Resistance to Different Antibiotics
Acquired resistance to ampicillin is conferred to Esch. coli by a plasmid-encoded, Tn3-associated TEM-1 β-lactamase. First described in 1965, this mobile gene has spread so extensively throughout the world that 40–60% of both hospital and community strains are now resistant by this mechanism. Up to 50% of these ampicillin-resistant organisms are also resistant to the combination of amoxicillin with clavulanic acid, either because of hyperproduction of TEM-1 β-lactamase or by production of a mutant, inhibitor-resistant TEM enzyme. Other plasmidencoded β-lactamases are seen in Esch. coli with increasing frequency, including extended-spectrum β-lactamases of the TEM, SHV and AmpC families. Fluoroquinolone resistance in Esch. coli is an increasingly common problem in Europe and has reached prevalence rates as high as 50% in Turkey, and 40% in Hong Kong. Intestinal carriage was found in 25% of healthy individuals in Spain. Fluoroquinolone-resistant Esch. coli is particularly common in patients with complicated urinary tract infections and in neutropenic patients developing bacteremia during fluoroquinolone prophylaxis.
Esch. coli has been recognized as the major source of ESBLs with a higher increase in prevalence in the community than in the hospital setting. This increase was initially due to the spread of multiple clones harboring different CTX-M enzymes into diverse genetics elements (integrons and transposons). These enzymes show higher hydrolyzing activity against cefotaxime than ceftazidime. They display high homology with chromosomal β-lactamases from Kluyvera species. The insertion sequences ISEcp1 and Orf513 contribute to their mobilization. Among the CTX-M, CTX-M-15 is the predominant enzyme found in the community and in long-term care facilities. This enzyme harbors the Asp240Gly substitution that confers an eight-fold higher level of resistance to ceftazidime than its parental CTX-M-3 enzyme. CTX-M-15 Esch. coli has emerged globally by acquisition of epidemic plasmids into highly virulent strains of the B2 phylogenetic subgroup, sequence type ST131, serogroup O25:H4. Co-resistance to fluoroquinolones is frequently mediated by qnr genes and aac (6′)-Ib-cr in these ESBL-producing strains.
In addition to ESBL, new variants of cephalosporinases called extended-spectrum AmpC (ESAC) β-lactamases, which confer resistance against oxyimino-cephalosporins including cefepime and cefpirome, have been described since 1995 in Ent. cloacae, Serratia marcescens and Esch. coli. Plasmid-encoded AmpC enzymes conferring resistance to third-generation cephalosporins (such as CMY-2) have become frequent in the USA but remain rare in Europe. Resistance to carbapenems by metallo-β- lactamase production (VIM-1) has been reported sporadically in clinical Esch. coli isolates from Spain and Greece.
Escherichia coli (E.coli) is a non-spore forming, Gram-negative, rod-shaped facultative anerobe, which is found in the human gastrointestinal tract. It belongs to the family of Enterobacteriaceae. E.coli is chemoorganotrophic and grows at 37°C. Pathogenic E.coli strains is associated with diarrhea, septicemia, meningitis and urinary tract infections. It inhibits the colonization of the gut by harmful bacteria. E.coli acts as an indicator of fecal contamination.
