Cross-resistance to lincosamides, streptogramins A and pleuromutilins in Streptococcus agalactiae isolates from the USA
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Cross-resistance to lincosamides, streptogramins A and pleuromutilins in Streptococcus agalactiae isolates from the USA

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  • Alternative Title:
    J Antimicrob Chemother
  • Personal Author:
  • Description:
    Background

    Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of meningitis, sepsis and pneumonia in neonates in the United States. GBS also causes invasive disease in older infants, pregnant women, children and young adults with underlying medical conditions, and older adults. Resistance to lincosamides in the absence of erythromycin resistance is rare in GBS, but has been previously reported in clinical isolates, both on its own or in combination with resistance to streptogramins A and pleuromutilins (L/LSA/LSAP phenotypes).

    Objectives

    To retrospectively screen the Active Bacterial Core surveillance (ABCs) GBS isolate collection for these phenotypes in order to identify the causal genetic determinants and determine whether their frequency is increasing.

    Methods

    Based on MIC data, 65 (0.31%) isolates susceptible to erythromycin (MIC ≤0.25 mg/L) and non-susceptible to clindamycin (MIC ≥0.5 mg/L) were identified among 21186 GBS isolates. Genomic DNA was extracted and WGS was performed. The presence of 10 genes previously associated with LSA resistance was investigated by read mapping.

    Results

    Forty-nine (75%) isolates carried the lsa(C) gene and expressed the LSAP phenotype, and 12 (18%) carried both the lnu(B) and lsa(E) genes and expressed the LSAP phenotype. The four remaining isolates were negative for all determinants investigated.

    Conclusions

    While the overall observed frequency of these phenotypes among our GBS isolates was quite low (0.31%), this frequency has increased in recent years. To the best of our knowledge, this is the first time the LSAP phenotype has been reported among GBS isolates from the USA.

  • Subjects:
  • Source:
    J Antimicrob Chemother. 72(7):1886-1892.
  • Pubmed ID:
    28333320
  • Pubmed Central ID:
    PMC5733627
  • Document Type:
    Journal Article
  • Funding:
    CC999999/Intramural CDC HHS/United States
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