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Staphylococcal food poisoning (SFP) is one of the most common food-borne diseases and results from the ingestion of staphylococcal enterotoxins (SEs) preformed in food by enterotoxigenic strains of Staphylococcus aureus. To date, more than 20 SEs have been described: SEA to SElV. All of them have superantigenic activity whereas half of them have been proved to be emetic, representing a potential hazard for consumers. This review, divided into four parts, will focus on the following: (1) the worldwide story of SFP outbreaks, (2) the characteristics and behaviour of S. aureus in food environment, (3) the toxinogenic conditions and characteristics of SEs, and (4) SFP outbreaks including symptomatology, occurrence in the European Union and currently available methods used to characterize staphylococcal outbreaks.

A study was carried out to estimate the proportion of diseases due to milk and milk products among food-borne diseases recorded in France and in other countries since 1980. Particular attention was given to whether the milk involved was heat-treated or not. Four etiologic agents were considered: Salmonella spp., Staphylococcus aureus, Listeria monocytogenes, and pathogenic Escherichia coli. An overview of food-borne disease annual reports from seven countries indicated that milk and milk products were implicated in 1-5% of the total bacterial outbreaks; however, details about the type of product and milk involved were usually not provided. When considering 60 outbreaks and four single cases described in the literature and implicating milk and milk products, confirmed or suspected food vehicles were distributed as follows: milk, 39.1%, cheese, 53.1%, other milk products, 7.8%. Overall, 32.8% of the food vehicles were made from pasteurised milk; 37.5% from raw milk; 10.9% from milk stated as "unpasteurised"; and 18.8% from unspecified milk. Salmonella spp. were responsible for 29 outbreaks, L. monocytogenes for 10 outbreaks and four well-documented single cases, pathogenic E. coli for 11 outbreaks, and S. aureus for 10 outbreaks. Analysis of unpublished data about food-borne disease outbreaks, listeriosis excluded, collected by the coordinator of the French surveillance system from 1992 to 1997, revealed 69 documented outbreaks for which milk and milk products were confirmed as the vehicle by the isolation of the etiologic agent. The food vehicles were distributed as follows: milk, 10%; cheese, 87%; others, 3%. UHT milk accounted for 1.5%, raw milk and raw milk products for 48%, and milk and milk products from unspecified milk for 50.5% of the 69 outbreaks. S. aureus was by far the most frequent pathogen associated with these outbreaks (85.5% of the outbreaks), followed by Salmonella (10.1%). This study demonstrates the limitations of the surveillance systems and the difficulties in estimating the contribution of milk and milk products to food-borne diseases. In particular, it was not possible to find out in many outbreaks what heat treatment, if any, the milk had undergone.

Staphylococcal poisoning is a common food-borne disease for which immunoassays to detect enterotoxins were developed, but these assays often lead to false diagnoses due to interferences or lack of specificity. Absolute quantitative mass spectrometry was for the first time successfully applied to an investigation of a staphylococcal outbreak due to coconut pearls.

A cytotoxin (CytK) has been isolated from a Bacillus cereus strain that caused a severe food poisoning outbreak killing three people. A protein of 34 kDa was highly cytotoxic, and the addition of other secreted proteins gave no synergistic effect. CytK was also necrotic and haemolytic. No known B. cereus enterotoxins were produced by this strain. A DNA sequence from 1.8 kb upstream to 0.2 kb downstream of the toxin gene was sequenced. The deduced amino acid sequence of the toxin showed similarity to Staphylococcus aureus leucocidins, gamma-haemolysin and alpha-haemolysin, Clostridium perfringens beta-toxin and B. cereus haemolysin II, all belonging to a family of beta-barrel channel-forming toxins. There was no sequence similarity between CytK and enterotoxins of B. cereus. The upstream sequence contained a partial sequence of a putative histidine kinase gene. A recognition site for PlcR, which regulates the transcription of enterotoxins HBL and Nhe of B. cereus, was found in the promoter region of the toxin. This new cytotoxin may be responsible for a disease that is similar to, although not as severe as, the necrotic enteritis caused by the beta-toxin of C. perfringens type C.