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PubMed1976

Laboratory diagnosis of botulism complicated by pyridostigmine treatment of the patient. A method for selectively removing interfering substances from clinical specimens.

In August 1974, a case of botulism occurred; home-canned potatoes and peas containing Clostridium botulinum, type A, were strongly incriminated as the vehicle of transmission. C. botulinum, type A, was isolated from a stool specimen of the patient, but the mouse neutralization test for botulinal toxin could not be completed because the stool extract contained a highly toxic, heat-stable substance that rapidly killed mice. Historical and laboratory evidence indicated that the substance was pyridostigmine bromide, a low-molecular-weight drug with which the patient had been treated after her disease was misdiagnosed as myasthenia gravis. A generally applicable method employing dialysis by which toxic SUBSTANCED of low molecular weigth could be selectively removed from specimens without diminishing the potency of botulinal toxin contained in them was developed. Dialysis rendered a pyridostigmine solution, a stool extract from the patient with botulism, and a stool extract from a person taking pyridostigmine virtually nontoxic to mice. Dialysis did not significantly alter the toxicity to mice of crude botulinal toxin; it selectively eliminated all or almost all pyridostigmine toxicity from a pyridostigmine-botulinal toxin mixture without altering the toxicity of the botulinal toxin.

Animals↗
PubMedDate not supplied

The clinical spectrum of infant botulism.

Infant botulism is the systemic illness that results when spores of Clostridium botulinum germinate in the infant's intestine and then produce botulinal toxin in vivo. As with other infectious diseases, infant botulism has a spectrum of clinical severity that ranges from a mild, outpatient illness to fulminant, sudden death. Most cases reported to date have been recognized in infants so weak and hypotonic that their need for hospital care was unquestioned; yet even this group of patients displayed a wide range in severity of illness. The outpatients were initially considered to be cases of "failure to thrive," while the fulminant cases were indistinguishable at autopsy from typical instances of the sudden infant death syndrome (SIDS, crib death). This article discusses the observed spectrum of clinical severity, the management of the hospitalized patient, and the manner in which sudden death might result from production of butulinal toxin in the intestine.

Anti-Bacterial Agents↗
PubMedDate not supplied

The sudden infant death syndrome and infant botulism.

Fecal and serum specimens taken from 30 cases of sudden infant death and from eight cases of nonsudden infant death that were diagnosed at a single facility in King County, Wash., were examined for the presence of Clostridium botulinum organisms and toxin. Organisms, but not toxin, were recovered from a fecal specimen in one case of sudden infant death, results that parallel those from studies previously reported by investigators in California. Studies made in our laboratory of a nonfatal case of infant botulism revealed that an estimated 366,000 mouse minimal lethal doses of toxin were excreted in feces collected by purging the infant. Organisms and toxin were excreted for at least 15 days after the infant was hospitalized. Observations made in our laboratory of atypical responses in mice to both fecal and serum extracts, coupled with recently described experiments in which mice were used as an animal model for infant botulism in humans, provide a biologically plausible foundation for the hypothesis that C. botulinum may be implicated etiologically in some sudden infant deaths. Additional microbiologic, physiologic, and toxicologic data are needed to adequately test this hypothesis.

Botulinum Toxins↗
PubMedDate not supplied

Epidemiologic characteristics of infant botulism in the United States, 1975-1978.

Between January 1, 1975, and July 31, 1978, 81 cases (47 type A, 34 type B) of infant botulism were reported to the Center for Disease Control (CDC), Atlanta, Georgia. Most cases occurred in the western states, with the majority in California and Utah, where active surveillance is in progress. Most of the cases reported have occurred in the fall months, but this pattern may be attributable to a reporting artifact. The median age at onset of illness was 10 weeks, with a range of three to 35 weeks. The case-fatality ratio was 3.7% (3 of 81). CDC has developed a reporting form for case investigation and has encouraged private physicians and state and territorial epidemiologists and laboratory directors to keep active surveillance of cases of infant botulism. State health departments and CDC are available for consultation regarding suspected cases of the illness.

Age Factors↗
PubMedDate not supplied

Human-derived immune globulins for the treatment of botulism.

The need for a human-derived immune globulin to replace the equine antitoxins currently used in the treatment of botulism is well recognized. A small group of individuals who had received multiple immunizations with pentavalent botulinal toxoid were plasmapheresed for the purpose of collecting a botulism-immune plasma of human origin to be fractionated for the production of immune globulin. Human-derived immune globulin will offer the advantage over equine antitoxins of not inducing reactions to foreign protein and of having a prolonged effective half-life.

Animals↗
PubMed1988

Food-borne botulism in Alaska, 1947-1985: epidemiology and clinical findings.

We reviewed records of all food-borne outbreaks of botulism in Alaska from 1947 through 1985. Fifty-nine confirmed or suspected outbreaks with 156 cases were reported. All outbreaks occurred in Alaska Natives and were associated with eating traditional Alaska Native foods. Forty-four (75%) of the outbreaks were laboratory confirmed and involved 133 persons. The overall annual incidence of confirmed or suspected botulism was 8.6 cases per 100,000 population. Seventeen persons died, an overall case-fatality rate of 11%. Type E toxin accounted for 32 (73%) laboratory-confirmed outbreaks; type A, six (14%); and type B, five (11%). Forty-one cases demonstrated botulinal toxin in one or more specimens (serum, gastric contents, or stool). Of the 41 botulinal toxin-positive persons, 38 (93%) had at least three of the commonly recognized pentad of signs or symptoms--nausea and vomiting, dysphagia, diplopia, dilated and fixed pupils, or dry mouth and throat--and 20 (49%) required respiratory assistance.

Adolescent↗
PubMed1981

Restaurant-associated type A botulism: transmission by potato salad.

In the period November 13-18, 1978, seven cases of type A botulism occurred in persons who had eaten in a restaurant in Colorado. The outbreak was recognized when two persons who had independently eaten at the restaurant were hospitalized with an illness compatible with botulism. Surveillance efforts identified five additional cases. Potato salad made at the restaurant and available for service during an 11-day period was epidemiologically incriminated as the vehicle of botulinal toxin transmission (p less than 0.00001). Laboratory studies showed that Clostridium botulinum spores on the surface of potatoes could survive baking in the manner used by the restaurant and that botulinal toxin could be produced in potatoes contaminated with C. botulinum spores.

Botulism↗
PubMedDate not supplied

Extracorporeal adsorption as a new approach to treatment of botulism.

Botulism is a paralytic disease caused by a toxin produced by the bacterium Clostridium botulinum. Outbreaks of the illness take place with a mortality rate of 10%, and the potential terrorist use of the toxin has become a serious concern. The current treatment includes administration of antitoxin, which can cause serious allergic reactions. Recently, we have successfully treated a 64 year old woman with the illness with IMMUSORBA TR350 (Asahi Medical, Tokyo, Japan), an extracorporeal adsorptive column containing polyvinylalcohol-tryptophan as an adsorptive agent, which has been widely used in Japan to treat myasthenia gravis and Guillain-Barre syndrome. Initially, the patient developed ocular muscle weakness and a variant of the Guillain-Barre syndrome was suspected. After extracorporeal treatment, her neurologic symptoms remarkably improved. After a series of treatments, botulinum toxin type B was isolated in the food she had eaten, establishing the diagnosis. An in vitro study revealed that the adsorptive column removed botulinum toxin to a significant extent. Our recent findings suggest that treatment with the adsorptive column TR350 can be a feasible option for botulism, which is a rare but potentially lethal disease.

Adsorption↗
PubMed1991

Audiologic findings in botulism poisoning.

Botulism poisoning results in a presynaptic failure of neuromuscular transmission, and may be expected to impair Eustachian tube and stapedius reflex function. The audiologic findings in five normal-hearing patients with type A botulism poisoning are presented. Results were varied. Two patients demonstrated type B or C tympanograms during the early stages, while three with normal middle ear function demonstrated marked bilateral or unilateral stapedius reflux threshold elevation. One patient had a reversible reflex decay, and the superimposition of a second stimulus upon the first resulted in complete recovery of reflex amplitude. A number of possible pathophysiological mechanisms are discussed.

Acoustic Impedance Tests↗
PubMed1981

Wound botulism.

Wound botulism, a potentially fatal disease, presents with signs and symptoms of food-borne botulism without the gastrointestinal manifestations. All cases have been associated with extremity wounds. The diagnosis is clinical, and aggressive ventilatory support is the cornerstone of successful therapy. A case is reported and the pathophysiology, diagnosis, and treatment are reviewed.

Adult↗
PubMed1977

Type A botulism from commercially canned beef stew.

Two of three persons who ate lunch together became ill with symptoms characteristic of botulism. One died before botulism was suspected and before specimens could be collected for laboratory testing, but a serum specimen from the other patient, who survived, yielded botulinal toxin, type A. The third person remained asymptomatic, but Clostridium botulinum type A was cultured from his stool. The three persons had shared two canned foods: home-canned green beans and commercially canned beef stew. The green beans were initially assumed to be the cause of the outbreak. However, the empty stew can was recovered from the garbage, and washings from the can yielded C botulinum, type A, and its toxin.

Aged↗
PubMed2006

A rare differential diagnosis in dysphagia: wound botulism.

The incidence of wound botulism is increasing dramatically among intravenous drug users. Efficient intensive care and early treatment with antitoxin is essential to avoid lethal courses. The clinical picture of botulism is of descending, symmetric, flaccid paralysis. Early symptoms include cranial nerve palsies resulting in blurred vision and diplopia, difficulty in focusing, ptosis, facial weakness, dysphagia, dysphonia, and dysarthria. Because patients presenting with dysarthria and dysphagia will often be seen by an ear, nose and throat specialist initially, this rare but upcoming neurologic disease must be considered in the differential diagnoses.

Adult↗
PubMed2005

A case of infant botulism with a possible link to infant formula milk powder: evidence for the presence of more than one strain of Clostridium botulinum in clinical specimens and food.

Infant botulism was confirmed in a 5-month-old female by both isolation of Clostridium botulinum type B and by detection of type B botulinum neurotoxin in rectal washout and faeces. DNA fingerprinting of nine isolates from faeces yielded two different amplified-fragment length polymorphism (AFLP) patterns. C. botulinum was isolated from two of 14 food and drink items from the patient's home: C. botulinum type A was recovered from an opened container of dried rice pudding and C. botulinum type B from opened infant formula milk powder. Ten C. botulinum type B isolates from the opened infant formula yielded four AFLP patterns, two of which were indistinguishable from the clinical isolates. Fifteen unopened foods were tested and C. botulinum type B of a unique AFLP pattern was recovered from one unopened infant formula of the same batch as the opened container. It is suggested that multiple C. botulinum were present in both food and the intestine during infant botulism.

Botulinum Toxins↗
PubMed2006

Botulism in a pregnant intravenous drug abuser.

A case of botulism is reported in a heroin-abusing parturient who initially presented with lethargy and slurred speech. The diagnostic difficulty, complications, intensive care and anaesthetic management of this case are discussed, with particular reference to the pregnancy and the effects of both botulism and its empirical treatment on the fetus. A short review is provided of a condition that has seen a marked increase in its incidence since 2000.

Adult↗
PubMed1993

Infant botulism: a review in South Australia (1980-89).

Between March 1980 and March 1989 there were six identified cases of infant botulism. The presenting symptoms were predominantly poor feeding, lethargy and constipation, and the presenting signs were predominantly hypotonia, weak gag reflex and respiratory difficulty. All required intensive care and prolonged hospital stays. Recovery was eventually complete in all cases. Infant botulism is an uncommon condition but early recognition with adequate intensive care usually results in complete recovery.

Botulism↗
PubMed1980

A report on the pathology of type A botulism.

An autopsy case of type A botulism, a sacrifice during the first outbreak in Japan, was presented. The patient exhibited typical neuromuscular symptoms and died on the 8th day from the onset of illness. Type A Clostridium botulinum was demonstrated from the stools and the toxin from the blood serum during the course of disease. The infection source of botulinus bacilli, however, was not clarified. The autopsy diagnoses were made as follows; 1) type A botulism, 2) bronchopneumonia, 3) respirator brain, 4) congestion, 5) hemorrhage in vagal nerve, myocardium and endometrium, 6) gastric erosion, 7) cloudy swelling of kidneys, 8) enterocolitis, 9) focal necrosis of liver and adrenals, 10) demyelination of cranial nerves, and 11) focal hyaline degeneration of striated and smooth muscles and myocardium. The botulinus toxin was confirmed from the samples of cardiac blood or autopsy.

Botulinum Toxins↗
PubMed1991

Infant botulism with Down syndrome.

A 4-month-old boy with Down syndrome and infant botulism is reported. He was admitted to our hospital with stridor and developed respiratory failure and generalized paralysis. Laboratory examination revealed botulinal toxin type A in his blood and feces. Clostridium botulinum organisms were found in the feces and in the honey which he had been fed. Anti-botulinal toxin was administered on the 10th day of illness. Artificial ventilation was given for 87 days and he survived. This is the 11th known case of infant botulism in Japan. It is possible that other cases remain undiagnosed.

Botulinum Antitoxin↗
PubMed1996

The first case of type B infant botulism in Japan.

A six-month-old girl with a 5 consecutive day history of constipation and poor feeding developed generalized weakness, poor head control, difficulties in sucking and swallowing, and cranial nerve dysfunction within a few days. These characteristic manifestations and clinical course prompted examination of the possibility of infant botulism, although no history of eating honey was obtained. Mouse bioassay performed with enema effluent demonstrated type B botulinum toxin. Culture of the effluent was positive for Clostridium botulinum type B. This is the first case of type B infant botulism in Japan.

Animals↗