Between July 1976 and February 1989, 50 incidents of suspected red kidney bean poisoning were reported in the UK. Nine incidents in which nausea, vomiting and diarrhoea developed within 1-7 h of ingestion, were confirmed by the detection of haemagglutinin in the beans. The diagnosis was made on a further 23 incidents on the basis of symptoms, incubation time and the description of preparation of beans prior to consumption. The haemagglutinin (lectin), which occurs naturally in the red kidney bean, is inactivated by thorough cooking of well soaked beans. In many of the outbreaks reported the implicated beans were consumed raw or following an inadequate heat process.
SUMMARYBetween 1976 and 1986, 258 incidents of suspected scombrotoxic fish poisoning were reported in Britain. Histamine analysis was carried out on 240 fish samples from these incidents, and 101 were found to contain > 5 mg histamine/I00 g fish. The symptoms most consistently reported were rash, diarrhoea, flushing and headache. In recent years there has been a decrease in the number of confirmed scombrotoxic outbreaks and a trend towards more sporadic incidents. Of fish samples with > 20 mg histamine/100 g, 94% were from incidents in which scombrotoxic symptoms were characteristic, but where fish had 5-20 mg/100 g only 38 % of incidents were clinically distinctive. Guidelines are presented based on the interpretation of quantitative histamine analysis of fish samples from scombrotoxic poisoning incidents.
Aims: To determine the incidence of sporadic and apparently non-food related diarrhoea associated with Clostridium perfringens enterotoxin. Methods: Enzyme linked immunosorbent assay (ELISA) and reversed phase latex agglutination (RPLA) were used to detect C perfringens enterotoxin in faecal specimens from 818 sporadic cases of diarrhoea.Results: C perfringens enterotoxin was identified as a cause of sporadic diarrhoea in 56 of 818 (6.8%) cases. Diarrhoea was prolonged (three days or more) in most cases. Ages ranged from 3 months to 89 years, although most patients were over 60 years of age. Conclusions: These results suggest that C perfringens may be a cause of sporadic cases of diarrhoea when causes such as food consumption or cross-infection are absent, particularly in the elderly. Greiner) were coated overnight at 4°C with rabbit IgG against enterotoxin in 0O1 M sodium carbonate buffer, pH 9-8. Unbound sites were blocked by 1% bovine serum albumin (BSA) (Sigma) in 0-1 M sodium carbonate buffer, pH 9-8, incubated overnight at 4°C. Test extracts were incubated undiluted with 0 05% Tween 20 (Sigma) and after dilution 1 in 10 in PBS, 0 05% Tween 20 for 75 minutes at room temperature. Each extract was also incubated with neutralising antibody. After washing, rabbit anti-enterotoxin conjugated to horseradish peroxidase in PBS, 0-05% Tween 20, 1% BSA was incubated for two hours at room temperature. The enzyme substrate solution contained 0-5 mg/ml orthophenyldiamine in citrate phosphate buffer (2-43 ml 0-1 M citric acid, 2-57 ml 0-2 M sodium phosphate, and 5-0 ml distilled water). The reaction was stopped by adding 100 ,ul 4 M H2so4 and the absorbance at 492 nm was read in a Titertek Multiskan MCC plate reader. Wells containing no absorbed antibody or no test extract were included in each plate and gave an absorbance of less than 0I10.A standard curve on each plate was used to calculate the enterotoxin concentration. This covered the full range of absorbance with enterotoxin concentrations between 0 1 ng/ml and 100 ng/ml. The coefficient of variance (100 x standard deviation/mean) for intra-assay measurement of enterotoxin concentration was 2-5%. The coefficient of variation of interassay measurements of enterotoxin concentration was between 4-4% and 11-2%.C perfringens spore counts were determined following alcohol shock.' Pure cultures of C perfringens isolated from enterotoxin positive faeces were sent to the PHLS Food Hygiene Laboratory for serological typing using a set of 609 on 7 May 2018 by guest. Protected by copyright.
SUMMARYThe largest recorded outbreak of foodborne botulism in the United Kingdom occurred in June 1989. A total of 27 patients was affected; one patient died. Twenty-five of the patients had eaten one brand of hazelnut yoghurt in the week before the onset of symptoms. This yoghurt contained hazelnut conserve sweetened with aspartame rather than sugar. Clostridium botulinum type B toxin was detected in a blown can of hazelnut conserve, opened and unopened cartons of hazelnut yoghurt, and one faecal specimen. Cl. botulinum type B was subsequently cultured from both opened and unopened cartons of the hazelnut yoghurt and from one faecal specimen. Investigations indicated that the processing of the conserve was inadequate to destroy Cl. botulinum spores. Control measures included the cessation of all yoghurt production by the implicated producer, the withdrawal of the firm's yoghurts from sale, the recall of cans of the hazelnut conserve, and advice to the general public to avoid the consumption of all hazelnut yoghurts.
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