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PubMed1984

Acute toxicity of aminoglycoside antibiotics as an aid in detecting botulism.

Gentamicin sulfate or neomycin sulfate injected intraperitoneally into 24- to 27-g mice at a dose of 6.2 mg per mouse elicited botulism-like responses in less than 30 min, but a dose of 3.1 mg per mouse had no observable effect. The normally nontoxic 3.1-mg aminoglycoside dose aggravated the illness induced by an earlier injection of Clostridium botulinum type A or B toxin; it was usually lethal in 2 to 20 min if the preexisting illness was moderate to severe and worsened the condition of mice for about 30 min if the preexisting botulism was mild. The aminoglycoside had no effect when given shortly after the botulinum toxin was injected intraperitoneally; the sensitized state followed a latent period. It rapidly produced botulism-like effects when given to mice which had responded to a mixture of botulinum toxin and another mouse toxic agent with an illness that did not include signs of botulism. An unexpected illness devoid of botulism-like effects was encountered during intestinal colonization of mice by C. botulinum. The appearance of botulism-like signs soon after 3.1 mg of gentamicin sulfate was injected supported other suggestions that this illness included botulism that was masked by the effects of a second cause.

Aminoglycosides↗
PubMed2005

Characterization of the neurotoxin produced by isolates associated with avian botulism.

Several varieties of birds are affected by type C botulism. We conducted neutralization tests of culture supernatants of isolates from cases of avian botulism. Whereas the toxin produced by isolates derived from mammalian botulism was neutralized only with type C antitoxin, the toxins of all isolates related to avian botulism were neutralized with both type C and D antitoxins. An analysis of nucleotide sequences with several strains revealed that the neurotoxin gene in the isolates from avian botulism comprises two thirds of the type C neurotoxin gene and one third of the type D neurotoxin gene. This indicates that the neurotoxin of avian isolates is a mosaic of type C and D neurotoxins. We prepared three sets of primers to differentiate the gene for the mosaic form from the conserved genes of type C and D neurotoxins. The results of polymerase chain reaction with these primers indicated that all avian botulism-related isolates and specimens possess the gene for the mosaic form of the neurotoxin. The toxins purified from avian and mammalian isolates exhibited the same degree of lethality in mice, but the former showed greater toxicity to chickens than the latter. These results indicate that the mosaic neurotoxin is probably a pathogenic agent causing some forms of avian botulism.

Amino Acid Sequence↗
PubMed1994

Use of sentinel mallards for epizootiologic studies of avian botulism.

Captive-reared mallards (Anas platyrhynchos) were used as sentinels to study the epizootiology of avian botulism at the Sacramento National Wildlife Refuge, Willows, California (USA) from 1986 to 1989. Sentinel mallards were wing-clipped, and 40 to 50 birds were confined in 1.6-ha enclosures in 11 selected wetlands (pools). Enclosures were searched intensively three to four times weekly from July through October. Sick and dead wild and sentinel birds were collected, necropsied, and tested for type C botulism toxin. Botulism epizootics occurred in sentinel mallards in 1986, 1987, and 1989, but only a few isolated cases of botulism were detected in 1988. In most epizootics, botulism also was detected simultaneously in wild birds using the same pool outside the enclosure. Epizootics in sentinels were initiated and perpetuated in the absence of vertebrate carcasses. A sex-specific trend in the probability of intoxication was detected, with males contracting botulism at a higher rate than females. Daily mortality rates of sentinels during botulism epizootics ranged from 0.0006 to 0.0600, with a mean of 0.0190. These rates would result in the daily loss of 0.6 to 60 birds per thousand at risk. The use of sentinel birds provided an effective means of gathering site-specific epizootiologic data.

Animals↗
PubMed2002

[Botulism disease].

Botulism is caused by a neurotoxin produced from the anaerobic, spore forming bacteria--clostridium botulinum. The disease is usually caused by toxins type A, B and E. Since the disease was first recognized in the beginning of the nineteenth century as food poisoning, different forms of intoxication were described. Infantile botulism, wound botulism, infectious botulism and inadvertent botulism are all clinical syndromes caused by the same toxin. The attempt to use the botulinum toxin as biological warfare agent is well known. Recently the potential terrorist use of botulinum toxin has become a real concern. Botulism is characterized by its classic triad: 1) symmetric descending flaccid paralysis with prominent bulbar palsies 2) afebrile patient 3) clear sensorium. The paralysis usually begins in the cranial nerves where blurred vision, dysarthia and dysphagia are the initial complaints. Diagnosis is based on clinical findings, history of suspicious exposure and supportive ancillary testing to rule out other causes of neurologic dysfunction that mimic botulism such as the Guillain-Barre syndrome, Myasthenia Gravis or cerebrovascular stroke. Laboratory confirmation of suspected cases is usually delayed and treatment should begin before confirmation is completed. The treatment includes supportive care, and the administration of antitoxin which reduces mortality if given early. Since community and emergency room physicians may be the first to treat patients with any type of botulinum intoxication, they must know how to diagnose and treat this rare but potentially lethal disease.

Bioterrorism↗
PubMed2002

[Botulism in Casablanca. (11 cases)].

Botulism is a rare but severe disease. Whereas until 1980, only one case of botulism had been reported in our department, in 1999, a real botulism epidemic took place in Morocco. To our knowledge, it's the first outbreak of that kind in Morocco. We report here an epidemiologic and descriptive study of 11 patients suffering from botulism, admitted at the Infectious Diseases department and in the Medical Intensive Care Unit of Ibn Rochd University Hospital, from August, the 10th to October, the 1st, 1999. Clinical diagnosis of botulism was made, at the admission, on ocular signs (diplopia, ptosis), swallowing troubles and/or muscle weakness. There was no fever, no trouble of conscience and normal reflexes, at the early stage of the disease. The average age of patients was of 23.9 years +/- 12.07. Three patients were first admitted in the Medical Intensive Care Unit. The period before symptom appearance varied between 7 and 96 hours. Dysphagia sore throat, dry mouth and dysphonia were always found in all patients, with normal conscience. The fever was noted in 3 cases, polypnea in 3 cases leading to respiratory assistance in 2 cases. Neurologic findings were dominated by ptosis and hypotonia. The search of botulism toxin B in blood was positive in 6 cases. The electromyography showed clear signs of botulism. The evolution was favourable in 10 cases. Respiratory complications were found in 2 cases and infectious complications in 4 cases. One patient died. The period of hospitalization varied between 10 to 24 days with an average stay of 15.8 days. Eating "mortadella" has been noticed in 7 patients) and investigations permitted to identify the factory of "mortadella" as well as the toxin's type B responsible for these poisoning. It appears clearly that it is important to reinforce hygiene controls. Physicians and specialists in public health must be aware of the severity of this illness, knowing that the recovery is shortened when the treatment is administered on an early stage of the disease.

Adolescent↗
PubMedDate not supplied

[Infant botulism and sudden infant death syndrome].

Infant botulism represents a distinct entity of botulism. Ingestion of the ubiquitously present spores of Clostridium botulinum leads to germination of the organism and neurotoxin production in the infant intestine. Symptoms typically develop gradually in contrast to classical food botulism in which an acute onset of symptoms shortly after the ingestion of preformed toxin in a food is characteristic. Microbiologically, the diagnosis is established by identification of Clostridium botulinum organism and toxin in stool specimen. However, positive results in these tests provide only indirect evidence for the clinical relevance of the neurotoxin since asymptomatic carriers have been found. The toxin irreversibly blocks the release of acetylcholin from the motoric end plate which results in muscle weakness and paralysis. Depending on the amount of toxin produced, infant botulism exhibits a broad clinical spectrum ranging from oligosymptomatic forms to a fulminant course with acute respiratory failure within hours leading to sudden death. Unrecognized mild forms or beginning muscle weakness can be a co-factor for other risk factors of sudden infant death (SIDS). In studies analyzing infants who died from SIDS, botulism bacteria or toxin were found in up to 20 % of cases. Infant botulism therefore represents an important differential diagnosis of unexplained and inconclusive muscular hypotonia in the first year of life.

Acetylcholine↗
PubMedDate not supplied

[Sudden death of twins: botulism because of contamination by pap vegetables].

Botulism is caused by the blockage of the neural transmission in the cholinergic synapses by botulinum neurotoxin (BoNT) which is produced by Clostridium botulinum or other Clostridia. The classic form of botulism occurs after the ingestion of food contaminated by BoNT. The course of the infection can be asymptomatic, mild with subtle paralysis ("failure to thrive") oder severe with generalized paralysis ("floppy infant"). Infected infants can also die sudden and unexpectedly. These deaths often are attributed to Sudden Infant Death Syndrome (SIDS), unless a thorough postmortem examination reveals Botulism. The rate of fatal Botulism falsely attributed to SIDS is not known, because it is difficult in most cases to show the causal relationship between contamination, disease and death. We report the sudden and unexpected simultaneous death of twins of 22 months which could be attributed to Botulism. Contamination of food, colonization of the gut by Clostridia and infection with specific pathomorphological changes could be proven. The initial suspicion of infanticide could be excluded. lt could be shown, that Botulism is a potential cause of simultaneous unexpected deaths in twins.

Botulinum Toxins↗
PubMed1986

The changing epidemiology of adult botulism in the United States.

All forms of botulism are rare in the United States, and, as a result, descriptions of the pertinent epidemiologic features and clinical spectrum of illness are limited. This review describes the epidemiologic characteristics of the 355 cases of botulism in adults reported in the United States between 1976 and 1984, outlines current therapy, and emphasizes newly recognized features of the disease. Evaluation of recent data for botulism demonstrates several new associations and trends. These include the occurrence of large restaurant-associated outbreaks, several newly identified vehicles for foodborne botulism, wound botulism in parenteral drug abusers, and botulism from an unknown source in patients with underlying gastrointestinal disease. Recognition of these unusual features can lead to more effective preventive measures and to early diagnosis, which is essential for effective treatment.

Botulism↗
PubMed2004

Wound botulism in the UK and Ireland.

There are three main, naturally occurring, epidemiological types of botulism: food-borne, intestinal colonization (infant botulism) and wound botulism. The neurological signs and symptoms are the same for all three epidemiological types and may include respiratory paralysis. Wound botulism is caused by growth of cells and release of toxin in vivo, is associated with traumatic wounds and abscesses and has been reported in drug users, such as those injecting heroin or sniffing cocaine. Up to the end of 1999 there were no confirmed cases of wound botulism in the UK. Between the beginning of 2000 and the end of December 2002, there were 33 clinically diagnosed cases of wound botulism in the UK and Ireland. All cases had injected heroin into muscle or by 'skin popping'. The clinical diagnosis was confirmed by laboratory tests in 20 of these cases. Eighteen cases were caused by type A toxin and two by type B toxin.

Adult↗
PubMed2005

Adult botulism type F in the United States, 1981-2002.

BACKGROUND: Clostridium botulinum neurotoxin types A, B, and E cause most cases of the paralytic disease botulism. Little is known about the epidemiology, clinical features, or microbiology of botulism type F. METHODS: Cases of adult type F botulism were identified by review of data collected by CDC's National Botulism Surveillance System between 1981 and 2002. A case was either an individual whose serum or stool demonstrated type F toxin or whose stool culture yielded an organism producing toxin type F. A detailed review of cases' medical charts and laboratory data from CDC and local health departments was performed. RESULTS: Between 1981 and 2002, 1,269 cases of botulism among adults and infants were reported to CDC; 13 (1%) were adult type F. The median age of type F cases was 54 years; 7 (54%) were female. None were part of outbreaks. A toxigenic Clostridium baratii was identified in 9 (69%) of 13 cases. Among 11 cases for which clinical data were available, all required mechanical ventilation for a median duration of 17 days (range, 10 to 84); 8 (73%) were intubated within 24 hours of symptom onset. All patients had nearly complete or complete quadriplegia at the nadir of neurologic dysfunction, which occurred on average on day 5. On average by day 8, improvement in neuromuscular function was noted. The median duration of acute hospitalization was 31 days (range, 20 to 60). No deaths were reported. In only one case was a possible foodborne etiology identified. CONCLUSIONS: Toxigenic C baratii are the sole documented causes of type F botulism in the United States since 1981. These cases are characterized by a fulminant course with rapid progression to respiratory failure and paralysis, making early recognition and intervention critical to appropriate management.

Adult↗
PubMed1981

Patient recovery from type A botulism: morbidity assessment following a large outbreak.

A large outbreak of foodborne botulism provided an opportunity to study the recovery from type A botulism in a group of 27 patients. Patients were interviewed either nine or 13 months after the outbreak, and a written questionnaire was mailed at 24 months, to obtain information on each patient's symptom complex and on subsequent symptom resolution. Recovery from symptoms of botulism was slow. Patients reported that resolution of 50 per cent of their original symptoms occurred by an average of 5 months. Thirteen of 14 patients contacted 13 months after onset of botulism reported some persistent symptoms. This study, although limited to interview data, strengthens the concept of a prolonged recovery phase in botulism, as previously suggested in individual case reports. Physicians and other health workers caring for patients with botulism should anticipate physical and psychological problems resulting from a lengthy and difficult convalescent period.

Adult↗
PubMed2004

Clostridium botulinum and the clinical laboratorian: a detailed review of botulism, including biological warfare ramifications of botulinum toxin.

OBJECTIVE: This review article is designed to thoroughly familiarize all health care professionals with the history, classification, epidemiology, clinical characteristics, differential diagnosis, diagnostic evaluation (including laboratory-based testing), treatment, and prognosis of botulism. It is especially targeted toward clinical laboratorians and includes a detailed enumeration of the important clinical laboratory contributions to the diagnosis, treatment, and monitoring of patients with botulism. Finally, the bioterrorism potential for botulism is discussed, with an emphasis on the clinical laboratory ramifications of this possibility. DATA SOURCES: Included medical periodicals and textbooks accessioned from computerized and manual medical literature searches. More than 1000 medical works published from the 1800s through 2003 were retrieved and reviewed in this process. DATA SYNTHESIS: Pertinent data are presented in textual and tabular formats, the latter including 6 tables presenting detailed information regarding the clinical parameters, differential diagnosis, diagnostic studies, laboratory testing, and therapeutic approaches to botulism. CONCLUSIONS: Because botulism is such a rare disease, a keen awareness of its manifestations and prompt diagnosis are absolutely crucial for its successful treatment. The bioterrorism potential of botulism adds further urgency to the need for all health care professionals to be familiar with this disease, its proper evaluation, and timely treatment; the need for such urgency clearly includes the clinical laboratory.

Biological Warfare↗
PubMed2003

Infant botulism--New York City, 2001-2002.

Infant botulism results from germination of swallowed spores of botulinum toxin-producing clostridia that colonize the large intestine temporarily. Four cases of type B infant botulism in one New York City (NYC) borough were diagnosed within a 12-month period during 2001-2002. All four patients resided in Staten Island (2000 population: 443,728). The annual incidence of infant botulism in the United States is two cases per 100,000 live births; incidence in NYC is four cases per 100,000 live births. Staten Island recorded 5,899 live births in 2000; incidence of infant botulism during this 12-month period was 68 cases per 100,000 live births. This report summarizes the investigation of these four cases; as expected with infant botulism, a common source of exposure was not identified. All four patients recovered after treatment and were discharged from local hospitals. State and local health departments should be notified promptly when infant botulism is suspected to arrange diagnostic testing.

Botulinum Toxins↗
PubMed2006

Wound botulism acquired in the Amazonian rain forest of Ecuador.

Wound botulism results from colonization of a contaminated wound by Clostridium botulinum and the anaerobic in situ production of a potent neurotoxin. Between 1943, when wound botulism was first recognized, and 1990, 47 laboratory-confirmed cases, mostly trauma-associated, were reported in the United States. Since 1990, wound botulism associated with injection drug use emerged as the leading cause of wound botulism in the United States; 210 of 217 cases reported to the Centers for Disease Control and Prevention between 1990 and 2002 were associated with drug injection. Despite the worldwide distribution of Clostridium botulinum spores, wound botulism has been reported only twice outside the United States, Europe, and Australia. However, wound botulism may go undiagnosed and untreated in many countries. We report two cases, both with type A toxin, from the Ecuadorian rain forest. Prompt clinical recognition, supportive care, and administration of trivalent equine botulinum antitoxin were life-saving.

Adult↗
PubMed1990

A review of botulism in China.

The epidemiological characteristics and etiology of botulism in China, as well as the distribution of different types of Clostridium botulinum in China, are described. Through 1989, 15 provinces and autonomous regions reported the occurrence of botulism. There were 2861 cases involved in 745 outbreaks. Among the cases 421 died, with a case fatality of 14.7%. The main epidemiological characteristics of botulism in China are: (i) the major foods causing botulism are homemade fermented bean products which accounted for 62.6% of the cases; (ii) the incubation period is longer (3 h-54 days) than that described in the western literature (mostly 2-7 days); (iii) the peak occurrence is from February to May; (iv) the progression of symptoms and signs is slower than that of western cases. All types of C. botulinum, with the exception of type G, have been found in China. The distribution of various types of C. botulinum is significantly different between southern and northern China; this is related to the latitude and is correlated with the prevalence of this disease. Most of the botulism outbreaks occurred above 30 degrees north latitude in northern China and outbreaks rarely occurred below 30 degrees north latitude. Nationwide surveys showed that the average detection rate of C. botulinum spores in soil and foods in the northern parts of China was 14.8%, while it was only 2.5% in the south. C. botulinum types A, B, E, and F, which are involved in human botulism, were frequently found in the North, while types C and D, which are involved only in animal intoxication, were found more frequently in the south.

Botulism↗
PubMed2026

Tracing and characterization of a family outbreak of subtype B2 botulism linked to homemade pickled eggs in Jinan, China.

Foodborne botulism (FB) results from the ingestion of food contaminated with botulinum neurotoxin. Here, we report a family outbreak of foodborne botulism caused by Clostridium botulinum subtype B2 linked to homemade pickled eggs. On August 13, 2024, the Jinan Center for Disease Control and Prevention and the Shanghe County Center for Disease Control and Prevention collaborated to investigate an outbreak of botulism poisoning related to a family gathering in Shanghe County, Jinan City. A total of 4 people attended the family gathering, three of whom developed clinical symptoms of botulism after consuming pickled eggs. The diagnosis of botulism was suspected through collaborative efforts by the Qilu Medical Prevention and Control Innovation Integration Mechanism and multidisciplinary consultations across multiple hospitals. We detected the bont gene using real-time quantitative PCR (qPCR) in Jinan CDC, determined the toxin serotype by mouse bioassay (MBA) in China CDC and performed whole-genome sequencing of bacterial strains isolated from patient feces, the homemade pickled eggs and soil in both laboratories. It was shown that the toxin type and bont gene were subtype B2, belonging to the ha gene cluster. The Clostridium botulinum strains isolated from two patients were closely related to the strains from the homemade pickled eggs through whole-genome single nucleotide polymorphism analysis. We also found that Clostridium botulinum strains from soil clustered into one branch with those from patients and food, suggesting that the source of Clostridium botulinum contamination may be from soil, although the contamination pathway was not clear. Importantly, our findings provided a basis for clinical antitoxin treatment, in which one patient successfully gave birth after recovery. These results underscore the importance of strengthening public education about the health risks associated with consuming homemade fermented or preserved foods and enhancing the laboratory detection capabilities.

Botulism↗
PubMed1986

Infant botulism. Three cases in a small town.

Through Dec 31, 1985, there have been six cases of infant botulism reported in Colorado. Three of these infants have lived in the same town of 800 people in western Colorado. Two of these three infants developed infant botulism within a six-month period in late 1981. The infants lived approximately 400 m apart; they had used the same crib at the time each developed botulism. A specimen from the crib yielded Clostridium botulinum, as did four soil samples from the town and house-dust samples from the home of a relative of the second infant. The third infant developed infant botulism in September 1984. This infant had not shared the crib. In this case, all seven samples of soil from various locations in the town yielded C botulinum, as did a sample of house dust from the home of this infant. The occurrence of these three cases in such a small town seems unlikely to be only coincidental. Investigations and reports of other such clusters may provide insight into modes of transmission of infant botulism.

Beds↗