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Encephalitozoon (E.) cuniculi has been occasionally identified as a cause of neurological or renal disease in dogs, but cases are not well documented in the United States. The medical records from a state veterinary diagnostic laboratory for 19 cases of fatal encephalitozoonosis in puppies were reviewed. Clinical histories included depression, inappetence, and progressive neurological signs of short duration. Histopathological evaluation showed brain and renal lesions typical of encephalitis and nephritis, respectively. Molecular analyses of parasites from 13 cases confirmed the identity of the organisms as E. cuniculi strain III. This parasite may be an underdiagnosed cause of fatal canine neurological or renal disease.

Infection with the zoonotic vector-borne protozoal parasite Trypanosoma cruzi causes Chagas disease in humans and dogs throughout the Americas. Despite the recognized importance of various wildlife species for perpetuating Trypanosoma cruzi in nature, relatively little is known about the development of cardiac disease in infected wildlife. Using a cross-sectional study design, we collected cardiac tissue and blood from hunter-donated wildlife carcasses- including raccoon (Procyon lotor), coyote (Canis latrans), gray fox (Urocyon cinereoargenteus), and bobcat (Lynx rufus) – from central Texas, a region with established populations of infected triatomine vectors and increasing diagnoses of Chagas disease in domestic dogs. Based on PCR analysis, we found that 2 bobcats (14.3%), 12 coyotes (14.3%), 8 foxes (13.8%), and 49 raccoons (70.0%) were positive for T. cruzi in at least one sample (right ventricle, apex, and/or blood clot). Although a histologic survey of right ventricles showed that 21.1% of 19 PCR-positive hearts were characterized by mild lymphoplasmocytic infiltration, no other lesions and no amastigotes were observed in any histologic section. DNA sequencing of the TcSC5D gene revealed that raccoons were infected with T. cruzi strain TcIV, and a single racoon harbored a TcI/TcIV mixed infection. Relative to other wildlife species tested here, our data suggest that raccoons may be important reservoirs of TcIV in Texas and a source of infection for indigenous triatomine bugs. The overall high level of infection in this wildlife community likely reflects high levels of vector contact, including ingestion of bugs. Although the relationship between the sylvatic cycle of T. cruzi transmission and human disease risk in the United States has yet to be defined, our data suggest that hunters and wildlife professionals should take precautions to avoid direct contact with potentially infected wildlife tissues.

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Six dogs were diagnosed with protein-losing enteropathy (PLE). There was no evidence of inappropriate inflammatory infiltrates or lymphangiectasia in multiple mucosal biopsies of the small intestine of 4 of the dogs. The 5th and 6th dogs had obvious lymphangiectasia and a moderate infiltrate of inflammatory cells in the intestinal mucosa. All 6 dogs had a large number of dilated intestinal crypts that were filled with mucus, sloughed epithelial cells, and/or inflammatory cells. Whether PLE occurs in these dogs because of protein lost from the dilated crypts into the intestinal lumen or whether the dilated crypts are a mucosal reaction due to another undetermined lesion that is responsible for alimentary tract protein loss is unknown. However, when large numbers of dilated intestinal crypts are present, they appear to be associated with PLE even if there are no other remarkable lesions in the intestinal mucosa.Key words: Gastroduodenoscopy; Hypoalbuminemia; Intestinal biopsy; Lymphangiectasia P rotein-losing enteropathy (PLE) is a syndrome in which there is excessive loss of protein from the gastrointestinal tract. In general, PLE is only recognized after animals become hypoalbuminemic, 1,2 although enteropathies in people can produce excessive alimentary protein loss without causing abnormal serum protein concentrations. PLE has been well described in the dog, and certain breeds, such as the Lundehund, 3 Basenji, 4 and Soft-coated Wheaten Terrier 5 appear to be at increased risk of PLE. Various intestinal lesions may be associated with PLE, including lymphangiectasia, immunoproliferative enteropathy, lymphocyticplasmacytic enteritis, eosinophilic enteritis, gastrointestinal ulceration/erosion, giardiasis, chronic intussusception, small intestinal bacterial overgrowth, neoplasia, hypoalbuminemia causing mucosal edema, increased activation of tissue plasminogen activator, systemic lupus erythematosus, vascular lesions in the intestinal mucosa, and chemotherapy/ radiation therapy. [6][7][8][9][10][11][12][13][14][15][16][17][18][19] Most of these diseases can be diagnosed by gross examination or by light microscopic examination of small intestinal tissue samples. However, some of these diseases such as systemic lupus erythematosus or small intestinal bacterial overgrowth cannot reliably be identified with biopsy and routine histopathology. 15,20 Although lesions of small intestinal crypts have been associated with PLE in 1 dog, this dog also had absence of villi and large areas of mucosal ulceration. 21 In this paper, we describe 6 dogs with PLE in which a large number of intestinal crypts were dilated and filled with mucus, with or without inflammatory cellular debris. None of our dogs had discernable ulceration or lack of villi. The purpose of this report is to document this histologic lesion and its apparent association with PLE in the dog. Materials and MethodsThe cases reported were examined at Texas A&M University between 1989 and 1999, and at Michigan State University in 1997. All dogs had panhypoproteinemia...

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The G M2 gangliosidoses are a group of lysosomal storage diseases caused by defects in the genes coding for the enzyme hexosaminidase or the G M2 activator protein. Four Jacob sheep from the same farm were examined over a 3-year period for a progressive neurologic disease. Two lambs were 6-month-old intact males and 2 were 8-month-old females. Clinical findings included ataxia in all 4 limbs, proprioceptive deficits, and cortical blindness. At necropsy, the nervous system appeared grossly normal. Histologically, most neurons within the brain, spinal cord, and peripheral ganglia were enlarged, and the cytoplasm was distended by foamy to granular material that stained positively with Luxol fast blue and Sudan black B stains. Other neuropathologic findings included widespread astrocytosis, microgliosis, and scattered spheroids. Electron microscopy revealed membranous cytoplasmic bodies within the cytoplasm of neurons. Biochemical and molecular genetic studies confirmed the diagnosis of G M2 gangliosidosis. This form of G M2 gangliosidosis in Jacob sheep is very similar to human Tay-Sachs disease and is potentially a useful animal model.

Melarsomine dihydrochloride is highly effective against both sexes of adult and L5 Dirofilaria immitis. Common adverse reactions include injection site irritation and reluctance to move. Neurologic complications associated with i.m. injection of melarsomine dihydrochloride for treatment of heartworm disease in 3 dogs are described. Different degrees of neurologic complications have been identified; the pathophysiologic features are unknown. It is speculated that the compound migrates out of the injection site via fascial planes and causes an ascending inflammation along nerve roots. The resulting extradural cord compression secondary to extensive inflammation and necrosis of epidural fat could induce a variety of neurologic deficits. Alternatively, inappropriate injection technique may result in direct contact of melarsomine with neural tissue. A heightened awareness of proper injection technique might prevent the development of most neurologic complications.