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Nosocomial Acinetobacter baumannii Infections: Microbiological and Clinical Epidemiology

Daniel Villers, MD; Eric Espaze, MD; Marianne Coste-Burel, PharmD; Frederic Giauffret, MD; Emmanuelle Ninin, MD; Francoise Nicolas, MD; and Herve Richet, MD
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From the Institut de Biologie des Hopitaux de Nantes and Hotel Dieu, Nantes, France. Acknowledgments: The authors thank Jerome Tokars, MD, MPH, for manuscript review and assistance with data analysis and Dominique Gautreau, Anny Blin, and Michele Fleury for technical assistance. Grant Support: In part by grant 931305 from the Institut National de la Sante et de la Recherche Medicale. Requests for Reprints: Daniel Villers, MD, Service de Reanimation Medicale, Hotel Dieu, Centre Hospitalier Universitaire de Nantes, 44035 Nantes Cedex 01, France. Current Author Addresses: Drs. Villers, Giauffret, and Nicolas: Service de Reanimation Medicale, Hotel Dieu, Centre Hospitalier Universitaire de Nantes, 44035 Nantes Cedex 01, France. Drs. Espaze, Coste-Burel, Ninin, and Richet: Laboratoire de Bacteriologie, Virologie, Hygiene Hospitaliere, Institut de Biologie des Hopitaux de Nantes, 9, Quai Moncousu, 44035 Nantes Cedex 01, France.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1998;129(3):182-189. doi:10.7326/0003-4819-129-3-199808010-00003
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Background: Acinetobacter baumannii is an important opportunistic pathogen that is rapidly evolving toward multidrug resistance and is involved in various nosocomial infections that are often severe. It is difficult to prevent A. baumannii infection because A. baumannii is ubiquitous and the epidemiology of the infections it causes is complex.

Objective: To study the epidemiology of A. baumannii infections and assess the relation between fluoroquinolone use and the persistence of multidrug-resistant clones.

Design: Three case–control studies and a retrospective cohort study.

Setting: A 20-bed medical and surgical intensive care unit.

Patients: Acinetobacter baumannii was isolated from 45 patients in urine (31%), the lower respiratory tract (26.7%), wounds (17.8%), blood (11.1%), skin (6.7%), cerebrospinal fluid (4.4%), and sinus specimens (2.2%). One death was due to A. baumannii infection.

Measurements: Antimicrobial resistance pattern and molecular typing were used to characterize isolates. The incidence of A. baumannii infection and the use of fluoroquinolones were calculated annually.

Results: Initially, 28 patients developed A. baumannii infection. Eleven isolates had the same antimicrobial susceptibility profile, genotypic profile, or both (epidemic cases), and 17 were heterogeneous (endemic cases). A surgical procedure done in an emergency operating room was the main risk factor for epidemic cases, whereas previous receipt of a fluoroquinolone was the only risk factor for endemic cases. The opening of a new operating room combined with the restriction of fluoroquinolone use contributed to a transitory reduction in the incidence of infection. When a third epidemiologic study was done, previous receipt of a fluoroquinolone was again an independent risk factor and a parallel was seen between the amount of intravenous fluoroquinolones prescribed and the incidence of endemic infection.

Conclusion: Epidemic infections coexisted with endemic infections favored by the selection pressure of intravenous fluoroquinolones.


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Figure 1.
Ribotype patterns of Acinetobacter baumannii strains after EcoR1 digestion and hybridization with the labeled pKK3535 riboprobe.

Lanes A, B, C, and D: Raoul 1 size marker; lanes 1 through 7: pattern R1 (epidemic strains); lanes 8 through 14: pattern R2 (endemic strains from the second and third case–control studies); and lanes 15 and 16: sporadic strains. Kb = kilobase pairs.

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Figure 2.
Repetitive polymerase chain reaction patterns of Acinetobacter baumannii after digestion with ERIC II.Figure 1

Lanes A, B, and C: 1-kilobase DNA ladder size marker. Lanes 1 through 16: Isolates are shown in the same order as in . Bp = base pairs.

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Figure 3.
Epidemic curve.Acinetobacter baumannii

infections in an intensive care unit, 1989-1993. OR = operating room.

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Figure 4.
Amount of fluoroquinolones given (white bars) compared with incidence of Acinetobacter baumannii infections per admission (solid line) in an intensive care unit, 1991-1994.
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Figure 5.
Mode of fluoroquinolone administration compared with incidence of Acinetobacter baumannii infections per admission (solid line) in patients in an intensive care unit, 1991-1994.

White bars represent oral administration of fluoroquinolone; striped bars represent intravenous administration of fluoroquinolone.

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