Nterobacteriaceae organisms with chromosomal ampC genes. Sequence analysis with the S.
Nterobacteriaceae organisms with chromosomal ampC genes. Sequence analysis in the S. marcescens ampC 5 UTR predicted a stemloop structure that gives stability to S. marcescens ampC mRNA (248). Generally, the expression of AmpC is low from S. marcescens and also other members from the Enterobacteriaceae (73, 97). Induction from the chromosomal ampC gene causes a rise in AmpC lactamase production and increases the MICs of various lactams (73, 97). Robust inducers of ampC in enteric bacteria such as S. marcescens contain cefoxitin, imipenem, ampicillin, amoxicillin, benzylpenicillin, and narrowspectrum cephalosporins, like cephalothin and cefazolin (97). Broadspectrum cephalosporins, like ceftazidime, cefotaxime, and ceftriaxone, along with other lactams, such as cefepime, cefuroxime, and aztreonam, are weak inducers (97). Overexpression of AmpC lactamase in S. marcescens as well as other Enterobacteriaceae, having said that, is most often due to a mutation or deletion in the induction cell wall recycling pathway (73, 97). These mutants, called derepressed mutants, are clinically vital and may well lead to therapy failures with lactam antibiotics (97, 244). When S. marcescens along with other Serratia species are usually not intrinsically resistant to broadspectrum cephalosporins, the use of these antimicrobials in treating Serratia infections is hazardous PD150606 web PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/10899433 because the emergence of derepressed ampC mutants happens a lot more generally with these agents than with other antimicrobials (97, 244). The 20 Clinical and Laboratory Requirements Institute (CLSI) Overall performance Requirements for Antimicrobial Susceptibility Testing (M00S2) (82) incorporates this warning concerning remedy with broadspectrum (thirdgeneration) cephalosporins: “Enterobacter, Citrobacter, and Serratia may perhaps develop resistance in the course of prolonged therapy with thirdgeneration cephalosporins. Hence, isolates that are initially susceptible may perhaps turn into resistant within three to four days after initiation of therapy. Testing of repeat isolates may well be warranted.” Some medical facilities may well use this as a statement if they decide to report broadspectrum cephalosporin susceptibilities for Serratia species. At my healthcare facility, we usually do not report broadspectrum cephalosporin susceptibility test results for Serratia species, while S. marcescens isolates from 2008 to 200 were 00 sensitive to ceftazidime and 97 sensitive to ceftriaxone (Table 4). An outbreak of a multiply antibioticresistant S. marcescens clone occurred in Italy from 200 to 2002 and might have been due to ampC derepression or induction. The outbreak occurred amongst 3 individuals, and two of your patients had been treated with a variety of lactams prior to isolation of S. marcescens. The S. marcescens clone within this cluster was resistant to penicillins, aztreonam, and expanded and broadspectrum cephalosporins and was sensitive to carbapenems and cefepime (26). An outbreak due to S. marcescens expressing an AmpClikelactamase, S4, was described in Taiwan from 999 to 2003. A total of 58 strains carried this S4 lactamase, and all have been recovered from individuals with bloodstream infections. Strains expressing S4 had been resistant to cefotaxime but not ceftazidime (420). Data on chromosomal ampC genes of other Serratia species are far 
more restricted. In one particular study, lactam sensitivity patterns indicated that isolates of S. liquefaciens, S. grimesii, and S. proteamaculans harbored chromosomal ampC genes (368). The sequence on the S. proteamaculans strain 568 genome indicates the presence of a chromosomal a.