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Bovine viral diarrhea (BVD) is one of the economically important diseases of cattle. For many years, different types of vaccines have been commercially available, yet this disease is hard to control in high-density population areas. Detection and isolation of bovine viral diarrhea virus (BVDV) from any potential reservoir is vital, especially when considering virus eradication from a herd or locale. One potential source is wild ruminants. Ear notches and lymph nodes were collected from the wild population of white-tailed deer (Odocoileus virginianus)during deer hunting season in Indiana and tested for BVDV with a commercial BVD antigen capture enzyme-linked immunosorbent assay. Two samples out of 745 collected samples were positive, and subsequently cp and ncp BVDV was isolated from 1 ear notch and 1 lymph node. These isolates were genotyped as type 1a and 1b based on sequence analysis of the 5′ untranslated region (UTR). The results of the present study indicate that the prevalence of BVDV in the white-tailed deer population of Indiana is about 0.3%. Wild ruminants infected with BVDV should be taken into consideration during an eradication program of BVDV from the livestock population.

Toxoplasmosis was diagnosed in a woodchuck (Marmota monax) and 2 American red squirrels (Tamiasciurus hudsonicus). The woodchuck was euthanized by a wildlife rescue organization in New York after progressive clinical signs of head tilt, circling, and rapid weight loss. Necropsy examination revealed acute subdural hemorrhage over the right cerebral hemisphere. Histologic lesions included meningoencephalitis, myocarditis, and hepatitis. Protozoal cysts were present in affected and unaffected neuroparenchyma. The squirrels were found dead, emaciated, and moderately infested with fleas near a park in northern Indiana. In both squirrels, the lungs were consolidated with numerous nodules up to 2 mm in diameter. Histologically, pneumonia and encephalitis were associated with intracellular and free protozoa. Additional histologic lesions included multifocal lymphoplasmacytic encephalitis with intralesional protozoa in both squirrels. The protozoa were positive with Toxoplasma gondii-specific immunohistochemistry and had ultrastructural features consistent with T. gondiiin both squirrels. A real-time polymerase chain reaction test using T. gondii–specific probes demonstrated protozoal DNA in the lung, brain, and kidney of the squirrels and in the brain and heart of the woodchuck. To the authors' knowledge, this is the first report of toxoplasmosis in woodchucks or American red squirrels. Because rodents are common near urban settlements, this finding underscores their role as important intermediate hosts for T. gondii.

Monkeypox with extensive lesions was diagnosed in a prairie dog that was involved in a recent human outbreak of monkeypox in the Midwestern United States. Gross lesions included oral ulcers, pulmonary consolidation, enlarged cervical and thoracic lymph nodes, and multifocal, small, white umbilicated plaques in the gastrointestinal wall. Microscopic lesions were extensive in the lungs and consisted of fibrinonecrotic bronchopneumonia with vasculitis and poorly defined eosinophilic intracytoplasmic inclusion bodies in cells thought to be alveolar epithelial cells, histiocytes, and fibroblasts. Multifocal necrotizing lesions, often accompanied by myxedema, were also present in most of the other examined organs. Aggregates of pox viral particles were observed within lesions by transmission electron microscopy. Monkeypox virus infection was confirmed by real-time polymerase chain reaction and virus culture at the Centers for Disease Control and Prevention. This report highlights the difficulties of rapid diagnosis of exotic or emerging diseases and further substantiates the prairie dog as an animal model of monkeypox.

Two experiments were conducted to study choline-methionine interactions in young swine. Seventy-two pigs in three replicates and 144 pigs in four replicates were utilized in Experiments 1 and 2, respectively. The factorial design of both experiments included 0 and 330 mg/kg dietary choline. Methionine levels of .12% and .32% in Experiment 1 and of .32%, .52% and .72% in Experiment 2 were used. Methionine supplemented pigs gained faster (P<.01) and were more efficient (P<.05), and choline supplemented pigs gained faster (P<.01) and had a higher hematocrit (P<.05) in Experiment 1 than controls. Methionine supplementation increased daily gain (P<.01) (.72 >.32) or (P<.05) (.32 >.52) and decreased plasma urea (P<.05) (.72 <.32 = .52) in Experiment 2, with a trend toward a similar choline effect in both criteria. There were no differences in plasma triglycerides, plasma cholesterol, plasma alkaline phosphatase or plasma urea in Experiment 1. Gross and histological examination of tissues and organs (liver, kidney, spleen, heart, lung, brain, skeletal muscle, thyroid, adrenals, thymus, bone marrow, joints, gastro-intestinal system) of 12 necropsied pigs (three per treatment) of Experiment 1 revealed no differences. There were no differences in feed intake, feed conversion, or hematocrit in Experiment 2. Neither experiment showed differences in hemoglobin, hematocrit:hemoglobin ratio, plasma total phospholipids or plasma phosphatidylcholine. There was no choline-methionine interaction. These results showed that choline supplementation is required in an 11% protein, semi-purified diet (.13% cystine) when .32% methionine was present.

L6 myoblasts were used as an in vitro model to investigate the role of moniliformin and its interaction with monensin in turkey knockdown syndrome and sudden death syndromes in poultry. Cell viability and microscopic and ultrastructural alterations noted in L6 myoblasts cultured in the presence of moniliformin (0.0–0.3 µg/µl) were compared to those observed in parallel cultures also containing one of the following compounds: selenium (0–0.004 ng/µl), thiamine (0–0.3 µg/µl), or pyruvate (0–0.46 µg/µl). Marked dilation of the RER, membranous whorls, glycogen deposition, membrane-bound cytoplasmic inclusions and necrosis were observed in myoblasts exposed to 0.03/2-0.30 µg moniliformin/µl medium. Supplementation of medium with thiamine and pyruvate, or selenium, provided significant protection to cells exposed to 0.0–0.3 µg/µl or 0.0–0.15 µg moniliformin/µl, respectively. Dose-dependent differences in protein and ATP production were not detected. Myoblasts grown in medium containing 0–0.15 µg moniliformin/µl and 7.5–50.0 µM A23187, beauvericin or monensin had degrees of cytotoxicity similar to parallel cultures receiving only an ionophore. L6 myoblasts were a useful model of moniliformin toxicosis. The findings of this study suggest cytotoxicity due to moniliformin in L6 myoblasts may be due in part to oxidative damage and altered pyruvate metabolism, and that moniliformin does not predispose myoblasts to ionophore toxicosis. This study supports the results of in vivo investigations in poultry that moniliformin and monensin do not act synergistically to induce knockdown or monensin toxicosis.

Chronic exposure to moniliformin results in the development of myocardial hypertrophy and degeneration. The cause of this hypertrophy is unknown. However, moniliformin-induced hypoxia or altered function of cardiac pyruvate dehydrogenase, rather than direct cardiostimulation have been proposed as potential mechanisms. Isolated guinea pig atria were used in a cumulative concentration-response model to evaluate the direct effect of moniliformin on the rate and force of atrial contraction. Moniliformin did not affect the rate or force of atrial contraction. These results are consistent with the hypothesis that moniliformin does not have a cardiostimulatory effect. Therefore cardiac stimulation, e.g. stimulation of beta-adrenergic receptors, is unlikely to be the cause of the myocardial hypertrophy observed hi poultry chronically intoxicated with moniliformin.

A procedure for performing a thorough necropsy examination of feeder pigs or adult swine is presented. Lesions encountered in various organ systems due to various disease states are included, along with those changes of inconsequential or artifactual status.

A retrospective study of 256 cases of naturally acquired Streptococcus suisinfections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was performed to determine the epidemiologic factors and antibiotic susceptibility patterns associated with S. suisserotypes 1–8 and 1/2. A standardized computer form was used to record the history, signalment, and clinical signs obtained from the records of selected cases and the microscopic lesions identified after review of the histopathology slides for each case. A computer statistics package (SAP) was used to evaluate the data. Although the number of recovered S. suisisolates increased in the fall and winter months, most serotypes were readily isolated throughout the year; only serotypes 1, 4, 7, and 1/2 increased in frequency of isolation in the fall, winter, and spring months. The majority (6 1.1%) of infected pigs in this study were < 12 weeks of age. More than 75% of pigs infected with serotypes 1, 6, 7, and 1/2 were < 12 weeks of age. There was extensive overlap in the age distributions for pigs with each serotype, and statistically significant differences for most serotypes were not observed. Fifty percent of pigs infected with S. suisserotypes 1 and 1/2 were 3–10 weeks of age, 50% of pigs infected with serotype 2 were 6–14 weeks of age, and 50% of pigs infected with serotypes 3, 4, 5, 7, and 8 were 2–16 weeks of age. Isolates of S. suiswere not uniformly susceptible to penicillin, and a large percentage of isolates were resistant to many antibiotics in common usage. The results of this study indicated that the various serotypes of S. suiscould not be readily separated based on antibiograms, epidemiologic factors (herd size, breed, etc.), or geographic location.

Cytomegalic cells with intranuclear inclusions were identified in lung tissue from one of two weanling Western lambs with pneumonia and Mycoplasma ovipneumoniae infection. On the basis of light and electron microscopy, cytomegalovirus infection was diagnosed. Arrays of viral particles whose morphology was consistent with that of viruses of the herpes group were in the intranuclear inclusions of cytomegalic cells.

A retrospective study of 256 cases of naturally acquired Streptococcus suisinfections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was undertaken to describe the clinical signs, lesions, and coexisting organisms associated with S. suisserotypes 1–8 and 1/2. Infected pigs generally had clinical signs and gross lesions referable to either the respiratory system or to the central nervous system (CNS), but not both. Neurologic signs were inversely related to gross lesions in the respiratory tract (R2= −0.19, P= 0.003), as were respiratory signs and gross lesions in the CNS (R2= −0.19, P= 0.003). Suppurative bronchopneumonia was the most common gross lesion observed (55.2%, overall). Fibrinous and/or suppurative pleuritis, epicarditis, pericarditis, arthritis, peritonitis, and polyserositis were also reported. In 68% of the pigs, other bacteria in addition to S. suiswere isolated. Escherichia coli(35.0%) and Pasteurella multocida(30.0%) were the most commonly recovered bacterial agents. Mycoplasma and viral agents were identified less often, and their role in the development of streptococcosis was difficult to assess. In pigs infected with serotypes 2–5, 7, 8, and 1/2, suppurative meningitis with suppurative or nonsuppurative encephalitis, suppurative bronchopneumonia, fibrinopurulent epicarditis, multifocal myocarditis, and cardiac vasculitis were the most common microscopic lesions observed, whereas pigs infected with serotype 1 generally presented with suppurative meningitis and interstitial pneumonia. Microscopic lesions were morphologically similar among serotypes and were also similar to those reported with other pyogenic bacteria. The distribution of clinical signs and the gross and microscopic lesions in pigs infected with S. suisvaried among serotypes. However, these differences were not statistically significant and could not be used to distinguish between the various serotypes. These findings suggest that in pigs infected with S. suis,suppurative or fibrinopurulent inflammation in brain, heart, lungs, and serosae predominates and that bacterial culture is needed to confirm a diagnosis of streptococcosis in swine and to differentiate this disease from those caused by other pyogenic bacteria.

Systemic infection of mature beef cows with Salmonella typhimuriumresulted in death of cows, abortions, and premature births. Salmonella typhimuriumwas isolated from the kidney, liver, and spleen of cows but not from an aborted fetus. Diarrhea was not a prominent clinical feature of the epizootic. The source of the salmonella was not determined.