EFFECT OF EXPERIMENTAL INFLUENZA-A VIRUS-INFECTION ON ISOLATION OF STREPTOCOCCUS-PNEUMONIAE AND OTHER AEROBIC-BACTERIA FROM THE OROPHARYNGES OF ALLERGIC AND NONALLERGIC ADULT SUBJECTS

Intranasal challenge with both influenza A virus and Streptococcus pne umoniae promotes otitis media with S. pneumoniae in chinchillas. We in vestigated whether influenza A virus infection promotes oropharyngeal colonization with S. pneumoniae and other middle ear pathogens by sele ctively inhibiting commensal bacteria. On study day 0, 12 allergic and 15 nonallergic adult subjects were intranasally inoculated with influ enza A/Kawasaki (H1N1) virus, Every subject was infected with the viru s as demonstrated by nasal shedding or seroconversion, Average upper r espiratory symptom scores and nasal secretion weights from the entire subject group were elevated between days 2 and 6 (acute phase) and wer e not significantly different between allergic and nonallergic subject s. S. pneumoniae was not isolated from any subject prior to the virus challenge but was isolated in heavy density from 4 (15%) subjects on d ay 6 (P = 0.055). Staphylococcus aureus was isolated more frequently f rom the nonallergic subjects than from the allergic subjects on days 2 (80 versus 25%, respectively) 4, (67 versus 17%, respectively), and 6 (73 versus 25%, respectively) (P < 0.05). The isolation rates of othe r middle ear pathogens were not significantly different before virus c hallenge and during the acute and resolution phases (days 27 to 30) of the experimental infection for the entire subject group or either the allergic or nonallergic subgroup. Densities and isolation rates of co mmensal bacteria from the entire subject group were similar throughout the observational period. These results suggest that the virus infect ion promoted S. pneumoniae colonization of the oropharynx and that non allergic persons may be more vulnerable to colonization with S. aureus than allergic persons. The altered colonization rates were not attrib uted to inhibition of commensal bacteria.