RESUMO A Peritonite Infecciosa Felina (PIF) é uma doença progressiva e fatal de felinos domésticos e selvagens, causada pelo vírus da Peritonite Infecciosa Felina (FIPV). A doença é caracterizada por uma reação imunomediada contra o vírus em vários órgãos. Este trabalho descreveu um relato de caso de epicardite fibrinosa causada pelo FPIV. Um gato macho, com três anos de idade, veio a óbito e foi recebido para necropsia. Macroscopicamente, foi observado exsudato fibrinoso esbranquiçado, friável, multifocal, medindo até 2 centímetros de espessura, no epicárdio, principalmente no ápice cardíaco. Microscopicamente, foi observado no epicárdio um infiltrado inflamatório misto, multifocal, composto por macrófagos, plasmócitos e linfócitos, associado a deposição de fibrina. A imuno-histoquímica foi positiva para o FIPV nas áreas de inflamação no epicárdio. Os autores descrevem o segundo relato de caso na literatura científica de epicardite causada pelo FIPV em um gato. Portanto, a epicardite deve ser considerada como diagnóstico diferencial em doenças cardíacas em Medicina Felina.

ABSTRACT Feline Infectious Peritonitis (FIP) is a progressive and fatal disease in domestic and wild cats, caused by Feline Infectious Peritonitis Virus (FIPV). The disease is characterized by an immunomediated reaction against the virus in various organs. This work described a case report of fibrinous epicarditis caused by FIPV. A male cat, three years old, died and was received to be necropsied. Grossly, soft, multifocal to coalescing, whitish fibrinous exudate, measuring up the 2 centimeters of thickness, was observed in the epicardium, mostly at the apex of the heart. Microscopically, severe, multifocal to coalescing inflammatory infiltrate was observed in the epicardium, composed mainly by macrophages, plasmocytes and lymphocytes, associated with fibrin deposition. Immunohistochemistry was performed for FIPV and was positive in the areas of inflammation in the epicardium. To the author´s knowledge, this is the second report of epicarditis due to FIPV in a cat. Therefore, epicarditis should be considered a differential diagnosis of cardiac diseases in Feline Medicine.

RESUMO A ocorrência de coccidiose clínica em aves está relacionada com a competência do sistema imune. Com o objetivo de avaliar a ocorrência natural de coccidiose em aves imunossuprimidas, foram selecionados frangos de corte, de ambos os sexos, com a 35 a 38 dias de vida para constituir 3 grupos - grupo I (n = 25), formado por aves sem coccidiose e negativas para coccídias no exame de fezes; grupo II (n = 25), formado por aves com coccidiose e positivas para coccídias no exame de fezes, e grupo III (n = 25), formado por aves sem coccidiose, negativas para coccídias no exame de fezes e submetidas à imunossupressão com dexametasona (4 mg/kg/dia por 4 dias, via subcutânea). Realizou-se o diagnóstico de coccidiose com a técnica de centrífugo-flutuação com solução saturada de sacarose para investigação de oocistos nas fezes e pela análise macro e microscópica das lesões intestinais observadas após a necropsia. A resposta imune foi avaliada pela reação de hipersensibilidade basofílica cutânea (CBH) à fitoemaglutinina (PHA) e pela relação entre o peso corporal e o peso da bursa de Fabricius ou do baço. Os frangos dos grupos II e III apresentaram menor reação CBH à PHA que os do grupo I, evidenciando-se diminuição da resposta imune. As aves do grupo III mostraram diminuição significante do peso da bursa de Fabricius e do baço em relação aos animais dos outros grupos. As espécies de coccídias encontradas foram E. acervulina e E. maxima nos animais dos grupos II e III, sendo ainda observada E. tenella nas aves do grupo III. A imunossupressão induzida pela dexametasona aumentou a suscetibilidade à coccidiose de ocorrência natural em frangos de corte criados comercialmente.

ABSTRACT The purpose of this study was to evaluate the occurrence of clinical coccidiosis in broilers immunosuppressed with dexamethasone. Male and female broiler chickens, from 35 to 38 days old were divided into 3 groups – group I (n = 25), including chickens without coccidiosis and negative for coccidia in fecal examination; group II (n = 25), including birds with coccidiosis and positive for coccidia in fecal examination; group III (n = 25), constituted by chickens with no coccidiosis, negative for coccidia in fecal examination and immunosuppressed with dexamethasone (4 mg/kg/day for 4 days, subcutaneous route). The diagnosis of coccidiosis was achieved using the centrifugal floatation technique in sucrose solution to investigate the presence of oocystis in stools, as well as by the observation of macroscopic and microscopic changes in the gut after necropsy. The immune response was evaluated by determination of cutaneous basophil hypersensitivity (CBH) response to phytohemagglutinin (PHA) and of the weight ratio of bursa of Fabricius and spleen in relation to body weight. Broilers from group II and III presented decreased CBH reaction to PHA in relation to group I, suggesting a decrease of the immune response. In addition, chickens from group III presented a significant decrease in the weight of the bursa of Fabricius and of the spleen. The coccidian types were E. acervulina and E. maxima in chickens from groups II and III, as well as E. tenella in chickens treated with dexamethasone. Immunosuppression induced by dexamethasone increased susceptibility to natural coccidiosis in commercially raised broiler chicks.

Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 µL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively).