ENTEROTOXEMIA (PULPY KIDNEY OR OVEREATING DISEASE) IN GOAT & SHEEP

Enterotoxemia caused by Clostridium perfringens type D affects sheep and goats of all ages (from one week to several years of age). There are two common times when this disease most often occurs. The first occurs when young animals nurse an abundant milk supply while grazing on improved pastures or being fed high quality hays and/or concentrates (grains). The second corresponds with thefinishing or feedlot period where an animal is fed a high grain diet. Enterotoxemia is one of the most common causes of death in feeding lambs. In “explosive” outbreaks, losses may range from 10 to 40%. In unvaccinated feeder lambs, one can expect a minimum of 1% of the lambs to die from this disease, with an average death loss of between 2-2.5%.

Enterotoxemia is one of the very important diseases and in some areas it is the most prevalent disease of goats. Despite the fact that it is also called ”Overeating Disease” it is not caused by overeating. Actually, the cause (etiology) of the disease is the toxin (poison) produced by the bacterium Clostridium perfringens type C or type D.

Most of our knowledge about the disease comes from sheep. There are some important differences in purpose and manner of raising (management systems) that exist between sheep and goats that should be kept in mind when one reads and applies sheep information on goats. First, the disease usually occurs in single (rarely in twins) lambs of a high milk producing ewe; all the milk is consumed by that lamb. In contrast, most goat births are twins, triplets or quadruplets and in the best caprine management systems, the kids are removed from their mother soon after birth. Thus, the type of birth is no factor in goats. Second, dairy kids are seldom fed large amounts of high energy diets for meat production and therefore do not have the same opportunity (unless accidentally or by mismanagement) of exposure to grain. Finally, goats are natural browsers (eat from bushes and trees with their head reaching out or up); they do graze but do not consume as much lush feed (usually in a pasture) as rapidly as sheep. Summarizing, the well understood predisposing factors in the sheep disease are not strictly applicable to goats.

The disease is caused by the bacterium Clostridium perfringens type D. It is normally present in low numbers in the bowel of most animals. Under circumstances brought about by heavy volume and high quality feeding, the organism grows rapidly and produces a powerful poison (toxin). This toxin is absorbed through the intestinal wall and causes death in a few hours. In many instances, deaths occur so quickly that owners do not observe sick animals. Any situation that causes a decrease in the movement of material out of the intestines will give the organism time to overgrow and produce lethal toxin levels in the animal.

The following list identifies common conditions that can cause an animal to develop fatal enterotoxemia:

A sudden change of feed

Feeding a diet too high inenergy (excessive carbohydrates, starches, and sugars)

Irregular feeding

Increasing the amount of concentrate too rapidly

A heavy parasite burden in the animal

A situation where large amounts of undigested or partially digested food in the gut devitalizes the intestinal tract and allows greater toxin absorption

A lack of natural or acquiredimmunity

Deaths from enterotoxemia usually occur suddenly. In some cases, the animal may be sick for several hours or even a day or longer before it dies. Affected lambs and kids may experience neurological signs such as trembling, stiff limbs, and convulsive movements. Sometimes the animal becomes comatose, with death taking place quietly. Diarrhea may be present in some cases, particularly in goats.

While the symptoms described above are suggestive of enterotoxemia, they also may be seen in other diseases that cause sudden death, such as acuteacidosis or grain founder, polioencephalomalacia, listeriosis, acute pasteurellosis, tetanus, and blackleg. Therefore, it is important that the cause of such deaths be promptly and correctly diagnosed.

A diagnosis of enterotoxemia is suggested when the sudden death of concentrate-fed animals that have not been vaccinated for Clostridium perfringens type D has occurred.Necropsy findings can also help lead to a diagnosis. If a necropsy or post-mortem is done immediately or shortly after death, few changes may be observed, particularly if the animal died suddenly. When changes are observed, they usually include congestion and fluid in the lungs, and an increase in fluid in the heart sac (pericardial sac) with clots of gelatinous material (fibrin). Smallhemorrhages and blood splashes will be seen under the clear membrane which lines the outer and inner muscle walls of the heart. The tissues of the kidney can be filled with fluid and deteriorate rapidly. This is where the term “pulpy kidney” arises. The carcass decomposes rapidly and is distended with gas. Urine from an animal that died from enterotoxemia is usually positive for high levels of glucose (sugar) when tested. This disease can be confirmed by laboratory tests performed on the dead animal. It is wise to seek the counsel of a veterinarian to help in establishing a correct diagnosis and to outline control measures.

For some animals already affected, oral antibiotics (sulfas) can be beneficial. Because recognizing sick animals is difficult and treatment is often unrewarding, emphasis should be placed on prevention.

To prevent this disease, efforts should be focused on management and vaccination:

Make the adjustment from range or pasture to feedlot conditions gradual. Place lambs/kids on either alfalfa hay or prairie hay first, and then gradually accustom them to concentrates.

Check animals for parasites and de-worm prior to vaccination. A burden of parasites interferes with the production of protective antibodies from the vaccines.

Have plenty of feed for the lambs/kids at all times. This prevents them from overeating at one given time.

All lambs/kids from mothers that have been vaccinated previously, should be vaccinated at 6-8 weeks of age with a Clostridium perfringenstype D toxoid vaccine; repeat this vaccine in 3-4 weeks. Lambs/kids from mothers that have not been vaccinated, should receive their first vaccine at 1-3 weeks of age; repeat this vaccine twice, every 3-4 weeks.

All adult animals should have an annual booster with a Clostridium perfringens type D toxoid vaccine 4-6 weeks prior to the lambing/kidding season. In pregnant animals, this will help boost antibodies shed in the colostrum.

All adult goats should be vaccinated a minimum of twicea year. They require more frequent vaccination because they do not respond as well as sheep do to the vaccine.

Vaccinate lambs soon after their arrival in the feedlot. Allow at least 10-14 days after vaccination for immunity to develop. Under certain conditions, re-vaccination (booster dose) is required 3-4 weeks later.