A single Legionella pneumophila genotype in the freshwater system in a ship experiencing three separate outbreaks of legionellosis in 6 years.

BACKGROUND: Recurrent legionella outbreaks at one and the same location are common. We have identified a single Legionella pneumophila genotype associated with recurrent Legionella outbreaks over 6 years. METHODS: Field emergency surveys following Legionella outbreaks were performed on a vessel in 2008, 2009 and 2013. Water samples from both the distribution and technical parts of the potable water system were analyzed with respect to L. pneumophila [Real-Time PCR, cultivation, serotyping and genotyping (PFGE)] and free-living amoebae, (FLA). RESULTS: Legionella pneumophila serogroup 1 was present in the ship's potable water system during every outbreak. Genotyping of the 2008 survey material showed two separate PFGE genotypes while those in 2009 and 2013 demonstrated the presence of only one of the two genotypes. FLA with intracellular L. pneumophila of the same genotype were also detected. Analyses of the freshwater system on a ship following three separate Legionella outbreaks, for L. pneumophila and FLAs, revealed a single L. pneumophila genotype and FLA (Hartmanella). CONCLUSIONS: It is reasonable to assume that the L. pneumophila genotype detected in the freshwater system was the causal agent in the outbreaks onboard. Persistence of an apparently low-pathogenic L. pneumophila genotype and FLA in a potable water system represent a potential risk for recurrent outbreaks.

Legionella pneumophila in Norwegian naval vessels.

BACKGROUND: Little is known about the occurrence of Legionella pneumophila in water supply systems on board ships. Our aim was to study the occurrence of L. pneumophila in the water supply system on board Norwegian naval vessels as the basis for framing preventive strategies against Legionella infection. MATERIAL AND METHOD: Water samples were collected from technical installations and from the water distribution network on board 41 vessels and from ten water filling (bunkering) stations, the sampling taking place in two rounds separated by a one-year interval. The samples were subjected to analysis, including serotyping and genotyping, with a view to identifying the presence of L. pneumophila and of free-living amoebae. RESULTS: L. pneumophila was found in 20 out of a total of 41 vessels in the first round of sampling, and live L. pneumophila serogroup 1 was isolated in seven of the 20 vessels. Free-living amoebae were found in the water supply system in most of the vessels, including all the vessels with L. pneumophila. The same genotype of L. pneumophila was identified in the water in bunkering stations and in the water on board the vessels. INTERPRETATION: L. pneumophila was not present in all the vessels, but all the vessels where the bacterium was found were also contaminated with free-living amoebae. We have demonstrated the probability of the fresh water from bunkering stations being the source of the contamination. In framing preventive strategies, importance should therefore be attached to identifying the source of contamination and the presence of free-living amoebae, as a premise for the establishment and growth of L. pneumophila in onboard water supply systems.

Concentration of circulating autoantibodies against HSP 60 is lowered through diving when compared to non-diving rats.

OBJECTIVE: Skin and ear infections, primarily caused by Pseudomonas aeruginosa (P. aeruginosa), are recurrent problems for saturation divers, whereas infections caused by P. aeruginosa are seldom observed in healthy people outside saturation chambers. Cystic fibrosis (CF) patients suffer from pulmonary infections by P. aeruginosa, and it has been demonstrated that CF patients have high levels of autoantibodies against Heat shock protein 60 (HSP60) compared to controls, probably due to cross-reacting antibodies induced by P. aeruginosa. The present study investigated whether rats immunised with P. aeruginosa produced autoantibodies against their own HSP60 and whether diving influenced the level of circulating anti-HSP60 antibodies. METHODS: A total of 24 rats were randomly assigned to one of three groups ('immunised', 'dived' and 'immunised and dived'). The rats in group 1 and 3 were immunised with the bacteria P. aeruginosa, every other week. Groups 2 and 3 were exposed to simulated air dives to 400 kPa (4 ata) with 45 min bottom time, every week for 7 weeks. Immediately after surfacing, the rats were anaesthetised and blood was collected from the saphenous vein. The amount of anti-HSP60 rat antibodies in the serum was analysed by enzyme linked immunosorbent assay. RESULTS: The immunised rats (group 1) showed a significant increase in the level of autoantibodies against HSP60, whereas no autoantibodies were detected in the dived rats (group 2). The rats both immunised and dived (group 3) show no significant increase in circulating autoantibodies against HSP60. A possible explanation may be that HSP60 is expressed during diving and that cross-reacting antibodies are bound.

Relationships between indoor environments and nasal inflammation in nursing personnel.

In this study, the authors sought to address the relationships between measured indoor environmental factors and nasal patency (i.e., minimum cross-sectional area) and volume and markers of nasal inflammation in nasal lavage fluid. Clinical data were obtained for 115 females who worked at 36 geriatric nursing departments. The indoor climates in the nursing departments were characterized by high room temperatures (median = 23 degrees C), low relative air humidities (median = 24%), and high air exchange rates indicated by low carbon dioxide levels (median = 570 ppm). Evidence of microbial amplification was observed in the ventilation unit in 3 of the departments. Decreased nasal patency was observed relative to microbial amplification in the ventilation units (minimum cross-sectional area 1 = 0.80 cm2 vs. 0.64 cm2, p = .003, minimum cross-sectional area 2 = 0.80 cm2 vs. 0.67 cm2, p = .02) and in relation to elevated indoor temperature (volume 1 = 3.46 cm3 vs. 3.22 cm3, p = .03). The authors concluded that the indoor environment may have affected the nasal mucosa of nursing personnel, thus causing nasal mucosal swelling. The results support the view that fungal contamination of air-supply ducts may be a source of microbial pollution, which can affect the nasal mucosa.