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Understanding and overcoming antibiotic resistance
Richardson, Lauren A
PLoS Biology, 2017-08, Vol.15 (8), p.e2003775-e2003775
[Periódico revisado por pares]
United States: Public Library of Science
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Título:
Understanding and overcoming antibiotic resistance
Autor:
Richardson, Lauren A
Assuntos:
Animals
;
Anti-Bacterial Agents - pharmacology
;
Antibiotic resistance
;
Antibiotics
;
Bacteria
;
Bacteria - drug effects
;
Bacteria - genetics
;
Bacteria - pathogenicity
;
Bacterial Infections - drug therapy
;
Bacterial Infections - microbiology
;
Bacterial Proteins - genetics
;
Bacterial Proteins - metabolism
;
Biology
;
Biology and Life Sciences
;
Dosage and administration
;
Drug dosages
;
Drug resistance
;
Drug Resistance, Bacterial - genetics
;
Enzymes
;
Evolution
;
Gene Expression Regulation, Bacterial
;
Genes, Bacterial - genetics
;
Humans
;
Library collections
;
Medical research
;
Medicine and Health Sciences
;
Mutation
;
Open access
;
Open Highlights
;
Pathogens
;
Pharmaceutical research
;
Plasmids
;
Staphylococcus infections
;
Streptococcus infections
;
Studies
;
Virulence - genetics
É parte de:
PLoS Biology, 2017-08, Vol.15 (8), p.e2003775-e2003775
Notas:
new_version
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
LR is a current paid employee at Public Library of Science.
Descrição:
Most classes of antibiotics on the market were discovered in the mid-to-late 20th century. [...]there is a limited arsenal of drugs to fight resistant bacteria, and bacteria can be resistant to multiple drugs at a time. In a PLOS Biology article, scientists show that intracellular expression of an antibiotic-metabolizing enzyme in a non-pathogenic strain of bacteria can provide resistance to the pathogen Streptococcus pneumoniae when the two types of bacteria are grown together, both in vitro and in vivo [3]. Methicillin-resistant Staphylococcus aureus (MRSA) is the most common antibiotic resistant infection in humans, and the most frequent mechanism of resistance in MRSA is via the acquisition of mecA (Fig 2). mecA is a member of the penicillin-binding protein family that doesn’t bind [Beta]-lactams (like penicillin) effectively and is thus immune to its effects. In an article published in PLOS Computational Biology, the authors use mathematical modelling of within-host infection dynamics to understand the interaction between the host immune response and antibiotic treatment [11].
Editor:
United States: Public Library of Science
Idioma:
Inglês
Links
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