Experimental yellow fever virus infection in the squirrel monkey (Saimiri spp.) I: gross anatomical and histopathological findings in organs at necropsy.

BACKGROUND: Non-human primates contribute to the spread of the yellow fever virus (YFV) and the establishment of transmission cycles in endemic areas. OBJECTIVE: To describe the severe histopathological aspects of YFV infection, 10 squirrel monkeys were infected with YFV and blood, brain, liver, kidney, spleen, heart, lung, lymph node and stomach were collected at 1-7, 10, 20 and 30 days post-infection (dpi). METHODS: Histopathological analysis and detection of the genome and viral antigens and neutralising antibodies were performed by RT-PCR, immunohistochemistry and neutralisation test, respectively. FINDINGS: Only one animal died from the experimental infection. The genome and viral antigens were detected in all investigated organs (1-30 dpi) and the neutralising antibodies from seven to 30 dpi. The brain contained perivascular haemorrhage (6 dpi); in the liver, midzonal haemorrhage and lytic necrosis (6 dpi) were observed. The kidney had bleeding in the Bowman's capsule and tubular necrosis (6 dpi). Pyknotic lymphocytes were observed in the spleen (1-20 dpi), the lung had haemorrhage (2-6 dpi), in the endocardium it contained nuclear pyknosis and necrosis (2-3 dpi) and the stomach contained blood in the lumen (6 dpi). MAIN FINDINGS: Squirrel monkeys reliably reproduced the responses observed in human cases of yellow fever and, therefore, constitute an excellent experimental model for studies on the pathophysiology of the disease.

Experimental yellow fever virus infection in the squirrel monkey (Saimiri spp. ) I: gross anatomical and histopathological findings in organs at necropsy

BACKGROUND Non-human primates contribute to the spread of the yellow fever virus (YFV) and the establishment of transmission cycles in endemic areas. OBJECTIVE To describe the severe histopathological aspects of YFV infection, 10 squirrel monkeys were infected with YFV and blood, brain, liver, kidney, spleen, heart, lung, lymph node and stomach were collected at 1-7, 10, 20 and 30 days post-infection (dpi). METHODS Histopathological analysis and detection of the genome and viral antigens and neutralising antibodies were performed by RT-PCR, immunohistochemistry and neutralisation test, respectively. FINDINGS Only one animal died from the experimental infection. The genome and viral antigens were detected in all investigated organs (1-30 dpi) and the neutralising antibodies from seven to 30 dpi. The brain contained perivascular haemorrhage (6 dpi); in the liver, midzonal haemorrhage and lytic necrosis (6 dpi) were observed. The kidney had bleeding in the Bowman's capsule and tubular necrosis (6 dpi). Pyknotic lymphocytes were observed in the spleen (1-20 dpi), the lung had haemorrhage (2-6 dpi), in the endocardium it contained nuclear pyknosis and necrosis (2-3 dpi) and the stomach contained blood in the lumen (6 dpi). MAIN FINDINGS Squirrel monkeys reliably reproduced the responses observed in human cases of yellow fever and, therefore, constitute an excellent experimental model for studies on the pathophysiology of the disease.

Reemerging of natural infection by Trypanosoma evansi in horses in Arari, Marajó Island, Brazil / Reemergência da infecção natural por Trypanosoma evansi em cavalos, na região do Arari, Ilha do Marajó, Brazil

ABSTRACT: Two outbreaks of trypanosomiasis by Trypanosoma evansi in horses in the municipality of Chaves, Marajó Island, Pará State, Brazil are reported. The first outbreak occurred in April 2011 in a farm with 147 horses; of these, 47 (31.97%) got sick, and 40 (27.21%) died. The second outbreak occurred in May 2012 and involved nine properties. Of a total of 679 horses, 209 (30.07%) got sick, and 183 (26.97%) died. The main clinical signs observed in these horses were weight loss, abdominal edema, toe dragging, and pelvic muscle atrophy. Necropsy was performed in two horses, one from each outbreak. Macroscopic alterations were not seen in the horse from the first outbreak; however, the horse from the second outbreak exhibited emaciation, pallor and icterus, as well as enlarged spleen with prominent white pulp at cut surface. Histopathology of the central nervous system of both animals revealed mild to severe, diffuse lymphoplasmacytic encephalitis, with presence of Mott cells. Immunohistochemistry for T. evansi revealed structures similar to intralesional trypomastigote forms. Between November and December of 2013, an epidemiological survey was carried out in the municipalities of Cachoeira do Arari, Santa Cruz do Arari, Salvaterra, Soure, and Chaves. Only Santa Cruz do Arari and Chaves had reported cases of the disease. Blood samples were collected from 243 horses for detection of T. evansi DNA by polymerase chain reaction (PCR) and 20 were positive.

RESUMO: São relatados dois surtos de tripanossomíase por Trypanosoma evansi , em cavalos no município de Chaves, Ilha do Marajó, Pará, Brasil. O primeiro surto ocorreu em abril de 2011 em uma fazenda com 147 cavalos, em que 47 (31,97%) adoeceram e 40 (27,21%) morreram. O segundo ocorreu em maio de 2012 e envolveu nove propriedades. De um total de 679 cavalos, 209 (30,07%) adoeceram e 183 (26,97%) morreram. Os principais sinais clínicos observados foram perda de peso, edema abdominal, emboletamento dos membros e atrofia da musculatura da região pélvica e membros posteriores. A necropsia foi realizada em dois cavalos, um de cada surto. O equino do primeiro surto não apresentou lesões macroscópicas, enquanto o segundo, do segundo surto, apresentava emagrecimento, palidez e icterícia, aumento do baço com protrusão da polpa branca ao corte. O sistema nervoso central de ambos os animais revelou uma leve à severa encefalite linfoplasmocitária, difusa, com presença de células de Mott. A imunohistoquímica para T. evansi revelou estruturas similares a formas tripomastigotas nas lesões. Entre novembro e dezembro de 2013, um levantamento epidemiológico foi realizado nos municípios de Cachoeira do Arari, Santa Cruz do Arari, Salvaterra, Soure e Chaves. Somente Santa Cruz do Arari e Chaves relataram casos da doença. Foram coletadas amostras de sangue de 243 equinos e realizada a reação em cadeia de polimerase (PCR) para a detecção do DNA de T. evansi das quais 20 foram positivas.

Fotossensibilizaçäo hepatógena em bovinos no Sul do Rio Grande do sul / Hepatogenous photosensitization in cattle in southern Rio Grande do Sul, Brazil

Säo descritos aspectos epidemiológicos e patológicos de 19 surtos de fotossensibilizaçäo observados em bovinos na regiäo sul do Rio Grande do Sul, no período entre 1984 e 1997. A doença, ocorre, principalmente, nos meses de outono e primavera com morbidade de 0,08 por cento a 64 por cento e mortalidade de 0 a 14 por cento. Todas as categorias säo afetadas e as áreas onde ocorrem os surtos se caracterizam por campos planos e baixos, freqüentemente utilizados para o plantio de arroz irrigado ou pastagens de azevém, trevo e aveia ou, ainda, em áreas similares com vegetaçäo nativa. A enfermidade caracteriza-se, clinicamente, por depressäo, anorexia, salivaçäo intensa e fotossensibilizaçäo observada nas áreas de pele despigmentadas e desprovidas de pêlos como o focinho, ao redor dos olhos, virilha, úbere e vulva. Nos casos severos, observam-se lesöes caracterizadas por ressecamento, rachaduras e desprendimento da pele, principalmente do dorso e membros, deixando à mostra superfície ulcerada. As lesöes macroscópicas säo características de insuficiência hepática, observando-se icterícia, fígado aumentado de tamanho com coloraçäo amarelada, aumento de tamanho da vesícula biliar, presença de líquido nas cavidades e, em alguns casos, edema do tecido subcutâneo e peritônio. As lesöes histológicas caracterizam-se, principalmente, por lesöes degenerativas do parênquima hepático, observando-se tumefaçäo e vacuolizaçäo difusa ou zonal dos hepatócitos. Observa-se, também, apoptose ou focos de necrose destribuídos aleatoriamente pelo parênquima, presença de megalócitos e, ainda, fibroplasia dos espaços porta e proliferaçäo de células de ductos biliares. A enfermidade é caracterizada como fotossensibilizaçäo hepatógena relacionada a dano primário ao parênquima hepático, de etiologia näo determinada, uma vez que foram descartadas as principais causas conhecidas de fotossensibilizaçäo de origem hepática em bovinos.