Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BOTULISM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2002

Botulism among Alaska natives in the Bristol Bay area of southwest Alaska: a survey of knowledge, attitudes, and practices related to fermented foods known to cause botulism.

OBJECTIVES: Botulism cases due to traditional Alaska Native fermented foods occur periodically in Southwest Alaska. In this population, we conducted a survey on knowledge, attitudes, and practices related to botulism and fermented foods. METHODS: We interviewed 140 adults randomly chosen from nine villages. Data collected included fermented food consumption frequency; knowledge about the cause and symptoms of botulism; and fermented food preparation methods. RESULTS: Most respondents (81%) had eaten Alaska Native fermented foods at least once. Over 70% identified botulism as a foodborne illness, and over 87% believed eating certain Native fermented foods could cause botulism. One-third of fermented food preparers used plastic containers for fermentation. To prevent botulism, 45% vwould consider boiling fermented foods, and 65% would not eat foods fermented in plastic or glass containers. CONCLUSIONS: Despite high awareness of botulism in this population, one-third of fermented food preparers use plastic containers, a practice which may increase the risk of botulism. Misconceptions and acceptable prevention messages about botulism, such as using traditional nonplastic fermentation methods, were identified and included in an educational video.

Adolescent↗
PubMed1999

Outbreak of type A botulism and development of a botulism surveillance and antitoxin release system in Argentina.

CONTEXT: Botulism is an important public health problem in Argentina, but obtaining antitoxin rapidly has been difficult because global supplies are limited. In January 1998, a botulism outbreak occurred in Buenos Aires. OBJECTIVES: To determine the source of the outbreak, improve botulism surveillance, and establish an antitoxin supply and release system in Argentina. DESIGN, SETTING, AND PARTICIPANTS: Cohort study in January 1998 of 21 drivers of a specific bus route in urban Buenos Aires. MAIN OUTCOME MEASURE: Occurrence of botulism and implication of a particular food as the vehicle causing this outbreak. RESULTS: Nine (43%) of 21 bus drivers developed botulism, presenting with gastroenteritis, symptoms of acute cranial nerve dysfunction including ptosis, dysphagia, blurred vision, and motor weakness. One driver experienced respiratory failure. Type A toxin was detected from 3 of 9 patients' serum samples. All drivers received botulism antitoxin; there were no fatalities. Consumption of matambre (Argentine meat roll) was significantly associated with illness. Among 11 persons who ate matambre, 9 developed illness, compared with none of those who did not eat it (P<.001). The matambre had been cooked in water at 78 degrees C to 80 degrees C for 4 hours, sealed in heat-shrinked plastic wrap, and stored in refrigerators that did not cool adequately. Subsequently, a botulism surveillance and antitoxin release system was established. CONCLUSIONS: Insufficient cooking time and temperatures, storage in heat-shrinked plastic wrap, and inadequate refrigeration likely contributed to Clostridium botulinum spore survival, germination, and toxin production. A rapid-response botulism surveillance and antitoxin release system in Argentina should provide more timely distribution of antitoxin to patients and may serve as a model for other nations.

Adult↗
PubMed1985

Epidemiologic study of infant botulism in Pennsylvania: Report of the Infant Botulism Study group.

The majority of the almost 400 confirmed cases of infant botulism in the United States have occurred in California, Pennsylvania, and Utah. In Pennsylvania, 44 of 53 (83%) cases occurred within a geographic area of Southeastern Pennsylvania which represents one tenth of the Commonwealth's area and one third of the population at risk for infant botulism. In Southeastern Pennsylvania, a map of the residences of cases circumscribes a discrete ring around Philadelphia. A case-control study performed to seek host-related risk factors, identifies the significant associations of botulism with infants who are white, breast-fed, and born at term into two-parent families with hospitalization insurance. County control studies were performed to identify differences in host-related factors between areas of high and low prevalence of botulism. Although some "protection" could be afforded Philadelphia infants by their feeding and family characteristics, the differences in case rates between Philadelphia and the botulism "ring counties" cannot be explained entirely by host-related factors. Further, the absence of botulism in counties just outside of the botulism "ring," where infants were found to have identical potential risk factors, suggests that an uneven distribution of botulinal spores in the environment is the most significant determinant of case rate.

Botulism↗
PubMed1994

Development of infant botulism in a 3-year-old female with neuroblastoma following autologous bone marrow transplantation: potential use of human botulism immune globulin.

Infant botulism is a rare disease caused by the release of toxin produced in the intestinal tract by Clostridium botulinum. The disease primarily affects infants under 1 year of age. We report a 3-year-old child with stage IV neuroblastoma who developed symptoms of progressive motor weakness, bulbar palsy and respiratory failure 42 days after autologous BMT. The diagnosis of infant botulism was established by identifying botulism toxin in the stool. Human botulism immune globulin (HBIG) was administered. Following the diagnosis, the patient made significant recovery over the next 7 weeks and was successfully extubated from mechanical ventilation. However, her neuroblastoma eventually recurred and she subsequently died of progressive disease. Although the etiology of the development of infant botulism in this case following autologous BMT still remains unclear, alteration of the intestinal microbial environment from gut sterilization and laminar airflow room isolation or, alternatively, immune suppression during pre- and post-autologous BMT and activation of endogenous spores may have contributed to the development of this disease. The use of HBIG in children with botulism over 1 year of age may be beneficial.

Bone Marrow Transplantation↗
PubMed1985

Botulism and botulism-like illness in chronic drug abusers.

From 1982 to 1983 we received reports of a neurologic illness characterized by a symmetric descending paralysis in six drug abusers from widely separated geographic areas. Botulism was confirmed in two patients; type B botulinal toxin was found and Clostridium botulinum was isolated from a small abscess in one, and type A botulinal toxin was found in the serum of the other. The clinical illness in the remaining four patients, although not laboratory confirmed, was also compatible with botulism. None of the patients had histories suggestive of foodborne botulism, and wound botulism was suspected as the cause of illness. There are several reports of tetanus associated with parenteral drug abuse; wound botulism is another toxin-mediated clostridial infection that may occur as a complication of chronic drug abuse.

Abscess↗
PubMed1991

Distinction between Clostridium botulinum type A strains associated with food-borne botulism and those with infant botulism in Japan in intraintestinal toxin production in infant mice and some other properties.

Two strains of Clostridium botulinum type A associated with food-borne botulism and six strains associated with infant botulism in Japan were compared in intraintestinal toxin production in infant mice, in vitro toxin and hemagglutinin production, molecular sizes of the toxins, and some other properties. The infant botulism-associated strains, producing M toxin (Mr 300 kDa) but no hemagglutinin, showed significantly lower 50% infective doses in infant mouse intestines. The antigenicities of the toxin differed between the two groups, while the biochemical properties of the cultures did not. Besides infant botulism-associated strains, this set of properties were found only in a strain isolated from honey of South American origin.

Animals↗
PubMed1984

Antitoxin levels in botulism patients treated with trivalent equine botulism antitoxin to toxin types A, B, and E.

Serum levels of equine-botulism antitoxin to toxin types A, B, and E were measured in four type-A botulism patients who had received equine-botulism antitoxin. High circulating levels capable of neutralizing in excess of 1 X 10(8), 9 X 10(7), and 6 X 10(6) 50% mouse lethal doses of toxin of types A, B, and E, respectively, were detected. There was little depletion of type-A antitoxin even though two of the patients had circulating type-A toxin before treatment. The half-life for antitoxin persistence for one patient was calculated as being 6.5, 7.6, and 5.3 days for antitoxin types A, B, and E, respectively. Antitoxin levels were not proportionate to the amount (range, 2-4 vials) injected and did not appear to be affected by whether the route of administration was iv or im. Peak serum levels of antitoxin were 10-1,000 times higher than amounts needed to neutralize the toxin measured in the serum of these and other patients with botulism.

Botulinum Antitoxin↗
PubMed1996

Experience with the use of an investigational F(ab')2 heptavalent botulism immune globulin of equine origin during an outbreak of type E botulism in Egypt.

During an outbreak of type E foodborne botulism in Cairo in 1991, an investigational equine F(ab')2 "despeciated" heptavalent botulism immune globulin (dBIG) was provided to the Egyptian Ministry of Health by the U.S. Army. Of 54 patients known to have been treated with antitoxins, 4 received commercially available trivalent antitoxins, 45 received dBIG, and 5 received both commercial antitoxin and dBIG. Physicians recorded side effects in 10 (22%) of 45 patients who received dBIG; in nine cases, reactions were considered "mild," and in one case they were believed to be serum sickness. In contrast, possible serum sickness during hospitalization was recorded for two of four patients who were receiving commercial antitoxins. No complications of therapy were noted for any patient who was receiving both antitoxin types. In a separate study, 31 patients were contacted about their reactions to the antitoxin by telephone after discharge from the hospital. Seven (54%) of 13 patients attributed symptoms that they experienced while they were hospitalized to receipt of dBIG, while four (44%) of nine patients who indicated that they had received commercial antitoxins and one (20%) of five who received both commercial antitoxin and dBIG reported side effects before discharge. Data on the efficacy of the antitoxins were not obtained. In our experience, equine dBIG was at least as safe as commercially available antitoxins in treating type E foodborne botulism.

Antitoxins↗
PubMed1998

Clinical spectrum of botulism.

Botulism is a paralyzing disease caused by the toxin of Clostridium botulinum. The toxin produces skeletal muscle paralysis by producing a presynaptic blockade to the release of acetylcholine. Recent studies have pinpointed the site of action of the several types of botulinum neurotoxin at the nerve terminal. Since the discovery of the toxin about 100 years ago, five clinical forms of botulism have been described: 1) classic or foodborne botulism; 2) wound botulism; 3) infant botulism; 4) hidden botulism; 5) inadvertent botulism. A clinical pattern of descending weakness is characteristic of all five forms. Almost all human cases of botulism are caused by one of three serotypes (A, B, or E). Classic and wound botulism were the only two forms known until the last quarter of this century. Wound botulism was rare until the past decade. Now there are increasing numbers of cases of wound botulism in injecting drug users. Infant botulism, first described in 1976, is now the most frequently reported form. In infant botulism spores of Clostridium botulinum are ingested and germinate in the intestinal tract. Hidden botulism, the adult variant of infant botulism, occurs in adult patients who usually have an abnormality of the intestinal tract that allows colonization by Clostridium botulinum. Inadvertent botulism is the most recent form to be described. It occurs in patients who have been treated with injections of botulinum toxin for dystonic and other movement disorders. Laboratory proof of botulism is established with the detection of toxin in the patient's serum, stool, or wound. The detection of Clostridium botulinum bacteria in the stool or wound should also be considered evidence of clinical botulism. Electrophysiologic studies can provide presumptive of botulism in patients with the clinical signs of botulism. Electrophysiologic testing can be especially helpful when bioassay studies are negative. The most consistent electrophysiologic abnormality is a small evoked muscle action potential in response to a single supramaximal nerve stimulus in a clinically affected muscle. Posttetanic facilitation can be found in some affected muscles. Single-fiber EMG studies typically reveal increased jitter and blocking, which become less marked following activation. The major treatment for severe botulism is advance medical and nursing supportive care with special attention to respiratory status.

Botulinum Toxins↗
PubMed1998

Botulism in the United States: a clinical and epidemiologic review.

Botulism is caused by a neurotoxin produced from the anaerobic, spore-forming bacterium Clostridium botulinum. Botulism in humans is usually caused by toxin types A, B, and E. Since 1973, a median of 24 cases of foodborne botulism, 3 cases of wound botulism, and 71 cases of infant botulism have been reported annually to the Centers for Disease Control and Prevention (CDC). New vehicles for transmission have emerged in recent decades, and wound botulism associated with black tar heroin has increased dramatically since 1994. Recently, the potential terrorist use of botulinum toxin has become an important concern. Botulism is characterized by symmetric, descending, flaccid paralysis of motor and autonomic nerves, usually beginning with the cranial nerves. Blurred vision, dysphagia, and dysarthria are common initial complaints. The diagnosis of botulism is based on compatible clinical findings; history of exposure to suspect foods; and supportive ancillary testing to rule out other causes of neurologic dysfunction that mimic botulism, such as stroke, the Guillain-Barré syndrome, and myasthenia gravis. Laboratory confirmation of suspected cases is performed at the CDC and some state laboratories. Treatment includes supportive care and trivalent equine antitoxin, which reduces mortality if administered early. The CDC releases botulism antitoxin through an emergency distribution system. Although rare, botulism outbreaks are a public health emergency that require rapid recognition to prevent additional cases and to effectively treat patients. Because clinicians are the first to treat patients in any type of botulism outbreak, they must know how to recognize, diagnose, and treat this rare but potentially lethal disease.

Antitoxins↗