Eosinophilic mediastinitis, myositis, pleuritis, and pneumonia of cattle associated with migration of first-instar larvae of Hypoderma lineatum.

Migrating first-instar larvae of Hypoderma lineatum are a frequent cause of focal inflammatory lesions in connective tissues of the mediastinum, parietal and visceral pleura, peritoneum, lungs, diaphragm, and other loci. The lesions are characterized grossly by foci of yellowish or greenish gelatinous edema and microscopically by infiltration of the edematous tissue by a dense array of eosinophils. Lesions were recognized during a period of several weeks in late spring; the timing was attributable to events in the life cycle of the fly. The larvae, which were small (approximately 1 x 4.5 mm), transparent, and unobtrusive, were recovered from lesions in 12 of 20 cattle in which careful parasitologic examination was made.

Malignant catarrhal fever in an Indian gaur and greater kudu: experimental transmission, isolation, and identification of a herpesvirus.

Herpesviruses were isolated in bovine cell cultures from buffy coat cells obtained from an Indian gaur (Bos gaurus) and a greater kudu (Tragelaphus strepsiceros) with clinical signs of the head and eye form of malignant catarrhal fever (MCF). Both animals were from herds housed in a zoologic park in Oklahoma. Serial transmission of the head and eye form of MCF was accomplished by using whole blood from the gaur into a Hereford-Angus heifer, then whole blood from the heifer into a Holstein calf, and finally, whole blood from the calf into a white-tailed deer (Odocoileus virginianus). A herpesvirus was isolated in bovine cell cultures inoculated with buffy coat cells from the heifer, and 2 deer inoculated with this herpesvirus developed the head and eye form of MCF. A deer inoculated with whole blood from the greater kudu also developed clinical signs of MCF, and a herpesvirus was subsequently recovered from the deer. Clinical signs of MCF included a mucopurulent catarrh, pyrexia (38.8 to 42.1 C), anorexia, and corneal opacity, and death occurred between postinoculation days 15 and 21.

Characteristics of the herpesvirus of malignant catarrhal fever isolated from captive wildebeest calves.

A herpesvirus was isolated from buffy coat cells from a newborn wildebeest (Connochaetes gnou) and from tissues of a 12-day-old wildebeest during the 1982 calving season of a captive, inbred herd maintained in a zoologic collection. Both wildebeests were clinically healthy, and there was no herd record that malignant catarrhal fever (MCF) existed. Each viral isolate produced cytopathologic changes in bovine kidney cell cultures (intranuclear inclusions and massive syncytia). The viral-infected cell cultures contained antigens of MCF virus detected by immunofluorescence. The morphology of each viral isolate as determined by electron microscopy was that of a herpesvirus. Suspensions of 4 to 5 ml of disrupted cell culture material which contained virus from each wildebeest were inoculated (IV) into white-tailed deer (Odocoileus virginianus). Each deer became clinically ill within 28 days. Both deer had mucoid catarrh and a febrile response (40.5 to 41 C). Each also seroconverted to MCF virus. The histopathologic change in the tissues from the 2 inoculated deer was vasculitis. At 16 to 17 days after the deer were inoculated, a syncytial-forming virus was isolated from each deer from buffy coat cells fused with polyethylene glycol (1000) to bovine fetal kidney cells. The virus was identified as MCF virus by immunofluorescence and production of antibody to MCF virus. The presence of virus in the inbred wildebeest herd established this species as a reservoir or latent carrier of African MCF virus at the zoologic park.

Experimental malignant catarrhal fever (African form) in white-tailed deer.

White-tailed deer (Odocoileus virginianus) were experimentally infected with the African form of malignant catarrhal fever (AMCF) virus by inoculation of whole blood from experimentally infected cattle, from whole blood obtained from a greater kudu (Tragelaphus strepsiceros) and from virus isolated in cell culture. The incubation period from AMCF in experimentally infected deer ranged from 13 to 18 days. Clinical disease was characterized by lacrimation, an elevated body temperature, conjunctivitis and swelling of the external lymph nodes. Histologic lesions were primarily characterized by widespread vasculitis and lymphadenopathy. The organs most severely affected were liver, lymphoid tissue, brain and lungs. Successful recovery and identification of AMCF virus was accomplished from one experimentally infected deer.

Visual defects in white-tailed deer from Michigan six case reports.

Six cases of unrelated visual defects in free-ranging white-tailed deer (Odocoileus virginianus) from Michigan are described. Two were congenital, two were of infectious etiology, one from central nervous neoplasia, and one from degenerative changes in lenses of both eyes.

Feline infectious peritonitis with spinal cord involvement in two cats.

Two cats from the same household had posterior paresis and hypergammaglobulinemia. Histologic evaluation of the spinal cords revealed a pyogranulomatous reaction consistent with that reported for feline infectious peritonitis.

Lead arsenate poisoning in a herd of beef cattle.

Lead arsenate poisoning was diagnosed in 2 beef heifers and was suspected in 6 other cattle from the same herd that had died previously and were not examined. Clinical signs in affected cattle included staggering, dehydration, hemorrhage, acidemia, and shock. Diagnosis was by arsenic and lead analysis of urine samples and kidney and liver tissue digests. Both examined heifers died within 4 days of onset of clinical signs. These cattle had been moved from an area with poor grazing conditions to a pasture with abundant forage. This pasture had an open shed that contained an open sack of lead arsenate insecticide. Old stores of this inorganic insecticide may still exist on farms or ranches, and are a hazard to livestock.

Isolation of wine influenza virus in Oklahoma.

Three isolations of swine influenca virus were made from 2 swine herds in west-central Oklahoma. Many swine in these herds had signs of respiratory tract disease, and in 1 herd, some affected animals also had diarrhea. Two isolations were made in swine testicle cell line and 1 in embryonating chicken eggs. All 3 strains were cytopathogenic for swine testicle cells.

Necropsy of the feeder and stocker calf.

Frequently occurring diseases are discussed in 2- to 12-month-old pastured or feedlot cattle. Emphasis is on gross necropsy lesions that are significant in differential diagnosis. Where applicable, practical laboratory tests that are helpful in confirming a diagnosis are described. Information about proper selection and preservation of tissues for submission to a diagnostic laboratory is included.

An epizootic of cerebral nematodiasis in rabbits due to Ascaris columnarus.

An epizootic of cerebral nematodiasis due to ascaris columnaris occurred in a commercial rabbitry, and 80 diseased rabbits died or were killed. The morbidity was high in groups of recently purchased rabbits and in the offspring of 12 breeder rabbits. The breeder rabbits which had been on the farm for more than a yr survived the outbreaks. Wild animals and birds had access to the facilities, but raccoons and skunks were never observed. A columnaris larvae were found on histopathologic examination. and live larvae were recovered from brains of 2 diseased rabbits.

Selenium toxicosis in three California sea lions (Zalophus californianus).

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.