Emergence of PER-2 and VEB-1a in Acinetobacter baumannii Strains in the Americas

Abstract

Antimicrobial treatment of Acinetobacter infections may be limited because of the emergence of extended-spectrum ␤-lactamase (ESBL)-and carbapenemase-producing multiresistant strains (7,13). Non-TEM-, non-SHV-derived ESBLs (such as PER and VEB) have been documented in Acinetobacter isolates from Europe and Asia (7) but not yet from the Americas.Recently, an increasing trend has been documented in carbapenem and extended-spectrum cephalosporin resistance in Acinetobacter isolates in Buenos Aires. Indeed, data from the Whonet-Argentina Network showed that, in 2004, more than 80% of Acinetobacter isolates were resistant to extendedspectrum cephalosporins. In addition, imipenem resistance increased from 5% to 54%, in the period from 2000 to 2004 (M. Galas, unpublished results). National ESBL surveillance is performed by Whonet-Argentina Network participants using a modification of the CLSI antibiogram (8), consisting of a synergy test with ceftazidime or cefepime and amoxicillin-clavulanic acid (distance between disks, 20 mm, center to center).FAV-1 and M5179 were the first putative ESBL-producing Acinetobacter baumannii strains isolated at two hospitals in Buenos Aires in 2000 and 2003, respectively. FAV-1 was a colonizer from the urine of a patient hospitalized for lung transplantation. M5179 was from the peritoneal fluid of a patient with hemolytic-uremic syndrome. Strains were confirmed to be A. baumannii by using the API 20NE system (bioMérieux, Marcy l'Etoile, France) combined with their ability to grow at 44°C.MICs (micrograms per milliliter) for FAV-1 and M5179 determined by agar dilution (10) were, respectively, as follows: ticarcillin, 1,024 and 1, 024; piperacillin, 512 and 256; piperacillin-tazobactam, 512 and 0.5; ampicillin-sulbactam, 8 and 8; cefotaxime, 64 and 64; cefotaxime-clavulanate, 64 and 8; ceftazidime, 64 and 512; ceftazidime-clavulanate, 16 and 2; cefepime, 64 and 64; cefepime-clavulanate, 16 and 4; aztreonam, 512 and 512; imipenem, 8 and 0.5; meropenem, 8 and 0.5; amikacin, 128 and 32; gentamicin, 2 and 32; trimethoprimsulfamethoxazole, 128 and 8; ciprofloxacin, 32 and 0.12; rifampin, 2 and Ͼ32; minocycline, 0.5 and Ͻ0.25. EDTA (0.4 mM) did not affect carbapenem MICs.Attempts to transfer the ceftazidime (FAV-1 and M5179) or imipenem (FAV-1) resistance marker by conjugation or electroporation to Escherichia coli ER1793 (6) were unsuccessful.Isoelectric focusing analysis (6) revealed ESBL bands at pIs of 5.4 (FAV-1) and 7.4 (M5179) and narrow-spectrum ␤-lactamase bands at pIs of 6.9, 9.4 (FAV-1), and 5.4 (M5179). A band at a pI of 9.4 was inhibited by oxacillin (1 mM) (probable

Genetic basis of antibiotic resistance in pathogenic Acinetobacter species

“…ISCR1 possesses a promoter sequence named P CR1-1 at its right extremity that is responsible for the expression of bla PER-7 (12). PER-2, which is distantly related to PER-1, has been found exclusively in South American isolates of A. baumannii, associated with a single copy of ISPa12 (13).…”

Phenotypic ESBL Detection in <i>Acinetobacter baumannii</i>: A Real Challenge

“…Cephalosporinases seems to be the predominant β-lactamases in A. baumannii isolates (Vila et al, 1993;Bergogne-Berezin and Towner, 1996). ESBLs in A. baumannii are widely reported from many countries, such as India, France, Turkey, Korea, Belgium and Latin America, the United Kingdom, and the United States (Poirel et al, 1999;Vahaboglu et al, 2001;Yong et al, 2003;Capoor et al, 2005;Naas et al, 2006;Pasteran et al, 2006;Litake et al, 2009;Joshi and Litake, 2013). Rapidly growing resistance among clinical isolates suggests a need to detect resistance mechanisms in this organism.…”

Susceptibility, phenotypes of resistance, and extended-spectrum β-lactamases in Acinetobacter baumannii strains

“…PER-1 producing Acinetobacter baumannii has been reported from France, Belgium, Romania, Russia and Hungary [10,19,[27][28][29]. Subsequent variants have been described in the PER family in various bacteria (also in A. baumannii), among which PER-2 is found to predominate in some South American countries [30,31]. Most strains of A. baumannii with the bla PER-1 gene, investigated in various countries, do not exhibit a consanguineous relationship to one another, something that is suggested by a clonal model of spread of this mechanism of resistance [9,11].…”