The incidence and RNA electropherotypes of rotavirus in stools or rectal swabs of children with diarrhea were studied for three rotavirus seasons (1981 through 1984) in Philadelphia, Pa. We used a simplified RNA analysis method involving polyacrylamide gel electrophoresis followed by silver staining. Phosphate-buffered saline suspensions of the stools and swab eluates were examined directly by polyacrylamide gel electrophoresis-silver staining analysis and enzyme-linked immunoadsorbent assay (Rotazyme; Abbott Laboratories); electron microscopy was performed on solid stool specimens. The RNA analysis results were compared with electron microscopy and enzyme-linked immunosorbent assay results and exhibited a sensitivity and specificity greater than or equal to that of electron microscopy or the enzyme-linked immunosorbent assay. Ten different electropherotypes were detected among the 68 rotavirus RNA-positive specimens examined over the 3-year study. The predominant electropherotype was different in each season. Our results indicate that the polyacrylamide gel electrophoresis-silver nitrate strain RNA analysis of simple unextracted stool suspensions is a uniquely useful diagnostic technique; it rapidly provides both a definitive positive result and immediate determination of the RNA electropherotype, which is of value for epidemiological study.

Haemophilus influenzae type b is responsible for an estimated 15 000 to 20 000 cases of meningitis per year in the United States, mainly in children 2 months to 5 years old.1-4 The mortality rate from meningitis due to H influenzae type b infections ranges from 5% to 10%. Despite antibiotic treatment, up to 35% of survivors have permanent neurologic sequelae. In addition to meningitis, H influenzae type b is responsible for other invasive infections, including epiglottitis, septicemia, cellulitis, septic arthritis, osteomyelitis, pneumonia, pericarditis, and otitis media; approximately 30 000 cases H influenzae diseases occur annually in the United States. The diseases peak in incidence between 6 and 12 months of age, with almost one half of the cases occurring before 1 year of age. About 75% of disease caused by H influenzae type b occurs in children younger than 24 months old. The incidence of disease is higher in children of certain groups, including blacks, Hispanics, Eskimos and Native Americans, young children attending day-care facilities, patients with asplenia or antibody-deficiency syndromes, and children of lower socioeconomic status.5 There is considerable evidence that antibody to the capsular polysaccharide (polyribosylribitol-phosphate [PRP]) of H influenzae type b is protective.6-8 These antibodies activate complement for bactericidal antibody,9,10 induce opsonophagocytic activity,11,12 and protect infant rats from bacteremia due to challenge with H influenzae type b.13,14 It has been demonstrated clinically that antibodies induced by vaccination of older children with PRP are protective.7,15 The level of antibodies correlated with protection has been estimated to be 0.05 to 0.15 µg/mL after natural infection16 or after passive acquisition via immunoglobulin17 and 1.0 µg/mL for vaccine-induced protection.18

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