Why do domestic pigs suddenly die mysteriously with a belly swollen like a drum? How is it treated?
For people, there is nothing more feared than falling ill, and likewise what worries farmers most is livestock and poultry getting sick, as this brings huge losses. Today the editor will introduce to you: Why do domestic pigs suddenly die mysteriously with a belly swollen like a drum? How is it treated? Sick pigs often show no signs of onset, the abdominal circumference rapidly distends, there is evidence of abdominal pain, rapid breathing, inability to stand, accompanied by symptoms of elevated body temperature. Some pigs eat normally in the evening when they fall ill, and by morning they are dead with a stiff body, a swollen and raised abdomen, and white foam flowing from the mouth and nose.
This is the most common Clostridium welchii disease of pigs in breeding production. The disease has many alternative names, such as: clostridial enteritis of pigs, infectious necrotic enteritis of pigs, and enterotoxemia of piglets, commonly known as red dysentery of piglets. The disease is an infectious disease caused by Clostridium perfringens, and pigs of all ages and either sex can be affected, and it can occur in all four seasons. The incidence rate is not high, but the mortality rate is extremely high, making it an important disease that seriously harms the pig farming industry.
Many cases of sudden death in healthy pigs are related to this bacterium, with acute onset, short course, no preceding symptoms, and sudden death. Postmortem examination shows obvious abdominal distension, cyanosis of the ear tips, hooves, and nose and lips, and the skin of the dead pig is pale.
If the pig's feed trough and water trough share the same source, and if the pig has leftover feed, it is prone to souring and molding and producing Clostridium perfringens; after the pig eats it, a large amount of harmful gas is produced in the intestinal tract and cannot be discharged in time, causing gastrointestinal bloating, compressing the internal organs and leading to blood circulation disorders, resulting in insufficient blood supply to the brain and death by oxygen deprivation and suffocation. In some cases, overfeeding weakens digestive function, so that a large amount of gas cannot be expelled and also causes bloating.
Differential diagnosis
Constipation. In modern production, sows are often placed in gestation stalls; due to insufficient exercise and less feeding of green fodder, constipation is likely to occur. This leads to bloating and ultimately death. This should be distinguished from this disease.
Colibacillosis. Its symptoms are similar to those of yellow and white dysentery in piglets. However, on necropsy of Clostridium welchii disease, the intestinal tract shows obvious bleeding and the jejunum segment shows obvious gas distension, with bubbles on the serosal layer, lymph node hemorrhage, pinpoint hemorrhages in the kidneys, and severe meningeal hemorrhage.
Clostridium botulinum poisoning. The clinical similarities between the two diseases are sudden onset and acute death. However, abdominal bloating is obvious in Clostridium welchii disease. Clostridium botulinum poisoning is mainly caused by eating rotten feed. The better the body condition and the fuller the pig eats, the deeper the poisoning.
Epidemiological characteristics
Rabbits of all ages and breeds can be infected and develop the disease, with young rabbits aged 1-3 months being more commonly affected, and purebred wool rabbits and rex rabbits being more susceptible. The disease occurs regardless of season. The digestive tract is the main route of infection.
Symptoms
The special symptom of this disease is severe diarrhea. The feces of affected rabbits are initially deformed and softened, then quickly turn into blood-tinged jelly-like, black or brown thin feces, with a foul fishy odor, and the area around the anus, the hind limbs, and the tail are contaminated by the thin feces; the coat is rough and disordered, the spirit is poor, there is refusal to eat, dehydration, no change in body temperature, and finally emaciation and death.
Pathological changes
Necropsy shows shedding of the gastric fundus mucosa, with ulcers of varying sizes. The intestinal mucosa shows diffuse hemorrhage, the small intestine is filled with gas, and the intestinal wall is thin and transparent. The cecum and colon are filled with gas and dark green thin contents, with a putrid odor. The liver becomes brittle, and the spleen is dark brown. The blood vessels on the surface of the heart are engorged and appear tree-branch-like.
The carcass is dehydrated and emaciated, the abdominal cavity has a fishy foul odor, the stomach contains accumulated food and gas, the gastric fundus mucosa is shed, and there are hemorrhages and black ulcers of varying sizes. The intestinal wall shows diffuse congestion or hemorrhage, the small intestine is filled with gas and thin contents, and the intestinal wall is thin and transparent. The mesenteric lymph nodes are congested and edematous, the cecal serosa shows obvious hemorrhage, and the cecum and colon are filled with gas and dark green watery feces, with a fishy foul odor. The epicardial blood vessels are engorged, appearing tree-branch-like. The liver and kidneys are congested, degenerated, and brittle. The bladder often contains tea-colored urine.
Laboratory diagnosis
Smears were made from the jejunum, ileum, cecal contents, intestinal mucosa, heart blood, and liver lesion tissues of dead rabbits, subjected to Gram staining, and examined under the microscope, showing Gram-positive large bacilli with blunt rounded ends, with no spores seen. The intestinal contents were inoculated onto blood agar medium and cultured anaerobically at 37°C for 24h, showing round colonies with double hemolytic rings, 1.5-3mm in diameter, light gray in color. The cultured strain was taken for biochemical reactions; the bacterium decomposes glucose, lactose, maltose, sucrose, and fructose, producing acid and gas, and does not ferment mannitol. Eight healthy adult rabbits were selected, divided into 4 groups, and inoculated intraperitoneally with 24h broth culture containing 550 million bacteria per milliliter at 3 different doses of 0.3ml, 0.6ml, and 1ml, while the control group was injected intraperitoneally with 1ml of normal saline. After the pure culture was inoculated into the rabbits, all test groups showed reduced appetite or no eating, depressed spirit, and thin feces, with severe cases passing watery feces. The rabbits in the test groups all died within 16h after challenge, while the control group remained normal. The clinical symptoms after inoculation were mainly characterized by diarrhea, the same as the clinical symptoms of naturally affected rabbits, and the pathological changes of the rabbits killed after inoculation were consistent with those of natural cases. Smears of lesion materials, examined under the microscope after Gram staining, showed Gram-positive large bacilli with blunt rounded ends.
Prevention and treatment
Proper feeding can reduce the occurrence of this disease; using a diet with lower energy and higher fiber can significantly reduce diarrhea mortality. Once a sick rabbit or a suspected sick rabbit is found, it should be isolated or culled immediately. For prevention, Clostridium welchii aluminum hydroxide inactivated vaccine can be used, with each rabbit injected subcutaneously with 2 milliliters, immunity begins to develop after 7 days, and the immunity period is 4~6 months.
For the treatment of this disease, oral administration of oxytetracycline and tetracycline both have a certain effect. In addition, treatment of this disease with hyperimmune serum also has a relatively good effect. The method is, after finding that a sick rabbit has diarrhea, depending on the size of the sick rabbit, inject each rabbit subcutaneously with 5~10 milliliters of hyperimmune serum, once a day, and recovery can be achieved after 2~3 consecutive days.