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Prior studies have failed to detect a convincing association between histologic lesions of inflammation and clinical activity in dogs with inflammatory bowel disease (IBD). We hypothesized that use of a simplified histopathologic scoring system would improve the consistency of interpretation among pathologists when describing histologic lesions of gastrointestinal inflammation. Our aim was to evaluate the correlation of histopathologic changes to clinical activity in dogs with IBD using this new system. Forty-two dogs with IBD and 19 healthy control dogs were enrolled in this retrospective study. Endoscopic biopsies from the stomach, duodenum, ileum, and colon were independently scored by 8 pathologists. Clinical disease activity was scored using the Canine Inflammatory Bowel Disease Activity Index (CIBDAI) or the Canine Chronic Enteropathy Clinical Activity Index (CCECAI), depending on the individual study center. Summative histopathological scores and clinical activity were calculated for each tissue (stomach, duodenum, ileum, and colon) and each tissue histologic score (inflammatory/morphologic feature). The correlation between CCECAI/CIBDAI and summative histopathologic score was significant ( P < .05) for duodenum ( r = 0.42) and colon ( r = 0.33). In evaluating the relationship between histopathologic scores and clinical activity, significant ( P < .05) correlations were observed for crypt dilation ( r = 0.42), lamina propria (LP) lymphocytes ( r = 0.40), LP neutrophils ( r = 0.45), mucosal fibrosis ( r = 0.47), lacteal dilation ( r = 0.39), and villus stunting ( r = 0.43). Compared to earlier grading schemes, the simplified scoring system shows improved utility in correlating histopathologic features (both summative histology scores and select histologic scores) to IBD clinical activity.

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Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a "dogseating position". Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the "dog-seating position". The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidinbiotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

Plant sources are receiving special attention as feedstuffs in aquafeeds because of fish meal and oil shortage. However, studies about the effects of dietary fibre in fish are scarce. The inclusion of plant ingredients containing different levels of dietary fibre -broken rice (BR), ground corn (GC), wheat bran (WB), citrus pulp (CP) and soybean hulls (SH) were evaluated for the omnivores jundia´catfish and Nile tilapia. Tilapia is a typical omnivore with long intestines, whereas jundia´has short intestines and no pyloric ceca. Fibrous sources (CP, WB and SH) were less digestible for both species than the starchy ones (BR and GC). However, jundia´presented less ability to utilize the starch and protein from plant sources than tilapia. Growth of tilapia followed plant sources digestibility but no significant differences were detected for jundia´, probably because of its slower growth rate. Muscle layer was thicker in the distal intestine of jundia´fed CP diet, which possibly indicates an adaptation to propel the large volume of viscous digesta along the intestine. Therefore, despite its lower ability to utilize starchy plant sources, jundia´showed an adaptive capacity to utilize fibrous diets, which is in agreement with its omnivorous feeding habit.

Os bovinos afetados tinham idade média de 5 anos (2-8 anos) e a evolução clínica variou de 3-18 meses. Os sinais clínicos observados em todos os bovinos foram de disfunções cerebelares caracterizadas por hipermetria, incoordenação, quedas, tremores musculares, convulsões esporádicas e permanência em estação com os membros em base ampla. Em um bovino foi observada hemorragia traumática subdural no encéfalo e em outro, atrofia macroscópica do cerebelo. As lesões histológicas eram confinadas ao cerebelo e consistiram de vacuolização parcial ou total do pericário dos neurônios de Purkinje com ocasionais esferóides axonais na camada de células granulares e na substância branca cerebelar. Nos casos avançados, havia acentuada perda dos neurônios de Pukinje e proliferação dos astrócitos de Bergmann. O estudo morfométrico do número de neurônios de Purkinje e da espessura da camada molecular revelou um decréscimo no número de células de Purkinje que se correlacionou com conseqüente diminuição da espessura da camada molecular. Nineteen cases of Solanum fastigiatum (Solanaceae) poisoning in cattle from three municipalites in the State of Rio Grande do Sul, Brazil, occurring from 2003 to 2005, are described. Morbidity and mortality rates were respectively 6.7% and 3.4%. Average age of affected cattle was five-yearold (2 to 8-year-old) and duration of clinical courses was 3-18 months. Clinical signs observed in all affected cattle were cerebellar deficits characterized by hypermetry, incoordination, falls, muscle tremors, transitory seizures and wide base stance. One affected bovine had encephalic traumatic subdural hemorrhage and another had gross atrophy of the cerebellum. Histologically, lesions were restricted to the cerebellum and consisted of partial or complete vacuolation of the perikaria of Purkinje neurons with occasional axonal spheroids in the granular cell layer and in the white matter of the cerebellum. In advanced cases there were extensive loss of cerebellar Purkinje neurons and proliferation of the Bergmann's glia. The morphometric evaluation of the numbers of Purkinje neurons and of the thickness of the cerebellar molecular layer indicated decreased numbers of Purkinje neurons with consequent decrease in the molecular layer thickness.INDEX TERMS: Poisonous plants, Solanum fastigiatum, Solanaceae, lysosomal storage diseases, central nervous system, diseases of cattle, neuropathology.

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