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To describe an outbreak of encephalomyelitis caused by West Nile virus (WNV) in horses in northern Indiana. Design--Case series. Animals--170 horses. Procedures--Horses with clinical signs suggestive of encephalomyelitis caused by WNV were examined. Date, age, sex, breed, and survival status were recorded. Serum samples were tested for anti-WNV antibodies, and virus isolation was attempted from samples of brain tissue. Climate data from local weather recording stations were collected. An epidemic curve was constructed, and case fatality rate was calculated. Results--The most common clinical signs were ataxia, hind limb paresis, and muscle tremors and fasciculations. Eight horses had been vaccinated against WNV from 2 to 21 days prior to the appearance of clinical signs. West Nile virus was isolated from brain tissue of 2 nonvaccinated horses, and anti-WNV IgM antibodies were detected in 132 nonvaccinated horses; in 2 other nonvaccinated horses, anti-WNV antibodies were detected and WNV was also isolated from brain tissue. Thirty-one (22.8%) horses died or were euthanatized. The peak of the outbreak occurred on September 6, 2002. Ambient temperatures were significantly lower after the peak of the outbreak, compared with prior to the peak. Conclusions and Clinical Relevance The peak risk period for encephalomyelitis caused by WNV in northern Indiana was mid-August to mid-September. Reduction in cases coincided with decreasing ambient temperatures. Because of a substantial case fatality rate, owners of horses in northern Indiana should have their horses fully protected by vaccination against WNV before June. In other regions of the United States with a defined mosquito breeding season, vaccination of previously non- vaccinated horses should commence at least 4 months before the anticipated peak in seasonal mosquito numbers, and for previously vaccinated horses, vaccine should be administered no later than 2 months before this time. (J Am Vet Med Assoc 2004;225:84–89) [ABSTRACT FROM AUTHOR]

Presents a response by Doctor Charlotte Edinboro and coauthors to a letter to the editor regarding their article about feline hyperthyroidism in the March 15, 2004 issue of "Journal of the American Veterinary Medical Association."

Details the epidemiologic study of relationships between consumption of commercial canned food and risk of hyperthyroidism in cats, using the Veterinary Medical Database. Estimates of the prevalence of feline hyperthyroidism from 1978 to 1997; Findings suggesting that the increasing prevalence of feline hyperthyroidism is not solely the result of aging of the cat population and that canned foods may play a role.

Infection with Baylisascaris procyonis, the common roundworm of raccoons, was found to be the cause of an epizootic of fatal CNS disease in domestic rabbits (Oryctolagus cuniculus). Clinical signs included torticollis, ataxia, tremors, and falling. Gross lesions were limited to white, raised nodules (1 to 1.5 mm) on the epicardium, endocardium, and liver serosa, and they were found to be larval granulomas. Microscopic lesions included multifocal myocarditis, multifocal hemorrhagic tracks and associated necrosis and inflammation in the liver, multifocal eosinophilic myositis, focal nephritis, and mild interstitial pneumonia; larval granulomas were seen in the heart, liver, lung, and mandibular salivary gland. Lesions in the brain consisted of multifocal areas of necrosis and inflammation in the cerebrum, cerebellum, midbrain, and medulla, with accompanying perivascular leukocyte aggregates and neuronal and axonal degeneration. Large numbers of large ascarid larvae were seen in the brain. Epidemiologically, infection was linked to the use of contaminated straw from a barn used by raccoons. On the basis of this study as well as that of similar studies, it was concluded that barn use and contamination by raccoons may be an important source of infection of animals and possibly man with this parasite.

Following vaccination for distemper, using a modified live-virus vaccine developed for dogs, 2 young kinkajous (Potos flavus) developed diarrhea, then central nervous system disease. Clinical signs included myoclonus, head trembling, loss of muscular coordination, and convulsions. One kinkajou gradually recovered; the other seemed to recover, then relapsed and was euthanatized. Microscopic lesions included those of interstitial pneumonia and enteritis and multifocal lymphocytic inflammation, gliosis, spongiosis, and swollen and degenerating axons in the cerebral, cerebellar, and brain stem white matter. Similar lesions were found at all caudally, as exemplified by complete destruction of the dorsal funiculi and dorsal horns of the gray matter of the upper sacral cord segments. Eosinophilic intranuclear inclusions were seen histologically in the glia in the spinal cord, midbrain, and cerebellum, and were confirmed as canine distemper viral inclusions by the fluorescent antibody method. It was concluded that modified live canine distemper virus vaccines should be used with caution or not at all in kinkajous.

Experiments were conducted to define the pathogenic potential of Salmonella heidelberg in weanling pigs. Oral inoculation with S heidelberg resulted in severe catarrhal enterocolitis with accumulation of large amounts of fluid in the small intestine and colon. Salmonella heidelberg was demonstrated, with fluorescence microscopy and bacteriologic cultural techniques, to colonize the ileum, to invade ileal mucosal enterocytes, and to reach mesenteric lymph nodes and extraintestinal tissues by 8 hours. In 5 pigs, intestinal loops were surgically prepared and inoculated with S heidelberg (to determine its invasiveness). Microscopically, there were atrophy of villi, erosion of enterocytes, and neutrophilic infiltration in the lamina propria. Ultrastructurally, intracellular bacteria were demonstrated in villous and cryptal enterocytes, as well as in macrophages of the lamina propria. Bacteria were morphologically intact, occurred free and membrane-bound and caused no detectable cytotoxic effect to the cell.

Twenty-six 4-week-old pigs were randomly allotted to 4 groups: group 1--orally inoculated with Salmonella typhimurium; group 2--orally dosed with S choleraesuis; and groups 3 and 4, with surgically constructed intestinal loops--loops inoculated with either S typhimurium or S choleraesuis. One pig each from groups 1 and 2 was killed at 8, 12, 24, 48, 72, 96, and 120 hours after inoculation. One pig each from groups 3 and 4 was killed at 2, 4, 6, 8, 12, and 24 hours after intestinal loop inoculation. Inoculation of S typhimurium resulted in acute enterocolitis of variable severity, whereas inoculation of S choleraesuis resulted initially in septicemia followed by formation of large necrotic and ulcerative lesions in the colonic mucosa. The most consistent systemic lesion of S choleraesuis infection was interstitial pneumonia and multifocal hepatic necrosis. Salmonella typhimurium and S choleraesuis were ultrastructurally within enterocytes of ligated ileal loops. Intracellular bacteria were morphologically intact, occurred free in the cytoplasm and membrane bound, and caused no detectable cytotoxic effect to the cell. Both S typhimurium and S choleraesuis penetrated the intestinal mucosa and were isolated from mesenteric lymph nodes at 2 hours after inoculation.

Cats (n = 4) were subjected to a bilateral osteotomy overlying the frontal sinuses. The right sinus of each cat served as a control, and the left sinus was filled with autogenous fat harvested from the subcutaneous region of the ventral part of the abdomen. All 4 cats were euthanatized at 200 days. The experiment was designed to determine whether satisfactory obliteration of the left frontal sinus could be accomplished without the benefit of intraoperative magnification. Grossly, obliteration of all 4 sinuses was accomplished in 3 of 4 cats. Light microscopy revealed fluid and/or regrowth of mucous membrane, both considered to be unfavorable sequelae. Although some fat retained viability in the sinus (50% in one cat, 40% in another), most of the obliteration was from mixed fibrous-adipose tissue or bony ingrowth. The clinical significance of this study was not determined, since all 4 cats were free of sinusitis before adipose tissue implantation.

At 4 days of age, 7 gnotobiotic pigs were orally inoculated with broth cultures of both Campylobacter sputorum subsp mucosalis (CSM) and Campylobacter hyointestinalis (CH). One pig was killed and evaluated each week for 7 weeks. Forty-eight hours after inoculation, CH and CSM were recovered from the feces of the pigs; thereafter, only CH was recovered. Organisms morphologically typical of Campylobacter sp were observed on the mucosal surface and on the crypt epithelial cells of the ileum, cecum, and colon from post-inoculation weeks (PIW) 2 through 7. Bacteria were clustered around the surface opening of goblet cells in pigs at PIW 6 and 7. Crypt epithelial cell proliferation and intracellular bacteria were not seen, except in 1 pig (killed at PIW 7) in which intracellular bacteria were seen only in the cecum. Therefore, CSM and CH did not induce porcine proliferative enteritis in gnotobiotic pigs.

Infection with larvae of Baylisascaris procyonis, the raccoon ascarid, was the cause of neurologic disease affecting young pheasants on a commercial pheasant ranch in Wisconsin. The disease was chronic and insidious, affecting 1% to 2% of the birds over a period of 2 years. Histologic lesions in the brain consisted of multifocal areas of necrosis and inflammation associated with Baylisascaris larvae. Onset of the disease at the farm correlated with introduction of chopped straw as bedding for the young birds. The straw was from a neighbor's barn and was contaminated with raccoon feces that contained B procyonis eggs. Cessation of use of the contaminated straw resulted in cessation of CNS disease in pheasants on the ranch.

Cerebrospinal nematodiasis and visceral larva migrans were diagnosed in an Australian (Latham's) brush turkey (Alectura lathami) that died at the Indianapolis Zoo following a progressive neurologic disease. Histologically, multifocal areas of malacia, necrosis, and inflammation were seen in sections of cerebrum, cerebellum, and midbrain; lesions were most severe in the cerebellum. A large granuloma in a lung contained cross sections of a large ascarid larva identified as Baylisascaris. The CNS lesions were typical of larval migration, as documented in other avian species. An epizootiologic investigation indicated that Baylisascaris procyonis was the etiologic agent and that the bird had acquired the parasite through contact with fecal contamination from wild raccoons at the St Louis Zoo, where the bird had been raised.

Immunologic deficiency was suspected in an 18-month-old Standardbred horse with persistent fever, multifocal bacterial infection, and neutropenia with a large number of immature neutrophils. Serum protein electrophoresis revealed marked depression of the gamma-globulin fraction (0.2 g/100 ml). Immunologic testing and histologic examination of lymphoid tissues identified the immune deficit as agammaglobulinemia. Serum concentrations of immunoglobulin (Ig)G and IgG(T) were initially low and declined with time; IgM and IgA were not detectable. The horse failed to produce antibodies when inoculated with foreign antigens but had a positive cell-mediated skin reaction to intradermal phytolectin injection, and lymphocytes responded normally to in vitro stimulation by mitogens. Histologic examination of lymphoid tissues revealed absence of germinal centers and plasma cells.

A young woodchuck (Marmota monax) with a history of CNS dysfunction and abnormal behavior was submitted frozen to the Animal Disease Diagnostic Laboratory, Purdue University, as a rabies suspect. The woodchuck was negative for rabies by the fluorescent antibody test. Histologically, multifocal areas of necrosis, malacia, and inflammation were seen in sections of cerebrum, midbrain, and cerebellum, accompanied by marked perivascular cuffing with eosinophils and lymphocytes. Sections of lung contained parasitic granulomas, one of which contained a large ascarid larva identified as Baylisascaris sp. The CNS lesions were typical of parasite migration, and resembled those commonly associated with infection with Baylisascaris larvae of raccoon or skunk origin. Cerebrospinal nematodiasis was diagnosed as the cause of the nervous disorder.