dc.contributor.author
Castañeda-García, Alfredo
dc.contributor.author
Blázquez, Jesús
dc.contributor.author
Rodríguez-Rojas, Alexandro
dc.date.accessioned
2018-06-08T10:43:37Z
dc.date.available
2018-01-25T12:27:41.092Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/20973
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-24270
dc.description.abstract
Bacterial infections caused by antibiotic-resistant isolates have become a
major health problem in recent years, since they are very difficult to treat,
leading to an increase in morbidity and mortality. Fosfomycin is a broad-
spectrum bactericidal antibiotic that inhibits cell wall biosynthesis in both
Gram-negative and Gram-positive bacteria. This antibiotic has a unique
mechanism of action and inhibits the initial step in peptidoglycan
biosynthesis by blocking the enzyme, MurA. Fosfomycin has been used
successfully for the treatment of urinary tract infections for a long time,
but the increased emergence of antibiotic resistance has made fosfomycin a
suitable candidate for the treatment of infections caused by multidrug-
resistant pathogens, especially in combination with other therapeutic
partners. The acquisition of fosfomycin resistance could threaten the
reintroduction of this antibiotic for the treatment of bacterial infection.
Here, we analyse the mechanism of action and molecular mechanisms for the
development of fosfomycin resistance, including the modification of the
antibiotic target, reduced antibiotic uptake and antibiotic inactivation. In
addition, we describe the role of each pathway in clinical isolates. View
Full-Text
en
dc.rights.uri
http://creativecommons.org/licenses/by-nc-sa/3.0/
dc.subject
fosfomycin resistance
dc.subject
molecular mechanisms
dc.subject.ddc
500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie
dc.title
Molecular Mechanisms and Clinical Impact of Acquired and Intrinsic Fosfomycin
Resistance
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Antibiotics. - 2 (2013), 2, S. 217-236
dcterms.bibliographicCitation.doi
10.3390/antibiotics2020217
dcterms.bibliographicCitation.url
http://www.mdpi.com/2079-6382/2/2/217
refubium.affiliation
Biologie, Chemie, Pharmazie
de
refubium.mycore.fudocsId
FUDOCS_document_000000028875
refubium.note.author
Der Artikel wurde in einer reinen Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000009369
dcterms.accessRights.openaire
open access