Spread of a carbapenem- and colistin-resistant Acinetobacter baumannii ST2 clonal strain causing outbreaks in two Sicilian hospitals.

BACKGROUND: Infections caused by multidrug-resistant (MDR) Acinetobacter baumannii have become an important healthcare-associated problem, particularly in intensive care units (ICUs). AIM: To investigate the emergence of carbapenem- and colistin-resistant A. baumannii infections in two Sicilian hospitals. METHODS: From October 2008 to May 2011, a period which included two Italian Nosocomial Infections Surveillance in ICUs network (SPIN-UTI) project surveys, all carbapenem-resistant A. baumannii isolates from the ICUs of two hospitals in Catania, Italy, were prospectively collected. Minimum inhibitory concentrations (MICs) were measured by agar dilution, and phenotypic testing for metallo-ß-lactamase (MBL) production was performed. Carbapenem resistance genes and their genetic elements were identified by polymerase chain reaction and sequencing. Genotypic relatedness was assessed by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing. Patient-based surveillance was conducted using the SPIN-UTI protocol and previous antibiotic consumption was recorded. FINDINGS: Twenty-six carbapenem-resistant A. baumannii were identified. Imipenem and meropenem MICs ranged from 4 to >32 mg/L, and 15 isolates exhibited high-level colistin resistance (MICs >32 mg/L). PFGE demonstrated that all isolates belonged to a unique clonal type and were assigned to ST2 of the international clone II. They harboured an intrinsic blaOxA-51-like carbapenemase gene, blaOxA-82, which was flanked upstream by ISAba1. CONCLUSIONS: The dissemination of clonally related isolates of carbapenem-resistant A. baumannii in two hospitals is described. Simultaneous resistance to colistin in more than half of the isolates is a problem for effective antibiotic treatment. Prior carbapenem and colistin consumption may have acted as triggering factors.

Clusters of imipenem-resistant Acinetobacter baumannii clones producing different carbapenemases in an intensive care unit.

During a 2-year period (April 2005-March 2007), 31 intensive care unit (ICU) patients in a Greek hospital were infected or colonised with imipenem-resistant isolates of Acinetobacter baumannii. Twelve patients died, with imipenem-resistant A. baumannii infection contributing to the death of seven patients. The 31 representative A. baumannii isolates were multidrug-resistant and clustered in four distinct clones, each of which contained different carbapenemase genes: clone I was predominant and contained bla(VIM-1), bla(OXA-58) and the intrinsic bla(OXA-66) gene; clone II contained bla(VIM-4), bla(OXA-58) and the intrinsic bla(OXA-69) gene; clone III contained bla(OXA-58) and the intrinsic bla(OXA-69) gene; and clone IV contained only the intrinsic bla(OXA-66) gene. ISAba1 was not associated with the intrinsic bla(OXA-51-like) alleles, whereas ISAba3 was found upstream and downstream of bla(OXA-58) in isolates of clone I, and upstream of bla(OXA-58) in isolates of clone III, but was not detected in isolates of clone II. PCR, curing and hybridisation experiments indicated that the bla(VIM) alleles were chromosomally located, whereas the bla(OXA-58) alleles were plasmid-located. This study provides the first description of the clonal spread of multidrug-resistant A. baumannii isolates carrying bla(VIM-1) and bla(VIM-4) metallo-beta-lactamase genes, and revealed that distinct carbapenem-resistant A. baumannii clusters bearing different carbapenemase genes may emerge and cause severe infections, even in a well-defined regional hospital setting.

Fatal massive hemolysis as the first manifestation of Clostridium perfringens septicemia in a patient with non-systematic or local predisposing disorder.

We report a case of fulminant massive hemolysis due to Clostridium perfringens septicemia in an elderly patient with non-systematic or local predisposing disorder. The patient presented with atypical symptoms but the progress of the disease was extremely rapid and he died almost 3h after his hospital admission. A focal infection or a possible portal of bacterial access was not found.