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Treatment is in the form of supportive care. If there is light-headedness, the victim should lie with feet partly elevated. If there is severe wheezing, then intramuscular epinephrine should be given, 0.5–1 ml at dilution of 1/1000 (standard medical emergency kit). An intravenous antihistamine like diphenhydramine should be given if needed.
There is no effective treatment or antidote for ciguatera poisoning. The mainstay of treatment is supportive care. There is some evidence that calcium channel blockers like nifedipine and verapamil are effective in treating some of the symptoms that remain after the initial sickness passes, such as poor circulation and shooting pains through the chest. These symptoms are due to the cramping of arterial walls caused by maitotoxin Ciguatoxin lowers the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart contraction, and changing the senses of hot and cold. Some medications such as amitriptyline may reduce some symptoms, such as fatigue and paresthesia, although benefit does not occur in every case.
Mannitol was once used for poisoning after one study reported symptom reversal. Follow-up studies in animals and case reports in humans also found benefit from mannitol. However, a randomized, double-blind clinical trial found no difference between mannitol and normal saline, and based on this result, mannitol is no longer recommended.
Long term management of chronic Ciguatera includes avoiding trigger food and environmental triggers, and managing symptoms with medications and or lifestyle.
Caution may be needed with anesthesia and should be discussed with your healthcare providers.
Various Caribbean folk and ritualistic treatments originated in Cuba and nearby islands. The most common old-time remedy involves bed rest subsequent to a guanabana juice enema. Other folk treatments range from directly porting and bleeding the gastrointestinal tract to "cleansing" the diseased with a dove during a Santería ritual. In Puerto Rico, natives drink a tea made from mangrove buttons, purportedly high in B vitamins, to flush the toxic symptoms from the system. There has never been a funded study of these treatments.
An account of ciguatera poisoning from a linguistics researcher living on Malakula island, Vanuatu, indicates the local treatment: "We had to go with what local people told us: avoid salt and any seafood. Eat sugary foods. And they gave us a tea made from the roots of ferns growing on tree trunks. I don't know if any of that helped, but after a few weeks, the symptoms faded away."
Senescent leaves of "Heliotropium foertherianum" (Boraginaceae), also known as octopus bush, a plant used in many Pacific islands as a traditional medicine to treat ciguatera fish poisoning, contain rosmarinic acid and derivatives, which are known for their antiviral, antibacterial, antioxidant and anti-inflammatory properties. Rosmarinic acid may remove the ciguatoxins from their sites of action, as well as being an anti-inflammatory.
Prevention is mainly the role of the state, through the definition of strict rules of hygiene and a public services of veterinary surveying of animal products in the food chain, from farming to the transformation industry and delivery (shops and restaurants). This regulation includes:
- traceability: in a final product, it must be possible to know the origin of the ingredients (originating farm, identification of the harvesting or of the animal) and where and when it was processed; the origin of the illness can thus be tracked and solved (and possibly penalized), and the final products can be removed from the sale if a problem is detected;
- enforcement of hygiene procedures such as HACCP and the "cold chain";
- power of control and of law enforcement of veterinarians.
In August 2006, the United States Food and Drug Administration approved Phage therapy which involves spraying meat with viruses that infect bacteria, and thus preventing infection. This has raised concerns, because without mandatory labelling consumers would not be aware that meat and poultry products have been treated with the spray.
At home, prevention mainly consists of good food safety practices. Many forms of bacterial poisoning can be prevented by cooking it sufficiently, and either eating it quickly or refrigerating it effectively. Many toxins, however, are not destroyed by heat treatment.
Techniques that help prevent food borne illness in the kitchen are hand washing, rinsing produce, preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between , called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containers
for quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of or until hot or steaming to kill bacteria.
The term alimentary mycotoxicoses refers to the effect of poisoning by Mycotoxins (The term 'mycotoxin' is usually reserved for the toxic chemical products produced by fungi that readily colonize crops) through food consumption. Mycotoxins sometimes have important effects on human and animal health. For example, an outbreak which occurred in the UK in 1960 caused the death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal. In the USSR in World War II, 5,000 people died due to Alimentary Toxic Aleukia (ALA). The common foodborne Mycotoxins include:
- Aflatoxins – originated from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of Aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result in necrosis, cirrhosis, and carcinoma. In the US, the acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5 μg/kg. The official document can be found at FDA's website.
- Altertoxins – are those of Alternariol (AOH), Alternariol methyl ether (AME), Altenuene (ALT), Altertoxin-1 (ATX-1), Tenuazonic acid (TeA) and Radicinin (RAD), originated from Alternaria spp. Some of the toxins can be present in sorghum, ragi, wheat and tomatoes. Some research has shown that the toxins can be easily cross-contaminated between grain commodities, suggesting that manufacturing and storage of grain commodities is a critical practice.
- Citrinin
- Citreoviridin
- Cyclopiazonic acid
- Cytochalasins
- Ergot alkaloids / Ergopeptine alkaloids – Ergotamine
- Fumonisins – Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and Esophageal cancer in humans. For human and animal health, both the FDA and the EC have regulated the content levels of toxins in food and animal feed.
- Fusaric acid
- Fusarochromanone
- Kojic acid
- Lolitrem alkaloids
- Moniliformin
- 3-Nitropropionic acid
- Nivalenol
- Ochratoxins – In Australia, The Limit of Reporting (LOR) level for Ochratoxin A (OTA) analyses in 20th Australian Total Diet Survey was 1 µg/kg, whereas the EC restricts the content of OTA to 5 µg/kg in cereal commodities, 3 µg/kg in processed products and 10 µg/kg in dried vine fruits.
- Oosporeine
- Patulin – Currently, this toxin has been advisably regulated on fruit products. The EC and the FDA have limited it to under 50 µg/kg for fruit juice and fruit nectar, while limits of 25 µg/kg for solid-contained fruit products and 10 µg/kg for baby foods were specified by the EC.
- Phomopsins
- Sporidesmin A
- Sterigmatocystin
- Tremorgenic mycotoxins – Five of them have been reported to be associated with molds found in fermented meats. These are Fumitremorgen B, Paxilline, Penitrem A, Verrucosidin, and Verruculogen.
- Trichothecenes – sourced from Cephalosporium, Fusarium, Myrothecium, Stachybotrys and Trichoderma. The toxins are usually found in molded maize, wheat, corn, peanuts and rice, or animal feed of hay and straw. Four trichothecenes, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and deoxynivalenol (DON) have been most commonly encountered by humans and animals. The consequences of oral intake of, or dermal exposure to, the toxins will result in Alimentary toxic aleukia, neutropenia, aplastic anemia, thrombocytopenia and/or skin irritation. In 1993, the FDA issued a document for the content limits of DON in food and animal feed at an advisory level. In 2003, US published a patent that is very promising for farmers to produce a trichothecene-resistant crop.
- Zearalenone
- Zearalenols
Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with clinical complications.
Erythromycin can be used in children, and tetracycline in adults. Some studies show, however, that erythromycin rapidly eliminates "Campylobacter" from the stool without affecting the duration of illness. Nevertheless, children with dysentery due to "C. jejuni" benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms. Quinolones are effective if the organism is sensitive, but high rates of quinolone use in livestock means that quinolones are now largely ineffective.
Antimotility agents, such as loperamide, can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided. Trimethoprim/sulfamethoxazole and ampicillin are ineffective against "Campylobacter".
The infection is usually self-limiting, and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections.
Botulism is generally treated with botulism antitoxin and supportive care.
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.
In some abnormal 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.
Bacteremia should be treated for 2 weeks, meningitis for 3 weeks, and brain abscess for at least 6 weeks. Ampicillin generally is considered antibiotic of choice; gentamicin is added frequently for its synergistic effects. Overall mortality rate is 20–30%; of all pregnancy-related cases, 22% resulted in fetal loss or neonatal death, but mothers usually survive.
Electrolytes may be replenished with oral rehydration supplements (typically containing salts sodium chloride and potassium chloride).
Appropriate antibiotics, such as ceftriaxone, may be given to kill the bacteria but are not necessary in most cases. Azithromycin has been suggested to be better at treating typhoid in resistant populations than both fluoroquinolone drugs and ceftriaxone. Antibiotic resistance rates are increasing throughout the world, so health care providers should check current recommendations before choosing an antibiotic.
The main means of prevention is through the promotion of safe handling, cooking and consumption of food. This includes washing raw vegetables and cooking raw food thoroughly, as well as reheating leftover or ready-to-eat foods like hot dogs until steaming hot.
Another aspect of prevention is advising high-risk groups such as pregnant women and immunocompromised patients to avoid unpasteurized pâtés and foods such as soft cheeses like feta, Brie, Camembert cheese, and bleu. Cream cheeses, yogurt, and cottage cheese are considered safe. In the United Kingdom, advice along these lines from the Chief Medical Officer posted in maternity clinics led to a sharp decline in cases of listeriosis in pregnancy in the late 1980s.
In adults, botulism can be treated by passive immunization with a horse-derived antitoxin, which blocks the action of the toxin circulating in the blood. 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. In infants, horse-derived antitoxin is sometimes avoided for fear of infants developing serum sickness or lasting hypersensitivity to horse-derived proteins. 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. This human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism. 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.
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.
Scombroid food poisoning is a foodborne illness that results from eating spoiled (decayed) fish. Along with ciguatera, it is listed as a common type of seafood poisoning. The toxin believed to be responsible is histamine, formed as the flesh of the fish begins to decay. As histamine is also the natural agent involved in allergic reactions, scombroid food poisoning often gets misidentified as a food allergy.
The syndrome is named after Scombridae family of fish, which includes mackerels, tunas and bonitos, because early descriptions of the illness noted an association with those species; however, the Centers for Disease Control and Prevention (CDC) have identified other, nonscombroid vectors, such as mahi-mahi and amberjack. Scombroid syndrome can result from inappropriate handling of fish during storage or processing. Cooking the food does not prevent illness, because histamine is not destroyed at normal cooking temperatures.
Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.
The FDA has published guidelines to help reduce the chance of food-borne salmonellosis. Food must be cooked to 68–72 °C (145–160 °F), and liquids such as soups or gravies must be boiled. Freezing kills some "Salmonella", but it is not sufficient to reliably reduce them below infectious levels. While "Salmonella" is usually heat-sensitive, it does acquire heat resistance in high-fat environments such as peanut butter.
Individuals can try minor changes of diet to exclude foods causing obvious reactions, and for many this may be adequate without the need for professional assistance. For reasons mentioned above foods causing problems may not be so obvious since food sensitivities may not be noticed for hours or even days after one has digested food. Persons unable to isolate foods and those more sensitive or with disabling symptoms should seek expert medical and dietitian help. The dietetic department of a teaching hospital is a good start. (see links below)
Guidance can also be given to your general practitioner to assist in diagnosis and management. Food elimination diets have been designed to exclude food compounds likely to cause reactions and foods commonly causing true allergies and those foods where enzyme deficiency cause symptoms. These elimination diets are not everyday diets but intended to isolate problem foods and chemicals. Avoidance of foods with additives is also essential in this process.
Individuals and practitioners need to be aware that during the elimination process patients can display aspects of food addiction, masking, withdrawals, and further sensitization and intolerance. Those foods that an individual considers as 'must have every day' are suspect addictions, this includes tea, coffee, chocolate and health foods and drinks, as they all contain food chemicals. Individuals are also unlikely to associate foods causing problems because of masking or where separation of time between eating and symptoms occur. The elimination process can overcome addiction and unmask problem foods so that the patients can associate cause and effect.
It takes around five days of total abstinence to unmask a food or chemical, during the first week on an elimination diet withdrawal symptoms can occur but it takes at least two weeks to remove residual traces. If symptoms have not subsided after six weeks, food intolerance is unlikely to be involved and a normal diet should be restarted. Withdrawals are often associated with a lowering of the threshold for sensitivity which assists in challenge testing, but in this period individuals can be ultra-sensitive even to food smells so care must be taken to avoid all exposures.
After two or more weeks if the symptoms have reduced considerably or gone for at least five days then challenge testing can begin. This can be carried out with selected foods containing only one food chemical, to isolate it if reactions occur. In Australia, purified food chemicals in capsule form are available to doctors for patient testing. These are often combined with placebo capsules for control purposes. This type of challenge is more definitive. New challenges should only be given after 48 hours if no reactions occur or after five days of no symptoms if reactions occur.
Once all food chemical sensitivities are identified a dietitian can prescribe an appropriate diet for the individual to avoid foods with those chemicals. Lists of suitable foods are available from various hospitals and patient support groups can give local food brand advice. A dietitian will ensure adequate nutrition is achieved with safe foods and supplements if need be.
Over a period of time it is possible for individuals avoiding food chemicals to build up a level of resistance by regular exposure to small amounts in a controlled way, but care must be taken, the aim being to build up a varied diet with adequate composition.
In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.
There is emerging evidence from studies of cord bloods that both sensitization and the acquisition of tolerance can begin in pregnancy, however the window of main danger for sensitization to foods extends prenatally, remaining most critical during early infancy when the immune system and intestinal tract are still maturing. There is no conclusive evidence to support the restriction of dairy intake in the maternal diet during pregnancy in order to prevent. This is generally not recommended since the drawbacks in terms of loss of nutrition can out-weigh the benefits. However, further randomised, controlled trials are required to examine if dietary exclusion by lactating mothers can truly minimize risk to a significant degree and if any reduction in risk is out-weighed by deleterious impacts on maternal nutrition.
A Cochrane review has concluded feeding with a soy formula cannot be recommended for prevention of allergy or food intolerance in infants. Further research may be warranted to determine the role of soy formulas for prevention of allergy or food intolerance in infants unable to be breast fed with a strong family history of allergy or cow's milk protein intolerance. In the case of allergy and celiac disease others recommend a dietary regimen is effective in the prevention of allergic diseases in high-risk infants, particularly in early infancy regarding food allergy and eczema. The most effective dietary regimen is exclusively breastfeeding for at least 4–6 months or, in absence of breast milk, formulas with documented reduced allergenicity for at least the first 4 months, combined with avoidance of solid food and cow's milk for the first 4 months.
Prevention is through use of Stock coryza-free birds. In other areas culling of the whole flock is a good means of the disease control. Bacterin also is used at a dose of two to reduce brutality of the disease. Precise exposure has also has been used but it should be done with care. Vaccination of the chicks is done in areas with high disease occurrence. Treatment is done by using antibiotics such as erythromycin, Dihydrostreptomycin, Streptomycin sulphonamides, tylosin and Flouroquinolones .
The medications prescribed for acute toxoplasmosis are the following:
- Pyrimethamine — an antimalarial medication
- Sulfadiazine — an antibiotic used in combination with pyrimethamine to treat toxoplasmosis
- Combination therapy is usually given with folic acid supplements to reduce incidence of thrombocytopaenia.
- Combination therapy is most useful in the setting of HIV.
- Clindamycin
- Spiramycin — an antibiotic used most often for pregnant women to prevent the infection of their children.
(other antibiotics, such as minocycline, have seen some use as a salvage therapy).
If infected during pregnancy, spiramycin is recommended in the first and early second trimesters while pyrimethamine/sulfadiazine and leucovorin is recommended in the late second and third trimesters.
In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not reach the bradyzoites in sufficient concentration.
The medications prescribed for latent toxoplasmosis are:
- Atovaquone — an antibiotic that has been used to kill "Toxoplasma" cysts inside AIDS patients
- Clindamycin — an antibiotic that, in combination with atovaquone, seemed to optimally kill cysts in mice
The 1951 Pont-Saint-Esprit mass poisoning, also known as Le Pain Maudit, occurred on 15 August 1951, in the small town of Pont-Saint-Esprit in southern France. More than 250 people were involved, including 50 persons interned in asylums and resulted in 7 deaths. A foodborne illness was suspected, and among these it was originally believed to be a case of "cursed bread" ("pain maudit").
Most academic sources accept ergot poisoning as the cause of the epidemic, while a few theorize other causes such as poisoning by mercury, mycotoxins, or nitrogen trichloride.
Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has an approximate relapse rate of 40%. Recent expert opinion is that Whipple's disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms.
There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting
contaminated premises.
Shortly after the incident, in September 1951, scientists writing in the "British Medical Journal" declared that “the outbreak of poisoning” was due to eating bread made from rye grain that was infected with the fungus. The victims appeared to have one common connection. They had eaten bread from the bakery of Roch Briand who was subsequently blamed for using flour made from rye.