We describe a case of proven donor transmission of carbapenem-resistant Acinetobacter baumannii, which resulted in severe infectious complications after lung transplantation. A single blaOXA-23 positive strain, belonging to a new multilocus sequence type (ST231), was isolated from donor and recipient, who died 65 days after transplantation. This report highlights the current challenges associated with the potential transmission of multidrug-resistant infections through organ transplantation.

Carbapenem-resistance mechanisms are a challenge in the treatment of Pseudomonas aeruginosa infections. We investigated changes in P. aeruginosa carbapenem-resistance determinants over a time period of eight years after the emergence of São Paulo metallo-β-lactamase in a university hospital in Rio de Janeiro, Brazil. Patients admitted to the intensive care unit (ICU) were screened for P. aeruginosa colonisation and followed for the occurrence of infections from April 2007 to April 2008. The ICU environment was also sampled. Isolates were typed using random amplified polymorphic DNA, pulsed-field gel electrophoresis and multilocus sequence typing. Antimicrobial susceptibility was determined by disk diffusion and E-test, production of carbapenemases by a modified-CarbaNP test and presence of carbapenemase-encoding genes by polymerase chain reaction. Non-carbapenemase resistance mechanisms studied included efflux and AmpC overexpression by PAβN and cloxacillin susceptibility enhancement, respectively, as well as oprD mutations. From 472 P. aeruginosa clinical isolates (93 patients) and 17 isolates from the ICU environment, high genotypic diversity and several international clones were observed; one environment isolate belonged to the blaSPM-1 P. aeruginosa epidemic genotype. Among isolates from infections, 10 (29%) were carbapenem resistant: none produced carbapenemases, three exhibited all non-carbapenemase mechanisms studied, six presented a combination of two mechanisms, and one exclusively displayed oprD mutations. Carbapenem-resistant P. aeruginosa displayed a polyclonal profile after the SPM-1 epidemic genotype declined. This phenomenon is connected with blaSPM-1 P. aeruginosa replaced by other carbapenem-resistant pathogens.

Fever and a petechial rash are strongly associated with meningococcal disease in the city of Rio de Janeiro. Early antibiotic therapy is indicated and, consequently, a reduction of confirmed cases by culture, Gram stain, and latex agglutination test is expected. We evaluated a multiplex PCR assay to identify Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenzae in biological samples from cases of non-culture proven meningitis with a petechial rash at presentation. To detect DNA in cerebrospinal fluid (n = 71) or blood (n = 5), a PCR screen was performed, based on the crgA, ply and bexA targets, respectively. Of the total, 70 CSF and 3 blood samples (96%) were positive by PCR for the presence of N. meningitidis DNA. Another PCR assay predicted in 82% of these samples N. meningitidis serogroups A (2%), B (60%), C (7%), X (3%), Y (2%), 29E (2%) or W135 (24%). In non-culture proven meningitis, PCR was found to be a valuable adjunct for the demonstration of meningococcal aetiology.

The main objective of this study was to assess the frequency and possible sources of colonization and infection by Acinetobacter in the intensive care unit (ICU) of a university hospital in Rio de Janeiro, Brazil, and characterize the isolates for relatedness to internationally and locally disseminated lineages. Patients consecutively admitted to the ICU from April 2007 to April 2008 were screened for colonization and infection. Species were identified by rpoB sequencing. The presence of acquired and intrinsic carbapenemase genes was assessed by polymerase chain reaction (PCR). Strains were typed by random amplification of polymorphic DNA (RAPD)-PCR, pulsed-field gel electrophoresis, and multilocus sequence typing (MLST) using the schemes hosted at the University of Oxford (UO) and Institut Pasteur (IP). Of 234 patients, 98 (42%) had at least one specimen positive for the Acinetobacter isolate, and 24 (10%) had infection. A total of 22 (92%) infections were caused by Acinetobacter baumannii and one each (4%) by Acinetobacter nosocomialis and Acinetobacter berezinae. A. baumannii isolates from 60 patients belonged to RAPD types that corresponded to MLST clonal complexes (CCs) 109/1 (UO/IP scheme, known as International Clone I), CC 110/110 (UO/IP), CC 113/79 (UO/IP), and CC 104/15 (UO/IP). Most CCs were carbapenem resistant and carried the bla(OXA-23)-like gene. Strains were introduced by patients transferred from other wards of the same hospital (11 patients, 18%) or acquired from cross-transmission within the ICU (49 patients, 82%). A. nosocomialis lineage sequence type 260 colonized 10% of the whole study population. A. baumannii have become established in this hospital as a part of a global epidemic of successful clones. Once introduced into the hospital, such clones have become entrenched among patients in the ICU.

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