bacteria. the spores require warm temperatures, a protein source, an anaerobic 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, but 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. botulinum inhibits the release within the nervous system of acetylcholine, a neurotransmitter, responsible for communication between motor neurons and muscle cells. all forms of botulism lead to paralysis that typically starts with the muscles of the face and then spreads towards the limbs. in severe forms, botulism 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 identify the source and take steps to prevent further cases from occurring. botulinum toxin a, c, and e cleave the snap-25, ultimately leading to paralysis. diagnosis for botulism in babies, diagnosis should be made on signs and symptoms. confirmation of the diagnosis is made by testing of a stool or enema specimen with the mouse bioassay. in people whose history and physical examination suggest botulism, 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. prevention although the vegetative form of the bacteria is destroyed by boiling, 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. a recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. in older children and adults the normal intestinal bacteria suppress development of c. botulinum. while commercially canned goods are required to undergo a "botulinum cook" in a pressure cooker at 121 °c (250 °f) for 3 minutes, and thus rarely cause botulism, there have been notable exceptions. two were the 1978 alaskan salmon outbreak and the 2007 castleberry's food company outbreak. foodborne botulism is the rarest form, accounting for only around 15% of cases (us) and has more frequently resulted 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. other, much rarer sources of infection (about every decade in the us) include garlic or herbs stored covered in oil without acidification, chili peppers, improperly handled baked potatoes wrapped in aluminum foil, tomatoes, and home-canned or fermented fish. when canning or preserving food at home, attention should be paid to hygiene, pressure, temperature, refrigeration and storage. when making home preserves, only acidic fruit such as apples, pears, stone fruits and berries should be used. tropical fruit and tomatoes are low in acidity and must have some acidity added before they are canned. low-acid foods have ph values higher than 4.6. they include red meats, seafood, poultry, milk, and all fresh vegetables except for most tomatoes. most mixtures of low-acid and acid foods also have ph values above 4.6 unless their recipes include enough lemon juice, citric acid, or vinegar to make them acidic. acid foods have a ph of 4.6 or lower. they include fruits, pickles, sauerkraut, jams, jellies, marmalades, and fruit butters. although tomatoes usually are considered an acid food, some are now known to have ph values slightly above 4.6. figs also have ph values slightly above 4.6. therefore, if they are to be canned as acid foods, these products must be acidified to a ph of 4.6 or lower with lemon juice or citric acid. properly acidified tomatoes and figs are acid foods and can be safely processed in a boiling-water canner. 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. metal cans containing food in which bacteria are growing may bulge outwards due to gas production from bacterial growth or the food inside may be foamy or have a bad odor; cans with any of these signs 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 be discarded. contamination of a canned food solely with c. botulinum may not cause any visual defects to the container, such as bulging. only assurance of sufficient thermal processing during production, and absence of a route for subsequent contamination, should be used as indicators of food safety. the addition of nitrites and nitrates to processed meats such as ham, bacon, and sausages reduces growth and toxin production of c. botulinum. vaccine vaccines are under development, but they have disadvantages, and in some cases there are concerns that they may revert to dangerous native activity. as of 2017 work to develop a better vaccine was being carried out, but the us fda had not approved any vaccine against botulism. treatment botulism is generally treated with botulism antitoxin and supportive care. supportive care for botulism includes monitoring of respiratory function. respiratory failure due to paralysis may require mechanical ventilation for 2 to 8 weeks, plus intensive medical and nursing care. after this time, paralysis generally improves as new neuromuscular connections are formed. in some abdominal cases, physicians may try to remove contaminated food still in the digestive tract by inducing vomiting or using enemas. wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. antitoxin botulinum antitoxin consists of antibodies that neutralize botulinum toxin in the circulatory system by passive immunization. this prevents additional toxin from binding to the neuromuscular junction, but does not reverse any already inflicted paralysis. in adults, a trivalent antitoxin containing antibodies raised against botulinum toxin types a, b, and e is used most commonly; however, a heptavalent botulism antitoxin has also been developed and was approved by the u.s. fda in 2013. in infants, horse-derived antitoxin is sometimes avoided for fear of infants developing serum sickness or lasting hypersensitivity to horse-derived proteins. to avoid this, a human-derived antitoxin has been developed and approved by the u.s. fda in 2003 for the treatment of infant botulism. this human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism. however, the danger of equine-derived antitoxin to infants has not been clearly established, and one study showed the equine-derived antitoxin to be both safe and effective for the treatment of infant botulism. trivalent (a,b,e) botulinum antitoxin is derived from equine sources utilizing whole antibodies (fab and fc portions). in the united states, this antitoxin is available from the local health department via the cdc. the second antitoxin, heptavalent (a,b,c,d,e,f,g) botulinum antitoxin, is derived from "despeciated" equine igg antibodies which have had the fc portion cleaved off leaving the f(ab')2 portions. this less immunogenic antitoxin is effective against all known strains of botulism where not contraindicated. prognosis the paralysis caused by botulism can persist for two to eight weeks, during which supportive care and ventilation may be necessary to keep the patient alive. botulism can be fatal in five to ten percent of people who are affected. however, if left untreated, botulism is fatal in 40 to 50 percent of cases. infant botulism typically has no long-term side effects but can be complicated by treatment-associated adverse events. the case fatality rate is less than two percent for hospitalized babies. epidemiology globally, botulism is fairly rare, with approximately 1,000 identified cases yearly. united states in the united states an average of 145 cases are reported each year. of these, roughly 65% are infant botulism, 20% are wound botulism, and 15% are foodborne. infant botulism is predominantly sporadic and not associated with epidemics, but great geographic variability exists. from 1974 to 1996, for example, 47% of all infant botulism cases reported in the u.s. occurred in california. between 1990 and 2000, the centers for disease control and prevention reported 263 individual foodborne cases from 160 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 events (~69%) with canned asparagus being the most frequent cause. two restaurant-associated outbreaks affected 25 people. 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. 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. all data regarding botulism antitoxin releases and laboratory confirmation of cases in the us are recorded annually by the centers for disease control and prevention and published on their website. on 2 july 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. between 31 march and 6 april 1977, 59 individuals developed type b botulism. all who fell ill had eaten at the same mexican restaurant in pontiac, michigan, and had consumed a hot sauce made with improperly home-canned jalapeño peppers, either by adding it to their food, or by eating nachos that had been prepared with the hot sauce. the full clinical spectrum (mild symptomatology with neurologic findings through life-threatening ventilatory paralysis) of type b botulism was documented. in april 1994, the largest outbreak of botulism in the united states since 1978 occurred in el paso, texas. thirty people were affected; 4 required mechanical ventilation. all ate food from a greek restaurant. the attack rate among people who ate a potato-based dip was 86% (19/22) compared with 6% (11/176) among people who did not eat the dip (relative risk = 13.8; 95% confidence interval , 7.6–25.1). the attack rate among people who ate an eggplant-based dip was 67% (6/9) compared with 13% (24/189) among people who did not (rr = 5.2; 95% ci, 2.9–9.5). botulism toxin type a was detected in 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. food handlers should be informed of the potential hazards caused by holding foil-wrapped potatoes at ambient temperatures after cooking. in 2002, fourteen alaskans ate muktuk (whale blubber) from a beached whale, resulting in eight of them developing botulism, with two of the affected requiring mechanical ventilation. beginning in late june 2007, 8 people contracted botulism poisoning by eating canned food