AN INQUIRY INTO THE ETIOLOGY OF ACUTE BRONCHIOLITIS OF INFANTS

Abstract

Tracheal aspirates and nasopharyngeal swabs obtained from 51 infants under 2 years of age with acute bronchiolitis were subjected to a careful bacteriologic study. The cases in this series were encountered during the 13 month period from November 1, 1951, to December 1, 1952. H. influenzae was recovered from 36 of the 51 infants. Of these, 26 proved to be H. influenzae type a and 6 proved to be H. influenzae type b. The four remaining were rough untypable strains. An increase in type specific antibody measured by a slide agglutination technic and by the Quellung reaction could be demonstrated in 46 infants. No increase in antibody titer could be demonstrated in 5. An increase in antibody titer to H. influenzae type a was demonstrated in 37 and to H. influenzae type b in 9 of the series. Combined bacteriologic and serologic evidence indicating that H. influenzae type a was involved in the infectious process was obtained in 26 cases. An increase in antibody titer to type a only was demonstrated in 11 others. In two from whom rough nontypable strains were isolated, an increase in titer to type a was demonstrated. Evidence for infection with type a was thus obtained in 37 of the 51 infants. From 2 infants H. influenzae type a was recovered but no increase in antibody titer could be demonstrated. Combined bacteriologic and serologic evidence for infection with H. influenzae type b was obtained in 5 infants. An increase in titer to type b was demonstrated in 2 others. A titer increase to type b was demonstrated in 2 more from whom rough untypable strains were isolated. Evidence for infection with type b was thus obtained in 9 of the 51 infants. H. influenzae type b without evidence of titer increase was obtained in one. No H. influenzae were isolated nor could an increase in antibody titer be demonstrated in the remaining 2 infants of the series. Cold hemagglutinin reactions were negative in 36 pairs of sera tested. No increase in antihemagglutinating titer to influenza virus A or B could be detected in 46 paired sera. A fourfold, but not greater, increase in antihemagglutination titer to influenza virus C was detected in 5 patients of the series. Reversion of rough untypable H. influenzae to smooth specifically typable strains was achieved by culturing the micro-organisms in chick embryos infected with influenza virus type A. It is postulated that H. influenzae types a and b must be strongly considered as participating in the pathogenesis of acute bronchiolitis of early infancy. Whether other bacterial or viral agents alone or a combination of bacteria and viruses can be implicated in the etiology of this disease must be determined by further investigation.