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PubMed2004

Public perceptions and risk communications for botulism.

Formative research findings from 10 focus group interviews on botulism are described. Data were collected from a diverse sample of people throughout the United States in 2003, as part of a collaborative multisite initiative sponsored by the Centers for Disease Control and Prevention to improve communications materials on bioterrorism agents. Focus group guides included questions on knowledge, action, emotions, and information seeking in response to a series of scenarios on a hypothetical terrorist attack using botulinum toxin. Data were collected, transcribed, coded, and analyzed using content domains based on risk and health communications theories. Initial participant responses to scenarios were emotional, changing into immediate health and survival concerns conceptualized as information specific to the agent and event. Knowledge about botulism was low, and participants wanted clear, concise, and actionable messages. Broadcast media, the internet, and community-based sources were cited as sources of information. Findings have implications for botulism preparedness messages and for general public risk communications.

Attitude to Health↗

PubMed2004

Development and application of Real-Time PCR assays to detect fragments of the Clostridium botulinum types A, B, and E neurotoxin genes for investigation of human foodborne and infant botulism.

Real-time PCR assays for detection of Clostridium botulinum neurotoxin (BoNT) gene fragments specific to BoNTA, B, and E were developed as alternatives to the mouse bioassay. The expected specificities of the PCR assays were demonstrated by in silico analysis as well as empirical testing of target DNA extracted from 83 pure cultures of C. botulinum, and 44 bacteria from other species. The sensitivities of the assays were found to be equivalent to 16, 10, and 141 genomes for BoNT A, B, and E, respectively. The assays were shown to be applicable to both purified DNA, as well as crude DNA extracted from cultures and enrichment broths. The assays were evaluated using DNA extracted directly from clinical and food specimens as well as from inoculated broths using material collected from seven confirmed and one suspected case of botulism. The appropriate BoNT genes were detected in material from seven of the eight cases of botulism and provided a supportive diagnosis faster than the conventional bioassay. These assays have already proven useful for pubic health microbiological investigation of suspected cases of human botulism by substantially improving the diagnostic process.

Base Sequence↗

PubMedDate not supplied

Differential diagnosis of infant botulism.

Clinical investigations of infants hospitalized with botulism demonstrate a remarkable uniformity of complaints and physical findings. Constipation precedes a course of progressive weakness and cranial nerve dysfunction. Examination reveals hypotonia, hyporeflexia, and a variable pattern of involvement of the motor cranial nerves. Initial laboratory investigations should include electrodiagnostic tests, because findings of an incremental response to rapid, repetitive nerve stimulation and of brief, small-amplitude motor units on electromyography are virtually pathognomonic of botulism in the infant. Differential diagnosis includes disorders that may produce generalized depression of the central nervous system, such as septicemia, meningitis, metabolic disturbances, and intoxications. Specific involvement of the neuromuscular system includes acute polyneuropathies, diseases of the anterior horn cell, congenital myopathies or muscular dystrophy, and neonatal myasthenia gravis. Recent studies have expanded the clinical spectrum of infant botulism to include some cases of sudden infant death syndrome and otherwise nonspecific constipation.

Action Potentials↗

PubMedDate not supplied

Laboratory aspects of infant botulism in California.

Infant botulism is the newly recognized form of the disease in which illness results from the production of toxin in the infant's intestines. Between the recognition of infant botulism as a distinct clinical entity in 1976 and the end of 1978, 50 cases were identified in California. The diagnosis of botulism was established by the identification of botulinal toxin in and the isolation of Clostridium botulinum from stool specimens of the affected infants. Thirty cases were type A and 20 were type B. Fecal excretion of toxin and organisms was monitored during hospitalization and after discharge from the hospital. Stools from family members and from 160 age-matched control infants did not contain botulinal toxin. A total of 396 food and drug samples, as well as 159 environmental and miscellaneous items, were examined. None of the foods or drugs tested contained preformed toxin. However, C. botulinum organisms were isolated from the nine samples of honey, five of soil, and one of vacuum cleaner dust.

Botulinum Toxins↗

PubMedDate not supplied

Botulism and tetanus: selected epidemiologic and microbiologic aspects.

Botulism is rare in both developing and developed countries. During 1980 only 89 cases (18 food borne, 68 infant, 2 wound, 1 unspecified) were reported in the United States. Coproexamination is essential for laboratory confirmation of infant botulism. Botulinal antitoxins of equine origin are used for treating food-borne and wound botulism but are usually not recommended for infant cases. Tetanus is much more common in some developing countries than in developed countries. During 1980 only 95 cases of tetanus were reported in the United States; in 68 (72%) of these cases, the patient was 50 years or older, and in only two (2.1%) cases was the patient younger than one year. Tetanus neonatorum is a major problem in some developing countries. Diagnosis of tetanus is based primarily on clinical findings, but laboratory studies can be helpful, especially in epidemiologic investigations. Human hyperimmune immunoglobulin is now used in the treatment of tetanus.

Adolescent↗

PubMed1988

An outbreak of type A foodborne botulism in Taiwan due to commercially preserved peanuts.

Until recently, botulism was not recognized as an important public health problem in Taiwan. In 1986, an outbreak of type A foodborne botulism resulted in nine cases, two of them fatal. The vehicle in this outbreak was commercially preserved peanuts processed by an improperly equipped, unlicensed cannery. A single batch of peanuts was implicated; however, we could not determine why this particular batch was contaminated. Efforts to recall the product were hampered by a lack of distribution records. Mass media announcements were used to warn the public about the outbreak, and preliminary data suggest the ensuing publicity improved botulism surveillance. The local preference for low-acid preserved foods, increasing consumerism, the shortage of adequately trained inspectors are factors which probably contributed to this outbreak. Stricter enforcement of food sanitation policies are needed to meet the changing situation in Taiwan.

Adult↗

PubMed1989

Foodborne botulism: an international outbreak.

We report an outbreak of fishborne botulism caused by type E Clostridium botulinum. The eight cases, six in Israel and two in New York City, resulted from the consumption of ribbetz or kapchunka, a freshwater whitefish soaked in brine and air-dried, that was processed commercially in New York. Half the cases were males; the age range was 9 to 77 years. Five of the victims were hospitalized; the oldest died, and two others required ventilatory assistance. Laboratory confirmation of botulism was obtained in three cases. Prolonged lack of refrigeration during transatlantic flight and packaging contributing to an anaerobic environment were felt to be contributing environmental factors in the Israeli cases. Rapid communication and full cooperation between Israeli and US health authorities limited the extent of the outbreak. Despite adequate understanding of how foodborne botulism may be avoided, outbreaks still occur, particularly among people consuming certain high-risk or ethnic foods.

Adolescent↗

PubMed1980

Quantitative evidence of intestinal colonization by Clostridium botulinum in four cases of infant botulism.

Infant botulism is an infectious form of a disease heretofore principally known as food-borne intoxication. Previous epidemiologic and laboratory studies have shown that infant botulism results from the ingestion of spores of Clostridium botulinum that subsequently germinate in the infant intestine and produce botulinal toxin. A quantitative study of the fecal microflora of four infants with infant botulism revealed the presence of C. botulinum in numbers as high as 6.0 x 10(8) colony-forming units (cfu)/g. At various times after the onset of illness, the numbers of C. botulinum that were recovered from feces ranged from 10(3) to 10(8) cfu/g and constituted from 0.01% to 3.3% of the total fecal flora. It was concluded that the large numbers of C. botulinum found in patients' feces could occur only as a consequence of in vivo spore germination and outgrowth.

Botulinum Toxins↗

PubMed1986

Two cases of type E infant botulism caused by neurotoxigenic Clostridium butyricum in Italy.

The first two confirmed cases of type E infant botulism occurred in two 16-week-old girls in Rome, Italy. The original diagnosis for the first patient was intestinal blockage due to an ileocecal invagination, which was treated surgically. Postoperatively, the patient became unresponsive and required ventilatory assistance. A diagnosis of infant botulism was then made. The second infant presented to the same hospital 7 1/2 months later with profound weakness, hypotonicity, mydriasis, and areflexia. This case was recognized as possible botulism at admission. Both cases were confirmed by detection and identification of type E botulinal toxin in stool specimens and in enrichment cultures of those specimens. The toxigenic organisms isolated were quite different from Clostridium botulinum type E. The apparent causative organism in each case resembles Clostridium butyricum but produces a neurotoxin that is indistinguishable from type E botulinal toxin by its effects on mice and by its neutralization with type E botulinal antitoxin.

Botulinum Toxins↗

PubMed1992

Clinical and laboratory comparison of botulism from toxin types A, B, and E in the United States, 1975-1988.

Cases of adult botulism (n = 309) were studied to identify clinical differences between toxin types and to evaluate the sensitivity of diagnostic laboratory testing. Patients with illness from type E toxin had the shortest incubation periods. Sporadic case-patients were more severely ill: 85% required intubation compared with only 42% in multiperson outbreaks. Of patients with type A botulism, 67% required intubation compared with 52% with type B and 39% with type E. Toxin testing was positive for 40%-44% of serum and stool specimens obtained within 3 days of toxin ingestion and for 15%-23% of specimens obtained thereafter, while 37% of stool specimens obtained > 3 days after toxin ingestion were positive by culture. Patients with type A botulism have more severe illness. In general, specimens obtained early are more likely to be positive by toxin assay, and stool cultures are more sensitive than toxin detection for specimens obtained later in the illness.

Botulinum Toxins↗

PubMed1993

A massive outbreak of type E botulism associated with traditional salted fish in Cairo.

In April 1991, 91 hospitalized patients in Cairo were reported to the Egyptian Ministry of Health with botulism intoxication. To define the spectrum of illness and identify a food vehicle, 45 patients were interviewed and a case-control investigation was conducted among families of 5 hospitalized patients. Clinical specimens and specimens of implicated food were tested for toxin and cultured for Clostridium botulinum. Hospitalized patients had symptoms consistent with botulism; 18 (20%) of 91 reported patients died. Illness was associated with eating faseikh (uneviscerated, salted mullet fish; lower 95% confidence limit of odds ratio = 6.6, P < .001). All 5 case-families purchased faseikh from one shop. Very high levels of type E botulinal toxin were detected in faseikh reported to be purchased from the implicated shop; C. botulinum type E was isolated from cultures of clinical specimens and from the faseikh. This is the first documented outbreak of botulism in Egypt and the largest type E outbreak ever reported.

Adolescent↗

PubMed1997

Endogenous antibody production to botulinum toxin in an adult with intestinal colonization botulism and underlying Crohn's disease.

A patient with obstruction of the terminal ileum from Crohn's disease developed complete paralysis in week 1 of hospitalization. Features initially suggested Guillain-Barre syndrome, but botulinum toxin was identified in serum and stool specimens from week 1 and type A toxin-producing Clostridium botulinum in stool specimens from weeks 3 to 19, confirming botulism due to intestinal colonization. In week 19, the inflamed small bowel was resected, and C. botulinum disappeared from the stool. In week 31, the patient was able to breath without assistance. Testing for an active immune response with neutralizing antibodies to C. botulinum at week 19 was positive; these antibodies remained at a protective level for >1 year. Intestinal colonization botulism, rare in adults, should be considered for patients with descending paralysis, especially those with a preceding alteration in small bowel function. An active immune response to botulinum toxin with production of protective antibodies has not been demonstrated previously in a patient with botulism and may have contributed to this patient's recovery.

Aged↗

PubMed1978

Botulism type B: epidemiologic aspects of an extensive outbreak.

Between March 31 and April 6, 1977, 59 individuals developed type B botulism. All ill persons had eaten at the same Mexican restaurant and all had consumed a hot sauce made with improperly home-canned jalapeno peppers, either by adding it to their food, or by eating a nacho that had had hot sauce used in its preparation. There was a highly significant association between illness and consumption of hot sauce when a comparison was made between ill persons and well controls: 4% of all restaurant patrons eating at the restaurant during the outbreak period became ill with botulism; however, approximately two-thirds of those actually exposed to the toxic hot sauce became ill. Disease severity was statistically correlated with incubation periods. No differences in disease severity were found between persons of different age groups. The full clinical spectrum (mild symptomatology with neurologic findings through life-threatening ventilatory paralysis) of type B botulism was documented.

Adolescent↗

PubMed1994

[A case report of infant botulism without a history of honey ingestion].

A 66-day-old female with infant botulism is reported. She was admitted to our hospital with respiratory failure. Laboratory examinations detected botulinal toxin type A in her feces. This was the first case with no history of honey ingestion among the 13 cases of infant botulism reported in Japan. It is possible that other cases, in which honey had not been consumed, remain undiagnosed. Further studies may be needed to clarify the factors necessary to cause infant botulism.

Botulism↗

PubMed2006

Laboratory diagnostics of botulism.

Botulism is a potentially lethal paralytic disease caused by botulinum neurotoxin. Human pathogenic neurotoxins of types A, B, E, and F are produced by a diverse group of anaerobic spore-forming bacteria, including Clostridium botulinum groups I and II, Clostridium butyricum, and Clostridium baratii. The routine laboratory diagnostics of botulism is based on the detection of botulinum neurotoxin in the patient. Detection of toxin-producing clostridia in the patient and/or the vehicle confirms the diagnosis. The neurotoxin detection is based on the mouse lethality assay. Sensitive and rapid in vitro assays have been developed, but they have not yet been appropriately validated on clinical and food matrices. Culture methods for C. botulinum are poorly developed, and efficient isolation and identification tools are lacking. Molecular techniques targeted to the neurotoxin genes are ideal for the detection and identification of C. botulinum, but they do not detect biologically active neurotoxin and should not be used alone. Apart from rapid diagnosis, the laboratory diagnostics of botulism should aim at increasing our understanding of the epidemiology and prevention of the disease. Therefore, the toxin-producing organisms should be routinely isolated from the patient and the vehicle. The physiological group and genetic traits of the isolates should be determined.

Adult↗

PubMed1982

Quantitation of Clostridium botulinum organisms and toxin in the feces of an infant with botulism.

A 4-month-old boy presented with symptoms and signs characteristic of infant botulism. Examination of feces revealed Clostridium botulinum type B and type B toxin. The numbers of C. botulinum and the amount of toxin in feces were measured throughout the 4-week period in hospital. The maximum numbers and amounts were detected in a fecal specimen collected 16 days after admission: this contained 8.4 X 10(6) C. botulinum type B colony-forming units and 61,440 mouse 100% lethal doses of type B toxin per g (wet weight) of feces. This latter figure is the highest fecal toxin titer reported yet for a case of infant botulism. By day 16, however, substantial improvement in the patient's clinical condition had occurred. This suggests that initiation of recovery from infant botulism is not necessarily preceded by a reduction in the numbers of C. botulinum organisms and the quantity of toxin in the gut.

Action Potentials↗

PubMed1991

Type F botulism due to neurotoxigenic Clostridium baratii from an unknown source in an adult.

Type F botulism was confirmed in a 54-year-old male with signs compatible with botulism who reported to the emergency unit of a hospital. Botulinal neurotoxin was detected in the patient's serum and fecal specimens, and a neurotoxigenic organism whose physiologic characteristics correspond to those of Clostridium baratii was isolated. The toxin produced by the isolate was neutralized by type F botulinal antitoxin and cross-neutralized with lower efficiency by type E antitoxin. The patient's food history was not suggestive of botulism, and it seems likely that the illness was due to colonization of the gut.

Botulinum Toxins↗

PubMed2002

Botulism due to Clostridium baratii type F toxin.

Botulism results from consumption of preformed toxin or in vivo toxin elaboration in wounds or intestine. Of U.S. food-borne botulism cases since 1950, the majority were due to toxin A, but a significant number of suspect cases were never confirmed by culture or toxin detection. We report here a possible case of food-borne botulism attributed to toxin F production by a Clostridium baratii organism isolated from food consumed by the patient. The isolation of a toxin-producing Clostridium species other than Clostridium botulinum from food and stool requires deviation from the usual laboratory protocols, which may account for the lack of complete laboratory confirmation of clinically diagnosed cases.

Adult↗