Changes in histamine and microbiological analyses in fresh and frozen tuna muscle during temperature abuse.

Temperature abuse of tuna (Thunnus alalunga) was carried out in order to assess the histamine buildup in fish-processing facilities where fish can be exposed to high temperatures for short periods of time. Histamine production was studied in tuna loins under different storage and abuse conditions. Tuna was stored at 0-2 degrees C, 3-4 degrees C, and 6-7 degrees C, and abused for 2 h daily at 20 degrees C and 30 degrees C for 7-12 days. Loins abused at 30 degrees C for 2 h daily contained potentially toxic histamine concentrations (67-382 mg kg(-1)) when stored at a low refrigeration temperature (0-2 degrees C), whereas when stored at 6-7 degrees C, the loins contained highly toxic histamine concentrations (544.5-4156.6 mg kg(-1)). Lower histamine concentrations (23-48 mg kg(-1) in loins stored at 0-2 degrees C and 124.7-2435.8 mg kg(-1) in loins stored at 6-7 degrees C) were observed in temperature-abused loins that were initially frozen. An increase over time was observed in most microbial counts tested. Bacteria isolated from the temperature-abused loins showed a varied ability of histamine production, with Morganella morganii, Klebsiella oxytoca, Staphylococcus hominis, and Enterococcus hirae being the most active histamine-producing bacteria.

Molecular characterization of Clostridium perfringens isolates from humans with sporadic diarrhea: evidence for transcriptional regulation of the beta2-toxin-encoding gene.

Clostridium perfringens type A food poisoning is caused by C. perfringens isolates carrying a chromosomal enterotoxin gene (cpe), while non-food-borne gastrointestinal (GI) diseases, such as antibiotic-associated diarrhea (AAD) and sporadic diarrhea (SD), are caused by C. perfringens plasmid cpe isolates. A recent study reported the association of beta2 toxin (CPB2) with human GI diseases, and particularly AAD/SD, by demonstrating that a large percentage of AAD/SD isolates, in contrast to a small percentage of food poisoning isolates, carry the beta2-toxin gene (cpb2). This putative relationship was further tested in the current study by characterizing 14 cpe+ C. perfringens fecal isolates associated with recent cases of human SD in England (referred to hereafter as SD isolates). These SD isolates were all classified as cpe+ type A, and 12 of the 14 cpe+ isolates carry their cpe gene on the plasmid and 2 carry it on the chromosome. Interestingly, cpb2 is present in only 12 plasmid cpe isolates; 11 isolates carry cpe and cpb2 on different plasmids, but cpe and cpb2 are located on the same plasmid in one isolate. C. perfringens enterotoxin is produced by all 14 cpe+ SD isolates. However, only 10 of the 12 cpe+/cpb2+ SD isolates produced CPB2, with significant variation in amounts. The levels of cpb2 mRNA in low- to high-CPB2-producing SD isolates differed to such an extent (30-fold) that this difference could be considered a major cause of the differential level of CPB2 production in vitro by SD isolates. Furthermore, no silent or atypical cpb2 was found in a CPB2 Western blot-negative isolate, 5422/94, suggesting that the lack of CPB2 production in 5422/94 was due to low expression of cpb2 mRNA. This received support from our observation that the recombinant plasmid carrying 5422/94 cpb2, which overexpressed cpb2 mRNA, restored CPB2 production in F4969 (a cpb2-negative isolate). Collectively, our present results suggest that CPB2 merits further study as an accessory toxin in C. perfringens-associated SD.

Wound botulism in the UK and Ireland.

There are three main, naturally occurring, epidemiological types of botulism: food-borne, intestinal colonization (infant botulism) and wound botulism. The neurological signs and symptoms are the same for all three epidemiological types and may include respiratory paralysis. Wound botulism is caused by growth of cells and release of toxin in vivo, is associated with traumatic wounds and abscesses and has been reported in drug users, such as those injecting heroin or sniffing cocaine. Up to the end of 1999 there were no confirmed cases of wound botulism in the UK. Between the beginning of 2000 and the end of December 2002, there were 33 clinically diagnosed cases of wound botulism in the UK and Ireland. All cases had injected heroin into muscle or by 'skin popping'. The clinical diagnosis was confirmed by laboratory tests in 20 of these cases. Eighteen cases were caused by type A toxin and two by type B toxin.

Food poisoning associated with biotoxins in fish and shellfish.

PURPOSE OF REVIEW: In recent times the number of blooms of algae that produce toxins has increased in frequency, intensity and geographical distribution. This review describes some of the illnesses caused by fish and shellfish contaminated with toxins produced by marine algae and by bacteria. RECENT FINDINGS: The increase in toxic algal blooms may be a result of increased awareness, aquaculture, eutrophication, or transport of cysts in ship ballast. Improved chemical methods for the detection of algal toxins are now being developed, and so the number of toxins recognized is increasing. Toxicological data on some of these algal toxins are lacking. Despite the increase in occurrence of algal toxins, scombrotoxic poisoning remains the most common cause of food poisoning associated with the consumption of fish and shellfish. This may be real or it may be a reflection of lack of suitable tests for algal toxins or under-recognition by workers in health care. SUMMARY: The major problem worldwide in this field is the lack of pure toxins for use in developing and standardizing chemical methods for toxin detection. Such methods would permit increased testing of both food and clinical specimens, and hence would prevent the entry of toxic food into the food chain and increase laboratory confirmation of incidents of illness.