sequential emergence of resistance to multiple antimicrobial agents in kpc-producing-klebsiella pneumoniae

نویسندگان

marcela nastro department of clinical biochemistry, bacteriology laboratory, hospital de clinicas jose de san martin, school of pharmacy and biochemistry, university of buenos aires, buenos aires, argentina; bacteriology laboratory, hospital de clinicas jose de san martin, school of pharmacy and biochemistry, university of buenos aires, buenos aires, argentina. tel: +54-1159508670, fax: +54-1159508694, [email protected]

carlos hernan rodriguez department of clinical biochemistry, bacteriology laboratory, hospital de clinicas jose de san martin, school of pharmacy and biochemistry, university of buenos aires, buenos aires, argentina

claudia barberis department of clinical biochemistry, bacteriology laboratory, hospital de clinicas jose de san martin, school of pharmacy and biochemistry, university of buenos aires, buenos aires, argentina

carlos vay department of clinical biochemistry, bacteriology laboratory, hospital de clinicas jose de san martin, school of pharmacy and biochemistry, university of buenos aires, buenos aires, argentina

چکیده

introduction klebsiella pneumoniae is one of the most important gram-negative bacteria causing hospital-acquired infections. case presentation in this report is presented a patient with an abdominal infection caused by carbapenemase producing-klebsiella pneumonia (k. pneumonia). in spite of administrating the combination therapy, successive resistance to last-resort antimicrobial agents (colistin and tigecycline) was observed. the use of combination therapy, in four successive isolates recovered from this patient, was analyzed by killing curves. the genetic relatedness among the isolates was assessed. conclusions all four isolates were klebsiella pneumoniae carbapenemase (kpc) positive and showed resistance to all β-lactams including carbapenems and to other antimicrobial agents like aminoglycosides, fluoroquinolones, minocycline and trimetoprim-sulfametoxazol (tms). isolates 1 and 2 showed susceptibility to colistin, whereas isolate 3 was colistin-resistant and isolate 4 became tigecycline-resistant as well. synergy was only observed with colistin plus rifampicin and with the triple combination of colistin, rifampicin and fosfomycin. the four isolates were indistinguishable genotypically. we described the sequential emergence of resistance to colistin and tigecycline in kpc-producing-k. pneumonia (kpc-kp) isolates that occurred under treatment with these antimicrobial agents despite the use of combination therapy.

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عنوان ژورنال:
international journal of infection

جلد ۱، شماره ۲، صفحات ۰-۰

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