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JAC Advance Access originally published online on June 21, 2007
Journal of Antimicrobial Chemotherapy 2007 60(2):445; doi:10.1093/jac/dkm127
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Correspondence

Comment on: Emergence of multidrug-resistant Gram-negative bacteria during selective decontamination of the digestive tract on an intensive care unit

F. Abecasis1, S. Kerr1, R. E. Sarginson1,*, L. Silvestri2, M. A. de la Cal3, D. Zandstra4, A. Beishuizen5, V. Damjanovic6 and H. K. F. van Saene7

1 Paediatric Intensive Care Unit, Alder Hey Children's Hospital, Liverpool, UK 2 Department of Anaesthesia and Intensive Care, Gorizia, Italy 3 Intensive Care Unit, University Hospital of Getafe, Getafe, Madrid, Spain 4 Department of Intensive Care, OLVG, Amsterdam, The Netherlands 5 Department of Intensive Care, VU Medical Center, Amsterdam, The Netherlands 6 Department of Medical Microbiology, University of Liverpool, Liverpool, UK 7 Department of Medical Microbiology, University of Liverpool and Department of Clinical Microbiology and Infection Control, Alder Hey Children's Hospital, Liverpool, UK


* Corresponding author. Tel: +44-151-252-5223; Fax: +44-151-252-5460; E-mail: richard.sarginson{at}rlc.nhs.uk

Keywords: tobramycin resistance , paromomycin , ESBLs

Sir,

We read with interest the paper by Al Naiemi et al.1 claiming a link between the emergence of aerobic Gram-negative bacilli (AGNB), producing extended-spectrum ß-lactamase (ESBL), and selective decontamination of the digestive tract (SDD). In particular, the parenteral component of SDD, cefotaxime, is considered a risk factor for the emergence of strains carrying ESBL.1 The authors concluded that they had identified an outbreak of plasmid-mediated ESBL genes during SDD treatment, presumably by horizontal transfer, although there is no clear evidence of transmission of different strains among the patients. It appears that all the evidence of a link with SDD is, at best, circumstantial.

There are many reports describing endemicity of ESBL-producing AGNB in intensive care units that do not use SDD.2 Additionally, the use of most parenteral antimicrobials that suppress the patient's indigenous gut flora has been shown to promote the subsequent overgrowth of ESBL-producing AGNB in the gut.2,3

Unfortunately, Al Naiemi et al. have omitted the basic demographic data, which would allow us to appreciate the magnitude of the endemicity of the ESBL-producing AGNB. Only four patients were involved, each of them carried a different strain and only one of the patients became infected. The impact of polymyxin E/tobramycin on the abnormal carrier state of ESBL-producing AGNB was not reported.

We believe that the issue is not the parenteral component, cefotaxime, but the susceptibility of the ESBL-producing AGNB to the enteral aminoglycoside component of SDD, tobramycin. Polymyxin E alone has not been shown to successfully clear AGNB, irrespective of their resistance pattern.4 All ESBL-producing AGNB isolated within the first week of admission were resistant to tobramycin. This suggests that they were present in the patient prior to admission, despite not being detected in the admission surveillance. SDD is considered to be effective only if surveillance cultures show the eradication of all AGNB.4 Two enteral antimicrobials, which are active against AGNB, are required to successfully decontaminate patients.4 If the ESBL-producing AGNB are resistant to tobramycin, there is a need to adjust SDD therapy.5 Neomycin6 and paromomycin have been successfully used as replacements for tobramycin. The ICU in Getafe (Madrid) experienced an episode of endemicity of carriage and infection due to a multiresistant Serratia. The strain was resistant to the enteral antimicrobials, polymyxin E and tobramycin. Both were discontinued and replaced by paromomycin. Endemicity was controlled within a week.

When a macrolide was added to polymyxin E, the combination failed to render the critically ill patient free of ESBL-producing AGNB, as these organisms were resistant to erythromycin.2

The traditional enteral polymyxin E/tobramycin combination is not a panacea and would need to be modified in the case of endemicity of ESBL-producing, tobramycin-resistant AGNB.5

Transparency declarations

None to declare.

References

1 Al Naiemi N, Heddema ER, Bart A, et al. Emergence of multidrug-resistant Gram-negative bacteria during selective decontamination of the digestive tract on an intensive care unit. J Antimicrob Chemother (2006) 58:853–6.[Abstract/Free Full Text]

2 Decré D, Gachot B, Lucet JC, et al. Clinical and bacteriologic epidemiology of extended-spectrum ß-lactamase-producing strains of Klebsiella pneumoniae in a medical intensive care unit. Clin Infect Dis (1998) 27:834–44.[Web of Science][Medline]

3 Pultz NJ, Stiefel U, Donskey CJ. Effects of daptomycin, linezolid and vancomycin on establishment of intestinal colonization with vancomycin-resistant enterococci and extended-spectrum-ß-lactamases-producing Klebsiella pneumoniae in mice. Antimicrob Agents Chemother (2005) 49:3513–6.[Abstract/Free Full Text]

4 Sanchez M, Pizer BP, Alcock SR. Enteral antimicrobials. In: Infection Control in the Intensive Care Unit—van Saene HKF, Silvestri L, de la Cal MA, eds. (2005) Second Edition. Milan, Italy: Springer. 171–87.

5 Brun-Buisson C, van Saene HKF. SDD and the novel extended-broad-spectrum ß-lactamases. J Antimicrob Chemother (1991) 28:145–7.[Free Full Text]

6 Brun-Buisson C, Legrand P, Rauss A, et al. Intestinal decontamination for control of nosocomial multiresistant gram-negative bacilli. Study of an outbreak in an intensive care unit. Ann Intern Med (1989) 110:873–81.[Abstract/Free Full Text]


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This Article
Right arrow Extract Freely available
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Right arrow All Versions of this Article:
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dkm127v1
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