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What are the symptoms of organophosphate pesticide poisoning?

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What are the symptoms of organophosphate pesticide poisoning? Please explain. Organophosphorus compounds are a type of insecticide widely used in agriculture and healthcare, and most have varying degrees of toxicity. They can enter the bodies of fur-bearing economic animals through the digestive tract, respiratory tract, skin, and mucous membranes, causing poisoning. Organophosphate pesticides that can cause poisoning include 1605, 1059, trichlorfon, dichlorvos, dimethoate, and more than 10 other types. Feeding grain, wild grass, or vegetables after organophosphate pesticides have been spread on them, or feed contaminated by them; spreading organophosphate pesticides near fur-bearing economic animal farms, with liquid splashing and being inhaled by the animals; using utensils previously used to prepare organophosphate pesticides to mix feed, or drinking water contaminated by them, can all cause organophosphate poisoning in fur-bearing economic animals. In addition, feeding the meat carcasses and by-products of livestock, poultry, and other animals that died from organophosphate pesticide poisoning, or using organophosphate pesticides to treat internal and external parasitic diseases in animals with improper dosage or excessively high concentration, can also cause poisoning. According to the amount of poison, the course of poisoning, and the manifestations, it can be divided into acute poisoning and chronic poisoning. In acute poisoning, the sick animal has difficulty breathing, salivates, foams at the mouth, sheds tears, snorts, and the conjunctiva and oral mucosa become cyanotic: the pupils constrict; diarrhea occurs with thin feces containing blood, with frequent defecation and urination; the skin feels cool; the animal is highly sensitive to external stimuli, in a state of excitement, with hearing loss and inhibited visual responses; the hind limbs are paralyzed, unable to stand, and walking is difficult. Muscle groups throughout the body show spasmodic contractions of varying degrees, skeletal muscles tremble, the whole body becomes weak, and death usually results from paralysis of the respiratory center or heart failure. In chronic poisoning, the sick animal shows reduced eating or even refusal to eat, gradually becomes emaciated, has movement disorders and uncoordinated movements: long-term diarrhea with shed intestinal mucosa or blood in the feces, increased respiratory secretions, leading to difficulty breathing, and finally a drop in body temperature and death. Necropsy shows cyanosis of the visible mucous membranes, a large amount of mucous secretions in the oral cavity, pulmonary congestion and edema, and bronchi filled with foamy mucus. Parenchymal organs are congested and hemorrhagic, meninges are congested, and gastrointestinal mucosa is shed with hemorrhagic spots or hemorrhagic patches. Based on a history of contact with organophosphate pesticides and typical symptoms such as excessive salivation, constricted pupils, muscle tremors, and difficulty breathing, a preliminary diagnosis can be made. It is best to collect pathological materials for toxicological identification to establish a final diagnosis. To prevent this disease, organophosphate pesticides must be properly stored and used. When deworming animals, the dosage and concentration must be correctly mastered, care must be strengthened, and licking or biting each other must be strictly prevented. When using trichlorfon to treat internal parasites in animals, it must never be given together with alkaline drugs. When crops sprayed with organophosphate pesticides are used as feed, they should be thoroughly washed clean and first subjected to a safety test before they can be fed to animals. It is forbidden to feed fur-bearing economic animals with the meat carcasses and by-products of livestock, poultry, and other animals (rabbits, dead foxes, rats, fish, etc.) that died from organophosphate poisoning. For acute poisoning, rescue should be carried out quickly. For poisoning caused by oral ingestion of organophosphate pesticides, immediately use 2-3% sodium bicarbonate solution, 1-2% soda water, or 0.1% potassium permanganate solution (potassium permanganate cannot be used for 1605 poisoning) for repeated gastric lavage to remove unabsorbed poison, but if poisoning is caused by oral trichlorfon, alkaline solution must not be used for gastric lavage; instead, use 1:5000 potassium permanganate solution or physiological saline for gastric lavage. For symptomatic treatment, to relieve spasms, barbiturate can be injected subcutaneously (10% sodium isoamylbarbiturate solution), 10 mg per kg body weight for mink, and 30-50 mg per kg body weight for silver-black foxes. It is best to use it once every few days, for several consecutive times. Pralidoxime at 30 mg per kg body weight, diluted with 5% glucose solution and physiological saline, should be injected slowly intravenously, and acts rapidly. However, it must never be combined with alkaline drugs.

What are the symptoms of organophosphate pesticide poisoning? Please explain.


Organophosphorus compounds are a type of insecticide widely used in agriculture and healthcare, and most have varying degrees of toxicity. They can enter the bodies of fur-bearing economic animals through the digestive tract, respiratory tract, skin, and mucous membranes, causing poisoning. Organophosphate pesticides that can cause poisoning include 1605, 1059, trichlorfon, dichlorvos, dimethoate, and more than 10 other types. Feeding grain, wild grass, or vegetables after organophosphate pesticides have been spread on them, or feed contaminated by them; spreading organophosphate pesticides near fur-bearing economic animal farms, with liquid splashing and being inhaled by the animals; using utensils previously used to prepare organophosphate pesticides to mix feed, or drinking water contaminated by them, can all cause organophosphate poisoning in fur-bearing economic animals. In addition, feeding the meat carcasses and by-products of livestock, poultry, and other animals that died from organophosphate pesticide poisoning, or using organophosphate pesticides to treat internal and external parasitic diseases in animals with improper dosage or excessively high concentration, can also cause poisoning. According to the amount of poison, the course of poisoning, and the manifestations, it can be divided into acute poisoning and chronic poisoning. In acute poisoning, the sick animal has difficulty breathing, salivates, foams at the mouth, sheds tears, snorts, and the conjunctiva and oral mucosa become cyanotic: the pupils constrict; diarrhea occurs with thin feces containing blood, with frequent defecation and urination; the skin feels cool; the animal is highly sensitive to external stimuli, in a state of excitement, with hearing loss and inhibited visual responses; the hind limbs are paralyzed, unable to stand, and walking is difficult. Muscle groups throughout the body show spasmodic contractions of varying degrees, skeletal muscles tremble, the whole body becomes weak, and death usually results from paralysis of the respiratory center or heart failure. In chronic poisoning, the sick animal shows reduced eating or even refusal to eat, gradually becomes emaciated, has movement disorders and uncoordinated movements: long-term diarrhea with shed intestinal mucosa or blood in the feces, increased respiratory secretions, leading to difficulty breathing, and finally a drop in body temperature and death. Necropsy shows cyanosis of the visible mucous membranes, a large amount of mucous secretions in the oral cavity, pulmonary congestion and edema, and bronchi filled with foamy mucus. Parenchymal organs are congested and hemorrhagic, meninges are congested, and gastrointestinal mucosa is shed with hemorrhagic spots or hemorrhagic patches. Based on a history of contact with organophosphate pesticides and typical symptoms such as excessive salivation, constricted pupils, muscle tremors, and difficulty breathing, a preliminary diagnosis can be made. It is best to collect pathological materials for toxicological identification to establish a final diagnosis. To prevent this disease, organophosphate pesticides must be properly stored and used. When deworming animals, the dosage and concentration must be correctly mastered, care must be strengthened, and licking or biting each other must be strictly prevented. When using trichlorfon to treat internal parasites in animals, it must never be given together with alkaline drugs. When crops sprayed with organophosphate pesticides are used as feed, they should be thoroughly washed clean and first subjected to a safety test before they can be fed to animals. It is forbidden to feed fur-bearing economic animals with the meat carcasses and by-products of livestock, poultry, and other animals (rabbits, dead foxes, rats, fish, etc.) that died from organophosphate poisoning. For acute poisoning, rescue should be carried out quickly. For poisoning caused by oral ingestion of organophosphate pesticides, immediately use 2-3% sodium bicarbonate solution, 1-2% soda water, or 0.1% potassium permanganate solution (potassium permanganate cannot be used for 1605 poisoning) for repeated gastric lavage to remove unabsorbed poison, but if poisoning is caused by oral trichlorfon, alkaline solution must not be used for gastric lavage; instead, use 1:5000 potassium permanganate solution or physiological saline for gastric lavage. For symptomatic treatment, to relieve spasms, barbiturate can be injected subcutaneously (10% sodium isoamylbarbiturate solution), 10 mg per kg body weight for mink, and 30-50 mg per kg body weight for silver-black foxes. It is best to use it once every few days, for several consecutive times. Pralidoxime at 30 mg per kg body weight, diluted with 5% glucose solution and physiological saline, should be injected slowly intravenously, and acts rapidly. However, it must never be combined with alkaline drugs.
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