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The first human cases were recognized in 1994 and 1999. The Hendra cases followed close contact with sick horses in Australia, and the Nipah cases occurred in pig farmers in Malaysia. Patients developed encephalitis and pneumonitis. The case-fatality rate was about 50%. Animal reservoirs include fruit bats, swine, horses, and possibly dogs. Person-to-person spread is not evident. [CCDM, p. 245-7] Eleven abattoir workers developed encephalitis or pneumonia and one died after Nipah virus infections in Singapore in 1999. All infected workers had direct contact with live pigs. [J Infect Dis 2000;181(5):1760-3] There are only 3 reported cases of Hendra virus infecting humans. Findings included fever, myalgia, headache, lethargy, vertigo, meningitis, pharyngitis, stiff neck, vomiting, low back pain, and seizures. The patient with meningitis had CSF pleocytosis with a predominance of neutrophils. Other lab abnormalities were thrombocytopenia and elevated liver function tests. Patients infected with Nipah virus had pneumonia and encephalitis with signs of brain stem dysfunction (areflexia, hypotonia, myoclonus, and ataxia). Patients with severe disease had sepsis, gastrointestinal bleeding, and renal failure. MRI is sensitive for detecting encephalitis in Nipah infected patients. Lab abnormalities included leukopenia, thrombocytopenia, elevated liver function tests, and CSF lymphocytic pleocytosis. Ribavirin may reduce mortality in Nipah virus infections. Hendra and Nipah viruses appear to be old viruses that emerged because of habitat changes of flying foxes (fruit bats). [PPID, p. 2038-44] |
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