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- W2463023882 abstract "Haemophilus influenzae is one of the important pathogens causing respiratory tract infections, pneumonia, and meningitis. Genotypic(g) beta-lactamase-nonproducing ampicillin resistance (gBLNAR) H. influenzae has rapidly increased since 2000 years in Japan. The resistant percentage exceeded 60% in Hib isolates from meningitis in 2009. The affinity of beta-lactam antibiotics for penicillin-binding proteins-3 (PBP3) that involved in septal peptidoglycan synthesis deceased in the resistant strains. Three amino acid substitutions, Ser385Thr, Asn526Lys and Arg517His in PBP3 encoded by ftsI gene are especially responsible for beta-lactam resistance in the gBLNAR. Susceptibilities of cephalosporin agents including cefotaxime for gBLNAR were apparently decreased than the ampicillin and carbapenem antibiotics. Though fluoroquinolone resistant isolates are rare (< 1%) in H. influenzae, strains of levofloxacin and ciprofloxacin MIC with > or = 8 microg/mL were isolated from elderly patients with CAP. These strains possessed amino acid substitutions of Ser84Phe and Asp88Asn in GyrA and Glu88Lys in ParC. It is important to practice rapidly identification of these resistant strains at routine work." @default.
- W2463023882 created "2016-07-22" @default.
- W2463023882 creator A5005158249 @default.
- W2463023882 date "2012-02-01" @default.
- W2463023882 modified "2023-09-23" @default.
- W2463023882 title "[Mechanisms of beta-lactam and quinolone resistance in Haemophilus influenzae]." @default.
- W2463023882 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22413526" @default.
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