Botulism wound

Botulism is a disease caused by ingestion of foods contaminated with Clostridium botulinum (food-borne botulism) or, very rarely, by wound infection (wound botulism) or colonization of the intestinal tract with Clostridium botulinum (infant botulism). The toxins block the release of acetylcholine. Botulism is characterized by generalized muscular weakness, which first affects eye and throat muscles and later extends to all skeletal muscles. Flaccid paralysis can lead to respiratory failure. 

Botulism is a potent neurotoxin produced from Clostridium botulinum that is an anaerobic, spore-forming bacterium. There are three different types ofbotulism Foodborne botulism occurs when a person ingests a pre-formed toxin that leads to illness within a few hours or days. Foodborne botulism is a public health emergency because the contaminated food may still be available. Infant botulism occurs in a small number of susceptible infants each year who harbor C. botulinum in their intestinal tract. Wound botulism occurs when wounds are infected with C. botulinum that secretes the toxin. Approximately 100 cases of the three types of botulism are reported within the United States each year about 5 percent are wound botulism, 25 percent are foodborne botulism, and a full 70 percent are infant botulism. Death can result from respiratory failure, but those who survive may have fatigue and shortness of breath for years. 

Botulism Toxin that occurs in the form of food-borne botulism, wound botulism, and infant botulism one of the most toxic substances known to man. 

Wound botulism occurs where C. botulinum spores germinate in wound infections and develop into vegetative cells. In such cases, neurotoxin is produced which leads to the onset of neurological symptoms. According to the Centers for Disease Control and Prevention, 23 cases of wound botulism (13.6% of all botulism cases) were reported in 2001 in the U.S. Wound botulism has also been diagnosed after intravenous drug injection (Rundervoort et al., 2003). 

Botulism is a neuroparalytic, primarily foodborne illness first described in 1897 (GDC, 1998). The disease is caused by a toxin produced by the anaerobic bacterium Clostridium botulinum. Although botulism is rare, it can kill rapidly and foodborne botulism is a public health emergency carrying significant risk for widespread disease and death, as potentially preventable deaths may occur if the source of botulism is not discovered and eliminated. There are classically four major types of botulism foodborne botulism, infantile botulism, wound botulism, and intestinal botulism. 

Foodborne botulism accounts for approximately 1,000 cases per year worldwide, of which approximately 30 occur in the United States. Home processed foods account for 94% of U.S. cases. Infantile botulism, a form of the disease in which C. botulinum spores are ingested by infants due to food contamination, occurs in approximately 60 children per year in the United States, more than half of which are in California. Wound botulism, typically involving intravenous drug users who either inject drugs intravenously or in the subcutaneous tissue (a practice known as skin-popping ), is reported one to three times per year in the United States. It can also occur in other types of contaminated wounds such as a severe crush injury or other areas of contaminated avascular tissue. Botulism due to intestinal colonization by C. botulinum is extremely rare only seven cases have been reported in the literature (CDC, 1998). 

Infantile Botulism—Ingestion ot botulism spores, often in honey, produces flaccid paralysis, poor feeding and suck reflexes, floppy baby syndrome. Wound Botulism—Contamination of wounds with C. botulinum spores can produce systemic symptoms. THERAPY Ventilatory support (often for weeks) Trivalent botulinum antitoxin Enemas and cathartics... 

The basie syndrome of BoNT intoxieation is similar for all naturally oeeurring forms, as well as for inhalation exposure and does not vary appreeiably among serotypes (Simpson, 1986 Habermann and Dreyer, 1986 Hatheway et al, 1984 Jankovie and Brin, 1997). Based upon documented laboratory evidenee, human BoNT intoxication is caused by exposure primarily to serotypes A, B, E, and to a much lesser extent to serotype F disease manifests mostly as a result of foodbome, infant, and wound botulism (Habermann and Dreyer, 1986 Simpson, 1986). BoNTs are also lethal from inhalation of aerosohzed toxin, although this form is not generally observed in nature. 

Sandrock, C.E., Murin, S. (2001). Clinical predictors of respiratory failure and long-term outcome in black tar heroin-associated wound botulism. Chest 120 562-6. 

Weber, J.T., Goodpasture, H.C., Alexander, H., Werner, S.B., Hatheway, C.L., Tauxe, R.V. (1993). Wound botulism in a patient with a tooth abscess case report and review. Clin. Infect. Dis. 16 635-9. 

An immediate rise in serum potassium occurs after the administration of suxamethonium. The rise is normally small, 0.5mmol/l or less (4). However, in some cases it can be larger, and cases of cardiac arrest associated with hyperkalemia have been reported in critically ill patients after prolonged immobilization (153-161). Cardiac arrest also occurred in a patient with wound botulism (162). 

The authors suggested that suxamethonium should be avoided in patients with suspected botulism and in patients with muscle weakness of unknown origin. Wound botulism had been observed before in drug users... 

Chakravarty EF, Kirsch CM, Jensen WA, Kagawa FT. Cardiac arrest due to succinylcholine-induced hyperkalemia in a patient with wound botulism. J Clin Anesth 2000 12(l) 80-2. 

Passaro DJ, Werner SB, McGee J, Mac Kenzie WR, Vugia DJ. Wound botulism associated with black tar heroin among injecting drug users JAMA 1998 279(ll) 859-63. 

Synonyms Clostridium botulinum-, Foodborne (classic) botulism Infant botulism Wound botulism Unclassified botulism... 

Ingestion is the primary exposure pathway for botulism. Wound botulism occurs when the bacterium encounters devitalized human tissue, synthesizes toxin, and thus causes disease. Intestinal (adult and infant types) botulism involves ingestion of spores or the live bacterium and, due to impaired intrinsic defenses, the gastrointestinal tract becomes colonized with Clostridium botulinum. In infant type, the mucosal surface of the intestines is susceptible to colonization due to multiple factors including decreased acidity of the stomach and lack of bile of acids, which are natural barriers. In adult-type intestinal botulism, patients have had surgical vagotomy/... 

Baymiller S (2001) Botulism in critical care A case study in wound botulism. American Journal of Critical Care 10(3) 172-180. 

Wound botulism, a relatively rare form of the disease, results from the production of toxin by organisms that multiply in a contaminated wound. Wounds associated with botulism may not appear obviously infected (38). Before 1980, wound botulism was most likely associated with complicated wounds, such as extensive crush injuries, compound fractures and other wounds associated with avascular areas. Since 1980, most cases have occurred in illicit drug users, including intravenous drug users with contaminated needle puncture sites or drug users with nasal and sinus wounds secondary to chronic cocaine sniffing (38). In 2001, there were 23 reported cases of wound botulism in the United States, with one death (39). 

Botulinum intoxication generally results from ingestion of preformed toxin elaborated in contaminated foods (foodborne) or from colonization by C. botuUnum of deep wounds with subsequent production of toxin (wound botulism) (Mershon and Dowell, 1973 Snydman, 1989). A third form. 

Wound botuhsm is relatively rare, accounting for only 5% of all outbreaks. The majority of these are caused by serotype A, and the remainder by serotype B (Shapiro et al., 1998). The neurological symptoms of wound botulism differ httle from those of foodbome botulism except for the general absence of G1 symptoms. Historically, this form of botulism was so uncommon that it was not even recognized until the last half of the twentieth century. From its discovery in 1943 until 1990, only 47 incidences of wound botulism were documented (Weber et al., 1993). An examination of these cases indicated that wounds susceptible to C. botulinum are generally deep with avascular areas but need not appear obviously infected or necrotic. Additional risk factors include compound fractures and extensive crush injuries (Mershon and Dowell, 1973). Contamination of wounds with... 

From 1980 to the present time, wound botulism has been observed predominantly in illicit drug users following repeated subcutaneous administration of black tar heroin, or in individuals with nasal or sinus lesions from chronic cocaine abuse (Anderson et al., 1997). During the last decade alone, wound botulism from black tar heroin has exceeded the total reported wound botulism cases during the preceding 40 years by a factor of almost three (Sandrock and Murin, 2001). 

Anderson, M.W., Sharma, K., and Feeney, C.M. 1997. Wound botulism associated with black tar heroin. Acad. Emerg. Med. 4 805-809. 

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