Antimicrobial Resistant Streptococcus pneumoniae

Prevalence, Mechanisms, and Clinical Implications

Regine Cherazard, Marcia Epstein, Thien Ly Doan, Tanzila Salim, Sheena Bharti, Miriam A. Smith

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)e361-e369
JournalAmerican Journal of Therapeutics
Volume24
Issue number3
DOIs
StatePublished - May 1 2017
Externally publishedYes

Fingerprint

Streptococcus pneumoniae
Fluoroquinolones
Macrolides
Anti-Bacterial Agents
Sulfamethoxazole Drug Combination Trimethoprim
Penicillin Resistance
Bacterial Genomes
Tetracyclines
Clindamycin
Trimethoprim Resistance
Lincosamides
beta-Lactam Resistance
Penicillin-Binding Proteins
Drug Compounding
Mutation
Information Storage and Retrieval
Otitis Media
beta-Lactams
Microbial Drug Resistance
Bacteremia

Keywords

  • Antibiotic resistance
  • Streptococcus pneumoniae

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Antimicrobial Resistant Streptococcus pneumoniae : Prevalence, Mechanisms, and Clinical Implications. / Cherazard, Regine; Epstein, Marcia; Doan, Thien Ly; Salim, Tanzila; Bharti, Sheena; Smith, Miriam A.

In: American Journal of Therapeutics, Vol. 24, No. 3, 01.05.2017, p. e361-e369.

Research output: Contribution to journalArticle

Cherazard, Regine ; Epstein, Marcia ; Doan, Thien Ly ; Salim, Tanzila ; Bharti, Sheena ; Smith, Miriam A. / Antimicrobial Resistant Streptococcus pneumoniae : Prevalence, Mechanisms, and Clinical Implications. In: American Journal of Therapeutics. 2017 ; Vol. 24, No. 3. pp. e361-e369.
@article{e520787e01a44690810bcde89d578195,
title = "Antimicrobial Resistant Streptococcus pneumoniae: Prevalence, Mechanisms, and Clinical Implications",
abstract = "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.",
keywords = "Antibiotic resistance, Streptococcus pneumoniae",
author = "Regine Cherazard and Marcia Epstein and Doan, {Thien Ly} and Tanzila Salim and Sheena Bharti and Smith, {Miriam A.}",
year = "2017",
month = "5",
day = "1",
doi = "10.1097/MJT.0000000000000551",
language = "English (US)",
volume = "24",
pages = "e361--e369",
journal = "American Journal of Therapeutics",
issn = "1075-2765",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Antimicrobial Resistant Streptococcus pneumoniae

T2 - Prevalence, Mechanisms, and Clinical Implications

AU - Cherazard, Regine

AU - Epstein, Marcia

AU - Doan, Thien Ly

AU - Salim, Tanzila

AU - Bharti, Sheena

AU - Smith, Miriam A.

PY - 2017/5/1

Y1 - 2017/5/1

N2 - 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.

AB - 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.

KW - Antibiotic resistance

KW - Streptococcus pneumoniae

UR - http://www.scopus.com/inward/record.url?scp=85018815975&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85018815975&partnerID=8YFLogxK

U2 - 10.1097/MJT.0000000000000551

DO - 10.1097/MJT.0000000000000551

M3 - Article

VL - 24

SP - e361-e369

JO - American Journal of Therapeutics

JF - American Journal of Therapeutics

SN - 1075-2765

IS - 3

ER -