{"title":"[MULTIRESISTANT BACTERIA].","authors":"B Bedenić, S Sardelić, M Ladavac","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The most important multiresistant bacteria causing treatment failures are extended-spectrum β-lactamase and/or plasmid-mediated\nAmpC β-lactamase positive Enterobacteriaceae, carbapenemase producing Acinetobacter baumannii and Pseudomonas\n(P.) aeruginosa, methicillin-resistant Staphylococcus (S.) aureus, penicillin-resistant Streptococcus pneumoniae, and van-comycin-\nresistant Enterococcus spp. Extended-spectrum β-lactamases hydrolyze oxyimino-caphalosporins and aztreonam, are\nmostly produced by Enterobacteriaceae, and are encoded on transferable plasmids which often contain resistance genes to\nnon--lactam antibiotics. Plasmid-mediated AmpC β-lactamases descend from the chromosomal ampC gene transferred to the\nplasmid. Those -lactamases confer resistance to first, second and third generation of cephalosporins, monobactams, and to\n-lactam--lactamase inhibitor combinations. Enterobacteriaceae may develop resistance to carbapenems due to the hyperproduction\nof ESBLs or plasmid-mediated AmpC β-lactamases in combination with porin loss or due to the production of carbapenemases\nof class A (KPC, IMI, NMC, SME), B (metallo-β-lactamases from VIM, IMP or NDM series), and D (OXA-48 β-lactamase).\nCarbapenemases found in Acinetobacter spp. belong to molecular class A (KPC), B (metallo-β-lactamases of IMP, VIM, NDM or\nSIM family) and D (OXA enzymes). The most frequent mechanism of carbapenem resistance in Acinetobacter spp. is through the\nproduction of OXA-enzymes but other various mechanisms including decreased permeability and efflux pump overexpression\ncould also be involved. Carbapenem-resistance in P. aeruginosa is usually mediated by the production of metallo-β-lactamases of\nIMP, VIM, GIM, SPM or NDM series, loss of OprD outer membrane protein and/or upregulation of MexAB or MexCD efflux pumps.\nMethicillin-resistance in S. aureus occurs as the result of the acquisition of mecA gene that encodes novel PBP2a protein. Expression\nof PBP2a renders bacteria resistant to all -lactams including cephalosporins (with the exception of ceftaroline and ceftobiprole)\nand carbapenems. Most strains of penicillin resistant Streptococcus pneumoniae are often resistant to cephalosporins\nand antibiotics from other classes, presenting a serious problem in treating invasive infections. The most important therapeutic\nproblem in enterococci is development of resistance to vancomycin.</p>","PeriodicalId":35756,"journal":{"name":"Acta Medica Croatica","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Medica Croatica","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
The most important multiresistant bacteria causing treatment failures are extended-spectrum β-lactamase and/or plasmid-mediated
AmpC β-lactamase positive Enterobacteriaceae, carbapenemase producing Acinetobacter baumannii and Pseudomonas
(P.) aeruginosa, methicillin-resistant Staphylococcus (S.) aureus, penicillin-resistant Streptococcus pneumoniae, and van-comycin-
resistant Enterococcus spp. Extended-spectrum β-lactamases hydrolyze oxyimino-caphalosporins and aztreonam, are
mostly produced by Enterobacteriaceae, and are encoded on transferable plasmids which often contain resistance genes to
non--lactam antibiotics. Plasmid-mediated AmpC β-lactamases descend from the chromosomal ampC gene transferred to the
plasmid. Those -lactamases confer resistance to first, second and third generation of cephalosporins, monobactams, and to
-lactam--lactamase inhibitor combinations. Enterobacteriaceae may develop resistance to carbapenems due to the hyperproduction
of ESBLs or plasmid-mediated AmpC β-lactamases in combination with porin loss or due to the production of carbapenemases
of class A (KPC, IMI, NMC, SME), B (metallo-β-lactamases from VIM, IMP or NDM series), and D (OXA-48 β-lactamase).
Carbapenemases found in Acinetobacter spp. belong to molecular class A (KPC), B (metallo-β-lactamases of IMP, VIM, NDM or
SIM family) and D (OXA enzymes). The most frequent mechanism of carbapenem resistance in Acinetobacter spp. is through the
production of OXA-enzymes but other various mechanisms including decreased permeability and efflux pump overexpression
could also be involved. Carbapenem-resistance in P. aeruginosa is usually mediated by the production of metallo-β-lactamases of
IMP, VIM, GIM, SPM or NDM series, loss of OprD outer membrane protein and/or upregulation of MexAB or MexCD efflux pumps.
Methicillin-resistance in S. aureus occurs as the result of the acquisition of mecA gene that encodes novel PBP2a protein. Expression
of PBP2a renders bacteria resistant to all -lactams including cephalosporins (with the exception of ceftaroline and ceftobiprole)
and carbapenems. Most strains of penicillin resistant Streptococcus pneumoniae are often resistant to cephalosporins
and antibiotics from other classes, presenting a serious problem in treating invasive infections. The most important therapeutic
problem in enterococci is development of resistance to vancomycin.
期刊介绍:
ACTA MEDICA CROATICA publishes original contributions to medical sciences, that have not been previously published. All manuscripts should be written in English.