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Journal of Clinical Microbiology, March 1999, p. 758-761, Vol. 37, No. 3
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Spread of Amikacin Resistance in Acinetobacter baumannii Strains Isolated in Spain Due to an Epidemic Strain

Jordi Vila,1,* Joaquim Ruiz,1 Margarita Navia,1 Berta Becerril,2 Isabel Garcia,3 Sofia Perea,4 Inmaculada Lopez-Hernandez,5 Isabel Alamo,6 Frederic Ballester,7 Anna M. Planes,8 Jesus Martinez-Beltran,9 and Teresa Jimenez De Anta1

Department de Microbiologia, Institut d' Investigació Biomèdica August Pi i Sunyer, Hospital Clínic, Facultat de Medicina, Universitat de Barcelona, 08036 Barcelona,1 Servicio de Microbiología, Hospital Virgen del Rocio, 41013 Seville,2 Servicio de Microbiología, Hospital de la Princesa, 28006 Madrid,3 Servicio de Microbiologia, Hospital 12 de Octubre, 28041 Madrid,4 Departamento de Microbiología y Epidemiología Infecciosa, Hospital Virgen Macarena, 41008 Seville,5 Servicio de Microbiología, Hospital Nuestra Señora del Pino, 35005 Las Palmas, Grand Canary Islands,6 Servicio de Microbiología, Hospital de Sant Joan de Reus, 43201 Reus, Tarragona,7 Servicio de Microbiología, Hospital del Valle Hebrón, 08035 Barcelona,8 and Servicio de Microbiología, Hospital Ramón y Cajal, 28034 Madrid,9 Spain

Received 29 April 1998/Returned for modification 2 July 1998/Accepted 8 December 1998

Sixteen amikacin-resistant clinical Acinetobacter baumannii isolates from nine different hospitals in Spain were investigated to determine whether the high incidence of amikacin-resistant A. baumannii was due to the dissemination of an amikacin-resistant strain or to the spread of an amikacin resistance gene. The epidemiological relationship studied by repetitive extragenic palindromic PCR and low-frequency restriction analysis of chromosomal DNA showed that the same clone was isolated in eight of nine hospitals, although other clones were also found. The strains were studied for the presence of the aph(3')-VIa and aac(6')-I genes, which encode enzymes which inactivate amikacin, by PCR. All 16 clinical isolates had positive PCRs with primers specific for the amplification of the aph(3')-VIa gene, whereas none had a positive reaction for the amplification of the aac(6')-I gene. Therefore, the high incidence of amikacin resistance among clinical A. baumannii isolates in Spain was mainly due to an epidemic strain, although the spread of the aph(3')-VI gene cannot be ruled out.

* Corresponding author. Mailing address: Laboratori de Microbiologia, Hospital Clinic, Facultat de Medicina, Universitat de Barcelona, Villarroel, 170, 08036 Barcelona, Spain. Phone: 34-3-2275522. Fax: 34-3-2275454. E-mail: vila{at}medicina.ub.es.

Journal of Clinical Microbiology, March 1999, p. 758-761, Vol. 37, No. 3
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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