Search

Six yearling American bison (Bison bison bison) bulls and one yearling ewe (Ovis aries) were inoculated intradermally and subcutaneously with 2 x 10(5) plaque forming units (pfu) of bluetongue (BT) virus serotype 11. Two uninoculated yearling bison bulls served as negative controls. Blood samples were collected for serology and virus isolation on 0, 4, 7, 11 and 14 days post-inoculation (dpi) and every 2 wk thereafter to 127 dpi. Every 4 wk a new ewe was inoculated with a pooled sample of whole blood from the six infected bison, and each sheep was monitored for 28 days for clinical signs of BT and seroconversion. Bluetongue viremia was detected in all six inoculated bison starting at 4 to 28 dpi and was no longer detectable from 42 dpi onward. Pooled blood samples collected at 28, 56, 84 and 112 dpi from the six infected bison were not infectious for sheep. The six infected bison seroconverted by 11 to 28 dpi on a competitive enzyme-linked immunosorbent assay and by 28 dpi on the serum neutralization test, and all remained seropositive thereafter. No clinical signs or lesions attributable to BT were observed in the infected bison or controls. There was evidence that a small amount of epizootic hemorrhagic disease virus type 2 had been present in the BT virus inoculum; reasons are given for concluding that this did not affect the results of the BT study.

In order to determine whether elk (Cervus elaphus) could be infected with and shed bovine viral diarrhea virus (BVDV) and to determine whether BVDV could cause disease in elk, two groups of five yearling elk each and two control cattle were experimentally inoculated intranasally with type 1 Singer strain or a virulent type 2 isolate of BVDV, strain 24515. Virulence of the type 2 isolate was confirmed by inoculation of a control bovine cow which developed diarrhea, dehydration, severe thrombocytopenia, hemorrhages, and enteritis with intestinal necrosis. None of the elk inoculated with type 1 or type 2 BVDV developed clinical signs of illness. However, all elk became infected as demonstrated by viremia, nasal shedding, and/or seroconversion. One uninoculated, in-contact elk contracted type 1 BVDV and seroconverted. Thus, although BVDV does not appear capable of producing disease in nonpregnant elk, the species is susceptible to infection and can shed and transmit BVDV.

Four moose (Alces alces) were inoculated conjunctivally with B. abortus biovar 1 to determine their susceptibility to brucellosis, and to describe the serology, bacteriology, hematology, clinical chemistry, and pathology associated with infection. All moose became infected. Two moose were killed at day 70 post-exposure, one (83F) died acutely at day 85, and one was killed at day 166. None of the moose had clinical signs, except for 83F immediately before death. Infected moose were readily detected serologically by the buffered antigen plate test, Brewer card test, standard tube agglutination test, and complement fixation test as used for brucellosis in cattle. With the exception of samples from 83F taken 24 hours before death, clinical chemistry, and hematology results were stable for all moose, and similar to normal values seen in cattle. Lesions seen in all moose were indicative of endotoxemia, and moose 83F died of acute endotoxic shock. Brucella abortus biovar 1 was isolated from several tissues in all moose, most notably from lymph nodes where counts often exceeded 4 x 10(4) colony forming units per g of tissue. Thus infection with B. abortus will kill moose, and progression of the disease is likely rapid under field conditions. Moose appear to be a dead-end host for brucellosis.

Four of five reindeer (Rangifer tarandus tarandus) obtained from a Besnoitia sp.- infected herd at the Assiniboine Park Zoo in Winnipeg, Manitoba, Canada, in October 1989, had evidence of mild dermatitis over the articular surfaces of carpal and tarsal joints. Cysts of Besnoitia sp., either surrounded by inflammatory reactions or without evident host response, were present within the dermis, submucosa of the nasal turbinates, periosteum, tendons, testes and hooves. The light microscopic and histochemical features of Besnoitia sp. from reindeer were indistinguishable from those of other Besnoitia spp. described in cattle, rodents and horses. The Besnoitia sp. cysts and organisms from reindeer were unique in that bradyzoite membrane micropores and cytoplasmic enigmatic bodies were not observed. Two cats were fed cysts of Besnoitia sp. but no oocysts were detected in feces for 90 days post-infection.