1) Specific foods that have been associated with the botulinum toxin include canned corn, peppers, greenbeans, soups, beets, asparagus, mushrooms, ripe olives, spinach, tuna, chicken and chicken livers, liver pate, luncheon meats, ham, sausage, stuffed eggplant, lobster, and smoked and salted fish (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
2) Prepared foods which have been left out of the refrigerator and eaten without sufficient re-heating have also caused botulism (CDC, 1995). Although home preparations remain the major sources of botulism outbreaks, there has been an increase in commercially prepared products resulting in botulism outbreaks. Due to recent changes in methods to preserve food products by using vacuum-packed and refrigerated or heat-treated foods at an inadequate temperature, the development of neurotoxinogenic clostridium has increased in both the US and Europe. In Italy, an outbreak of clostridium occurred in the late 1990's with commercially prepared mascarpone. In the US, outbreaks have occurred in commercially prepared cheese sauce, fish and pate(Abgueguen et al, 2003).
3) CASE REPORT/INFANT: Foodborne botulism occurred in a 6-month-old infant following exposure to improperly prepared home-canned baby food contaminated with Botulinum toxin A (Armada et al, 2003).
4) CASE REPORT: Recurrent botulism (headaches, slurred speech, diplopia and blurred vision, dysphagia, and generalized weakness) was reported in a 71-year-old man who repeatedly consumed homemade hot chili pepper sauce contaminated with botulinum toxin type B (Bilusic et al, 2008).
5) CASE SERIES: Foodborne botulism occurred in 5 patients who consumed roasted home-canned mushrooms. Four of the five patients recovered following symptomatic and supportive treatment. Only one patient received botulinum trivalent antitoxin. The fifth patient developed cardiac arrest and could not be resuscitated (Cengiz et al, 2006).
6) CASE SERIES: Foodborne botulism was identified in 8 patients who consumed commercially canned hot dog chili sauce from June to August, 2007. Three of the patients were from Texas, 3 from Ohio, and 2 from Indiana. Botulinum toxin type A was identified from the left-over chili sauce that was consumed by the two patients from Indiana and from one of the Ohio patients. The median amount of time from symptom onset to clinical diagnosis was 8 days (ranging from 4 to 21 days), with all patients hospitalized and 7 requiring mechanical ventilation. Five of the 8 patients received botulinum antitoxin and there were no deaths reported (Juliao et al, 2013).

1) Over 500 cases of infant botulism have been reported in the US since 1979 (Long, 1985), making it the predominant form of botulism recognized in the US (Bartlett, 1986).
2) It has been estimated that 4% to 13% of all SIDS cases are victims of infant botulism (Jagoda & Renner, 1990).

1) Many infants who have developed botulism have been exposed to honey which commonly contains botulinum spores. Most cases of infant botulism occur in infants 6 months of age or less; susceptibility may decrease as normal flora develops (Abrutyn, 1994).
2) In infant botulism the toxin is produced in and absorbed from the intestine following germination of ingested spores (Abrutyn, 1994). Severity ranges from mild illness to severe paralysis with respiratory failure.
3) The US Center for Disease Control suggests that infants under the age of 6 months not be given honey and the Honey Industry Council extends that limit to one year. Of 20 cases reported to officials during early 1984, 8 had eaten honey, and 6 of the 8 honey samples contained spores (Anon, 1984). Individual cases of infant botulism following ingestion of small amounts of honey have been reported in the literature (Noda et al, 1988; Beushausen et al, 1994).

1) In a prospective study to determine risk factors for infant botulism, the following were observed: for infants 2 months of age and older ingestion of corn syrup (odds ratio = 5.2), breast-feeding (odds ratio = 3.8), and less than one bowel movement/day for at least 2 months (odds ratio = 2.9) were associated with disease (Spika et al, 1989).

1) Infant botulism was confirmed in a 6-week-old infant following ingestion of dark Karo syrup; C. botulinum toxin B was detected in both the syrup and the infant's stool (Maselli et al, 1992).

1) Although honey has been defined as one source of spores, most cases cannot be attributed to a certain food (Hurst & Marsh, 1993; Abrutyn, 1994). Thompson et al (1980) suggested that infant botulism results from infant exposure to air-borne soil containing botulinum spores.

a) ADULT DOSE (17 years of age or greater): One vial, prepared in a 1:10 dilution in NS and administered as an IV infusion, starting at a rate of 0.5 mL/min for the first 30 minutes, then doubling the rate every 30 minutes as tolerated, to a maximum infusion rate of 2 mL/min.
b) CHILDREN (1 to 16 years) GREATER THAN 30 KILOGRAMS: Children receive 20% to 100% of the adult dose based on body weight. For a child more than 30 kg use the following formula: weight (kg) +30 = % of adult dose to administer. Use entire contents of a vial to prepare a 1:10 dilution in NS in an IV bag and then administer the recommended percentage of the prepared product by slow IV infusion beginning at a rate of 0.01 mL/kg/min for first 30 minutes, not to exceed a total rate of 0.5 mL/min. Monitor vital signs, and if tolerated, the infusion rate may be increased by 0.01 mL/kg/min every 30 minutes to a rate of 0.03 mL/kg/min (do not exceed a rate of 2 mL/min).
c) CHILDREN (1 to 16 years) UP TO 30 KILOGRAMS: Children receive 20% to 100% of the adult dose based on body weight. For a child more than 30 kg use the following formula: 2 x weight (kg) = % of adult dose to administer. Use entire contents of a vial to prepare a 1:10 dilution in NS in an IV bag and then administer the recommended percentage of the prepared product by slow IV infusion beginning at a rate of 0.01 mL/kg/min for first 30 minutes, not to exceed a total rate of 0.5 mL/min. Monitor vital signs, and if tolerated, the infusion rate may be increased by 0.01 mL/kg/min every 30 minutes to a rate of 0.03 mL/kg/min (do not exceed a rate of 2 mL/min).
d) INFANT (less than 1 year): Administer 10% of the adult dose (ie, 10% of 1 single-use vial), regardless of body weight. Use entire contents of a vial to prepare a 1:10 dilution in NS in an IV bag and then administer 10% of the prepared product by slow IV infusion beginning at a rate of 0.01 mL/kg/min for the first 30 minutes. Monitor vital signs, and if tolerated, infusion rate may be increased by 0.01 mL/kg/min every 30 minutes to a maximum rate of 0.03 mL/kg/min.

a) WOUND BOTULISM: Standard wound cleaning and surgical debridement of devitalized tissue is required along with antimicrobial therapy.

a) Ocular symptoms (acute presbyopia, mydriasis, diplopia, and dryness of lacrimal secretions) were commonly reported in a retrospective review of 108 cases of type B botulism in France (Roblot et al, 1994).

a) CASE SERIES: A review of botulism surveillance data in California from 1993 to 2006 identified 17 heroin users with recurrent wound botulism. Black tar heroin use was specified in 88% of the users. Fourteen patients reported 1 recurrence and 3 patients reported 2 recurrences. The most common signs and symptoms included visible wound, dysarthria, respiratory distress, diplopia, and dysphagia (Yuan et al, 2011).
b) CASE SERIES: Blurred vision and diplopia were reported in 5 of 8 patients who were associated with a foodborne botulism outbreak following consumption of commercially canned hot dog chili sauce (Juliao et al, 2013).

a) BOTULINUM TOXIN: Ptosis was the most commonly reported side effect (44%) in blepharospasm patients treated with local injection of botulinum toxin type A (Denislic et al, 1994).

a) CASE REPORT: Difficulty swallowing with pain, hoarseness, and generalized weakness were initial complaints of a 31-year-old man with a history of parenteral drug abuse. Signs and symptoms indicated pharyngitis; however, neurological symptoms consistent with botulism developed over the next 24 hours, and the patient was diagnosed with wound botulism. The patient admitted to black tar heroin use (no wound sites were found); serum samples were positive for botulinum toxin serotype A. The patient recovered following antitoxin administration and supportive care (Cohen & Hern, 2000).

a) BOTULINUM TOXIN: Dysphagia was the most commonly reported side effect (29.3%) in torticollis patients treated with local injection of botulinum toxin type A (Denislic et al, 1994).

a) Cardiac arrest may occur in patients with respiratory failure. It is not known whether arrest is secondary to hypoxia or due to a direct effect of botulinum toxin on the myocardium (Frean et al, 2004; Beaty & Graefner, 1977). In one series of patients with type A botulism, cardiac arrest was the cause of death in 7 of 19 patients (Tacket et al, 1984).
b) CASE REPORT: A 25-year-old woman collapsed in her home after consuming roasted home-canned mushrooms suspected to be contaminated with botulinum toxin. The patient developed cardiac arrest at presentation to the emergency department and subsequently died (Cengiz et al, 2006).

a) Experimental and clinical evidence suggests that botulinum toxin may exert a direct cardiac effect. Intraventricular conduction delay, nonspecific ST-T wave changes, and dysrhythmias, including sudden death from ventricular fibrillation, have been reported (Koenig et al, 1967).

a) SUMMARY
b) CASE REPORTS

a) Descending muscle weakness with progressive respiratory weakness is an important clue to the diagnosis, particularly in type A botulism, in which pulmonary involvement is the rule (Schmidt-Nowara et al, 1983). The primary cause of death in botulism patients is respiratory or bulbar paralysis (Sanders et al, 1983). Respiratory weakness may be difficult to detect clinically (Schmidt-Nowara et al, 1983).

a) CASE REPORT: Two children experienced vomiting and abdominal pain approximately 12 hours after consuming a meal of fish packaged in a tin can. Both patients also developed facial and limb muscle weakness, rapidly progressing to respiratory paralysis and cardiac arrest. The 12-year-old girl died on route to the hospital. The 8-year-old boy developed generalized flaccid paralysis and was mechanically ventilated at the hospital. After 10 days of ventilation, with no neurological improvement, respiratory support was removed and brain death was confirmed via an EEG (Frean et al, 2004). It was determined that corrosion damage of the tin can allowed entry of Clostridium botulinum type A toxin to the tinned food.

a) In one outbreak, aspiration pneumonia occurred in 9 of 34 patients (25%), all of whom had a respiratory arrest and were mechanically ventilated (Schmidt-Nowara et al, 1983). In 8 cases, pneumonia occurred before or shortly after intubation, but not during the course of assisted ventilation. The ninth patient developed pneumonia after premature extubation.

a) INFANT

a) Weakness and possible paralysis of the muscles of respiration can result in shortness of breath (Werner & Chin, 1973; Schmidt-Nowara et al, 1983). In one outbreak, 11 of 31 patients (35%) overall and 7 of 11 (64%) who received ventilatory assistance were dyspneic at presentation (Schmidt-Nowara et al, 1983). Shortness of breath can be intensified by activity and relieved by periods of rest (Mann et al, 1981).

a) DYSPNEA: Many patients may experience dyspnea of varying degrees for a year or more after onset of botulism, despite essentially normal pulmonary function. The association between dyspnea and fatigue reported in one series suggested that dyspnea may be due to a residual defect of ventilatory muscle, such as the development of fatigue with sustained respiratory effort (Schmidt-Nowara et al, 1983).
b) COMPLETE ATELECTASIS was reported in an infant exposed to a small amount of honey (Kothare & Kassner, 1995).

a) Systemic neurologic symptoms usually occur within 72 hours of GI symptoms but may be delayed up to 8 days. Early onset of neurologic symptoms, particularly ocular, generally indicates a more severe infection and worse prognosis (Sanders et al, 1983; MacDonald et al, 1985).
b) EARLY EFFECTS: Ocular effects, dizziness, and slurred speech are common (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Bilusic et al, 2008). Slurred speech was reported in 7 of 8 patients who were associated with a foodborne botulism outbreak following consumption of commercially canned hot dog chili sauce (Juliao et al, 2013).
c) Because botulism may occur in a variety of settings, the diagnosis should be suspected in any patient with bilateral descending paralysis, even when traditional epidemiologic features of botulism are absent (MacDonald et al, 1986).
d) Weakness typically spreads symmetrically and in a descending pattern involving the cranial nerves, both upper and lower extremities, and respiratory muscles; sensation is usually intact. The patient remains mentally clear (Sanders et al, 1983; Paterson et al, 1992).
e) Some patients with botulism may have atypical neurologic findings, eg, paresthesias and depressed or absent deep tendon reflexes (Hughes et al, 1981). In type E botulism, GI signs may be more prominent than neurologic signs (Badhey et al, 1986).

a) Respiratory paralysis and failure can occur (Center for Food Safety and Applied Nutrition (CFSAN), 2012; CDC, 1992; Abrutyn, 1994; Anon, 1995), particularly in type A botulism (Frean et al, 2004; Schmidt-Nowara et al, 1983). It has also been reported in a case of infantile type B botulism (Hurst & Marsh, 1993).

a) Seizures have been reported in infant botulism. The authors speculated that seizures occurred secondary to hyponatremia (Schreiner et al, 1991).

a) Dizziness usually is an early complaint, occurring either at the same time as early gastrointestinal and musculoskeletal symptoms or after a 12- to 72-hour delay (Cengiz et al, 2006; Werner & Chin, 1973). Postural dizziness is a relatively frequent symptom resulting from cholinergic blockade (Koenig et al, 1967).

a) In most cases, cranial nerve involvement marks the onset of foodborne botulism (Abrutyn, 1994). Lower cranial nerve involvement with slurring of speech and dysarthria are common early effects (Terranova et al, 1979; Ruthman et al, 1985; Schmidt-Nowara et al, 1983).
b) Unilateral and bilateral cranial nerve palsies have been described with wound botulism (Royl et al, 2007; Horowitz et al, 1998).
c) Cranial neuropathy and descending paralysis was reported in a patient following consumption of botulinum toxin type A-contaminated chili (Kalluri et al, 2003).

a) Oculomotor disturbances, usually bilateral (Werner & Chin, 1973; Terranova et al, 1979), are the earliest definitive symptoms (Werner & Chin, 1973). Extraocular muscle weakness, particularly of the lateral rectus (cranial nerve VI) is common (Terranova et al, 1979).
b) Unilateral and bilateral cranial nerve palsies have been described with wound botulism (Royl et al, 2007; Horowitz et al, 1998).

a) In the later stages weakness of striated muscle groups occurs, especially in the extremities. Weakness typically spreads symmetrically and in a descending pattern involving both the upper and lower extremities (Bilusic et al, 2008; Sanders et al, 1983; Werner & Chin, 1973; Schmidt-Nowara et al, 1983; Ruthman et al, 1985; Terranova et al, 1979). Weakness ranges from mild impairment to complete flaccid paralysis (Royl et al, 2007; Frean et al, 2004; Schaffner, 1985).
b) CASE REPORT: Complete paralysis with hypotonia and areflexia was reported in a 31-year-old woman 68 hours after consuming roasted home-canned mushrooms suspected of being contaminated with Clostridium botulinum. Due to difficulties in procurement, the patient was given one 10-mL vial of trivalent equine antitoxin 96 hours after ingestion. With continued supportive care, the patient gradually regained movement in her arms and legs on day 12 and was able to spontaneously open her eyes on day 15 (Cengiz et al, 2006).
c) Some patients may present with atypical findings, including asymmetric extremity weakness; this occurred in 17% of patients in one outbreak (Hughes et al, 1981) and has been reported with wound botulism (Horowitz et al, 1998).
d) Loss of the gag reflex, lethargy, weak cry, and poor sucking ability are common in infant botulism (Ramroop et al, 2012; Schmidt & Schmidt, 1992; Graf et al, 1992).
e) CASE REPORT: A 6-month-old infant presented to the emergency department with decreased appetite, lethargy, and progressive muscle weakness and hypotonicity, requiring mechanical ventilation. Due to an acute onset of rapidly progressive descending paralysis and a concern for botulism, the patient received human botulism immune globulin. An electromyelogram showed a presynaptic block of neuromuscular transmission, which was consistent with the speculative diagnosis of botulism. Although Clostridium botulinum was not detected in the child's stools on hospital day 1 or from enema fluid on hospital day 5, testing of leftover jars of home-canned baby food detected the presence of botulinum toxin type A. The patient gradually improved and was extubated approximately 6 weeks after hospital admission (Kalluri et al, 2003).
f) CASE REPORT: A 3-day-old infant presented to the emergency department with a 24-hour history of constipation, poor sucking, weak cry, and difficulty in breathing. The infant rapidly developed respiratory failure, necessitating intubation, and a progressive decrease in neurological status with the development of acute flaccid paralysis. Toxin assay and culture of a stool sample indicated the presence of Clostridium baratii type F, confirming the diagnosis of infant botulism. Interview of the mother revealed that symptoms began the day that the infant, who was normally breastfed, was given formula. The infant received botulinum heptavalent antitoxin, resulting in extubation 2 days later and recovery of his reflexes and muscle tone (Al-Sayyed, 2009). The authors thought the source of infection in this case may have been due to environmental factors and might have been related to the father's occupation in construction and working underground.
g) CASE SERIES: An outbreak of foodborne botulism, involving 8 individuals, occurred following consumption of commercially canned hot dog chili sauce. Muscle weakness was reported in all 8 patients (Juliao et al, 2013).

a) CASE REPORT: A 6-year-old child with cerebral palsy developed fever, malaise, choking, constipation, eyelid ptosis, mucous discharge, and an absence of deep tendon reflexes after therapeutic administration of botulinum toxin for treatment of spasticity related to the cerebral palsy. Due to the progressive severity of the patient's symptoms, she was eventually placed on mechanical ventilation (Beseler-Soto et al, 2003). Similar symptoms appeared 5 months previously following a dose of botulinum toxin, but the symptoms were less severe and were thought to be related to a respiratory infection.

a) Babinski sign and other pathologic reflex responses are absent (Werner & Chin, 1973).

a) Somnolence occasionally occurs, but patients are usually alert and oriented. In one outbreak of type B botulism involving 4 patients, all were strikingly somnolent but could be easily aroused (Koenig et al, 1967).

a) The sensory examination in patients with botulism should reveal no deficits (Werner & Chin, 1973; Stahl et al, 1980); however, paresthesias may be a subjective complaint. Paresthesias were present in 14% of patients in one outbreak (Hughes et al, 1981).

a) Bilateral facial nerve palsies have been reported (Paterson et al, 1992; CDC, 1995).
b) Unilateral facial nerve palsy has been described with wound botulism (Horowitz et al, 1998).
c) CASE REPORT: A 3-month-old infant developed progressively worsening lethargy, cough, and stridor, with constipation and clear mucous secretions. A nasal aspirate polymerase chain reaction was positive for respiratory syncytial virus. Although oxygenation improved with supportive care, the patient could not be weaned from ventilation. Seven days post admission, the patient continued to remain ventilated with development of bilateral ptosis and facial diplegia. Suspecting infant botulism, a stool sample was sent for testing, and botulism immune globulin was administered. Two days later, testing of the sample confirmed the presence of Clostridium botulinum toxin type A. Although the patient improved over the next 3 weeks, he continued to have decreased tone, a weak cry, and uncoordinated feeding mechanics at discharge 1 month later (Quinn et al, 2013).

a) BOTULINUM TOXIN TYPE A
b) BOTULINUM TOXIN TYPE B

a) INCIDENCE: Nausea and vomiting are early symptoms occurring in approximately 50% of patients (Kalluri et al, 2003; Beaty & Graefner, 1977; Badhey et al, 1986). Nausea is a rare complaint in type A botulism, occurs variably with type B, and is frequent and severe with type E (Koenig et al, 1967). Although most reports state that GI complaints are rare in cases of type A botulism, one report suggests that GI effects are common (Hughes et al, 1981).
b) CASE REPORT: Nausea, vomiting, and abdominal pain occurred in a 33-year-old man approximately 6 hours after consuming ham contaminated with botulinum toxin type B (Merz et al, 2003).
c) CASE SERIES: An outbreak of foodborne botulism, involving 8 individuals, occurred following consumption of commercially canned hot dog chili sauce. Nausea, vomiting, and abdominal pain were reported in 3, 1, and 1 patient, respectively (Juliao et al, 2013).

a) INCIDENCE: Vomiting occurs in approximately 50% of patients (Beaty & Graefner, 1977). Early regurgitation of gastric contents may remove significant quantities of botulinum toxin (Koenig et al, 1967).
b) CASE REPORT: Two children developed vomiting and abdominal pain 12 hours after consuming a meal of fish packaged in a tin can. Both patients also developed facial and limb muscle weakness, rapidly progressing to respiratory paralysis and cardiac arrest. The 12-year-old girl died on route to the hospital. The 8-year-old boy developed generalized flaccid paralysis and was mechanically ventilated at the hospital. After 10 days of ventilation, with no neurological improvement, respiratory support was removed and brain death was confirmed via an EEG (Frean et al, 2004). It was determined that corrosion damage of the tin can allowed entry of Clostridium botulinum type A toxin to the tinned food.

a) Abdominal pain and constipation are common in adults and infants (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Bilusic et al, 2008; Fenicia et al, 2004; Merz et al, 2003; Beseler-Soto et al, 2003; Kalluri et al, 2003; Werner & Chin, 1973; Schmidt & Schmidt, 1992; Anon, 1995) and can be severe in foodborne illness (Abrutyn, 1994). Abdominal cramps may be an early symptom of foodborne botulism and may occur before or after onset of paralysis (Frean et al, 2004; Sanders et al, 1983; Abrutyn, 1994). Cramping symptoms often last throughout the illness (Sanders et al, 1983).

a) Marked abdominal distention with absent bowel sounds may be present due to paralytic ileus (Werner & Chin, 1973; Schaffner, 1985). GI symptoms are often more prominent in type E botulism (Badhey et al, 1986).

a) Diarrhea has occurred with infant botulism (Hurst & Marsh, 1993).
b) Diarrhea was reported in 44% of patients (n=16) following consumption of botulinum toxin type A-contaminated chili (Kalluri et al, 2003).
c) Diarrhea occurred in 2 of 8 patients involved in a foodborne botulism outbreak following consumption of commercially canned hot dog chili sauce (Juliao et al, 2013).

a) Poor feeding or refusal to feed from 24 to 72 hours has been reported in some cases of pediatric botulism (Ramroop et al, 2012; Beseler-Soto et al, 2003; Hurst & Marsh, 1993; Graf et al, 1992).

a) SUMMARY: The presence of Meckel's diverticulum may be a risk factor in the development of intestinal colonization of the botulinum toxin (Fenicia et al, 1999).

a) BACKGROUND: There are infrequent reports of gastrointestinal colonization by C botulinum spores in adults resulting in cases of adult infectious botulism (the in vivo toxin that is produced is similar to that of infant botulism). Several factors may be related to this form of botulism: gastrointestinal tract abnormalities (eg, achlorhydria), antimicrobial therapy that may disrupt the normal gastrointestinal flora, and a history of abdominal surgery (eg, gastrectomy) (Shapiro et al, 1998; Li et al, 1999).
b) CASE REPORT: A 12-year-old girl was exposed to foodborne Clostridium botulinum type Ab after eating a contaminated canned meat product and developed flaccid quadriplegia. Treatment with botulinum antitoxin (types A-G) was delayed approximately 1 week after exposure, and the patient had a protracted hospital course (discharged to home on hospital day 425). She developed obstinate constipation for more than 6 months. C botulinum type Ab was isolated from the stool specimen on hospital day 122, and toxin was detected in stool but not serum suggesting that the initial foodborne intoxication became intestinal colonization-type botulism. Serum for the patients on hospital day 250 detoxified type A toxin, suggesting she was producing botulinum antitoxin (Kobayashi et al, 2003).
c) CASE REPORT: In a woman with a history of cystic fibrosis (CF), the development of infant botulism was thought to be associated with CF, which can alter GI motility, along with the long-term use of antibiotic therapy (Li et al, 1999).
d) CASE REPORT: A 3-month-old infant with a history of gastrointestinal reflux and constipation developed infant botulism caused by Clostridium botulinum type A with an enterovirus infection. Although the infant was given honey few days before hospitalization, samples of this honey showed 0.2 spores/g of Clostridium botulinum type B, indicating that this food was probably not the source of infection. The authors suggested that an association could exist between the enterovirus-induced alteration of the bowel-mucosal immunity and the susceptibility to C botulinum colonization. In addition, it has been hypothesized that enterovirus may induce modifications of mucin favoring the earlier development of strictly anaerobic strains (Fenicia et al, 2004).

a) Urinary retention is common following foodborne illness (Merz et al, 2003; Abrutyn, 1994) and may result from cholinergic blockade (Koenig et al, 1967). This occurs primarily in type E botulism (Badhey et al, 1986).

a) CASE REPORT: A 33-year-old man experienced erectile dysfunction, as an autonomic symptom, approximately 24 hours after ingesting ham contaminated with botulinum toxin type B. Approximately 10 weeks after onset, the patient's erectile dysfunction improved by 80%, with complete resolution 4 weeks later (Merz et al, 2003).

a) The CDC reports that the number of cases of wound botulism with C botulinum steadily increased in California during the 1990s. Only one case was not related to injection of black tar heroin. Unlike botulinum toxin (inactivated by heat), spores of C botulinum which could be in the heroin or in the liquid (usually water) in which the heroin is dissolved are not destroyed by heating (CDC, 1995).
b) PATHOPHYSIOLOGY: C botulinum spores can germinate in an anaerobic environment with subsequent multiplication of the organism, followed by production and absorption of the toxin in vivo (Shapiro et al, 1998).
c) CLINICAL MANIFESTATIONS: Symptoms appear similar to those seen in foodborne botulism, except that gastrointestinal symptoms are absent. The incubation period is slightly longer (7 days {range 4 to 14 days}) (Shapiro et al, 1998).
d) MORTALITY: A 10% (n=4 patients) fatality rate was reported in a retrospective review of cases of wound botulism (Mechem & Walter, 1994). In another report, case fatality rate has been estimated to be 15% (Shapiro et al, 1998).
e) MORBIDITY: Of the remaining 36 patients, all had significant morbidity requiring prolonged medical treatment (Mechem & Walter, 1994).
f) OTHER SOURCES: Most cases of wound botulism involve type A toxin (MacDonald et al, 1985; Athwal et al, 2001). However, in a recent case report of wound botulism following IV drug abuse, Clostridium perfringens grew from the wound material. Blood cultures were negative for the botulinum toxin. Symptoms were consistent with previous reports of wound botulism (Scheibe et al, 2002).
g) CASE SERIES
h) CASE REPORTS

a) TOOTH ABSCESS: Despite dental treatment a 5-year-old developed ongoing pain and swelling in a molar. Three months after initial treatment, an abscess was drained followed shortly by neurological and respiratory symptoms. A diagnosis of type A botulism was confirmed. The family reported that the child often played in their garden and would then place his dirty hands in his mouth (Weber et al, 1993a).

a) Wound botulism can occur following crush injuries, deep muscle lacerations, or compound fractures treated with open reduction. Fever can be present secondary to abscess or soft tissue infection thought to harbor the clostridial organism (Mechem & Walter, 1994).

a) CASE REPORT: Dry palms and soles were reported in a 33-year-old man who consumed ham contaminated with botulinum toxin type B. Symptoms gradually disappeared within 10 weeks after onset (Merz et al, 2003).

a) Patients with botulism typically experience weakness and fatigue for a long period after illness onset. Weakness may be described as an overall lack of energy, difficulty with self-pacing, and excessive fatigue at the end of the day or week. In some cases, symptoms may reappear if the person becomes fatigued (Mann et al, 1981; Schmidt-Nowara et al, 1983). Patients may report the need to rest periodically during the day and may be unable to return to work (Schmidt-Nowara et al, 1983).

a) A syndrome of inappropriate secretion of antidiuretic hormone has been reported in cases of botulism. All of these patients were on a ventilator when this occurred (Schreiner et al, 1991).

a) Electromyography is useful in confirming the diagnosis (Cherington, 1974; Gutmann et al, 1992).
b) Maselli et al (1992) conducted an in vitro microelectrode study in the case of an infant botulism exposure which indicated that the toxin interferes with the process of synaptic vesicle release following a normal entry of calcium into the motor nerve terminal (Maselli et al, 1992).

a) Experimental and clinical evidence suggests that botulinum toxin may exert a direct cardiac effect. Intraventricular conduction delay, nonspecific ST-T wave changes, and arrhythmias, including sudden death from ventricular fibrillation, have been reported (Koenig et al, 1967).

a) Monitor continuous pulse oximetry and cutaneous pCO2 (this may be the most sensitive indicator of clinical deterioration in infants).
b) Vital capacity and inspiratory force are the most appropriate clinical indexes of pulmonary function in botulism patients as arterial blood gases may show only minor abnormalities despite substantial loss of ventilatory reserve. Patients with a vital capacity of less than 30% predicted are at risk of developing ventilatory failure and require close monitoring. Intubation and assisted ventilation are indicated with a further decline in vital capacity (Schmidt-Nowara et al, 1983).
c) Bedside spirometry to determine FVC and MIF should be considered at the time of admission and sequentially in suspected patients.

a) WOUND CULTURES: Clostridium botulinum, although a fastidious organism, can be found in wound cultures (Burningham, 1992; (Athwal et al, 2000).
b) STOOL: In suspected cases, assay stool for the presence of botulinum toxin and culture for C. botulinum.
c) FOOD: Assay the suspected source for botulinum toxin and culture for C. botulinum.

a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) Theoretically, although activated charcoal actively binds to the C. botulinum, it remains uncertain what clinical effect this treatment would have on the course of the disease, such as interfering with other proteins in the gut which may have denaturing and detoxifying effects on the neurotoxin present.
b) However, based on these results, activated charcoal is recommended for treatment since it may inactivate type A botulinum toxin.

a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) In a review of 55 cases of infant botulism, the following indications were used for endotracheal tube REMOVAL: MIP of more than -25 to -30 centimeters water and vital capacity of more than 10 to 15 milliliters/kilogram; and evidence of gag reflex by the appearance of coughing and swallowing (Schreiner et al, 1991).
b) TRACHEOSTOMY: In a review of 55 cases of infant botulism, the indications for tracheostomy included: expected long intubation period; inability of the infant to maintain the endotracheal tube; lack of improvement after prolonged ventilation; and prevention of subglottic stenosis (Schreiner et al, 1991).

a) Heptavalent botulinum antitoxin (HBAT), containing equine-derived antibody to botulinum toxin types A through G, is approved in the United States for treatment of suspected or documented exposure to botulinum toxin in adult and pediatric patients. To report suspected botulism cases, healthcare providers should call their State Health Department. For assistance in the diagnosis, management, laboratory and epidemiological evaluation of botulism, the State Health Department should call the CDC Emergency Operations Center at 770-488-7100 (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013; Centers for Disease Control and Prevention, 2010).
b) USA: Available from CDC via state and local state health departments. For assistance in the diagnosis, management, laboratory and epidemiological evaluation of botulism, and to obtain antitoxin, the state health department should call 770-488-7100. Antitoxin is released from CDC quarantine stations located in airports throughout the US. States of California and Alaska control release of antitoxin independently of CDC because of the relatively large number of botulism cases in those states and need for local storage of antitoxin in isolated areas of Alaska. In most cases in the US, antitoxin is administered to the patient within 12 hours of decision to release the product.
c) INTERNATIONALLY: The CDC has an agreement with the Pan American Health Organization to supply botulism antitoxin to other countries in the Western Hemisphere (with exception of Canada, which maintains its own supply). There is no reliable source of antitoxin elsewhere in the world.

a) ADULT (17 YEARS OR OLDER): For treatment of symptomatic botulism following suspected or documented exposure to botulinum neurotoxin, the recommended dose in adults is botulism equine heptavalent antitoxin 1 vial prepared in a 1:10 dilution in NS and administered by slow IV infusion at a starting rate of 0.5 mL/min for the first 30 minutes. Monitor vital signs, and if tolerated, infusion rate may be doubled every 30 minutes to a maximum rate of 2 mL/min (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013).
b) CHILD (1 YEAR TO 16 YEARS): For treatment of symptomatic botulism following suspected or documented exposure to botulinum neurotoxin, the recommended dose of botulism equine heptavalent antitoxin in children is a percentage of the adult dose (ie, a percentage of a single-use vial) based on the child's body weight (see table below). Use entire contents of a vial to prepare a 1:10 dilution in NS in an IV bag and then administer the recommended percentage of the prepared product by slow IV infusion beginning at a rate of 0.01 mL/kg/min for first 30 minutes, not to exceed a total rate of 0.5 mL/min. Monitor vital signs, and if tolerated, the infusion rate may be increased by 0.01 mL/kg/min every 30 minutes to a rate of 0.03 mL/kg/min (do not exceed a rate of 2 mL/min). For patients at risk of an acute hypersensitivity reaction, begin administration at the lowest rate achievable (ie, less than 0.01 mL/min) and monitor. If a patient develops discomfort or infusion-related adverse reactions, decrease infusion rate (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013).
c) INFANTS (LESS THAN 1 YEAR): For treatment of symptomatic botulism following suspected or documented exposure to botulinum neurotoxin, the recommended dose of botulism equine heptavalent antitoxin in infants is 10% of the adult dose (ie, 10% of 1 single-use vial), regardless of body weight. Use entire contents of a vial to prepare a 1:10 dilution in NS in an IV bag and then administer 10% of the prepared product by slow IV infusion beginning at a rate of 0.01 mL/kg/min for the first 30 minutes. Monitor vital signs, and if tolerated, infusion rate may be increased by 0.01 mL/kg/min every 30 minutes to a maximum rate of 0.03 mL/kg/min. For patients at risk of an acute hypersensitivity reaction, begin administration at the lowest rate achievable (ie, less than 0.01 mL/min) and monitor. If a patient develops discomfort or infusion-related adverse reactions, decrease infusion rate (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013).

a) Prior to administering any serum or antitoxin, the manufacturer advises that the healthcare provider determine if the patient has a history of asthma or hay fever (especially when near horses), has any known or suspected hypersensitivity to horse serum, or has had prior exposure to horse serum. Patients with such histories are at greater risk of serious anaphylactic reactions if given the heptavalent botulinum antitoxin (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013).

a) Consider performing a skin sensitivity test in patients at risk of acute hypersensitivity reaction (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013):

a) Closely observe for evidence of allergic reaction. Careful observation is particularly important in cases with a history of sensitization.

a) Recently, the increased use of botulinum toxins for the treatment of neurologic diseases, hyperhidrosis and cosmetic purposes has resulted in the development of antibodies to these products (or byproducts (eg, botulinum toxoid)). The existence of antibodies, could potentially interfere with antitoxin efficacy, if treatment became necessary (Gruchalla & Jones, 2003).

a) INDICATIONS
b) RECOMMENDATIONS: Skin testing for hypersensitivity to horse serum should precede antitoxin administration. Review package insert with public health authorities before using antitoxin, as the dose and safety precautions have changed over time (Arnon, 2001, per Working Group on Civilian Biodefense).
c) AVAILABLE FORM: Heptavalent botulinum antitoxin (HBAT), containing equine-derived antibody to botulinum toxin types A through G, is approved in the United States for treatment of suspected or documented exposure to botulinum toxin in adult and pediatric patients (Prod Info BAT Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) Equine intravenous injection solution, 2013; Centers for Disease Control and Prevention, 2010).
d) PRECAUTIONS: Use only in patients who have had sensitivity tests for equine serum. Skin testing for hypersensitivity to horse serum should be done initially; patients who react to this test should be desensitized prior to treatment. During infusion of antitoxin, diphenhydramine and epinephrine should be available for rapid administration in case of adverse reaction.

a) In two reported cases in which it was used, one infant was thought to have foodborne botulism, and the other had an anaphylactic reaction (Arnon, 1980; Johnson et al, 1979).
b) In another case, a 3-day-old infant developed infant botulism caused by Clostridium baratii type F from an uncertain cause (possibly environmental; the father worked in construction (primarily underground)). The patient developed respiratory failure, necessitating intubation, and acute flaccid paralysis. Following administration of botulinum heptavalent antitoxin, the patient was extubated 2 days later with recovery of his reflexes and muscle tone (Al-Sayyed, 2009).

a) The neuromuscular blockade antagonist, 4-aminopyridine has been used in addition to regular supportive care and antitoxin therapy. This agent, however, has shown only a transient improvement in reversing peripheral muscle paralysis, and had no effect at all on respiratory muscle. A constant infusion of 4-aminopyridine did allow prolonged reversal of peripheral paralysis, but caused convulsive phenomena following the treatment (Shi & Wang, 2004; Ball et al, 1979).

a) EFFICACY: Guanidine hydrochloride acts by increasing the release of acetylcholine from nerve endings. Improvement has been seen in approximately 50% of cases, primarily in ocular findings and limb muscles, with minimal or no respiratory improvement (Puggiari & Cherington, 1978). Due to the lack of respiratory improvement, significant nausea and epigastric pain associated with guanidine use, and the lack of a parenteral form, guanidine is rarely used clinically (Goldfrank & Flomenbaum, 1998).
b) Roblot et al (1994) conducted a retrospective review of botulism cases over a 25-year period treated with either serotherapy or guanidine. Guanidine was used in 31% (n=33) of cases and guanidine along with antiserum was used in 29% (n=31) of cases. Intolerance to the therapy was reported in two cases: psychomotor agitation and muscular pain, respectively. Recovery was complete in all cases (Roblot et al, 1994).
c) DOSE: 10 to 35 milligrams/kilogram/day orally in 4 divided doses (Roblot et al, 1994).

a) National Animal Poison Control Center (NAPCC), 1717 S. Philo Road, Suite 36, Urbana, IL 61802.
b) NAPCC is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel, and poison center staff for a fee. A veterinary toxicologist is available for consultation.
c) Two 24 hour phone numbers: (900) 680-0000 or 1-800-548-2423 are available. The charge is $30 per case. The 800 or 900 lines can be charged to a major credit card. 900 lines are billed directly to caller's phone bill. NAPCC will make follow-up calls as needed in critical cases at no extra charge.

a) DECONTAMINATION -
b) EMESIS AND LAVAGE -
c) ACTIVATED CHARCOAL -
d) CATHARTIC

a) DECONTAMINATION
b) EMESIS -
c) ACTIVATED CHARCOAL
d) CATHARTIC

a) HORSES - A recumbent patient should be muzzled to avoid aspiration of food or bedding. A slurry of alfalfa meal, dextrose, cottage cheese, and electrolytes given via nasogastric tube has been used for up to a month for alimentation. Extremely anxious animals may have to be sedated with xylazine or other sedatives (Robinson, 1987).
b) CATTLE - Carbamylcholine has been administered in cattle to stimulate gastrointestinal motility (Beasley et al, 1990).

1) Begin treatment immediately.
2) Do not handle the animal unnecessarily.
3) Sample vomitus, blood, and feces for analysis.
4) Remove the patient and other animals from the source of contamination.
5) Treatment should always be done on the advice and with the consultation of a veterinarian. Additional information regarding treatment of poisoned animals may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
6) ANIMAL POISON CONTROL CENTERS

1) DOGS/CATS
2) RUMINANTS/HORSES/SWINE

1) Treatment is symptomatic and supportive.

1) GENERAL

1) A large outbreak of type C botulism occurred in a herd of cattle in Northern Ireland. 80 of 150 cattle became ill and 68 died. The source of the toxin was traced to the feed, ensiled poultry litter, that contained decomposing poultry carcasses (Neill et al, 1989; McLoughlin et al, 1988).
2) Eight horses on the same farm developed symptoms of bulbar paralysis, and four of these later died. Spoiled alfalfa silage was the source of the illness, and C. botulinum type B toxin was isolated (Haagsma et al, 1990).
3) Type A toxin was isolated from rumen contents of zebu cattle who died in an outbreak of botulism in Brazil. More than 60 animals died after gnawing on bones that contained C. botulinum; cattle will ingest skeletal materials if they are mineral-deprived (Schocken-Iturrino et al, 1990).
4) No source of toxin could be identified in an epidemic of type C botulism among captive baboons in an English safari park. 36 baboons died; the toxin was isolated from gastric contents (Lewis et al, 1990).

1) Vaccination with types B or C toxoid is available for horses and is recommended once yearly in adults living on infected soil. Foals can be protected by inoculating mares three times prior to foaling (Robinson, 1987).