Format

Send to

Choose Destination
Acta Otolaryngol. 2005 Feb;125(2):180-3.

Evaluation of mutations in penicillin binding protein-3 gene of non-typeable Haemophilus influenzae isolated from the nasopharynx of children with acute otitis media.

Author information

1
Department of Otolaryngology--Head and Neck Surgery, Wakayama Medical University, Wakayama, Japan.

Abstract

CONCLUSION:

Younger children tend to harbor more resistant strains because they are exposed to these pathogens more often through contacts with siblings or attendance at day-care centers and are frequently treated with antibiotics. The high prevalence of BLNAR strains should be taken into account in the treatment of AOM in young children.

OBJECTIVE:

Non-beta-lactamase-producing ampicillin-resistant (BLNAR) strains with mutations in penicillin-binding protein (PBP) genes of Haemophilus influenzae have been prevalent recently among younger children.

MATERIAL AND METHODS:

We investigated mutations in the ftsI gene encoding PBP-3 of H. influenzae isolated from the nasopharynx of children with acute otitis media (AOM) using polymerase chain reaction (PCR).

RESULTS:

Strains containing the bla gene (beta-lactamase-producing ampicillin-resistant) were identified in 4.7% of cases. Strains with mutations in the ftsI gene (BLNAR) were identified in 23.3% of cases. Strains without mutations in the ftsI gene and that did not contain the bla gene (non-beta-lactamase-producing ampicillin-susceptible) were identified in 70.7% of cases. Strains with both expression of the bla gene and mutations in the ftsI gene (beta-lactamase-producing amoxicillin clavulanate-resistant) were identified in 1.3% of cases. The MICs of ampicillin against the strains evaluated in this study were 0.5-2.0 microg/ml. Cefditoren-pivoxil had the lowest MIC90 against the strains (0.06 microg/ml). Strains with mutations in the ftsI gene (BLNAR) were broadly identified among young children.

PMID:
15880950
DOI:
10.1080/00016480410020301
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center