Effect of antibiotics on adherence of Haemophilus influenzae type b
Janet R. Gilsdorf, J M Jesperson
Abstract
Janet R. Gilsdorf, J M Jesperson
Abstract
During antibiotic therapy for serious Haemophilus influenzae type b infections in children, respiratory mucosal colonization with this organism is suppressed but not eradicated. To define possible mechanisms contributing to this suppression, the ability of six antibiotics to influence the adherence of H. influenzae type b to human epithelial cells was investigated. In assays in which the organisms were grown in broth containing 0.5 X the MIC of rifampin, ampicillin, clindamycin, chloramphenicol, lincomycin, or trimethoprim-sulfamethoxazole, all drugs except rifampin significantly reduced bacterial adherence. In assays in which nonreplicating organisms were exposed to the antibiotics, all six drugs reduced the adherence of the bacteria. In assays in which the epithelial cells were exposed to the antibiotics, all drugs reduced bacterial adherence. In addition, the presence of ampicillin, chloramphenicol, lincomycin, or trimethoprim-sulfamethoxazole appeared to facilitate the release of organisms adherent to epithelial cells. Thus, antibiotics appear to inhibit adherence of H. influenzae type b to human epithelial cells and may interfere with bacterial or epithelial cell binding sites. These observations may explain the suppression of H. influenzae type b mucosal colonization that occurs during antibiotic treatment of patients with systemic H. influenzae type b infections.
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During antibiotic therapy for serious Haemophilus influenzae type b infections in children, respiratory mucosal colonization with this organism is suppressed but not eradicated. To define possible mechanisms contributing to this suppression, the ability of six antibiotics to influence the adherence of H. influenzae type b to human epithelial cells was investigated. In assays in which the organisms were grown in broth containing 0.5 X the MIC of rifampin, ampicillin, clindamycin, chloramphenicol, lincomycin, or trimethoprim-sulfamethoxazole, all drugs except rifampin significantly reduced bacterial adherence. In assays in which nonreplicating organisms were exposed to the antibiotics, all six drugs reduced the adherence of the bacteria. In assays in which the epithelial cells were exposed to the antibiotics, all drugs reduced bacterial adherence. In addition, the presence of ampicillin, chloramphenicol, lincomycin, or trimethoprim-sulfamethoxazole appeared to facilitate the release of organisms adherent to epithelial cells. Thus, antibiotics appear to inhibit adherence of H. influenzae type b to human epithelial cells and may interfere with bacterial or epithelial cell binding sites. These observations may explain the suppression of H. influenzae type b mucosal colonization that occurs during antibiotic treatment of patients with systemic H. influenzae type b infections.
Key concepts: Microbiology, Antibiotics, Lincomycin, Ampicillin, Haemophilus influenzae, Trimethoprim, Clindamycin, Chloramphenicol