Aetiology and risk factors of community-acquired pneumonia in hospitalized patients in Norway.

BACKGROUND AND AIMS: In Norway, data on the aetiology of community-acquired pneumonia (CAP) in hospitalized patients are limited. The aims of this study were to investigate the bacterial aetiology of CAP in hospitalized patients in Norway, risk factors for CAP and possible differences in risk factors between patients with Legionnaire's disease and pneumonia because of other causes. METHODS: Adult patients with radiologically confirmed CAP admitted to hospital were eligible for the study. Routine aerobic and Legionella culture of sputum, blood culture, urinary antigen test for Legionella pneumophila and Streptococcus pneumoniae, polymerase chain reaction detection of Chlamydophila pneumoniae, Mycoplasma pneumoniae and Bordetella pertussis from throat specimens, and serology for L. pneumophila serogroup 1-6 were performed. A questionnaire, which included demographic and clinical data, risk factors and treatment, was completed. RESULTS: We included 374 patients through a 20-month study period in 2007-2008. The aetiological agent was detected in 37% of cases. S. pneumoniae (20%) was the most prevalent agent, followed by Haemophilus influenzae (6%) and Legionella spp. (6%). Eight Legionella cases were diagnosed by urinary antigen test, of which four also had positive serology. In addition, 13 Legionella cases were diagnosed by serology. The degree of comorbidity was high. An increased risk of hospital-diagnosed Legionella pneumonia was found among patients with a diagnosis of chronic congestive heart failure. CONCLUSION: Our results indicate that S. pneumoniae is the most common bacterial cause of pneumonia in hospitalized patients, and the prevalence of Legionella pneumonia is probably higher in Norway than recognized previously.

Characterization of the extent of a large outbreak of Legionnaires' disease by serological assays.

BACKGROUND: In May 2005, a long-distance outbreak of Legionnaires' disease (LD) caused by Legionella pneumophila serogroup 1 occurred in south-east Norway. The initial outbreak investigation without serology identified 56 laboratory-confirmed LD cases of whom 10 died. However, 116 patients with community-acquired pneumonia might belong to the outbreak based on epidemiological investigations, but acute laboratory tests other than serology were negative or not performed. To assess the true extent of the outbreak, we evaluated two serological assays in order to reclassify the 116 patients with indeterminate case status. METHODS: Two polyvalent antibody tests, a serogroup 1-6 immunofluorescence assay (IFA) and a serogroup 1-7 enzyme-linked immunosorbent assay (ELISA) were used. They were evaluated with cases defined as culture- or urinary antigen positive LD patients (n=40) and non-cases defined as confirmed non-LD patients (n=39) and healthy control subjects (n=62). The 116 patients, who were negative in culture, polymerase chain reaction and/or urinary antigen tests, were analysed by the same serological assays. Antibodies to the outbreak strain were determined by immunoblotting. RESULTS: In the evaluation study, the sensitivity and specificity of a ≥4-fold IFA titre change was 38% and 100%, respectively, with corresponding values of 30% and 99% for seroconversion in ELISA. A single high positive IFA titre yielded sensitivity and specificity of 73% and 97%, respectively, with corresponding values of 68% and 96% for a single high immunoglobulin (Ig) G and/or IgM in ELISA. Based on this evaluation, the following serological testing identified 47 more LD cases, and the outbreak thus comprised 103 cases with a case fatality rate of 10%. About the same proportion (70%) of the urinary antigen positive and negative LD cases had antibodies to the serogroup-specific lipopolysaccharide of the outbreak strain. In addition to the 103 LD cases, Legionella infection could not be verified or excluded in 32 patients based on epidemiology and/or lack of microbiological sampling. CONCLUSIONS: The acute-phase tests (culture, polymerase chain reaction, and urinary antigen) identified less than 55% of the 103 patients in this outbreak. Serological testing thus remains an important supplement for diagnosis of LD and for determination of outbreak cases.

Resistance rates of metronidazole and other antibacterials in Helicobacter pylori from previously untreated patients in Norway.

The aim of the study was to describe the antimicrobial resistance rate of Helicobacter pylori isolated from previously untreated patients in Norway, including the application of two different methods for the determination of metronidazole susceptibility. Altogether 102 isolates obtained in 2008 and 2009 from previously untreated patients suspected of H. pylori related disease, were examined applying a standardized European study protocol. The activity of amoxicillin, tetracycline, clarithromycin, metronidazole, rifabutin and levofloxacin was recorded after an incubation period of 72-96 h in a microaerobic atmosphere. Strains resistant to metronidazole were re-examined for metronidazole resistance applying anaerobic conditions for the first 24 h. None of the isolates were resistant to amoxicillin or tetracycline, whereas 5, 9% were resistant to clarithromycin and 22, 5% resistant to metronidazole tested conventionally. Applying local standards the metronidazole resistance rate fell to 7, 8%, highlighting the importance of the methodology applied for metronidazole susceptibility testing.

Emergence of OXA-carbapenemase- and 16S rRNA methylase-producing international clones of Acinetobacter baumannii in Norway.

This study was designed to investigate the molecular epidemiology and antibiotic-resistance characteristics of 11 carbapenem-resistant clinical isolates of Acinetobacter baumannii obtained in Norway between 2004 and 2009. Interestingly, all the isolates were linked with recent hospitalization outside Norway. The epidemiological status was investigated by multilocus sequence typing (MLST), multiplex PCR assays for major international clones, typing of blaOXA-51-like variants and PFGE. The genotypic-resistance characteristics, including the occurrence of OXA-carbapenemase-encoding and 16S rRNA methylase-encoding genes and class 1 integrons, were investigated by PCR assays and sequencing. Seven isolates were found to harbour blaOXA-66 and belong to MLST clonal complexes (CCs) CC2P (Pasteur Institute scheme) and CC92B (Bartual scheme), and international clone II. One isolate harboured blaOXA-69, and belonged to CC1P, CC109B and international clone I. Two isolates belonged to sequence group 9, probably a subgroup of international clone I, and one isolate belonged to sequence group 4, a proposed novel international clone. All isolates contained an acquired OXA-carbapenemase-encoding gene: blaOXA-23-like (n=9), blaOXA-24-like (n=1) and blaOXA-58-like (n=1). Four isolates with high-level aminoglycoside-resistance contained the 16S rRNA methylase-encoding armA gene. Class 1 integrons with six different variable regions were detected. Sequence analysis of gene cassettes identified four aminoglycoside (aacA4, aac(6')-Im, aadA1 and aacC1), two chloramphenicol (catB8 and cm1A5), one ß-lactamase (blaOXA-20) and one rifampicin (arr-2) resistance gene in various combinations. In conclusion, the occurrence of A. baumannii isolates producing OXA carbapenemase and 16S rRNA methylase in Norway was related to the worldwide distribution of international clones I and II, and the emergence of novel international clones.

An outbreak of legionnaires disease caused by long-distance spread from an industrial air scrubber in Sarpsborg, Norway.

BACKGROUND: On 21 May 2005, the Norwegian health authorities were alerted by officials from a local hospital that several recent patients had received the diagnosis of legionnaires disease; all patients resided in 2 neighboring municipalities. We investigated the outbreak to identify the source and to implement control measures. METHODS: We interviewed all surviving case patients and investigated and harvested samples from 23 businesses with cooling towers and other potential infection sources. The locations of the businesses and the patients' residences and movements were mapped. We calculated attack rates and risk ratios among people living within various radii of each potential source. Isolates of Legionella pneumophila were compared using molecular methods. RESULTS: Among 56 case patients, 10 died. The case patients became ill 12-25 May, resided up to 20 km apart, and had not visited places in common. Those living up to 1 km from a particular air scrubber had the highest risk ratio, and only for this source did the risk ratio decrease as the radius widened. Genetically identical L. pneumophila serogroup 1 isolates were recovered from patients and the air scrubber. The air scrubber is an industrial pollution-control device that cleans air for dust particles by spraying with water. The circulating water had a high organic content, pH of 8-9, and temperature of 40 degrees C. The air was expelled at 20 m/s and contained a high amount of aerosolized water. CONCLUSIONS: The high velocity, large drift, and high humidity in the air scrubber may have contributed to the wide spread of Legionella species, probably for >10 km. The risk of Legionella spread from air scrubbers should be assessed.