RESUMO
Two groups of rhesus monkeys were inoculated with either 10(5) (group 1) or 10(3) (group 2) plaque-forming units of Machupo virus, the etiologic virus of Bolivian hemorrhagic fever. The monkeys were observed for clinical signs; body temperatures, viremias, hematologic changes, and virus-neutralizing antibody were measured. The onset of clinical signs for groups 1 and 2 occurred on days 4-6 and 7-10, respectively, with fever, anorexia, and depression. These and other signs became more severe, and all of the monkeys died; the respective mean times to death for groups 1 and 2 were 14.3 and 19.5 days. Hematocrit, neutrophil, and lymphocyte values decreased in both groups until a few days before death and then increased slightly. Viremias in the two groups peaked on days 13 and 16, respectively, and persisted until death; the sole exception was one monkey in group 2 that developed neutralizing antibody by day 21. The response of the rhesus monkey to Machupo virus thus provides a useful model for the study of Bolivian hemorrhagic fever.
Assuntos
Modelos Animais de Doenças , Febre Hemorrágica Americana , Febres Hemorrágicas Virais , Macaca mulatta , Macaca , Animais , Arenavirus do Novo Mundo/isolamento & purificação , Temperatura Corporal , Haplorrinos , Febre Hemorrágica Americana/sangue , Febre Hemorrágica Americana/diagnóstico , Febre Hemorrágica Americana/etiologiaRESUMO
Gross and microscopic lesions associated with Bolivan hemorrhagic fever virus infection in the rhesus monkey were studied in 10 animals which died following inoculation. Gross lesions included skin rash, lymphadenopathy, splenomegaly, meningeal edema, hydropericardium and enlarged friable livers. Hemorrhagic manifestations of the infection were not consistently observed, but hemorrhages were present in the skin, heart, brain and nares in some monkeys. Histopathologic lesions were fairly consistent. Hepatic necrosis with the presence of acidophilic hyaline bodies, necrotizing enteritis, epithelial necrosis and adrenal cortical necrosis were present in all monkeys. Those monkeys which died after the seventeenth day of infection had nonsupurative meningoencephalitis; lymphoid necrosis was present in 3 monkeys that died after day 18. Other microscopic lesions included myocardial degeneration, lymphoid and reticuloendothelial cell hyperplasia and lymphoid depletion. Most of the histopathologic lesions described in human autopsy material were reproduced; however, the necrosis in the skin and oral mucosa, mucosa of the gastrointestinal tract and the adrenal cortex have not been described in man. Despite these apparent discrepancies the results of this investigation indicate that the rhesus monkey is a good experimental model for the study of Bolivian hemorrhagic fever infection.