Jump to content

Clostridium botulinum

From Wikipedia, the free encyclopedia

Clostridium botulinum
Clostridium botulinum stained with gentian violet.
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Bacillota
Class: Clostridia
Order: Eubacteriales
Family: Clostridiaceae
Genus: Clostridium
Species:
C. botulinum
Binomial name
Clostridium botulinum

Clostridium botulinum is a gram-positive,[1] rod-shaped, anaerobic, spore-forming, motile bacterium with the ability to produce botulinum toxin, which is a neurotoxin.[2][3]

C. botulinum is a diverse group of pathogenic bacteria. Initially, they were grouped together by their ability to produce botulinum toxin and are now known as four distinct groups, C. botulinum groups I–IV. Along with some strains of Clostridium butyricum and Clostridium baratii, these bacteria all produce the toxin.[2]

Botulinum toxin can cause botulism, a severe flaccid paralytic disease in humans and other animals,[3] and is the most potent toxin known to science, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans.[4][5]

C. botulinum is commonly associated with bulging canned food; bulging, misshapen cans can be due to an internal increase in pressure caused by gas produced by bacteria.[6]

C. botulinum is responsible for foodborne botulism (ingestion of preformed toxin), infant botulism (intestinal infection with toxin-forming C. botulinum), and wound botulism (infection of a wound with C. botulinum). C. botulinum produces heat-resistant endospores that are commonly found in soil and are able to survive under adverse conditions.[2]

Microbiology

[edit]

C. botulinum is a Gram-positive, rod-shaped, spore-forming bacterium.[1] It is an obligate anaerobe, the organism survives in an environment that lacks oxygen. However, C. botulinum tolerates traces of oxygen due to the enzyme superoxide dismutase, which is an important antioxidant defense in nearly all cells exposed to oxygen.[7] C. botulinum is able to produce the neurotoxin only during sporulation, which can happen only in an anaerobic environment.

C. botulinum is divided into four distinct phenotypic groups (I-IV) and is also classified into seven serotypes (A–G) based on the antigenicity of the botulinum toxin produced.[8][9] On the level visible to DNA sequences, the phenotypic grouping matches the results of whole-genome and rRNA analyses,[10][11] and setotype grouping approximates the result of analyses focused specifically on the toxin sequence. The two phylogenetic trees do not match because of the ability of the toxin gene cluster to be horizontally transferred.[12]

Serotypes

[edit]
Main article: Botulinum toxin

Botulinum neurotoxin (BoNT) production is the unifying feature of the species. Seven serotypes of toxins have been identified that are allocated a letter (A–G), several of which can cause disease in humans. They are resistant to degradation by enzymes found in the gastrointestinal tract. This allows for ingested toxins to be absorbed from the intestines into the bloodstream.[5] Toxins can be further differentiated into subtypes on the bases of smaller variations.[13] However, all types of botulinum toxin are rapidly destroyed by heating to 100 °C for 15 minutes (900 seconds). 80 °C for 30 minutes also destroys BoNT.[14][15]

Most strains produce one type of BoNT, but strains producing multiple toxins have been described. C. botulinum producing B and F toxin types have been isolated from human botulism cases in New Mexico and California.[16] The toxin type has been designated Bf as the type B toxin was found in excess to the type F. Similarly, strains producing Ab and Af toxins have been reported.[12]

Evidence indicates the neurotoxin genes have been the subject of horizontal gene transfer, possibly from a viral (bacteriophage) source. This theory is supported by the presence of integration sites flanking the toxin in some strains of C. botulinum. However, these integrations sites are degraded (except for the C and D types), indicating that the C. botulinum acquired the toxin genes quite far in the evolutionary past. Nevertheless, further transfers still happen via the plasmids and other mobile elements the genes are located on.[17]

Toxin types in disease

[edit]

Only botulinum toxin types A, B, E, F and H (FA) cause disease in humans. Types A, B, and E are associated with food-borne illness, while type E is specifically associated with fish products. Type C produces limber-neck in birds and type D causes botulism in other mammals.[18] No disease is associated with type G.[19] The "gold standard" for determining toxin type is a mouse bioassay, but the genes for types A, B, E, and F can now be readily differentiated using quantitative PCR.[20] Type "H" is in fact a recombinant toxin from types A and F. It can be neutralized by type A antitoxin and no longer is considered a distinct type.[21]

A few strains from organisms genetically identified as other Clostridium species have caused human botulism: C. butyricum has produced type E toxin[22] and C. baratii had produced type F toxin.[23] The ability of C. botulinum to naturally transfer neurotoxin genes to other clostridia is concerning, especially in the food industry, where preservation systems are designed to destroy or inhibit only C. botulinum but not other Clostridium species.[12]

Metabolism

[edit]

Many C. botulinum genes play a role in the breakdown of essential carbohydrates and the metabolism of sugars. Chitin is the preferred source of carbon and nitrogen for C. botulinum.[24] Hall A strain of C. botulinum has an active chitinolytic system to aid in the breakdown of chitin.[24] Type A and B of C. botulinum production of BoNT is affected by nitrogen and carbon nutrition.[25][26][27] There is evidence that these processes are also under catabolite repression.[28]

Groups

[edit]

Physiological differences and genome sequencing at 16S rRNA level support the subdivision of the C. botulinum species into groups I-IV.[10] Some authors have briefly used groups V and VI, corresponding to toxin-producing C. baratii and C. butyricum. What used to be group IV is now C. argentinense.[29]

Phenotypic groups of toxin-producing Clostridium[11][29]
Property Group I Group II Group III C. argentinense C. baratii C. butyricum
Proteolysis (casein) + - - + - -
Saccharolysis - + - -
Lipase + + + - - -
Toxin Types A, B, F B, E, F C, D G F E
Toxin gene chromosome/plasmid chromosome/plasmid bacteriophage plasmid chromosome[30] chromosome[31]
Close relatives
  • C. beijerinckii
  • C. butyricum
 N/A (already a species)

Although group II cannot degrade native protein such as casein, coagulated egg white, and cooked meat particles, it is able to degrade gelatin.[32]

Human botulism is predominantly caused by group I or II C. botulinum.[32] Group III organisms mainly cause diseases in non-human animals.[32]

Laboratory isolation

[edit]

In the laboratory, C. botulinum is usually isolated in tryptose sulfite cycloserine (TSC) growth medium in an anaerobic environment with less than 2% oxygen. This can be achieved by several commercial kits that use a chemical reaction to replace O2 with CO2. C. botulinum (groups I through III) is a lipase-positive microorganism that grows between pH of 4.8 and 7.0 and cannot use lactose as a primary carbon source, characteristics important for biochemical identification.[33]

Transmission and sporulation

[edit]

The exact mechanism behind sporulation of C. botulinum is not known. Different strains of C. botulinum can be divided into three different groups, group I, II, and III, based on environmental conditions like heat resistance, temperature, and biome.[34] Within each group, different strains will use different strategies to adapt to their environment to survive.[34] Unlike other clostridial species, C. botulinum spores will sporulate as it enters the stationary phase.[35] C. botulinum relies on quorum-sensing to initiate the sporulation process.[35] C. botulinum spores are not found in human feces unless the individual has contracted botulism,[36] but C. botulinum cannot spread from person to person.[37]

Motility structures

[edit]

The most common motility structure for C. botulinum is a flagellum. Though this structure is not found in all strains of C. botulinum, most produce peritrichous flagella.[38] When comparing the different strains, there is also differences in the length of the flagella and how many are present on the cell.[38]

Growth conditions and prevention

[edit]
See also: Botulism § Prevention

C. botulinum is a soil bacterium. The spores can survive in most environments and are very hard to kill. They can survive the temperature of boiling water at sea level, thus many foods are canned with a pressurized boil that achieves even higher temperatures, sufficient to kill the spores.[39][40] This bacteria is widely distributed in nature and can be assumed to be present on all food surfaces. Its optimum growth temperature is within the mesophilic range. In spore form, it is a heat resistant pathogen that can survive in low acid foods and grow to produce toxins. The toxin attacks the nervous system and will kill an adult at a dose of around 75 ng.[41] Botulinum toxin can be destroyed by holding food at 100 °C for 10 minutes; however, because of its potency, this is not recommended by the USA's FDA as a means of control.[42]

Botulism poisoning can occur due to preserved or home-canned, low-acid food that was not processed using correct preservation times and/or pressure.[43] Growth of the bacterium can be prevented by high acidity, high ratio of dissolved sugar, high levels of oxygen, very low levels of moisture, or storage at temperatures below 3 °C (38 °F) for type A. For example, in a low-acid, canned vegetable such as green beans that are not heated enough to kill the spores (i.e., a pressurized environment) may provide an oxygen-free medium for the spores to grow and produce the toxin. However, pickles are sufficiently acidic to prevent growth;[44] even if the spores are present, they pose no danger to the consumer.

Honey, corn syrup, and other sweeteners may contain spores, but the spores cannot grow in a highly concentrated sugar solution; however, when a sweetener is diluted in the low-oxygen, low-acid digestive system of an infant, the spores can grow and produce toxin. As soon as infants begin eating solid food, the digestive juices become too acidic for the bacterium to grow.[45]

The control of food-borne botulism caused by C. botulinum is based almost entirely on thermal destruction (heating) of the spores or inhibiting spore germination into bacteria and allowing cells to grow and produce toxins in foods. Conditions conducive of growth are dependent on various environmental factors. Growth of C. botulinum is a risk in low acid foods as defined by having a pH above 4.6[46] although growth is significantly retarded for pH below 4.9.[47]

Taxonomic history

[edit]
Genomic information
NCBI genome ID726
Ploidyhaploid
Genome size3.91 Mb
Number of chromosomes2 (1 plasmid)
Year of completion2007

C. botulinum was first recognized and isolated in 1895 by Emile van Ermengem from home-cured ham implicated in a botulism outbreak.[48] The isolate was originally named Bacillus botulinus, after the Latin word for sausage, botulus. ("Sausage poisoning" was a common problem in 18th- and 19th-century Germany, and was most likely caused by botulism.)[49] However, isolates from subsequent outbreaks were always found to be anaerobic spore formers, so Ida A. Bengtson proposed that both be placed into the genus Clostridium, as the genus Bacillus was restricted to aerobic spore-forming rods.[50]

Since 1959, all species producing the botulinum neurotoxins (types A–G) have been designated C. botulinum. Substantial phenotypic and genotypic evidence exists to demonstrate heterogeneity within the species, with at least four clearly-defined "groups" (see § Groups) straddling other species, implying that they each deserve to be a genospecies.[51][29]

The situation as of 2018 is as follows:[29]

  • C. botulinum type G (= group IV) strains are since 1988 their own species, C. argentinense.[52]
  • Group I C. botulinum strains that do not produce a botulin toxin are referred to as C. sporogenes. Both names are conserved names since 1999.[53] Group I also contains C. combesii.[54]
  • All other botulinum toxin-producing bacteria, not otherwise classified as C. baratii or C. butyricum,[55] is called C. botulinum. This group still contains three genogroups.[29]

Smith et al. (2018) argues that group I should be called C. parabotulinum and group III be called C. novyi sensu lato, leaving only group II in C. botulinum. This argument is not accepted by the LPSN and would cause an unjustified change of the type strain under the Prokaryotic Code.[29] Dobritsa et al. (2018) argues, without formal descriptions, that group II can potentially be made into two new species.[11]

The complete genome of C. botulinum ATCC 3502 has been sequenced at Wellcome Trust Sanger Institute in 2007. This strain encodes a type "A" toxin.[56]

Diagnosis

[edit]

Physicians may consider the diagnosis of botulism based on a patient's clinical presentation, which classically includes an acute onset of bilateral cranial neuropathies and symmetric descending weakness.[57][58] Other key features of botulism include an absence of fever, symmetric neurologic deficits, normal or slow heart rate and normal blood pressure, and no sensory deficits except for blurred vision.[59][60] A careful history and physical examination is paramount to diagnose the type of botulism, as well as to rule out other conditions with similar findings, such as Guillain–Barré syndrome, stroke, and myasthenia gravis.[61] Depending on the type of botulism considered, different tests for diagnosis may be indicated.

  • Foodborne botulism: serum analysis for toxins by bioassay in mice should be done, as the demonstration of the toxins is diagnostic.[62]
  • Wound botulism: isolation of C. botulinum from the wound site should be attempted, as growth of the bacteria is diagnostic.[63]
  • Adult enteric and infant botulism: isolation and growth of C. botulinum from stool samples is diagnostic.[64] Infant botulism is a diagnosis which is often missed in the emergency room.[65]

Other tests that may be helpful in ruling out other conditions are:

Pathology

[edit]

Foodborne botulism

[edit]

Signs and symptoms of foodborne botulism typically begin between 18 and 36 hours after the toxin gets into your body, but can range from a few hours to several days, depending on the amount of toxin ingested. Symptoms include:[69][70]

  • Double vision
  • Blurred vision
  • Ptosis
  • Nausea, vomiting, and abdominal cramps
  • Slurred speech
  • Trouble breathing
  • Difficulty in swallowing
  • Dry mouth
  • Muscle weakness
  • Constipation
  • Reduced or absent deep tendon reactions, such as in the knee

Wound botulism

[edit]

Most people who develop wound botulism inject drugs several times a day, so determining a timeline of when onset symptoms first occurred and when the toxin entered the body can be difficult. It is more common in people who inject black tar heroin.[71] Wound botulism signs and symptoms include:[70][72]

  • Difficulty swallowing or speaking
  • Facial weakness on both sides of the face
  • Blurred or double vision
  • Ptosis
  • Trouble breathing
  • Paralysis

Infant botulism

[edit]

If infant botulism is related to food, such as honey, problems generally begin within 18 to 36 hours after the toxin enters the baby's body. Signs and symptoms include:[65][70]

  • Constipation (often the first sign)
  • Floppy movements due to muscle weakness and trouble controlling the head
  • Weak cry
  • Irritability
  • Drooling
  • Ptosis
  • Tiredness
  • Difficulty sucking or feeding
  • Paralysis[70]

Beneficial effects of botulinum toxin

[edit]

Purified botulinum toxin is diluted by a physician for treatment of:[73]

  • Congenital pelvic tilt
  • Spasmodic dysphasia (the inability of the muscles of the larynx)
  • Achalasia (esophageal stricture)
  • Strabismus (crossed eyes)
  • Paralysis of the facial muscles
  • Failure of the cervix
  • Blinking frequently
  • Anti-cancer drug delivery[74]

Adult intestinal toxemia

[edit]

A very rare form of botulism that occurs by the same route as infant botulism but is among adults. Occurs rarely and sporadically. Signs and symptoms include:[75]

  • Abdominal pain
  • Blurred vision
  • Diarrhea
  • Dysarthria
  • Imbalance
  • Weakness in arms and hand area[76]

Treatment

[edit]

In the case of a diagnosis or suspicion of botulism, patients should be hospitalized immediately, even if the diagnosis and/or tests are pending. Additionally if botulism is suspected, patients should be treated immediately with antitoxin therapy in order to reduce mortality. Immediate intubation is also highly recommended, as respiratory failure is the primary cause of death from botulism.[77][78][79]

In North America, an equine-derived heptavalent botulinum antitoxin is used to treat all serotypes of non-infant naturally occurring botulism. For infants less than one year of age, botulism immune globulin is used to treat type A or type B.[80][81]

Outcomes vary between one and three months, but with prompt interventions, mortality from botulism ranges from less than 5 percent to 8 percent.[82]

Vaccination

[edit]

There used to be a formalin-treated toxoid vaccine against botulism (serotypes A-E), but it was discontinued in 2011 due to declining potency in the toxoid stock. It was originally intended for people at risk of exposure. A few new vaccines are under development.[83]

Use and detection

[edit]

C. botulinum is used to prepare the medicaments Botox, Dysport, Xeomin, and Neurobloc used to selectively paralyze muscles to temporarily relieve muscle function. It has other "off-label" medical purposes, such as treating severe facial pain, such as that caused by trigeminal neuralgia.[84]

Botulinum toxin produced by C. botulinum is often believed to be a potential bioweapon as it is so potent that it takes about 75 nanograms to kill a person (LD50 of 1 ng/kg,[41] assuming an average person weighs ~75 kg); 1 kilogram of it would be enough to kill the entire human population.

A "mouse protection" or "mouse bioassay" test determines the type of C. botulinum toxin present using monoclonal antibodies. An enzyme-linked immunosorbent assay (ELISA) with digoxigenin-labeled antibodies can also be used to detect the toxin,[85] and quantitative PCR can detect the toxin genes in the organism.[20]

C. botulinum in different geographical locations

[edit]

A number of quantitative surveys for C. botulinum spores in the environment have suggested a prevalence of specific toxin types in given geographic areas, which remain unexplained.

Location
North America Type A C. botulinum predominates the soil samples from the western regions, while type B is the major type found in eastern areas.[86] The type-B organisms were of the proteolytic type I. Sediments from the Great Lakes region were surveyed after outbreaks of botulism among commercially reared fish, and only type E spores were detected.[87][88][89] In a survey, type-A strains were isolated from soils that were neutral to alkaline(average pH 7.5), while type-B strains were isolated from slightly acidic soils (average pH 6.23).
Europe C. botulinum type E is prevalent in aquatic sediments in Norway and Sweden,[90] Denmark,[91] the Netherlands, the Baltic coast of Poland, and Russia.[86] The type-E C. botulinum was suggested to be a true aquatic organism, which was indicated by the correlation between the level of type-E contamination and flooding of the land with seawater. As the land dried, the level of type E decreased and type B became dominant [92]

In soil and sediment from the United Kingdom, C. botulinum type B predominates. In general, the incidence is usually lower in soil than in sediment. In Italy, a survey conducted in the vicinity of Rome found a low level of contamination; all strains were proteolytic C. botulinum types A or B.[93]

Australia C. botulinum type A was found to be present in soil samples from mountain areas of Victoria.[94] Type-B organisms were detected in marine mud from Tasmania.[95] Type-A C. botulinum has been found in Sydney suburbs and types A and B were isolated from urban areas. In a well-defined area of the Darling-Downs region of Queensland, a study showed the prevalence and persistence of C. botulinum type B after many cases of botulism in horses.

References

[edit]
  1. ^ a b Tiwari A, Nagalli S (2021). "Clostridium Botulinum". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 31971722. Retrieved 2021-09-23.
  2. ^ a b c Peck MW (2009). "Biology and genomic analysis of Clostridium botulinum". Advances in Microbial Physiology. 55: 183–265, 320. doi:10.1016/S0065-2911(09)05503-9. ISBN 978-0-12-374790-7. PMID 19573697.
  3. ^ a b Lindström M, Korkeala H (April 2006). "Laboratory diagnostics of botulism". Clinical Microbiology Reviews. 19 (2): 298–314. doi:10.1128/cmr.19.2.298-314.2006. PMC 1471988. PMID 16614251.
  4. ^ Košenina S, Masuyer G, Zhang S, Dong M, Stenmark P (June 2019). "Crystal structure of the catalytic domain of the Weissella oryzae botulinum-like toxin". FEBS Letters. 593 (12): 1403–1410. doi:10.1002/1873-3468.13446. PMID 31111466.
  5. ^ a b (2010). Chapter 19. Clostridium, Peptostreptococcus, Bacteroides, and Other Anaerobes. In Ryan K.J., Ray C (Eds), Sherris Medical Microbiology, 5th ed. ISBN 978-0-07-160402-4
  6. ^ Schneider KR, Silverberg R, Chang A, Goodrich Schneider RM (9 January 2015). "Preventing Foodborne Illness: Clostridium botulinum". edis.ifas.ufl.edu. University of Florida IFAS Extension. Retrieved 7 February 2017.
  7. ^ Doyle MP (2007). Food Microbiology: Fundamentals and Frontiers. ASM Press. ISBN 978-1-55581-208-9.
  8. ^ Peck MW, Stringer SC, Carter AT (April 2011). "Clostridium botulinum in the post-genomic era". Food Microbiology. 28 (2): 183–191. doi:10.1016/j.fm.2010.03.005. PMID 21315972.
  9. ^ Shukla HD, Sharma SK (2005). "Clostridium botulinum: a bug with beauty and weapon". Critical Reviews in Microbiology. 31 (1): 11–18. doi:10.1080/10408410590912952. PMID 15839401. S2CID 2855356.
  10. ^ a b Austin JW (January 1, 2003). "Clostridium | Occurrence of Clostridium botulinum". Clostridium. Academic Press. pp. 1407–1413. doi:10.1016/B0-12-227055-X/00255-8. ISBN 978-0-12-227055-0. Retrieved February 19, 2021.
  11. ^ a b c Dobritsa AP, Kutumbaka KK, Samadpour M (September 2018). "Reclassification of Eubacterium combesii and discrepancies in the nomenclature of botulinum neurotoxin-producing clostridia: Challenging Opinion 69. Request for an Opinion". International Journal of Systematic and Evolutionary Microbiology. 68 (9): 3068–3075. doi:10.1099/ijsem.0.002942. PMID 30058996.
  12. ^ a b c Hill KK, Smith TJ (2012). "Genetic Diversity Within Clostridium botulinum Serotypes, Botulinum Neurotoxin Gene Clusters and Toxin Subtypes". Botulinum Neurotoxins. Current Topics in Microbiology and Immunology. Vol. 364. pp. 1–20. doi:10.1007/978-3-642-33570-9_1. ISBN 978-3-642-33569-3. PMID 23239346.
  13. ^ Peck MW, Smith TJ, Anniballi F, Austin JW, Bano L, Bradshaw M, et al. (January 2017). "Historical Perspectives and Guidelines for Botulinum Neurotoxin Subtype Nomenclature". Toxins. 9 (1): 38. doi:10.3390/toxins9010038. PMC 5308270. PMID 28106761.
  14. ^ Notermans S, Havellar AH (1980). "Removal and inactivation of botulinum toxin during production of drinking water from surface water". Antonie van Leeuwenhoek. 46 (5): 511–514. doi:10.1007/BF00395840. S2CID 21102990.
  15. ^ Montecucco C, Molgó J (June 2005). "Botulinal neurotoxins: revival of an old killer". Current Opinion in Pharmacology. 5 (3): 274–279. doi:10.1016/j.coph.2004.12.006. PMID 15907915.
  16. ^ Hatheway CL, McCroskey LM (December 1987). "Examination of feces and serum for diagnosis of infant botulism in 336 patients". Journal of Clinical Microbiology. 25 (12): 2334–2338. doi:10.1128/JCM.25.12.2334-2338.1987. PMC 269483. PMID 3323228.
  17. ^ Poulain B, Popoff MR (January 2019). "Why Are Botulinum Neurotoxin-Producing Bacteria So Diverse and Botulinum Neurotoxins So Toxic?". Toxins. 11 (1): 34. doi:10.3390/toxins11010034. PMC 6357194. PMID 30641949.
  18. ^ Meurens F, Carlin F, Federighi M, Filippitzi ME, Fournier M, Fravalo P, et al. (2023-01-05). "Clostridium botulinum type C, D, C/D, and D/C: An update". Frontiers in Microbiology. 13: 1099184. doi:10.3389/fmicb.2022.1099184. PMC 9849819. PMID 36687640.
  19. ^ (2013). Chapter 11. Spore-Forming Gram-Positive Bacilli: Bacillus and Clostridium Species. In Brooks G.F., Carroll K.C., Butel J.S., Morse S.A., Mietzner T.A. (Eds), Jawetz, Melnick, & Adelberg's Medical Microbiology, 26th ed. ISBN 978-0-07-179031-4
  20. ^ a b Satterfield BA, Stewart AF, Lew CS, Pickett DO, Cohen MN, Moore EA, et al. (January 2010). "A quadruplex real-time PCR assay for rapid detection and differentiation of the Clostridium botulinum toxin genes A, B, E and F". Journal of Medical Microbiology. 59 (Pt 1): 55–64. doi:10.1099/jmm.0.012567-0. PMID 19779029.
  21. ^ Maslanka SE, Lúquez C, Dykes JK, Tepp WH, Pier CL, Pellett S, et al. (February 2016). "A Novel Botulinum Neurotoxin, Previously Reported as Serotype H, Has a Hybrid-Like Structure With Regions of Similarity to the Structures of Serotypes A and F and Is Neutralized With Serotype A Antitoxin". The Journal of Infectious Diseases. 213 (3): 379–385. doi:10.1093/infdis/jiv327. PMC 4704661. PMID 26068781.
  22. ^ Aureli P, Fenicia L, Pasolini B, Gianfranceschi M, McCroskey LM, Hatheway CL (August 1986). "Two cases of type E infant botulism caused by neurotoxigenic Clostridium butyricum in Italy". The Journal of Infectious Diseases. 154 (2): 207–211. doi:10.1093/infdis/154.2.207. PMID 3722863.
  23. ^ Hall JD, McCroskey LM, Pincomb BJ, Hatheway CL (April 1985). "Isolation of an organism resembling Clostridium barati which produces type F botulinal toxin from an infant with botulism". Journal of Clinical Microbiology. 21 (4): 654–655. doi:10.1128/JCM.21.4.654-655.1985. PMC 271744. PMID 3988908.
  24. ^ a b Sebaihia M, Peck MW, Minton NP, Thomson NR, Holden MT, Mitchell WJ, et al. (July 2007). "Genome sequence of a proteolytic (Group I) Clostridium botulinum strain Hall A and comparative analysis of the clostridial genomes". Genome Research. 17 (7): 1082–1092. doi:10.1101/gr.6282807. PMC 1899119. PMID 17519437.
  25. ^ Leyer GJ, Johnson EA (October 1990). "Repression of toxin production by tryptophan in Clostridium botulinum type E". Archives of Microbiology. 154 (5): 443–447. Bibcode:1990ArMic.154..443L. doi:10.1007/BF00245225. PMID 2256780.
  26. ^ Patterson-Curtis SI, Johnson EA (June 1989). "Regulation of neurotoxin and protease formation in Clostridium botulinum Okra B and Hall A by arginine". Applied and Environmental Microbiology. 55 (6): 1544–1548. Bibcode:1989ApEnM..55.1544P. doi:10.1128/aem.55.6.1544-1548.1989. PMC 202901. PMID 2669631.
  27. ^ Schantz EJ, Johnson EA (1992). "Properties and use of botulinum toxin and other microbial neurotoxins in medicine". Microbiological Reviews. 56 (1): 80–99. doi:10.1128/MMBR.56.1.80-99.1992. ISSN 0146-0749. PMC 372855. PMID 1579114.
  28. ^ Johnson EA, Bradshaw M (November 2001). "Clostridium botulinum and its neurotoxins: a metabolic and cellular perspective". Toxicon. 39 (11): 1703–1722. Bibcode:2001Txcn...39.1703J. doi:10.1016/S0041-0101(01)00157-X. PMID 11595633.
  29. ^ a b c d e f Smith T, Williamson CH, Hill K, Sahl J, Keim P (September 2018). "Botulinum Neurotoxin-Producing Bacteria. Isn't It Time that We Called a Species a Species?". mBio. 9 (5). doi:10.1128/mbio.01469-18. PMC 6156192. PMID 30254123.
  30. ^ Mazuet C, Legeay C, Sautereau J, Bouchier C, Criscuolo A, Bouvet P, et al. (February 2017). "Characterization of Clostridium Baratii Type F Strains Responsible for an Outbreak of Botulism Linked to Beef Meat Consumption in France". PLOS Currents. 9. doi:10.1371/currents.outbreaks.6ed2fe754b58a5c42d0c33d586ffc606 (inactive 2024-09-12). PMC 5959735. PMID 29862134.{{cite journal}}: CS1 maint: DOI inactive as of September 2024 (link)
  31. ^ Hill KK, Xie G, Foley BT, Smith TJ, Munk AC, Bruce D, et al. (October 2009). "Recombination and insertion events involving the botulinum neurotoxin complex genes in Clostridium botulinum types A, B, E and F and Clostridium butyricum type E strains". BMC Biology. 7 (1): 66. doi:10.1186/1741-7007-7-66. PMC 2764570. PMID 19804621.
  32. ^ a b c Carter AT, Peck MW (May 2015). "Genomes, neurotoxins and biology of Clostridium botulinum Group I and Group II". Research in Microbiology. 166 (4): 303–317. doi:10.1016/j.resmic.2014.10.010. PMC 4430135. PMID 25445012.
  33. ^ Madigan MT, Martinko JM, eds. (2005). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 978-0-13-144329-7.
  34. ^ a b Portinha IM, Douillard FP, Korkeala H, Lindström M (January 2022). "Sporulation Strategies and Potential Role of the Exosporium in Survival and Persistence of Clostridium botulinum". International Journal of Molecular Sciences. 23 (2): 754. doi:10.3390/ijms23020754. PMC 8775613. PMID 35054941.>
  35. ^ a b Shen A, Edwards AN, Sarker MR, Paredes-Sabja D (November 2019). Fischetti VA, Novick RP, Ferretti JJ, Portnoy DA, Braunstein M, Rood JI (eds.). "Sporulation and Germination in Clostridial Pathogens". Microbiology Spectrum. 7 (6). doi:10.1128/microbiolspec.GPP3-0017-2018. PMC 6927485. PMID 31858953.
  36. ^ Dowell VR (1977). "Coproexamination for Botulinal Toxin and Clostridium botulinum". JAMA. 238 (17): 1829. doi:10.1001/jama.1977.03280180033021. Retrieved 2024-04-11.
  37. ^ "Botulism". www.who.int. Retrieved 2024-04-16.
  38. ^ a b Paul CJ, Twine SM, Tam KJ, Mullen JA, Kelly JF, Austin JW, et al. (May 2007). "Flagellin Diversity in Clostridium botulinum Groups I and II: a New Strategy for Strain Identification". Applied and Environmental Microbiology. 73 (9): 2963–2975. Bibcode:2007ApEnM..73.2963P. doi:10.1128/AEM.02623-06. ISSN 0099-2240. PMC 1892883. PMID 17351097.
  39. ^ "Prevent Botulism". Centers for Disease Control and Prevention (CDC). 2019-06-06. Retrieved 2023-04-23.
  40. ^ "Botulism: take care when canning low-acid foods". extension.umn.edu. Retrieved 2023-04-23.
  41. ^ a b Fleming DO. Biological Safety: principles and practices. Vol. 2000. ASM Press. p. 267.
  42. ^ "Chapter 13: Clostridium botulinum Toxin Formation" (PDF). Fda.gov. Archived (PDF) from the original on 2021-02-08. Retrieved 18 March 2022.
  43. ^ "Home Canning and Botulism". Centers for Disease Control and Prevention. Retrieved 14 April 2021.
  44. ^ Ito KA, Chen JK, Lerke PA, Seeger ML, Unverferth JA (July 1976). "Effect of acid and salt concentration in fresh-pack pickles on the growth of Clostridium botulinum spores". Applied and Environmental Microbiology. 32 (1): 121–124. Bibcode:1976ApEnM..32..121I. doi:10.1128/aem.32.1.121-124.1976. PMC 170016. PMID 9898.
  45. ^ "Botulism". The Lecturio Medical Concept Library. Retrieved 5 July 2021.
  46. ^ "Guidance for Commercial Processors of Acidified & Low-Acid Canned Foods". U.S. Food and Drug Administration. Retrieved 8 October 2016.
  47. ^ Odlaug TE, Pflug IJ (March 1979). "Clostridium botulinum growth and toxin production in tomato juice containing Aspergillus gracilis". Applied and Environmental Microbiology. 37 (3): 496–504. Bibcode:1979ApEnM..37..496O. doi:10.1128/aem.37.3.496-504.1979. PMC 243244. PMID 36843.
  48. ^ van Ergmengem E (1897). "Über einen neuen anaeroben Bacillus und seine Beziehungen Zum Botulismus". Zeitschrift für Hygiene und Infektionskrankheiten. 26: 1–8.
  49. ^ Erbguth FJ (March 2004). "Historical notes on botulism, Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxin". Movement Disorders. 19 (Suppl 8): S2–S6. doi:10.1002/mds.20003. PMID 15027048. S2CID 8190807.
  50. ^ Bengston IA (1924). "Studies on organisms concerned as causative factors in botulism". Bulletin (Hygienic Laboratory (U.S.)). 136: 101 fv.
  51. ^ Uzal FA, Songer JG, Prescott JF, Popoff MR (21 June 2016). "Taxonomic Relationships among the Clostridia". Clostridial Diseases of Animals. pp. 1–5. doi:10.1002/9781118728291.ch1. ISBN 978-1-118-72829-1.
  52. ^ Suen JC, Hatheway CL, Steigerwalt AG, Brenner DJ (1988). "Clostridium argentinense sp.nov.: a genetically homogeneous group composed of all strains of Clostridium botulinum type G and some nonttoxigenic strains previously identified as Clostridium subterminale or Clostridium hastiforme". International Journal of Systematic Bacteriology. 38: 375–381. doi:10.1099/00207713-38-4-375.
  53. ^ "Rejection of Clostridium putrificum and conservation of Clostridium botulinum and Clostridium sporogenes-Opinion 69. Judicial Commission of the International Committee on Systematic Bacteriology". International Journal of Systematic Bacteriology. 49 Pt 1 (1): 339. January 1999. doi:10.1099/00207713-49-1-339. PMID 10028279.
  54. ^ "Species: Clostridium combesii". lpsn.dsmz.de.
  55. ^ Arahal DR, Busse HJ, Bull CT, Christensen H, Chuvochina M, Dedysh SN, et al. (August 2022). "Judicial Opinions 112-122". International Journal of Systematic and Evolutionary Microbiology. 72 (8). doi:10.1099/ijsem.0.005481. PMID 35947640. S2CID 251470203.
  56. ^ "Clostridium botulinum A str. ATCC 3502 genome assembly ASM6358v1". NCBI.
  57. ^ Cherington M (June 1998). "Clinical spectrum of botulism". Muscle & Nerve. 21 (6): 701–710. doi:10.1002/(sici)1097-4598(199806)21:6<701::aid-mus1>3.0.co;2-b. PMID 9585323.
  58. ^ Cai S, Singh BR, Sharma S (April 2007). "Botulism diagnostics: from clinical symptoms to in vitro assays". Critical Reviews in Microbiology. 33 (2): 109–125. doi:10.1080/10408410701364562. PMID 17558660. S2CID 23470999.
  59. ^ "Diagnosis and Treatment | Botulism". CDC. Retrieved 2017-10-08.
  60. ^ "Botulism: Rare but serious food poisoning". Mayo Clinic. Retrieved 2017-11-18.
  61. ^ Rao AK, Sobel J, Chatham-Stephens K, Luquez C (May 2021). "Clinical Guidelines for Diagnosis and Treatment of Botulism, 2021". MMWR. Recommendations and Reports. 70 (2): 1–30. doi:10.15585/mmwr.rr7002a1. PMC 8112830. PMID 33956777.
  62. ^ Lindström M, Korkeala H (April 2006). "Laboratory diagnostics of botulism". Clinical Microbiology Reviews. 19 (2): 298–314. doi:10.1128/CMR.19.2.298-314.2006. PMC 1471988. PMID 16614251.
  63. ^ Akbulut D, Grant KA, McLauchlin J (September 2005). "Improvement in laboratory diagnosis of wound botulism and tetanus among injecting illicit-drug users by use of real-time PCR assays for neurotoxin gene fragments". Journal of Clinical Microbiology. 43 (9): 4342–4348. doi:10.1128/JCM.43.9.4342-4348.2005. PMC 1234055. PMID 16145075.
  64. ^ Dezfulian M, McCroskey LM, Hatheway CL, Dowell VR (March 1981). "Selective medium for isolation of Clostridium botulinum from human feces". Journal of Clinical Microbiology. 13 (3): 526–531. doi:10.1128/JCM.13.3.526-531.1981. PMC 273826. PMID 7016901.
  65. ^ a b Antonucci L, Locci C, Schettini L, Clemente MG, Antonucci R (September 2021). "Infant botulism: an underestimated threat". Infectious Diseases. 53 (9): 647–660. doi:10.1080/23744235.2021.1919753. PMID 33966588.
  66. ^ O'Suilleabhain P, Low PA, Lennon VA (January 1998). "Autonomic dysfunction in the Lambert-Eaton myasthenic syndrome: serologic and clinical correlates". Neurology. 50 (1): 88–93. doi:10.1212/wnl.50.1.88. PMID 9443463. S2CID 39437882.
  67. ^ Mechem CC, Walter FG (June 1994). "Wound botulism". Veterinary and Human Toxicology. 36 (3): 233–237. PMID 8066973.
  68. ^ Taraschenko OD, Powers KM (June 2014). "Neurotoxin-induced paralysis: a case of tick paralysis in a 2-year-old child". Pediatric Neurology. 50 (6): 605–607. doi:10.1016/j.pediatrneurol.2014.01.041. PMID 24679414.
  69. ^ Lonati D, Schicchi A, Crevani M, Buscaglia E, Scaravaggi G, Maida F, et al. (August 2020). "Foodborne Botulism: Clinical Diagnosis and Medical Treatment". Toxins. 12 (8): 509. doi:10.3390/toxins12080509. PMC 7472133. PMID 32784744.
  70. ^ a b c d "Botulism Symptoms". Mayo Clinic. June 13, 2015. Retrieved January 25, 2016.
  71. ^ "Injection Drug Use and Wound Botulism | Botulism | CDC". www.cdc.gov. 2022-05-31. Retrieved 2024-04-17.
  72. ^ Schulte M, Hamsen U, Schildhauer TA, Ramczykowski T (October 2017). "Effective and rapid treatment of wound botulism, a case report". BMC Surgery. 17 (1): 103. doi:10.1186/s12893-017-0300-4. PMC 5658925. PMID 29073888.
  73. ^ Chiu SY, Patel B, Burns MR, Legacy J, Shukla AW, Ramirez-Zamora A, et al. (2020-02-27). "High-dose Botulinum Toxin Therapy: Safety, Benefit, and Endurance of Efficacy". Tremor and Other Hyperkinetic Movements. 10. doi:10.5334/tohm.527. ISSN 2160-8288. PMID 32149014.
  74. ^ Arnon SS, Schechter R, Inglesby TV, Henderson DA, Bartlett JG, Ascher MS, et al. (February 2001). "Botulinum toxin as a biological weapon: medical and public health management". JAMA. 285 (8): 1059–1070. doi:10.1001/jama.285.8.1059. PMID 11209178.
  75. ^ Harris RA, Anniballi F, Austin JW (January 2020). "Adult Intestinal Toxemia Botulism". Toxins. 12 (2): 81. doi:10.3390/toxins12020081. PMC 7076759. PMID 31991691.
  76. ^ "Botulism". Centers for Disease Control and Prevention. Retrieved 23 October 2016.
  77. ^ Witoonpanich R, Vichayanrat E, Tantisiriwit K, Wongtanate M, Sucharitchan N, Oranrigsupak P, et al. (March 2010). "Survival analysis for respiratory failure in patients with food-borne botulism". Clinical Toxicology. 48 (3): 177–183. doi:10.3109/15563651003596113. PMID 20184431. S2CID 23108891.
  78. ^ Sandrock CE, Murin S (August 2001). "Clinical predictors of respiratory failure and long-term outcome in black tar heroin-associated wound botulism". Chest. 120 (2): 562–566. doi:10.1378/chest.120.2.562. PMID 11502659.
  79. ^ Wongtanate M, Sucharitchan N, Tantisiriwit K, Oranrigsupak P, Chuesuwan A, Toykeaw S, et al. (August 2007). "Signs and symptoms predictive of respiratory failure in patients with foodborne botulism in Thailand". The American Journal of Tropical Medicine and Hygiene. 77 (2): 386–389. doi:10.4269/ajtmh.2007.77.386. PMID 17690419.
  80. ^ "Botulism - Guide for Healthcare Professionals". Health Canada. 2012-07-18. Retrieved 2023-11-01.
  81. ^ "Investigational Heptavalent Botulinum Antitoxin (HBAT) to Replace Licensed Botulinum Antitoxin AB and Investigational Botulinum Antitoxin E". www.cdc.gov. Retrieved 2023-11-01.
  82. ^ Varma JK, Katsitadze G, Moiscrafishvili M, Zardiashvili T, Chokheli M, Tarkhashvili N, et al. (August 2004). "Signs and symptoms predictive of death in patients with foodborne botulism--Republic of Georgia, 1980-2002". Clinical Infectious Diseases. 39 (3): 357–362. doi:10.1086/422318. PMID 15307002. S2CID 20675701.
  83. ^ Sundeen G, Barbieri JT (September 2017). "Vaccines against Botulism". Toxins. 9 (9): 268. doi:10.3390/toxins9090268. PMC 5618201. PMID 28869493.
  84. ^ Guardiani E, Sadoughi B, Blitzer A, Sirois D (February 2014). "A new treatment paradigm for trigeminal neuralgia using Botulinum toxin type A". The Laryngoscope. 124 (2): 413–417. doi:10.1002/lary.24286. PMID 23818108.
  85. ^ Sharma SK, Ferreira JL, Eblen BS, Whiting RC (February 2006). "Detection of type A, B, E, and F Clostridium botulinum neurotoxins in foods by using an amplified enzyme-linked immunosorbent assay with digoxigenin-labeled antibodies". Applied and Environmental Microbiology. 72 (2): 1231–1238. Bibcode:2006ApEnM..72.1231S. doi:10.1128/AEM.72.2.1231-1238.2006. PMC 1392902. PMID 16461671.
  86. ^ a b Hauschild AH (1989). "Clostridium botulinum.". In Doyle MP (ed.). Food-borne Bacterial Pathogens. New York: Marcel Dekker. pp. 111–189.
  87. ^ Bott TL, Johnson J, Foster EM, Sugiyama H (May 1968). "Possible origin of the high incidence of Clostridium botulinum type E in an inland bay (Green Bay of Lake Michigan)". Journal of Bacteriology. 95 (5): 1542–7. doi:10.1128/jb.95.5.1542-1547.1968. PMC 252172. PMID 4870273.
  88. ^ Eklund MW, Peterson ME, Poysky FT, Peck LW, Conrad JF (February 1982). "Botulism in juvenile coho salmon (Oncorhynchus kisutch) in the United States". Aquaculture. 27 (1): 1–11. Bibcode:1982Aquac..27....1E. doi:10.1016/0044-8486(82)90104-1.
  89. ^ Eklund MW, Poysky FT, Peterson ME, Peck LW, Brunson WD (October 1984). "Type E botulism in salmonids and conditions contributing to outbreaks". Aquaculture. 41 (4): 293–309. Bibcode:1984Aquac..41..293E. doi:10.1016/0044-8486(84)90198-4.
  90. ^ Johannsen A (April 1963). "Clostridium botulinum in Sweden and the adjacent waters". Journal of Applied Bacteriology. 26 (1): 43–47. doi:10.1111/j.1365-2672.1963.tb01153.x.
  91. ^ Huss HH (April 1980). "Distribution of Clostridium botulinum". Applied and Environmental Microbiology. 39 (4): 764–9. Bibcode:1980ApEnM..39..764H. doi:10.1128/aem.39.4.764-769.1980. PMC 291416. PMID 6990867.
  92. ^ Portinha IM, Douillard FP, Korkeala H, Lindström M (January 2022). "Sporulation Strategies and Potential Role of the Exosporium in Survival and Persistence of Clostridium botulinum". International Journal of Molecular Sciences. 23 (2): 754. doi:10.3390/ijms23020754. PMC 8775613. PMID 35054941.
  93. ^ Creti R, Fenicia J, Aureli P (May 1990). "Occurrence of Clostridium botulinum in the soil of the vicinity of Rome". Current Microbiology. 20 (5): 317–321. doi:10.1007/bf02091912.
  94. ^ Eales CE, Gillespie JM (August 1947). "The isolation of Clostridium botulinum type A from Victorian soils". The Australian Journal of Science. 10 (1): 20. PMID 20267540.
  95. ^ Ohye DF, Scott WJ (1957). "Studies in the physiology of Clostridium botulinum type E". Australian Journal of Biological Sciences. 10: 85–94. doi:10.1071/BI9570085.

Further reading

[edit]
[edit]
Retrieved from "https://en.wikipedia.org/w/index.php?title=Clostridium_botulinum&oldid=1245282238"