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Botulismo
Botulism1and2.JPG
Un niño de 14 años con botulismo, caracterizado por debilidad de los músculos oculares y párpados caídos que se muestran en la imagen de la izquierda, y pupilas dilatadas e inmóviles que se muestran en la imagen de la derecha. Este joven estaba plenamente consciente.
Pronunciación
EspecialidadEnfermedad infecciosa , gastroenterología
SíntomasDebilidad, dificultad para ver, cansancio , dificultad para hablar [1]
ComplicacionesInsuficiencia respiratoria [2]
Inicio habitual12 a 72 horas [2]
DuraciónVariable [2]
CausasClostridium botulinum [1]
Método de diagnósticoEncontrar la bacteria o su toxina [1]
Diagnóstico diferencialMiastenia gravis , síndrome de Guillain-Barré , esclerosis lateral amiotrófica , síndrome de Lambert Eaton [3]
PrevenciónPreparación adecuada de los alimentos, sin miel para niños menores de un año [1]
TratamientoAntitoxina , antibióticos, ventilación mecánica [1]
Pronóstico~ 7.5% de riesgo de muerte [1]

El botulismo es una rara y potencialmente fatal enfermedad causada por una toxina producida por la bacteria Clostridium botulinum . [1] La enfermedad comienza con debilidad, visión borrosa, sensación de cansancio y dificultad para hablar. [1] Esto puede ir seguido de debilidad de los brazos, los músculos del pecho y las piernas. [1] También pueden ocurrir vómitos, hinchazón del abdomen y diarrea. [1] La enfermedad generalmente no afecta la conciencia ni causa fiebre . [1]

El botulismo se puede transmitir de varias formas. [1] Las esporas bacterianas que lo causan son comunes tanto en el suelo como en el agua. [1] Producen la toxina botulínica cuando se exponen a niveles bajos de oxígeno y ciertas temperaturas. [1] El botulismo transmitido por los alimentos ocurre cuando se ingieren alimentos que contienen la toxina. [1] El botulismo infantil ocurre cuando la bacteria se desarrolla en los intestinos y libera la toxina. [1] Por lo general, esto solo ocurre en niños menores de seis meses, ya que los mecanismos de protección se desarrollan después de ese tiempo. [1] El botulismo por heridas se encuentra con mayor frecuencia entre quienes se inyectan drogas ilegales . [1]En esta situación, las esporas ingresan a una herida y, en ausencia de oxígeno, liberan la toxina. [1] No se transmite directamente entre personas. [1] El diagnóstico se confirma al encontrar la toxina o la bacteria en la persona en cuestión. [1]

La prevención se realiza principalmente mediante la preparación adecuada de los alimentos. [1] La toxina, aunque no el organismo, se destruye calentándola a más de 85 ° C (185 ° F) durante más de 5 minutos. [1] La miel puede contener el organismo, por lo que no se debe administrar miel a niños menores de 12 meses. [1] El tratamiento es con una antitoxina . [1] En aquellos que pierden la capacidad de respirar por sí mismos, la ventilación mecánica puede ser necesaria durante meses. [1] Se pueden usar antibióticos para el botulismo de heridas. [1] La muerte ocurre en el 5 al 10% de las personas. [1] El botulismo también afecta a muchos otros animales. [1]La palabra proviene del latín botulus , que significa salchicha. [4] Las primeras descripciones del botulismo se remontan al menos a 1793 en Alemania. [5]

Signos y síntomas [ editar ]

La debilidad muscular del botulismo comienza característicamente en los músculos inervados por los nervios craneales, un grupo de doce nervios que controlan los movimientos oculares , los músculos faciales y los músculos que controlan la masticación y la deglución . Por tanto , puede producirse visión doble , caída de ambos párpados , pérdida de la expresión facial y problemas para tragar. Además de afectar los músculos voluntarios , también puede causar alteraciones en el sistema nervioso autónomo . Esto se experimenta como sequedad de boca y garganta (debido a la disminución de la producción de saliva), hipotensión postural.(disminución de la presión arterial al ponerse de pie, con el consiguiente mareo y riesgo de desmayos) y, finalmente, estreñimiento (debido a la disminución del movimiento hacia adelante del contenido intestinal ). [6] Algunas de las toxinas (B y E) también precipitado náuseas , vómitos , [6] y dificultad con la que habla . La debilidad luego se extiende a los brazos (comenzando en los hombros y siguiendo a los antebrazos) y piernas (nuevamente desde los muslos hasta los pies). [6]

El botulismo severo conduce a un movimiento reducido de los músculos de la respiración y, por lo tanto, a problemas con el intercambio de gases . Esto puede experimentarse como disnea (dificultad para respirar), pero cuando es grave puede provocar insuficiencia respiratoria , debido a la acumulación de dióxido de carbono no exhalado y su efecto depresor resultante sobre el cerebro. Esto puede provocar un compromiso respiratorio y la muerte si no se trata. [6]

Los médicos con frecuencia piensan en los síntomas del botulismo en términos de una tríada clásica: parálisis bulbar y parálisis descendente, falta de fiebre y sentidos claros y estado mental ("sensorium claro"). [7]

Botulismo infantil [ editar ]

Un bebé con botulismoː a pesar de no estar dormido o sedado, no puede abrir los ojos ni moverse; también tiene un llanto débil.

El botulismo infantil (también conocido como síndrome del bebé flácido ) se reconoció por primera vez en 1976 y es la forma más común de botulismo en los Estados Unidos. Los bebés son susceptibles al botulismo infantil en el primer año de vida, y más del 90% de los casos ocurren en bebés menores de seis meses. [8] El botulismo infantil es el resultado de la ingestión de esporas de C. botulinum y la posterior colonización del intestino delgado. El intestino del bebé puede ser colonizado cuando la composición de la microflora intestinal (flora normal) es insuficiente para inhibir competitivamente el crecimiento de C. botulinum y los niveles de ácidos biliares (que normalmente inhiben el crecimiento de clostridios) son más bajos que en etapas posteriores de la vida. [9]

El crecimiento de las esporas libera toxina botulínica , que luego se absorbe en el torrente sanguíneo y se lleva a todo el cuerpo, causando parálisis al bloquear la liberación de acetilcolina en la unión neuromuscular . Los síntomas típicos del botulismo infantil incluyen estreñimiento, letargo, debilidad, dificultad para alimentarse y un llanto alterado, que a menudo progresa hasta una parálisis flácida descendente completa . Aunque el estreñimiento suele ser el primer síntoma del botulismo infantil, por lo general se pasa por alto. [10]

La miel es un reservorio dietético conocido de esporas de C. botulinum y se ha relacionado con el botulismo infantil. Por esta razón, la miel no se recomienda para bebés menores de un año. [9] Sin embargo, se cree que la mayoría de los casos de botulismo infantil son causados ​​por la adquisición de esporas del entorno natural. Clostridium botulinum es una bacteria ubicua que habita en el suelo. Se ha demostrado que muchos pacientes con botulismo infantil viven cerca de un sitio de construcción o un área de alteración del suelo. [11]

Se ha informado de botulismo infantil en 49 de 50 estados de EE. UU. (Todos excepto Rhode Island), [8] y se han reconocido casos en 26 países de los cinco continentes. [12]

Complicaciones [ editar ]

El botulismo infantil no tiene efectos secundarios a largo plazo, pero puede complicarse con infecciones adquiridas en el hospital .

El botulismo puede provocar la muerte por insuficiencia respiratoria . Sin embargo, en los últimos 50 años, la proporción de pacientes con botulismo que mueren ha disminuido de aproximadamente un 50% a un 7% debido a la mejora de la atención de apoyo. Un paciente con botulismo severo puede requerir ventilación mecánica (soporte respiratorio a través de un ventilador), así como cuidados médicos y de enfermería intensivos, a veces durante varios meses. La persona puede requerir terapia de rehabilitación después de salir del hospital. [13]

Porque [ editar ]

Una microfotografía de la bacteria Clostridium botulinum .

Clostridium botulinum is an anaerobic, Gram positive, spore-forming rod. Botulinum toxin is one of the most powerful known toxins: about one microgram is lethal to humans when inhaled.[14] It acts by blocking nerve function (neuromuscular blockade) through inhibition of the excitatory neurotransmitter acetylcholine's release from the presynaptic membrane of neuromuscular junctions in the somatic nervous system. This causes paralysis. Advanced botulism can cause respiratory failureparalizando los músculos del pecho; esto puede progresar a un paro respiratorio . [15] Además, se bloquea la liberación de acetilcolina de las membranas presinápticas de las sinapsis nerviosas muscarínicas . Esto puede conducir a una variedad de signos y síntomas autónomos descritos anteriormente.

En todos los casos, la enfermedad es causada por la toxina botulínica producida por la bacteria C. botulinum en condiciones anaeróbicas y no por la propia bacteria. El patrón de daño se produce porque la toxina afecta primero a los nervios que se activan (despolarizan) con mayor frecuencia. [dieciséis]

Los mecanismos de entrada al cuerpo humano de la toxina botulínica se describen a continuación.

Colonización del intestino [ editar ]

La forma más común en los países occidentales es el botulismo infantil. Esto ocurre en bebés que están colonizados con la bacteria en el intestino delgado durante las primeras etapas de su vida. Luego, la bacteria produce la toxina, que se absorbe en el torrente sanguíneo. El consumo de miel durante el primer año de vida ha sido identificado como un factor de riesgo para el botulismo infantil; es un factor en una quinta parte de todos los casos. [6] La forma adulta de botulismo infantil se denomina toxemia intestinal adulta y es extremadamente rara. [6]

Comida [ editar ]

La toxina producida por la bacteria en recipientes de alimentos que no se han conservado adecuadamente es la causa más común de botulismo transmitido por alimentos. El pescado encurtido sin la salinidad o acidez de la salmuera que contiene ácido acético y altos niveles de sodio , así como el pescado ahumado almacenado a una temperatura demasiado alta, presenta un riesgo, al igual que los alimentos enlatados incorrectamente.

Food-borne botulism results from contaminated food in which C. botulinum spores have been allowed to germinate in low-oxygen conditions. This typically occurs in improperly prepared home-canned food substances and fermented dishes without adequate salt or acidity.[17] Given that multiple people often consume food from the same source, it is common for more than a single person to be affected simultaneously. Symptoms usually appear 12–36 hours after eating, but can also appear within 6 hours to 10 days.[18]

Wound[edit]

El botulismo por heridas resulta de la contaminación de una herida con las bacterias, que luego secretan la toxina en el torrente sanguíneo. Esto se ha vuelto más común en los consumidores de drogas intravenosas desde la década de 1990, especialmente en las personas que consumen heroína de alquitrán negro y en los que se inyectan heroína en la piel en lugar de en las venas. [6] El botulismo por heridas representa el 29% de los casos.

Inhalación [ editar ]

Se han descrito casos aislados de botulismo tras la inhalación por parte de trabajadores de laboratorio. [ cita requerida ]

Inyección [ editar ]

Symptoms of botulism may occur away from the injection site of botulinum toxin.[19] This may include loss of strength, blurred vision, change of voice, or trouble breathing which can result in death.[19] Onset can be hours to weeks after an injection.[19] This generally only occurs with inappropriate strengths of botulinum toxin for cosmetic use or due to the larger doses used to treat movement disorders.[6] Following a 2008 review the FDA added these concerns as a boxed warning.[20]

Mechanism[edit]

The toxin is the protein botulinum toxin produced under anaerobic conditions (where there is no oxygen) by the bacterium Clostridium botulinum.

Clostridium botulinum is a large anaerobic Gram-positive bacillus that forms subterminal endospores.[21]

There are eight serological varieties of the bacterium denoted by the letters A to H. The toxin from all of these acts in the same way and produces similar symptoms: the motor nerve endings are prevented from releasing acetylcholine, causing flaccid paralysis and symptoms of blurred vision, ptosis, nausea, vomiting, diarrhea or constipation, cramps, and respiratory difficulty.

Botulinum toxin is broken into eight neurotoxins (labeled as types A, B, C [C1, C2], D, E, F, and G), which are antigenically and serologically distinct but structurally similar. Human botulism is caused mainly by types A, B, E, and (rarely) F. Types C and D cause toxicity only in other animals.[22]

In October 2013, scientists released news of the discovery of type H, the first new botulism neurotoxin found in forty years. However, further studies showed type H to be a chimeric toxin composed of parts of types F and A (FA).[23]

Some types produce a characteristic putrefactive smell and digest meat (types A and some of B and F); these are said to be proteolytic; type E and some types of B, C, D and F are nonproteolytic and can go undetected because there is no strong odor associated with them.[21]

When the bacteria are under stress, they develop spores, which are inert. Their natural habitats are in the soil, in the silt that comprises the bottom sediment of streams, lakes and coastal waters and ocean, while some types are natural inhabitants of the intestinal tracts of mammals (e.g., horses, cattle, humans), and are present in their excreta. The spores can survive in their inert form for many years.[24]

Toxin is produced by the bacteria when environmental conditions are favourable for the spores to replicate and grow, but the gene that encodes for the toxin protein is actually carried by a virus or phage that infects the bacteria. Unfortunately, little is known about the natural factors that control phage infection and replication within the bacteria.[25]

The spores require warm temperatures, a protein source, an anaerobic environment, and moisture in order to become active and produce toxin. In the wild, decomposing vegetation and invertebrates combined with warm temperatures can provide ideal conditions for the botulism bacteria to activate and produce toxin that may affect feeding birds and other animals. Spores are not killed by boiling, but botulism is uncommon because special, rarely obtained conditions are necessary for botulinum toxin production from C. botulinum spores, including an anaerobic, low-salt, low-acid, low-sugar environment at ambient temperatures.[26]

Botulinum inhibits the release within the nervous system of acetylcholine, a neurotransmitter, responsible for communication between motor neurons and muscle cells. All forms of botulism lead to paralysis that typically starts with the muscles of the face and then spreads towards the limbs.[6] In severe forms, botulism leads to paralysis of the breathing muscles and causes respiratory failure. In light of this life-threatening complication, all suspected cases of botulism are treated as medical emergencies, and public health officials are usually involved to identify the source and take steps to prevent further cases from occurring.[6]

Botulinum toxin A, C, and E cleave the SNAP-25, ultimately leading to paralysis.

Diagnosis[edit]

For botulism in babies, diagnosis should be made on signs and symptoms. Confirmation of the diagnosis is made by testing of a stool or enema specimen with the mouse bioassay.

In people whose history and physical examination suggest botulism, these clues are often not enough to allow a diagnosis. Other diseases such as Guillain–Barré syndrome, stroke, and myasthenia gravis can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can be cultured from tissues. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony.[27]

Prevention[edit]

Although the vegetative form of the bacteria is destroyed by boiling,[28][29] the spore itself is not killed by the temperatures reached with normal sea-level-pressure boiling, leaving it free to grow and again produce the toxin when conditions are right.[30][31]

A recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. In older children and adults the normal intestinal bacteria suppress development of C. botulinum.[32]

While commercially canned goods are required to undergo a "botulinum cook" in a pressure cooker at 121 °C (250 °F) for 3 minutes, and thus rarely cause botulism, there have been notable exceptions. Two were the 1978 Alaskan salmon outbreak and the 2007 Castleberry's Food Company outbreak. Foodborne botulism is the rarest form though, accounting for only around 15% of cases (US)[33] and has more frequently been from home-canned foods with low acid content, such as carrot juice, asparagus, green beans, beets, and corn. However, outbreaks of botulism have resulted from more unusual sources. In July 2002, fourteen Alaskans ate muktuk (whale meat) from a beached whale, and eight of them developed symptoms of botulism, two of them requiring mechanical ventilation.[34]

Other, much rarer sources of infection (about every decade in the US[33]) include garlic or herbs[35] stored covered in oil without acidification,[36] chili peppers,[33] improperly handled baked potatoes wrapped in aluminum foil,[33] tomatoes,[33] and home-canned or fermented fish.

When canning or preserving food at home, attention should be paid to hygiene, pressure, temperature, refrigeration and storage. When making home preserves, only acidic fruit such as apples, pears, stone fruits and berries should be bottled. Tropical fruit and tomatoes are low in acidity and must have some acidity added before they are bottled.[37]

Low-acid foods have pH values higher than 4.6. They include red meats, seafood, poultry, milk, and all fresh vegetables except for most tomatoes. Most mixtures of low-acid and acid foods also have pH values above 4.6 unless their recipes include enough lemon juice, citric acid, or vinegar to make them acidic. Acid foods have a pH of 4.6 or lower. They include fruits, pickles, sauerkraut, jams, jellies, marmalades, and fruit butters.[38]

Although tomatoes usually are considered an acid food, some are now known to have pH values slightly above 4.6. Figs also have pH values slightly above 4.6. Therefore, if they are to be canned as acid foods, these products must be acidified to a pH of 4.6 or lower with lemon juice or citric acid. Properly acidified tomatoes and figs are acid foods and can be safely processed in a boiling-water canner.[38]

Oils infused with fresh garlic or herbs should be acidified and refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Because the botulism toxin is destroyed by high temperatures, home-canned foods are best boiled for 10 minutes before eating.[39] Metal cans containing food in which bacteria are growing may bulge outwards due to gas production from bacterial growth; such cans should be discarded.[40]

Any container of food which has been heat-treated and then assumed to be airtight which shows signs of not being so, e.g., metal cans with pinprick holes from rust or mechanical damage, should be discarded. Contamination of a canned food solely with C. botulinum may not cause any visual defects to the container, such as bulging, or the food. Only assurance of sufficient thermal processing during production, and absence of a route for subsequent contamination, should be used as indicators of food safety.

The addition of nitrites and nitrates to processed meats such as ham, bacon, and sausages reduces growth and toxin production of C. botulinum,[41] although such additives are now known to be carcinogenic.

Vaccine[edit]

Vaccines are under development, but they have disadvantages, and in some cases there are concerns that they may revert to dangerous native activity.[1] As of 2017 work to develop a better vaccine was being carried out, but the US FDA had not approved any vaccine against botulism.[42][43]

Treatment[edit]

Botulism is generally treated with botulism antitoxin and supportive care.[1]

Supportive care for botulism includes monitoring of respiratory function. Respiratory failure due to paralysis may require mechanical ventilation for 2 to 8 weeks, plus intensive medical and nursing care. After this time, paralysis generally improves as new neuromuscular connections are formed.[44]

In some abdominal cases, physicians may try to remove contaminated food still in the digestive tract by inducing vomiting or using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria.[45]

Antitoxin[edit]

Botulinum antitoxin consists of antibodies that neutralize botulinum toxin in the circulatory system by passive immunization.[46] This prevents additional toxin from binding to the neuromuscular junction, but does not reverse any already inflicted paralysis.[46]

In adults, a trivalent antitoxin containing antibodies raised against botulinum toxin types A, B, and E is used most commonly; however, a heptavalent botulism antitoxin has also been developed and was approved by the U.S. FDA in 2013.[15][47] In infants, horse-derived antitoxin is sometimes avoided for fear of infants developing serum sickness or lasting hypersensitivity to horse-derived proteins.[48] To avoid this, a human-derived antitoxin has been developed and approved by the U.S. FDA in 2003 for the treatment of infant botulism.[49] This human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism.[49][50] However, the danger of equine-derived antitoxin to infants has not been clearly established, and one study showed the equine-derived antitoxin to be both safe and effective for the treatment of infant botulism.[48]

Trivalent (A,B,E) botulinum antitoxin is derived from equine sources utilizing whole antibodies (Fab and Fc portions). In the United States, this antitoxin is available from the local health department via the CDC. The second antitoxin, heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, is derived from "despeciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This less immunogenic antitoxin is effective against all known strains of botulism where not contraindicated.[51]

Prognosis[edit]

The paralysis caused by botulism can persist for 2 to 8 weeks, during which supportive care and ventilation may be necessary to keep the person alive.[44] Botulism is fatal in 5% to 10% of people who are affected.[1] However, if left untreated, botulism is fatal in 40% to 50% of cases.[50]

Infant botulism typically has no long-term side effects but can be complicated by treatment-associated adverse events. The case fatality rate is less than 2% for hospitalized babies.[52]

Epidemiology[edit]

Globally, botulism is fairly rare,[1] with approximately 1,000 cases yearly.[53]

United States[edit]

In the United States an average of 145 cases are reported each year. Of these, roughly 65% are infant botulism, 20% are wound botulism, and 15% are foodborne.[54] Infant botulism is predominantly sporadic and not associated with epidemics, but great geographic variability exists. From 1974 to 1996, for example, 47% of all infant botulism cases reported in the U.S. occurred in California.[54]

Between 1990 and 2000, the Centers for Disease Control and Prevention reported 263 individual foodborne cases from 160 botulism events in the United States with a case-fatality rate of 4%. Thirty-nine percent (103 cases and 58 events) occurred in Alaska, all of which were attributable to traditional Alaska aboriginal foods. In the lower 49 states, home-canned food was implicated in 70 events (~69%) with canned asparagus being the most numerous cause. Two restaurant-associated outbreaks affected 25 persons. The median number of cases per year was 23 (range 17–43), the median number of events per year was 14 (range 9–24). The highest incidence rates occurred in Alaska, Idaho, Washington, and Oregon. All other states had an incidence rate of 1 case per ten million people or less.[55]

The number of cases of food borne and infant botulism has changed little in recent years, but wound botulism has increased because of the use of black tar heroin, especially in California.[56]

All data regarding botulism antitoxin releases and laboratory confirmation of cases in the US are recorded annually by the Centers for Disease Control and Prevention and published on their website.[54]

  • On July 2, 1971, the U.S. Food and Drug Administration (FDA) released a public warning after learning that a New York man had died and his wife had become seriously ill due to botulism after eating a can of Bon Vivant vichyssoise soup.
  • Between March 31 and April 6, 1977, 59 individuals developed type B botulism. All ill persons had eaten at the same Mexican restaurant in Pontiac, Michigan and all had consumed a hot sauce made with improperly home-canned jalapeño peppers, either by adding it to their food, or by eating a nacho that had had hot sauce used in its preparation. The full clinical spectrum (mild symptomatology with neurologic findings through life-threatening ventilatory paralysis) of type B botulism was documented.[57]
  • In April 1994, the largest outbreak of botulism in the United States since 1978 occurred in El Paso, Texas. Thirty persons were affected; 4 required mechanical ventilation. All ate food from a Greek restaurant. The attack rate among persons who ate a potato-based dip was 86% (19/22) compared with 6% (11/176) among persons who did not eat the dip (relative risk [RR] = 13.8; 95% confidence interval [CI], 7.6–25.1). The attack rate among persons who ate an eggplant-based dip was 67% (6/9) compared with 13% (24/189) among persons who did not (RR = 5.2; 95% CI, 2.9–9.5). Botulism toxin type A was detected from patients and in both dips. Toxin formation resulted from holding aluminum foil-wrapped baked potatoes at room temperature, apparently for several days, before they were used in the dips. Food handlers should be informed of the potential hazards caused by holding foil-wrapped potatoes at ambient temperatures after cooking.[58]
  • In 2002, fourteen Alaskans ate muktuk (whale blubber) from a beached whale, resulting in eight of them developing botulism, with two of the affected requiring mechanical ventilation.[59]
  • Beginning in late June 2007, 8 people contracted botulism poisoning by eating canned food products produced by Castleberry's Food Company in its Augusta, Georgia plant. It was later identified that the Castleberry's plant had serious production problems on a specific line of retorts that had under-processed the cans of food. These issues included broken cooking alarms, leaking water valves and inaccurate temperature devices, all the result of poor management of the company. All of the victims were hospitalized and placed on mechanical ventilation. The Castleberry's Food Company outbreak was the first instance of botulism in commercial canned foods in the United States in over 30 years.[citation needed]
  • One person died, 21 cases were confirmed, and 10 more were suspected in Lancaster, Ohio when a botulism outbreak occurred after a church potluck in April 2015. The suspected source was a salad made from home-canned potatoes.[60]
  • A botulism outbreak occurred in Northern California in May 2017 after 10 people consumed nacho cheese dip served at a gas station in Sacramento County. One man died as a result of the outbreak.[61]

United Kingdom[edit]

The largest recorded outbreak of foodborne botulism in the United Kingdom occurred in June 1989. A total of 27 patients were affected; one patient died. Twenty-five of the patients had eaten one brand of hazelnut yogurt in the week before the onset of symptoms. Control measures included the cessation of all yogurt production by the implicated producer, the withdrawal of the firm's yogurts from sale, the recall of cans of the hazelnut conserve, and advice to the general public to avoid the consumption of all hazelnut yogurts.[62]

China[edit]

From 1958–1983 there were 986 outbreaks of botulism in China involving 4,377 people with 548 deaths.[63]

Qapqal disease[edit]

After the Chinese Communist Revolution in 1949, a mysterious plague (named Qapqal disease) was noticed to be affecting several Sibe villages in Qapqal Xibe Autonomous County. It was endemic with distinctive epidemic patterns, yet the underlying cause remained unknown for a long period of time.[64] It caused a number of deaths and forced some people to leave the place.[65]

In 1958, a team of experts were sent to the area by the Ministry of Health to investigate the cases. The epidemic survey conducted proved that the disease was primarily type A botulism,[66] with several cases of type B.[64] The team also discovered that, the source of the botulinum was local fermented grain and beans as well as raw meat food called mi song hu hu.[65] They promoted the improvement of fermentation techniques among local residents, and thus eliminated the disease.

Canada[edit]

From 1985-2015 there was an outbreak of 91 confirmed cases of foodborne botulism in Canada, 85% of which were in Inuit communities, especially Nunavik and First Nations of the coast of British Columbia from eating traditionally prepared marine mammal and fish products.[67]

Ukraine[edit]

In 2017, there were 70 cases of botulism with 8 deaths in Ukraine. The previous year there were 115 cases with 12 deaths. Most cases were the result of dried fish, a common local drinking snack.[68]

Vietnam[edit]

In 2020, several cases of botulism were reported in Vietnam. All of them were related to a product containing contaminated vegetarian pâté. Some patients have been put on life support.[69][70]

Other susceptible species[edit]

Botulism can occur in many vertebrates and invertebrates. Botulism has been reported in rats, mice, chicken, frogs, toads, goldfish, aplysia, squid, crayfish, drosophila, leeches, etc.[71]

Death from botulism is common in waterfowl; an estimated 10,000 to 100,000 birds die of botulism annually. The disease is commonly called "limberneck". In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. An enzootic form of duck botulism in Western USA and Canada is known as "western duck sickness".[72] Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock.

Botulism seems to be relatively uncommon in domestic mammals; however, in some parts of the world, epidemics with up to 65% mortality are seen in cattle. The prognosis is poor in large animals that are recumbent.

In cattle, the symptoms may include drooling, restlessness, uncoordination, urine retention, dysphagia, and sternal recumbency. Laterally recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur. Phosphorus-deficient cattle, especially in southern Africa, are inclined to ingest bones and carrion containing clostridial toxins and consequently suffer lame sickness or lamsiekte.

A recent study has demonstrated an effective vaccine against cattle botulism associated with Clostridium botulinum serotypes C and D.[73]

The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.

Clostridium botulinum type C toxin has been incriminated as the cause of grass sickness, a condition in horses which occurs in rainy and hot summers in Northern Europe. The main symptom is pharynx paralysis.[74]

Domestic dogs may develop systemic toxemia after consuming C. botulinum type C exotoxin or spores within bird carcasses or other infected meat[75] but are generally resistant to the more severe effects of Clostridium botulinum type C. Symptoms include flaccid muscle paralysis; dogs with breathing difficulties will require more intensive care monitoring. Muscle paralysis can lead to death due to cardiac and respiratory arrest.[76]

Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.[77]

In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates.

See also[edit]

  • List of foodborne illness outbreaks

References[edit]

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External links[edit]

Wikipedia's health care articles can be viewed offline with the Medical Wikipedia app.
  • BOTULISM in the United States, 1889–1996. Handbook for Epidemiologists, Clinicians and Laboratory Technicians. Centers for Disease Control and Prevention. National Center for Infectious Diseases, Division of Bacterial and Mycotic Diseases 1998.
  • NHS choices
  • CDC Botulism: Control Measures Overview for Clinicians
  • University of California, Santa Cruz Environmental toxicology – Botulism
  • CDC Botulism FAQ
  • FDA Clostridium botulinum Bad Bug Book
  • USGS Avian Botulism
Classification
D
  • ICD-10: A05.1
  • ICD-9-CM: 005.1,040.41,040.42
  • MeSH: D001906
  • DiseasesDB: 2811
External resources
  • MedlinePlus: 000598
  • eMedicine: article/213311
  • Patient UK: Botulism