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Botulism outbreaks

Dodds, K.L., Restaurant-associated botulism outbreaks in North America, Food Control, 1, 139-141, 1990. [Pg.213]

Ihe smoked fish industry was responsible for several botulism outbreaks in the 1960 s, but it has produced millions of pounds of safe products since that time after processing techniques were modified (21). [Pg.64]

Human foodbome botulism outbreaks have typically been linked to the consumption of toxin-contaminated home-prepared or home-preserved foods (Maselli, 1998). The vast majority of foodbome botulism cases are attributed to toxin types A, B, or E. Maselli (1998) reports that type B is the most prevalent (52%) in the USA, followed by type A (34%) and type E (12%), while the CDC (1998) suggests 37.6% of all foodbome botulism outbreaks since 1950 were caused by... [Pg.411]

The natural epidemiology of foodbome botulism provides additional insight into the similarities and discrepancies between the human disease and that represented in various animal models. In the USA, around 25% of reported human botulism cases are classified as foodbome and 72% are infant (Mackle et al., 2001). Human type A and B foodbome botulism cases occur worldwide and constitute the vast majority of reported human intoxications (Maselli, 1998). The majority of other botulism cases are attributed to serotype E and are typically associated with the consumption of contaminated seafood. Generalizations have been made regarding the geographic distribution of the most common C. botulinum strains within the USA. Most human foodbome botulism outbreaks occurring west of the Mississippi are due to type A toxin type B strains are more prevalent east of the Mississippi while type E strains are typically isolated to Alaska and the Pacific Northwest (Amon et al, 2001 Richardson et al, 2004). [Pg.412]

The onset of symptoms in botulism depends upon the amount of toxin ingested or inhaled and the related kinetics of absorption. Time to onset can range from as early as 2 h to as long as 8 days, although symptoms typically appear between 12 and 72 h after consumption of toxin-contaminated food (Lecour et ah, 1988 Amon et ah, 2001). In a review of 13 foodbome botulism outbreaks involving 50 patients from 1970 to 1984, the incubation period ranged from 10 h to 6 days (Lecour et al, 1988). [Pg.419]

Notify the public health department of a botulism outbreak. [Pg.343]

For some particularly risky foods, even the most careful hygiene and sanitation are insuificient to prevent contamination, and a definitive microbe-killing step must be included in the process. For example, early in the century, large botulism outbreaks occurred when canned foods were cooked... [Pg.130]

Espelund, M., and D. Klaveness. Botulism Outbreaks in Natural Environments—An Update. Frontiers in Microbiology 5(11 June 2014) 287. doi 10.3389/fmicb.2014.00287. [Pg.193]

Anniballi, R, Fiore, A., Lofstrom, C., et al., 2013. Management of animal botulism outbreaks from clinical suspicion to practical countermeasures to prevent or minimize outbreaks. Biosecur. Bioterror. 11 (Suppl. 1), S191-S199. [Pg.789]

Detection and identification of the botulism neurotoxin have been essential for diagnosis of the illness and for identifying the causative food. When van Ermengem showed the lethality for animals of the ham that caused the Ellezelles botulism outbreak in 1895 (73), the bioassay naturally became the standard test for botulism neurotoxin. The mouse is very sensitive, and the mouse LD50 determined by i.p. injection became the quantitative unit. [Pg.481]


See other pages where Botulism outbreaks is mentioned: [Pg.203]    [Pg.203]    [Pg.64]    [Pg.166]    [Pg.133]    [Pg.426]    [Pg.412]    [Pg.412]    [Pg.413]    [Pg.413]    [Pg.426]    [Pg.76]    [Pg.394]    [Pg.385]    [Pg.366]    [Pg.367]    [Pg.367]    [Pg.367]    [Pg.381]   
See also in sourсe #XX -- [ Pg.102 ]




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