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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."

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.

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.