Diarrhea, scours (Neonatal Diarrhea Complex)

Diarrhea or scours is the most common cause of disease and death in kids 1 to 30 days of age. Diarrhea is usually associated with intensive rearing of goats under conditions of overcrowding and poor sanitation. Extreme weather conditions during the kidding season can predispose young kids to diarrhea. While diarrhea can affect meat goats, it is more common in dairy kids that are weaned early, group penned, crowded, and housed in a damp, dirty environment. Diarrhea causes a loss of body water and electrolytes and can result in death if not treated quickly.

Major causes of diarrhea are bacterial (E. coli, Clostridium perfringens type C, Campylobacter jejuni, Salmonella); parasitic (coccidia, cyrptosporidia, giardia, strongyloides); viral (coronavirus, rotavirus); and noninfectious (milk replacer, antibiotics). While the cause is often assumed to be a specific bacteria (E. coli), surveys of diarrhea in young kids have consistently failed to identify specific causes in the majority of cases.

Cryptosporidia seems to be the most common cause of diarrhea in kids less than a month old. Cryptosporidiosis can occur alone or in conjunction with other pathogenic bacteria, viruses, and protozoa. Cryptosporidia is difficult to treat because there are no drugs available to control it. Infection is usually from consuming fecal matter from infected animals, even from a different livestock species. A fuller discussion of Cryptosporidiosis is in the section on Internal and External Parasites later in this chapter.

Older kids (>1 month) are prone to diarrhea caused by coccidia and other internal parasites (Giaridia). Nutritional causes of diarrhea in young kids are often associated with husbandry and feeding practices, mainly seen in dairy kids due to overfeeding, milk replacers, etc. Under most circumstances, outbreaks of diarrhea are probably not caused by any one factor but by a combination of factors, hence, the name “Neonatal Diarrhea Complex.”

Signs and symptoms

Affected kids develop a loose stool. The consistency can vary from pasty to watery. Kids quickly become dehydrated from loss of body fluid and electrolytes and become progressively weaker. Terminally, kids are severely dehydrated, lie on their side, have cool extremities, and are unwilling to drink.

Treatment, prevention, and control

With increasing fluid loss, the kid goes into progressive shock, cannot maintain body temperature, and dies. Causes of death in uncomplicated cases of neonatal scours are dehydration, electrolyte losses, and hypothermia. Treatment consists of supplying the kid with fluids to restore normal fluid and electrolyte levels. Commercially available electrolyte and alkalinizing products are available. Initially, milk can be removed from the diet and electrolytes given. Milk is then gradually reintroduced to the kid in small feedings alternated with electrolytes. Electrolyte solutions should continue to be used until the stool returns to a near normal consistency. Injectable antibiotics such as Naxcel or Exenel can be given to prevent the infection from becoming blood-borne. Oral antibiotics are commonly used to treat diarrhea and scours but their efficacy is not well proven. Be aware that feeding electrolytes alone for more than 2 days will result in a significant caloric deficit. It is critical that the goat be kept warm.

The keys to preventing scours are to reduce exposure of kids to pathogens causing the disease and to increase resistance of kids to the disease-causing agents. To reduce exposure to pathogens, ensure that kidding takes place on fresh pasture and a clean, dry area. Assist with kidding if necessary and ensure that all navels are dipped in iodine. Monitor nursing behavior and force feed colostrum if no nursing is seen within 6 hours of birth. Avoid congregating kids to prevent overcrowding conditions. Use separate kidding and nursery areas. Resistance can be strengthened by optimum pre-kidding maternal nutrition and following a prescribed vaccination schedule. This will strengthen antibody production in the dam and improve resistance gained by the kid through colostrum. If deemed necessary, oral E. coli, corona and rota virus vaccines can be given to newborn kids before they nurse the doe.

Enterotoxemia, overeating disease

Overeating disease is an important and highly fatal disease that mostly affects young kids. It is not caused by overeating but by the toxin produced by the bacteria Clostridium perfringens Type C or Type D. C. perfringens is found widely in the environment and in the intestinal tract in normal quantities. Under certain conditions, the organisms proliferate in the intestine and produce toxin in lethal quantities. This most commonly occurs when goats have a sudden exposure to grain or large increases in the quantity of milk consumed. At these times, the passage rate for food through the intestinal tract is slowed, providing ideal conditions for C. perfringens to grow.

Signs and symptoms

A typical history is of a young, vigorous kid found dead. The affected kid has a consistent history of nursing a heavy milking doe or being on full feed. Animals have actually been observed to drop to the ground, convulse, and be dead within a matter of minutes.

Adults appear to be more resistant to the disease as a result of continuous exposure; however, the resistance can be overwhelmed. A typical history for an older animal dying from overeating disease is that the animal was sick and off feed from some other disease (e.g., parasitism). As the animal recovers it quickly increases feed intake resulting in a mild grain overload. This allows the proliferation of C. perfringens and ultimately the death of the goat.

Treatment, prevention and control

There is usually no opportunity to treat animals with enterotoxemia. Specific antitoxin (CD&T) is available for treatment and should be given according to label directions. Affected animals should be treated with high levels of penicillin (6 cc/100 lbs) and fluids.

All goat herds need to have a regular vaccination program for overeating disease. This includes annual vaccination of does roughly 30 days prior to expected parturition to protect the newborn for the first 1 to 2 months of life. Kids are given a series of two vaccinations at 4 and 8 weeks of age. A booster dose is given at the time of weaning or when going on full feed. See the Meat Goat Vaccination Schedule in the Meat Goat Herd Health – Procedures and Prevention chapter.

Milk fever, parturient paresis, hypocalcemia

Milk fever is a disease more commonly associated with dairy goats. It is not a fever but is due to inadequate amounts of calcium available in the blood stream for use in milk production during early lactation. This usually occurs in does with high milk production and ones fed high levels of calcium in late pregnancy. In milk fever, the doe cannot mobilize calcium from her bones as quickly as it is needed for milk production necessitating the use of blood calcium. When blood calcium levels drop too low, milk fever occurs. High levels of dietary calcium fed in late pregnancy prevent the doe’s metabolic system from becoming accustomed to mobilizing bone calcium. Does having triplets or quadruplets may be more prone to milk fever

Signs and symptoms

Milk fever usually occurs close to kidding, up to about 3 weeks after birth, but can occur before kidding. Animals will show a wobbly gait, foot dragging, and muscle incoordination. Some animals will be unable to stand and, if prior to kidding, be too weak to deliver.

Treatment, prevention, and control

Treatment consists of intravenous calcium therapy with 50 to 100 cc of 25% calcium borogluconate. Some veterinarians prefer to give an additional 50 to 100 cc subcutaneously after the intravenous treatment. Oral calcium preparations are used in mild cases. Prevent milk fever by feeding a low calcium diet the last month of gestation. This prepares the doe’s metabolic system to mobilize calcium from its skeleton.

Paratuberculosis, Johne’s disease

Paratuberculosis or Johne’s disease is a chronic wasting and diarrhea disease of ruminants caused by the bacteria Mycobacterium avium subspecies paratuberculosis (M. johnei). The organism is capable of living on infected premises for up to a year and the same bacterial strain can infect any ruminant. This means that goats sharing pastures with infected cattle are susceptible.

The primary mode of transmission is via the fecal oral route with kids most susceptible to infection. In general, it is safe to assume that if the doe is infected her kids will also be infected. Infected animals shed the bacteria for months or years prior to developing clinical signs. This results in heavy contamination of pastures before it is known that the disease is present.

Signs and symptoms

Signs rarely occur prior to 1 year of age with peak incidence of disease at 2 to 3 years of age. Goats will show weight loss, loss of appetite, depression, and general wasting. Watery diarrhea is seen in cattle but is a rare finding in goats. As the disease progresses, anemia and bottle jaw (swelling of tissues under the jaw) may develop. Affected goats also seem to become more susceptible to internal parasites such as the barberpole worm (Haemonchus contortus).

Johne’s disease is suspected whenever a goat is losing weight for unknown reasons. The diagnosis may be confirmed by biopsy, necropsy, bacterial culture, or one of several serologic (blood) tests.

Treatment, prevention, and control

There are no treatments available for Johne’s disease. Prevent by not allowing infected ruminants (cattle, goats, sheep, etc.) on your premises. Purchase animals from farms with no history of Johne’s disease and blood test all incoming ruminants. Remove any that test positive. There is a vaccine licensed for use in the prevention of paratuberculosis. It is apparently effective but produces large swellings at the injection site that last for years. Vaccination will also cause hypersensitivity to the tuberculosis test. In order to use the vaccine you must to obtain permission from your State Veterinarian.

Eradication of Johne’s disease is difficult. Identification of animals in your herd is problematic in that blood tests will give both false positives and false negatives. Fecal culture or DNA probe testing will not give false positives; however, these tests may miss up to 50% of infected animals. Multiple tests or several different tests are required. A second problem is the contamination of pastures and housing. These should be free from diseased animals for at least 12 months before housing disease-free goats. Ensure that kids are not exposed to the feces of infected adults by housing them separately and have fecal-free feed troughs, boots, and clothes at all times.

Pregnancy toxemia, ketosis

Ketosis, pregnancy disease, pregnancy toxemia, or twinning disease usually occurs during the last few weeks of gestation and is caused by the competition for glucose between the doe and her rapidly growing fetus(es). It is more commonly seen in does carrying more than two kids or overly fat does, although very thin animals can be affected. Because the uterus, fetuses, placenta, and other pregnancy tissues take up an increasing amount of abdominal space there is less and less room for feed consumption. If a doe is overly fat, she also has less room to hold feed. Thus, feed intake decreases and the doe is forced to break down fat stores for energy. Ketones are a chemical by-product of fat breakdown. While the body can use small amounts of ketones, excessive amounts cause the appearance of ketosis.

Signs and symptoms

Does with pregnancy toxemia are depressed, weak, and have poor muscle coordination. They may also star gaze and grind their teeth. Animal may have a strong smell of ketones (sweetish smell) on their breath.

Treatment, prevention, and control

Treatment consists of 2 to 3 ounces of propylene glycol twice a day. If the does are too weak to stand, treatment may not be successful in getting them up until they deliver their kids. Induce parturition around 145 days in gestation to have live viable kids. Have a veterinarian perform a Caesarian section if they are close to term to try and save the doe and kids.

Prevent by not letting does get overly fat early in gestation. Feed good quality grains or grain by-products and good quality hay. If a particular doe is very large or has a history of having more than two kids, increase her energy intake.

Acidosis, carbohydrate engorgement, grain overload

Goats frequently fall victim to the disorder called grain overload that leads to acidosis. This is a condition which affects all ruminants and results from the over consumption of highly fermentable carbohydrates such as cereal grains and many pelleted diets. The bacteria in the rumen are responsible for digestion of the majority of what a goat eats. Under normal conditions of a steady diet these bacteria become very specialized at their task. If the diet is changed very quickly, rapid, dramatic, and often fatal changes occur within the rumen. As the excessive carbohydrates are metabolized, they are broken into small particles which draw water into the rumen resulting in dehydration. As they are fermented, the rumen pH decreases from a normal of 6.0 to 7.0 to very low (acid) levels (pH of 3.5 to 4.5). This acid solution kills many of the ruminal bacteria and damages the wall of the rumen itself.

These rapid dietary changes occur from improper feeding often as a result of two facts of goat husbandry. The first is that some goat owners extrapolate principles of human nutrition to their goats. While knowing that humans do not suffer from eating too much corn, flour, and the like, they do not realize that this can be fatal to goats. The second reason is the inquisitive nature of goats and their skill at getting into places where they should not be. This allows them to gain access to grain stores and consume them free-choice.

Signs and symptoms

Affected goats become dehydrated, their rumens become distended with fluid, and in the later stages of disease they develop diarrhea. The ruminal inflammation due to the acidic conditions is painful and goats act uncomfortable, grind their teeth, and may vocalize. Generally, signs develop 6 to 12 hours after the overconsumption of carbohydrates.

Death can result from the dehydration, acidosis, and electrolyte disturbances associated with the disease. Alternatively, during the course of the grain overload, a large amount of undigested food travels to the intestinal tract. This provides an ideal environment for Clostridium perfringens to proliferate and produce deadly toxins causing overeating disease (enterotoxemia). As a sequel to acidosis, the rumen can be damaged severely enough that bacteria gain access to the liver and cause liver abscesses. This will cause ill thrift and chronic weight loss in affected goats.

Treatment, prevention, and control

In mild cases, goats should be given hay and not fed any grain or concentrate. The grain or concentrate feedstuffs can then be reintroduced into the diet gradually. Alkalinizing agents such as oral antacids (10 to 20 grams or 0.7 ounces magnesium oxide, 50 grams or 1.75 ounces magnesium hydroxide, or 20 grams or 0.7 ounces sodium bicarbonate) can be given or a solution of 2 to 4 teaspoons of baking soda in a quart of water can be used. However, if too much feed is in the rumen these will act only temporarily.

In severe cases, goats should be given intravenous fluids containing 5% sodium bicarbonate. Large amounts of oral fluids should be avoided because they will not be absorbed and may actually increase rumen distension and discomfort. A stomach tube can be passed into the rumen and the contents washed with water and the fluid removed. Alkalinizing agents can be used as in mild cases. In very severe cases, surgery must be done to remove the consumed feed. Thiamine (500 mg IM, three times daily) has been shown to be helpful in recovery. Anti-inflammatory drugs can be given to make the goat more comfortable.

Normal rumen bacteria flora can be reestablished by transferring some rumen contents from a healthy goat, or cow, into the rumen of the sick goat. This may be done by tubing the animals though it would be wise to consult a veterinarian. Various probiotics (e.g., Biosol) or live culture yoghurt will have some beneficial effect. The diet for the recovering goat should be forages only for at least 3 weeks.

Prevention is by gradual adaptation of the rumen to changes in diet. This process should take a period of 3 weeks of gradually increasing grain intake. At high levels of grain intake (feedlot or dairy goats), feed frequent small meals rather than fewer larger ones. Maintain a rigid feeding time to avoid simple rumen upset. All stored grains must be kept in well secured goat proof buildings.

Bloat, ruminal tympany

Bloat is the accumulation of free gas or froth in the rumen due to the inability of goats to rid themselves of gas produced by ruminal microorganisms during the breakdown of feedstuffs. This condition is always an emergency.

There are two causes of bloat but both have the same symptoms and effects. Frothy bloat can be caused by feeding on rapidly growing legumes and small grain pastures (wheat, barley, oats, rye). This occurs most often when goats are suddenly changed to grazing these types of pastures with no adaptation period. Frothy bloat can also occur when animals consume too much finely ground grain. Free gas bloat is caused by consumption of a diet that causes excessive gas production, such as a high grain diet, or blockage of the esophagus due to choking, a foreign object, swollen lymph nodes, nerve damage, etc.

Signs and symptoms

The gas trapped in the rumen causes the left side of the animal, where the rumen is just under the skin, to swell. The goat will experience pain, discomfort, and have difficulty breathing. If left untreated, the internal pressure will make it increasingly difficult to breath and the animal will die from a lack of oxygen.

Treatment, prevention, and control

Treatment consists of relieving the pressure caused by the gas. For mild cases, a stomach tube can be used to free the trapped gas. If this is not effective, remove the tube and look for the presence of froth at the end. Frothy bloat can be treated by orally giving through the stomach tube:

1. Poloxalene (Therabloat), 30 ml or 1 ounce,
2. Diocytyl sodium sulfosuccinate (DSS), 30 ml or 1 ounce,
3. Detergent, such as liquid hand soap or dishwashing soap, 10 ml in 1 to 2 ounces of water, or
4. Mineral or vegetable oil, 3 to 4 ounces or 1 to 1 ½ cups.

Severe bloat should be treated using a trocar and cannula or very large gauge needle to pierce the left side of the animal releasing the gas. This should only be done in extreme emergencies as animals treated in this way may later encounter problems due to infection that can lead to death. If performed, antibiotics should be administered.

Prevent bloat by avoiding sudden dietary changes. If animals will graze lush pastures, feed hay or forage prior to grazing to prevent goats from gorging themselves. In cases where frothy bloat may be a problem, poloxalene can be provided in a mineral supplement. Ionophores such as monensin, lasalocid, or decoquinate can be fed. Free gas bloat can be prevented by slow adaptation to high grain diets allowing ruminal microbes to adapt.

Two types of trocar and cannula

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