Encefalomielite equina do leste no Distrito Federal e entorno

Background: Eastern equine encephalitis (EEE) is a highly lethal zoonotic disease caused by Eastern equine encephalitis virus (EEEv), an RNA virus of the genus Alphavirus, family Togaviridae. The transmission of these alphaviruses is through mosquitoes, mainly species of Culex, Aedes, Anopheles and Culiseta. Horses and humans are considered accidental hosts and the main reservoirs are birds and some wild rodents. The disease has been identified in Brazil by serological studies, but investigations with clinico-pathological descriptions are scarce. The present study aimed to describe the epidemiology and clinical-pathological findings of four cases of EEE in horses from Midwestern Brazil. Materials, Methods & Results: Four confirmed cases of EEE in horses from the necropsy and histopathology files of the Laboratory of Veterinary Pathology (LPV) of the University of Brasilia (UnB) were reviewed. Cases occurred between January 2005 and April 2012. Samples of brain and spinal cord samples were fixed in formalin 10%, processed routinely for histopathology, and stained by hematoxylin and eosin (HE). Immuno-histochemistry (IHC) with the peroxidase streptoavidin-biotin method was done to confirm the diagnosis of EEEv infection in all cases. The slides were incubated with the anti-EEEv monoclonal primary antibody (overnight, 1:100 dilution). The disease affected both young and adult horses. One case occurred in the summer and the other three in the fall. Clinical signs more frequently observed included circling, blindness, paresis, paralysis, somnolence, ataxia, head pressing, and recumbence. Clinical course varied from two to fifteen days (average eight days). Gross findings were not observed at necropsy of the four horses. The main histopathological changes were noted in the telencephalic lobes, thalamus and basal nuclei, and included multifocal meningoencephalitis, necrotizing vasculitis, thrombosis, swelling of endothelial cells, gliosis, neuronal necrosis, and neuronophagia. In all cases, moderate, granular, and positive immunoreaction to EEEv was observed in perikaryon of neurons, astrocytes and inflammatory cells (mainly lymphocytes) of the perivascular cuffs. Similar reaction was observed in the brain of positive control horse. EEE diagnosis was confirmed by immunohistochemistry. Discussion: In the current study, the four cases of EEEv infection occurred in the summer and fall, suggesting seasonality of the disease. In Midwestern Brazil, these periods present high rainfall indices facilitating the proliferation and survival of the vector insects. Similar epidemiological features were observed in other outbreaks of the disease elsewhere. All horses of this study presented typical clinical signs of neurological disease, as detected in other investigations carried out in Brazil and United States of America. Usually, no gross lesions are noted in EEE cases. When these gross changes are observed, traumatic hemorrhages can be observed. Histopathology and IHC findings were conclusive for the diagnosis of EEE. This study demonstrates, for the first time, that EEE occur in the Distrito Federal of Brazil, and in one neighboring city. These results enlarge the Brazilian areas with clinico-pathological description of this important arboviral disease and reinforce the importance of keeping in place epidemiologic and anatomopathological investigations across the country for control and prevention of these infectious diseases.