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PubMedDate not supplied

Clinical electrophysiology of infantile botulism.

Infantile botulism is a recently recognized cause of acute hypotonic paresis and respiratory failure in young infants. Electrophysiological testing has proven useful in early diagnosis in suspected cases by demonstrating abnormal neuromuscular transmission as is known to occur in botulism. Twenty-five infants with bacteriologically proven botulism were studied by uniform methods in our laboratory and characteristic electrophysiological abnormalities were found. Repetitive stimulation at 20 and 50 Hz was the most specific single test; 23 patients (92%) showed incremental responses. Stimulation at low rates was less specific. Concentric needle electromyography provided useful supplemental information. Short-duration, low-amplitude motor unit potentials were prominent in 22 patients (92%) accompanied by abnormal spontaneous activity in 13 patients (54%). Compound muscle action potential amplitudes were usually reduced, but motor and sensory conduction studies were otherwise normal. Electrodiagnostic testing demonstrated one or more characteristic abnormalities in all cases of infantile botulism. This constellation of electrophysiological abnormalities, combined with an appropriate clinical picture, was so distinctive as to allow early presumptive diagnosis of infant botulism, before the results of bacteriological testing were available.

Action Potentials↗
PubMed2002

[Botulism: the agent, mode of action of the botulinum neurotoxins, forms of acquisition, treatment and prevention].

The botulinum neurotoxins are produced by anaerobic, spore-forming bacteria belonging to the Clostridium genus. They are synthesised as a single chain protein (150 kDa), which is not or weakly active. The active form results from a proteolysis cleaving the precursor in a light chain (about 50 kDa) and a heavy chain (about 100 kDa), which are linked by a disulfide bridge. The heavy chain is involved in the recognition of a specific neuronal surface receptor and mediates the internalization of the light chain into the cytosol. The light chain is responsible for the intracellular activity. It catalyses the proteolysis of SNARE proteins, which are involved in the exocytosis of synaptic vesicles containing acetylcholine. Hence, the release of acetylcholine at the neuromuscular junction is blocked, leading to a flaccid paralysis. Human botulism, usually type A, B or E, is associated with intoxination, ingestion of preformed toxin in food, with digestive toxi-infection, mainly in newborns (infant botulism), or with wound contamination (wound botulism). The treatment of botulism is usually symptomatic. The specific treatment is based on the serotherapy or on the use of purified specific antibodies. The vaccination against botulism is efficient. However, since the botulinum neurotoxins are widely used for the treatment of numerous dystonias, a generalised vaccination is not conceivable.

Bacterial Vaccines↗
PubMed1982

[Diagnostic and therapeutic problems of botulism in infants (author's transl)].

The incidence of botulism remains high. This disease is burdened by a high lethality rate. It is of significant importance for the patient that therapy is instituted sufficiently early. Botulism is an intoxication with the toxin of Clostridium botulinum. In babies, botulism can be caused also by peroral infection with the bacteria or spores. It appears that intestinal germination to toxin-forming bacteria can occur in babies only. Since honey is very frequently contaminated with Clostridium botulinum spores, honey should be eliminated from baby food. The signs manifested in botulism in infants are similar to those in somewhat older children and adults: increasing muscular hypotonia, apathy, pareses of the cranial nerves, and, finally, respiratory insufficiency through paresis of the respiratory musculature. The authors report on their own observations in cases of botulism, and on current possibilities of treatment.

Age Factors↗
PubMed2003

An outbreak of foodborne botulism associated with food sold at a salvage store in Texas.

Foodborne botulism is caused by potent neurotoxins of Clostridium botulinum. We investigated a large outbreak of foodborne botulism among church supper attendees in Texas. We conducted a cohort study of attendees and investigated the salvage store that sold the implicated foods. We identified 15 cases of botulism (40%) among 38 church supper attendees. Nine patients (60%) had botulinum toxin type A detected in stool specimens. The diagnosis was delayed in 3 cases. Fifteen (63%) of 24 attendees who ate a chili dish developed botulism (relative risk, undefined; P<.001). The chili dish was prepared with "brand X" or "brand Y" frozen chili, "brand Z" canned chili, and hot dogs. An unopened container of brand X chili yielded type A toxin. Brand X chili was purchased at a salvage store where perishable foods were inadequately refrigerated. Our investigation highlights the need to improve clinicians' awareness of botulism. More rigorous and more unannounced inspections may be necessary to detect food mishandling at salvage stores.

Adolescent↗
PubMed1999

Clostridium difficile colitis associated with infant botulism: near-fatal case analogous to Hirschsprung's enterocolitis.

We present the first five reported cases of Clostridium difficile-associated diarrhea (CDAD) in children with infant botulism caused by Clostridium botulinum. We compare two fulminant cases of colitis in children with colonic stasis, the first caused by infant botulism and the second caused by Hirschsprung's disease. In both children, colitis was accompanied by hypovolemia, hypotension, profuse ascites, pulmonary effusion, restrictive pulmonary disease, and femoral-caval thrombosis. Laboratory findings included pronounced leukocytosis, hypoalbuminemia, hyponatremia, coagulopathy, and, when examined in the child with infant botulism, detection of C. difficile toxin in ascites. CDAD recurred in both children, even though difficile cytotoxin was undetectable in stool after prolonged initial therapy. Four children who had both infant botulism and milder CDAD also are described. Colonic stasis, whether acquired, as in infant botulism, or congenital, as in Hirschsprung's disease, may contribute to the susceptibility to and the severity of CDAD.

Botulism↗
PubMed1993

Wound botulism in a patient with a tooth abscess: case report and review.

We describe a case of wound botulism associated with a tooth abscess in a 5-year-old boy. We reviewed the literature and reports to the Centers for Disease Control and Prevention (Atlanta) of laboratory-confirmed cases of wound botulism. From 1943 through 1990, 47 cases were reported. Type A botulinus toxin was identified in 32 cases, type B in 13, types A and B in 1, and an unknown type in 1. Botulism was associated with wounds from trauma, use of injectable drugs, and surgery. Sinusitis after use of intranasal cocaine has also been associated with botulism. Treatment for wound botulism includes prompt debridement of the wound for eliminating anaerobic conditions, intensive care, and treatment with antitoxin.

Botulinum Toxins↗
PubMed1992

Characterization of the neurotoxin isolated from a Clostridium baratii strain implicated in infant botulism.

Botulism is widely known to result from ingestion of food containing botulinum neurotoxin produced in situ by certain strains of Clostridium botulinum. Infant botulism caused by C. botulinum, unlike the food-borne intoxication, is the toxicoinfectious form of botulism (S. S. Arnon, p. 331-345, in G. E. Lewis, ed., Biomedical Aspects of Botulism, 1981). The strain of Clostridium baratii implicated in infant botulism produced a neurotoxin that was neutralized with antiserum for botulinum neurotoxin serotype F (J. D. Hall, L. M. McCroskey, B. J. Pincomb, and C. L. Hatheway, J. Clin. Microbiol. 21:654-655, 1985). We developed a procedure to culture the toxigenic C. baratii (strain 6341) in dialysis bags and a simple purification scheme (precipitation of 900-ml culture supernatant with ammonium sulfate and two anion-exchange chromatographic steps at pH 5.5 and 8.0) that yielded up to 150 micrograms of purified neurotoxin. It is an approximately 140-kDa single-chain protein and has the following sequence of amino acid residues at the N terminus: Pro-Val-Asn-Ile-Asn-Asn-Phe-Asn-Tyr-Asn-Asp-Pro-Ile-Asn-Asn-Thr-Thr-Ile- Leu. Comparison of this amino acid sequence with those of the botulinum neurotoxin serotypes A, B, and E showed 40 to 50% identical residues in comparable positions. The specific toxicity of the neurotoxin, approximately 2 x 10(6) 50% lethal doses for mice per mg of protein injected, was not enhanced significantly by mild trypsinization, although the protease cleaved the neurotoxin within a disulfide loop that generated at least two primary fragments, approximately 47 and approximately 86 kDa, that remained linked by an interchain disulfide. These two fragments resembled the light and heavy chains of the well-characterized neurotoxin serotypes A, B, C, D, E, and F produced by C. botulinum.

Amino Acid Sequence↗
PubMed1980

Cultural and physiological characteristics and antimicrobial susceptibility of Clostridium botulinum isolates from foodborne and infant botulism cases.

Isolates Clostridium botulinum from foodborne and infant botulism cases in the United States were compared on the basis of toxigenicity, cultural and biochemical characteristics, metabolic products, and susceptibility to antimicrobial agents. Seventy-eight strains, including 42 from foodborne and 36 from infant botulism sources, were examined. Cultures on anaerobic blood agar exhibited circular, spindle, and rhizoid (medusa head) colonies. Overall, the characteristics of isolates from foodborne and infant botulism cases were quite similar. We concluded that it was not possible to differentiate C. botulinum isolates associated with foodborne botulism from those recovered from infant botulism cases. All of the 78 strains produced an unidentified indole derivative(s), detected with paradimethylaminocinnamaldehyde reagent, and hydrocinnamic acid, detected by gas-liquid chromatography; all exhibited a high degree of resistance to cycloserine, sulfamethoxazole, and trimethoprim. These characteristics should prove to be useful in the isolation and identification of C. botulinum from mixed microbial populations.

Anti-Bacterial Agents↗
PubMed1987

Examination of feces and serum for diagnosis of infant botulism in 336 patients.

In the 12-year period 1975 to 1987, feces from 336 infants were examined for botulinal neurotoxin and Clostridium botulinum. All the infants had illnesses which prompted their physicians to consider infant botulism in the diagnosis. Stool specimens from 113 of the infants yielded organisms that produced botulinal neurotoxins assumed to be responsible for the illness. The types of botulinal toxin in the confirmed cases were distributed as follows: 38 A, 69 B, 2 atypical B, 1 E, 1 F, 1 A + B, and 1 B + F. The type A and B toxins in a single infant were produced by two different strains of organism, and the type B and F toxins in another infant were produced by a single strain. The physiological characteristics of all the isolated toxigenic organisms except two were consistent with those of group I (proteolytic) C. botulinum. The toxigenic isolate from the infant with type E botulism was identified as C. butyricum, and that from the infant with type F botulism was identified as C. barati. Toxin of the same type as produced by the isolated organisms was identified in feces of 98 of 111 culture-positive infants. Botulinal toxin was identified in the serum of 9 of 67 culture-positive infants (8 of 22 infants with type A organisms; 1 of 43 infants with type B organisms; neither of 2 infants with A + B or atypical type B organisms). Botulinal toxin was not detected in feces (206 infants) or in serum (114 infants) of the culture-negative infants. The culture-positive infants had clinical features and a course of illness consistent with those of infant botulism. Most of the culture-negative infants probably had illnesses other than botulism, but specimens might have been obtained late in some infants' illnesses, when the organism had disappeared.

Botulinum Toxins↗
PubMedDate not supplied

Tracheotomy for infant botulism.

Botulism is a serious intoxication caused by ingestion of food containing preformed botulinus toxin and characterized by rapidly progressive bulbar paralysis, generalized weakness, and respiratory insufficiency. In 1976 a distinct clinical entity of infant botulism was recognized. The disease apparently results from intraintestinal toxin production which produces a defect in neuromuscular transmission by interfering with release of acetylcholine at cholinergic synapses. Five cases of infant botulism were identified at the Children's Hospital of Philadelphia between 1975 and 1977. Initial symptoms included constipation, slow feeding, lethargy and weak cry. Four of the patients progressed to respiratory insufficiency requiring nasotracheal intubation. Three of the infants with respiratory failure required tracheotomy. Because infants with respiratory failure may require support for months, we recommend that a tracheotomy be performed early in the management to avoid the complications associated with prolonged intubation. The effectiveness of antitoxin or antibiotics to treat infant botulism remains questionable and therefore prolonged respiratory supportive care is the mainstay of therapy. In addition, we offer guidelines for decannulation in cases of infant botulism. None of the patients in our series could be decannulated prior to initial discharge from the hospital.

Botulism↗
PubMed1980

Wound botulism.

It is well recognized that food contamination can result in botulism either from ingestion of performed toxin, in classical botulism, or through absorption of toxin from bacteria within the gut, in infant botulism. Botulism due to contamination of wounds with Clostridium botulinum is not commonly recognized. We report a case of wound botulism occurring in an eight-year-old boy, characterized by early ptosis, dysphagia and dysarthria and then followed by progressive generalized paralysis and fixed dilated pupils, but with intact sensorium. Management consisted of early wound debridement and prolonged intensive respiratory and nutritional support. Recovery was complete.

Botulism↗
PubMed1988

Botulism from chopped garlic: delayed recognition of a major outbreak.

Diagnosis of botulism in two teenaged sisters in Montreal led to the identification of 36 previously unrecognized cases of type B botulism in persons who had eaten at a restaurant in Vancouver, British Columbia, during the preceding 6 weeks. A case-control study implicated a new vehicle for botulism, commercial chopped garlic in soybean oil (P less than 10(-4)). Relatively mild and slowly progressive illness, dispersion of patients over at least eight provinces and states in three countries, and a previously unsuspected vehicle had contributed to prolonged misdiagnoses, including myasthenia gravis (six patients), psychiatric disorders (four), stroke (three), and others. Ethnic background influenced severity of illness: 60% of Chinese patients but only 4% of others needed mechanical ventilation (P less than 10(-3]. Trypsinization of serum was needed to show toxemia in one patient. Electromyography results with high-frequency repetitive stimulation corroborated the diagnosis of botulism up to 2 months after onset. Although botulism is a life-threatening disease, misdiagnosis may be common and large outbreaks can escape recognition completely.

Botulinum Toxins↗
PubMed1999

Botulism: heart rate variation, sympathetic skin responses, and plasma norepinephrine.

BACKGROUND: Botulism may involve the autonomic nervous system. METHODS: We assessed the autonomic function of 6 botulism patients with heart rate variations, sympathetic skin responses, and plasma norepinephrine. RESULTS: Two weeks after onset, all the patients had absent sympathetic skin response in the palm and sole. Compared with controls, the heart rate variation of botulism patients was significantly decreased at rest (3.1 +/- 1.2% vs. 20.9 +/- 2.0%, p = 0.0018) and during deep breathing (4.3 +/- 2.3% vs. 29.7 +/- 2.6%, p = 0.0018). The botulism patients had significantly lower plasma norepinephrine levels (supine 29.2 +/- 10.1 pg/ml vs. 257.5 +/- 65.8 pg/ml, p = 0.0018; standing 40.3 +/- 13.1 pg/ml vs. 498.5 +/- 85.6 pg/ml, p = 0.0018). The heart rate variation and sympathetic skin response was greatly improved 6 months after onset. CONCLUSIONS: Heart rate variation, absence of sympathetic skin response, and low plasma norepinephrine are all manifestations of autonomic dysfunction in botulism patients.

Adult↗
PubMed2003

Outbreak of botulism type E associated with eating a beached whale--Western Alaska, July 2002.

Botulism is a neuroparalytic illness caused by toxins produced by the bacterium Clostridium botulinum, an obligate anaerobe found commonly in the environment. Intoxication with toxin type E is associated exclusively with eating animal foods of marine (salt or fresh water) origin. Persons who eat raw or fermented marine fish and mammals are at high risk for botulism from type E toxin. On July 17, 2002, the Alaska Division of Public Health investigated a cluster of suspected botulism cases among residents of a fishing village in Alaska. This report summarizes the findings of the outbreak investigation, which linked disease to eating raw muktuk (skin and a pink blubber layer) from a beached whale (Figure). To avoid delays in treatment, health-care providers evaluating patients suspected of having botulism should base treatment decisions on clinical findings. Public health authorities should be notified immediately about any suspected botulism case.

Adolescent↗
PubMed2003

[Botulism toxin, bioterrorist weapon].

BOTULISM AND BIOWARFARE: Botulism is a severe neuro-paralysing infection due to a toxin produced by Clostridium botulinum. The use of the botulinum toxin for terrorist aims in the form of aerosols is a perfectly credible eventuality. The botulinum toxin is the most potent toxin known; it is easy to produce and can lead to massive destruction. DEPENDING ON THE CONTAMINATION: The clinical forms of botulism depend on the mode of contamination. Botulism through inhalation can only be the result of a deliberate act using an aerosol. The clinical symptomatology is identical to that of the other forms. PREVENTION: In the case of a bio-terrorist attack with an aerosol of botulinum toxin, the subjects exposed should be vaccinated as a prophylactic measure with trivalent antitoxin vaccine (types A, B and E). This vaccine must be administered as rapidly as possible in symptomatic patients. A single case of botulism acquired by inhalation corresponds to an act of terrorism.

Administration, Oral↗
PubMed1956

The status of botulism as a world health problem.

The author reviews the international literature and brings up to date the published statistical data on botulism-a disease which, owing to its spectacular nature and high case-fatality rate, appears to occupy a place out of proportion to its frequency as a cause of death in some regions.Without exception, botulism is caused by carelessness in the preparation and preservation of vegetable and animal foods. Local customs of eating such food uncooked, in the form of salads, watery conserves, poorly cured or inadequately smoked pork and salted fish products create the botulism problem.The risk of botulism exists wherever the telluric incidence of Type A, B, and E spores is high. Surveys to appraise the extent of Clostridium botulinum in the soils of Asia and Africa are urgently needed so that the magnitude of the potential problem in these areas can be properly evaluated.Food processors must not relax in the use of properly calculated thermal processes now available for every food commodity. Agencies that promote or give instruction in preservation of food in the home should be thoroughly familiar with the most effective, practical, and inexpensive methods of preventing botulism.

Africa↗
PubMedDate not supplied

Mechanical ventilation in foals with botulism: 9 cases (1989-2002).

"Shaker foal" disease, toxicoinfectious botulism of foals, was 1st described as a clinical entity in 1967. The reported mortality rate was 90%, with death occurring within 24-72 hours of the onset of the characteristic clinical signs. The mortality rate decreased when equine-origin botulism antitoxin became available; however, a certain percentage of foals continued to die of respiratory failure. Mechanical ventilation is an important part of the treatment of infant botulism and is essential to the survival of many affected infants. We report a retrospective study of 9 foals with toxicoinfectious botulism where early mechanical ventilation was employed as part of the treatment. Foals receiving mechanical ventilation were progressively acidemic and had increased PaCO2 tensions before mechanical ventilation. These arterial blood gas abnormalities were ameliorated with mechanical ventilation. One foal was euthanized for economic reasons; survival in treated foals was 87.5%. Mechanical ventilation of foals with botulism and respiratory failure appears to be an effective therapy.

Animals↗
PubMed1992

[Botulism: a case report].

Botulism is an acute form of poisoning that results from ingestion of a toxin produced by Clostridium botulinum. Botulism toxin causes their major effect by blocking neuromuscular transmission in autonomic and motor nerve terminals. Guillain Barre Syndrome, Myasthenia Graves, Lambert Eaton Myasthenic Syndrome, acute poliomyelitis and diphtheria must be considered in the differential diagnosis. Electrodiagnostic studies have been shown to be of value in differentiating botulism from other paralytic diseases. Identification of the toxin in the patients serum is diagnostic. The treatment of botulism is mainly supportive. In this study we have discussed a patient who was treated in our clinic as a botulism from unknown source, the differential diagnosis from other paralytic diseases.

Botulism↗