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.     

Intestinal toxemia botulism in two young people, caused by Clostridium butyricum type E.

Two unconnected cases of type E botulism involving a 19-year-old woman and a 9-year-old child are described. The hospital courses of their illness were similar and included initial acute abdominal pain accompanied by progressive neurological impairment. Both patients were suspected of having appendicitis and underwent laparotomy, during which voluminous Meckel's diverticula were resected. Unusual neurotoxigenic Clostridium butyricum strains that produced botulinum-like toxin type E were isolated from the feces of the patients. These isolates were genotypically and phenotypically identical to other neurotoxigenic C. butyricum strains discovered in Italy in 1985-1986. No cytotoxic activity of the strains that might explain the associated gastrointestinal symptoms was demonstrated. The clinical picture of the illness and the persistence of neurotoxigenic clostridia in the feces of these patients suggested a colonization of the large intestine, with in vivo toxin production. The possibility that Meckel's diverticulum may predispose to intestinal toxemia botulism may warrant further investigation.     

Botulism in Brazil, 2000-2008: epidemiology, clinical findings and laboratorial diagnosis

Botulism is a rare and potentially lethal illness caused by Clostridium botulinum neurotoxin. We describe the findings of a laboratorial investigation of 117 suspected cases of botulism reported to the surveillance system in Brazil from January 2000 to October 2008. Data on the number and type of samples analyzed, type of toxins identified, reporting of the number of botulism cases and transmission sources are discussed. A total of 193 clinical samples and 81 food samples were analyzed for detection and identification of the botulism neurotoxin. Among the clinical samples, 22 (11.4%) presented the toxin (nine type A, five type AB and eight with an unidentified type); in food samples, eight (9.9%) were positive for the toxin (five type A, one type AB and two with an unidentified type). Of the 38 cases of suspected botulism in Brazil, 27 were confirmed by a mouse bioassay. Laboratorial botulism diagnosis is an important procedure to elucidate cases, especially food-borne botulism, to confirm clinical diagnosis and to identify toxins in food, helping sanitary control measures.     

Bichat guidelines for the clinical management of botulism and bioterrorism-related botulism

Botulism is a rare but serious paralytic illness caused by botulinum toxin, which is produced by the Clostridium botulinum. This toxin is the most poisonous substance known. It 100,000 times more toxic than sarin gas. Eating or breathing this toxin causes illness in humans. Four distinct clinical forms are described: foodborne, wound, infant and intestinal botulism. The fifth form, inhalational botulism, is caused by aerosolised botulinum toxin that could be used as a biological weapon. A deliberate release may also involve contamination of food or water supplies with toxin or C. botulinum bacteria. By inhalation, the dose that would kill 50% of exposed persons (LD50) is 0.003 microgrammes/kg of body weight. Patients with respiratory failure must be admitted to an intensive care unit and require long-term mechanical ventilation. Trivalent equine antitoxins (A,B,E) must be given to patients as soon as possible after clinical diagnosis. Heptavalent human antitoxins (A-G) are available in certain countries.     

Foodborne botulism in a six-month-old infant caused by home-canned baby food

Previously reported cases of botulism in infants have been diagnosed as infant botulism; that is, botulism caused by intestinal colonization by Clostridium botulinum with intraluminal production and absorption of toxin. Foodborne botulism is caused by ingestion of preformed toxin. We describe an unusual case of foodborne botulism in a 6-month-old infant caused by the ingestion of improperly prepared home-canned baby food. This represents the youngest age of onset for foodborne botulism in the United States of which we are aware and illustrates the need to rule out foodborne botulism, which represents a public health emergency, regardless of the patient's age. The diagnosis could have been readily missed or delayed in this case because the weakness was rapidly progressive rather than insidious, as is typical of infant botulism.     

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.     

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.     

Surveillance of foodborne botulism in Poland: 1960-1998

Human foodborne botulism, in contrast to the other two forms of botulism (wound and infant botulism), is an intoxication that results when preformed botulinum toxin is ingested. Sporadic cases and family and general outbreaks occur when food products are     

An outbreak of botulism in a family in Eastern Anatolia associated with eating süzme yoghurt buried under soil

Cases of botulism in a family in eastern Anatolia were studied. In late September 2005, an outbreak of botulism developed in our region, first in 2 patients, a teenage boy and his mother, in whom the disease culminated in respiratory insufficiency and death. An additional 8 cases of botulism were identified later; most of them presented to our medical centre the next d. These patients with milder symptoms recovered gradually. All the patients received anti-botulinum toxin. The investigation of the source of the outbreak showed an unexpected vehicle for botulism infection in the these patients, süzme (condensed) yoghurt buried under soil. Type A botulinal toxin was detected in the yoghurt sample. The clinical diagnosis was also confirmed by a mouse bioassay performed with the serum samples of the patients. The most common symptoms were dry mouth, difficulty in speaking and swallowing, and change in voice quality. The 10 identified patients with botulism constitutes the largest-ever outbreak of botulism reported in Turkey to date. The present study shows the importance of considering a diagnosis of botulism soon after patients present with acute cranial nerve dysfunction and of promptly treating suspected cases with antitoxin.     

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.     

Early and late pulmonary complications of botulism

Pulmonary complications of botulism were studied in an outbreak of 34 cases of type A botulism in New Mexico in 1978. Hospital record review, standardized questionnaires, and pulmonary function tests were used to define pulmonary complications during the acute illness and the patient's status one year later. Pulmonary involvement was documented in 81% of patients. Ventilatory failure occurred in 11, aspiration pneumonia in nine, and death in two patients. Difficulties in the diagnosis of ventilatory insufficiency were identified. At one year, most patients had residual symptoms, including easy fatigability in 68% and exertional dyspnea in 46%. However, only minor pulmonary function abnormalities were present. This study confirms the generally favorable prognosis of botulism and provides clinical guidance for the diagnosis and management of pulmonary complications in botulism.     

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.     

云南省宁蒗县不明原因猝死病例调查研究

目的探讨云南省宁蒗县不明原因猝死病例的死因。方法对云南省宁蒗县不明原因猝死病例进行现场流行病学调查,采集样本进行病理学、病毒学等相关检验及分析研究。结果猝死病例的临床表现类似阿-斯综合征发作,心电图示窦性心动过速、Q-T间期延长、ST段改变、室颤,病理检验主要以心肌间质水肿、弥漫性炎细胞浸润、心肌纤维断裂、心肌灶性坏死以及其他脏器炎细胞浸润等改变为主;同发病例的临床表现亦类似阿-斯综合征发作,心电图示Q-T间期延长、室扑,粪便标本病毒分离阴性,但是从中检测到了埃可病毒11型(ECHO11)的基因片段。结论猝死病例及同发病例与既往报道的云南地方性爆发性心肌炎类似,心肌炎性改变可能诱发快速心律失常,引起阿-斯综合征发作,最后导致发病甚至猝死。     

Histopathological study of pancreatic duct in acute fulminant pancreatitis

AIM: To study the pathological changes in the pancreas of acute fulminant pancreatitis patients suffering from sudden death. METHODS: Pancreatic duct specimens taken at autopsy from 30 patients with acute fulminant pancreatitis were examined under a light microscope for histopathological changes, with those of 30 other patients who died of other diseases as controls. RESULTS: Among the 30 cases of acute fulminant pancreatitis, 29 (96.7%) were non-inflammatory including hemorrhagic necrotic type (2 cases) and one were inflammatory. The pathological findings showed that all the above types had pancreatic ductal changes, including the accumulation of shed ductal epithelial cells, eosinophilic materials in the ductal lumen and the presence of ductules in the wall of the pancreatic duct. In the control group, except for 1 case presenting ductules, there were no other changes observed. CONCLUSION: Abnormal structural changes can cause damage to the ductal system of the pancreas, leading to an escape of activated proteolytic and lipolytic enzymes into the interstitial tissues and resulting in edema, ischemia, hemorrhage, necrosis and development of acute fulminant pancreatitis, which is an important cause of sudden death.     

An outbreak of foodborne botulism in Ontario

Botulism is a rare paralytic illness resulting from a potent neurotoxin produced by Clostridium botulinum. Botulism in Canada is predominately due to C botulinum type E and affects mainly the First Nations and Inuit populations. The most recent outbreak of botulism in Ontario was in Ottawa in 1991 and was caused by C botulinum type A. We report an outbreak of foodborne type B botulism in Ontario, which implicated home-canned tomatoes. The outbreak was characterized by mild symptoms in two cases and moderately severe illness in one case. The investigation shows the importance of considering the diagnosis of botulism in patients presenting with cranial nerve and autonomic dysfunction, especially when combined with gastrointestinal complaints; it also highlights the importance of proper home canning technique.Key Words: Botulism, Clostridium botulinum, Pyo-mediastinitis, OutbreakBotulism is a neuroparalytic illness resulting from a potent toxin produced by the bacterium Clostridium botulinum (1 ). Foodborne botulism results from the ingestion of foods contaminated with one of three preformed toxins (A, B or E). Although foodborne botulism is a rare disease, its manifestations can be severe and can progress rapidly. Because of the potential severity of the disease and the possibility of exposure of a large number of people to contaminated products, foodborne botulism is a public health emergency requiring rapid investigation. Hauschild and Gauvreau published a thorough summary of all the botulism outbreaks in Canada between 1971 and 1984 (2 ). There were 61 outbreaks with 122 cases and 22 deaths. The Botulism Reference Service for Canada also summarized the botulism outbreaks in Canada between 1976 and 1987, in the year 1989, and between 1995 and 1997 (3 -17 ). In the three most recent reports, in 1995, 1996 and 1997, there were five to seven outbreaks per year with 13, 10 and 18 cases, respectively (15 -17 ). All of the outbreaks have been in Quebec, North West Territories, Yukon, British Columbia and Nunavut, and have primarily affected the First Nations population, particularly the Inuit. Fifty-nine per cent of the outbreaks were due to contaminated mammal meat (seal, whale, walrus) and 23% were due to fermented salmon eggs or fish. Only three (16%) outbreaks were due to home-canned foods and one (5%) was due to a commercial product. The majority (90%) of outbreaks in Canada are due to serotype E. The most recent outbreak of botulism in Ontario was in Ottawa in 1991 and was due to serotype A; however, the outbreak was never reported (KL Dodds, personal communication). Three cases were involved in this outbreak, which was caused by home-canned asparagus. The last reported case of botulism in Ontario was in 1972 (2 ). It was a case of type B botulism related to contaminated home-salted pork.This report summarizes the investigation and outcome of an outbreak of foodborne type B botulism in Ontario that implicated home-canned tomatoes. The outbreak was characterized by relatively mild symptoms in two cases and moderately severe illness in one case and was caused by an unlikely food vehicle. The investigation shows the importance of considering the diagnosis of botulism soon after patients present with acute cranial nerve dysfunction, autonomic dysfunction and gastrointestinal complaints; it also highlights the importance of proper home canning techniques.     

Epidemiology and risk factors for notifiable Clostridium botulinum infections in Taiwan from 2003 to 2020

Botulinum toxin is produced by Clostridium botulinum, a gram-positive anaerobic bacterium. This study aimed to examine the epidemiological characteristics, including sex, age, season in which infection occurred, place of residence, and epidemiological trends, of confirmed botulism cases in Taiwan from 2003 to 2020. This study examined the annual summary data on reported botulism in Taiwan’ s Center for Disease Control from 2003 to 2020 available to the public on the internet. We found that there were 50 confirmed domestic cases of botulism. The incidence of botulism ranged from 0 to 0.48 per 1000,000 from 2003 to 2020 and peaked in 2008 and 2010. During the 18-year investigation period in which 6-year intervals were used, the study results showed a decreasing trend (2003–2008, 2009–14, and 2015–2020, had 22, 19, 9 cases each). In terms of patients’ gender, age, and place of residence, most of the patients were females (56%), were aged ≥ 50 years (48%), and resided in Taipei and northern Taiwan (44%). The number of botulism cases in Taiwan from 2012 to 2020 compared with other years (from 2003 to 2011) found that there were significant differences among patients within an age group of <20 years (P = .003, odds ratio = 18.500, and 95% confidence interval = 3.287–104.111), and there were significant differences among patients whose place of residence was Taipei metropolitan area (P = .025, odds ratio = 5.667, and 95% confidence interval = 1.248–25.734). During 2003 to 2009, there was no case of botulism among those aged <20 years. Over the last 10 years, botulism in children showed an increasing trend. A total of 9 children were found to have botulism during 2010 to 2020; most of these children were male (66.7%) and were infected during spring and summer (66.7%). This study is the first to report the number of confirmed domestic cases with botulism from surveillance data from Taiwan’s Center for Disease Control during 2003 to 2020. This study also found that the place of residence and age were associated with an increased risk of botulism in Taiwan. This information may be useful for policymakers and clinical experts to direct prevention- and control-based activities regarding botulism that result in the most severe illness and the greatest burden on Taiwanese.     

云南省地方性猝死的死因调查分析

目的调查云南省地方性猝死(亦称云南省地方性爆发性心肌炎,曾称云南省爆发性病毒性心肌炎)的死亡性质,为有效防治该病提供依据。方法以临床医学检查及现场流行病学调查为主要方法,调查15例死者的发病与死亡经过,并对5例死者做尸解,进行病理诊断以确定死因;同时对死者所在病区居民157人进行查体、心电图、X线检查、心肌酶学检查及现场流行病学调查,以确定各调查点的现有患者,为分析死亡原因提供重要依据。结果2004年调查的15例死者中,死因为克山病者10例,疑似克山病者2例,死于肺性脑病者2例,无法确定死因者1例;检诊病区居民共计157例,查出克山病现患5例,其中3例为新检出者。在所检查的死者和居民中均未发现可以诊断病毒性心肌炎或爆发性病毒性心肌炎的患者。结论在2004年所调查的15例云南省地方性猝死死者中有10例死者的死因确定为克山病。     

Exacerbation of bacterial toxicity to infant ferrets by influenza virus: possible role in sudden infant death syndrome

Of several toxins examined, only staphylococcal alpha and gamma toxin, endotoxin, and diphtheria toxins were lethal for 5-day-old ferrets. Their toxicities were enhanced in animals infected at 1 day old with influenza virus, from 3-fold with staphylococcal gamma toxin through 14-fold for staphylococcal alpha toxin, 84-fold for endotoxin, and 219-fold for diphtheria toxin. No increased viral replication occurred in any tissue; thus the effects of the toxins were exacerbated by the infection, not vice versa. Neonates died suddenly without clinical symptoms as in human babies dying from the sudden infant death syndrome (SIDS). Pathologic examination showed inflammation in the upper respiratory tract, lung edema and collapse, and early bronchopneumonia in the toxin- and influenza virus-treated animals but not in those treated with toxin or virus alone. Thus, bacterial toxins could play a role in SIDS, this being more likely with a concomitant influenza virus infection.     

Infant botulism was confirmed in Ehime Prefecture

The third case of infant botulism in Japan is reported. A four-month-old baby boy suddenly had weakness of suckling force, constipation and generalized hypotonicity. He was the product of normal gestation, labor and delivery. Growth and development were normal until he was nineteen weeks old. He received fruit-juice and honey daily. By bacteriological examination, Clostridium botulism type A was isolated from his feces and the honey which he had received. Type A toxin was detected from his feces but not from his serum.     

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.