Bjørn G. Iversen

An Outbreak of Pseudomonas aeruginosa Infection Caused by Contaminated Mouth Swabs

BACKGROUND Pseudomonas aeruginosa is an opportunistic bacterium that can cause severe infection in susceptible patients. During the winter of 2001-2002, we investigated an outbreak of P. aeruginosa infection among patients in several hospitals across Norway. METHODS A nationwide outbreak investigation was performed with case finding, questionnaires, and product sampling. All available clinical and environmental P. aeruginosa strains were genotyped. Detailed information was collected from patients with the outbreak strain or with any P. aeruginosa in blood or cerebrospinal fluid samples. To identify risk factors, we conducted a case-control study among patients with P. aeruginosa isolated from blood or cerebrospinal fluid samples during October 2001-December 2002. Case patients were patients infected with the outbreak genotype, and control subjects were patients infected with other genotypes. RESULTS A total of 231 patients from 24 hospitals were identified as having the outbreak strain; 39 of these patients had positive blood culture results. Seventy-one patients (31%) died while hospitalized; all of the patients who died had severe underlying disease. Among 39 case patients and 159 control subjects, use of the moist mouth swab (adjusted odds ratio, 5.3; 95% confidence interval, 2.0-13.6) and receipt of mechanical ventilation (adjusted odds ratio, 6.4; 95% confidence interval, 2.3-17.2) were associated with infection due to the outbreak strain. Genotypically identical strains of P. aeruginosa were identified in 76 mouth swabs from 12 different batches and from the production line. CONCLUSIONS Contamination of mouth swabs during production caused the largest-ever outbreak of P. aeruginosa infection in Norway. Susceptible patient groups should use only documented quality-controlled, high-level-disinfected products and items in the oropharynx.

Meticillin-resistant Staphylococcus aureus in Norway, a low-incidence country, 2006-2010.

BACKGROUND Antibiotic resistance is a global public health threat. Norway has managed to keep the incidence of resistant bacteria at a low level in both the healthcare system and the community. Reporting of both individual cases and meticillin-resistant Staphylococcus aureus (MRSA) outbreaks is mandatory. All isolates are genotyped. AIM To describe the epidemiology of MRSA in Norway and to analyse how MRSA is spreading in a low-incidence country. METHODS All cases of laboratory-confirmed MRSA colonisation and infection reported in Norway from 2006 to 2010 were subject to epidemiological analysis. FINDINGS A total of 3620 cases of MRSA were found. Around one-third of the cases were imported, one-third acquired in the Norwegian healthcare system and one-third acquired in the community. Twelve percent of the cases were linked to known outbreaks. The total incidence of infected and colonized patients is slowly increasing. The numbers of severe infections remain stable at around 20 cases annually and the proportion of MRSA cases associated with healthcare has decreased. CONCLUSION MRSA is still rare in the Norwegian population and the strategic objective of preventing MRSA from becoming a permanent part of the bacterial flora in hospitals and nursing homes has so far been met.

Meningococcal disease in Norway 1992-1995. Epidemiology and fatality.

We analysed data on all cases of meningococcal disease (MCD) reported to the Norwegian Notification System for Infectious Diseases during the period 1992-1995. For 1994, additional information on fatalities was gathered. Notifications were received from laboratories and clinicians. A total of 586 patients were included. The incidence decreased from 4.6 per 100000 in 1992 to 2.4 in 1994, and then rose to 3.7 in 1995. The initial decrease, a trend also observed in previous years, was seen in both main serogroups B and C. This decline was broken with the increase of serogroup B in 1995. MCD predominantly affects children below 5 years and teenagers. In 1994, 17/105 (16%) patients died. Main risk factors for fatal outcome were age above 30 years (adjusted odds ratio (OR) 19.8; 95% confidence interval (CI) 2.4-164), septicaemia (adjusted OR 9.5; 95% CI 2.2-41) and disease caused by strains B:15 (adjusted OR 6.4; 95% CI 1.2-35) or C:2a (adjusted OR 10.1; 95% CI 1.6-62). We conclude that the incidence of MCD in Norway is unpredictable and that the case fatality rate is substantially higher than previously believed.

Effect of Vaccines and Antivirals during the Major 2009 A(H1N1) Pandemic Wave in Norway – And the Influence of Vaccination Timing

To evaluate the impact of mass vaccination with adjuvanted vaccines (eventually 40% population coverage) and antivirals during the 2009 influenza pandemic in Norway, we fitted an age-structured SEIR model using data on vaccinations and sales of antivirals in 2009/10 in Norway to Norwegian ILI surveillance data from 5 October 2009 to 4 January 2010. We estimate a clinical attack rate of approximately 30% (28.7–29.8%), with highest disease rates among children 0–14 years (43–44%). Vaccination started in week 43 and came too late to have a strong influence on the pandemic in Norway. Our results indicate that the countermeasures prevented approximately 11–12% of potential cases relative to an unmitigated pandemic. Vaccination was found responsible for roughly 3 in 4 of the avoided infections. An estimated 50% reduction in the clinical attack rate would have resulted from vaccination alone, had the campaign started 6 weeks earlier. Had vaccination been prioritized for children first, the intervention should have commenced approximately 5 weeks earlier in order to achieve the same 50% reduction. In comparison, we estimate that a non-adjuvanted vaccination program should have started 8 weeks earlier to lower the clinical attack rate by 50%. In conclusion, vaccination timing was a critical factor in relation to the spread of the 2009 A(H1N1) influenza. Our results also corroborate the central role of children for the transmission of A(H1N1) pandemic influenza.

Pseudomonas aeruginosa contamination of mouth swabs during production causing a major outbreak

BackgroundIn 2002 we investigated an outbreak comprising 231 patients in Norway, caused by Pseudomonas aeruginosa and linked to the use of contaminated mouth swabs called Dent-O-Sept. Here we describe the extent of contamination of the swabs, and identify critical points in the production process that made the contamination possible, in order to prevent future outbreaks.MethodsEnvironmental investigation with microbiological examination of production, ingredients and product, molecular typing of bacteria and a system audit of production.ResultsOf the 1565 swabs examined from 149 different production batches the outbreak strain of P. aeruginosa was detected in 76 swabs from 12 batches produced in 2001 and 2002. In total more than 250 swabs were contaminated with one or more microbial species. P. aeruginosa was detected from different spots along the production line. The audit revealed serious breeches of production regulations. Health care institutions reported non-proper use of the swabs and weaknesses in their purchasing systems.ConclusionBiofilm formation in the wet part of the production is the most plausible explanation for the continuous contamination of the swabs with P. aeruginosa over a period of at least 30 weeks. When not abiding to production regulations fatal consequences for the users may ensue. For the most vulnerable patient groups only documented quality-controlled, high-level disinfected products and items should be used in the oropharynx.

Nationwide study of invasive Pseudomonas aeruginosa infection in Norway: Importance of underlying disease

OBJECTIVE Pseudomonas aeruginosa is an opportunistic pathogen that may cause invasive disease. We describe the epidemiology of invasive P. aeruginosa infection in Norway and identify associated clinical factors. METHODS All patients with invasive P. aeruginosa and Pseudomonas not identified at the species level (Pseudomonas spp.) in Norway 1992-2002 were included. Detailed information was collected for all cases during 1999-2002. Population and health institution statistics were obtained from national databases. RESULTS In 1999-2002 the incidence rate was 3.16 per 100 000 person-years at risk or 0.20 per 1000 hospital stays. For hospital-acquired infection the rate was 671 per 100 000 person-years as compared with 1.13 for community-acquired infection, and 37 in nursing homes. The highest risk for invasive Pseudomonas disease was found in patients with malignant neoplasms of lymphoid and haematopoietic tissue (risk per 1000 hospital stays 1.9; 95% CI 1.5-2.3) and other diseases of blood and blood-forming organs (2.2; 95% CI 1.2-3.7). The case fatality rate was 35%. CONCLUSIONS The incidence of invasive P. aeruginosa infection in this population-based study was much lower than in most single-hospital studies. The nationwide study design and prudent antibiotic use may explain some of the difference. Infection risk is strongly associated with certain underlying diseases.

Disease caused by the new influenza A(H1N1) virus

BACKGROUND A new A(H1N1) influenza virus was detected in April 2009. The virus is now causing a pandemic of influenza. The article presents an overview of symptoms, complications, vulnerable groups, diagnosis and treatment. MATERIAL AND METHODS The overview is based on literature identified through a search in PubMed (using PubMeds own search strategy) and on official reports from WHO and the disease control centres of EU and the USA. RESULTS The new influenza A(H1N1) has so far mainly affected young people, only few people over 60 years. The clinical presentation is similar to that of ordinary influenza; but nausea, vomiting and diarrhoea seem to be more common. The reported risk of complications and case fatality are low, but hospitalisation, pneumonia and deaths have occurred, also in previously healthy young individuals. Antiviral treatment with oseltamivir or zanamivir is likely to be as effective as in ordinary influenza. INTERPRETATION Mild cases may be underrepresented in the published literature. It is important to keep up-to-date on international reports on the nature of the disease in order to best prepare clinicians to diagnose and treat patients when the epidemic hits Norway with full force.

Evaluation of the national surveillance system for point-prevalence of healthcare-associated infections in hospitals and in long-term care facilities for elderly in Norway, 2002-2008

BackgroundSince 2002, the Norwegian Institute of Public Health has invited all hospitals and long-term care facilities for elderly (LTCFs) to participate in two annual point-prevalence surveys covering the most frequent types of healthcare-associated infections (HAIs). In a comprehensive evaluation we assessed how well the system operates to meet its objectives.MethodsSurveillance protocols and the national database were reviewed. Data managers at national level, infection control practitioners and ward personnel in hospitals as well as contact persons in LTCFs involved in prevalence data collection were surveyed.ResultsThe evaluation showed that the system was structurally simple, flexible and accepted by the key partners. On average 87% of hospitals and 32% of LTCFs participated in 2004-2008; high level of data completeness was achieved. The data collected described trends in the prevalence of reportable HAIs in Norway and informed policy makers. Local results were used in hospitals to implement targeted infection control measures and to argue for more resources to a greater extent than in LTCFs. Both the use of simplified Centers for Disease Control and Prevention (CDC) definitions and validity of data seemed problematic as compliance with the standard methodology were reportedly low.ConclusionsThe surveillance system provides important information on selected HAIs in Norway. The system is overall functional and well-established in hospitals, however, requires active promotion in LTCFs. Validity of data needs to be controlled in the participating institutions before reporting to the national level.

Evaluation of the national campaign to improve hand hygiene in nursing homes in Norway.

1. World Health Organization. WHO guidelines on hand hygiene in health care. Geneva: WHO; 2009. 2. Magiorakos AP, Leens E, Drouvot V, et al. Pathways to clean hands: highlights of successful hand hygiene implementation strategies in Europe. Euro Surveill 2010; 15. pii1⁄419560. 3. Muller MP, Detsky AS. Public reporting of hospital hand hygiene compliance – helpful or harmful? JAMA 2010;304:1116–1117. 4. Pittet D, Hugonnet S, Harbarth S, et al. Effectiveness of a hospital-wide programme to improve compliance with hand hygiene. Lancet 2000;356:1307–1312. 5. Sax H, Allegranzi B, Uckay I, Larson E, Boyce J, Pittet D. My five moments for hand hygiene: a user-centred design approach to understand, train, monitor and report hand hygiene. J Hosp Infect 2007;67:9–21. 6. Sax H, Allegranzi B, Chraiti MN, Boyce J, Larson E, Pittet D. The World Health Organizationhandhygieneobservationmethod.Am J Infect Control2009;37:827–834. 7. Edmond MB, Goodell A, Zuelzer W, Sanogo K, Elam K, Bearman G. Successful use of alcohol sensor technology to monitor and report hand hygiene compliance. J Hosp Infect 2010;76:364–365. 8. Hugonnet S, Perneger TV, Pittet D. Alcohol-based handrub improves compliance with hand hygiene in intensive care units. Arch Intern Med 2002;162:1037–1043.

Contaminated mouth swabs caused a multi-hospital outbreak of Pseudomonas aeruginosa infection.

Pseudomonas aeruginosa is a gram-negative, obligate aerobic rod-shaped bacterium with minimal nutritional requirements. It is often found in moist environments and can cause infections in immunocompromised or otherwise- susceptible hosts (1, 2). Numerous outbreaks have been associated with faulty or unclean medical equipment or products (3-9) and with personnel and environmental reservoirs (10-16), as well as with cross-contamination within the hospital (13, 17, 18). (Published: 20 April 2010) Citation: Journal of Oral Microbiology 2010, 2 : 5123 - DOI: 10.3402/jom.v2i0.5123