Botulism

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Botulism is a poisoning caused by a bacterial neurotoxin, botulinum toxin, produced by the bacterium Clostridium botulinum. The most common route of intoxication is food, generally due to the ingestion of poorly prepared or improperly preserved food. The disease can also be acquired through contamination of open wounds, or as a side effect of the deliberate use of the toxin in the treatment of neuromuscular diseases or in cosmetics.

Etymology

Although the Dictionary of the Spanish language states that the term comes from the Latin botulus, which means "sausage", other sources indicate that the meaning is "sausage" or "sauce".

History

The incidence of botulism was described by Justinus Kerner between 1817 and 1822 (he called it "sausage poison" or "fat poison"). Because of this, it was then called "Kerner's disease". The incidence of the disease in Baden-Wurttemberg was quite considerable and between 1793 and 1827, 234 cases were recorded. Up to the year 1853, 400 cases with 150 deaths were added. However, it would not be until 1895 that Emile Pierre van Ermengem, professor of bacteriology at the University of Ghent, discovered Clostridium botulinum .

Causes

The toxin is produced by the bacterium Clostridium botulinum, which is found in contaminated areas such as untreated soil and water. Clostridium botulinum is an anaerobic bacterium whose spores are capable of surviving in contaminated food that has been subjected to incorrect manufacturing processes and/or inadequate storage.

Botulinum toxin is one of the most toxic substances known, so it is possible that just by tasting contaminated food, serious poisoning can occur that can even lead to death.

There are several types of botulinum toxin, which are designated with letters: A, B, C, D, E, F and G, according to their affinity for nervous tissue, with type A toxin having the highest affinity.

Botulinum bacteria need low acid or alkaline media for their development: with pH values higher than 4.5.

Among the foods most exposed to botulism are raw meat or fish preserved by poor salting or smoking processes. To avoid the risks associated with the proliferation of Clostridium botulinum and toxin synthesis, nitrites and nitrates have been used for a long time as food additives, which effectively inhibit it. It can also proliferate. Clostridium botulinum in some vegetables with low acidity or that can lose their natural acidity due to the action of other microorganisms, when they have been preserved with insufficient heat treatment to destroy the spores of the bacteria. This occasionally happens in home canning, but is very rare in industrially canned foods.

The home preservation of compotes and jellies provides a good example:

"The use of a large amount of sugar is essential to the preservation process because sugar helps kill the bacteria that cause botulism [...] when a bacterial cell is in a hypertonic (high concentration) of sugar, intracellular water tends to leave the bacterial cell towards the more concentrated solution, by osmosis. This process, known as <<crenation>>, causes the cell to shrink and eventually die. The natural acidity of the fruits also inhibits bacterial growth". (Chang, 2010, p.536).

Botulism has also been described in laboratory workers due to inhalation of the toxin in aerosolized form, drug addicts are also exposed to various forms of botulism: intravenously (syringes or contaminated drug), or by nasal inhalation of drug contaminated that gives rise to chronic sinusitis.

Pathogenesis

Botulinum toxin acts by blocking the release of acetylcholine at the level of the myoneural plate, preventing the transmission of the nerve impulse. In this way, it causes a flaccid paralysis of the skeletal muscles and a parasympathetic failure.

In food poisoning, the pre-formed toxin is ingested and absorbed by endocytosis through the gastrointestinal tract. In the infant, the ingested spores germinate in the intestine, since there is no inhibitory flora, and they produce the toxin that is later absorbed. After being absorbed from the gastrointestinal tract or from the wound, the toxin is carried via the lymphatics or blood to its sites of action: the cholinergic nerve endings. Since it does not cross the blood-brain barrier, it only acts on the peripheral nervous system, especially at the neuromuscular plate or junction, and on the autonomic nervous system.

In wound botulism, the toxin is produced in the wound when the bacteria find suitable conditions there to germinate and develop. The process is very similar to the development of tetanus.

Mechanism of action of the toxin

The active portion of the toxin has peptidase activity that is specific for proteins that make up the structure of the synaptic vesicle that contains the neurotransmitter and are involved in exocytosis. The action of the toxin prevents the exocytosis of the neurotransmitter and thus the nerve impulse is blocked. Recovery of nerve function requires regeneration of the motor neuron terminal and the formation of new motor endings.

There are 3 steps:

  1. The H-chain of the toxin binds to receptors in the presynaptic membrane.
  2. Toxin penetrates by an active mechanism similar to endocytosis.
  3. Within the nerve cell, toxin interferes with the release of acetylcholine, necessary for the excitation of the muscle.

Fragment A of the released toxin cleaves the synaptobrevin protein, which helps calcium with the fusion of the synaptic vesicle to the pre-synaptic membrane; therefore the neurotransmitter acetylcholine will not be released, causing muscle paralysis and death when the respiratory muscles are affected.

Clinical picture

Symptoms usually appear 8 to 36 hours after consuming the contaminated food. There is no fever with this infection.

In adults, symptoms may include

  • Palpebral Ptosis
  • Midriasis (both pupils dilated, not reactive)
  • Abdominal colics, not always present.
  • Respiratory difficulty that can lead to respiratory failure
  • Difficulty swallowing and talking
  • Double vision
  • Dryness in the mouth
  • Nausea
  • Temporary Absence of Breath
  • Vomits
  • Weakness with paralysis (equal on both sides of the body)
  • Constipation
  • Mental lucidity decrease

Symptoms in babies may include:

  • Constipation
  • Weakness, loss of muscle tone
  • Weak plain
  • Poor feeding or soft or null suction
  • Midriasis
  • Respiratory difficulty
  • Mental lucidness despite weakness

Diagnosis

Exams of gastric contents and fecal matter are performed. The finding of toxin in blood is rare. Once a food survey has been carried out to establish what the suspected food could be, it is analyzed to determine if it contains botulinum toxin and to what type it belongs.

Treatment

Treatment is directed at respiratory support (to avoid respiratory arrest), administering trivalent equine botulinum antitoxin ABE to neutralize the effect of circulating toxin, and applying supportive therapy. It may be necessary to intubate the patient and Intravenous fluids need to be administered if swallowing difficulty persists.

Complications and clinical prognosis

When treatment is received early, the risk of death is reduced. This disease can be complicated by prolonged weakness, as well as nervous system dysfunction that can last up to a year. It is believed that there is approximately a 5% mortality in infants, but this is not reliably established.

Prevention

To avoid this disease, commercial canned goods are forced to submit to strict technological standards that vary according to the product, its composition and packaging. Temperatures of 121 °C (250 °F) for the minutes established in these standards can ensure proper sterilization.

The vegetative form of the bacterium that causes botulism is destroyed at much lower temperatures (75-80 °C), but not the spores that do require such high temperatures to be inactivated. But there is a pH limit, which is 4.5, below which the spores cannot develop, so if a food is acidified bringing its pH below 4.5, it will be enough to preserve it with a conventional heat treatment with temperatures of 90-100 °C, since it will only be necessary to destroy the vegetative forms of Clostridium Botulinum.

Home canners must follow strict hygiene procedures to reduce contamination of foods, especially low-acid foods such as carrot juice, asparagus, green beans, bell peppers, eggplant, mushrooms, beets, corn etc Although it is considered that whenever feasible, it is better to discourage the production of home canning due to the problems that this entails when the correct technology is not applied.

Do not home-can low-acid foods, such as meat, fish, and most vegetables; there are no problems with fruits, since they are of high acidity (peach, apricot, pear, quince, cherries, etc.). Oils infused with garlic or herbs should be refrigerated.

In general, consumers are advised to take precautions with canned or preserved food, not eat food from swollen or dented cans or homemade cans that are poorly closed with air or sausages of dubious origin. Likewise, all aseptic or antiseptic measures must be taken to avoid wound contamination and in the case of using botulinum to treat wrinkles or to treat neuromuscular diseases, it must be verified that the product used is the appropriate one, that is, the authorized one. for that purpose, as well as the suitability of who applies it.

The bacterium that causes botulism is Clostridium botulinum and it can develop in food if it has the right conditions, but it does not cause any alteration to the food, that is, it does not change the taste, the smell, the taste, does not produce gas. But botulinum toxin is thermolabile, that is, it is destroyed by heat, so when in doubt about any canned food, pour the contents of the can into a pot and boil it for 10 minutes; in this way the botulinum toxin is destroyed.

Botulism in Animals

In addition to being a human disease, botulism affects many animals, both vertebrates and invertebrates. Horses (particularly foals), sheep, chickens, lions, or baboons, for example, can be infected with Clostridium botulinum, mainly neurotoxic types A and B, or C/D in the Mediterranean area. The survival rate of horses (over six months of age) with botulism treated in a specialized veterinary hospital is almost 50%. These animals are especially sensitive to the disease and in certain areas vaccination and periodic control of food and water are recommended. Some strains of the bacterium can endophytically colonize clover white (Trifolium repens), a forage plant and eaten by cattle. The presence of the bacterium in pack animals is a public health problem in developing countries. Proper pasteurization of inactive dairy products more than 99.5% of botulinum toxins.

Work is underway to develop a chimeric recombinant vaccine against bovine botulism types C and D. In Brazil, the effect of a vaccine of these characteristics has been evaluated on populations of Bubalus bubalis, an introduced species that is of considerable importance for Brazilian farmers. Animals that perform pica are more prone to developing the infection.

Notable is avian botulism, which attacks 117 species of animals from 22 different families. It affects waterfowl, especially Anatidae. In different localities of Catalonia, this disease is quite common. The transmission mechanism between birds is the ingestion of carrier slugs or necrophagous dipteran larvae contaminated with the bacterium, developed on the remains of other birds killed by the toxin and which they act as vectors. The characteristic symptoms of the disease in these animals are weakness and progressive paresis that evolves to a flaccid paralysis of the legs, wings, neck and eyelids and that ends up making flight and walking impossible. They cannot maintain normal neck posture and drown if in water. Avian botulism is considered an emerging disease in Europe, especially in poultry. French researchers have developed a new PCR technique in real time optimized to detect, with high sensitivity and excellent specificity, different varieties of botulism in samples of fetuses of domestic and wild origin.

The decomposition of plants, algae or animals in certain soils or bogs creates the anaerobic environment in which the bacteria are created and feed saprophytically. Neurotoxic type E spores can be found in the digestive tract of fish of the lakes, which represents a danger for the fish-eating species or the people who consume these affected fish.

Additional bibliography

  • Moreno Izco, Isabel (2008, Gen). Botulism. A: E-Book of Emergencies, 12. Infectious diseases. Navarro Health Service. ISBN 9788469069585. Consultation on August 30, 2017.
  • Bertorini, Tulio E. (2010). Neuromuscular Disorders: Management and Treatment E-Book. Treatment and Management of Disorders of the Neuromuscular Junction, pp: 307-342 (in English). Saunders. ISBN 9781437703726.
  • Jeffery, Iain A.; Karim, Shahnawaz (2017; Oct 6 PubMed). Botulism Bookshelf (in English). StatPearls Publishing LLC. p. 6. Consultation on 4 November 2017.
  • Middlebrook, John L.; Franz, David R. (1997). Botulism Toxins. A: Textbook of Military Medicine. Part I, Medical Aspects of Chemical and Biological Warfare. Chap 33, pp: 643-654 (in English). Office of The Surgeon General. Department of the Army, USA. ISBN 978-9997320919. Archived from the original on December 22, 2010. Consultation on 24 November 2017.

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