Caprine arthritis encephalitis (CAE)

Caprine arthritis encephalitis (CAE), caused by a retrovirus, can affect all breeds of goats but is most common in the dairy goat industry. Up to 80% of all dairy goat herds tested have infected animals compared with only up to 10% of meat goat herds. The CAE virus is transmitted from an infected adult goat to kids through consumption of colostrum and milk. There is also evidence to suggest that CAE can be transmitted directly from goat to goat possibly through saliva, nasal secretions, urine, feces, venereal transmission from infected bucks, and mechanical transmission (needles, tattooing equipment, etc.). While generally not a deadly disease, CAE can result in lost production, particularly in older goats. CAE is not an important disease in most meat goat herds at the present time.

Signs and symptoms

There are four forms of the disease, a CNS or “central nervous system” form that affects kids, an arthritic form that affects adults, a pneumonia form, and a mastitic form. The arthritic form in older goats is most commonly seen.

In the CNS form, young kids (2 to 4 months of age) develop a weakness in the rear legs, stumble, and finally cannot rise. The unused leg muscles lose strength and terminally affected kids are unable to sit up and can only lie on their sides. Throughout the course of the disease, kids remain bright and alert and will continue eating and drinking with assistance.

In the arthritic form, goats will have one or more swollen joints. The knee joints are most frequently affected followed by the hocks and stifles. Lameness results and goats may eventually walk on their knees. Affected goats gradually lose weight and condition, have poor hair coats, swollen knees, and have signs of joint pain particularly during cold weather.

The pneumonia form is usually seen during advanced pregnancy when the animal is stressed. The mastitic form occurs in adult does and is also known as “hard bag.” At the time of parturition the udder is swollen, firm, and hard but contains very little milk.

Treatment, prevention, and control

There is no treatment. Infected animals can be assisted by good nutrition, nursing care, and pain relief with anti-inflammatory drugs.

Prevention and control consist of purchasing CAE-free animals, culling infected animals, raising CAE-free kids, and preventing potential goat-to-goat transmission. Blood tests can detect CAE and animals can be tested prior to purchase. Periodic blood testing is required to monitor herd CAE status as animals will seroconvert (meaning they will blood test positive for the disease) at different times. An animal may test negative and three months later test positive. Once an animal tests positive, it will not revert to negative status. Repeated annual or biannual testing and strict culling is necessary to keep a herd CAE-free.

To raise CAE-free kids, remove them from affected dams at birth and feed pasteurized colostrum and milk, feed bovine colostrum and milk, or feed artificial products. Colostrum can be heat treated by raising the temperature to 133°F [56oC] for 60 minutes or 165°F [74°C] for 15 seconds. Milk is pasteurized by treating at 145°F [63°C] for 30 minutes or 165°F [74°C] for 15 seconds. The temperature is critical for colostrum because a higher temperature will denature colostral proteins that provide disease immunity and a lower temperature will not kill the virus. Pasteurization can be accomplished using a water bath heated by an electric frying pan or by equipment purchased for the task. It is probably not safe to feed unpasteurized milk from test negative does.

Finally, because there is evidence that any body fluid from an infected goat is a possible source of the disease, separation of infected and uninfected animals is important. Disinfect anything that could transmit body fluids (milk, saliva, feces, blood, or nasal discharges) between goats. This includes milking machines, tattoo needles, etc.

Contagious footrot

Footrot in goats is caused by infection with two bacteria, Dichelobacter nodosus (from the feet of infected animals) and Fusobacterium necrophorum (commonly found in the environment). Footrot can occur throughout the U.S. but is particularly prevalent in the southern states. The source of D. nodosus is the hooves of chronically infected carriers that occur in approximately 10% of affected small ruminants. Because of D. nososus’ short life span outside the hoof (usually less than four days), pastures or paths left alone by sheep and goats can be considered to be noninfectious after two weeks in wet/warm environments and after one week in a dry environment.

Outbreaks of footrot occur only when pastures are continually wet and mean daily temperatures are above 50°F [10°C]. Wet conditions soften tissues surrounding the hoof and can lead to infection or dermatitis making the skin more permeable to infectious bacteria. In an outbreak, 70 to 90% of all animals in the herd will be affected. About 10% of the animals will remain infected for life and 20% will remain uninfected. Those animals infected early in the course of the outbreak tend to stay infected for long periods of time; those infected late in the outbreak typically recover spontaneously in a short period. Resistance can be enhanced by selective breeding for footrot resistance, vaccination, maintaining feet in a dry condition, routine foot trimming, and administering zinc to animals deficient in that element.

Signs and symptoms

Both a mild (benign) and a severe (virulent) form of footrot may occur. In the mild form, often called foot scald, skin between the hooves will be inflamed, swollen, and damaged. There may be some secretions and the skin may have a “cooked meat” appearance. Lameness is mild and the problem responds readily to treatment and usually disappears spontaneously when the feet are exposed to dry conditions. Usually only a few animals are affected.

Severe, or virulent, footrot is caused by strains of the bacteria which rapidly digest the keratinized tissues found in the hoof wall. Initially, the foot is red, swollen, and moist and the goat experiences moderate lameness. As the infection progresses, the layers of the hoof separate and exude a dark, foul-smelling pus. Walking on the affected foot causes movement of the separated hoof layers resulting in severe pain. The animal will limp or walk on its knees. An affected animal may have a fever and will lose productivity.

Treatment, prevention, and control

Treatment, prevention, and control generally consist of combinations of antibiotic use, foot baths, foot trimming, and possibly vaccination. The use of injectable antibiotics is highly effective and penicillin, erythromycin, florphenicol, or oxytetracyline can be given under the advice of your veterinarian. Treated goats should be kept in a dry environment for at least 24 hours following treatment. In dry environments, topical treatment of antibiotics (5% tincture of tetracycline) or antiseptics (10% zinc sulfate, 10% copper sulfate solution) is adequate for benign footrot where small flocks of animals are involved or when routine foot trimming is being done. These can be applied with a brush or spray. Some commercial products for good hoof health are also available. Ensure good, prolonged contact with infected tissues.

– Foot baths

Large goat herds are treated more practically with foot baths. In an outbreak, goats should be treated weekly for four weeks. Separate infected from noninfected animals, treat, and then place on separate pastures. Preventive use of foot baths during the transmission season is recommended for herds with endemic footrot. Troughs must be deep enough to allow complete coverage of the foot and can be made from concrete, fiberglass, or plastic-lined wood. Foam rubber or wool can be placed in the solution to prevent splashing of caustic substances. Goats are adept at walking on small ledges so sides should be smooth. As goats can jump long distances, foot baths should be at least 8 to 10 feet long (~ 3 meters). Provisions should be made for drainage and proper solution disposal so as to prevent environmental contamination.

Copper sulfate (5%) and zinc sulfate (10%) are commonly used foot bath chemicals. Zinc sulfate is generally preferred as it does not stain hair and has less toxicity concerns than copper sulfate. Zinc sulfate is also not decomposed by organic matter to the extent seen with copper sulfate meaning that the solution need not be changed as frequently. Both chemicals are slow to penetrate the hoof and soaking periods of an hour or longer are necessary. Using a detergent, such as dishwashing detergent, in the solution may help penetration. Dry foot baths (85% limestone, 15% zinc sulfate) can also be beneficial.

– Foot trimming

Routine foot trimming is crucial in the prevention and treatment of footrot. Overgrown hooves provide an anaerobic environment for D. nodosus to grow and stress the foot increasing the chance of damaging skin and allowing entry of bacteria. In treatment, it is crucial to pare the feet adequately to expose infected areas when topical disinfectants are used. Do not trim so severely as to cause bleeding. Blood stop powder can help stop bleeding.

– Eradication

Eradicating footrot can be difficult, particularly in wet, moist environments. A typical program includes:

• Trim and examine the feet of all animals. Clean and disinfect hoof shears between animals by using alcohol, dilute iodine, or chlorhexidine.
• Run both groups through a foot bath, standing in the solution for a minimum of 30 minutes, then place on clean pastures.
• Repeat treatment weekly for two to four weeks.
• Cull those animals that do not respond to treatment.
• Consult your veterinarian on a potential vaccination regime.
• Select breeding animals that are less affected.

Once the program has been completed, monitor the herd on a monthly basis and remove relapsing animals. New additions to the herd should be checked for lesions and treated appropriately. Animals returning from shows should be foot bathed prior to re-entry into the herd.

A multivalent vaccine for footrot (Footvax) is available and can decrease the duration, severity, and incidence of footrot. However, its effectiveness is highly variable and repeated injections may be needed to maintain resistance.

Nutritional muscular dystrophy, white muscle disease

White muscle disease is caused by a deficiency of the mineral selenium and(or) vitamin E. Kids from does consuming a selenium-deficient diet are most affected. Selenium deficiency can occur when animals graze or are fed feedstuffs grown in low selenium-containing soils. White muscle disease affects both heart and skeletal muscle, usually in young, fast-growing animals under 6 months of age. Both selenium and vitamin E protect cell membranes from oxidation and to a certain degree act together and substitute for one another. A deficiency of one or both will overwhelm the abilities of the remaining compound(s) to protect body cells.

Signs and symptoms

Animals with the heart muscle affected will show signs of weakness, respiratory distress, rapid heart beat, and sudden death, particularly after exercise. Animals with the skeletal form will be stiff, stand with difficulty, and reluctant to move. Muscles, particularly in the hind legs, will be hard and painful. Upon necropsy (autopsy), the heart and skeletal muscles may have white streaks.

Treatment, prevention, and control

Treatment consists of injections of a product containing selenium and vitamin E such as Bo-Se. This can be repeated 24 hours later.

White muscle disease can be prevented by providing supplemental selenium and vitamin E, particularly if soils in your area are deficient. Supplements can be fed as additions to the regular diet or in a mineral mixture. Dietary concentrations of Se should be no more than 0.1 to 0.3 parts per million (ppm). Follow recommended guidelines on selenium feeding.

For additional protection, or in animals with an unknown history, Bo-Se may be injected subcutaneously shortly prior to kidding at 2.5cc/100 lbs live weight.

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