Enterotoxemia.docx

**Enterotoxaemia** **Enterotoxaemia** also known as overeating or pulpy kidney disease is a highly significant and costly disease problem for the sheep industry. Proper preventive practices are strongly recommended to sheep producers in order to avoid death loss from this disease. It is a condition...

**Enterotoxaemia** **Enterotoxaemia** also known as overeating or pulpy kidney disease is a highly significant and costly disease problem for the sheep industry. Proper preventive practices are strongly recommended to sheep producers in order to avoid death loss from this disease. It is a condition caused by the absorption of a large amount of toxins from the intestines. Clostridium perfringens types C & D are bacteria normally found in the soil and as part of the normal microflora in the gastrointestinal tract of a healthy sheep and goats. Under certain conditions, these bacteria can rapidly reproduce in the animals, producing large quantities of toxins. The toxins cause enterocolitis (inflammation of the intestine), increase the permeability of the blood vessels and become absorbed in the blood. They circulate in the bloodstream, promoting swelling in the lungs and kidneys, giving the condition the name pulpy kidney disease. Young animals are most susceptible. Sudden and high mortality rates are concentrated in lambs and kids. Although adult animals are also susceptible to enterotoxemia, they develop immunity due to frequent exposure to these toxins.  **Etiology** *Clostridium perfringens* is a normal inhabitant of the intestinal tract of sheep and most mammals. Certain conditions appear to trigger excessive bacterial growth, and thus lethal amounts of toxin are produced. Predisposing conditions often appear to be nutritional and occur most often in the early stages of feeding in feedlot lambs. Excessive concentrate ingestion, generally exceeding 3/4 pound per head per day, is a common history in flocks of affected animals. Other management factors that allow lambs to rapidly engorge, such as irregular feeding or inadequate bunk space, also increase the risk of enterotoxemia. Consumption of large amounts of milk by nursing lambs is also thought to contribute to the occurrence of this disease. These organisms are normally "laying low" in the small and large intestine they are present in relatively low numbers and appear to be in a relatively quiescent state in the normal, healthy animal. -When kids and lambs excessively consume milk or feed with high quantities of grain. -While recovering from an illness or distress; when natural immunity is compromised. -As a consequence of heavy infestations of gastrointestinal parasites, such as nematodes (worms) and coccidian. -When animals have a diet rich in grains and low in dry matter (hay or green grass). -When animals have any condition or disease that slows the peristalsis (motility of the gastrointestinal tract). -**A change in the diet **of the animal trigger them to cause disease. Most commonly, the change that triggers disease is an increase in the amount of grain, protein supplement, milk or milk replacer (for lambs and kids), and/or grass that the sheep or goat is ingesting. Collectively, these feeds are rich in starch, sugar, and/or protein. Unusually high levels of these nutrients reach the intestine; ***Clostridium perfringens*** undergoes explosive growth, increasing its numbers rapidly within the intestine. As the organism grows in number, it releases very potent toxins (bacterial poisons) that harm the animal. These toxins can cause damage to the intestine as well as numerous other organs. This can result in fatalities, particularly in the non-vaccinated animal or in the newborn lamb or kid whose dam has not been vaccinated. **Clinical signs:** enterotoxemia in sheep and goats include: - Most frequent in young animals, the peracute form is characterized by sudden death that occurs 12 hours after the first signs of the disease appear. Sudden death occurs only minutes after a lamb or a kid shows signs of central nervous system alteration. These signs are excitement and convulsion, followed by death. Loss of appetite Abdominal discomfort, shown by kicking at the belly and arching the back Profuse diarrhea (watery consistence with or without blood) - While in acute case, the animals may go off of feed and become lethargic. - Affected animals may show signs of stomach pain, such as kicking at their belly, repeatedly laying down and getting up, laying on their sides. - Diarrhea may develop; in some cases, there is blood visible in the loose stool. - Animals may lose the ability to stand, lay on their sides, and extend their legs, with their head and neck extended back over their withers. This posture is caused by the effects of the toxins on the brain. Death commonly occurs within minutes to hours after this sign is seen. - Because enterotoxemia can progress so quickly, animals may be found dead with no previous signs of disease. **Diagnosis** Enterotoxemia must be differentiated from other acute, fatal diseases of sheep, such as blackleg, bloat, or acute poisonings. Clinical signs of grain overload, or acidosis, are similar to those of enterotoxemia. Grain overload losses occur from overconsumption of concentrate rations whereas enterotoxemia losses, even though often precipitated by eating high concentrate rations, occur from Clostridium perfringens toxin production. It is essential to differentiate enterotoxemia from grain overload; however, at times both can occur simultaneously in the same flock. Diagnosis is based on clinical signs, and history of sudden death that can be confirmed by necropsy. Diagnosis can be confirmed by positive identification of enterocolitis (inflammation of the intestine). Clostridium perfringens types C & D from the feces, and gut content and kidneys cultured and isolated from the affected animals. The presence of glucosuria (high levels of sugar in the urine) can indicate enterotoxemia. Postmortem data are important for the diagnosis of enterotoxemia. Therefore, dead animals should be submitted to necropsy and their tissues sent to a diagnostic laboratory for confirmation of the clinical diagnosis. A postmortem examination of the large and small intestines can identify a high collection of watery blood and fibrinous clots, and numerous ulcers on the mucosa (internal layer of the intestines). The brain and kidney tissues may show softening. Post mortem examinations are needed to confirm the diagnosis. Type C enterotoxemia primarily shows a discolored, hemorrhagic small intestine. Type D enterotoxemia may or may not show small hemorrhagic spots in the intestines. Fluid around the heart is a frequent finding. The lungs are often congested and fluid filled. Urine is also often found to be high in sugar content. Other conditions may be present, but are found less consistently. Laboratory confirmation is accomplished through culturing large numbers of the *Clostridium perfringens* organisms. They can be found microscopically in scrapings or tissue of the intestines, and thus are a valuable diagnostic aid. **Treatment** Treatment of affected individual animals is usually ineffective, thus prevention is essential. Antitoxins produced by commercial companies can be given either orally or by injection. Administration of antibiotics such as penicillin may be recommended, but is frequently of little value after clinical signs appear. Other supportive therapy, such as fluids, vitamins, or cortisone, may be prescribed. Flock treatment primarily involves a ration change that reduces or eliminates concentrate feeding and increases the amount of roughage fed for a period of time. Feeding of concentrates may be gradually increased after dangers of enterotoxemia have passed.. **Prevention** Prevention of enterotoxemia is far more likely to be successful than trying to treat the disease. All animals in a herd should be vaccinated against enterotoxemia. Vaccination will reduce the chances that animals will contract enterotoxemia. **Vaccination** Vaccination is the cornerstone to prevention of this disease. For sheep and goats, there are multiple vaccines available that induce immunity to the toxins generated by Clostridium perfringens types C and D. Because tetanus is also an important disease to prevent in sheep and goats, many veterinarians recommend that sheep and goats be vaccinated with a vaccine that also induces protection against tetanus. These vaccines are often termed "three-way" vaccines because they induce protection against the three bacteria involved:  Clostridium perfringens type C (enterotoxemia), type D (enterotoxemia) and Clostridium tetani (the bacterium that causes tetanus). Vaccinate pregnant animals with C/ D&T vaccines during the fourth month of pregnancy. This procedure will enrich the colostrum with antibodies that will protect the newborn against enterotoxemia. All young animals should be vaccinated at four weeks of age and then 30 days later. Vaccinate bucks and all adult animals once a year. Do not vaccinate goats within 21 days before slaughter. Vaccinate animals that appear healthy; avoid vaccinating animals sick with fever or worms. These animals may not respond well to the vaccine because their immune systems may be weakened. Keep good records of the herd. Avoid causing stress to the animals during vaccination. In case of anaphylaxis caused by a vaccine, use epinephrine or its equivalent. **Feeding Strategies** **Smart feeding strategies**  Since the causative bacteria proliferate in the intestine in response to ingestion of abnormally high levels of starch, sugar, or protein, need to be careful how feed certain feedstuffs that contain high levels of these nutrients, such as grains, silage, milk or milk replacer, and protein supplements. Complete feeds -- such as pellets designed to be fed to induce gain in lambs or kids -- can also trigger this disease if fed in excess. When feeding these high-risk feedstuffs, divide the daily allotment for each animal into as many small feedings as is feasible (three to four feedings), rather than providing such feeds in a single, large meal. It is also advisable to feed roughages such as hay before feeding these higher-risk feeds, simply to allow the animals to become full on hay beforehand. This helps to limit the potential for overeating on high-risk feedstuffs, such as grain. **Always make feed changes slowly**. If the plan to increase the amount of grain fed to a flock or herd, always do so in gradual increments over several days. This helps the bacteria in the stomach to accommodate to the diet, making it less likely that the troublesome bacteria will get access to the nutrients. Divide herd or flock as necessary, and make sure to provide an adequate number of feeding sites or feeder space to enable all animals an equal chance to eat.For animals being turned out onto pasture after being fed hay or other stored feeds, a conservative thumb rule is to begin by allowing only about 10 minutes of grazing time on the first day. Double this with each subsequent day -- it will take about a week for them to work up to a full 24 hours on pasture. **Heavily milking dams** may need to be fed more roughage and less concentrate to limit the excessive milk production that might endanger their offspring. Keep the feed schedule consistent to lactating does and ewes to limit fluctuations in milk volume for their nursing offspring.