- Email: [email protected]
Wound botulism
CASE REPORT
Wound Botulism From the Department of Emergency Medicine, Division of Toxicology, * and the Department of Microbiology, t Valley Medical Center, FresnoCentral San Joaquin Valley Medical Education Program, University of Cal{fi~rnia, San Francisco School of Medicine; and lhe Fresno Regional Poison Control Center, Fresno Community Hospital; r Cal{Jbrnia. Recdved.]br publication October 18, 1993. Revision received March I l, 1994. AcceptedJor publication March 29, 1994.
Mark D Burningham,MD* Frank G Walter, MD, FACEP* Crawford Mechem, MD* Judy Haber, PhDt Brent R Ekins, PharmD*
Wound botulism is a rare infectious and toxicologic complication of trauma and IV drug abuse. Only 39 cases have been reported in detail in the English literature. This case report describes a patient with wound botulism who presented to four medical facilities before receiving definitive diagnosis and treatment. Although his history and physical examination were consistent with wound botulism, diagnosis and therapy were delayed because this rare disease was not considered initially in the differential diagnosis. Wound botulism should be considered in trauma patients and IV drug abusers who present with cranial nerve palsies and descending paresis.
Presented at the Annual Scient{lic Meeting of the American and Canadian Associations q] Poison Control Centcrs, The American Academy of Clinical Toxicology, and the American Board of Medical ToxicoloGy, Tampa, Florida, September 1992.
[Burningham MD, Walter FG, Mechem C, Haber J, Ekins BR: Wound botulism. Ann EmergMed Becember 1994;24:11841187.]
Copyright 9 by the American College of Emergency Physicians.
Wound botulism can be defined as clinical evidence of botulism following trauma, with a resultant infected wound and no history suggestive of food-borne illness. Colonization of a wound by Clostridium botulinum also can cause symptoms without a clinically apparent infection.2 A detailed history and physical examination are the keys to diagnosing wound botulism and initiating treatment. Wound cultures and serum analysis for botulinum toxin are confirmatory; other tests and laboratory findings are nonspecific. Treatment must be initiated based on a presumptive clinical diagnosis while awaiting definitive laboratory results. Management of the patient with wound botulism involves aggressive ventilatory support, local wound care, and administration of antitoxin. Tetanus prophylaxis and antibiotics also should be considered. This is the 40th case of wound botulism reported in detail in the English literature and the second published case documenting isolation of the botufinum toxin from serum and the bacterium from wound culture in an IV drug abuser. 3,4
1184
INTRODUCTION
ANNALS OF EMERGENCY MEDICINE
24:6
DECEMBER 1994
WOUND
BOTULISM
Burningham et al
CASE REPORT
A 43-year-old IV heroin abuser presented to four separate medical facilities over a 2-week period. He complained of skin abscesses and progressive weakness. He was treated with oral dicloxacillin at the first facility, was discharged without treatment at the second, and received naloxone at the third. He then presented to our emergency department. His complaints included progressive dysphagia, dysarthria, diplopia, and extremity weakness. He denied pain and other symptoms. He was taking 30 mg methadone daily and 500 mg dicloxacillin four times daily as prescribed at his methadone clinic. His medical history was significant for years of IV drug abuse with several previous forearm abscesses. The patient's physical examination revealed blood pressure, 152/80 mm Hg; pulse, 120; respirations, 28; and tympanic temperature, 35.3~ He was dyspneic and unable to sit without assistance. Dysarthria was pronounced, and his gag reflex was minimal. Chest excursion and air movement were poor. Skin abscesses were noted in his right antecubital fossa and left volar forearm. Neurologic examination revealed the patient to be alert and oriented. He had paresis of cranial nerves Ill through VII and IX through XII. Motor function was very weak proximally, with only trace movement of the shoulder, trunk, and pelvic musculature. He was able to move his distal extremities against slight resistance. Sensory function was normal. Coordination was impaired due to weakness. Deep-tendon reflexes were symmetrically diminished but present. Plantar stimulation of the feet resulted in plantar flexion. Significant laboratory findings included arterial blood gases with Pao2, 71 mm Hg; hemoglobin saturation, 93%; Pac%, 46 mm Hg; and pH, 7.33 on room air. His WBC count was 22,300/mm 3. Creatine phosphokinase was 534 U/L. Electrolytes were normal. Gram stains from his abscesses showed no organisms. Cerebral spinal fluid analysis was normal, as were plasma and RBC cholinesterase levels and whole-blood lead levels. Computed tomography of the head, with and without contrast, was normal. Electromyography and nerve conduction studies were performed on distal extremities only and were normal. The patient's weakness did not improve during a Tensilon | (ICN Pharmaceuticals, Costa Mesa, California) test. A presumptive diagnosis of wound botulism was made in the ED. Therapy included 0.5 mL tetanus toxoid IM, 250 units tetanus immune globulin IM, and 4 million units aqueous penicillin G IV The Centers for Disease Control and Prevention and the California Department of
DECEMBER 1994
24:6
ANNALS OF EMERGENCY MEDICINE
Health Services were called to obtain Trivalent (A, B, E) Botulinum Antitoxin (Connaught Laboratories Limited, Willowdale, Ontario, Canada). The patient was taken from the ED to the operating room, where he was intubated and his abscesses were debrided surgically. The botulinum antitoxin was flown in from the San Francisco branch of the Centers for Disease Control and Prevention and arrived after surgery. The patient was given an initial dose of one vial IV and one vial IM. Each vial contains 21,500 IU (type A, 7,500; type B, 5,500; type E, 8,500). This dose was repeated the next day for worsening ptosis and weakness of extraocular muscles. The patient's signs and symptoms stabilized after the second dose. Wound cultures subsequently grew Clostridium botulinum, and serum analysis revealed type A botulinum toxin. The patient was hospitalized I 11 days with 76 days of ventilator support. He was discharged home with a tracheostomy and gastrostomy. He made a full recovery. DISCUSSION C botulinum is an anaerobic, spore-forming, Gram-positive bacterium found in soil. Its toxin, botulin, is a heat-stable, high molecular weight protein. Eight immunologically distinct toxins have been identified, designated A, B, C 1, C2, and D through G. 5,6 All reported cases of wound botulism have involved types A, B, or both. 1 Botulism is a poisoning characterized by cranial nerve paralysis and descending paralysis with sensory sparing. The mechanism of action involves botulinum toxin binding to the distal synaptic cell membrane of cholinergic nerves. The toxin is endocytosed and appears to block the calcium-mediated release of acetylcholine into the synaptic cleft. Nerve function may be impaired for months until new nerve endings regenerate. The blockade is most pronounced in the cranial nerves and muscles of respiration. 6,7 The incubation period between injury and neurologic symptoms has been reported as from 4 to 18 days, with a median of 7 days. 2 A detailed history and physical examination are the keys to diagnosing wound botulism and initiating treatment. The most common symptoms are dyspnea, dysphagia, dysphonia or dysarthria, and diplopia. The most common signs are descending paralysis and respiratory insufficiency. The differential diagnosis for wound botulism includes the following: the Eaton-Lambert syndrome, hypermagnesemia, and aminoglycoside toxicity, s,9 all of which have similar electromyographic findings. 9,w The Miller Fisher variant of the Guillain-Barr~ syndrome, which occurs in
1185
WOUND
BOTULISM
Burningham et al
approximately 4% of patients with the syndrome, is characterized by descending paralysis. 11 Diphtheria must be considered in unimmunized patients. Myasthenia gravis may present with cranial nerve dysfunction that is rapidly reversible with the administration of edrophonium. 12 Tetanus can produce cranial nerve deficits, but affects primarily the central nervous system and produces spasticity 2 Cerebrovascular accidents, especially those affecting the brainstem, produce symptoms that mimic botulism. The rapid onset characteristic of vascular events should distinguish them from the insidious onset of botulism. Tick paralysis generally produces ascending rather than descending paralysis.13 Poliomyelitis presents with a more asymmetric ascending paralysis, often affecting primarily the lower extremities with associated cerebrospinal fluid pleocytosis and modest protein elevation, r Still other causes to be considered in the differential diagnosis include organophosphate and lead poisoning, and paralytic shellfish toxicity with saxitoxin or tetrodotoxin. ~'* Wound cultures and serum assay for botulinum toxin are confirmatory. Other tests and laboratory findings are nonspecific. Isolation of the C botulinum organism is by standard anaerobic culture techniques. The MicroScan WalkAway (Baxter Diagnostics Inc, Deerfield, Illinois), the instrument used in our hospital to identify cultured bacteria, is unable to biochemically distinguish between some species of clostridia and will identify C botulinum as C sporogenes. Therefore, botulism must not be ruled out based on automated wound cultures and identification techniques. The clostridial isolates must be analyzed for botulin. Initial wound Gram stains may provide supportive evidence but will not distinguish C botulinum from other Clostridium species. Electrophysiologic studies may support the diagnosis of botulism but cannot be used to exclude it. Typical electromyographic findings in botulism include diminished response to a single stimulus, but potentiation of the action potential during repetitive stimulation. Only botulism, the Eaton-Lambert syndrome, aminoglycoside toxicity, and hypermagnesemia produce thiselectromyographic constellation. 9J5,16 Other electrophysiologic findings in wound botulism include normal motor conduction velocity, distal motor latencies, and sensory nerve action potentials. 6 The edrophonium test is not definitive in distinguishing wound botulism from other causes of neuromuscular blockade. Of 19 cases in which Tensilon | testing was mentioned, six patients (32%) showed at least partial improvement. 2,1r, t 8 The mainstay of therapy is ventilator,/support; local wound care, including debridement; botulinum antitoxin
1186
administration; and coincidental tetanus prophylaxis. Trivalent (A, B, E) botulinum antitoxin should be administered as soon as possible in cases that are clinically compatible with wound botulism even though results of definitive diagnostic tests will not yet be available. As botulin is produced, it is rapidly and irreversibly bound to cholinergic nerve membranes. Botulinum antitoxin is ineffective once the toxin is endocytosed. 2,16 It binds only to free toxin and therefore can only arrest progression of nerve dysfunction. Timely administration of antitoxin can prevent progression of paralysis while definitive debridement of the organism is pursued. Trivalent (A, B, E) botulinum antitoxin is available on an emergency basis from the Centers for Disease Control and Prevention in Atlanta (404-639-3356, Monday through Friday, 8 AM tO 4:30 PM; or 404-639-2888 after hours and on weekends and holidays). High-dose IV penicillin is recommended by some authors, but there is no evidence that antibiotics affect the disease course or outcome. 1a In fact, wound botulism has been diagnosed twice in patients already taking oral penicillin; our patient was the second.5,18 Sellin 6 raised the theoretical concern that antibiotic-induced cell lysis may increase toxin release. However, penicillin is used commonly to treat other clostridial infections, and its use seems reasonable, especially if the patient has fever, leukocytosis, or cellulitis. Aminoglycosides should be avoided because of the potential for aminoglycoside-induced neuromuscular blockade in these already compromised patients. 19 When appropriate respiratory support is provided, the prognosis for patients with wound botulism is favorable. To date, 4 of 39 (10%) previously published cases resulted in death. While mortality is low, morbidity is pronounced. Ventilator support was required in 23 of the 39 previous cases, ranging from 24 hours to 3 months. Eleven of the 23 patients required ventilator support for 30 days or more. Length of hospitalization among survivors also was protracted, with no patient being discharged in less than 4 weeks. The longest documented hospitalization was for 171 days, 2~ Long-term outcome among survivors is good. Patients with mild cases generally are free of neurologic sequelae in 2 to 3 months. Seriously affected patients may have more gradual resolution of their deficits over a course of months to years. 2~ SUMMARY
Wound botulism is a rare disease with serious morbidity and a 10% mortality rate. Initial diagnosis should be based on history and physical examination, and treatment
ANNALS OF EMERGENCY MEBICINE
2 4 : 6 DECEMBER 1994
WOUND
BOTULISM
Burningham et al
should be initiated without waiting for results of definitive tests. We describe a case that emphasizes that concurrent antibiotic therapy does not preclude the diagnosis. Our patient was taking a course of oral dicloxacillin for skin abscesses when his symptoms began. Wound botulism should be considered when a trauma victim or IV drug abuser develops cranial nerve palsies and descending paralysis.
Reprint no. 47/1/60283 Address for reprints: Mark D Burningham, MD Idaho Emergency Physicians 2312 N Cole, Ste B Boise, Idaho 83704 208-322-1730
REFERENCES 1. MacDonald KL, Cohen ML, Blake PA: The changing epidemiologyof adult botulism in the United States Am J Epidemiol 1986;124:794-799. 2. Merson MH, Dowell VR: Epidemiologic,clinical and laboratoryaspectsof wound botulism. N Engl J Mad 1973;289:1005-1010. 3. E[stonHR, Wang M, Log LL: A~m abscessescaused by Clostridium botulinum. J C/in Micrc;biol 1991:29:2678-2679. 4. Bumingham MD, Walter FG, Mechem CC, et ah Wound botulism. VetHum Toxicol 1992;34:347. 5. SakaguchiG: Clostridium botufinum toxins. Pharmacol Ther1982;19:165-194. 6. Sellin LC: Botulism--An update. Mil Mad 1984;149:12-16. 7. HathawayCL: Toxigenic clostridia. Clin Microbiol Rev 1990;3:66-98. 8. McQuillan MP, Cantor HE, O'RourkeJR: Myastbenic syndromeassociatedwith antibiotics. Arch Neurol 1968;18:402-415. 9. DeJesus PV, Slater R, Spitz LK, et al: Neuromuscularphysiologyof wound botulism. Arch Neurol 1973;29:425-431. 10. Lewis SW, Pierson DJ, CaryJM, et al: Prolongedrespiratoryparalysis in wound botulism. Chest 1979;75:59-61. 11. RodenbergH, Grattoe M, Bennett J, et al: Left upper extremity weakness in an 18-year-old man. Ann EmergMed 1991;20:672-679. 12. SwedbergJ, Wendel TH, Deiss F: Wound botulism. WestJ Med1987;147:335-338. 13. McCarthyJD, FleischmannJ, GeorgeWL: Fever,dyspnea,and slurred speechfollowing lower extremity trauma (clinical conference).Rev Infect Dis 1991;13:172-176. 14. Slovis CM: Food poisoning, in Haddad LM, Winchester JF (eds): Clinical Management of Poisoning andDrug Overdose,ed 2. Philadelphia, WB SoundersCo, 1990, p 612-623. 15. MacDonald KL, Rutherford GW, Friedman SM, et al: Botulism and botulism-like illness in chronic drug abusers.Ann Intern Med 1985;102:616-618. 16. Wapen BD, Gutmann L: Wound botulism: A case report. JAMA 1974;227:1416-1417. 17. Cherington M, Ginsburg S: Wound botulism. Arch Surg 1975;110:436-438. 18. Edell T, Sullivan CP, Osborn KM, et al: Wound botulism associatedwith a positive Tensilon| test. West J Med1983;139:218-219. 19. Santos IS, Swanson P, GlasgowLA: Potentiationof Clostridium botufinum toxin by aminoglycoside antibiotics. Pediatrics 1981;68:50-54. 20. Thorne EL, Kropp RJ: Wound botulism: A life-threateningcomplication of band injuries. Plast Reconstr Surg 1983;71:548-551.
DECEMBER 1994
24:6
ANNALS OF EMERGENCY MEDICINE
1187
Wound Botulism From the Department of Emergency Medicine, Division of Toxicology, * and the Department of Microbiology, t Valley Medical Center, FresnoCentral San Joaquin Valley Medical Education Program, University of Cal{fi~rnia, San Francisco School of Medicine; and lhe Fresno Regional Poison Control Center, Fresno Community Hospital; r Cal{Jbrnia. Recdved.]br publication October 18, 1993. Revision received March I l, 1994. AcceptedJor publication March 29, 1994.
Mark D Burningham,MD* Frank G Walter, MD, FACEP* Crawford Mechem, MD* Judy Haber, PhDt Brent R Ekins, PharmD*
Wound botulism is a rare infectious and toxicologic complication of trauma and IV drug abuse. Only 39 cases have been reported in detail in the English literature. This case report describes a patient with wound botulism who presented to four medical facilities before receiving definitive diagnosis and treatment. Although his history and physical examination were consistent with wound botulism, diagnosis and therapy were delayed because this rare disease was not considered initially in the differential diagnosis. Wound botulism should be considered in trauma patients and IV drug abusers who present with cranial nerve palsies and descending paresis.
Presented at the Annual Scient{lic Meeting of the American and Canadian Associations q] Poison Control Centcrs, The American Academy of Clinical Toxicology, and the American Board of Medical ToxicoloGy, Tampa, Florida, September 1992.
[Burningham MD, Walter FG, Mechem C, Haber J, Ekins BR: Wound botulism. Ann EmergMed Becember 1994;24:11841187.]
Copyright 9 by the American College of Emergency Physicians.
Wound botulism can be defined as clinical evidence of botulism following trauma, with a resultant infected wound and no history suggestive of food-borne illness. Colonization of a wound by Clostridium botulinum also can cause symptoms without a clinically apparent infection.2 A detailed history and physical examination are the keys to diagnosing wound botulism and initiating treatment. Wound cultures and serum analysis for botulinum toxin are confirmatory; other tests and laboratory findings are nonspecific. Treatment must be initiated based on a presumptive clinical diagnosis while awaiting definitive laboratory results. Management of the patient with wound botulism involves aggressive ventilatory support, local wound care, and administration of antitoxin. Tetanus prophylaxis and antibiotics also should be considered. This is the 40th case of wound botulism reported in detail in the English literature and the second published case documenting isolation of the botufinum toxin from serum and the bacterium from wound culture in an IV drug abuser. 3,4
1184
INTRODUCTION
ANNALS OF EMERGENCY MEDICINE
24:6
DECEMBER 1994
WOUND
BOTULISM
Burningham et al
CASE REPORT
A 43-year-old IV heroin abuser presented to four separate medical facilities over a 2-week period. He complained of skin abscesses and progressive weakness. He was treated with oral dicloxacillin at the first facility, was discharged without treatment at the second, and received naloxone at the third. He then presented to our emergency department. His complaints included progressive dysphagia, dysarthria, diplopia, and extremity weakness. He denied pain and other symptoms. He was taking 30 mg methadone daily and 500 mg dicloxacillin four times daily as prescribed at his methadone clinic. His medical history was significant for years of IV drug abuse with several previous forearm abscesses. The patient's physical examination revealed blood pressure, 152/80 mm Hg; pulse, 120; respirations, 28; and tympanic temperature, 35.3~ He was dyspneic and unable to sit without assistance. Dysarthria was pronounced, and his gag reflex was minimal. Chest excursion and air movement were poor. Skin abscesses were noted in his right antecubital fossa and left volar forearm. Neurologic examination revealed the patient to be alert and oriented. He had paresis of cranial nerves Ill through VII and IX through XII. Motor function was very weak proximally, with only trace movement of the shoulder, trunk, and pelvic musculature. He was able to move his distal extremities against slight resistance. Sensory function was normal. Coordination was impaired due to weakness. Deep-tendon reflexes were symmetrically diminished but present. Plantar stimulation of the feet resulted in plantar flexion. Significant laboratory findings included arterial blood gases with Pao2, 71 mm Hg; hemoglobin saturation, 93%; Pac%, 46 mm Hg; and pH, 7.33 on room air. His WBC count was 22,300/mm 3. Creatine phosphokinase was 534 U/L. Electrolytes were normal. Gram stains from his abscesses showed no organisms. Cerebral spinal fluid analysis was normal, as were plasma and RBC cholinesterase levels and whole-blood lead levels. Computed tomography of the head, with and without contrast, was normal. Electromyography and nerve conduction studies were performed on distal extremities only and were normal. The patient's weakness did not improve during a Tensilon | (ICN Pharmaceuticals, Costa Mesa, California) test. A presumptive diagnosis of wound botulism was made in the ED. Therapy included 0.5 mL tetanus toxoid IM, 250 units tetanus immune globulin IM, and 4 million units aqueous penicillin G IV The Centers for Disease Control and Prevention and the California Department of
DECEMBER 1994
24:6
ANNALS OF EMERGENCY MEDICINE
Health Services were called to obtain Trivalent (A, B, E) Botulinum Antitoxin (Connaught Laboratories Limited, Willowdale, Ontario, Canada). The patient was taken from the ED to the operating room, where he was intubated and his abscesses were debrided surgically. The botulinum antitoxin was flown in from the San Francisco branch of the Centers for Disease Control and Prevention and arrived after surgery. The patient was given an initial dose of one vial IV and one vial IM. Each vial contains 21,500 IU (type A, 7,500; type B, 5,500; type E, 8,500). This dose was repeated the next day for worsening ptosis and weakness of extraocular muscles. The patient's signs and symptoms stabilized after the second dose. Wound cultures subsequently grew Clostridium botulinum, and serum analysis revealed type A botulinum toxin. The patient was hospitalized I 11 days with 76 days of ventilator support. He was discharged home with a tracheostomy and gastrostomy. He made a full recovery. DISCUSSION C botulinum is an anaerobic, spore-forming, Gram-positive bacterium found in soil. Its toxin, botulin, is a heat-stable, high molecular weight protein. Eight immunologically distinct toxins have been identified, designated A, B, C 1, C2, and D through G. 5,6 All reported cases of wound botulism have involved types A, B, or both. 1 Botulism is a poisoning characterized by cranial nerve paralysis and descending paralysis with sensory sparing. The mechanism of action involves botulinum toxin binding to the distal synaptic cell membrane of cholinergic nerves. The toxin is endocytosed and appears to block the calcium-mediated release of acetylcholine into the synaptic cleft. Nerve function may be impaired for months until new nerve endings regenerate. The blockade is most pronounced in the cranial nerves and muscles of respiration. 6,7 The incubation period between injury and neurologic symptoms has been reported as from 4 to 18 days, with a median of 7 days. 2 A detailed history and physical examination are the keys to diagnosing wound botulism and initiating treatment. The most common symptoms are dyspnea, dysphagia, dysphonia or dysarthria, and diplopia. The most common signs are descending paralysis and respiratory insufficiency. The differential diagnosis for wound botulism includes the following: the Eaton-Lambert syndrome, hypermagnesemia, and aminoglycoside toxicity, s,9 all of which have similar electromyographic findings. 9,w The Miller Fisher variant of the Guillain-Barr~ syndrome, which occurs in
1185
WOUND
BOTULISM
Burningham et al
approximately 4% of patients with the syndrome, is characterized by descending paralysis. 11 Diphtheria must be considered in unimmunized patients. Myasthenia gravis may present with cranial nerve dysfunction that is rapidly reversible with the administration of edrophonium. 12 Tetanus can produce cranial nerve deficits, but affects primarily the central nervous system and produces spasticity 2 Cerebrovascular accidents, especially those affecting the brainstem, produce symptoms that mimic botulism. The rapid onset characteristic of vascular events should distinguish them from the insidious onset of botulism. Tick paralysis generally produces ascending rather than descending paralysis.13 Poliomyelitis presents with a more asymmetric ascending paralysis, often affecting primarily the lower extremities with associated cerebrospinal fluid pleocytosis and modest protein elevation, r Still other causes to be considered in the differential diagnosis include organophosphate and lead poisoning, and paralytic shellfish toxicity with saxitoxin or tetrodotoxin. ~'* Wound cultures and serum assay for botulinum toxin are confirmatory. Other tests and laboratory findings are nonspecific. Isolation of the C botulinum organism is by standard anaerobic culture techniques. The MicroScan WalkAway (Baxter Diagnostics Inc, Deerfield, Illinois), the instrument used in our hospital to identify cultured bacteria, is unable to biochemically distinguish between some species of clostridia and will identify C botulinum as C sporogenes. Therefore, botulism must not be ruled out based on automated wound cultures and identification techniques. The clostridial isolates must be analyzed for botulin. Initial wound Gram stains may provide supportive evidence but will not distinguish C botulinum from other Clostridium species. Electrophysiologic studies may support the diagnosis of botulism but cannot be used to exclude it. Typical electromyographic findings in botulism include diminished response to a single stimulus, but potentiation of the action potential during repetitive stimulation. Only botulism, the Eaton-Lambert syndrome, aminoglycoside toxicity, and hypermagnesemia produce thiselectromyographic constellation. 9J5,16 Other electrophysiologic findings in wound botulism include normal motor conduction velocity, distal motor latencies, and sensory nerve action potentials. 6 The edrophonium test is not definitive in distinguishing wound botulism from other causes of neuromuscular blockade. Of 19 cases in which Tensilon | testing was mentioned, six patients (32%) showed at least partial improvement. 2,1r, t 8 The mainstay of therapy is ventilator,/support; local wound care, including debridement; botulinum antitoxin
1186
administration; and coincidental tetanus prophylaxis. Trivalent (A, B, E) botulinum antitoxin should be administered as soon as possible in cases that are clinically compatible with wound botulism even though results of definitive diagnostic tests will not yet be available. As botulin is produced, it is rapidly and irreversibly bound to cholinergic nerve membranes. Botulinum antitoxin is ineffective once the toxin is endocytosed. 2,16 It binds only to free toxin and therefore can only arrest progression of nerve dysfunction. Timely administration of antitoxin can prevent progression of paralysis while definitive debridement of the organism is pursued. Trivalent (A, B, E) botulinum antitoxin is available on an emergency basis from the Centers for Disease Control and Prevention in Atlanta (404-639-3356, Monday through Friday, 8 AM tO 4:30 PM; or 404-639-2888 after hours and on weekends and holidays). High-dose IV penicillin is recommended by some authors, but there is no evidence that antibiotics affect the disease course or outcome. 1a In fact, wound botulism has been diagnosed twice in patients already taking oral penicillin; our patient was the second.5,18 Sellin 6 raised the theoretical concern that antibiotic-induced cell lysis may increase toxin release. However, penicillin is used commonly to treat other clostridial infections, and its use seems reasonable, especially if the patient has fever, leukocytosis, or cellulitis. Aminoglycosides should be avoided because of the potential for aminoglycoside-induced neuromuscular blockade in these already compromised patients. 19 When appropriate respiratory support is provided, the prognosis for patients with wound botulism is favorable. To date, 4 of 39 (10%) previously published cases resulted in death. While mortality is low, morbidity is pronounced. Ventilator support was required in 23 of the 39 previous cases, ranging from 24 hours to 3 months. Eleven of the 23 patients required ventilator support for 30 days or more. Length of hospitalization among survivors also was protracted, with no patient being discharged in less than 4 weeks. The longest documented hospitalization was for 171 days, 2~ Long-term outcome among survivors is good. Patients with mild cases generally are free of neurologic sequelae in 2 to 3 months. Seriously affected patients may have more gradual resolution of their deficits over a course of months to years. 2~ SUMMARY
Wound botulism is a rare disease with serious morbidity and a 10% mortality rate. Initial diagnosis should be based on history and physical examination, and treatment
ANNALS OF EMERGENCY MEBICINE
2 4 : 6 DECEMBER 1994
WOUND
BOTULISM
Burningham et al
should be initiated without waiting for results of definitive tests. We describe a case that emphasizes that concurrent antibiotic therapy does not preclude the diagnosis. Our patient was taking a course of oral dicloxacillin for skin abscesses when his symptoms began. Wound botulism should be considered when a trauma victim or IV drug abuser develops cranial nerve palsies and descending paralysis.
Reprint no. 47/1/60283 Address for reprints: Mark D Burningham, MD Idaho Emergency Physicians 2312 N Cole, Ste B Boise, Idaho 83704 208-322-1730
REFERENCES 1. MacDonald KL, Cohen ML, Blake PA: The changing epidemiologyof adult botulism in the United States Am J Epidemiol 1986;124:794-799. 2. Merson MH, Dowell VR: Epidemiologic,clinical and laboratoryaspectsof wound botulism. N Engl J Mad 1973;289:1005-1010. 3. E[stonHR, Wang M, Log LL: A~m abscessescaused by Clostridium botulinum. J C/in Micrc;biol 1991:29:2678-2679. 4. Bumingham MD, Walter FG, Mechem CC, et ah Wound botulism. VetHum Toxicol 1992;34:347. 5. SakaguchiG: Clostridium botufinum toxins. Pharmacol Ther1982;19:165-194. 6. Sellin LC: Botulism--An update. Mil Mad 1984;149:12-16. 7. HathawayCL: Toxigenic clostridia. Clin Microbiol Rev 1990;3:66-98. 8. McQuillan MP, Cantor HE, O'RourkeJR: Myastbenic syndromeassociatedwith antibiotics. Arch Neurol 1968;18:402-415. 9. DeJesus PV, Slater R, Spitz LK, et al: Neuromuscularphysiologyof wound botulism. Arch Neurol 1973;29:425-431. 10. Lewis SW, Pierson DJ, CaryJM, et al: Prolongedrespiratoryparalysis in wound botulism. Chest 1979;75:59-61. 11. RodenbergH, Grattoe M, Bennett J, et al: Left upper extremity weakness in an 18-year-old man. Ann EmergMed 1991;20:672-679. 12. SwedbergJ, Wendel TH, Deiss F: Wound botulism. WestJ Med1987;147:335-338. 13. McCarthyJD, FleischmannJ, GeorgeWL: Fever,dyspnea,and slurred speechfollowing lower extremity trauma (clinical conference).Rev Infect Dis 1991;13:172-176. 14. Slovis CM: Food poisoning, in Haddad LM, Winchester JF (eds): Clinical Management of Poisoning andDrug Overdose,ed 2. Philadelphia, WB SoundersCo, 1990, p 612-623. 15. MacDonald KL, Rutherford GW, Friedman SM, et al: Botulism and botulism-like illness in chronic drug abusers.Ann Intern Med 1985;102:616-618. 16. Wapen BD, Gutmann L: Wound botulism: A case report. JAMA 1974;227:1416-1417. 17. Cherington M, Ginsburg S: Wound botulism. Arch Surg 1975;110:436-438. 18. Edell T, Sullivan CP, Osborn KM, et al: Wound botulism associatedwith a positive Tensilon| test. West J Med1983;139:218-219. 19. Santos IS, Swanson P, GlasgowLA: Potentiationof Clostridium botufinum toxin by aminoglycoside antibiotics. Pediatrics 1981;68:50-54. 20. Thorne EL, Kropp RJ: Wound botulism: A life-threateningcomplication of band injuries. Plast Reconstr Surg 1983;71:548-551.
DECEMBER 1994
24:6
ANNALS OF EMERGENCY MEDICINE
1187