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The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.
The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.

[[Domestic dog]]s may develop systemic toxemia after consuming C. botulinum type C exotoxin or spores within bird carcasses or other infected meat<ref>{{cite web|url=http://www.vetbook.org/wiki/dog/index.php/Botulism |title=Dogs / Botulism |publisher=http://vetbook.org/wiki/index.php/Main_Page |date=2012-08-12 |accessdate=2013-08-23}}</ref> but are generally resistant to the more severe effects of Clostridium botulinum type C.
Symptoms include flaccid muscle paralysis; dogs with breathing difficulties will require more intensive care monitoring. Muscle paralysis can lead to death due to cardiac and respiratory arrest.<ref>{{cite web|url=http://www.merckmanuals.com/vet/poultry/botulism_limberneck_western_duck_sickness/overview_of_botulism_in_poultry.html |title=Overview of botulism in poultry |publisher=http://www.merckmanuals.com/vet/index.html |date=2012-03-31 |accessdate=2013-08-23}}</ref>


Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.<ref>"Botulism." In the Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and CO., 1988, pp.442–444.</ref>
Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.<ref>"Botulism." In the Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and CO., 1988, pp.442–444.</ref>

Revision as of 09:47, 23 August 2013

Botulism
SpecialtyInfectious diseases Edit this on Wikidata

Botulism (Latin, botulus, "sausage") (pronounced /ˈbɒtʃ[invalid input: 'ʉ']lɪzəm/) is, in humans, a rare but sometimes fatal paralytic illness. Foodborne botulism is an intoxication caused by consuming food contaminated with the botulinum toxin; it is not passed on from person to person when the skin is intact. Infant botulism is a toxico-infection where the gastro-intestinal tract is colonized by spores prior to the protective intestinal bacterial flora having developed and wound botulism is found most often among substance abusers when spores enter a wound under the skin, and, in the absence of oxygen are activated and release toxin.[1]

General Information

The toxin is a protein produced under anaerobic conditions (where there is no oxygen) by the bacterium Clostridium botulinum, and affects a wide range of animals, including mammals, birds and fish.[2] In domestic fowl, such as ducks, chickens, etc. as well as in birds in the wild, the disease is known as Limberneck.[3]

Clostridium botulinum is a large anaerobic Gram-positive bacillus that forms subterminal endospores.[4]

There are seven serological varieties of the bacterium denoted by the letters A to G. The toxin from all of these acts in the same way and producing similar symptoms: acetylcholine is prevented from being released from the motor nerve endings causing flaccid paralysis and symptoms of blurred vision, ptosis, nausea, vomiting, diarrhea and/or constipation, cramps, respiratory difficulty.

Botulinum toxin is broken into 7 neurotoxins (labeled as types A, B, C [C1, C2], D, E, F, and G), which are antigenically and serologically distinct but structurally similar. Human botulism is caused mainly by types A, B, E, and (rarely) F. Types C and D cause toxicity only in other animals.[5]

Some types produce a characteristic putrefactive smell and digest meat (types A and some of B and F); these are said to be proteolytic; type E and some types of B, C, D and F are nonproteolytic and can go undetected because there is no strong odour associated with them[4]

When the bacteria are under stress, they develop spores, which are inert. Their natural habitats are in the soil, in the silt that comprises the bottom sediment of streams, lakes and coastal waters and in the ocean, while some types are natural inhabitants of mammalian (e.g., human, cattle, horses) intestinal tracts, and are present in their excreta. The spores can survive in their inert form for many years.[6]

Toxin is produced by the bacteria when environmental conditions are favourable for the spores to replicate and grow, but the gene that encodes for the toxin protein is actually carried by a virus or phage that infects the bacteria. Unfortunately, little is known about the natural factors that control phage infection and replication within the bacteria.[7]

The spores require warm temperatures, a protein source and an anaerobic (no oxygen) environment and moisture in order to become active and produce toxin. In the wild, decomposing vegetation and invertebrates combined with warm temperatures can provide ideal conditions for the botulism bacteria to activate and produce toxin that may affect feeding birds and other animals. Spores are not killed by boiling, however botulism is uncommon because special, rarely obtained conditions are necessary for botulinum toxin production from C. botulinum spores, including an anaerobic, low-salt, low- acid, low-sugar environment at ambient temperatures.[8]

The toxins enters the human body in one of three ways: by colonization of the digestive tract by the bacterium; in children (infant botulism)[citation needed] or adults (adult intestinal toxemia), by ingestion of toxin from foods (foodborne botulism) or by contamination of a wound by the bacterium (wound botulism).[9] Person to person transmission of botulism does not occur. Improperly preserved food is the most common form of foodborne botulism. Fish that has been pickled without the salinity or acidity of the brine (that contains acetic acid and high sodium levels) and smoked fish stored at too high a temperature present a risk, as does improperly canned food. Infants under one year should not be fed honey, a natural source of botulinum bacteria, as bacteria in the gut is not sufficiently developed.

Botulinum inhibits the body's production of acetylcholine within the nervous system, the chemical that produces a bridge across synapses, where nerve cell axons and dendrites connect with each other. All forms lead to paralysis that typically starts with the muscles of the face and then spreads towards the limbs.[9] In severe forms, it leads to paralysis of the breathing muscles and causes respiratory failure. In light of this life-threatening complication, all suspected cases of botulism are treated as medical emergencies, and public health officials are usually involved to prevent further cases from the same source.[9]

Signs and symptoms

The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. A group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).[9]

Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.[9]

In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis).[9] Some of the toxins (B and E) also precipitate nausea and vomiting.[9]

Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status ("clear sensorium").[10][self-published source?]

Infant botulism

Infant botulism was first recognized in 1976, and is the most common form of botulism in the United States. There are 80 to 100 diagnosed cases of infant botulism in the United States each year. Infants are susceptible to infant botulism in the first year of life, with more than 90% of cases occurring in infants younger than six months.[11] Infant botulism results from the ingestion of the C. botulinum spores, and subsequent colonization of the small intestine. The infant gut may be colonized when the composition of the intestinal microflora (normal flora) is insufficient to competitively inhibit the growth of C. botulinum and levels of bile acids (which normally inhibit clostridial growth) are lower than later in life.[12]

The growth of the spores releases botulinum toxin, which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of acetylcholine at the neuromuscular junction. Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding and an altered cry, often progressing to a complete descending flaccid paralysis. Although constipation is usually the first symptom of infant botulism, it is commonly overlooked.

Honey is the only known dietary reservoir of C. botulinum spores linked to infant botulism. For this reason honey should not be fed to infants less than one year of age.[12] Other cases of infant botulism are thought to be caused by acquiring the spores from the natural environment. Clostridium botulinum is a ubiquitous soil-dwelling bacterium. Many infant botulism patients have been demonstrated to live near a construction site or an area of soil disturbance.[citation needed]

Infant botulism has been reported in 49 of 50 US states,[11] and cases have been recognized in 26 countries on five continents.[13]

Complications

Infant botulism has no long-term side effects, but can be complicated by nosocomial adverse events. The case fatality rate is less than 1% for hospitalized infants with botulism.

Botulism can result in death due to respiratory failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50% to 7% due to improved supportive care. A patient with severe botulism may require mechanical ventilation (breathing support through a ventilator) as well as intensive medical and nursing care, sometimes for several months. Patients who survive an episode of botulism poisoning may have fatigue and shortness of breath for years and long-term therapy may be needed to aid their recovery.

Cause

C. botulinum is an anaerobic, Gram positive, spore-forming rod. Botulinium toxin is one of the most powerful known toxins: about one microgram is lethal to humans. It acts by blocking nerve function (neuromuscular blockade) through inhibition of the excitatory neurotransmitter acetyl choline's release from the presynaptic membrane of neuromuscular junctions in the somatic nervous system. This causes paralysis. Advanced botulism can cause respiratory failure by paralysing the muscles of the chest; this can progress to respiratory arrest.

In all cases illness is caused by the botulinium toxin produced by the bacterium C. botulinum in anaerobic conditions, and not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that fire (depolarise) at a higher frequency first.[14]

Four main modes of entry for the toxin are known. The most common form in Western countries is infant botulism. This occurs in small children who are colonized with the bacterium during the early stages of their lives. The bacterium then releases the toxin into the intestine, which is absorbed into the bloodstream. The consumption of honey during the first year of life has been identified as a risk factor for infant botulism; it is a factor in a fifth of all cases.[9] The adult form of infant botulism is termed adult intestinal toxemia, and is exceedingly rare.[9]

Foodborne botulism results from contaminated foodstuffs in which C. botulinum spores have been allowed to germinate in anaerobic conditions. This typically occurs in home-canned food substances and fermented uncooked dishes.[dubious – discuss] Given that multiple people often consume food from the same source, it is common for more than a single person to be affected simultaneously. Symptoms usually appear 12–36 hours after eating, but can also appear within 6 hours to 10 days.[15]

Wound botulism results from the contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream. This has become more common in intravenous drug users since the 1990s, especially people using black tar heroin and those injecting heroin into the skin rather than the veins.[9]

Isolated cases of botulism have been described after inhalation by laboratory workers and after cosmetic use of inappropriate strengths of Botox.[9]

Diagnosis

For infant botulism, diagnosis should be made on clinical grounds. Confirmation of the diagnosis is made by testing of a stool or enema specimen with the mouse bioassay.

Physicians may consider diagnosing botulism if the patient's history and physical examination suggest botulism. However, these clues are often not enough to allow a diagnosis. Other diseases such as Guillain-Barré syndrome, stroke, and myasthenia gravis can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can be cultured from tissues. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony.[16]

In animals

In cattle, the symptoms may include drooling, restlessness, uncoordination, urine retention, dysphagia, and sternal recumbency. Laterally recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur. Phosphorus-deficient cattle, especially in southern Africa, are inclined to ingest bones and carrion containing clostridial toxins and consequently suffer lame sickness or lamsiekte.

The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.

Domestic dogs may develop systemic toxemia after consuming C. botulinum type C exotoxin or spores within bird carcasses or other infected meat[17] but are generally resistant to the more severe effects of Clostridium botulinum type C. Symptoms include flaccid muscle paralysis; dogs with breathing difficulties will require more intensive care monitoring. Muscle paralysis can lead to death due to cardiac and respiratory arrest.[18]

Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.[19]

In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates.

Prevention

Although the botulinum toxin is destroyed by thorough cooking over the course of a few minutes,[2] the spore itself is not killed by the temperatures reached with normal sea-level-pressure boiling, leaving it free to grow and again produce the toxin when conditions are right.[20][21]

A recommended prevention measure for infant botulism is to avoid feeding honey to infants less than 12 months of age. In older children and adults the normal intestinal bacteria suppress development of C. botulinum.[22]

While commercially canned goods are required to undergo a "botulinum cook" in a pressure cooker at 121 °C (250 °F) for 3 minutes, and so rarely cause botulism, there have been notable exceptions such as the 1978 Alaskan salmon outbreak and the 2007 Castleberry's Food Company outbreak. Foodborne botulism is the rarest form though, accounting for only around 15% of cases (US)[23] and has more frequently been from home-canned foods with low acid content, such as carrot juice, asparagus, green beans, beets, and corn. However, outbreaks of botulism have resulted from more unusual sources. In July 2002, fourteen Alaskans ate muktuk (whale meat) from a beached whale, and eight of them developed symptoms of botulism, two of them requiring mechanical ventilation.[24]

Other, but much rarer sources of infection (about every decade in the US[23]) include garlic or herbs[25] stored covered in oil without acidification,[26] chilli peppers,[23] improperly handled baked potatoes wrapped in aluminum foil,[23] tomatoes,[23] and home-canned or fermented fish.

When canning or preserving food at home pay attention to hygiene, pressure, temperature, refrigeration and storage. When making home preserves bottle only acidic fruit such as apples, pears, stone fruits and berries. Tropical fruit and tomatoes are low in acidity and must have some acidity added before they are bottled[27]

Oils infused with fresh garlic or herbs should be acidified and refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Because the botulism toxin is destroyed by high temperatures, home-canned foods are best boiled for 10 minutes before eating.[28] Metal cans containing food in which bacteria, possibly botulinum, are growing may bulge outwards due to gas production from bacterial growth; such cans should be discarded.

Any container of food which has been heat-treated and then assumed to be airtight which shows signs of not being so, e.g., metal cans with pinprick holes from rust or mechanical damage, should also be discarded. Contamination of a canned food solely with C. botulinum may not cause any visual defects (e.g. bulging). Only sufficient thermal processing during production should be used as a food safety control.

Wound botulism can be prevented by promptly seeking medical care for infected wounds, and by avoiding punctures by unsterile things such as needles used for street drug injections. It is currently being researched at USAMRIID under BSL-434.

Treatment

Most infant botulism patients require supportive care in a hospital setting. The only drug currently available to treat infant botulism is Botulism Immune Globulin Intravenous-Human (BIG-IV or BabyBIG). BabyBIG was developed by the Infant Botulism Treatment and Prevention Program at the California Department of Public Health.[29]

The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a ventilator for weeks, plus intensive medical and nursing care. After several weeks, the paralysis slowly improves. If diagnosed early, foodborne and wound botulism can be treated by inducing passive immunity with a horse-derived antitoxin, which blocks the action of toxin circulating in the blood.[30]

This can prevent patients from worsening, but recovery still takes many weeks. Physicians may try to remove contaminated food still in the stomach by inducing vomiting or by using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. Good supportive care in a hospital is the mainstay of therapy for all forms of botulism.[31]

Furthermore each case of food-borne botulism is a potential public health emergency in that it is necessary to identify the source of the outbreak and ensure that all persons who have been exposed to the toxin have been identified, and that no contaminated food remains.

There are two primary botulinum antitoxins available for treatment of wound and foodborne botulism. Trivalent (A,B,E) botulinum antitoxin is derived from equine sources utilizing whole antibodies (Fab & Fc portions). This antitoxin is available from the local health department via the CDC. The second antitoxin is heptavalent (A,B,C,D,E,F,G) botulinum antitoxin which is derived from "despeciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This is a less immunogenic antitoxin that is effective against all known strains of botulism where not contraindicated. This is available from the US Army. On 1 June 2006 the US Department of Health and Human Services awarded a $363 million contract with Cangene Corporation for 200,000 doses of heptavalent botulinum antitoxin over five years for delivery into the Strategic National Stockpile beginning in 2007.[32]

Prognosis

Infant botulism has no long-term side effects, but can be complicated by nosocomial adverse events. The case fatality rate is less than 1% for hospitalized infants with botulism.[citation needed]

Between 1910 and 1919 the death rate from botulism was 70% in the United States, dropping to 9% in the 1980s and 2% in the early 1990s, mainly because of the development of artificial respirators. Up to 60% of botulism cases are fatal if left untreated.[citation needed]

The World Health Organization (WHO) reports that the current mortality rate is 5% (type B) to 10% (type A). Other sources report that, in the U.S., the overall mortality rate is about 7.5%, but the mortality rate among adults over 60 is 30%. The mortality rate for wound botulism is about 10%. The infant botulism mortality rate is about 1.3%.[citation needed]

Death from botulism is common in waterfowl; an estimated 10,000 to 100,000 birds die of botulism annually. In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock. Some affected birds may recover without treatment.[citation needed]

Botulism seems to be relatively uncommon in domestic mammals; however, in some parts of the world, epidemics with up to 65% mortality are seen in cattle. The prognosis is poor in large animals that are recumbent. Most dogs with botulism recover within 2 weeks.[citation needed]

Epidemiology

Between 1990 and 2000, the Centers for Disease Control reported 263 individual 'cases' from 160 foodborne botulism 'events' in the United States with a case-fatality rate of 4%. Thirty-nine percent (103 cases and 58 events) occurred in Alaska, all of which were attributable to traditional Alaska aboriginal foods. In the lower 49 states, home-canned food was implicated in 70 (91%) events with canned asparagus being the most numerous cause. Two restaurant-associated outbreaks affected 25 persons. The median number of cases per year was 23 (range 17–43), the median number of events per year was 14 (range 9–24). The highest incidence rates occurred in Alaska, Idaho, Washington, and Oregon. All other states had an incidence rate of 1 case per ten million people or less.[33]

The number of cases of food borne and infant botulism has changed little in recent years, but wound botulism has increased because of the use of black tar heroin, especially in California.[34]

Outbreaks

Clostridium botulinum has been associated with one outbreak linked to venison jerky. The investigation done of this outbreak showed that toxin could be repeatedly demonstrated in the jerky, but the organism was only isolated once. It was never isolated from any of the raw materials used to make the jerky and no conclusions were drawn as to how the organism came to produce toxin within the product.

Outbreak in the US of type B botulism from home canned jalapeño peppers

Between March 31 and April 6, 1977, 59 individuals developed type B botulism. All ill persons had eaten at the same Mexican restaurant and all had consumed a hot sauce made with improperly home-canned jalapeño peppers, either by adding it to their food, or by eating a nacho that had had hot sauce used in its preparation. The full clinical spectrum (mild symptomatology with neurologic findings through life-threatening ventilatory paralysis) of type B botulism was documented. [35]

Outbreak in the UK from hazelnut yoghurt

The largest recorded outbreak of foodborne botulism in the United Kingdom occurred in June 1989. A total of 27 patients were 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. 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.[1]

Baked potato in El Paso, Texas

In April 1994, the largest outbreak of botulism in the United States since 1978 occurred in El Paso, Texas. Thirty persons were affected; 4 required mechanical ventilation. All ate food from a Greek restaurant. The attack rate among persons who ate a potato-based dip was 86% (19/22) compared with 6% (11/176) among persons who did not eat the dip (relative risk [RR] Å 13.8; 95% confidence interval [CI], 7.6 – 25.1). The attack rate among persons who ate an eggplant-based dip was 67% (6/9) compared with 13% (24/189) among persons who did not (RR Å 5.2; 95% CI, 2.9 – 9.5). Botulism toxin type A was detected from patients and in both dips. Toxin formation resulted from holding aluminum foil – wrapped baked potatoes at room temperature, apparently for several days, before they were used in the dips. Consumers should be informed of the potential hazards caused by holding foil-wrapped potatoes at ambient temperatures after cooking.[36]

Castleberry's Food Company outbreak

Main article: Castleberry's Food Company

Beginning in late June 2007, 8 people contracted botulism poisoning by eating canned food products produced by Castleberry's Food Company in its Augusta, Georgia plant. It was later identified that the Castleberry's plant had serious production problems on a specific line of retorts that had under-processed the cans of food. These issues included broken cooking alarms, leaking water valves and inaccurate temperature devices, all the result of poor management of the company.

All of the victims were hospitalized and placed on mechanical ventilation. The Castleberry's Food Company outbreak was the first instance of botulism in commercial canned foods in the United States in over 30 years.

Bon Vivant incident

Main article: 1971 Bon Vivant botulism case

On July 2, 1971, the U.S. Food and Drug Administration (FDA) released a public warning after learning that a New York man had died and his wife had become seriously ill due to botulism after eating a can of Bon Vivant vichyssoise soup.

US annual botulism statistics

All data regarding botulism antitoxin releases and laboratory confirmation of cases in the US are recorded annually by CDC Centers for Disease Control and Prevention and published on their website

In other species

Botulism can occur in many vertebrates and invertebrates. Botulism has been reported in rats, mice, chicken, frogs, toads, goldfish, aplysia, squid, crayfish, drosophila, leeches, etc.[37]

See also

References

  1. ^ It is important to distinguish between infection and intoxication. In most cases, botulism results from ingestion of the toxin (intoxication). In other cases (e.g. infant botulism, wound botulism), the disease results from the ingestion of spores or infection of an open wound with spores which then germinate and produce the bacterial cells that release the toxin. Questions and Answers on Botulism (WHO)
  2. ^ a b http://www.who.int/mediacentre/factsheets/fs270/en/
  3. ^ Merck Manual of Veterinary Medicine
  4. ^ a b University of California, Santa Cruz Environmental toxicology - Botulism
  5. ^ Divakara Kedlaya, MBBS Botulinum Toxin medscape
  6. ^ B. Q. Ward, B. J. Carroll, E. S. Garrett, G. B. Reese. (Technological Laboratory, U.S. Bureau of Commercial Fisheries, Pascagoula, Mississippi 39567) Survey of the U.S. Gulf Coast for the Presence of Clostridium botulinum Applied Microbiology, Vol. 15, No. 3; May 1967, pp 629-636
  7. ^ US government publications Field Manual of Wildlife Diseases - Chapter 38: Avian Botulism
  8. ^ International Commission on Microbiological Specifications for Foods. Clostridium botulinum. In: Micro-organisms in foods 5: characteristics of microbial pathogens. London, UK: Blackie Academic & Professional; 1996:68–111. quoted in Botulism From Drinking Prison-Made Illicit Alcohol — Utah 2011 CDC - Morbidity and Mortality Weekly Report (MMWR) / October 5, 2012 / Vol. 61 / No. 39 Bottom of p 783
  9. ^ a b c d e f g h i j k Sobel J (2005). "Botulism". Clin. Infect. Dis. 41 (8): 1167–73. doi:10.1086/444507. PMID 16163636. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ http://www.outbreakid.com/bioterrorism.htm
  11. ^ a b Arnon SS Infant Botulism In Feigin RD, CherryJD, Demmler GJ, Kaplan SL., eds. Textbook of Pediatric Infectious Diseases. 5th edition Philadelphia, PA: WB Saunders; 2004:1758–1766
  12. ^ a b Caya JG, Agni R, Miller JE (2004). "Clostridium botulinum and the clinical laboratorian: a detailed review of botulism, including biological warfare ramifications of botulinum toxin". Arch. Pathol. Lab. Med. 128 (6): 653–62. doi:10.1043/1543-2165(2004)128<653:CBATCL>2.0.CO;2. PMID 15163234. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ Koepke R, Sobel J and Arnon SS Global Occurrence of Infant Botulism, 1976–2006 Pediatrics 2008;122;e73-e82
  14. ^ Oxford Textbook of Medicine, 4th Ed., Section 7.55
  15. ^ "Facts About Botulism". Emergency Preparedness and Response. Centers for Disease Control and Prevention. Oct 14, 2001. Retrieved Jul 2 2011. {{cite web}}: Check date values in: |accessdate= (help)
  16. ^ Weber,J.T. "Botulism" In Infectious Diseases, 5th ed. Edited by P. D. Hpeprich, J. B. Lippincott Company, 1994, pp. 1185–1194.
  17. ^ "Dogs / Botulism". http://vetbook.org/wiki/index.php/Main_Page. 2012-08-12. Retrieved 2013-08-23. {{cite web}}: External link in |publisher= (help)
  18. ^ "Overview of botulism in poultry". http://www.merckmanuals.com/vet/index.html. 2012-03-31. Retrieved 2013-08-23. {{cite web}}: External link in |publisher= (help)
  19. ^ "Botulism." In the Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and CO., 1988, pp.442–444.
  20. ^ Toronto Star 2008Couple suing over tainted juice
  21. ^ FDA Guidance for Industry: Refrigerated carrot juice and other refrigerated low acid juices
  22. ^ Stephen S. Arnon; et al. (February 1979). "Honey and other environmental risk factors for infant botulism". The Journal of Pediatrics. 94 (2): 331–336. doi:10.1016/S0022-3476(79)80863-X. PMID 368301. {{cite journal}}: Explicit use of et al. in: |author= (help)
  23. ^ a b c d e http://www.cdc.gov/ncidod/aip/research/bot.html
  24. ^ Centers for Disease Control and Prevention (CDC) (2003). "Outbreak of botulism type E associated with eating a beached whale--Western Alaska, July 2002". MMWR Morb. Mortal. Wkly. Rep. 52 (2): 24–6. PMID 12608715. {{cite journal}}: Unknown parameter |month= ignored (help)
  25. ^ Oil Infusions and the Risk of Botulism, Colorado State University Cooperative Extension, Safefood new – Summer 1998 – Vol 2 / No. 4
  26. ^ Centers for Disease Control (CDC) (1985). "Update: international outbreak of restaurant-associated botulism--Vancouver, British Columbia, Canada". MMWR Morb. Mortal. Wkly. Rep. 34 (41): 643. PMID 3930945. {{cite journal}}: Unknown parameter |month= ignored (help)
  27. ^ Government of Western Australia. Department of Health. Public Health Botulism Fact Sheet
  28. ^ U.S. Food and Drug Administration. "Bad Bug Book: Foodborne Pathogenic Microorganisms and Natural Toxins Handbook Clostridium botulinum". Retrieved 12 January 2013.
  29. ^ Brook I (2007). "Infant botulism". J Perinatol. 27 (3): 175–80. doi:10.1038/sj.jp.7211651. PMID 17314986. {{cite journal}}: Unknown parameter |month= ignored (help)
  30. ^ Shapiro RL, Hatheway C, Swerdlow DL (1998). "Botulism in the United States: a clinical and epidemiologic review". Ann. Intern. Med. 129 (3): 221–8. doi:10.1059/0003-4819-129-3-199808010-00011. PMID 9696731. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  31. ^ Brook I. Botulism: the challenge of diagnosis and treatment. Rev Neurol Dis. 2006;3:182-9.
  32. ^ "HHS Awards BioShield Contract For Botulism Antitoxin". HHS Archive. Department of Health and Human Services. June 1, 2006. Retrieved July 2, 2011.
  33. ^ Sobel, Jeremy (September 2004). "Foodborne Botulism in the United States, 1990–2000". Centers for Disease Control. Retrieved September 29, 2010Template:Inconsistent citations {{cite journal}}: Cite journal requires |journal= (help)CS1 maint: postscript (link)
  34. ^ Passaro DJ, Werner SB, McGee J, Mac Kenzie WR, Vugia DJ (1998). "Wound botulism associated with black tar heroin among injecting drug users". JAMA. 279 (11): 859–63. doi:10.1001/jama.279.11.859. PMID 9516001. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  35. ^ William Terranova Joel G. Breman, Robert P. Locey (Director) and Sarah Speck Botulism type B: Epidemiologic Aspects of an Extensive Outbreak
  36. ^ *A Large Outbreak of Botulism: The Hazardous Baked Potato Frederick J. Angulo, Jonathan Getz, Jeffery P. Taylor, Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, Centers forKatherine A. Hendricks, Charles L. Hatheway,* Disease Control and Prevention, Atlanta, Georgia; Bureaus of Suzanne S. Barth, Haim M. Solomon, Ann E. Larson, Communicable Disease Control and Laboratories, Texas Department of Eric A. Johnson, Laurance N. Nickey, and Allen A. Ries Health, Austin, and El Paso City-County Health and Environmental District, El Paso, Texas; Division of Microbiological Studies, Food and Drug Administration, Washington, DC; Food Research Institute, University of Wisconsin, Madison, Wisconsin
  37. ^ Humeau Y, Doussau F, Grant NJ, Poulain B (2000). "How botulinum and tetanus neurotoxins block neurotransmitter release". Biochimie. 82 (5): 427–46. doi:10.1016/S0300-9084(00)00216-9. PMID 10865130. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

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