AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Follow-up
• Miscellaneous
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INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Botulism is an acute neurologic disorder with potentially life-threatening neuroparalysis that is caused by a neurotoxin produced by Clostridium botulinum (CB). The toxin binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions. Toxin binding blocks acetylcholine release, resulting in weakness, flaccid paralysis, and (often) respiratory arrest. Cure occurs following sprouting of new nerve terminals.

The 3 main clinical presentations of botulism include infant, food-borne, and wound. Additionally, because of the potency of the toxin, the possibility of botulism as a bioterrorism agent or biological weapon is a great concern.

Infant botulism (IB) arises from ingested botulism spores that germinate in the intestine and produce toxin. These spores typically come from bee honey or the environment. Most infants fully recover with supportive treatment; the infant mortality rate is less than 1%. Improperly canned or home-prepared foods are common sources of the toxin that can result in food-borne botulism (FBB). Wound botulism (WB) results from contamination of the wound with toxin-producing CB. FBB and WB occur predominantly in adults and are the focus of this article.

CB is an anaerobic gram-positive rod that survives in soil and marine sediment by forming spores. Under anaerobic conditions that permit germination, it synthesizes and releases a potent exotoxin. Microbiologically, the organism stains gram-positive in cultures less than 18 hours old. The organism may stain gram-negative after 18 hours of incubation, potentially complicating attempts at diagnosis. On a molecular weight basis, botulinum toxins are the most potent toxins known.

Eight antigenically distinct CB toxins are known, including A, B, C (alpha), C (beta), D, E, F, and G. Each strain of CB is limited to producing a single toxin type. Types A, B, E, and (rarely) F cause human disease. Toxins A and B are the most potent, and the consumption of small amounts of food contaminated with them has resulted in full-blown disease. During the last 20 years, toxin A has been the most frequent cause of food-borne outbreaks; toxins B and E follow in frequency. In 15% of CB outbreaks, the toxin type is not determined. Toxins C and D cause disease in a variety of animals. Type G toxin has been associated with sudden death but not with neuroparalytic illness. It was isolated from autopsy material from 5 patients in Switzerland in 1977.

Pathophysiology

The mechanism of action involves toxin-mediated blockade of neuromuscular transmission in cholinergic nerve fibers. This is accomplished by either inhibiting acetylcholine release at the presynaptic clefts of the myoneural junctions or by binding acetylcholine itself. Toxins are absorbed from the stomach and small intestine where they are not denatured by digestive enzymes. Subsequently, they are hematogenously disseminated and block neuromuscular transmission in cholinergic nerve fibers. The nervous, gastrointestinal, endocrine, and metabolic systems are predominantly affected. Because the motor end plate responds to acetylcholine, botulinum toxin ingestion results in hypotonia that manifests as descending symmetric flaccid paralysis and is usually associated with gastrointestinal symptoms of nausea, vomiting, and diarrhea. Cranial nerves are affected early in the course of disease. Later complications include paralytic ileus, severe constipation, and urinary retention.

WB results when wounds are contaminated with CB spores. It has occurred (1) after traumatic injury that involved soil contamination, (2) among injection drug users, particularly those who use black-tar heroin, and (3) after cesarean delivery. The wound may appear deceptively benign. Traumatized and devitalized tissue provides an anaerobic medium for the spores to germinate into vegetative organisms and produce neurotoxin, which then disseminates hematogenously. The nervous, endocrine, and metabolic systems are predominantly affected. Symptoms develop after an incubation period of 4-14 days, with a mean of 10 days. The clinical symptoms of WB are similar to those of FBB except that gastrointestinal symptoms (including nausea, vomiting, diarrhea) are uncommon.

Frequency

United States

The frequency is 0.034 cases out of 100,000 population, of which nearly 75% are associated with IB.

FBB incidences total 24 cases per year. WB incidences total 3 cases per year and 3 cases per year from the young adult cohort (aged 18-25 y). IB incidences total 71 cases per year, with a mean age of 3 months. FBB incidence totals 24 cases per year drawn from all age cohorts.

Toxin A is found predominantly west of the Mississippi River. Toxin B is found most commonly in the eastern United States. Toxin E is found in northern latitudes, such as the Pacific Northwest, the Great Lakes region, and Alaska. The native peoples have some of the highest rates of botulism in the world. Toxin E outbreaks frequently are associated with fish products.

International

Human botulism is found worldwide. Spores from organisms producing type A or B toxins are distributed widely in the soil and have been found throughout the world. Toxin type B commonly is found in Europe. Toxin G originally was isolated in Switzerland.

Mortality/Morbidity

• Mortality rates vary according to age of the patient and the type of botulism observed. In FBB, a 25% mortality rate exists overall; however, the rate is 10% in patients younger than 20 years. In WB, the mortality rate varies (15-17%); in IB, the mortality rate usually is less than 1%.
• The recovery period from botulism often is quite long (30-100 d). Some patients demonstrate residual weakness or autonomic dysfunction for 1 year after the onset of the illness. However, full neurologic recovery is usual. Permanent deficits may occur in those who sustain significant hypoxic insults.

Sex

Males present more frequently with WB than females. Males and females present with FBB in equal numbers.

Age

FBB and WB predominately occur in adults.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
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• Follow-up
• Miscellaneous
• Multimedia
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History

With the onset of symptoms, the disease quickly develops over several days. The magnitude of the neuromuscular impairment can advance hourly. Stabilization then occurs with subsequent recovery over a period of days to months. The mechanism of recovery is not fully understood but requires the generation of new presynaptic axons and the formation of new synapses because the original synapses are affected permanently. As with tetanus, recovery from botulism does not confer long-term immunity. Rare examples of a second episode in the same patient have been reported.

• Food-borne botulism
• • The diagnosis of FBB should be suspected in a patient who presents with an acute gastrointestinal illness associated with neurologic symptoms. Symptoms usually appear within 12-36 hours following consumption of contaminated food products. The severity of the illness varies from mild to severe, but death can occur within 24 hours.
  • Incubation periods usually are 18-36 hours. Depending on toxin dose, the incubation period ranges from 2 hours to 8 days. The onset of symptoms can be abrupt or can evolve over several days.
• Wound botulism
• • Patients with WB typically have a history of traumatic injury with wounds that are contaminated with soil.
  • Since 1994, the number of patients with WB and a history of chronic intravenous drug abuse has increased dramatically. In most cases, black tar heroin has been the implicated vehicle.
  • Rare cases of WB after cesarean delivery are documented.
  • WB is similar to FBB except that the incubation period is longer. Usually, the incubation period is 4-14 days, with a mean of 10 days. Unlike FBB, no gastrointestinal symptoms are involved with WB. Patients may be febrile, but this is more likely due to the wound infection rather than the WB syndrome. Often, the wound appears quite benign.

Physical

Over 90% of patients have 3-5 of the following signs or symptoms: nausea, vomiting, dysphagia, diplopia, dilated/fixed pupils, and an extremely dry mouth unrelieved by drinking fluids.

• Generally, the progression of the disease is as follows:
• • Preceding or following the onset of paralysis are nonspecific findings such as nausea, vomiting, abdominal pain, malaise, dizziness, dry mouth, dry throat, and, occasionally, sore throat. Except for nerves I and II, the cranial nerves are affected first.
  • Cranial nerve paralysis presents with blurred vision, diplopia, ptosis, extraocular muscle weakness or paresis, fixed/dilated pupils, dysarthria, dysphagia, and/or suppressed gag reflex. Additional neurologic manifestations include symmetric descending paralysis or weakness of motor and autonomic nerves.
  • Respiratory muscle weakness may be subtle or progressive, advancing rapidly to respiratory failure. Progressive muscle weakness occurs and often involves the muscles of the head and neck as well as intercostal diaphragmatic muscles and those of the extremities.
• The autonomic nervous system also is involved. Manifestations of this include the following:
• • Paralytic ileus advancing to severe constipation
  • Gastric dilation
  • Bladder distention advancing to urinary retention
  • Orthostatic hypotension
  • Reduced salivation
  • Reduced lacrimation
• Other neurologic findings include the following:
• • Changes in deep tendon reflexes, which may be either intact or diminished
  • Incoordination due to muscle weakness
  • Absence of pathologic reflexes and normal sensory and gait examinations
  • Normal results on mental status examination
• Many patients with FBB and WB are afebrile.

Causes

• WB is documented after traumatic injury involving contamination with soil, in people who chronically abuse intravenous drugs (eg, black tar heroin), and after cesarean delivery. WB illness can occur even after antibiotics are administered to prevent wound infection.
• FBB results from the ingestion of preformed neurotoxins; A, B, and E are the most common. On the average, approximately 24 cases of FBB are reported annually.
• • High-risk foods include home-canned or home-processed low-acid fruits and vegetables; fish and fish products; and condiments, such as relish and chili peppers.
  • Commercially processed foods and improperly handled fresh foods occasionally cause outbreaks of botulism.
  • Outbreaks in restaurants, schools, and private homes have been traced to uncommon sources, such as commercial pot-pies, baked potatoes, beef stew, turkey loaf, sautéed onions, chopped garlic in oil, and cheese sauce.

DIFFERENTIALS

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Other Problems to be Considered

The diseases most frequently confused with botulism are those that produce generalized weakness. Differentiating botulism from other diseases is essential for early initiation of therapy. A diagnosis of botulism should be considered in patients who are afebrile and mentally intact and who have symmetric descending paralysis without sensory findings. The diagnosis should be suspected on clinical grounds in the context of an appropriate history. Other conditions often confused with botulism include the following:

• Guillain-Barré syndrome
• Fisher variant of Guillain-Barré syndrome
• Myasthenia gravis
• Lambert-Eaton syndrome
• Poliomyelitis
• Tick paralysis
• Cerebrovascular disease of the brainstem
• Basilar artery stroke
• Encephalitis
• Diphtheria
• Neurasthenia
• Progressive external ophthalmoplegia
• Intracranial mass lesions
• Drugs, penicillamine
• Aminoglycosides: Very large doses can induce neuromuscular blockade.
• Poisonings by atropine, scopolamine, organophosphate insecticides, shellfish, amanita mushrooms, carbon monoxide, methyl alcohol, methyl chloride, and sodium fluoride
• Congenital neuropathy or myopathy

WORKUP

Section 5 of 11  

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Lab Studies

• Laboratory tests are not helpful in the routine diagnosis of botulism.
• White blood cell counts and erythrocyte sedimentation rates are normal.
• Cerebrospinal fluid is normal, except for occasional mild elevations in protein concentration.
• A mouse neutralization bioassay confirms botulism by isolating the botulism toxin.
• Toxin may be identified in serum, stool, vomitus, gastric aspirate, and suspected foods. CB may be grown on selective media from samples of stool or foods. Note that the specimens for toxin analysis should be refrigerated, but culture sample for CB should not be refrigerated.
• Because intestinal carriage is rare, identifying the organism or its toxin in vomitus, gastric fluid, or stool is strongly suggestive of the diagnosis.
• • Isolation of the organism from food without toxin is insufficient grounds for the diagnosis.
  • Only experienced personnel who have been immunized with botulinum toxoid should handle the specimens.
  • Because the toxin may enter the blood stream through the eye or via small breaks in the skin, precaution is warranted.
• For WB, wound cultures that grow the organism are suggestive of botulism.

Imaging Studies

• Imaging studies generally are not useful in the diagnosis of botulism.
• The only potential role for imaging studies (eg, CT scan, MRI) would be to rule out central nervous system (CNS) pathology, such as intracranial mass lesions, cerebrovascular disease of the brainstem, or basilar artery stroke, in patients in whom the presentation is atypical or vague.

Other Tests

• Mild nonspecific electrocardiogram abnormalities may occur.
• Results from nerve conduction studies are normal, and electromyography (EMG) reveals reduced amplitude of compound muscle action potentials.
• EMG may be useful in establishing a diagnosis of botulism, but the findings can be nonspecific and nondiagnostic, even in severe cases.
• • Characteristic findings in patients with botulism include brief low-voltage compound motor-units, small M wave amplitudes, and overly abundant action potentials. An incremental increase in M wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction.
  • Single fiber EMG may be a more useful and sensitive method for the rapid diagnosis of botulism intoxication, particularly when signs of general muscular weakness are absent.
• The results of the edrophonium chloride, or Tensilon, test for myasthenia gravis may be falsely positive in botulism. If positive, it typically is much less dramatically positive than in patients with myasthenia gravis.

TREATMENT

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Medical Care

• Rigorous and supportive care is essential for patients with botulism.
• Meticulous airway management is paramount, and respiratory failure is the most important threat to survival in patients with botulism.
• • Patients with symptoms or known exposure should be hospitalized and observed closely.
  • Sequential determinations of spirometry, pulse oximetry, vital capacity, and arterial blood gases should be made.
  • Respiratory failure can occur with unexpected rapidity.
  • Intubation and mechanical ventilation should be strongly considered when the vital capacity is less than 30% of predicted, especially when paralysis is progressing rapidly and hypoxemia with hypercarbia is present.
  • Many patients require intubation and ventilatory support for a few days to months.
  • Tracheostomy may prove necessary to manage secretions.
• If bowel sounds are present, cathartics and enemas are administered to remove unabsorbed botulinum toxin from the intestine.
• Magnesium salts, citrate, or sulfate, should not be administered because magnesium can potentiate the toxin-induced neuromuscular blockade.
• Stress ulcer prophylaxis also is a standard component of intensive care management.
• If an ileus is present, nasogastric suction and intravenous hyperalimentation are very helpful supportive measures. If no ileus is present, tube feeding can be used for nutritional supplementation.
• Foley catheter often is used for bladder incontinence. This must be monitored conscientiously and changed on a regular basis.
• Reducing the risk of nosocomial infections
• • Close observation for hospital-acquired infections, especially pneumonia (especially aspiration pneumonia) is necessary, as is precaution to prevent aspiration. Typically, aggressive pulmonary toilet with clearance of secretions, ventilatory support, and incentive spirometry are utilized.
  • Close observation for urinary tract infection is essential. Foley catheters should be changed on a regular basis.
  • Meticulous skin care is required to prevent decubital ulcers and skin breakdown.
  • Careful attention to peripheral and central intravenous catheters with regular site rotation to reduce the risks of thrombophlebitis, cellulitis, and line infections should be part of the supportive care.
• Deep venous thrombosis (DVT) prophylaxis also is a standard component of intensive care management.

Surgical Care

WB requires incision and thorough debridement of the infected wound, antitoxin therapy, and high-dose intravenous penicillin.

Consultations

• A nutrition consultation for hyperalimentation and tube feeding recommendations and monitoring should be obtained.
• Physical and occupational therapists are needed to work on range of motion exercises and assisted ambulation as tolerated.
• A psychiatrist and/or a psychologist is recommended for counseling, as needed; patients with prolonged hospitalization, slow recovery, and complications from the disease or from extended hospitalization are at increased risk for depression.
• Pastoral care is recommended, as needed.
• Physical medicine and rehabilitation consultants may be helpful in coordinating long-term rehabilitation planning once sustained recovery has begun.

Diet

• Nasogastric suction and intravenous hyperalimentation are important when an ileus is present. If no ileus is present or when the ileus resolves, tube feeding can be used for nutritional supplementation.
• Oral intake should be reinstituted gradually under the following conditions:
• • Respiratory status is stable without mechanical ventilation.
  • Swallowing safety has been assessed and confirmed with a swallowing study, as appropriate.
  • Ileus has resolved.

Activity

• Bedrest is required initially.
• Increase activity as tolerated.

MEDICATION

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Antibiotics are useful in WB, but they have no role in FBB.

Drug Category: Antibiotics

When botulism occurs from a wound infection, antibiotic therapy and meticulous debridement of the wound are essential.

Drug Name	Chloramphenicol (Chloromycetin)
Description	Alternate to penicillin. Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.
Adult Dose	50 mg/kg/d IV
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	Upon concurrent administration with barbiturates, chloramphenicol serum levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum chloramphenicol levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity; chloramphenicol levels may be increased or decreased
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Use only for indicated infections or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while on therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome)

Drug Name	Clindamycin (Cleocin)
Description	Alternative to penicillin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose	600 mg IV q8h
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
Interactions	Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Drug Category: Antitoxins

Essential in FBB and WB. Trivalent A-B-E antitoxin is available at the Centers for Disease Control and Prevention (CDC). The CDC phone numbers are 404-639-3670 or 639-2888 or 639-3753. Polyvalent antitoxin for toxins A, B, C, D, E, and F also is available for specific outbreaks. Because only equine antitoxin is available, all patients must be tested for hypersensitivity to equine serum. Twenty percent of patients will experience some degree of serum sickness or hypersensitivity reaction, and anaphylaxis also can occur. Patients who react to a test dose must be desensitized. Because of risk of adverse reactions, prophylactic antitoxin is not recommended for patients who are exposed to botulism toxin but who have no symptoms. These patients may undergo gastric lavage or induced vomiting in an attempt to eliminate the toxin prior to absorption.

FOLLOW-UP

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Further Inpatient Care

• Recovery of ventilatory and upper airway muscle strength in patients who develop respiratory failure is most significant over the first 12 weeks. The time for recovery typically ranges from 30-100 days. Artificial respiratory support may be required for months in severe cases.

Further Outpatient Care

• The most significant improvements in ventilatory and upper airway muscle strength occur over the first 12 weeks, and, in some patients, recovery may not be complete for as long as a year. Close follow-up is crucial.
• Follow-up with other consultants, such as physical medicine and rehabilitation, physical and occupational therapy, nutrition, and psychiatry, should be obtained as needed.

In/Out Patient Meds

• When botulism occurs from a wound infection, antibiotic therapy and meticulous debridement of the wound are essential.
• • Penicillin is the drug of choice.
  • Clindamycin and chloramphenicol are reasonable second-line agents.

Transfer

• Transfer is indicated if the patient's condition continues to deteriorate or if the initial hospital is unable to manage the complexities involved.

Deterrence/Prevention

• Prompt notification of public health authorities regarding a suspected case of botulism may prevent further consumption of a contaminated home-canned or commercial food product.
• FBB is best prevented by strict adherence to recommended home-canning techniques. High-temperature pressure cooking is essential to ensure spore elimination from low-acid fruits and vegetables. Although boiling for 10 minutes will kill bacteria and destroy the heat labile botulism toxin, the spores are resistant to heat and can survive boiling for 3-5 hours. Food contaminated by botulism toxins usually has a putrefactive odor; however, contaminated food also may look and taste completely normal. Hence, terminal heating of toxin-containing food can prevent illness and is an important preventive measure.
• WB due to intravenous drug abuse can be prevented by cessation of drug use.
• WB is best prevented by prompt, thorough debridement of contaminated wounds. Prophylactic use of antibiotics after trauma cannot be relied upon to prevent WB.

Complications

• Nosocomial infections
• • Hospital-acquired pneumonia, especially aspiration pneumonia, can occur. Atelectasis and poor secretion clearance also increase the risk of hospital-acquired pneumonia.
  • Urinary tract infection can occur from in-dwelling Foley catheters.
  • Skin breakdown and decubiti formation can occur.
  • Thrombophlebitis, cellulitis, and line infections can occur. These patients often have peripheral and central intravenous catheters for prolonged periods.
  • Fungal infections can occur; the predisposing factors are prolonged hospitalization, parenteral nutrition, and central venous catheters. DVT prophylaxis is essential to reduce the risk of these potential complications. DVT and pulmonary embolism (PE) are potential complications because patients can be bedridden for weeks to months.
  • Stress ulcers can occur and are common in the intensive care unit setting. Stress ulcer prophylaxis is essential to reduce the risk of this potential complication.
• Hypoxic tissue damage can lead to permanent neurologic deficits.
• Death

Prognosis

• Type A disease generally is more severe than type B or E.
• The mortality rate from botulism is higher among patients older than 60 years, as compared to younger patients. FBB mortality is 25%, except for patients younger than 20 years who have a mortality rate near 10%.
• The time for recovery typically ranges from 30-100 days. Artificial respiratory support may be required for months in severe cases. Full neurologic recovery usually occurs. Hypoxic insults, though infrequent, can result in permanent deficits. Some patients experience residual weakness and autonomic dysfunction for as long as a year after disease onset.
• Mortality is due to the following:
• • Delayed diagnosis and respiratory failure
  • Hospital complications such as nosocomial infections (usually pneumonia)

Patient Education

• When preserving food at home, kill C botulinum spores by pressure cooking at 250°F (120°C) for 30 minutes.
• • The toxin can be destroyed by boiling for 10 minutes or cooking at 175°F (80°C) for 30 minutes.
  • Do not eat or taste food from bulging cans, or, if food smells bad, discard it.
• Cessation of intravenous drug use prevents wound botulism due to this vehicle.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Incorrect diagnosis can lead to potential medical and legal problems. The diseases most frequently confused with botulism are those that produce generalized weakness.
• Botulism must be considered in patients who are afebrile and mentally intact and who have symmetric descending paralysis without sensory findings. The diagnosis must be suspected on clinical grounds in the context of an appropriate history.
• Incorrect diagnosis leads to inadequate treatment, as does failure to recognize the need for antitoxin therapy for cases of FBB and WB.
• Inadequate treatment greatly increases the risk of death.
• If death occurs due to failure to make the correct diagnosis, both the physician and hospital may be liable for medical malpractice.
• Failure to adequately debride the wound or administer penicillin in cases of WB is a potential pitfall.

MULTIMEDIA

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• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Bioterrorist Agents. Signs and symptoms. Chart courtesy of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright University of North Carolina at Chapel Hill, www.unc.edu/depts/spice/bioterrorism.html.
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REFERENCES

Section 11 of 11

• Authors and Editors
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• Follow-up
• Miscellaneous
• Multimedia
• References

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• Slater PE, Addiss DG, Cohen A, et al. Foodborne botulism: an international outbreak. Int J Epidemiol. Sep 1989;18(3):693-6. [Medline].
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• St Louis ME, Peck SH, Bowering D, et al. Botulism from chopped garlic: delayed recognition of a major outbreak. Ann Intern Med. Mar 1988;108(3):363-8. [Medline].
• Varma JK, Katsitadze G, Moiscrafishvili M, et al. Signs and symptoms predictive of death in patients with foodborne botulism--Republic of Georgia, 1980-2002. Clin Infect Dis. Aug 1 2004;39(3):357-62. [Medline].
• Weber JT, Goodpasture HC, Alexander H, et al. Wound botulism in a patient with a tooth abscess: case report and review. Clin Infect Dis. May 1993;16(5):635-9. [Medline].
• Wilcox PG, Morrison NJ, Pardy RL. Recovery of the ventilatory and upper airway muscles and exercise performance after type A botulism. Chest. Sep 1990;98(3):620-6. [Medline].

Article Last Updated: Apr 26, 2006