title: Severe sepsis facilitates intestinal colonization by extended-spectrum-β-lactamase-producing Klebsiella pneumoniae and transfer of the SHV-18 resistance gene to Escherichia coli during antimicrobial treatment.
abstract: Infections caused by multidrug-resistant pathogens are frequent and life threatening in critically ill patients. To investigate whether severe sepsis affects gut colonization by resistant pathogens and genetic exchange between opportunistic pathogens, we tested the intestinal-colonization ability of an extended-spectrum beta-lactamase-producing Klebsiella pneumoniae strain carrying the SHV-18 resistance gene and the transfer ability of the resistance gene to endogenous Escherichia coli under ceftriaxone treatment in rats with burn injury only or severe sepsis induced by burns plus endotoxin exposure. Without ceftriaxone treatment, the K. pneumoniae strain colonized the intestine in both septic and burned rats for a short time, with clearance occurring earlier in burn-only rats but never in sham burn rats. In both burned and septic rats, the colonization level of the challenge strain dropped at the beginning and then later increased during ceftriaxone treatment, after which it declined gradually. This pattern coincided with the change in resistance of K. pneumoniae to ceftriaxone during and after ceftriaxone treatment. Compared with burn-only injury, severe sepsis had a more significant effect on the change in antimicrobial resistance to ceftriaxone. Only in septic rats was the resistance gene successfully transferred from the challenge strain to endogenous E. coli during ceftriaxone treatment; the gene persisted for at least 4 weeks after ceftriaxone treatment. We concluded that severe sepsis can facilitate intestinal colonization by an exogenous resistant pathogen and the transfer of the resistance gene to a potential endogenous pathogen during antimicrobial treatment.
authors.affiliation: Critical Care and Emergency Department, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, People's Republic of China.
authors.forename: Jun
authors.initials: J
authors.lastname: Guan
authors.forename: Shaoze
authors.initials: S
authors.lastname: Liu
authors.forename: Zhaofen
authors.initials: Z
authors.lastname: Lin
authors.forename: Wenfang
authors.initials: W
authors.lastname: Li
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Liu
authors.forename: Dechang
authors.initials: D
authors.lastname: Chen
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002056:Burns / Q000188:drug therapy / Q000382:microbiology* / Q000473:pathology; D002443:Ceftriaxone / Q000494:pharmacology; D024901:Drug Resistance, Multiple, Bacterial; D004731:Endotoxins; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics*; D022761:Gene Transfer, Horizontal; D006358:Hot Temperature; D007422:Intestines / Q000382:microbiology / Q000473:pathology; D007710:Klebsiella Infections / Q000188:drug therapy / Q000382:microbiology* / Q000473:pathology; D007711:Klebsiella pneumoniae / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000139:chemically induced / Q000188:drug therapy / Q000382:microbiology* / Q000473:pathology; D001618:beta-Lactamases / Q000235:genetics* / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D004731:Endotoxins; D002443:Ceftriaxone; C413409:SHV-18 beta-lactamase; D001618:beta-Lactamases