Gastrointestinal ulcer mainly refers to the keratinization, erosion and necrosis of the gastroesophageal mucosa, or autodigestion, the formation of circular ulcers, and even gastric perforation. Symptoms include anorexia, abdominal discomfort, abnormal bowel movements leading to constipation or diarrhea, and some cases of gastric bleeding and black feces. At the beginning of the disease, the stomach showed a slight bleeding, only indigestion, and people were often not aware of it. When the stomach is perforated, it can quickly die when accompanied by acute chronic peritonitis. Frequently distributed, individual pigs were killed in a group of pigs. The disease can occur at any age, but it is more common in pigs that grow faster than 50kg and in sows that are housed within monomer restriction columns. There is an onset throughout the year, but it is more common in hot summer and autumn seasons.
1. Causes
1.1 Feed Factors (1) Hard and hard to digest. (2) There is insufficient fiber in the feed. (3) The feed is crushed too finely. (4) Long-term feeding of feeds with high energy, especially high corn content. (5) Improper mixing of large amounts of irritating mineral mixtures in cereal diets. (6) The lack of vitamin E, vitamin B1, and selenium in feed. (7) There is too much unsaturated fatty acid in the feed. (8) Feed mildew.
1.2 Environmental stress and feeding and management factors (1) Noise, fear, sultry, pain, pregnancy, childbirth, too much to disturb the pig (if frequent transfer group, weighing). (2) The pig house is narrow and the range of activity is limited for a long time. (3) Poor ventilation and poor sanitation. (4) feeding is not regular, when full of hunger, suddenly change the feed.
1.3 Disease factors (1) are often secondary to chronic erysipelas, roundworm infections, copper poisoning, and fungal infections (especially Candida albicans infections). (2) Pigs commonly found in vitamin E deficiency and liver malnutrition. (3) physical weakness, excessive stomach acid.
2. Pathogenesis
The pathogenesis is more complicated. Due to the influence of poor digestive factors, the gastric wall tissue is stimulated, causing gradual histological changes in mucosal hyperemia, defects, and erosions: the gastric mucosal tissue that has been damaged and eroded, releases histamine, expands the capillary wall of the stomach, and promotes gastrin secretion The formation of a large number of acetylcholine and the production of acetylcholine stimulated the secretion of gastric juice and increased the acidity. Contrary to this, the protective mucus was extremely reduced or lacking. In the acidic gastric juice, pepsin acts as a digestive tissue. This leads to the formation and production of localized ulcers.
3, symptoms
3.1 Recessive and healthy pigs no different, no obvious symptoms, growth rate and feed conversion rate is almost unaffected. Found after slaughter.
3.2 Chronic appetite is reduced or not eaten. The sick pig's body surface and visible mucous membrane are obviously pale. Hemorrhagic or vomiting bloody, arched or prone, hesitate because of weakness and progressive thin. Constipation at the beginning, after the coal tar-like excrement, occult blood test positive. The condition sometimes deteriorates, sometimes relieves, causing digestive disorders and abdominal pain. A few cases have chronic peritonitis symptoms. Duration of 7 to 30 days.
3.3 acute acute exacerbation of this disease, due to ulcer bleeding, the sick pigs can suddenly die; also some sick pigs in a strong exercise, mutual bite, before and after delivery into a sudden vomiting blood, coal tar-like bloody stool, body temperature, shortness of breath, abdominal pain Anxiety, body surface and mucous membranes pale, physical weakness, and death due to prostration. When a sick pig causes peritonitis due to gastric perforation, it usually dies within 1-2 days after the onset of symptoms.
4, necropsy lesions
Ulcers mainly in the esophagus of the stomach, but also in the stomach and pyloric area of ​​varying degrees of congestion, bleeding and size of the amount of different forms often have erosive spots and well-defined, round edges of neat circular ulcers. There are blood clots in the stomach and fresh blood that has not coagulated, there is cellulose exudate, fresh blood is often found in the intestines. In disease-free pigs, early lesions had hyperkeratosis and epithelial shedding without true ulcer formation. The stomach of a sick pig often has more fluid contents than the normal stomach; there is also bile reflux from the duodenum to the stomach to yellowen the gastric mucosa. Hemorrhagic diseased pigs caused by chronic gastric ulcers. Splenomegaly due to extramedullary hematopoiesis. Some ulcer healing pigs can leave scars. If the stomach has been worn, diffuse or localized peritonitis can be seen. It is also common for decidual inflammation, and the contents of the abdominal cavity enter the chest cavity to show iliac lesions.
5, diagnosis
The prenatal diagnosis of the disease is difficult, especially in early diagnosis. Symptoms that are of diagnostic significance are: faeces become dark, and skin and mucous membranes are markedly pale. The only evidence is to take suspected feces for occult blood tests. It should be distinguished from hemorrhagic enteritis syndrome and acute swine dysentery.
6, treatment
The principle of treatment is to eliminate the etiological factors, neutralize gastric acid, and protect the gastric mucosa. Pigs with milder symptoms should be kept quiet and relieve stress. Injectable sedatives, such as: chlorpromazine hydrochloride, 1 to 3 mg per kilogram of body weight. Neutralizes acid in stomach and prevents gastric mucosal damage. Antioxidant such as magnesium aluminum silicate or magnesium oxide can be used to reduce the acidity of stomach contents. To protect ulcers, prevent bleeding, and promote healing, it is advisable to take nitric acid bismuth 5 to 10 g three times a day before feeding. Can also oral tannic acid protein, each 2 ~ 5g, 2 or 3 times a day, once every 5 to 7 days. In addition, in order to maintain the normal emptying of the restaurant, sodium polyacrylate can be used for 5~20g/day in Beverage Service, or 0.5%~5% of the feed can be mixed in the feed for 5~7 days. If the pig is extremely anemic, confirmed as gastric perforation or diffuse peritonitis, it loses its therapeutic value and should be eliminated as soon as possible.
7, prevention
Take corresponding measures for the cause of morbidity: (1) Avoid the feed being crushed too fine, and the grain size of the feed should be above 500 μm. (2) Reduce the amount of corn in the diet and feed powder instead of pellet feed. (3) The addition of grass powder or oat hull to the feed makes the amount of crude fiber in the diet reach 7%. (4) Ensure the content of vitamin E, vitamin B1 and selenium in the feed. (5) When copper is used as a growth promoter, 11010-6 zinc carbonate is added to the feed as a copper-induced ulcer additive. (6) Polyacrylic acid sodium mixed with a concentration of 0.1% to 0.2% to change the physical state of the feed so that it can stay normal in the stomach. (7) Avoid psychological stress, reduce frequent shifts, transport, drive, and prevent pigs from biting each other. (8) Keep the pig houses cool in winter and cool in summer, strengthen ventilation, and keep the density appropriately. Pighouses should have enough space to allow pigs to freely move.
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