C. botulinum is a diverse group ofpathogenic 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 ofClostridium butyricum andClostridium baratii, these bacteria all produce the toxin.[6]
Botulinum toxin can causebotulism, a severeflaccid paralytic disease in humans and other animals.[7] The botulinum toxin is the most potent toxin known in scientific literature, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans.[8][9]
C. botulinum is commonly associated with bulgingcanned food; misshapen cans can be due to an internal increase in pressure caused by gas produced by bacteria.[10]C. botulinum can also grow in traditionally aged meats (e.g.igunaq)[11] andcarrion (e.g. deadbeachedwhale).[12]
C. botulinum is responsible for food-bornebotulism (ingestion of preformed toxin), infant botulism (intestinal infection with toxin-formingC. botulinum), and wound botulism (infection of a wound withC. botulinum).C. botulinum produces heat-resistantendospores that are commonly found in soil and are able to survive under adverse conditions.[6]
C. botulinumis anobligate anaerobe, requiring an environment that lacksoxygen. However,C. botulinum tolerates traces of oxygen due to the enzymesuperoxide dismutase, which is an important antioxidant defense in nearly all cells exposed to oxygen.[13]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 distinctphenotypic groups (I-IV) and is also classified into sevenserotypes (A–G) based on theantigenicity of the botulinum toxin produced.[14][15] On the level visible to DNA sequences, the phenotypic grouping matches the results of whole-genome andrRNA analyses,[16][17] and setotype grouping approximates the result of analyses focused specifically on the toxin sequence. The twophylogenetic trees do not match because of the ability of the toxingene cluster to be horizontally transferred.[18]
Botulinum neurotoxin (BoNT) production is the unifying feature of the species. Sevenserotypes oftoxins 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.[9] Toxins can be further differentiated into subtypes on the bases of smaller variations.[19]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.[20][21]
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 inNew Mexico andCalifornia.[22] 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.[18]
Evidence indicates the neurotoxin genes have been the subject ofhorizontal gene transfer, possibly from a viral (bacteriophage) source. This theory is supported by the presence of integration sites flanking the toxin in some strains ofC. botulinum. However, these integrations sites are degraded (except for the C and D types), indicating that theC. 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.[23]
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.[24] No disease is associated with type G.[25] The "gold standard" for determining toxin type is a mousebioassay, but the genes for types A, B, E, and F can now be readily differentiated usingquantitative PCR.[26] 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.[27]
A few strains from organisms genetically identified as otherClostridium species have caused human botulism:C. butyricum has produced type E toxin[28] andC. baratii has produced type F toxin.[29] The ability ofC. botulinum to naturally transfer neurotoxin genes to other clostridia is concerning, especially in thefood industry, where preservation systems are designed to destroy or inhibit onlyC. botulinum but not otherClostridium species.[18]
ManyC. 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 forC. botulinum.[30] Hall A strain ofC. botulinum has an active chitinolytic system to aid in the breakdown of chitin.[30] Type A and B ofC. botulinum production of BoNT is affected by nitrogen and carbon nutrition.[31][32][33] There is evidence that these processes are also under catabolite repression.[34]
ProteolyticClostridium often rely onamino acids as carbon and energy sources. They carry out a unique metabolic process calledStickland Fermentation.[35] In this process, two amino acids are used in complementary roles. One will serve as anelectron donor, and the other amino acid serves as anelectron acceptor. Not only does this reaction create precursors for other metabolic pathways, but it also regeneratesNAD+,[35] an important oxidizing agent in theEmbden-Meyerhof-Parnas pathway. Utilizing amino acids as a carbon source and regenerating NAD+ allowsC. botulinum to thrive in anaerobic environments.
Physiological differences and genome sequencing at 16SrRNA level support the subdivision of theC. botulinum species into groups I-IV.[16] Some authors have briefly used groups V and VI, corresponding to toxin-producingC. baratii andC. butyricum. What used to be group IV is nowC. argentinense.[36]
Phenotypic groups of toxin-producingClostridium[17][36]
In the laboratory,C. botulinum is usually isolated in tryptose sulfitecycloserine (TSC) growth medium in an anaerobic environment with less than 2% oxygen. This can be achieved by severalcommercial kits that use a chemical reaction to replace O2 with CO2.C. botulinum (groups I through III) is alipase-positive microorganism that grows betweenpH of 4.8 and 7.0 and cannot uselactose as a primary carbon source, characteristics important for biochemical identification.[40]
Sporulation and germination inClostridium botulinum is a majorvirulence factor, allowing the bacteria to be prevalent in a wide variety of environments, and botulism to exist in many forms.[41] The exact mechanism behindsporulation and germination ofC. botulinum is not known, but the study ofBacillus subtilus can be used to give a general prediction of the mechanism.[41]
Different strains ofC. botulinum can be divided into three different groups, group I, II, and III, based on environmental conditions like heat resistance, temperature, and biome.[42] Within each group, different strains will use different strategies to adapt to their environment to survive.[42] Unlike other clostridial species,C. botulinumspores will sporulate as it enters the stationary phase.[43]C. botulinum relies onquorum-sensing to initiate the sporulation process.[43]
C. botulinum begins sporulation once its sporulation protein becomes phosphorylated.[41] Thephosphorylation activates the stage I and II sporulation genes that haltcell division, and begin creation of an asymmetricseptum and the spore.[41] The cell forms spore layers until the spore is fully mature, after which, the cell is covered inexosporium.[41] Group I cells have a thick yet loose exosporium layer that allows the spore to be heat-resistant, while group III have a thin yet tight exosporium layer that leaves the cell with a moderate amount of heat-resistance.[41]
Germination will begin if specific nutrients called germinants interact with receptors found within the spore.[41] Once the germinants are bound to the cell, the cell begins tohydrolyze itself to rehydrate its core and create a vegetative cell.[41]C. botulinum spores are not found in human feces unless the individual has contracted botulism,[44] butC. botulinum cannot spread from person to person.[45]
The most common motility structure forC. botulinum is aflagellum. Though this structure is not found in all strains ofC. botulinum, most produceperitrichous flagella.[46] When comparing the different strains, there are also differences in the length of the flagella and how many are present on the cell.[46]
Genomic analyses of C.botulinum have shown many strains to harbor mutations in flagellar genes, including flaA, which encodes theflagellin protein, and flhA and flgN, which are involved in flagellarbiosynthesis. These mutations can changemotility to varying extents, and in some cases, may modify the structure of the flagellum without fully impairing its function. Flagella are important in colonization and movement in gut environments, but also have immunogenic properties that make the bacterium more visible to host defenses. As a result, strains may downregulating flagellar production or acquire mutations that change flagellar assembly, so they can be used for motility but also evade the immune system during colonization.[47]
C. botulinum is asoil 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.[48][49] This bacteria is widely distributed in nature and can be assumed to be present on all food surfaces. Its optimum growth temperature is within themesophilic 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 thenervous system and will kill an adult at a dose of around 75 ng.[50] 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.[51]
Botulism poisoning can occur due to preserved or home-canned, low-acid food that was not processed using correct preservation times and/or pressure.[52] Growth of the bacterium can be prevented by highacidity, high ratio of dissolvedsugar, high levels ofoxygen, very low levels ofmoisture, or storage at temperatures below 3 °C (38 °F) for type A. For example, in a low-acid, canned vegetable such asgreen 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;[53] 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-aciddigestive 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.[54]
The control of food-borne botulism caused byC. 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 variousenvironmental factors.Growth ofC. botulinum is a risk in low acid foods as defined by having a pH above 4.6[55] although growth is significantly retarded for pH below 4.9.[56]
C. botulinum is very resilient against many mechanisms offood processing because of theendospores that it produces. These endospores allow the bacteria to survive extreme conditions such as heat, cold, and high or low acidity. These endospores have multiple thick protective layers which allow the bacteria to survive in a dormant state for very long periods of time.[57] The endospores can remain dormant in the bacteria, and in this state they are harmless. As endosporesgerminate when they are subject to environments with low oxygen, they multiply producing the neurotoxin that causes botulism.[58]
C. botulinum was first recognized and isolated in 1895 byEmile van Ermengem from home-curedham implicated in a botulism outbreak.[59] The isolate was originally namedBacillus 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.)[60] However, isolates from subsequent outbreaks were always found to beanaerobic spore formers, soIda A. Bengtson proposed that both be placed into the genusClostridium, as the genusBacillus was restricted toaerobic spore-forming rods.[61]
Since 1959, all species producing the botulinum neurotoxins (types A–G) have been designatedC. botulinum. Substantialphenotypic andgenotypic evidence exists to demonstrateheterogeneity within thespecies, with at least four clearly defined "groups" (see§ Groups) straddling other species, implying that they each deserve to be a genospecies.[62][36]
All other botulinum toxin-producing bacteria, not otherwise classified asC. baratii orC. butyricum,[66] is calledC. botulinum. This group still contains three genogroups.[36]
Smithet al. (2018) argues that group I should be calledC. parabotulinum and group III be calledC. novyisensu lato, leaving only group II inC. botulinum. This argument is not accepted by theLPSN and would cause an unjustified change of thetype strain under theProkaryotic Code. (The current type strain ATCC 25763 falls into group I.)[36] Dobritsaet al. (2018) argues, without formal descriptions, that group II can potentially be made into two new species.[17]
The complete genome ofC. botulinum ATCC 3502 has been sequenced atWellcome Trust Sanger Institute in 2007. This strain encodes a type "A" toxin.[67]
Physicians may consider the diagnosis of botulism based on a patient's clinical presentation, which classically includes an acute onset of bilateralcranial neuropathies and symmetric descending weakness.[68][69] 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.[70][71] 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 asGuillain–Barré syndrome,stroke, andmyasthenia gravis.[72] 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.[73]
Wound botulism: isolation ofC. botulinum from the wound site should be attempted, as growth of the bacteria is diagnostic.[74]
Adult enteric and infant botulism: isolation and growth ofC. botulinum from stool samples is diagnostic.[75] Infant botulism is a diagnosis which is often missed in the emergency room.[76]
Other tests that may be helpful in ruling out other conditions are:
Signs and symptoms of foodborne botulism typically begin between 18 and 36 hours after the toxin gets into the body, but can range from a few hours to several days, depending on the amount of toxin ingested. Symptoms include:[80][81]
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.[82] Wound botulism signs and symptoms include:[81][83]
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:[76][81]
Constipation (often the first sign)
Floppy movements due to muscle weakness and trouble controlling the head
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:[86]
Most cases of botulism in animals come from foodborne botulism, though wound botulism is also common.[88] Foodborne botulism comes from ingestion of infected material, like raw or decaying vegetation, carcasses, or larvae that have consumed infected material.[88] Ruminants have longer incubation times for foodborne botulism when compared to animals with less complex stomachs.[88] Wound botulism occurs when a wound becomes infected with Clostridium botulinum that is allowed to germinate and produce toxins.[88]
Toxicoinfection can also cause botulism cases as Clostridium botulinum cells infect the lower intestine and begin to produce toxins.[88] The toxin is either expelled as feces from the animal, not causing any harm but spreading the toxin, or, if in close proximity to the beginning of the small intestine, causes symptoms to present in the host.[88]
Botulism symptoms in cattle and horses can begin with weakness or trembling in the hindquarters which progresses into full body paralysis and eventually death.[88] Avian botulism is characterized by the inability of the animal to fly, walk, lift its neck, or close its inner eyelid, followed by death.[88] Small carnivores, like foxes, mink, and ferrets, are prone to botulism and will present flaccid paralysis, then die.[88] An infected fish will have each of its fins paralyzed over time until the tail fin is fully paralyzed, preventing swimming, killing the fish.[88]
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.[89][90][91]
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.[92][93]
Outcomes vary between one and three months, but with prompt interventions, mortality from botulism ranges from less than 5 percent to 8 percent.[94]
Despite these interventions, there is currently no approved pharmacological treatment that reverses botulinum neurotoxin once it has enteredneurons. Due to this limitation, early antitoxin administration and supportive care is critical. Ongoing research investigates several therapeutic strategies; for example, recombinant vaccines based on the heavy-chain (HC) domains of BoNTs have provided protective immunity in animals and shown promise in early clinical trials. However, no human vaccine is currently licensed. Veterinary vaccines are available to prevent outbreaks in livestock.[95]
Antibody-based therapies are also under development. Traditional equine antitoxins, though effective, carry risks of serum sickness. Humanpolyclonal antibodies isolated from immunized volunteers and novel camelidsingle-domain antibodies are two alternatives, which may provide safer and longer-lasting protection. Additionally, small-molecule inhibitors targeting the metalloprotease activity of the toxin’s light chain are being explored as potential post-exposure therapies.[95]
Clinical outcomes also depend on the toxinserotype involved. Type A toxins typically cause the most prolonged paralysis, while type E toxins are associated with shorter disease courses. Although BoNTs induce paralysis, they do not destroy neurons; with adequate ventilation and intensive care, patients can fully recover asnerve terminals regenerate.[95]
Due to the extreme potency of botulinumneurotoxins, much of this therapeutic research is framed in context of biodefense preparedness against the potential use of BoNTs as biological weapons.[95]
There used to be a formalin-treatedtoxoid 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.[96]
C. botulinum is used to prepare the medicamentsBotox,Dysport,Xeomin, andNeurobloc 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 bytrigeminal neuralgia.[97]
Botulinum toxin produced byC. botulinum is often believed to be a potentialbioweapon as it is so potent that it takes about 75nanograms to kill a person (LD50 of 1 ng/kg,[50] assuming an average person weighs ~75 kg); 1 kilogram of it would be enough to kill theentire human population.
A number ofquantitativesurveys forC. botulinumspores in the environment have suggested a prevalence of specific toxin types in given geographic areas, which remain unexplained.
Location
North America
Type AC. botulinum predominates thesoil samples from the western regions, while type B is the major type found in eastern areas.[99] The type-B organisms were of the proteolytic Group I.Sediments from theGreat Lakes region were surveyed after outbreaks of botulism among commercially rearedfish, and only type E spores were detected.[100][101][102] In a survey, type-A strains were isolated from soils that wereneutral toalkaline (average pH 7.5), while type-B strains were isolated from slightlyacidic soils (average pH 6.23).
Europe
C. botulinum type E is prevalent in aquatic sediments inNorway andSweden,[103]Denmark,[104] theNetherlands, the Baltic coast ofPoland, andRussia.[99] The type-EC. botulinum was suggested to be a trueaquatic 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.[105]
In soil and sediment from the United Kingdom,C. botulinum type B predominates. In general, the incidence is usually lower in soil than insediment. In Italy, a survey conducted in the vicinity ofRome found a low level of contamination; all strains wereproteolytic (Group I)C. botulinum types A or B.[106]
Australia
C. botulinum type A was found to be present in soil samples from mountain areas ofVictoria.[107] Type-B organisms were detected in marine mud fromTasmania.[108] Type-AC. botulinum has been found inSydney suburbs and types A and B were isolated fromurban areas. In a well-defined area of theDarling-Downs region ofQueensland, a study showed the prevalence and persistence ofC. botulinum type B after many cases of botulism inhorses.
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