What are the characteristics of sheep struck (enterotoxemia) and how is it prevented and treated?
Sheep struck is a toxemia caused by Clostridium welchii type C, clinically characterized by acute death, peritonitis and ulcerative enteritis.
I. Pathogen
Clostridium welchii, also known as "Bacillus aerogenes capsulatus," belongs taxonomically to the genus Clostridium. This bacterium is Gram-positive, can form a capsule in the animal body, and its spores are located in the center of the bacterial cell. This bacterium can produce multiple exotoxins such as alpha, beta, epsilon and iota; based on toxin-antitoxin neutralization tests, Clostridium welchii can be divided into 5 toxin types: a, b, C, D and E. Sheep struck is caused by Clostridium welchii type C.
II. Epidemiological characteristics
This disease occurs in adult sheep, with sheep aged 1 to 2 years being more frequently affected. It is often prevalent in low-lying, damp areas and in winter and spring, and is mainly transmitted through the digestive tract. It occurs as an endemic disease.
III. Clinical symptoms
Clostridium welchii type C enters the digestive tract of sheep with contaminated feed or drinking water, multiplies in the small intestine, especially the duodenum and jejunum, and mainly produces beta toxin, causing the sheep to develop the disease. The course of the disease is short, and sudden death often occurs before symptoms are seen. Sometimes affected sheep are found lagging behind the flock or lying down, showing restlessness, weakness or spasms, and die within a few hours.
IV. Pathological changes
On necropsy, the mucosa of the duodenum and jejunum shows severe congestion and erosion, and ulcers of varying sizes may be seen in some segments. There is often fluid accumulation in the body cavities, which readily forms fibrinous floccules when exposed to air. There are petechial hemorrhages on the serosa. Eight hours after death, blood-stained fluid accumulates between the skeletal muscles, with muscular hemorrhage and gas clefts; these changes are very similar to the lesions of blackleg.
V. Laboratory diagnosis
Collect body cavity exudate, spleen and other diseased materials for bacteriological examination; take small intestine contents for toxin testing to determine the bacterial type.
VI. Differential diagnosis
This disease should be differentiated from other diseases of the sheep bradsot group, anthrax, pasteurellosis and similar diseases. Differentiation is mainly carried out through etiological examination and toxin testing.
VII. Prevention and control measures
1 In areas where the disease commonly occurs, regularly vaccinate each year with the "sheep bradsot, enterotoxemia and struck triple vaccine" or the "sheep bradsot, enterotoxemia, struck, lamb dysentery and black disease pentavalent vaccine." Regardless of size, all sheep are injected subcutaneously or intramuscularly with 5 ml; immunity develops 2 weeks after vaccination, and the protective period lasts up to half a year.
2 Strengthen feeding management and prevent attacks by severe cold. On frosty days, do not turn the sheep out to pasture too early in the morning, and avoid feeding on frost-covered forage.
3 When the disease occurs, isolate affected sheep promptly and move the flock to high, dry pasture or grassland, which can reduce or stop the occurrence of the disease.
4 The course of this disease is short, and treatment is often too late. For cases with a somewhat longer course, penicillin can be injected intramuscularly at 800,000 to 1,000,000 units per dose, twice a day for 2 to 3 consecutive days; sulfadiazine can be given orally at 5.6 grams per dose for 3 to 4 consecutive doses; 10% to 20% lime milk can also be given orally at 500 to 1000 ml for 1 to 2 consecutive doses. If necessary, 10 ml of 10% caffeine sodium benzoate can be added to 500 to 1000 ml of 5% to 10% glucose solution for intravenous drip infusion.