National collaborative study of the prevalence of antimicrobial resistance among clinical isolates of Haemophilus influenzae

G. V. Doern, J. H. Jorgensen, C. Thornsberry, D. A. Preston, T. Tubert, J. S. Redding, L. A. Maher

Research output: Contribution to journalArticlepeer-review

161 Scopus citations


A total of 2,811 clinical isolates of Haemophilus influenzae were obtained during 1986 from 30 medical centers and one nationwide private independent laboratory in the United States. Among these, 757 (26.9%) were type b strains. The overall rate of β-lactamase-mediated ampicillin resistance was 20.0%. Type b strains were approximately twice as likely as non-type b strains to produce β-lactamase (31.7 versus 15.6%). The MICs of 12 antimicrobial agents were determined for all isolates. Ampicillin resistance among strains that lacked β-lactamase activity was extremely uncommon (0.1%). Percentages of study isolates susceptible to cefamandole, cefaclor, cephalothin, and cephalexin were 98.7, 94.5, 87.3, and 43.3%, respectively. For 14 strains (0.5% of the total), chloramphenicol MICs were ≥8.0 μg, and thus the strains were considered resistant. All of these resistant strains produced chloramphenicol acetyltransferase. In addition, all 14 strains were resistant to tetracycline; 11 produced β-lactamase. The percentage of isolates susceptible to tetracycline was 97.7%. In contrast, erythromycin and sulfisoxazole were relatively inactive. The combination of erythromycin-sulfisoxazole (1/64) was more active than erythromycin alone but essentially equivalent in activity to sulfisoxazole alone. Finally, small numbers of clinical isolates of H. influenzae were resistant to trimethoprim-sulfamethoxazole and rifampin.

Original languageEnglish (US)
Pages (from-to)180-185
Number of pages6
JournalAntimicrobial agents and chemotherapy
Issue number2
StatePublished - 1988
Externally publishedYes

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases


Dive into the research topics of 'National collaborative study of the prevalence of antimicrobial resistance among clinical isolates of Haemophilus influenzae'. Together they form a unique fingerprint.

Cite this