Eurosurveillance - Volume 16, Issue 4, 27 January 2011

In an asylum seeker centre in Schleswig-Holstein, a resident was diagnosed with furuncle caused by a Panton-Valentine leukocidine (PVL)-positive community-acquired meticillin-resistant Staphylococcus aureus (CA-MRSA). As a result of active case finding, 232 of 427 persons (54% of all residents) were screened for MRSA and two further PVL-positive CA-MRSA cases were identified.

A cluster of three fatal cases of invasive meningococcal disease due to Neisseria meningitidis serogroup B in a town in Suffolk, United Kingdom, during December 2009 to January 2010 was reported to the local Health Protection Unit. This paper describes the investigation undertaken to identify any potential epidemiological links among the cases, to determine if this was an outbreak and to consider whether to implement community-wide interventions and control measures. Case epidemiological information in addition to serogroup and genosubtyping (porA gene sequencing) data of the infecting organism was gathered on all cases in this reported cluster. Genosubtyping was also retrospectively requested for all serogroup B cases confirmed in Suffolk during 2009. Extensive investigation failed to establish an epidemiological link among the cluster of fatal cases of serogroup B invasive meningococcal disease in Suffolk. By demonstrating a number of distinct strains, the genosubtyping of isolates proved to be useful in the public health management of this incident by serving to exclude a community outbreak and preventing unnecessary mass chemoprophylaxis.

From May 2009 to January 2010, the Virology Laboratory at the University Hospital of Bordeaux received more than 4,000 nasopharyngeal samples from the Aquitaine region (south-west France) for the diagnosis of pandemic influenza A(H1N1)2009. Eighty-three infected patients deteriorated and were admitted to intensive care units. Our study focused on 24 of these patients. Positivity for influenza A(H1N1)2009 was monitored by realtime PCR and duration of viral shedding was determined. The first available sample of each patient was analysed for bacterial, fungal and viral co-infection. We observed six bacterial (or bacterial/fungal) co-infections and one viral co-infection with respiratory syncytial virus. The samples were analysed for the presence of the neuraminidase H275Y (N1 numbering) mutation, which confers resistance to oseltamivir, by realtime PCR of the neuraminidase gene. No H275Y mutation was observed in any of the viral strains screened in this study. In parallel, a fragment of the haemagglutinin gene encoding amino acid residues 173 to 362 was sequenced to detect mutations that had been reported to increase the severity of the disease. Two patients were infected by strains bearing the D222G (H3 numbering) mutation. The viral shedding of A(H1N1)2009 in this study ranged from four to 28 days with a median of 11 days.