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I. Milder toxin poisoning
Food or feed contaminated by mold toxin due to long-term eating (lasting more than 20 to 30 days).
more chronic pass, anorexia, loss, spirit and discipline, unwillingness, weight loss, stool is soft or intermittent diarrhea, gastrointestinal function is serious Disorder, jaundice (fat degeneration, biliary hyperplasia), weakness, ascites, failure of the liver, fatty degeneration.
Feeding a mildew feed in breeding period can lead to a public, female fox is not estrus or decrease in breeding, and the sperm activity is lowered, leading to the empty, infertility; feeding a mildew in pregnancy, causing pregnancy Animal recessive abortion and small production.
There is no effectary antidote, mainly in prevention, avoiding food of a mildew. The symptomatic treatment is: eating low-fat diet, using anti-fat liver drugs, add choline in feed, add 0.05% to feed, or 20 ~ 40 mg / kg weight, orally, add microecological preparations in feed Increase animal resistance.
II, botulinum poisoning
The botulinum poisoning is also known as the botulinum clostridosis, which is a human and animal suffering from a human body that absorbs a botulinum clostridosis. It is characterized by sporty neurons and paralysis and stoakal paralysis.
(1) Pathogen and epidemiology
Bothalastubility is a special anaerobic Gram-positive bacterium. The bacteria can produce poisonous toxins during animal bodies, meat, feed, and canned food. The toxins can withstand gastric acid, gastric protease and trypsin, so it is not destroyed in the digestive tract. The toxins can be destroyed at 80 ° C for 30 minutes or 100 ° C for 5 to 20 minutes. In the solid food, it is necessary to boil for 2 hours, and the bacteria discovery has a, B, C, E Ti-type, and various toxins. Both of which are generated by the same type, usually in non-vertebrates in the adjacent non-vertebrae, which is mainly non-vertebrates, which are most likely to cause a variety of mammals.
The sputum of the botulinums is widely distributed in nature, soil, water, air, animal intestines, feces, corruption bodies, corruption feed and various plants, therefore infected with animals. From nature. This disease is mainly used to eat corruption, deteriorated fish and corruptionThe body causes a pathogenesis.
(2) The severity of the clinical signs of the botulinum poisoning is different from the amount of toxin and the sensibility of the individual. The first appearance is from the posterior limb to the forelimbs, thereby causing the limbs to be paralyzed, but the tail is still swinging, the reflection is weakened, the muscle tension is reduced, the pupil is large, the reaction is slow, and the tension of the mandibular muscle is reduced, thereby causing the mandible. Difficult to swallow, saliva flow, noise, visual obstacles, eyelid reflection, and low. Can cause conjunctivitis and ulcerative keratitis. Most seriously poisoned animals, abdominal muscles and diaphragm tensile tensile tension, but the breathing is difficult, the heart rate is fast, the arrhythmia, constipation and urinary retention. After an animal ingestion of contaminated food, the incubation period is from several hours to 6 days. The sooner of poisoning symptoms, the more the condition is, and it will eventually die due to poor breathing.
(3) Pathological changes
The body is thin, and there is often a chewing food in the mouth, stink, tongue outlet cavity, the stomach with bone tablets, earth block or stone tablets. The throat and the episode of the mucosa have gray-yellow coating, and there is bleeding on the mucosa. The gastric mucosa has a trucosynthymosis and a small bleeding, and the endometrium has a small bleeding, and the pulmonary congestion edema changes.
According to clinical symptoms and fed corruption, preliminary diagnosis is performed, and the diagnosis must be examined to inspect the presence of non-toxins in the feed and bodies.
After poisoning, the disease is short, the mortality rate is high, should be actively rescued.
1. Anti-toxin treatment
The use of botulinum antitoxin in the case of the first effect, the toxin type of the botulinumisuria poisoning of the fur animal is C-type, so it can be used in intravenous or muscle injection with C-type antitoxins. Manual. Anti-toxin can be stored 40 days in the blood, so it is not necessary to use it again.
2. The symptomatic treatment
discharges gastrointestinal content, reducing the absorption of toxins, can be washed with 0.01% potassium permanganate water or deep enema, or jade laxative. Animals with fewer than ingestion of toxicity, immediately replace the feed, and intramuscularly, intramuscin to reduce the number of closses of the intestine. Animals that have weakened heart should be strong and dehydrated animal response.
(6) Preventive measures
botox is heated 80 ° C, 30 minutes or 100 ° C, and it can be eliminated for 10 minutes. Do not let the animals close to the humetine, feeding the animals should be boiled to prevent the disease. In addition, Vinimicin antibiotics feed additives are added to feed, and the dose is 20 to 30 ppm, which can effectively inhibit the reproduction of Clostridia.
Three, Huangquisin Poisoning
Huangquisin poisoning is an acute or chronic poisoning caused by animals to eat after pollution of xylushic or parasite and produce toxins.
There are more than 20 kinds of yellowlaxins that have been found, and B1, B2, G1, and G2 is stronger, under ultraviolet light, B1, B2 blue purple fluorescence, G1, G2 yellow-green fluorescence has carcinogenic effects.
The maximum damage to the liver is the strongest in B1, and the mixing kinetic energy oxidase system in the hepatocyte endogenic network is converted to the catalysis of the mixed kinetic energy oxidase system in the hepatocyte in the body. Toxin B1, combined with DNA and RNA and mutation, and normal hepatocytes transformed into cancer cells. The most easily contaminated feed is a plant seed and by-product such as peanut, corn, soybeans, cottonseed. Any food, forage feed, etc., which pollutes Huang Sika and parasitic cocci, may have a yellow belaxin, and there is no foundation of fungi, fungus and spores, and agricultural and sideline products can also be found. If the animals eat these feed containing yellowed toxin, they will cause disease.
Submerged poisoning is chronic through, and the late stage of disease exhibits clinical symptoms, such as spiritual depth, no food, gastrointestinal dysfunction, intermittent diarrhea, body temperature Normal, mucous membrane pale or yellow-stained, and then died soon after you were filling.
(3) Pathological changes
Deadwood’s belly is fresh and red, liver swollen yellow, hard, kidney, pale, gastrointestinal mucosa bleeding.
According to the feed and food and pathological examination of the froquochromatin, the disease is preliminary, and the feed sample is required to be tested.
No detoxification agent, mainly in prevention, avoid feeding of moldy deteriorationAnd food, allograms of glucose, vitamin C, vitamin B12 mixture, can alleviate poisonous animal symptoms.
Four, organophosphorus and urethane poisoning
organophosphorus include tri-phosphorus, phosphorus, fly phosphorus, dichlorvos, diazine, music, enemy kill phosphorus, chloride phosphorus, Marahi phosphorus, a sixty-five, phosphate ammonium, flyfly phosphorus, dude phosphorus and enemy passengers. Carbamates include West Vibes, furan, mixer, killing, destroy pests and disabled.
The above drug is acetyl cholecymide anase active inhibitor, which can cause poisoning of crop pesticide or animal systemic in vitro parasitic drugs, animal contact or emblem.
are different due to the intake of the drug and the individual sensitivity. The incidence is that there is soon that the feeding of toxicity is soon, and the death is very fast. Viscinogenosis, nicotine poisoning and central nervous system poisonous type three categories. Its main symptom is a mortar, mouth spitruff, muscle spontaneous contraction, tremor, and tribute. Severe people will have convulsions, vomiting, diarrhea, pupil shrinking, tears, increased respiratory secretions, shrinking bronchogenesis, difficulty breathing, hair, coma death. The poisoning is lighter, the spirit is depressed, it is lying in the cage, the head and cavity, do not eat, if it does not take 1 to 2 days to die.
(3) Pathological changes
The mine of acute poisoning death, the lungs have bleeding, the spleen has bleeding spots, the gastrointestinal mucosa is severely bleeding, and the hepatic bleeding is black.
1. The intravenous sulfate, the dose is 0.1 mg / kg body weight, and 1 sub-skin injection is made in the same dose. In order to control the extensive mitizen activity, it is repeated once every 1 to 2 hours. If the animals have a hair, you can’t use atropine before the mapping correction.
2. Intravenous injection of phosphorus, dose of 20 mg / kg body weight, the injection duration must be more than 12 hours. If necessary, it can be repeated for 1 time after 12 hours, and the carbamate poisoning is disabled.
If the body surface contacts poisoning, it is possible to brush the hair with soapy water. If you swallow in poison poisoning, taking salt diarrhea after washing the stomach. For severe cases, severe hypoxia and ventilator can be incomplete, and the tracheal intubation and artificial breathing are required. Exciting or unrestThe convulsions can use sedatives, such as Babhta drugs that can enhance organic phosphorus toxicity and convulsions, by infusion, correcting water, electrolyte metabolism and acid-base balance disorders by infusion, correcting water, electrolyte metabolism It can also be done to feed the support therapy.
Five, phosphate poisoning
Phosphatedride is a kind of kinemate, due to a mouse, poisoning bait or swallowing mouse, poisoning dose 20 ~ 40 mg / kg body weight.
First is an appetite risk, then vomiting (vomit phosphorus in dark), accompanied by diarrhea, abdominal pain, feces mixed with blood, in the dark Also phosphorus, exhalation, and vomit emit acetylene odor or garlic odor, animal irritability, breathing extremely difficult and pulmonary edema. The illness of the illness is excessively excited, and the heterogeneous seizures may be in a coma.
no effects treatment. Can be affixed with 0.2% to 0.5% sulfate solution, reminded its vomiting, laminated with a 1: 5000 potassium permanganate solution, intravenous 5% glucose saline, but is disabled when pulmonary edema occurs, intravenous glucose aqueous solution 500 ml contains 1 to 5 mg of an isoproporous, observation.
Sixth, acetunpassoxin poisoning
pyrubane pixorin is generally used to murry. Toxic: Separabenzyl xyloxin 5 ~ 50 mg / kg body weight, composite is 1 ~ 5 mg / kg body weight. The name of the mercaulin-killing drug used in my country has served as the sodium of the enemy. The coumarin is high temperature, 100 ° C, 30 minutes is not damaged.
Choosing coumarin kiroster toxic or coumarin poisoning mice can also be poisoned by seeds that are eaten into pixamin. . After the animal is eating a poxylin, it enters the blood circulation through the gastrointestinal agility to reach the blood circulation, and the coagulation time is prolonged, increase the brittleness and permeability of capillaries, and thus poisoning Animal manner has more bleeding and osmaste.
The animals after poisoning are mainly shown in multiple internal bleeding and excessive blood symptoms. External bleeding is mainly in the oral mucosa, the small traumatic bleeding on the tongue and the skin and the injection pinhole. Pregnant animals are not coveredA large amount of red blood is discharged. Non-pregnancy animals are only manifested in internal bleeding, with a more common hematoma on an intracellular membrane and a longitudinal thrust, a large hematoma is formed on a veneer and a longitudinal pleural pleural, a part of the blood seepage chest, and the blood is not solidified or semi-coagulation state in the chest. Pregnant animal is bleeding, forming a large hematoma on the fluffy film around the fetus, and there are several large hematoma, and there is still a lot of unsolved blood in the uterine cavity. Spleen essential hemorrhage, some animal bladder mucosa and serum, intestinal mucosa and enteric membrane submershed. Poisonous animal liver is light yellow, crisp and slightly large.
In the early days of poisoning, normal appetite, the animal spirit is slightly poor, with the increase of bleeding, the animal spirit is depressed, the film is pale, the lying is reluctant, and the pulse is weak. In the later, shock, animal breathing, paralyzed, paralyzed, paralyzed, paralyzed, paralyzed, paralyzed, paralyzed, paralyzed, paralyzed, paralyzed. Animals who have died in acute inner bleeding, they have not seen symptoms before living, often died in the night at night.
Immediately find out the cause, eliminate the drugs that can be eaten in a coumarin toxic or feed and immediately stop bleeding, maintain blood volume and restoring liver function. treatment.
Intravenous vitamin K1 emulsion, injected 3 times a day, 15 to 30 mg each time, continuously for 6 to 7 days, then changed to oral vitamin K1, about 5 days for medication. The effect of using vitamin K1 alone is not ideal, and if the vitamin K1 is used with vitamin K3, it can improve the efficacy.
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