Carbapenem-resistant Acinetobacter baumannii and Klebsiella pneumoniae across a hospital system: impact of post-acute care facilities on dissemination

Federico Perez, Andrea Endimiani, Amy J Ray, Brooke K Decker, Christopher J Wallace, Kristine M Hujer, David J Ecker, Mark D Adams, Philip Toltzis, Michael J Dul, Anne Windau, Saralee Bajaksouzian, Michael R Jacobs, Robert A Salata, Robert A Bonomo, Federico Perez, Andrea Endimiani, Amy J Ray, Brooke K Decker, Christopher J Wallace, Kristine M Hujer, David J Ecker, Mark D Adams, Philip Toltzis, Michael J Dul, Anne Windau, Saralee Bajaksouzian, Michael R Jacobs, Robert A Salata, Robert A Bonomo

Abstract

Background: Resistance to carbapenems among Acinetobacter baumannii and Klebsiella pneumoniae presents a serious therapeutic and infection control challenge. We describe the epidemiology and genetic basis of carbapenem resistance in A. baumannii and K. pneumoniae in a six-hospital healthcare system in Northeast Ohio.

Methods: Clinical isolates of A. baumannii and K. pneumoniae distributed across the healthcare system were collected from April 2007 to April 2008. Antimicrobial susceptibility testing was performed followed by molecular analysis of carbapenemase genes. Genetic relatedness of isolates was established with repetitive sequence-based PCR (rep-PCR), multilocus PCR followed by electrospray ionization mass spectrometry (PCR/ESI-MS) and PFGE. Clinical characteristics and outcomes of patients were reviewed.

Results: Among 39 isolates of A. baumannii, two predominant genotypes related to European clone II were found. Eighteen isolates contained bla(OXA-23), and four isolates possessed bla(OXA-24/40). Among 29 K. pneumoniae isolates with decreased susceptibility to carbapenems, two distinct genotypes containing bla(KPC-2) or bla(KPC-3) were found. Patients with carbapenem-resistant A. baumannii and K. pneumoniae were elderly, possessed multiple co-morbidities, were frequently admitted from and discharged to post-acute care facilities, and experienced prolonged hospital stays (up to 25 days) with a high mortality rate (up to 35%).

Conclusion: In this outbreak of carbapenem-resistant A. baumannii and K. pneumoniae across a healthcare system, we illustrate the important role post-acute care facilities play in the dissemination of multidrug-resistant phenotypes.

Figures

Figure 1
Figure 1
(a) PFGE of ApaI macrorestriction of representative A. baumannii isolates, demonstrating PFGE type A (Ab21, Ab30, Ab31, Ab33, Ab37, Ab40, Ab41 and Ab53), type B (Ab20, Ab22 and Ab39), type C (Ab69, Ab76 and Ab79), type D (Ab51 and Ab83) and type E (Ab52). (b) Dendrogram describing percentage similarity and band patterns of A. baumannii by rep-PCR, interpreted using the Kullback–Leibler method. Similarity within group 1 (1–13) and within group 2 (14–29) is >95%. Similarity between the two groups is >90%. Also in this figure, ST by PCR/ESI-MS, PFGE types, carbapenemase genes detected and distribution by location in hospital ward, medical intensive care unit (MICU), cardiac intensive care unit (CICU), surgical intensive care unit (SICU) and long-term acute care hospital (LTACH) are shown.
Figure 1
Figure 1
(a) PFGE of ApaI macrorestriction of representative A. baumannii isolates, demonstrating PFGE type A (Ab21, Ab30, Ab31, Ab33, Ab37, Ab40, Ab41 and Ab53), type B (Ab20, Ab22 and Ab39), type C (Ab69, Ab76 and Ab79), type D (Ab51 and Ab83) and type E (Ab52). (b) Dendrogram describing percentage similarity and band patterns of A. baumannii by rep-PCR, interpreted using the Kullback–Leibler method. Similarity within group 1 (1–13) and within group 2 (14–29) is >95%. Similarity between the two groups is >90%. Also in this figure, ST by PCR/ESI-MS, PFGE types, carbapenemase genes detected and distribution by location in hospital ward, medical intensive care unit (MICU), cardiac intensive care unit (CICU), surgical intensive care unit (SICU) and long-term acute care hospital (LTACH) are shown.
Figure 2
Figure 2
(a) PFGE of XbaI macrorestriction of selected K. pneumoniae isolates, demonstrating PFGE type A (Kp01, Kp03, Kp04, Kp05, Kp07, Kp23, Kp24, Kp27 and Kp47) and type B (Kp17, Kp18, Kp22, Kp32, Kp40, Kp42, Kp48 and Kp54). L corresponds to lambda ladder. (b) Dendrogram describing percentage similarity and band patterns of K. pneumoniae by rep-PCR, interpreted using the Kullback–Leibler method. Similarity within group 1 (1–17) and within group 2 (19–28) is ∼95%. Similarity between the two groups is ∼85%. Also in this figure, the type of blaKPC detected, PFGE types, results of susceptibility testing against amikacin (AMK) and gentamicin (GEN) and location in hospital ward, medical intensive care unit (MICU), surgical intensive care unit (SICU) and long-term acute care hospital (LTACH).
Figure 2
Figure 2
(a) PFGE of XbaI macrorestriction of selected K. pneumoniae isolates, demonstrating PFGE type A (Kp01, Kp03, Kp04, Kp05, Kp07, Kp23, Kp24, Kp27 and Kp47) and type B (Kp17, Kp18, Kp22, Kp32, Kp40, Kp42, Kp48 and Kp54). L corresponds to lambda ladder. (b) Dendrogram describing percentage similarity and band patterns of K. pneumoniae by rep-PCR, interpreted using the Kullback–Leibler method. Similarity within group 1 (1–17) and within group 2 (19–28) is ∼95%. Similarity between the two groups is ∼85%. Also in this figure, the type of blaKPC detected, PFGE types, results of susceptibility testing against amikacin (AMK) and gentamicin (GEN) and location in hospital ward, medical intensive care unit (MICU), surgical intensive care unit (SICU) and long-term acute care hospital (LTACH).

Source: PubMed

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