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Antimicrobial Resistant Streptococcus pneumoniae

Prevalence, Mechanisms, and Clinical Implications

Cherazard, Regine MD1; Epstein, Marcia MD2; Doan, Thien-Ly PharmD3; Salim, Tanzila MBBS1; Bharti, Sheena DO2; Smith, Miriam A. MD, MBA1,*

American Journal of Therapeutics: May 2017 - Volume 24 - Issue 3 - p e361–e369
doi: 10.1097/MJT.0000000000000551
Systematic Review and Clinical Guidelines

Background: Streptococcus pneumoniae is a major cause of pneumonia, meningitis, sepsis, bacteremia, and otitis media. S. pneumoniae has developed increased resistance to multiple classes of antibiotics.

Study Design: Systematic literature review of prevalence, mechanisms, and clinical implications in S. pneumoniae resistance.

Areas of Uncertainty: Since S. pneumoniae resistance to penicillin was first reported with subsequent development of resistance to other classes of drugs, selection of appropriate antibiotic treatment is challenging.

Data Sources: We searched PubMed (English language) for citations to antibiotic resistance in S. pneumoniae published before March 1, 2016.

Results: We present a review of S. pneumoniae resistance to beta-lactams, macrolides, lincosamides, fluoroquinolones, tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX). There has been a steady decline in susceptibility of S. pneumoniae to commonly used beta-lactams. Phenotypic expression of penicillin resistance occurs as a result of a genetic structural modification in penicillin-binding proteins. Between 20% and 40% of S. pneumoniae isolates are resistant to macrolides. Macrolide resistance mechanisms include ribosomal target site alteration, alteration in antibiotic transport, and modification of the antibiotic. Approximately 22% of S. pneumoniae isolates are resistant to clindamycin. Similar to macrolide resistance, clindamycin involves a target site alteration. The prevalence of fluoroquinolone resistance is low, although increasing. S. pneumoniae resistance to fluoroquinolones occurs by accumulated mutations within the bacterial genome, increased efflux, or acquisition of plasmid-encoded genes. S. pneumoniae resistance has also increased for the tetracyclines. The primary mechanism is mediated by 2 genes that confer ribosomal protection. The prevalence of TMP-SMX resistance is around 35%. As with fluoroquinolones, resistance to TMP-SMX is secondary to mutations in the bacterial genome.

Conclusions: Effective treatment of resistant S. pneumoniae is a growing concern. New classes of drugs, newer formulations of older drugs, combination antibiotic therapy, nonantibiotic modalities, better oversight of antibiotic usage, and enhanced preventive measures hold promise.

1Department of Medicine, Long Island Jewish Hospital Forest Hills, Northwell Health, Forest Hills, NY;

2Department of Medicine, Division of Infectious Disease, North Shore University Hospital, Northwell Health, Manhasset, NY; and

3Department of Pharmacy, Long Island Jewish Medical Center, Northwell Health, New Hyde Park, NY.

Address for correspondence: Chair, Department of Medicine, Long Island Jewish Hospital Forest Hills, 102-01 66th Road, Forest Hills, NY 11375. E-mail:

The authors have no conflicts of interest to declare.

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