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Journal of Clinical Microbiology, April 2008, p. 1566-1567, Vol. 46, No. 4
0095-1137/08/$08.00+0     doi:10.1128/JCM.02299-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

LETTER TO THE EDITOR

Prevalence of Fecal Carriage of Acquired Expanded-Spectrum Cephalosporin Resistance in Enterobacteriaceae Strains from Cattle in France

Top LETTER REFERENCES

 
In gram-negative pathogens, extended-spectrum beta-lactamases (ESBLs) confer resistance to penicillins, cephalosporins (including extended-spectrum cephalosporins), and aztreonam, but not to cephamycins and carbapenems, and are inhibited by beta-lactamase inhibitors (8). Recently, cefotaximases have become the most prevalent ESBLs worldwide (7) and have also been detected in animals (see, for instance, references 2 and 9).

Contrary to the human field (see, for instance, references 10, 11, and 13), little has been reported on the prevalence of fecal carriage of ESBL producers by animals (1, 3, 4, 12), and this issue was examined here by testing 1,264 nonduplicate specimens collected from cattle at farms and slaughterhouses in France.

From March to October 2006, fecal samples from 657 sick cattle (farm) were plated on agar supplemented with ceftazidime (1 µg/ml) or cefotaxime (1 µg/ml), 117 of which allowed colonies to grow. After determination of MICs with ESBL Etest strips, 52 ESBL or cephalosporinase producers were identified. Species identification revealed 41 Escherichia coli and 11 non-E. coli isolates, i.e., 7 of Acinetobacter sp., 2 of Pseudomonas aeruginosa, 1 of Citrobacter freundii, and 1 of Hafnia alvei. Antibiotic susceptibility testing, including a double-disk synergy test, confirmed an acquired bla-encoded phenotype in all of the E. coli isolates, whereas a natural phenotype was identified in all 11 non-E. coli isolates. The 41 E. coli isolates were tested by PCR for the bla_TEM, bla_SHV, bla_OXA, bla_CMY, and bla_CTX-M groups as described previously (9), revealing 17 ESBL producers (12 bla_CTX-M-1 isolates, 1 bla_CTX-M-15 isolate, 3 bla_CTX-M-14 isolates, and 1 bla_TEM-126 isolate), either alone (15 isolates) or with a bla_TEM gene (2 isolates).

Similarly, of the fecal samples collected from 607 healthy cattle at abattoirs from March 2005 to June 2006, 61 allowed colonies to grow, 46 of which were ESBL or cephalosporinase producers (35 E. coli and 11 non-E. coli isolates, i.e., 8 Acinetobacter sp. isolates, 1 Pseudomonas aeruginosa isolate, 1 Enterobacter cloacae isolate, and 1 Hafnia alvei isolate). Only the 35 E. coli isolates harbored an acquired bla-encoded phenotype, 25 of which produced ESBLs (21 had bla_CTX-M-1, 2 had bla_CTX-M-14, and 2 had bla_SHV-12), either alone (19 isolates) or with a bla_TEM gene (6 isolates).

Thus, the prevalence of E. coli producing acquired expanded-spectrum cephalosporinases was 6.2% and 5.8% in sick and healthy cattle, respectively (Table 1). All 42 ESBL-producing E. coli isolates were qnrA, -B, and -S negative by PCR, and most of them (39/42) showed unrelated pulsed-field gel electrophoresis patterns (not shown).

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TABLE 1. Cephalosporin resistance in E. coli isolates from sick and healthy cattle

The use of expanded-spectrum cephalosporins (such as ceftiofur) in veterinary medicine may select ESBL producers in animals. Most genes were of the CTX-M-1 group, so that the epidemiology in farm animals seems to mirror the trend observed in humans in France (5, 6). The absence of the qnr gene was reassuring, and the predominant absence of clonality may argue for multiple transferable genetic elements supporting ESBL-encoding genes.

Overall, our study indicates a worrisome prevalence of fecal carriage of cephalosporin resistance in cattle in France, with a higher prevalence of ESBL-producing E. coli at slaughterhouses compared to farms (Table 1).

 
This study was supported in part by a grant from the Direction Générale de l'Alimentation, Ministère de l'Agriculture, France.  We gratefully thank Vincent Jarlier and Jérôme Robert (Hôpital de la Pitié-Salpétrière, Paris, France) for helpful discussions and critical reading of the manuscript.

 
Published ahead of print on 13 February 2008.

Top LETTER REFERENCES

 

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						Jean-Yves Madec* Corinne Lazizzera Pierre Châtre Danièle Meunier Afssa Lyon 31, Ave. Tony Garnier 69364 Lyon Cedex 7, France Sylvie Martin LCAM 4, rue de Bort les Orgues 57078 Metz Cedex 3, France Gérard Lepage Marie-Françoise Ménard LVD53 224, rue du Bas des Bois 53014 Laval, France Patricia Lebreton Thomas Rambaud LVD76 Avenue du Grand Cours 76175 Rouen Cedex, France
						* Phone: 33 4 78 69 68 30 Fax: 33 4 78 61 91 45 E-mail: jy.madec{at}lyon.afssa.fr

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Journal of Clinical Microbiology, April 2008, p. 1566-1567, Vol. 46, No. 4
0095-1137/08/$08.00+0     doi:10.1128/JCM.02299-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Madec, J.-Y. Articles by Rambaud, T. Search for Related Content PubMed PubMed Citation Articles by Madec, J.-Y. Articles by Rambaud, T.