MENINGEAL DEERWORM INFECTION IN GOATS

Goat producers who live in areas where whitetail deer are abundant should be concerned about Meningeal Deerworm infection in their goats. Rainfall, swampy ground, and leaf litter compound the problems but the presence of white-tail deer are the key.

Sometimes called deerworm or brainworm, the parasite Parelaphostrongulus tenuis uses the whitetail deer as its host and passes through the deer's body without harming it. But with goats, the deerworm seems to "get lost" and winds up in the spinal canal . . . causing hind leg weakness and unsteadiness, progressing to hind leg dragging, inability to walk in a straight line, rear end wobbling from side to side, tremors, inability to stand, and paralysis. Once the larvae migrate over the body, the goat oftentimes but not always experiences intense itching and may begin chewing holes in its hide. There may be multiple small patches or one large patch of leathery skin, often behind the front leg of the body and moving up to the neck area. Shaving the hair off the sites where itching and chewing are occurring will usually reveal a straight line of hard nodules leading from the spine over which the skin has thickened. These are the subcutaneous larvae migrating throughout the goat's body. If the producer diagnoses the problem before paralysis occurs, full recovery is possible.

Goats who develop Meningeal Deerworm infection get it by ingesting the intermediate host, a slug or snail, while browsing in wet areas, such as ponds or swamps, or under dead leaves, branches, and trees. Warm weather in early winter and the resulting lack of snow cover has made this disease common in the eastern part of the United States. Goat producers who raise alpacas, llamas, or related ruminants may find that these camelids are even more susceptible to Meningeal Deerworm disease than goats or sheep.

The producer should suspect Meningeal Deerworm disease if the goat displays neurologic signs or any problem involving the spinal cord, from leg dragging to inability to get up. The disease can be a slow progression of symptoms or can strike suddenly. Pneumonia is a common secondary problem, since the goat is down and therefore inactive. The infected goat does not seem to be in pain, other than the itching; most goats eat and drink until death occurs.

Treatment involves very high dosages of Ivomec Plus or generic equivalent. Ivermectin paste or pour-on are not effective. Ivomec Plus or generic equivalent is recommended because if snails or slugs are present, so may also be liver flukes, and Ivomec Plus will handle both conditions at the same time. Ivomec Plus should be given at a rate of 1 cc per 25 pounds bodyweight for at least seven days, followed by a double-the-cattle dosage of fenbendazole (Safeguard/ Panacur) for five days. (Jeffers carries both dewormers.) Dosing too low means that the deerworm continues to do damage. Enough medication needs to remain in the goat's system so that the blood-brain barrier can be crossed in order to kill the larvae that have already penetrated the spinal column. If the goat is down and can't get up on its own, the chance for recovery is not good. An anti-inflammatory drug like Banamine can be useful in alleviating the inflammation of nerve tissue. Dexamethozone should also be used if paralysis is present, dosing at approximately 8 cc per 100 lbs bodyweight and stepping down one cc per day. Dex should be given into the muscle (IM). If the sick goat is a pregnant doe, use the dexamethasone and let her abort, because she isn't likely to survive if she is trying to grow fetuses while fighting this disease. If the producer is concerned about using Dexamethasone and Banamine at the same time, then use the Dex and forget the Banamine. When symptoms are found in one goat, the producer should either treat the entire herd or watch everyone closely daily for symptoms and begin treatment immediately if discovered.

This treatment, if utilized early in the disease, can stop its progression but cannot undo any nerve damage. Permanent spinal damage (including curvature), weakness in the hindquarters, and/or inability to deliver kids may be the residual effect of Meningeal Deerworm infection. Once the spinal cord is damaged, treatment can only do so much and the goat will never be back to full health. Producers should let at least one month pass before becoming convinced that the animal has been successfully treated.

In the northern and eastern parts of the United States, most infections occur in late summer/early fall or early winter, following a wet summer and mild fall. The larval migration of P. tenuis can take from ten days to over three months. If weather conditions produce wet ground, leaf litter or other slug habitat, and temperatures above 55*F, then meningeal deerworm is likely to appear six weeks after the first warm day and exist for the same number of days that the warm temperatures lasted. Said another way, if two weeks of warm weather occurs in November, watch for the appearance of meningeal deerworm in January. During these timeframes, some producers are using Ivomec Plus or its generic equivalent monthly for up to four months during the at-risk seasons.

Although laboratory testing of the cerebrospinal fluid produces an accurate diagnosis, the key to treatment of Meningeal Worm infection is early aggressive treatment. If all indications tell the producer that the goat is infected with P. tenuis, forget the testing and get on with treatment.

Prevention is difficult. The only proven preventative medication is administering Ivomec Plus or its generic equivalent monthly during slug and snail season. Because slugs and snails travel, ponds, swamps, and leafy wooded areas should be fenced off at least 200 yards from the areas to avoid so goats cannot become exposed to slugs and snails. Test for existence of slugs and snails by putting dry dog food in a small plastic cup, place it on the ground, and cover it with a bucket or box. Check the bucket or box at sunrise and sundown. If you find slugs, you have a potential Meningeal Deerworm problem in play.

Treatment can be unsuccessful, even when the disease is caught in its early stages. Prevention is the key to avoiding this devastating disease. This writer thanks Ray Kruse of Little Brush Creek Farm in Buffalo, Kentucky for his input based upon his experience with this disease.

Suzanne W. Gasparotto 12/8/09
ONION CREEK RANCH
Lohn, Texas 76852