Outbreak In Norway Research Articles

Outbreak of methicillin-resistant Staphylococcus aureus in two nursing homes in Central Norway

Until recently, infections with methicillin-resistant Staphylococcus aureus (MRSA) have mainly been associated with hospital outbreaks in Norway. However, increasingly cases are contracted outside hospitals. This paper reports the first two outbreaks of MRSA in two nursing homes in central Norway, affecting 23 residents and five staff members. Pulsed-field gel electrophoresis analysis showed that all strains from nursing home A were identical and that the strains from nursing home B were genotypically similar with one or two band differences. Multi-locus sequence typing (MLST) showed that the strains from the two nursing homes belong to clonal complex 45, with each strain being a single-locus variant of sequence type 45 (ST 45), a well-known European epidemic strain. No evident source of the two outbreaks was found, and there was no obvious connection between the two outbreaks. The latter is also supported by the minor differences observed by MLST, suggesting a connection at some time in the past. The outbreaks led to a heavier workload and economic strain on both nursing homes. The outbreak in nursing home A was brought to an end, whereas two residents remained colonized in nursing home B despite several eradication attempts. These outbreaks show the potential for MRSA spread in a nursing home. If the prevalence of MRSA in Norway continues to increase, nursing home staff and residents may have to be included in the groups to be screened for MRSA upon hospital admission.

Pathology of heart and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon Salmo salar

This is the first description of heart and skeletal muscle inflammation (HSMI), a novel disease affecting farmed Atlantic salmon Salmo salar in Norway. HSMI was first diagnosed in 1999, and there has since been a yearly increase in the number of recorded outbreaks. Atlantic salmon are commonly affected 5 to 9 mo after transfer to sea, but outbreaks have been recorded as early as 14 d following seawater transfer. Affected fish are anorexic and display abnormal swimming behaviour. Autopsy findings typically include a pale heart, yellow liver, ascites, swollen spleen and petechiae in the perivisceral fat. While mortality is variable (up to 20%), morbidity may be very high in affected cages. Until more accurate tests are available, HSMI is diagnosed on the basis of histopathology. The major pathological changes occur in the myocardium and red skeletal muscle, where extensive inflammation and multifocal necrosis of myocytes are evident. HSMI is transmissible and, although most likely caused by a virus, the causal agent has not yet been isolated. This paper describes clinical signs and pathology of HSMI from 3 field outbreaks in Norway. Microscopic lesions are compared and discussed in relation to published descriptions of pancreas disease (PD) and cardiomyopathy syndrome (CMS). It is concluded that HSMI is histopathologically distinguishable from PD and CMS.

Molecular characterization of Sp serotype strains of infectious pancreatic necrosis virus exhibiting differences in virulence

Infectious pancreatic necrosis virus (IPNV), a prototype virus of the family Birnaviridae, exhibits a high degree of antigenic variability, pathogenicity and virulence in salmonid species. The Genomic Segment A encodes all the structural (VP2 and VP3) and nonstructural (NS) proteins, whereas Segment B encodes the viral RNA-dependent RNA polymerase (VP1). We tested 3 different IPNV isolates (Sp103, Sp116 and Sp122) isolated during field outbreaks in Norway for their ability to cause mortality in fry and post-smolt of Atlantic salmon Salmo salar L. The cumulative mortality following experimental challenge in fry was 29% for Sp122 followed by 19% for Sp116 and 15% for Sp103. In post-smolt, the corresponding mortality rates were 79, 46 and 16%, respectively. Comparisons of the deduced amino acid sequences of Segments A and B of all 3 Sp strains revealed substitutions of residues in 13 positions, of which 6 are in VP2, 2 in VP3, and 5 in VP1. Our results suggest that these residues, especially those in the outer capsid VP2, may be involved in the virulence of IPNV. Genome Segment A of the Sp serotype is 3097 nucleotides long and contains a major open reading frame (ORF) encoding a polyprotein of 972 amino acids, which initiates at the second in-frame start codon at Position 119. This was ascertained by making mutants of Segment A clone using site-directed mutagenesis, followed by in vitro transcription-coupled translation reaction and immunoprecipitation analyses. In addition, Segment A also encodes a 15 kDa arginine-rich non-structural protein from a small ORF, preceding and partially overlapping the polyprotein ORF, which is truncated to 12 kDa in the virulent Sp122 strain. Moreover, Segment A could encode a novel, putative 25 kDa protein from another ORF between VP2 and VP4 coding regions, which is only detected in the Sp serotype. Segment B is 2777 nucleotides long and encodes in a single large ORF (a polypeptide of 844 amino acid residues), VP1.

Relationship between El Niño /South Oscillation (ENSO) and population outbreaks of some lemmings and voles in Europe

Ecologists have been puzzled by population cycles of lemmings and voles for the over 70 years. At present, our understanding and explanation to this phenomenon remain controversial. Recently, El Nino/South Oscillation has attracted attention of ecologists on its links with population outbreaks of terrestrial animals. This paper aims to investigate the statistical relationship between outbreaks of microtine rodents and ENSO events by scanning available literature. During 1862–1894, outbreaks of Norway lemmings in Norway tended to occur in the Southern Oscillation Index (SOI) peak years or 1 year after the SOI peak years with an approximate significance level (p = 0.057). During 1885–1931, outbreaks of voles in France tended to occur 1 year before the SOI peak years (p = 0.01). During 1946–1993, outbreaks of lemmings and voles in North Finland tended to occur 1 year before the SOI peak years with a significant level (p = 0.022); the peaks of population abundance corresponded well to the SOI trough years (equal to 1 year before the SOI peak years). Outbreaks of common voles in Poland during 1946–1975 tended to occur in the SOI peak years or 1 year before the SOI peak years (p = 0.011), and also tended to occur 1 year before the SOI peak years (p = 0.030). It was also found that the rodent outbreaks in Norway and France, rodent outbreaks in Finland and Poland synchronized well. It was suggested that the ENSO-related climate or food were key factors in causing outbreaks of microtine rodents in Europe.

Characterisation of a non-haemolytic enterotoxin complex from Bacillus cereus isolated after a foodborne outbreak

Three enterotoxic components have been isolated from a strain of Bacillus cereus which was involved in a large food poisoning outbreak in Norway in 1995. The components were purified by chromatography on three different columns. Three proteins of 39, 45 and 105 kDa, respectively, were found to be necessary for maximum cytotoxicity. The amino acid N-terminal sequences of the 39 and 45 kDa proteins were determined. The 45 kDa component was the same protein as the main antigen detected in the Bacillus Diarrhoeal Enterotoxin Visual Immunoassay (Tecra). The 39 kDa protein showed some similarity to the l 1 protein of haemolysin BL from B. cereus. Furthermore, the three toxic components were all recognised by a polyclonal antiserum reported to detect enterotoxin from B. cereus. The proteins were different from the B- and L 2-components of haemolysin BL, previously suggested to be a primary virulence factor, and had no detectable haemolytic activity.

Characterisation of a non-haemolytic enterotoxin complex from Bacillus cereus isolated after a foodborne outbreak.

Three enterotoxic components have been isolated from a strain of Bacillus cereus which was involved in a large food poisoning outbreak in Norway in 1995. The components were purified by chromatography on three different columns. Three proteins of 39, 45 and 105 kDa, respectively, were found to be necessary for maximum cytotoxicity. The amino acid N-terminal sequences of the 39 and 45 kDa proteins were determined. The 45 kDa component was the same protein as the main antigen detected in the Bacillus Diarrhoeal Enterotoxin Visual Immunoassay (Tecra). The 39 kDa protein showed some similarity to the L1 protein of haemolysin BL from B. cereus. Furthermore, the three toxic components were all recognised by a polyclonal antiserum reported to detect enterotoxin from B. cereus. The proteins were different from the B- and L2-components of haemolysin BL, previously suggested to be a primary virulence factor, and had no detectable haemolytic activity.

DNA fingerprinting and serotyping of Campylobacter jejuni isolates from epidemic outbreaks.

The aim of the present investigation was to compare DNA fingerprinting and serotyping (heat-stabile and heat-labile antigens) of isolates from epidemic outbreaks as well as of solitary isolates. Campylobacter jejuni isolates from two epidemic outbreaks in Sweden, one milkborne (35 isolates) and one waterborne (17 isolates), and one waterborne outbreak in Norway (11 isolates), as well as 30 solitary isolates from Swedish patients with gastroenteritis, were analyzed. A total of 93 isolates were analyzed. In the waterborne outbreak in Norway, only one serotype with one DNA pattern was found. In the milkborne outbreak in Sweden, two serotypes (HS2:HL4 and HSNT:HL4) with two different DNA patterns were found. The isolates from the waterborne outbreak in Sweden were different serotypes. For two isolates of the same serotype, different DNA patterns were seen. This was also recorded for isolates from solitary cases. It was concluded that serotyping is a useful tool in most epidemiological situations but sometimes lacks sufficient discriminatory power. DNA fingerprinting can add valuable epidemiological information to that supplied by serotyping and can in some situations provide sufficient epidemiological information when used alone.

Spectrum of disease in bacteraemic patients during a Streptococcus pyogenes serotype M-1 epidemic in Norway in 1988.

All 87 known cases of bacteraemia due to Streptococcus pyogenes (beta-haemolytic group A streptococci) occurring during the peak of a nationwide outbreak in Norway (population 4.2 million) between January and June 1988 were reviewed. Clinical features varied widely and appeared largely to be dependent on the patients' age. The case fatality rate ranged from 11% in the age group under 30 years to 44% in patients over 60 years. Clinical complications such as shock, severe renal or respiratory failure or serious local infection occurred particularly in 30-to 59-year old individuals. Shock was manifest in 32% of the patients and carried a 68% case fatality rate. Chronic heart disease in the elderly and pneumonia seemed to be associated with a fatal outcome. In the 25 patients (29%) who died the disease showed a fulminant course, 80% dying within 48 hours after admission. However, 56% of the patients had experienced symptoms for more than two days before admission, suggesting that early diagnosis and treatment might possibly have prevented the development of a serious disease. This study revealed a wide spectrum of clinical manifestations in bacteraemia cases in a unique epidemiological situation caused largely by a single serotype of Streptococcus pyogenes; 89% of the 27 preserved bacteraemia strains carried the M-1 antigen. The observations call attention to the ability of these organisms to cause fulminant clinical illness, indicating a probable increase in both invasiveness and toxicity of group A streptococci responsible for the epidemic.

Serotyping and biotyping of Campylobacter jejuni and Campylobacter coli from sporadic cases and outbreaks in Norway.

Of 172 thermophilic campylobacters isolated from human cases of gastroenteritis in Norway, 149 (86.6%) were classified as Campylobacter jejuni, whereas 23 isolates (13.4%) belonged to Campylobacter coli. C. jejuni biotype 1 comprised 66.3% and C. jejuni biotype 2 comprised 20.3% of the total number. Using 50 unabsorbed antisera, we were able to serotype 109 (80.1%) of 136 campylobacters on the basis of heat-stable antigens identified by means of passive hemagglutination. The typable strains fell into 36 different serotypes. A large proportion of the strains were isolated from travellers returning from abroad, a state of affairs which may have influenced the serotype and biotype distribution. Two family outbreaks were found to be caused by a bio-serotype common to all diseased members of the particular families. A third family outbreak and an outbreak among employees at a poultry processing plant each involved two distinct strains.

Bacillus cereus Food Poisoning

<i>Bacillus cereus</i>is a recent addition to the growing list of organisms known to cause food-borne disease. In the 1950s, Hauge¹published the first description of a food-borne<i>B cereus</i>outbreak based on his investigation of several outbreaks in Norway. Illness in these outbreaks was characterized preponderantly by diarrhea, with an incubation period of from ten to 12 hours. In the early 1970s, a second clinical syndrome associated with<i>B cereus</i>was identified in which vomiting was the primary symptom and in which the incubation period ranged from one to six hours.²Unlike outbreaks of diarrheal<i>B cereus</i>food-borne disease, which have been associated with a variety of foods, rice has been implicated as the vehicle in almost all reported outbreaks of the emetic syndrome. These two different clinical syndromes seem to be associated with two different toxins produced by the bacteria: one toxin is heat labile—causes fluid

British Food Journal Volume 52 Issue 8 1950

In both Norway and Sweden the law governing food hygiene is similar to that in Britain. Powers are vested in local authorities by one general Act couched in wide terms, and by more detailed regulations or byelaws drawn up as required. The degree of severity with which local authorities interpret the regulations varies, and in both countries the functions of central government in relation to food hygiene are mainly advisory. Outbreaks of food poisoning are rare. The various salmonella infections and the cattle diseases liable to infect food are well known, and the supervision in slaughterhouses and on farms is such that the organisms, if present, are identified. Salmonella out‐breaks due to infected imported dried eggs have also been traced. Yet such knowledge and careful supervision is common to other countries where notified outbreaks of food poisoning are comparatively numerous. Whether the relative absence of notified outbreaks in Norway and Sweden is entirely due to a higher standard of food hygiene, or to the prevailing custom of preparing food immediately before or even during a meal, is not clear. It is noticeable that in restaurants some time elapses between ordering a meal and receiving it, and that the food is always freshly prepared. In neither country are food handlers examined medically, except those in the milk trade, who are said to be examined every year. Some doubt exists about the value of this examination and the extent to which it is enforced, though in Stockholm enforcement would not be difficult as over 90 per cent of the milk supplied to that city is handled by one combine, controlled by the farmers' co‐operatives. In both countries all milk supplied in towns must be pasteurised, though bovine tuberculosis has been almost eliminated. Owing to a shortage of glass, milk is still sold “ loose ”, but it is hoped to introduce compulsory bottling in the near future. As the result of requests for more detailed instructions from Medical Officers of Health of small towns and country districts new regulations governing the sale of food have recently been drawn up. Restaurants, hotels and food shops must be licensed by local authorities; they are not licensed until they have been inspected and approved. The local authority can revoke a licence, but the proprietor of the establishment concerned has the right of appeal to the courts.