Resistance to Different Antibiotics
This organism is intrinsically resistant to ampicilli. It has the ability to cause hospital outbreaks of opportunistic infection, and it often exchanges plasmidborne resistances. K. pneumoniae is the most common nosocomial pathogen of it, and appears to have the greatest ability to receive and disseminate multiresistance plasmids. The ampicillin resistance of K. pneumoniae is mediated by chromosomal SHV-1 β-lactamase. In the 1970s, organisms carrying plasmid-borne aminoglycoside resistance often caused large outbreaks of hospital infection and sometimes disseminated their resistances to Enterobacter, Serratia and other enterobacterial species. These outbreaks diminished when the newer cephalosporins and aminoglycosides became available.
Resistance to carbapenems has been reported increasingly in K. pneumoniae. In the majority of cases, this was related to the spread of plasmid-encoded class A carbapenemases (KPC) and class B carbapenemases (VIM), especially in K. pneumoniae. Less commonly, carbapenem- resistant Enterobacteriaceae were due to high-level production of cephalosporinase- or oxacillinase-mediated resistance combined with other β-lactamases and porin mutation. The K. pneumoniae carbapenemase (KPC) was initially reported in North Carolina in 1996 and subsequently worldwide. Six variants of the blaKPC1/2 gene have been reported. Although these enzymes confer decreased susceptibility to all β-lactams, impaired outer membrane permeability is often required to achieve full resistance to carbapenems. The blaKPC genes have been identified within a Tn3-type transposon (Tn4001) in large transferable plasmids. These plasmids frequently carry aminoglycoside determinants and have been associated with ESBL (CTX-M-15) and the quinolone-resistance proteins QnrA and QnrB. Co-resistance to other non-β-lactam antibiotics limits therapeutic options for these strains. The blaKPC genes have been reported in other Enterobacteriaceae (Enterobacter spp., Esch. coli, K. oxytoca, C. freundii, P. mirabilis, Salmonella spp. and S. marcescens) and at chromosomal and plasmid locations in Ps. aeruginosa.
About 30% of hospital isolates of Enterobacter spp. show cephalosporinase hyperproduction. In the 1990s, ESBLproducing (mostly TEM-24), multiresistant Ent. aerogenes strains emerged as a common cause of nosocomial infection in France, Spain and Belgium. Epidemic strains were first reported in ICUs and have since disseminated hospital-wide to cause large regional epidemics. Many of these ESBLproducing strains remain susceptible only to carbapenems, which are the drugs of choice for treatment of serious infection with these organisms.
