Epidemiological Studies of Aseptic Meningitis Caused by Coxsackie Virus B5
- 1 September 1958
- journal article
- research article
- Published by American Public Health Association in American Journal of Public Health and the Nations Health
- Vol. 48 (9) , 1193-1200
- https://doi.org/10.2105/ajph.48.9.1193
Abstract
During the summer of 1956, Coxsackie virus B5 was found widely distributed in Iowa and was associated with several localized outbreaks of aseptic meningitis. The evidence that the B5 virus was etiologically related to the illnesses observed was reenforced by a detailed study of the outbreak that occurred in Mason City. In all, 193 cytopathogenic agents were isolated from fecal specimens of 329 individuals residing in different parts of the state. Of these 193 agents, over 50% were identified as Coxsackie B5 viruses; the others were 2 Coxsackie A9 ''viruses, 8 polioviruses and 6 as yet unidentified. Illnesses observed in the Mason City outbreak were aseptic meningitis and associated cases of minor illnesses. Increased morbidity was observed in early July with the peak occurring during the 2nd week of August. The overall attack rate based on a household survey was 8%, with the highest rate observed among children under 10 years of age. The secondary attack rate was 15%. In the Mason City study, Coxsackie virus B5 was recovered from feces of 75% of patients with aseptic meningitis and from feces of 71% of patients with minor illnesses. The virus was also recovered from oropharyngeal secretions of 12 patients and from spinal fluids of 2. Infection with Coxsackie virus B5 was invariably accompanied by development of homotypic neutralizing antibodies. Antibodies were detected in the serums of 89% of 56 persons with positive Coxsackie B5 virus isolations; 68% showing 4-fold or greater rise in titers. Virus and antibody studies performed on asymptomatic household contacts indicated that subclinical infection was a common experience. Coxsackie virus B5 was detected in the feces of 43% of 42 asymptomatic contacts, and type-specific antibody rise was demonstrated in 62% of 16 contacts who provided a history of no clinical illness.Keywords
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