The Short-Lived Epidemic of Botulism From Commercially Canned Foods in the United States, 1919 to 1925.

In 1919, three deadly outbreaks of botulism caused by consumption of canned olives packed in California captured national headlines. In all of the outbreaks, which occurred in separate locales, unsuspecting people died after consuming tainted food during a banquet or family meal. The press's sensational portrayal of canned food as hazardous aroused alarm among consumers at a time when commercial canning was becoming more common. Intent on restoring the image of their product as safe and wholesome, canning industry leaders funded a "botulism commission" of scientific experts in 1919 to investigate how to systematically eliminate the threat of botulism that had imperiled their business. The commissioners identified the scientific reasons for the outbreaks, and on the basis of their findings, the California Department of Public Health issued explicit recommendations for sterilization procedures intended to ensure safety. However, the department did not mandate inspections for all canneries. When commercially packed fruits and vegetables continued to cause botulism, industry leaders voluntarily backed a cannery inspection act to legally require all California canners to possess appropriate equipment and follow scientifically validated sterilization procedures. After the California legislature approved the act in 1925, canneries were inspected, regulations were enforced, and no further outbreaks occurred. This botulism epidemic is an example of a disease outbreak that was controlled when business interests became aligned with public health goals. The press's portrayal of afflicted persons as innocent victims and worthy citizens galvanized businessmen to implement safeguards to protect consumers from botulism intoxication. To preserve their customer base and salvage their corporations, leaders of the canning industry acknowledged the public health threat of their unregulated procedures and acted on the recommendations of scientists.

Molecular epidemiology of infant botulism in California and elsewhere, 1976-2010.

BACKGROUND: Infant botulism (IB), first identified in California in 1976, results from Clostridium botulinum spores that germinate, multiply, and produce botulinum neurotoxin (BoNT) in the immature intestine. From 1976 to 2010 we created an archive of 1090 BoNT-producing isolates consisting of 1012 IB patient (10 outpatient, 985 hospitalized, 17 sudden death), 25 food, 18 dust/soils, and 35 other strains. METHODS: The mouse neutralization assay determined isolate toxin type (56% BoNT/A, 32% BoNT/B). Amplified fragment-length polymorphism (AFLP) analysis of the isolates was combined with epidemiologic information. RESULTS: The AFLP dendrogram, the largest to date, contained 154 clades; 52% of isolates clustered in just 2 clades, 1 BoNT/A (n=418) and 1 BoNT/B (n=145). These clades constituted an endemic C. botulinum population that produced the entire clinical spectrum of IB. Isolates from the patient's home environment (dust/soil, honey) usually located to the same AFLP clade as the patient's isolate, thereby identifying the likely source of infective spores. C. botulinum A(B) strains were identified in California for the first time. CONCLUSIONS: Combining molecular methods and epidemiological data created an effective tool that yielded novel insights into the genetic diversity of C. botulinum and the clinical spectrum, occurrence, and distribution of IB in California.

[The route of botulinum toxin from cause of food poisoning to medical remedy]. / Botuliinin tie ruokamyrkytyksen aiheuttajasta lääkkeeksi.

Botulinum toxins are amongst the most poisonous substances known in nature. The discovery and development of this toxin into a medical remedy is one of the most fascinating stories in the history of medicine. German physician Justinus Kerner founded the theory of treating hyperactive disorders with botulinum toxin and Alan Scott was the one to make this happen successfully. Nowadays the toxin is widely used in different indications, and the research is still going on for discovering novel tools for treating e.g. pain.

Foodborne botulism in Canada, 1985-2005.

During 1985-2005, a total of 91 laboratory-confirmed outbreaks of foodborne botulism occurred in Canada; these outbreaks involved 205 cases and 11 deaths. Of the outbreaks, 75 (86.2%) were caused by Clostridium botulinum type E, followed by types A (7, 8.1%) and B (5, 5.7%). Approximately 85% of the outbreaks occurred in Alaska Native communities, particularly the Inuit of Nunavik in northern Quebec and the First Nations population of the Pacific coast of British Columbia. These populations were predominantly exposed to type E botulinum toxin through the consumption of traditionally prepared marine mammal and fish products. Two botulism outbreaks were attributed to commercial ready-to-eat meat products and 3 to foods served in restaurants; several cases were attributed to non-Native home-prepared foods. Three affected pregnant women delivered healthy infants. Improvements in botulism case identification and early treatment have resulted in a reduction in the case-fatality rate in Canada.

The unusual history and the urological applications of botulinum neurotoxin.

INTRODUCTION: Botulinum neurotoxin (BoNT) is probably the most potent biological toxin that can affect humans. Since its discovery by Justinus Kerner, BoNT has seen use in a wide range of cosmetic and non-cosmetic conditions such as cervical dystonia, cerebral palsy, migraines and hyperhidrosis. We tried to trace its history from its inception to its recent urological applications. MATERIALS AND METHODS: Historical articles about botulinum toxin were reviewed and a Medline search was performed for its urological utility. We hereby present a brief review of historical aspects of BoNT and its applications in urology. RESULTS: In 1793, the first known outbreak of botulism occurred due to 'spoiled' sausage in Wildebad, Germany. The German physician and poet Justinus Kerner published the first accurate description of the clinical symptoms of botulism (sausage poison). He was also the first to mention its potential therapeutic applications. In urology, BoNT has been used in bladder and urethral lesions with varying degree of success. Recently, BoNT applications were explained for prostatic disorders. BoNT applications in urology are in the treatment of detrusor external sphincter dyssynergia, detrusor overactivity, detrusor underactivity, spastic conditions of the urethral sphincter, chronic prostate pain, interstitial cystitis, non-fibrotic bladder outflow obstruction (including benign prostatic hyperplasia) and acute urinary retention in women. CONCLUSION: Justinus Kerner is the godfather of botulism research. The role of BoNT in urology has evolved exponentially and it is widely used as an adjuvant in voiding dysfunction. In the future, its utility will broaden and guide the urologist in managing various urological disorders.

Foodborne Botulism: Clinical Diagnosis and Medical Treatment.

Botulinum neurotoxins (BoNTs) produced by Clostridia species are the most potent identified natural toxins. Classically, the toxic neurological syndrome is characterized by an (afebrile) acute symmetric descending flaccid paralysis. The most know typical clinical syndrome of botulism refers to the foodborne form. All different forms are characterized by the same symptoms, caused by toxin-induced neuromuscular paralysis. The diagnosis of botulism is essentially clinical, as well as the decision to apply the specific antidotal treatment. The role of the laboratory is mandatory to confirm the clinical suspicion in relation to regulatory agencies, to identify the BoNTs involved and the source of intoxication. The laboratory diagnosis of foodborne botulism is based on the detection of BoNTs in clinical specimens/food samples and the isolation of BoNT from stools. Foodborne botulism intoxication is often underdiagnosed; the initial symptoms can be confused with more common clinical conditions (i.e., stroke, myasthenia gravis, Guillain-Barré syndrome-Miller-Fisher variant, Eaton-Lambert syndrome, tick paralysis and shellfish or tetrodotoxin poisoning). The treatment includes procedures for decontamination, antidote administration and, when required, support of respiratory function; few differences are related to the different way of exposure.

Human Botulism in France, 1875-2016.

Botulism is a rare but severe disease which is characterized by paralysis and inhibition of secretions. Only a few cases had been reported at the end of the 19th century in France. The disease was frequent during the second world war, and then the incidence decreased progressively. However, human botulism is still present in France with 10-25 cases every year. Food-borne botulism was the main form of botulism in France, whereas infant botulism (17 cases between 2004 and 2016) was rare, and wound and inhalational botulism were exceptional. Type B was the prevalent botulism type and was mainly due to consumption of home-made or small-scale preparations of cured ham and to a lesser extent other pork meat products. In the recent period (2000-2016), a wider diversity of botulism types from various food origin including industrial foods was reported. Severe cases of type A and F botulism as well as type E botulism were more frequent. Albeit rare, the severity of botulism justifies its continued surveillance and recommendations to food industry and consumers regarding food hygiene and preservation practices.

A brief history of botulism in South Africa.

When looking back into the history of botulism and contemplating the final understanding of the syndrome and the ultimate solutions, there are four facets that stand out clearly. The first is that much of the solution was guided by astute observations, curious travellers, committed veterinarians and particularly farmers themselves who were able to relate the occurrence of the condition to climatic and grazing conditions. Secondly, there was the identification of the osteophagia and pica syndrome which led to the feeding of bone-meal as a successful mitigating measure as well as the establishment that botulism was not due to a plant poisoning. Thirdly, the solution of the problem depended on the integration of experience and knowledge from diverse disciplines such as soil science, animal behaviour and husbandry, nutrition, botany and ultimately advanced bacteriology and the science of immunology. Finally it required the technical advancement to produce toxoids in large quantities and formulate effective aluminium hydroxide precipitated and oil emulsion vaccines.

The story of Clostridium botulinum: from food poisoning to Botox.

In the last fifty years, Clostridium botulinum has become notorious for its ability to produce the deadly botulinum neurotoxins. While botulinum toxin A, better known as Botox, is universally recognised by the public as a cosmetic enhancement tool, the botulinum neurotoxins are commonly used off-label for many medical conditions in ophthalmology, neurology and dermatology. The versatility of these botulinum toxins has made Clostridium botulinum one of the most widely known bacterial pathogens in medical history. This article outlines the discovery of botulinum toxins through to their present day applications in medicine.

[The men of the Andrée expedition probably died of botulism. A new hypothesis explains these mysterious deaths]. / Andrée-expeditionens män dog troligen av botulism. Ny hypotes förklarar de mystiska dödsfallen.

The last camp of the three members of the 1897 Swedish Andrée balloon expedition to the North Pole was found in Svalbard in 1930. The human remains and the paraphernalia of the expedition including diaries were brought to Sweden and are presently housed in a museum. The cause of the deaths has never been determined, but several hypotheses have been put forward over the years. Trichinosis, scurvy, and poisoning by carbon-monoxide, vitamin-A or lead are some of them. In this article it is argued that botulism is a plausible explanation which is in better accord with known facts.

Lamsiekte (botulism): solving the aetiology riddle.

The reason or reasons why it took Sir Arnold Theiler so many years to unravel the riddle of the aetiology of lamsiekte in cattle and whether P.R. Viljoen's lifelong grudge for receiving insufficient credit from Theiler for his research contribution was justified are analysed in this paper. By 1912, Theiler knew that Duncan Hutcheon had advocated the use of bonemeal as a prophylactic against the disease in the early 1880s. Hutcheon's colleague, J.D. Borthwick, had shown conclusively in a field experiment in 1895 that lamsiekte did not occur in cattle fed a liberal allowance of bonemeal; and bone-craving had been identified by Hutcheon and several farmers as being associated with the occurrence of the disease (a 'premonitory' sign). Hutcheon regarded a phosphate deficiency of the pastures as the direct cause of lamsiekte. However, Theiler did not accept this, was convinced that intoxication was involved and developed a 'grass toxin' theory. Viljoen (1918) also latched onto the grass toxin theory. He did not believe that osteophagia existed, stating categorically that he had not observed it on the experimental farm Armoedsvlakte where > 100 cases of lamsiekte had occurred during the > 3 years that he spent there. Moreover, he did not believe in the prophylactic value of bonemeal. However, careful analysis of a subsequent publication, of which he was a co-author, revealed that in late 1918 and early 1919 he reproduced the disease by drenching cattle with blowfly pupae and larvae as well as with crushed bones from decomposing bovine carcasses. For this breakthrough he did not get proper credit from Theiler. Reappointed to study lamsiekte on Armoedsvlakte in the autumn of 1919, Theiler, probably already aware that the toxin he was seeking was in the decomposing bones or carcass material rather than the grass, deliberately 'walked with the cattle' on the farm to encounter a classic manifestation of bone-craving (osteophagia). The penny then immediately dropped. Theiler, actually rationalising an hypothesis that was about four decades old, did so with a vengeance. Within less than two years he had reproduced lamsiekte by exposing cattle with natural bone-craving to rotten carcass material, had chemical proof that the grazing was phosphorus-deficient, had developed a satisfactory bonemeal prophylactic dosage programme, and the bacterial toxin concerned - perhaps the trickiest contribution - had been produced in culture. Hence the table was set for the later development of an excellent lamsiekte vaccine.