ACC-1 β-Lactamase–producing Salmonella enterica Serovar Typhi, India

نویسندگان

  • Bindiganavile N. Gokul
  • Godfred A. Menezes
  • Belgode N. Harish
چکیده

To the Editor: Typhoid fever, caused by Salmonella enterica sero-var Typhi, is a serious form of enteric fever. In 2000, the worldwide number of typhoid cases was estimated to be >21,000,000, and there were >200,000 deaths from this disease (1). Ciprofl oxacin is the fi rst-line drug of choice for treatment of patients with typhoid fever, but there has been an increase in strains resistant to ciprofl ox-acin (2) and resistance to third-generation cephalosporins has emerged (3). There are sporadic reports of high resistance to ceftriaxone in typhoidal salmonellae (3,4) in which CTX-M-15 and SHV-12 extended spectrum β-lactamases (ESBLs) have been reported. To date, there are no reports of AmpC β-lactamases in typhoidal salmonellae. AmpC β-lactamases confer resistance to a broad spectrum of β-lactams, which greatly limits therapeutic options. We investigated an isolate of S. Typhi by using serotyping, antimicrobial drug susceptibility testing , PCR screening for β–lactamase genes, and sequence analysis to con-fi rm the identity of the isolate and the β–lactamase gene involved in conferring resistance to this isolate. The isolate was obtained in Ban-galore, India, in August 2009, from the blood of a female patient (14 years of age) who was hospitalized because of signs and symptoms of enteric fever. She had no history of having received antimicrobial drugs. After a blood sample was cultured, the patient was empirically treated with ceftriaxone but did not clinically improve. Culture yielded gram-negative bacteria after 48 hours. The isolate was identifi ed by standard biochemical methods as S. Typhi. Identifi cation was confi rmed by using Salmonella spp. polyvalent O, O9, and H:d anti-sera (Murex Biotech, Dartford, UK). Susceptibility to antimicrobial drugs was assessed by using the Kirby-Bau-er disk diffusion method according to Clinical and Laboratory Standards Institute guidelines (www.clsi.org). The isolate was resistant to ampicil-It was susceptible to chloramphenicol, trimethoprim/sulfamethoxazole, na-lidixic acid, ciprofl oxacin, and mero-penem. Treatment was changed to cipro-fl oxacin (500 mg every 12 h for 7 d). The patient recovered within 72 hours and was discharged. MICs were determined for ciprofl oxacin, gatifl oxacin, ofl oxacin, ceftazidime, ceftriaxone, and amoxicillin/clavulanate by using the Etest (AB Biodisk, Solna, Swe-den) (Table). MIC for ceftriaxone was confi rmed by an agar dilution method (www.clsi.org). The isolate was tested for ESBLs by using a method with disks containing ceftazidime (30 μg) and ceftazidime/clavulanate (30 μg/10 μg). The AmpC disk test for detection of plasmid-mediated AmpC β-lactamase was conducted according to …

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عنوان ژورنال:

دوره 16  شماره 

صفحات  -

تاریخ انتشار 2010