Evidence map›Paper›PMID 3319506›Full record

ReviewDrugs1987

Mechanisms of resistance to cephalosporin antibiotics.

D M Livermore

Abstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Antimicrobial Treatment ofAntibiotics (Basel, Switzerland) · 2023
    Review
  9. Article
  10. Review
  11. Frontiers in microbiology · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Microorganisms · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Antimicrobial resistance to ceftazidime involving loss of penicillin-binding protein 3 in Burkholderia pseudomallei.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

D M LivermoreDepartment of Medical Microbiology, London Hospital Medical College.
Royal London Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cephalosporins, like other beta-lactams, bind to the bacterial penicillin-binding proteins (PBPs). These correspond to the D-ala-D-ala trans-, carboxy- and endo-peptidases responsible for catalysing the cross-linking of newly formed peptidoglycan. Resistance arises when the PBPs-and particularly the transpeptidases-are modified, or when they are protected by beta-lactamases or 'permeability barriers'. Target-mediated cephalosporin resistance can involve either reduced affinity of an existing PBP component, or the acquisition of a supplementary beta-lactam-insensitive PBP. beta-lactamases are produced widely by bacteria and may be determined by chromosomal or plasmid DNA. The chromosomal beta-lactamases are species-specific, but can be classified into a few broad groups. The plasmid-mediated enzymes cross interspecific and intergeneric boundaries. The level of beta-lactamase-mediated resistance relates to the amount of enzyme produced with or without induction; to the location of the enzyme (extracellular for Gram-positive organisms and periplasmic in Gram-negative ones); and to the kinetics of the enzyme's activity. In Gram-positive organisms the PBPs are located on the outer aspect of the cytoplasmic membrane and so shielding by permeability barriers is minimal. In Gram-negative cells, however, the PBPs are protected by the outer membrane, which most beta-lactams cross by diffusion through aqueous pores composed of 'porin' proteins. In enterobacteria, a clear correlation exists between porin quantity and cephalosporin resistance, suggesting that the outer membrane is the sole barrier to drug entry. Such relationships are less clear for Pseudomonas aeruginosa, where the cell may contain additional barriers between the outer membrane and the PBPs. Although elevated cephalosporin resistance often is attributed to a single factor (PBP-modification, beta-lactamase action or impermeability) an organism's response to a drug often reflects the interplay of several factors. Mathematical models can be proposed to describe this interplay.

Indexed as

BacteriaCephalosporinsDrug Resistance, MicrobialCephalosporins

Identifiers

PMID3319506
OpenAlexW1998067206

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.