Experimental St. Louis Encephalitis Virus Infection of Sloths and Cormorants

Charles SeymourGorgas Memorial Laboratory, Panamá 5, Republic of Panama

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Laura D. KramerGorgas Memorial Laboratory, Panamá 5, Republic of Panama

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Pauline H. PeraltaGorgas Memorial Laboratory, Panamá 5, Republic of Panama

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Experimental infection of 11 Bradypus variegatus and Choloepus hoffmanni sloths with St. Louis encephalitis (SLE) virus produced detectable viremias of seven to 27 (median 13) days duration and maximum titers of 2.7 to 6.5 (median 5.1) log10 median suckling mouse intracranial lethal doses (SMicLD50) per ml. Experimental SLE viremia onset was delayed and maximum titer depressed in two sloths concurrently infected with naturally acquired viruses. SLE viremias in four experimentally inoculated cormorants Phalacrocorax olivaceus were shoter, and of equal or lower titer, than in sloths. Colonized Culex pipiens quinquefasciatus mosquitoes were infected by feeding on sloths circulating at least 4.8 log10 SMicLD50 of SLE virus per ml, and subsequently transmitted the infection to mice and chicks. An uninoculated baby Bradypus became infected by contact transmission from its mother. The antibody response of sloths to SLE virus was slow, being undetectable until several weeks post-inoculation. However, both sloth species developed high and long-lasting neutralizing and hemagglutination-inhibition antibody titers. The complement-fixation antibody response in Bradypus was lower and slower to develop than in Choloepus. Sloths with naturally acquired SLE virus antibody did not become detectably viremic after experimental inoculation. Neither sloths nor cormorants become overtly ill from SLE virus infection.

Author Notes

Present address: St. Francis Hospital and Medical Center, 114 Woodland Street, Hartford, Connecticut 06105.

Present address: School of Public Health, University of California, Berkeley, California 94720.

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