Clostridium botulinum
Clostridium botulinum | |
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Clostridium botulinum stained with gentian violet .
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Scientific classification | |
Domain: | Bacteria |
Phylum: | Bacillota |
Class: | Clostridia |
Order: | Eubacteriales |
Family: | Lachnospiraceae |
Genus: | Clostridium |
Species: | C. botulinum
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Binomial name | |
Clostridium botulinum van Ermengem, 1896
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Clostridium botulinum is a
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
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
C. botulinum is a
C. botulinum is divided into four distinct
Serotypes
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
Only
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
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
Physiological differences and genome sequencing at 16S
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 |
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|
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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
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
The exact mechanism behind
Motility structures
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
Growth conditions and 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] This toxin is detoxified by holding food at 100 °C for 10 minutes.[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.
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
NCBI genome ID | 726 |
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Ploidy | haploid |
Genome size | 3.91 Mb |
Number of chromosomes | 2 (1 plasmid) |
Year of completion | 2007 |
C. botulinum was first recognized and isolated in 1895 by
Since 1959, all species producing the botulinum neurotoxins (types A–G) have been designated C. botulinum. Substantial phenotypic and
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
The complete genome of C. botulinum ATCC 3502 has been sequenced at
Diagnosis
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:
- Electromyography (EMG) or antibody studies may help with the exclusion of myasthenia gravis and Lambert–Eaton myasthenic syndrome (LEMS).[66]
- Collection of cerebrospinal fluid (CSF) protein and blood assist with the exclusion of Guillan-Barre syndrome and stroke.[67]
- Detailed physical examination of the patient for any rash or tick presence helps with the exclusion of any tick transmitted tick paralysis.[68]
Pathology
Foodborne botulism
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
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
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
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
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
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
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
C. botulinum is used to prepare the medicaments
A "mouse protection" or "mouse bioassay" test determines the type of C. botulinum toxin present using
C. botulinum in different geographical locations
A number of
Location | |
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North America | Type A C. botulinum predominates the acidic soils (average pH 6.23).
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Europe | C. botulinum type E is prevalent in aquatic sediments in Norway and Sweden,[90] Denmark,[91]</ref> 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 .
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Further reading
- Sobel J (October 2005). "Botulism". Clinical Infectious Diseases. 41 (8): 1167–1173. PMID 16163636.