Prevalence of carbapenemase-encoding genes including New Delhi metallo-ß-lactamase in Acinetobacter species, Algeria.

BACKGROUND: Nosocomial infections caused by carbapenem-resistant Acinetobacter spp are a global health problem. The aim of this study was to investigate the molecular epidemiology and the genetic support of carbapenem resistance in Acinetobacter spp clinical isolates recovered from three different hospitals in western Algeria from 2008 to 2012. METHODS: A total of 113 Acinetobacter spp isolates were identified by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry. Antimicrobial susceptibility testing was carried out, and minimum inhibitory concentrations (MICs) were determined by the dilution method on Mueller-Hinton agar for ß-lactams, aminoglycosides, fluoroquinolones, and colistin. The characterization of ß-lactamases was investigated by phenotypic tests for the detection of metallo-ß-lactamases and oxacillinases. Resistance genes were screened for by quantitative PCR and sequenced when positive. RESULTS: Among the 113 isolates, 80 (70.8%) were found to be resistant to imipenem with MICs ranging from 64 to 512µg/ml. The blaOXA-23-like gene was detected in 50% (40/80) of the isolates and the blaOXA-24-like gene was detected in 21.2% (17/80) of the isolates. In addition, the metallo-ß-lactamase blaNDM-1-like was detected in five isolates (6.2%). CONCLUSIONS: This study represents the first description of autochthonous Acinetobacter spp producing metallo-ß-lactamase blaNDM-1-like and oxacillinases blaOXA-23-like and blaOXA-24-like in western Algeria.

Plague outbreak in Libya, 2009, unrelated to plague in Algeria.

After 25 years of no cases of plague, this disease recurred near Tobruk, Libya, in 2009. An epidemiologic investigation identified 5 confirmed cases. We determined ribotypes, Not1 restriction profiles, and IS100 and IS1541 hybridization patterns of strains isolated during this outbreak. We also analyzed strains isolated during the 2003 plague epidemic in Algeria to determine whether there were epidemiologic links between the 2 events. Our results demonstrate unambiguously that neighboring but independent plague foci coexist in Algeria and Libya. They also indicate that these outbreaks were most likely caused by reactivation of organisms in local or regional foci believed to be dormant (Libya) or extinct (Algeria) for decades, rather than by recent importation of Yersinia pestis from distant foci. Environmental factors favorable for plague reemergence might exist in this area and lead to reactivation of organisms in other ancient foci.