Staphylococcus aureus Exotoxins and Their Detection in the Dairy Industry and Mastitis.

Staphylococcus aureus constitutes a major food-borne pathogen, as well as one of the main causative agents of mastitis in dairy ruminants. This pathogen can produce a variety of extracellular toxins; these include the shock syndrome toxin 1 (TSST-1), exfoliative toxins, staphylococcal enterotoxins (SE), hemolysins, and leukocidins. S. aureus expresses many virulence proteins, involved in evading the host defenses, hence facilitating microbial colonization of the mammary glands of the animals. In addition, S. aureus exotoxins play a role in the development of both skin infections and mastitis. Indeed, if these toxins remain in dairy products for human consumption, they can cause staphylococcal food poisoning (SFP) outbreaks. As a result, there is a need for procedures to identify the presence of exotoxins in human food, and the methods used must be fast, sensitive, reliable, and accurate. It is also essential to determine the best medical therapy for human patients suffering from S. aureus infections, as well as establishing the relevant veterinary treatment for infected ruminants, to avoid economic losses in the dairy industry. This review summarizes the role of S. aureus toxins in the development of mastitis in ruminants, their negative effects in the food and dairy industries, and the different methods used for the identification of these toxins in food destined for human consumption.

Effects of Lactic Acid and Salt on Enterotoxin A Production and Growth of Staphylococcus aureus.

Food poisoning caused by Staphylococcus aureus is responsible for staphylococcal enterotoxin (SE) produced in foods. Staphylococcal food poisoning is mostly caused by staphylococcal enterotoxin type A (SEA) among SEs. Growth/no growth for S. aureus under various environmental conditions was well studied with a logistic regression model so far. Recently we successfully described the boundaries of SEA production and growth of S. aureus in broth at various temperatures and salt concentrations with the model. In this study, the effects of lactic acid and salt on SEA production and growth of S. aureus was quantitatively studied. Consequently the boundaries of SEA production and growth of S. aureus cocktail in broth at various combinations of salt concentrations and pH values that were adjusted with lactic acid were successfully described with a logistic regression model. Here the cocktail was incubated in stationary culture at 30 °C and 10 °C. The maximum toxin production and cell growth of the cocktail were observed both at 5% salt in the pH range from 4.5 to 7.0. Also, the characteristics of individual strains of the cocktail in SEA production and growth at 30 °C and 10 °C were found to be specific to the strains. The present study revealed the effect of lactic acid and salt on SEA production and growth of S. aureus as well as the variety of SEA production and growth of S. aureus strains. These results would become useful information in food industry to prevent staphylococcal food poisoning. PRACTICAL APPLICATION: Boundaries of enterotoxin A production/no production and growth/no growth of staphylococcal cocktail at various combinations of pHs adjusted with lactic acid and salt concentrations were well described with a logistic regression model. The maximum toxin production and cell growth were observed both at 5% salt in the pH range from 4.5 to 7.0. A variety of the toxin production and cell growth were observed in terms of pH and salt concentration among individual strains of the cocktail.

Histamine release from intestinal mast cells induced by staphylococcal enterotoxin A (SEA) evokes vomiting reflex in common marmoset.

Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus are known as causative agents of emetic food poisoning. We previously demonstrated that SEA binds with submucosal mast cells and evokes mast cell degranulation in a small emetic house musk shrew model. Notably, primates have been recognized as the standard model for emetic assays and analysis of SE emetic activity. However, the mechanism involved in SEA-induced vomiting in primates has not yet been elucidated. In the present study, we established common marmosets as an emetic animal model. Common marmosets were administered classical SEs, including SEA, SEB and SEC, and exhibited multiple vomiting responses. However, a non-emetic staphylococcal superantigen, toxic shock syndrome toxin-1, did not induce emesis in these monkeys. These results indicated that the common marmoset is a useful animal model for assessing the emesis-inducing activity of SEs. Furthermore, histological analysis uncovered that SEA bound with submucosal mast cells and induced mast cell degranulation. Additionally, ex vivo and in vivo pharmacological results showed that SEA-induced histamine release plays a critical role in the vomiting response in common marmosets. The present results suggested that 5-hydroxytryptamine also plays an important role in the transmission of emetic stimulation on the afferent vagus nerve or central nervous system. We conclude that SEA induces histamine release from submucosal mast cells in the gastrointestinal tract and that histamine contributes to the SEA-induced vomiting reflex via the serotonergic nerve and/or other vagus nerve.

Assessment of Enterotoxin Production and Cross-Contamination of Staphylococcus aureus between Food Processing Materials and Ready-To-Eat Cooked Fish Paste.

This study evaluated Staphylococcus aureus growth and subsequent staphylococcal enterotoxin A production in tryptone soy broth and on ready-to-eat cooked fish paste at 12 to 37 °C, as well as cross-contamination between stainless steel, polyethylene, and latex glove at room temperature. A model was developed using Barany and Roberts's growth model, which satisfactorily described the suitable growth of S. aureus with R(2)-adj from 0.94 to 0.99. Except at 12 °C, S. aureus cells in TSB presented a lag time lower (14.64 to 1.65 h), grew faster (0.08 to 0.31 log CFU/h) and produced SEA at lower cell density levels (5.65 to 6.44 log CFU/mL) compare to those inoculated on cooked fish paste with data of 16.920 to 1.985 h, 0.02 to 0.23 log CFU/h, and 6.19 to 7.11 log CFU/g, respectively. Staphylococcal enterotoxin type A (SEA) visual immunoassay test showed that primary SEA detection varied considerably among different storage temperature degrees and media. For example, it occurred only during exponential phase at 30 and 37 °C in TSB, but in cooked fish paste it took place at late exponential phase of S. aureus growth at 20 and 25 °C. The SEA detection test was negative on presence of S. aureus on cooked fish paste stored at 12 and 15 °C, although cell density reached level of 6.12 log CFU/g at 15 °C. Cross-contamination expressed as transfer rate of S. aureus from polyethylene surface to cooked fish paste surface was slower than that observed with steel surface to cooked fish paste under same conditions. These results provide helpful information for controlling S. aureus growth, SEA production and cross-contamination during processing of cooked fish paste.

[Intoxications caused by Staphylococcal enterotoxin B]. / Zatrucia gronkowcowa enterotoksyna B.

Staphylococcal enterotoxin B (SEB) is one of exotoxins produced by Staphylococcus aureus. Depending on the type exposure SEB may cause a food or inhalant poisoning. The course of food poisoning is usually lighter and resolves spontaneously. The course of inhalant poisoning depends on the inhaled dose. It can be tough and demanding intensive treatment. Given the lack of specific therapy, led therapy is purely symptomatic.

Investigating an outbreak of staphylococcal food poisoning among travellers across two Australian states.

INTRODUCTION: Staphylococcus aureus is a common cause of staphylococcal food poisoning in Australia with several outbreaks associated with foods prepared by commercial caterers. Laboratory testing on cases of gastrointestinal illness caused by enterotoxin-producing S. aureus is not routinely done as this condition is self-limiting. Hence outbreaks of such illness may go undetected. METHODS: A retrospective cohort study was conducted among a group of tourists who were hospitalized in Sydney shortly after flying from Queensland. The group had consumed food prepared by a restaurant on the Gold Coast before transit. Laboratory analyses on stool specimens were conducted in Sydney. An environmental assessment of the restaurant in the Gold Coast was conducted, and environmental specimens were assessed for contamination. RESULTS: Epidemiological investigations linked the outbreak to a restaurant in the Gold Coast where the suspected food was produced. Stool samples from two of the hospitalized cases were confirmed to have enterotoxin-producing S. aureus, and several environmental samples were found to be contaminated with S. aureus as well. Investigations suggested that absence of hand washing and other unhygienic food handling at the implicated restaurant was the likely cause of this outbreak. CONCLUSION: Food poisoning due to toxin-mediated S. aureus is frequently undetected and underreported. Public health units should consider toxin-producing pathogens such as S. aureus when investigating outbreaks where vomiting is the predominant symptom and occurs rapidly after consuming food.

Enfermedades transmitidas por alimentos en Villa Clara / Foodborne diseases in Villa Clara

Introducción: las enfermedades transmitidas por alimentos constituyen, según la Organización Mundial de la Salud, uno de los problemas más extendidos en el mundo actual y una causa importante de disminución de la productividad para países, empresas, familias e individuos. Métodos: se realizó un estudio observacional descriptivo retrospectivo de las enfermedades transmitidas por alimentos en Villa Clara en el período del 2004 al 2008, con el propósito de caracterizarlas. Se trabajó con los 371 brotes reportados y toda la información se obtuvo a través de la vigilancia epidemiológica. Las variables utilizadas fueron: incidencia de brotes, tipo de brotes, lugar de ocurrencia, alimento implicado y agente causal. Los métodos utilizados fueron frecuencias absolutas, porcentajes, tasas de incidencia y chi cuadrado. Resultados: los brotes más frecuentes fueron los causados por alimentos, y se identificaron como principales causantes los cárnicos y los embutidos. La vivienda fue el lugar donde ocurrieron con mayor frecuencia. Predominó la procedencia estatal. Conclusiones: el principal agente causal de las enfermedades transmitidas por alimentos fue el Estafilococo aureus(AU)

Introduction: foodborne diseases are, according to the World Health Organization, one of the most widespread problems in the present world and an important cause for the decrease in productivity in countries, enterprises, families and individuals. Methods: a retrospective descriptive observational study of foodborne diseases in Villa Clara was conducted for the period 2004 2008 in order to characterize them. 371 reported outbreaks were processed and all the information was obtained thorough epidemiological surveillance. The variables used were: incidence of outbreaks, type of outbreaks, place of occurrence, implicated food and causative agent. The methods used were absolute frequencies, percentages, incidence rates and chi-square. Results: the most frequent outbreaks were the ones caused by food and meat and sausage were identified as the main causative agents. The houses were the places where they most frequently occurred. State origin predominated. Conclusions: the main causative agent of foodborne diseases was the Staphylococcus aureus(AU)

Brotes por Salmonella spp., Staphylococcus aureus y Listeria monocytogenes asociados al consumo de pollo / Outbreaks of Salmonella spp., Staphylococcus aureus and Listeria monocytogenes associated with poultry consumption. Systematic review.

Introducción. Las enfermedades transmitidas por alimentos son un serio problema de salud pública y, el pollo, uno de los alimentos asociados con ellas. Objetivo. Determinar la distribución y frecuencia de brotes alimentarios asociados al consumo de pollo contaminado por Salmonella spp., Listeria monocytogenes y Staphylococus aureus, mediante una revisión sistemática de la literatura científica. Materiales y métodos. Se buscaron los estudios de brotes asociados a Salmonella spp., S. aureus y L. monocytogenes, en las bases de datos Medline, Pubmed, Science Direct,SciELO,Librería Cochrane (CCRT),Biblioteca Virtual en Salud (BVS), Highwire,HINARI y MedicLatina. Se obtuvieron los datos para el cálculo de odds ratios (OR) mediante la elaboración de tablas de contingencia en el programa RevMan5™. Resultados. Siete artículos cumplieron con los criterios de inclusión y no se encontraron reportes de L. monocytogenes. El OR global fue de 3,01 (IC95% 2,37-3,81), lo que se interpreta como una asociación significativa entre el consumo de pollo contaminado y la infección alimentaria. Se presentó heterogeneidad en los estudios incluidos (p=0,03), por lo que fue necesario un análisis por subgrupos de microorganismos; para el caso de Salmonella spp., el OR fue de 2,67 (IC95% 2,09-3,41). No se hizo análisis para S. aureus por reportarse un solo artículo. Conclusiones. Se encontró un OR de 2,61, lo que indica que hay una fuerte asociación entre el consumo de pollo y la adquisición de salmonelosis. El principal factor de riesgo para adquirir salmonelosis es el consumo de pollo de asadero en los restaurantes.

Introduction. Food borne diseases are a serious public health problem. Poultry are often associated with these outbreaks. Objective. A systematic review of the literature is provided concerning the distribution and frequency of food borne outbreaks associated with consumption of chicken contaminated with Salmonella spp., Listeria monocytogenes and Staphylococcus aureus. Materials and methods. The search for studies of outbreaks associated with Salmonella, S. aureus and L. monocytogenes was conducted in Medline, Pubmed, Science Direct, Scielo, Cochrane Library (CCRT), Virtual Health Library (VHL), Highwire, HINARI and MedicLatina. Data were obtained for the calculation of odds ratio (OR) by preparing contingency tables using the RevMan5 program. Results. Seven articles met the inclusion criteria; however, no reports of L. monocytogenes were obtained. The overall OR was 3.01 (95% CI: 2.37, 3.81); this was interpreted as a significant association between the consumption of contaminated chicken and food poisoning. In the included studies heterogeneity (p= 0.03) was presented, so it took a subgroup analysis of microorganisms, in the case of Salmonella OR was 2.67 (95% CI: 2.09 -3.41). No analysis was made for S. aureus reported a single article. Conclusions. The OR indicated a strong association between chicken consumption and acquisition of salmonellosis. The main risk factor for acquiring salmonellosis is the consumption of chicken from grill restaurants.

Staphylococcal enterotoxin A has potent superantigenic and emetic activities but not diarrheagenic activity.

Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus are pyrogenic superantigenic toxins that are involved in human diseases including food poisoning and toxic shock syndrome. Although the superantigenic activity of SEs has been well characterized, its role and mechanism in clinical symptoms of food poisoning remain poorly understood. In this study, house musk shrews (Suncus murinus), a small emetic animal model, were used to study the role of SEs in clinical manifestations of food poisoning. Administration of SEA induced a potent emetic response in vivo and showed significant superantigenic activity in vitro in house musk shrews. However, SEA revealed no diarrheagenic activity. SEA directly injected into the intestinal loops of house musk shrews failed to induce fluid exudation and consequent dilation of the intestinal segments. Rabbit intestinal loop experiments were further carried out to confirm the results and also showed that SEA induced no fluid exudation and consequent dilation. Furthermore, the SEA-producing S. aureus also failed to induce fluid exudation in the administered loops of these animal models. These results indicate that SEA has potent superantigenic and emetic activities, but does not have a diarrheagenic activity.

Escherichia coli O157:H7 facilitates the penetration of Staphylococcus aureus into table eggs.

Fresh eggshells collected from a local farm were subjected to different levels of surface contamination with feces containing different levels (3 to 5 log10) of Escherichia coli O157:H7 or Staphylococcus aureus and incubated at 3 different temperatures (10, 25, and 32 °C). The penetration rates of contaminating bacteria were followed throughout the incubation period by tracing bacterial presence in shell, shell membranes, albumen, and yolk. The study revealed the ability of both E. coli O157:H7 and enterotoxigenic S. aureus to grow on shell in feces, penetrate the shell, and move and multiply within egg contents at different rates and periods depending on bacterial type and incubation conditions. High temperatures (25 and 32 °C) increased penetration rate, whereas storage at 10 °C decreased significantly the rate of penetration. High levels of contamination with E. coli O157:H7 also shortened the time needed for the penetration process. Results showed that when eggshells were contaminated with both organisms simultaneously, the penetration of E. coli O157:H7 preceded that of S. aureus and facilitated the invasion of the latter bacteria.

[Outbreaks of Salmonella spp., Staphylococcus aureus and Listeria monocytogenes associated with poultry consumption. Systematic review]. / Brotes por Salmonella spp., Staphylococcus aureus y Listeria monocytogenes asociados al consumo de pollo.

INTRODUCTION: Food borne diseases are a serious public health problem. Poultry are often associated with these outbreaks. OBJECTIVE: A systematic review of the literature is provided concerning the distribution and frequency of food borne outbreaks associated with consumption of chicken contaminated with Salmonella spp., Listeria monocytogenes and Staphylococcus aureus. MATERIALS AND METHODS: The search for studies of outbreaks associated with Salmonella, S. aureus and L. monocytogenes was conducted in Medline, PubMed, Science Direct, Scielo, Cochrane Library (CCRT), Virtual Health Library (VHL), Highwire, HINARI and MedicLatina. Data were obtained for the calculation of odds ratio (OR) by preparing contingency tables using the RevMan5 program. RESULTS: Seven articles met the inclusion criteria; however, no reports of L. monocytogenes were obtained. The overall OR was 3.01 (95% CI: 2.37, 3.81); this was interpreted as a significant association between the consumption of contaminated chicken and food poisoning. In the included studies heterogeneity (p= 0.03) was presented, so it took a subgroup analysis of microorganisms, in the case of Salmonella OR was 2.67 (95% CI: 2.09 -3.41). No analysis was made for S. aureus reported a single article. CONCLUSIONS: The OR indicated a strong association between chicken consumption and acquisition of salmonellosis. The main risk factor for acquiring salmonellosis is the consumption of chicken from grill restaurants.

Extended staphylococcal enterotoxin D expression in ham products.

Staphylococcal enterotoxin D (SED) is one of the most frequently recovered enterotoxins in staphylococcal food poisoning (SFP) outbreaks. The expression and production of SED were investigated in three ham products, i.e. boiled ham, smoked ham and dry-cured Serrano ham incubated at room temperature for seven days. Staphylococcus aureus was also, as a reference, grown in cultivation broth during optimal growth conditions for seven days. In boiled and smoked ham, continuous sed expression was observed throughout the incubation period with a second increase in sed expression found after five days of incubation. In smoked ham, nine times less SED per colony-forming unit of S. aureus was detected than in boiled ham. In boiled ham, the SED levels unpredictably decreased after three days of incubation. In the Serrano ham, SED was detected after five days of incubation although S. aureus growth was poor and sed expression was too low to determine. After five days of incubation, all three products contained enough SED to cause SFP. These results show that the specific production levels of SED vary in the different ham products, and that toxin production was in part uncoupled from bacterial growth.

Food poisoning and Staphylococcus aureus enterotoxins.

Staphylococcus aureus produces a wide variety of toxins including staphylococcal enterotoxins (SEs; SEA to SEE, SEG to SEI, SER to SET) with demonstrated emetic activity, and staphylococcal-like (SEl) proteins, which are not emetic in a primate model (SElL and SElQ) or have yet to be tested (SElJ, SElK, SElM to SElP, SElU, SElU2 and SElV). SEs and SEls have been traditionally subdivided into classical (SEA to SEE) and new (SEG to SElU2) types. All possess superantigenic activity and are encoded by accessory genetic elements, including plasmids, prophages, pathogenicity islands, vSa genomic islands, or by genes located next to the staphylococcal cassette chromosome (SCC) implicated in methicillin resistance. SEs are a major cause of food poisoning, which typically occurs after ingestion of different foods, particularly processed meat and dairy products, contaminated with S. aureus by improper handling and subsequent storage at elevated temperatures. Symptoms are of rapid onset and include nausea and violent vomiting, with or without diarrhea. The illness is usually self-limiting and only occasionally it is severe enough to warrant hospitalization. SEA is the most common cause of staphylococcal food poisoning worldwide, but the involvement of other classical SEs has been also demonstrated. Of the new SE/SEls, only SEH have clearly been associated with food poisoning. However, genes encoding novel SEs as well as SEls with untested emetic activity are widely represented in S. aureus, and their role in pathogenesis may be underestimated.

Multiple roles of Staphylococcus aureus enterotoxins: pathogenicity, superantigenic activity, and correlation to antibiotic resistance.

Heat-stable enterotoxins are the most notable virulence factors associated with Staphylococcus aureus, a common pathogen associated with serious community and hospital acquired diseases. Staphylococcal enterotoxins (SEs) cause toxic shock-like syndromes and have been implicated in food poisoning. But SEs also act as superantigens that stimulate T-cell proliferation, and a high correlation between these activities has been detected. Most of the nosocomial S. aureus infections are caused by methicillin-resistant S. aureus (MRSA) strains, and those resistant to quinolones or multiresistant to other antibiotics are emerging, leaving a limited choice for their control. This review focuses on these diverse roles of SE, their possible correlations and the influence in disease progression and therapy.

Staphylococcal enterotoxins.

Staphylococcus aureus (S. aureus) is a Gram positive bacterium that is carried by about one third of the general population and is responsible for common and serious diseases. These diseases include food poisoning and toxic shock syndrome, which are caused by exotoxins produced by S. aureus. Of the more than 20 Staphylococcal enterotoxins, SEA and SEB are the best characterized and are also regarded as superantigens because of their ability to bind to class II MHC molecules on antigen presenting cells and stimulate large populations of T cells that share variable regions on the ß chain of the T cell receptor. The result of this massive T cell activation is a cytokine bolus leading to an acute toxic shock. These proteins are highly resistant to denaturation, which allows them to remain intact in contaminated food and trigger disease outbreaks. A recognized problem is the emergence of multi-drug resistant strains of S. aureus and these are a concern in the clinical setting as they are a common cause of antibiotic-associated diarrhea in hospitalized patients. In this review, we provide an overview of the current understanding of these proteins.

[Raw milk-associated Staphylococcus aureus intoxication in children]. / Rohmilch-assoziierte Staphylococcus aureus Intoxikation bei Kindern.

Four hours after the consumption of raw goat milk, three Swiss children came down with emesis and diarrhea in July 2008. First investigations showed that the milk originated from a goat suffering from clinical mastitis (Staphylococcus aureus). In the milk sample from the untreated left udder, Staphylococcus aureus counts reached 5.0 x 10(7) CFU ml(-1). By PCR, the gene for the staphylococcal enterotoxin D was found in isolated strains. The consumption of raw milk is rarely associated with Staphylococcus aureus intoxications. Due to the flora naturally present in raw milk, Staphylococcus aureus normally cannot multiply sufficiently. However, in the present case, high Staphylococcus aureus counts were already present in the milk due to the mastitis of the goat. This amount sufficed to cause a Staphylococcus aureus intoxication in the children.

Diversity in Staphylococcus aureus enterotoxins.

The molecular mechanism of Staphylococcus aureus phathogenicity is complex and involves several toxins, including the famous staphylococcal enterotoxin (SE) and toxic shock syndrome toxin-1 (TSST-1). Although these toxins were discovered in specific clinical contexts of food poisoning and menstrual toxic shock syndrome, they share common biochemical and biological properties. As superantigens they are able to massively activate mononuclear cells and T cells regardless of the antigenic specificity of the T cells. To date, 19 different enterotoxins and related toxins have been described in S. aureus with some differences in structure and biological activity. It has been clearly demonstrated that most human S. aureus isolates harbor at least one gene encoding for these toxins. It is suspected that S. aureus produces SEs and TSST-1 in humans from colonization to infection, whatever the clinical situation. It is proposed that the production of SEs plays a role not only in classical staphylococcal infections but also in noninfectious diseases. This review will focus on recent findings related to staphylococcal superantigens and their impact on human diseases.

Risk evaluation for staphylococcal food poisoning in processed milk produced with skim milk powder.

The growth of S. aureus and the production of staphylococcal enterotoxin A (SEA) in skim milk concentrates stored at inappropriate temperatures in a recovery milk tank (tank for excess concentrated skim milk) used in the manufacture of skimmed milk powder were investigated. Also, it was estimated if a possible outbreak of food poisoning would occur if the contaminated skimmed milk powder was used in the manufacture of processed milk. Skim milk concentrates with milk solid content of 15, 25, and 35% were inoculated with S. aureus at 1-2 log CFU/ml and incubated at 15, 25, or 35 degrees C for 0 to 24 h with or without shaking. Bacterial growth and the level of SEA production were measured. At 35 degrees C with shaking, there was a significant difference (p<0.05) in one way layout analysis of variance, and it was demonstrated that the growth of S. aureus and SEA production could be milk solid content-dependent. Shaking accelerated the growth of S. aureus and SEA production at 35 degrees C. Generally, skim milk powder is produced by mixing a set percentage of skim milk concentrates (recovery milk) from the recovery milk tank into raw milk. If recovery milk contaminated with S. aureus at levels of 1-2 log CFU/ml is kept at 15 to 35 degrees C due to a power failure, it was estimated that processed milk consumption of 670-1200 ml, 420-1500 ml and 18-83 ml would trigger the onset of food poisoning symptoms when skim milk concentrates (recovery milk) are stored at 25 degrees C for 24 h, 35 degrees C for 10 h, and 35 degrees C for 24 h, respectively, during the production of the skim milk powder. Based on these consumption levels, it was concluded that, if recovery milk cannot be refrigerated and is stored at room temperature (25 to 35 degrees C), it must be used within 8 h and preferably within 6 h.

[Large-scale, acute, bacterial gastroenteritis caused by the enterotoxin of Staphylococcus aureus after a barbecue]. / Grootschalige, acute bacteriële gastro-enteritis door enterotoxine van Staphylococcus aureus na een barbecue.

UNLABELLED: EPIDEMIOLOGICAL OBSERVATION: On a warm day, during a barbecue that was attended by over 100 guests, a large number became rapidly ill with signs of acute gastroenteritis within a few hours after eating the prepared food. The characteristic symptoms were nausea, vomiting, syncope and in some cases in a later stage, diarrhoea. Sixty patients were transferred to hospitals. INVESTIGATION: Investigation revealed that the cause of this outbreak of gastroenteritis was an enterotoxin-A-producing strain of Staphylococcus aureus in a noodle dish. Both the food residues and the faeces from patients contained genotypically identical strains of S. aureus. They all had the gene for the gastroenteritis-inducing enterotoxin A from S. aureus. CONCLUSION: This case shows that the timely involvement of the different health authorities responsible for intervening in explosions of food poisoning is crucial for the clarification and treatment of such large-scale outbreaks. In the investigation of this outbreak, the municipal health authority co-operated with regional laboratories and the Food and Consumer Product Safety Authority/Inspectorate for Health Protection and Veterinary Public Health.