Moldy sweet potato poisoning (black spot sweet potato poisoning)

作者：admin  点击次数：7  发布时间：2025-05-08

(I) Etiology
Sweet potato (also known as sweet potato, sweet potato) black spot disease is caused by Ceracris fimbriala or Fusarium solani. They mostly parasitize on wounds, broken skin, and cracks of sweet potatoes. The infected parts are light yellow and turn brown or black after contact with air. The lesions are hard and slightly concave on the surface. They taste bitter. It can cause poisoning when eaten by humans or animals.
Sweet potatoes are contaminated by mold and produce toxins. When eaten by humans, they can cause mold food poisoning, which mainly occurs in rural areas. The parts of the sweet potatoes that are scratched or broken during harvesting, transportation, and storage are easily contaminated by bacteria. When stored under conditions of high temperature and humidity, molds grow and multiply and produce toxins. The toxins that cause sweet potato poisoning include ipomeamarone, ipomeamaronol, ipomeanine, 4-ipomeanol, etc. The toxins are highly heat-resistant and can cause poisoning whether eaten raw or cooked. The toxins are very stable in a neutral environment, but can be destroyed by acids and alkalis.
Sweet potato black spot was first discovered in the United States in 1890, introduced to Japan in 1919, and introduced to Gai County, Liaoning Province, my country from Kagoshima, Japan in 1937. Subsequently, the disease gradually spread from north to south and has now become one of the common and serious hazards in my country's sweet potato producing areas. According to statistics, the annual production loss caused by this disease in my country is 5%~10%, and the loss caused by serious damage is 20%~50%, or even higher. In addition, when the disease is eaten by livestock, it causes poisoning, and in severe cases, death. When the diseased potatoes are used as fermentation raw materials, they can poison yeast and saccharifying enzyme bacteria, delay the fermentation process, and reduce alcohol production and quality. The disease can be spread over long distances with the transportation of seedlings and seed potatoes. In order to prevent the expansion of the epidemic area, my country has listed the disease as a domestic quarantine object. (II) Symptoms of poisoning The incubation period of moldy sweet potato poisoning is relatively long, and it usually occurs 24 hours after eating. The incubation period is 1~24 hours. The main manifestations are: dizziness, headache, nausea, vomiting, abdominal pain, and diarrhea in mild cases; in severe cases, in addition to the above symptoms, there will be multiple vomiting and diarrhea, fever, muscle tremors, palpitations, dyspnea, blurred vision, dilated pupils, and even shock, coma, paralysis, and even death. In the early stage, the breathing is fast and shallow, and the frequency decreases but deepens later, and dyspnea occurs. The residual gas in the alveoli increases relatively, the alveoli rupture, and the gas enters the pulmonary interstitium, causing pulmonary interstitial emphysema, and causing lung enlargement, widening of the pulmonary interstitium, and filling of the interstitial lobule and the submucosal part of the lung with gas; there are punctate hemorrhages in the coronary sulcus of the heart; bleeding and necrosis of the gastrointestinal mucosa; enlarged liver and punctate hemorrhages in the liver parenchyma.
There is no special treatment for moldy sweet potato poisoning. The treatment principle is to take emergency measures and symptomatic treatment. The emergency measures are vomiting, gastric lavage, and catharsis to reduce the absorption of toxins. Symptomatic treatment is mainly rehydration, correction of gastroenteritis symptoms and neurological symptoms.
(III) Prevention According to the conditions and transmission routes of sweet potato black spot disease, comprehensive prevention and control measures should be taken, with the elimination of the initial infection source as the premise, the selection of disease-free seed potatoes as the basis, the cultivation of disease-free seedlings as the center, and safe storage as the guarantee, and agricultural prevention and control as the main and chemical prevention and control as the auxiliary. The main thing is to prevent sweet potatoes from being contaminated by mold, prevent the potato body from being injured during harvesting, transportation and storage, and maintain a low temperature and humidity during storage. Be able to identify and avoid eating moldy sweet potatoes. The surface of moldy sweet potatoes has round or irregular dark brown spots, the flesh becomes hard, and has a bitter and medicinal taste. Moldy sweet potatoes can cause poisoning whether eaten raw, cooked or made into dried potatoes. For sweet potatoes that are only slightly moldy, the skin and flesh of the moldy part can be removed, soaked and cooked, and then eaten in small quantities.
4. Ergot poisoning
As early as the middle of the 17th century, people realized that eating grains containing ergot (Frgot) could cause poisoning, namely ergolism. Ergot is a black and slightly curved sclerotium (Sclerotium) formed by the invasion of ergot fungus (Clauicepsprupurea) into the husk. The sclerotium is the dormant body of ergot fungus. If there is humid and warm weather during the harvest season, grains are easily infected by ergot fungus.
(I) Etiology
Food poisoning caused by eating grains containing ergot is called epi-ergot poisoning. Ergot is the dormant body of ergot fungus (Clavicepspurpurea). Ergot belongs to the phylum Ascomycota, class Pyromycetes, order Sphaerocephala, family Claviceps, and genus Claviceps. It is a fungus that causes diseases in Gramineae plants such as cereals. Its spores enter the ovary of the stamens, where they continue to reproduce and develop, forming hyphae. After 2 to 3 weeks, keratinization appears on the ears of wheat to form epidermis. Ergot contains ergot alkaloids. Ergot alkaloids are a nitrogen-containing substance that can cause blood vessels to constrict. Currently known ergometrine, ergobasinine, ergolamine, ergotaminine, ergocristine, ergocrisinine, etc. The degree of ergot's toxicity depends on the content of alkaloids in ergot, which is usually 0.015% to 0.017%, and the highest is 0.22%. The toxicity of ergot is very stable. It is not affected by storage for several years, and its toxicity is not destroyed during baking. Stowell first isolated ergotamine in 1918. Ergotamine is related to the characteristic gangrene symptoms caused by ergot poisoning. Large doses of ergotamine cause severe vasoconstriction and can lead to dry gangrene of the limbs.
Ergot fungi are easy to grow in humid, rainy and warm seasons. For example, if it rains continuously before and after wheat harvest, it will become moldy after harvesting, or if wheat is stored in a humid, warm and unventilated warehouse, it is easy for ergot fungi to grow and develop. Fresh ergot fungi are the most toxic and are not easily destroyed by high temperatures. Their toxicity can be maintained for 4 years. The grains that are susceptible to ergot infection are mainly rye, followed by wheat, barley, millet, corn, rice, oats, sorghum, etc. When a large amount of ergot is mixed in the grains and is not removed during processing, it can cause poisoning after consumption. Because the degree of grain contamination varies from region to region, ergot poisoning often occurs in a few villages or families.