Inquérito sorológico da infecção pelos vírus da encefalomielite equina no estado de Minas Gerais, Brasil / Serological survey of equine encephalomyelitis virus infection in the state of Minas Gerais, Brazil

Foi investigada a ocorrência da infecção pelos vírus da Encelafalomielite Equina do Leste (EEE), Encefalomielite Equina do Oeste (WEE) e Encefalomielite Equina Venezuelana (VEE) em equídeos não vacinados contra tais agentes, criados em dez delegacias regionais do estado de Minas Gerais (Almenara, Bambuí, Curvelo, Governador Valadares, Montes Claros, Oliveira, São Gonçalo do Sapucaí, Teófilo Otoni, Unaí e Viçosa), empregando-se a técnica de soroneutralização em microplacas. Dos 826 animais examinados, 30,2% ((250/826) foram soropositivos para EEE e 1,9% (16/826) para o zuelano de Encefalomielite Equina circulam na população equina do estado de Minas Gerais.

The occurrence of Equine Eastern Encephalomyelitis (EEE), Equine Western Encephalomyelitis (WEE) and Equine Venezuelan Encephalomyelitis (VEE) virus infection was investigated in equids not vaccinated against these viruses. The animals were distributed in ten regional districts of the state of Minas Gerais (Almenara, Bambuí, Curvelo, Governador Valadares, Montes Claros, Oliveira, São Gonçalo do Sapucaí, Teófilo Otoni, Unaí e Viçosa). Microplate serum neutralization test was used to detect antibodies against encephalitis virus. Two hundred and fifty animals (30.2%, 250/826) were EEE-seropositive, while 1.9% of them (16/826) were VEE-seropositive. No animals were found to be seropositive for WEE. In conclusion, either EEE or VEE viruses circulate in the equid population of the state of Minas Gerais.

Astrocytic and microglial response and histopathological changes in the brain of horses with experimental chronic Trypanosoma evansi infection / Resposta astrocítica e microglial e alterações histopatológicas no sistema nervoso central de eqüinos infectados cronicamente com Trypanosoma evansi

This study aimed to characterize astrocytic and microglial response in the central nervous system (CNS) of equines experimentally infected with T. evansi. The experimental group comprised males and females with various degrees of crossbreeding, ages between four and seven years. The animals were inoculated intravenously with 10(6) trypomastigotes of T. evansi originally isolated from a naturally infected dog. All equines inoculated with T. evansi were observed until they presented symptoms of CNS disturbance, characterized by motor incoordination of the pelvic limbs, which occurred 67 days after inoculation (DAI) and 124 DAI. The animals in the control group did not present any clinical symptom and were observed up to the 125th DAI. For this purpose the HE histochemical stain and the avidin biotin peroxidase method was used. Lesions in the CNS of experimentally infected horses were those of a wide spread non suppurative meningoencephalomyelitis.The severity of lesions varied in different parts of the nervous system, reflecting an irregular distribution of inflammatory vascular changes. The infiltration of mononuclear cells was associated with anisomorphic gliosis and reactive microglia was identified. The intensity of the astrocytic response in the CNS of the equines infected by T. evansi characterizes the importance of the performance of these cells in this trypanosomiasis. The characteristic gliosis observed in the animals in this experiment suggests the ability of these cells as mediators of immune response. The parasite, T. evansi, was not identified in the nervous tissues.

Este estudo objetivou caracterizar a participação astrocítica e microglial no sistema nervoso central (SNC) de eqüinos experimentalmente infectados com T. evansi. O grupo experimental foi formado por machos e fêmeas com vários graus de cruzamentos e idade variando entre quatro e sete anos. Os animais foram inoculados com 10(6) tripomastigotas de T. evansi, originalmente isolada de um cão infectado naturalmente. Todos os eqüinos inoculados foram observados até o aparecimento dos sintomas neurológicos, caracterizados por incoordenação motora dos membros pélvicos, o qual ocorreu entre 67 e 124 dias após a inoculação (DPI). Os animais do grupo controle não apresentaram sinais clínicos e foram observados até o 125º DPI. Para este propósito, foram utilizados os métodos histoquímicos (HE) e imunoistoquímicos do complexo avidina-biotina peroxidase (ABC). A lesão no sistema nervoso central (SNC) dos eqüinos infectados com T. evansi foi caracterizada como meningoencefalomielite não supurativa. A gravidade das lesões variou em diferentes segmentos do SNC, refletindo distribuição irregular das alterações vasculares. Infiltrado perivascular e meníngeo foi associado a gliose anisomórfica e microgliose reativa. A intensidade da resposta astrocítica no SNC dos equinos infectados com T. evansi caracteriza a importância da performance destas células nas tripanossomíases. A gliose observada nos animais deste experimento sugerem a habilidade destas células como mediadoras da resposta imune. T. evansi não foi identificado no parênquima do SNC.

Modulation of fibronectin expression in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis

Fibronectin (FN), a large family of plasma and extracellular matrix (ECM) glycoproteins, plays an important role in leukocyte migration. In normal central nervous system (CNS), a fine and delicate mesh of FN is virtually restricted to the basal membrane of cerebral blood vessels and to the glial limitans externa. Experimental autoimmune encephalomyelitis (EAE), an inflammatory CNS demyelinating disease, was induced in Lewis rats with a spinal cord homogenate. During the preclinical phase and the onset of the disease, marked immunolabelling was observed on the endothelial luminal surface and basal lamina of spinal cord and brainstem microvasculature. In the paralytic phase, a discrete labelling was evident in blood vessels of spinal cord and brainstem associated or not with an inflammatory infiltrate. Conversely, intense immunolabelling was present in cerebral and cerebellar blood vessels, which were still free from inflammatory cuffs. Shortly after clinical recovery minimal labelling was observed in a few blood vessels. Brainstem and spinal cord returned to normal, but numerous inflammatory foci and demyelination were still evident near the ventricle walls, in the cerebral cortex and in the cerebellum. Intense expression of FN in brain vessels ascending from the spinal cord towards the encephalon preceded the appearance of inflammatory cells but faded away after the establishment of the inflammatory cuff. These results indicate an important role for FN in the pathogenesis of CNS inflammatory demyelinating events occurring during EAE

Encefalomiopatía mitocondrial, acidosis láctica y apariencia de accidentes vasculares cerebrales / Mitochondrial, lactic acidosis and features of cerebrovascular disorders

En una paciente de 12 años de edad, aparentemente sana hasta los 9 años, con epilepsia progresiva, deterioro mental, acidosis láctica y déficit neurológicos que simulaban accidentes cerebrovasculares, la biopsia muscular demostró fibras rojas desflecadas y acúmulos de mitocondrias anormales, confirmando el diagnóstico de encefalomiopatía mitocondrial. Conviene pensar en este grupo de enfermedades en pacientes escolares con cefalea periódica, epilepsia mioclónica que responde mal al tratamiento, hipoacusia sensorioneural y deterioro mental. Las manifestaciones musculares pueden ser frecuentemente tardías