JAC Advance Access originally published online on September 19, 2007
Journal of Antimicrobial Chemotherapy 2007 60(5):1174-1176; doi:10.1093/jac/dkm366
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Correspondence |
Panresistant extended-spectrum ß-lactamase SHV-5-producing Acinetobacter baumannii from New York City
1 Service de Bactériologie-Virologie, Hôpital de Bicêtre, Assistance Publique/Hôpitaux de Paris, Faculté de Médecine Paris-Sud, Université Paris XI, 78 rue du Général Leclerc, 94275 K.-Bicêtre, France 2 Service de Bactériologie, Hôpital Cochin, Assistance Publique/Hôpitaux de Paris, Faculté de Médecine Paris Descartes, Université Paris V, 75014 Paris, France
* Corresponding author. Tel: +33-1-45-21-29-86; Fax: +33-1-45-21-63-40; E-mail: thierry.naas{at}bct.ap-hop-paris.fr
Keywords: ESBLs , inter-country spread , multidrug resistance , carbapenem resistance
Over the last decade, nosocomial infections of Acinetobacter baumannii have been described with an increasing trend towards multidrug resistance, mostly in intensive care units.1 The main mechanisms of resistance to extended-spectrum cephalosporins in A. baumannii are the overexpression of chromosome-encoded cephalosporinases and plasmid-encoded Ambler class A, B and D ß-lactamases.1 A. baumannii producing extended-spectrum ß-lactamases (ESBLs) have also been reported: PER-1 from Turkey, Korea, Russia, Romania, Belgium and France; VEB-1 from France and Belgium; TEM-116 and SHV-12 from China and the Netherlands; and CTX-M-2 from Korea.2,3 However, ESBL-producing A. baumannii strains remain susceptible to carbapenems.1,2 Recently, a carbapenem-resistant PER-1-producing strain from Russia has been described.2 Here, we report the first ESBL-producing A. baumannii isolate from the USA being susceptible only to colistin and rifampicin.
An 80-year-old man with a 5 year history of prostatic carcinoma and metastasis was admitted at the Cochin Hospital in Paris for acute urine retention in the right nephrostomy in February 2005. The bilateral nephrostomy was performed in December 2004 at a New York City hospital. Between his stay in New York and his emergency hospitalization in Paris, no hospitalization or antibiotic treatment is known. This patient also had urine and blood cultures with Klebsiella pneumoniae YC producing the plasmid-encoded class A carbapenemase KPC-2.4 At the day of his admission, cultures from rectal swabs revealed a carbapenem-resistant A. baumannii strain YC. During the same period of time, no other A. baumannii isolate with a similar antibiotic resistance pattern was recovered from the Cochin Hospital.
Disc diffusion susceptibility testing2 revealed that A. baumannii strain YC was susceptible only to rifampicin and colistin. No synergy image could be observed between clavulanic acid and cefepime- or ceftazidime-containing discs. The use of cloxacillin-containing Mueller-Hinton plates (200 mg/L) allowed detection of a synergy image, the signature of the presence of an ESBL. A. baumannii YC was resistant to all the ß-lactams tested (amoxicillin, ticarcillin, piperacillin, ceftazidime, aztreonam, cefepime and imipenem). The MIC of imipenem was >32 mg/L, and clavulanic acid addition (2 mg/L) decreased the ticarcillin MIC from >512 to 256 mg/L and the ceftazidime MIC from 512 to 128 mg/L, but did not affect the MIC values of imipenem. Furthermore, the MIC of tigecycline was 24 mg/L.
PCR experiments with primers for the detection of most of the Ambler class A, class B and class D ß-lactamase genes,2,4 followed by sequencing, identified the blaSHV-5 gene.5 A ß-lactamase extract from A. baumannii YC culture subjected to analytical isoelectric focusing2 identified two pI values (8.1 for SHV-5 and >8.5 for AmpC). A crude ß-lactamase extract of that isolate had no significant imipenem hydrolysis activity, suggesting that the carbapenem resistance was not ß-lactamase-mediated.2
Using a series of successive PCR primers, the surrounding sequences of the blaSHV-5 gene were found to be identical to those surrounding the blaSHV-5 gene in Enterobacteriaceae (Figure 1a).5 Several conserved genes, such as repF and deoR that originated from the K. pneumoniae chromosome, were found along with IS26 insertion elements, likely involved in the mobilization of the blaSHV-5 gene (Figure 1b). Attempts to demonstrate plasmids or transfer genes encoding SHV-5, as previously described, into azide-resistant Escherichia coli J53 or to rifampicin-resistant A. baumannii CIP7010 failed (data not shown), suggesting that the gene was probably chromosomally encoded.2
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The naturally occurring blaAMPC- and blaOXA-51-like genes of A. baumannii YC were also amplified and sequenced.1 The deduced amino acid sequences identified an AMPC ß-lactamase that has two amino acid changes (T341A and V376A) when compared with AMPC characterized from China (unpublished GenBank AQB45322) and a novel variant of the naturally occurring oxacillinase, OXA-113, point mutant derivative of OXA-71 (L167V). ISAba1 was inserted upstream of blaOXA-113 and blaAMPC genes, but also in front of the aminoglycoside resistance gene aac6'Ib (Figure 1c).
The emergence and spread of the ESBL-producing A. baumannii strains is worrisome, as it will enhance extensive use of carbapenems, thus increasing the risk of emergence of carbapenem-resistant isolates. A. baumannii YC is the second description of an ESBL-producing A. baumannii isolate being also resistant to carbapenems and the first description of an ESBL-producing A. baumannii isolate from the USA, a country where blaSHV-5 is the most prevalent ESBL gene in Enterobacteriaceae.6 Multidrug-resistant A. baumannii has emerged as a serious nosocomial pathogen in the New York area.7 A citywide surveillance revealed that approximately two of three isolates were resistant to carbapenem antibiotics.7 The decreased production of outer membrane porins, together with an increased expression of a class C cephalosporinase, appeared to be important factors leading to carbapenem resistance. It would be interesting to test these strains for the presence of blaSHV-5, especially as nothing could predict its presence on a routine antibiogram.
These results highlight the importance of international patient transfer in the spread of antimicrobial resistance. Rapid identification of A. baumannii YC and increased awareness and implementation of strict barrier precautions prevented this strain from spreading to other patients.
This work was funded by a grant from the Ministère de l'Education Nationale et de la Recherche (UPRES-EA3539), Université Paris Sud and by the European Community (6th PCRD, LSHM-CT-2005-018705).
None to declare.
Table S1 is available as Supplementary data at JAC Online (http://jac.oxfordjournals.org/).
Acknowledgements
We are grateful to Gaelle Cuzon for technical assistance.
References
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