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Phillip D. Levin, MBBChir; Charles L. Sprung, MD, FCCP; Andrew E. Simor, MD
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From the Department of Anesthesia and Critical Care Medicine (Drs Levin and Sprung), Hadassah Hebrew University Medical Center; and the Department of Microbiology (Dr Simor), Sunnybrook Health Sciences Center, and the Division of Infectious Diseases (Dr Simor), University of Toronto.

Correspondence to: Phillip D. Levin, MBBChir, Department of Anesthesia and Critical Care Medicine, POB 12000, Jerusalem 91120, Israel; e-mail: levinp@netvision.net.il


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(5):1286. doi:10.1378/chest.10-1720
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To the Editor:

We are complimented by Dr Meyers’ interest in our publications1-3 and appreciate her comments. Dr Meyer comments on differences in isolate counts in our various publications. Careful examination of the methodology of the articles reveals that the Infection Control Hospital Epidemiology article included isolates resistant only to ciprofloxacin, whereas the CHEST article included isolates resistant to all fluoroquinolones.

Unique isolates were defined as patient-, site-, and resistance-pattern-specific, meaning that a patient who was heavily colonized with Pseudomonas aeruginosa, for example, could harbor isolates in the surgical wound, sputum, urine, blood, and surveillance cultures (five isolates in this example of only one bacterial species). Further, even a single change in antibiotic sensitivity could double the number of unique isolates. This may have somewhat artificially inflated the number of resistant isolates reported.

For these reasons, counting isolates has significant limitations, and thus, the current research focused on patient acquisition of resistant bacteria, regardless of the site or the number of isolates involved. Considering patient acquisition of resistant organisms is, in our opinion, more clinically relevant and robust. When considered in this way, the number of patients acquiring ciprofloxacin-resistant bacteria in the Infection Control Hospital Epidemiology and CHEST reports is identical. Indeed, isolate distribution was included in the current study only to illustrate the huge differences in the load of resistant bacteria that existed between the Jerusalem and Toronto ICUs.

The high number of Acinetobacter baumanni isolates in Jerusalem may well have resulted from a very prolonged outbreak. However, we would suggest that the conditions in the Jerusalem ICU (whether related to end-of-life care decisions or not) contributed to the maintenance of the outbreak and further justified the comparison of the two ICUs.

As reported in the “Discussion” section of the article, combining the two populations (from Jerusalem and Toronto) is problematic. Although it is true that the populations are not identical, there is much in common between them. Further, performing separate regression analyses is limited because in the Toronto environment of low prevalence of resistant bacteria, few patients will acquire these bacteria, regardless of any other care consideration.

Regarding the fifth point, this is our hypothesis. Patients usually die within hours of withdrawal of therapy, so clearly there is limited opportunity for additional microbiologic studies or administration of antibiotics. In contrast, patients who die without withdrawal of therapy are obviously severely ill, are at high risk of infection, and receive more antibiotics. They are also present in the ICU for longer periods of time and can therefore act as a reservoir for resistant bacteria for the rest of the ICU.

To discover whether there really is a connection between end-of-life care and the acquisition of resistant bacteria will require a multicenter prospective study. We are currently planning such a study, to be performed during the coming winter under the aegis of the European Society of Intensive Care, and would welcome Dr Meyers’ support and participation.

Levin PD, Simor AE, Moses AE, Sprung CL. End-of-life treatment and bacterial antibiotic resistance: a potential association. Chest. 2010;1383:588-594. [CrossRef] [PubMed]
 
Levin PD, Fowler RA, Guest C, Sibbald WJ, Kiss A, Simor AE. Risk factors associated with resistance to ciprofloxacin in clinical bacterial isolates from intensive care unit patients. Infect Control Hosp Epidemiol. 2007;283:331-336. [CrossRef] [PubMed]
 
Levin PD, Shatz O, Sviri S, et al. Contamination of portable radiograph equipment with resistant bacteria in the ICU. Chest. 2009;1362:426-432. [CrossRef] [PubMed]
 

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References

Levin PD, Simor AE, Moses AE, Sprung CL. End-of-life treatment and bacterial antibiotic resistance: a potential association. Chest. 2010;1383:588-594. [CrossRef] [PubMed]
 
Levin PD, Fowler RA, Guest C, Sibbald WJ, Kiss A, Simor AE. Risk factors associated with resistance to ciprofloxacin in clinical bacterial isolates from intensive care unit patients. Infect Control Hosp Epidemiol. 2007;283:331-336. [CrossRef] [PubMed]
 
Levin PD, Shatz O, Sviri S, et al. Contamination of portable radiograph equipment with resistant bacteria in the ICU. Chest. 2009;1362:426-432. [CrossRef] [PubMed]
 
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