Rapidly Increasing Prevalence of β-Lactamase-Nonproducing, Ampicillin-Resistant Haemophilus influenzae Type b in Patients with Meningitis

Keiko Hasegawa, Naoko Chiba, Reiko Kobayashi, Somay Y. Murayama, Satoshi Iwata, Keisuke Sunakawa, Kimiko Ubukata

Research output: Contribution to journalArticle

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Abstract

A total of 395 Haemophilus influenzae strains from 226 Japanese institutions participating in the Nationwide Surveillance Study Group for Bacterial Meningitis were received from 1999 to 2002. All strains were analyzed by PCR to identify the resistance genes, and their susceptibilities to β-lactam agents were determined. Of these strains, 29.1% were β-lactamase nonproducing and ampicillin (AMP) susceptible (BLNAS) and lacked all resistance genes; 15.4% were β-lactamase producing and AMP resistant and had the blaTEM-1 gene; 30.6% were β-lactamase nonproducing and AMP resistant (low-BLNAR) and had a Lys-526 or His-517 amino acid substitution in ftsI encoding PBP 3; 13.9% were β-lactamase nonproducing and AMP resistant (BLNAR) and had an additional substitution of Thr-385 in ftsI; 9.1% were amoxicillin-clavulanic acid resistant (BLPACR I) and had the blaTEM-1 gene and a Lys-526 or His-517 amino acid substitution in ftsI; and 1.8% showed resistance similar to that of the BLPACR I group (BLPACR II) but had blaTEM-1 gene and ftsI substitutions, as was the case for the BLNAR strains. All but three strains were serotype b. The prevalence of BLNAR strains has increased rapidly: 0% in 1999, 5.8% in 2000, 14.1% in 2001, and 21.3% in 2002. The MICs at which 90% of BLNAR isolates were inhibited were as follows: AMP, 16 μg/ml; cefotaxime, 1 μg/ml; ceftriaxone, 0.25 μg/ml; and meropenem, 0.5 μg/ml. All of these values were higher than those for the BLNAS counterpart strains. The relatively wide distributions of the β-lactam MICs for BLNAR strains presumably reflect variations in ftsI gene mutations. Pulsed-field gel electrophoresis suggested the rapid spread of specific H. influenzae type b strains throughout Japan. Expedited vaccination, rapid identification, and judicious antibiotic use could slow their spread.

Original languageEnglish
Pages (from-to)1509-1514
Number of pages6
JournalAntimicrobial Agents and Chemotherapy
Volume48
Issue number5
DOIs
Publication statusPublished - 2004 May
Externally publishedYes

Fingerprint

Haemophilus influenzae type b
Ampicillin
Meningitis
Genes
Lactams
meropenem
Amino Acid Substitution
Amoxicillin-Potassium Clavulanate Combination
Bacterial Meningitides
Cefotaxime
Ceftriaxone
Pulsed Field Gel Electrophoresis
Haemophilus influenzae
Japan
Vaccination
Anti-Bacterial Agents
Polymerase Chain Reaction
Mutation

ASJC Scopus subject areas

  • Pharmacology (medical)

Cite this

Rapidly Increasing Prevalence of β-Lactamase-Nonproducing, Ampicillin-Resistant Haemophilus influenzae Type b in Patients with Meningitis. / Hasegawa, Keiko; Chiba, Naoko; Kobayashi, Reiko; Murayama, Somay Y.; Iwata, Satoshi; Sunakawa, Keisuke; Ubukata, Kimiko.

In: Antimicrobial Agents and Chemotherapy, Vol. 48, No. 5, 05.2004, p. 1509-1514.

Research output: Contribution to journalArticle

Hasegawa, Keiko ; Chiba, Naoko ; Kobayashi, Reiko ; Murayama, Somay Y. ; Iwata, Satoshi ; Sunakawa, Keisuke ; Ubukata, Kimiko. / Rapidly Increasing Prevalence of β-Lactamase-Nonproducing, Ampicillin-Resistant Haemophilus influenzae Type b in Patients with Meningitis. In: Antimicrobial Agents and Chemotherapy. 2004 ; Vol. 48, No. 5. pp. 1509-1514.
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abstract = "A total of 395 Haemophilus influenzae strains from 226 Japanese institutions participating in the Nationwide Surveillance Study Group for Bacterial Meningitis were received from 1999 to 2002. All strains were analyzed by PCR to identify the resistance genes, and their susceptibilities to β-lactam agents were determined. Of these strains, 29.1{\%} were β-lactamase nonproducing and ampicillin (AMP) susceptible (BLNAS) and lacked all resistance genes; 15.4{\%} were β-lactamase producing and AMP resistant and had the blaTEM-1 gene; 30.6{\%} were β-lactamase nonproducing and AMP resistant (low-BLNAR) and had a Lys-526 or His-517 amino acid substitution in ftsI encoding PBP 3; 13.9{\%} were β-lactamase nonproducing and AMP resistant (BLNAR) and had an additional substitution of Thr-385 in ftsI; 9.1{\%} were amoxicillin-clavulanic acid resistant (BLPACR I) and had the blaTEM-1 gene and a Lys-526 or His-517 amino acid substitution in ftsI; and 1.8{\%} showed resistance similar to that of the BLPACR I group (BLPACR II) but had blaTEM-1 gene and ftsI substitutions, as was the case for the BLNAR strains. All but three strains were serotype b. The prevalence of BLNAR strains has increased rapidly: 0{\%} in 1999, 5.8{\%} in 2000, 14.1{\%} in 2001, and 21.3{\%} in 2002. The MICs at which 90{\%} of BLNAR isolates were inhibited were as follows: AMP, 16 μg/ml; cefotaxime, 1 μg/ml; ceftriaxone, 0.25 μg/ml; and meropenem, 0.5 μg/ml. All of these values were higher than those for the BLNAS counterpart strains. The relatively wide distributions of the β-lactam MICs for BLNAR strains presumably reflect variations in ftsI gene mutations. Pulsed-field gel electrophoresis suggested the rapid spread of specific H. influenzae type b strains throughout Japan. Expedited vaccination, rapid identification, and judicious antibiotic use could slow their spread.",
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