Fatal herpesvirus infection in patas monkeys and a black and white colobus monkey

Fatal herpesvirus infections were diagnosed in 3 patas monkeys and 1 black and white colobus monkey over a 4-week period. Herpesvirus was isolated from 1 patas monkey and from the black and white colobus monkey. Both isolates had growth characteristics similar to Herpesvirus hominis and Herpesvirus simiae. The isolate from the colobus monkey antigenically appeared to be H simiae or H simiae-like, whereas the isolate from the patas monkey could not be conclusively identified with the antisera used. All affected animals were housed in close proximity to rhesus monkeys, the carrier host of H simiae.     

Hepatic and gastric amebiasis in black and white colobus monkeys

Three cases of hepatic amebiasis and one case of gastric amebiasis were diagnosed in black and white colobus monkeys during a 9-month period. The diagnosis was difficult because of the absence of trophozoites and cysts in the feces and because of few trophozoites found in many of the hepatic lesions. Indirect hemagglutination titers were diagnostic in 2 monkeys.     

Cervid herpesvirus 2 infection in reindeer: A review

Herpesviruses of the genus Varicellovirus are known to infect and cause disease in a variety of ruminant species, but the impact of cervid herpesvirus 2 (CvHV2) in reindeer (Rangifer tarandus) is mostly unknown. Reindeer is a circum-polar species with a total estimated number of more than 5 million animals. Mortality may reach high values, as in northern Norway, especially in calves (37%; 2005–2006), and disease can potentially account for some of this mortality. CvHV2 has been isolated during a natural outbreak of infectious keratoconjunctivitis, indicating an etiologal link. Serological screening has shown that CvHV2 infection is prevalent in Northern Norway and experimental infection studies have demonstrated that viremia, latency and vertical transmission occur for CvHV2. The present review aims at summarizing current knowledge on the epidemiology, pathogenesis and molecular virology of CvHV2.     

Allergic conjunctivitis in a juvenile black spider monkey.

Allergic conjunctivitis in a young spider monkey (Ateles fusciceps) was diagnosed on the basis of clinical signs, histomorphologic appearance of conjunctival biopsy specimens, and response to systemic corticosteroid therapy.     

Naturally occurring Sarcocystis neurona-like infection in a dog with myositis

Tissue stages similar to those of Sarcocystis neurona, the causative agent of equine protozoal myeloencephalitis, were identified in skeletal muscles of a dog. The dog, a 6-year-old Labrador retriever, was seropositive for Toxoplasma gondii infection and euthanized due to a history of polymyositis and progressive muscular atrophy. Histologically, 30, variably sized, microscopic, intracellular sarcocysts were observed in 60 sections of skeletal muscles taken from the neck, fore limbs and hind limbs. The cysts were only observed in inflamed skeletal muscles, but were mostly in myocytes at the periphery of areas infiltrated with leukocytes. Ultrastructurally, the cyst wall had villar protrusions consistent with sarcocysts. Immunohistochemistry with monoclonal S. neurona antibodies demonstrated positive labeling of zoites in merozoites or schizonts in the skeletal muscle interstitium, but no labeling of the sarcocysts. Initial PCR analysis with primers amplifying a genetic sequence encoding Apicomplexan 18s rRNA, and subsequent PCR analysis with differentiating primers indicated that the genetic sequences had 100% identity with sequences reported for S. neurona.     

Feline herpesvirus infection in a group of semi-captive cheetahs

Clinical disease caused by feline herpesvirus type-1 in wild felid species is similar to that in domestic cats. Herpesviruses are endemic in free-ranging lions in South Africa but actual clinical disease due to them has not been reported in free-ranging felids. The first reports of feline herpesvirus infection associated with clinical disease in wild felids came from Australia and the USA in 1970. Subsequent reports of clinical disease in cheetahs and other wild felid species were limited to captive animals. This report deals with clinical disease in a group of semi-captive cheetahs in which 18 animals were affected, and included 12 adult males, 4 adult females and 2 subadults. No mortalities occurred in this group, the most common clinical signs being sneezing, nasal discharge and loss of appetite.     

Fatal herpesvirus infection in commercial rabbits

Acute mortality occurred in two unrelated rabbitries. In the rabbits examined, an unidentified herpesvirus caused lesions that have not been reported previously in this species. The primary lesions were multifocal hemorrhagic dermatitis on the face and back, localized pneumonia, and severe splenic necrosis. Large eosinophilic, intranuclear inclusion bodies that were observed in tissue sections of skin, spleen, and lung were identified as herpes-like viral particles by electron microscopy, and herpesvirus was cultured on rabbit kidney cells. Intramuscular injection of tissue culture fluid containing virus resulted in mortality and severe illness in two seven-week-old domestic rabbits four and six days postinfection, respectively. The gross and microscopic lesions were reproduced and herpeslike viral inclusions were observed in skin lesions. Herpesvirus was recovered from lung, trachea, spleen, liver, and from the thigh muscle at the site of inoculation. The experimental infection also activated severe pasteurella septicemia. The herpesvirus isolate needs further characterization.     

Respiratory disease in foals and the epizootiology of equine herpesvirus type 2 infection

The epizootiology of equine herpesvirus type 2 (EHV-2) infection was investigated in Thoroughbred foals on a stud farm which in previous years had suffered economic loss due to respiratory disease. Sixteen pairs of foals and their dams were selected for this study and all of the foals became infected with EHV-2 by two to four months of age. These animals responded serologically to the virus infection as detected by an enzyme-linked immunosorbent assay (ELISA). EHV-2 infection persisted in these foals for two to six months with constant or intermittent virus recovery. This persistent infection stimulated continuous production of antibodies against EHV-2. As soon as the antibody levels reached their peak at five to six months, the isolation rate of EHV-2 from the nasal cavity of these animals decreased, and eventually by nine months of age virus could no longer be recovered. Respiratory disease was observed in ten of the 16 foals; and two severely affected animals died at two months of age. EHV-2 was isolated from both foals at ante and/or post mortem examination. It is postulated that EHV-2, either as an initiating agent or by means of immnunosuppression, caused the respiratory disease observed in these foals.