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Published on: February 23, 2014
Antimicrobial Resistant Streptococcus pneumoniae: Prevalence, Mechanisms, and Clinical Implications
Regine Cherazard1, Marcia Epstein, Thien-Ly Doan
11Department 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.
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.
Insights
Antibiotic resistance in Streptococcus pneumoniae is a growing concern, impacting treatment efficacy for common infections. This review details resistance trends and mechanisms, highlighting the need for new strategies.
Area of Science:
- Microbiology
- Infectious Diseases
- Pharmacology
Background:
- Streptococcus pneumoniae is a leading cause of serious infections like pneumonia and meningitis.
- Increasing antibiotic resistance in S. pneumoniae complicates treatment decisions.
Purpose of the Study:
- To review the prevalence, mechanisms, and clinical implications of antibiotic resistance in Streptococcus pneumoniae.
Main Methods:
- A systematic literature review was conducted using PubMed for English-language citations.
- The search focused on antibiotic resistance in S. pneumoniae published before March 1, 2016.
Main Results:
- Decreased susceptibility to beta-lactams, with resistance linked to altered penicillin-binding proteins.
- Prevalence of macrolide and clindamycin resistance ranges from 20-40% and 22% respectively, often due to target site alteration.
- Increasing fluoroquinolone resistance occurs via mutations, efflux, or gene acquisition. Tetracycline and trimethoprim-sulfamethoxazole (TMP-SMX) resistance, around 35% for TMP-SMX, is also increasing, primarily due to genomic mutations.
Conclusions:
- Effective treatment of resistant S. pneumoniae is a significant challenge.
- Promising strategies include novel antibiotics, updated drug formulations, combination therapies, non-antibiotic treatments, improved antibiotic stewardship, and enhanced prevention.
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