH Elaeophora schneideri

Five neonatal mule deer (Odocoileus hemionus) and five yearling mule deer were experimentally infected with Elaeorphora schneideri. Infections ranging from 2 to 31 parasites established in 9 of 10 animals. Evidence of elaeophorosis was not observed in any animal, indicating that mule deer are normal definitive hosts.

ORAL ADMINISTRATION OF DIAZEPAM AND PROMAZINE HYDROCHLORIDE TO IMMOBILIZE PRONGHORN

Oral tranquilizers were mixed with a grain bait and fed to pronghorn (Antilocapra americana) in an attempt to immobilize and thus facilitate their capture. Diazepam, administered at 6 mg/kg body weight immobilized a tame pronghorn fawn within 30 min. Tranquilization was still apparent after 8 h. A minimum dose of 23 mg/kg body weight was necessary to immobilize a wild adult pronghorn. Immobilization occurred after 60 min and tranquilization was apparent 24 h post ingestion. Excitement severely impeded the effect of the drug and although easily captured, the animal struggled wildly when handled. Wild pronghorn fawns showed moderate tranquilization when administered diazepam at 23 mg/kg body weight but were unapproachable. Doses of diazepam between 13 and 23 mg/kg body weight were used to capture tame yearling and adult pronghorn held in a 132 ha enclosure. A dose of 23 mg/kg body weight was excessive in that the animals did not recover for 48 to 54 h post ingestion and had difficulty maintaining a sternal bedding position. Diazepam at 13 mg/kg body weight failed to tranquilize the animals sufficiently for easy capture. Promazine hydrochloride at doses of 2 to 17 mg/kg body weight, given orally to wild pronghorn fawns and an adult, did not produce visible signs of tranquilization. Animals refused to eat bait containing doses of promazine hydrochloride greater than 17 mg/kg body weight.