Province/territory |
Serotype, no. cases |
Total |
|||||
---|---|---|---|---|---|---|---|
A |
B |
E |
F |
AB |
Unknown |
||
Quebec | 5 | 2 | 21 | 1 | 1 | 1 | 31 |
Ontario | 4 | 6 | 4 | 1 | 0 | 0 | 15 |
Alberta | 4 | 1 | 0 | 0 | 0 | 1 | 6 |
Nunavut | 0 | 0 | 5 | 0 | 0 | 0 | 5 |
British Columbia | 1 | 1 | 1 | 0 | 0 | 0 | 3 |
Northwest Territories | 0 | 0 | 3 | 0 | 0 | 0 | 3 |
Manitoba | 1 | 1 | 0 | 0 | 0 | 0 | 2 |
Saskatchewan | 1 | 0 | 0 | 0 | 0 | 0 | 1 |
Newfoundland and Labrador | 0 | 0 | 1 | 0 | 0 | 0 | 1 |
Total | 16 | 11 | 35 | 2 | 1 | 2 | 67 |
Table 1. Foodborne botulism cases by province or territory and BoNT serotype, Canada, 2006–2021
Food source |
Years |
Outbreaks |
Cases |
Deaths |
Serotype |
---|---|---|---|---|---|
Commercial retail foods | |||||
Carrot juice |
2006 | 1 | 2 | 0 | A |
Ground beef |
2009 | 1 | 2 | 0 | B |
Salted fish |
2012 | 1 | 3 | 0 | E |
Alfredo sauce |
2021 | 1 | 1 | 0 | AB |
Home-prepared foods | |||||
Spaghetti sauce |
2006 | 1 | 2 | 0 | A |
Watermelon jelly |
2011 | 1 | 1 | 0 | B |
Traditionally prepared Indigenous foods (traditional name) | |||||
Blubber in oil (misiraq) |
2006–2021 | 7 | 8 | 1 | E |
Meat and fat (igunaq) |
2006–2021 | 5 | 10 | 1 | E |
Beluga skin (muktuk) |
2006–2021 | 3 | 3 | 0 | E |
Aged meat |
2006–2021 | 3 | 3 | 0 | A, E |
Salmon eggs |
2013 | 1 | 1 | 1 | E |
Unknown* | 2006–2021 | 30 | 31 | 4 | A, B, E, F |
Table 2. Foodborne botulism outbreaks, cases, deaths, and serotype, by year and food source, Canada, 2006–2021
*Food was either not submitted for analysis or was submitted but not found to be toxic.
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During 2006–2021, Canada had 55 laboratory-confirmed outbreaks of foodborne botulism, involving 67 cases. The mean annual incidence was 0.01 case/100,000 population. Foodborne botulism in Indigenous communities accounted for 46% of all cases, which is down from 85% of all cases during 1990–2005. Among all cases, 52% were caused by botulinum neurotoxin type E, but types A (24%), B (16%), F (3%), and AB (1%) also occurred; 3% were caused by undetermined serotypes. Four outbreaks resulted from commercial products, including a 2006 international outbreak caused by carrot juice. Hospital data indicated that 78% of patients were transferred to special care units and 70% required mechanical ventilation; 7 deaths were reported. Botulinum neurotoxin type A was associated with much longer hospital stays and more time spent in special care than types B or E. Foodborne botulism often is misdiagnosed. Increased clinician awareness can improve diagnosis, which can aid epidemiologic investigations and patient treatment.
Human foodborne botulism is a neuroparalytic disease that results from ingestion of foods containing botulinum neurotoxin (BoNT) serotypes A, B, E, or F, produced by Clostridium botulinum groups I and II or, rarely, neurotoxigenic strains of C. baratii type F or C. butyricum type E.[1]. BoNTs prevent muscle contraction through cleavage of the proteins responsible for fusion of acetylcholine-containing synaptic vesicles in nerve terminals at neuromuscular junctions[2]
Clinical symptoms of botulism include symmetric cranial nerve palsies of the eyes, mouth, and throat. Paralysis can descend to the diaphragm, causing respiratory arrest that can necessitate use of mechanical ventilation[1]. In some instances, patients can take months or years to recover from prolonged disability caused by skeletal muscle paralysis[3]. Treatment options are limited to use of botulinum antitoxin (BAT) that binds to and neutralizes circulating BoNTs[4]. BAT is especially effective when administered early[5], and its use should be based on clinical diagnosis, rather than waiting for results from diagnostic tests.
Manifestations of botulism are classified according to the route of exposure to BoNTs. Wound botulism occurs when C. botulinum colonizes an infected wound, and intestinal toxemia botulism occurs in the adult intestinal tract when BoNTs are released in situ[6,7]. Infant botulism is a form of intestinal toxemia botulism that occurs in children <1 year of age[8]. Foodborne botulism is an acute intoxication resulting from ingestion of BoNTs preformed in foods supporting C. botulinum growth.C. botulinum endospores are widely distributed in soils throughout the world and survive heating processes that inactivate vegetative bacterial cells[9]. Foods contaminated with viable C. botulinum spores can germinate, grow, and produce BoNTs when they are stored under permissive growth conditions, including low oxygen, low acidity (pH >4.6), sufficient temperature (>10°C), and water activity (aw >0.93)[10]
Investigations of foodborne botulism provide valuable information regarding food sources and storage conditions that permit C. botulinum growth and BoNT production. Previous reports of foodborne botulism in Canada are available, including the periods of 1919–1973.,[11], 1971–1984[12] and 1985–2005[13] Here, we present a summary of foodborne botulism in Canada during 2006–2021, including incidence over the course of time, geographic distribution by province and territory, BoNT serotype, and food source when available. In addition, we used hospital records that match cases from laboratory-confirmed outbreaks to determine clinical disease outcomes.