Dinâmica das alterações do baço associadas ao estado clínico de cães com leishmaniose visceral / Dynamic of changes of the spleen associated with the clinical status ofdogs with visceral leishmaniasis

Foram avaliadas as alterações esplênicas de cães com leishmaniose visceral, sintomáticos e assintomáticos, em relação ao número de sinais clínicos observados nestes animais. Cães sintomáticos foram divididos em cinco grupos de acordo com o número de sinais clínicos presentes. Nos grupos com três ou mais sinais, houve hipertrofia e hiperplasia dos cordões esplênicos e depleção de células linfóides da bainha periarteriolar. No grupo de cães com apenas um sinal clínico houve depleção de folículos da polpa branca. Hiperplasia dos folículos foi observada em intensidade maior no grupo de cães mostrando mais de cinco sinais clínicos.Granulomas estavam presentes em maior intensidade no grupo de cães exibindo cinco sinais. Granulações eosinofílicas no citoplasma de células plasmáticas (corpúsculos de Russell) foram significativamente maiores no grupo de cães com cinco sinais clínicos em comparação com aqueles com apenas um, dois, três e quatro sinais clínicos e cães assintomáticos. Os resultados mostram que o baço apresenta profundas alterações morfológicas que podem influenciar a evolução da infecção.

Alterations in the spleen of dogs with symptomatic and asymptomatic leishmaniasis have been evaluated with respect to the number of clinical signs observed in such animals. Symptomatic dogs were divided into five groups according to the number of clinical signs presented. In groups with three or more signs, there was hypertrophy and hyperplasia of the splenic cords and depletion of periarteriolar lymphatic sheath cells. In the group of dog with only one clinical sign, a there was follicle depletion in the white pulp. Follicle hyperplasia was higher in the canine group showing more than five clinical signs. Granulomas were present in a greater quantity in the canine group exhibiting five signs. Eosinophil granulations in the cytoplasm of plasma cells (Russell bodies) were significantly greater in the canine group with five clinical manifestations compared to those with only one, two, three and four manifestations and to asymptomatic dogs. The results show that the spleen undergoes profound morphologic changes that can influence the outcome of infection.

Fiebre entérica en fase de fastigium: notas epicríticas acerca de un caso de autopsia / Enteric fever in fastigium phase; epicritic notes on a necropsy case

La fiebre tifoidea es una enfermedad sistémica de etiología infecciosa ocasionada por el bacilo gramnegativo Salmonella typhi. Se presenta el caso de una mujer de 19 años quien comenzó con fiebre, dolor abdominal y diarrea; posteriormente cursó con insuficiencia hepática, necrosis tubular aguda, rabdomiolisis y trombocitopenia. Falleció a los 3 días del ingreso hospitalario. Los hallazgos de autopsia fueron: ulceración de placas de Peyer, inflamación y necrosis de ganglios linfáticos mesentéricos, úlceras puntiformes en colon, hepatización pulmonar, congestión hepática, esplénica y renal, así como hemorragias maculares en mesencéfalo y puente. Los cortes histológicos evidenciaron grupos de macrófagos alrededor de focos de necrosis (nódulos tifoideos) en diversas localizaciones: aracnoides, parénquima cerebral, pulmón, hígado, bazo, riñón y médula ósea. Estos hallazgos permitieron concluir el diagnóstico de fiebre tifoidea en fase de fastigium. La fiebre tifoidea presenta 5 fases cuya expresión morfológica es resultado de una serie de interacciones entre Salmonella typhi y el sistema fagocítico mononuclear del hospedero.

Typhoid fever is a multisystemic disease of infectious etiology with the gramnegative rod Salmonella typhi as its causative agent. We present the case of a 19 year old woman who started with fever, abdominal cramps and diarrhea progressing to hepatic insufficiency, acute tubular necrosis, rhabdomyolysis and thrombocytopenia dying three days after hospital admission. Autopsy findings were as follows: Peyer's patches ulcers, necrosis and inflammation of mesenteric lymph nodes, dotted ulcers in colon, lung hepatisation, hepatic, splenic and renal congestion, as well as purpuric lesions in mesencephalon and pons. Microscopic examination revealed macrophage clusters surrounding spots of necrosis (typhoid nodules) in the next locations: arachnoid mater, brain parenchyma, lung, liver, spleen, kidney and bone marrow. These findings supported a diagnosis of typhoid fever at fastigum stage. Typhoid fever goes through 5 consecutive stages whose morphological expression is product of several interactions between Salmonella typhi and the mononuclear phagocyte system of its host.