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Eight of 9 juvenile raccoons at a rehabilitation center died without obvious prior clinical signs. Gross changes were unremarkable except for mildly distended intestines. Microscopically, crypt loss, distension, necrosis, and regeneration with intranuclear viral inclusions were observed in the small intestine, with marked lymphoid depletion and necrosis in Peyer patches and mesenteric lymph nodes. Immunohistochemistry with a canine parvovirus antibody showed intensive signals of parvoviral antigens in the crypts and lymphoid germinal centers. Metagenomic sequencing allowed assembly of a complete parvoviral genome with >99% identity to canine parvovirus 2a, as well as Salmonella enterica subsp. enterica. Also, S. enterica subsp. enterica serovar Thompson with multiple antimicrobial resistance was isolated from the intestinal contents. Concurrent infection with parvovirus and Salmonella should be included as a differential diagnosis in raccoons with sudden death.

A juvenile raccoon was euthanized because of severe neurologic signs. At postmortem examination, no significant gross lesions were present. Histologic evaluation demonstrated nonsuppurative encephalitis in thalamus, brainstem, and hippocampus, cerebellar Purkinje cell loss, as well as poliomyelitis and demyelination of the spinal cord. Parvovirus antigen–specific immunohistochemistry revealed immunopositive neurons in the brainstem, cerebral cortex, and hippocampus. A few Purkinje cells were also immunopositive. DNA extracted from formalin-fixed, paraffin-embedded brain tissue (thalamus, hippocampus, cerebral cortex) yielded a positive signal using PCR targeting both feline and canine parvovirus. Sequencing analyses from a fragment of the NS1 gene and a portion of the VP2 gene confirmed the presence of DNA of a recent canine parvovirus variant (CPV-2a–like virus) in the cerebellum. Our case provides evidence that a recent canine parvovirus (CPV) strain ( Carnivore protoparvovirus 1) can infect cerebral and diencephalic neurons and cause encephalitis in an otherwise healthy raccoon. Parvovirus-induced encephalitis is a differential diagnosis of rabies and canine distemper in raccoons with neurologic signs.

A juvenile raccoon ( Procyon lotor) was submitted dead to the Minnesota Veterinary Diagnostic Laboratory for rabies testing without history. The animal had marked hypoplasia of the cerebellum. Histology demonstrated that most folia lacked granule cells and had randomly misplaced Purkinje cells. Immunohistochemistry revealed the presence of parvoviral antigen in a few neurons and cell processes. PCR targeting feline and canine parvovirus yielded a positive signal. Sequencing analyses from a fragment of the nonstructural protein 1 ( NS1) gene and a portion of the viral capsid protein 2 ( VP2) gene confirmed the presence of DNA of a recent canine parvovirus variant (CPV-2a–like virus) in the cerebellum. Our study provides evidence that (canine) parvovirus may be associated with cerebellar hypoplasia and dysplasia in raccoons, similar to the disease that occurs naturally and has been reproduced experimentally by feline parvoviral infection of pregnant cats, with subsequent intrauterine or neonatal infections of the offspring.

Two 6-month-old raccoon kits, which had been rescued and fostered in preparation for return to the wild, became acutely ill and died 3 weeks before scheduled release. At necropsy, the kits had grossly enlarged livers and spleens, diffusely consolidated lungs, and generalized lymphadenopathy. Histologically, extensive infiltrates of macrophages containing yeast organisms were identified in lung, liver, kidney, spleen, lymph nodes, intestinal tissues, brain, adrenal gland, bone marrow, and thymus of both animals. Histiocytic inflammation with accompanying fibrosis was widespread, with necrotic foci evident in lungs, spleen, and intestinal sections. Fungal organisms were observed on sheep blood agar plates; however, repeated subcultures to fungal media designed to induce conidial structures for fungal identification were unsuccessful. Partial DNA sequencing of the 28S ribosomal RNA gene of the blood agar isolate identified 100% homology with Ajellomyces capsulatus (anamorphic name Histoplasma capsulatum). The kits were rescued and fostered in the San Francisco Bay area and it is likely that the exposure to H. capsulatum occurred in this area. Histoplasma sp. infection in wild mammal species is often used as an indication of spore contamination of a geographic region. Northern California is not known to be an endemic region for H. capsulatum, which is not a reportable disease in this state. The presence of severe, disseminated disease and the need for molecular identification associated with the isolate from a nonendemic region identified in the present report may indicate genetic adaptation and altered characteristics of this agent and may warrant further investigation.

A lethargic, wild, juvenile raccoon died and was subsequently presented for necropsy. The lungs had widely disseminated, finely granular, yellow–tan foci with moderate pulmonary, as well as, thoracic lymphadenopathy. Histopathology revealed numerous cross-sections of larval trematodes morphologically consistent with diplostomid mesocercariae and metacercariae as well as moderate alveolointerstitial pneumonia with a mixed population of eosinophils, macrophages, lymphocytes, and plasma cells. The presence of larval trematodes within lymphatics in multiple organs indicates a route of fluke migration. Live specimens of mesocercariae and metacercariae recovered from refrigerated lung tissue after 7 days were identified as Pharyngostomoides sp., an intestinal diplostomid parasite (trematode) of raccoons and other mammals that is similar in appearance and life cycle to Alaria spp.

To determine the transmissibility of transmissible mink encephalopathy (TME) agent to raccoons and to provide information about clinical course, lesions, and suitability of currently used diagnostic procedures for detection of transmissible spongiform encephalopathies (TSEs) in raccoons, 4 raccoon kits were inoculated intracerebrally with a brain suspension from mink experimentally infected with TME. One uninoculated raccoon kit served as a control. All 4 animals in the TME-inoculated group showed clinical signs of neurologic disorder and were euthanized between 21 and 23 weeks postinoculation (PI). Necropsy examinations revealed no gross lesions. Spongiform encephalopathy was observed by light microscopy, and the presence of protease-resistant prion protein (PrPres) was detected by immunohistochemistry and Western blot techniques. Scrapie-associated fibrils were observed by negative-stain electron microscopy in the brains of 3 of the 4 inoculated raccoons. These findings confirm that TME is experimentally transmissible to raccoons and that diagnostic techniques currently used for TSE in livestock detect prion protein in raccoon tissue. According to previously published data, the incubation period of sheep scrapie in raccoons is 2 years, whereas chronic wasting disease (CWD) had not shown transmission after 3 years of observation. Because incubation periods for the 3 US TSEs (scrapie, TME, and CWD) in raccoons appear to be markedly different, it may be possible to use raccoons for differentiating unknown TSE agents. Retrospective genotyping of raccoons using frozen spleens showed that the raccoon PrP gene is identical to the mink gene at codons 179 and 224. Further studies, such as the incubation periods of bovine spongiform encephalopathy and other isolates of scrapie, CWD, and TME in raccoons, are needed before the model can be further characterized for differentiation of TSE agents.

During a 2-year period (1995-1997), vacuoles were detected in neurons of 21/50 (42% preva- lence) raccoons (Procyon lotor) in Oregon. Age or sex predisposition was not apparent. Twenty of these raccoons were from within a radius of 40 km of Corvallis in western Oregon. Microscopically, the vacuoles were variable in size, were in the perikarya, and were consistently present in pontine nuclei. Brain tissues were negative for rabies virus antigen by fluorescent antibody test and for the protease-resistant protein prion by immunohistochemistry. Electron microscopic examination of the brain stem of selected animals revealed ac- cumulation of electron-dense material within neuronal perikarya. Light and electron microscopic examination indicated that the accumulated intracellular material had a high lipid content. These lesions suggest a form of neuronal storage condition. Further research is required to identify the composition of the intracellular lipid material, to elucidate the mechanism of neuronal vacuolation in raccoons, and to understand the basis for the apparent geographic restriction of this lesion. Raccoons (Procyon lotor) are nocturnal and are widespread throughout North America. They are high- ly adaptable omnivores and have managed to survive and increase their numbers in many urban and subur- ban areas. For this reason, they have been used as monitors of zoonotic diseases and environmental con- tamination. 2,7 Spongiform changes affecting the neuropil and neu- ronal cell bodies have been described in experimental and natural cases of rabies in skunks and foxes 3 and in a heifer. 5 Neuronal perikaryonic vacuolation is also seen in scrapie and related spongiform encephalopa- thes 6 and in lysosomal and acquired storage diseases of various animals. 11 Naturally occurring transmissible spongiform encephalopathy and storage diseases have not been documented in raccoons, but rabies is com- monly encountered in raccoons of the eastern United States. However, vacuolation of neurons or the neu- ropil has not been seen in raccoons with naturally ac- quired rabies 9 or in raccoons experimentally infected with either a dog or a raccoon isolate of the rabies virus. 10 Recently vacuolation in neurons of 2 raccoons from 2 different geographic locations in the USA has been described. 8 Here, we describe histopathologic changes in 21 additional raccoons from the same geographic area of Oregon from which 1 of the original cases was identified. 9

>> 12 provided an opportunity to examine a large number of raccoons for pathologic changes. This communication documents adrenal gland tumors in 8 raccoons. The animals used for this investigation were obtained from 4 different locations in the eastern USA. During a 5-year period (1986-1990), 322 raccoons (113 from Pennsylvania, 85 from Ohio, 73 from Virginia, 51 from South Carolina) were necropsied, and their tissues were examined histopathologically. The Pennsylvania raccoons were from raccoon rabies-enzootic areas and were rabies suspects. The raccoons from Ohio were obtained from the wild and were used for experimental evaluation of the V-RG vaccine, rabies pathogenesis, and adenovirus studies.

1. Batsaki J: 1968, Degenerative lesions of the heart. In: Pathology of the heart and blood vessels, ed. Gould S, p. 479–526. CTP, Springfield. 2. Bharati S, Rosen KM, Miller RA, Lev M: 1974, Conduction system examination in a case of spontaneous heart block in a dog. Am Heart J 88:596–600. 3. Denac M, Stunzi H, Mehring M: 1970, Atrio-ventricular compensatory rhythm in the dog following inhibition of development of the atrial musculature. Zentralbl Vet Med Reihe A 17: 920–924. 4. Frankel KA, Rosser RJ: 1976, The pathology of the heart in progressive muscular dystrophy: epimyocardial fibrosis. Hum Pathol 7:375–386. 5. Hisaoka T, Kawai S, Ohi H, et al.: 1990, Two cases of chronic myocarditis mimicking arrhythmogenic right ventricular dysplasia. Heart Vessels Suppl. 5:51–54. 6. Jeraj K, Ogburm PN, Edwards WD, Edwards JE: 1980, Atrial standstill, myocarditis and destruction of cardiac conduction system: clinicopathologic correlation in a dog. Am Heart J 99: 185–192. 7. Liu SK: 1982, Cardiac disease in the dog and cat, In: Pig model for biomedical research, ed. Roberts HR, Dodds WJ, pp. 110– 133. Pig Research Institute, Taiwan, Republic of China. 8. Marcus FI, Fontaine GH, Guiraudon G, et al.: 1982, Right ventricular dysplasia: a report of 24 adult cases. Circulation 65: 384–398. 9. Moriuchi T, Kagawa N, Mukoyama M, Hizawa K: 1993, Autopsy analyses of the muscular dystrophies. Tokushima J Exp Med 40:83–93. 10. Scott TM: 1977, Heart. In: Pathology, ed. Anderson WAD, Kissane JM, 7th ed., pp. 737–855. C. V. Mosby, St. Louis, MO. 11. Valentine BA, Cummings JF, Cooper BJ: 1989, Development of Duchenne-type cardiomyopathy. Morphologic studies in a canine model. Am J Pathol 135:671–678. 12. Vecht RJ, Carmichael DJS, Gopal R, Philip G: 1979, Uhl’s anomaly. Br Heart J 41:676–682.

4This communication documents the relevant gross, microscopic, and immunohistochemical findings of a proliferative skin lesion in 2 of the 53 raccoons with papillomavirus infection. These 2 raccoons were adult males which were live-trapped in an area where vaccine-laden baits were distributed. The raccoons were in good nutritional state and appeared healthy. However, on the dorsal aspects of all 4 paws, there were numerous small (1-2 mm in diameter), slightly raised, roughly circular lesions (Fig. 1). The lesions were lightly pigmented (gray), and occasionally coalesced. All the paws and representative tissues of all major organs were collected and placed into neutral buffered 10% formalin as previously described. 3,4 The tissues were embedded in paraffin, sectioned at 6 µm, and stained with hematoxylin and eosin (HE). Additional sequential sections were stained using the avidin-biotin complex (ABC) method for dection of papillomaviru s anti

2. Cunningham CC: 1973, Sarcocysts in the heart muscle of a foal. 6. Fayer R, Hounsel C, Giles RC: 1983, Chronic illness in a SarVet Rec 92:684. cocystis -infected pony. Vet Rec 113:216-217. 3. Dubey JP, Speer CA, Fayer R: 1989, Sarcocystosis of animals 7. Schneider T, Zimmermann U, Matuschka FR, et al.: 1985, Clinand man, p. 215. CRC Press, Boca Raton, FL. ical signs, serum-enzyme activity and the dynamics of antibody 4. Edwards GT: 1984, Prevalence of equine Sarcocystis in British titres in horses with experimental sarcosporidial infections. Zenhorses and a comparison of two detection methods. Vet Rec 115: tralbl Veterinaermed Reihe B 32:29-39. 265-267. 8. Tinling SP, Cardinet GH III, Blythe LL, et al.: 1980. A light and 5. Fayer R, Dubey JP: 1982, Development of Sarcocystis fayeri in electron microscopic study of sarcocysts in a horse. J Parasitol the horse. J Parasitol 68:856-860. 66:458-465.

Eosinophilic myositis is a relatively rare condition of cattle and sheep in which individual muscles or groups of muscles may be involved, or the lesions may be widespread through all muscles, including the heart The condition has been seen in pigs, and a case has been described in a monkey. A similar pathological entity confined to the muscles of mastication has been reported in dogs. Although Sarcocystis has often been implicated in ruminants and pigs, the specific cause of this condition remains unknown. We report here a case of generalized eosinophilic myositis with simultaneous infestation with Sarcocystis in a raccoon, and the results of a survey on the prevalence of muscle parasites in raccoons. Between July 1985 and February 1988, l01 adult raccoons of both sexes were examined at the Laboratory of Large Animal Pathology, University of Pennsylvania, Kennett Square, Pennsylvania. These raccoons were either suspect rabies cases (from Pennsylvania) or were part of a larger study on the development of an oral vaccinia-rabies glycoprotein recombinant viral vaccine (from Ohio).’ Whenever possible, prior to euthanasia of the raccoons, blood samples were obtained for routine hematology and blood chemistry. At the time of necropsy, a sample of cerebrospinal fluid (CSF) was obtained (within 15 min of euthanasia) for cytological examination. Also at the time of necropsy, besides other tissue samples, striated muscle samples from 5 different organs (heart, tongue, diaphragm, proximal esophagus, and masseter muscle) were fixed in 10% phosphate-buffered formalin. Examination of these muscles forms the basis of the present study. The tissues were processed routinely for histopathology for examination by light microscopy. Selected sections were stained with periodic acid-Schiff (PAS) and hematoxylin and eosin (HE). Samples of striated muscles were taken for electron microscopy, the results of which have been published elsewhere. Gross lesions were seen in the muscles of only 1 of the raccoons-an adult female used in the vaccine trial. The lesions consisted of numerous small (to 3 mm wide), pale white, streaklike to oval granulomatous areas, which were numerous and more prominent on the diaphragm and on the muscles of the abdomen and the thigh (Fig. 1). Histological examination of the striated muscles from different anatomical sites revealed presence of Sarcocystis (48 cases), Trichinella (3 cases), and Hepatozoon (in 1 raccoon). Heart muscle was the least likely tissue (12% positive), whereas the tongue (37% positive) was the most common place for