# goat dragging leg



## Taz's Arc (Aug 27, 2010)

Hello,

I'm a new member and before I've had opportunity to introduce myself my little guys having a problem.

I'm an accidental goat owner. They are pets and I've no real background except what I've managed to learn these past four years with two pygmy goats five hours away from a vet. 

I now have one pygmy goat (cougar took the other grrrr) and a new Nigerian dwarf/Saanen cross. There is a vet in my new town but are not large animal vets. 

Karuno is apx 19mths, 65pds, nurtured, and a few weeks ago he began to limp. As the doe pygmy has been a tad nasty since she became a precocious milker I initially thought she'd hit him a bit to hard. It appeared to be getting better then the past four days he began to drag his rear left leg. He is in no pain. I palpated and did bilateral compare and there were no issues or point tenderness. Checked his hooves, eyes, ears etc...it now is becoming a weakness in the hindquarters. The vet advised yest they know naught but believes it is neurological. They took blood for CAE but he has not been in contact with a heard of goats for a year. The Queen pygmy has not for four years and is very healthy.

They free range for the most part, get half cup of goat ration/day, hay, orchard grass, and veggies from the kitchen (garbarators) I have not noticed anything new in their diet.

I live on the northern tip of Vancouver Island British Columbia and there are no white tails - thinking p. tenuis meningeal worm.

I am very concerned any suggestions or assistance greatly appreciated!!!


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## StaceyRosado (Oct 5, 2007)

if he was much younger I would be thinking Floppy Kid but it could still be a selenium deficiency. 

testing for CAE is good - hope it comes back negative for you. They get that from their mom through the milk and sometimes they dotn show signs of the disease till years later.


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## cmjust0 (Oct 8, 2009)

The symptom you're describing -- "weakness in the hindquarters" -- sounds to me like either _ataxia_ or _paresis_. When I went looking for a differentiation, I came to find that paresis is probably more fitting here because it basically means 'weakness,' whereas ataxia is more descriptive of an uncoordinated state. When discussing paresis, the book "Goat Medicine" specifically mentions "dragging of one or more limbs..."

Here's the entire section from the book.. Forgive me for spelling errors...I couldn't copy/paste, so I had to type the whole thing from the book:

Neurogenic impairment of motor function leading to weakness may result from lesions of the brain stem, spinal cord, peripheral nerves, or neuromuscular junctions. Tetraparesis, paraparesis, hemiparesis, or involvement of a single limb may occur. Signs can include difficulty in rising, dragging of one or more limbs, trembling when standing, difficulty in standing for long periods, and collapse or buckling of the limbs. When hemiparesis is present, leaning, falling, or rolling to one side may be noted. Careful observation and thorough neurologic examination are necessary to distinguish ataxia from paresis when both are present.

Infectious causes of paresis include rabies, CAE or visna, listeriosis, and botulism. Parasitic causes include cerebrospinal nematodiasis with either Paralephostrongylus tenuis, Elaphostongylus spp., or Setaria digitata; coenurosis; and tick paralysis.

Metabolic and nutritional causes include milk fever, pregnancy toxemia, and enzootic ataxia or swayback. Toxic causes include plant poisonings by coyotillo (Karsinskia humboldtiana), locoweeds (Astragalus spp.), carpetweed (Kallstoemia hirsutissima), milkweed (Asclepias spp.), tropical soda apple (Solanum viarum), Ipomoea carnea, and maize contaminated with the fungus Diplodia maydis. Toxic causes other than plant poisoning include salt poisoning, bromide intoxication, boron toxicity, organophosphate and carbamate insecticide poisoning, and pentachlorophenal toxicity.

Neoplastic causes of paresis are uncommon but reports include lymphosarcoma sporadically associated with the brain or meninges (Craig et al. 1986) and malignant melanoma metastasized to the vertebral canal (Sockett et al. 1984).

Congenital or inherited causes include hydrocephalus and progressive paresis of Angora goats. Caprine encephalomyelomalacia, a disease of unknown etiology, can also produce paraparesis or tetraparesis.


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## Taz's Arc (Aug 27, 2010)

Wow thanks for typing that out!!! Helps me know where to focus research on. wow...happy to have come across this discussion forum!!


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## Taz's Arc (Aug 27, 2010)

He tested positive for CAE and what an awful progression...I kept hoping it was a false positive and tried many different possible solutions such as b shots to garlic. I spoke to the breeder I received him from and was advised that in all the years she's been breeding goats CAE has never shown in the offspring....either or I am now down to one pygmy goat that is spending way to much time with the german shepard...I expect her to start barking soon.


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## StaceyRosado (Oct 5, 2007)

oh I am so sorry :hug:


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## liz (Oct 5, 2007)

So sorry to hear that he tested positive :hug: 

CAE is a disease that most often does not show signs...neurologic affects of it though are often shown in kids and yearlings. I know it's hard to think of it this way but at least now you know what was wrong and I hope that your "barking pygmy" gets a goatie companion soon :hug:


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## farmgirl42 (Jan 3, 2010)

Aw, I'm so sorry to hear about your little guy. :hug:


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## e35378 (Aug 18, 2013)

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. Dexamethosone 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


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## toth boer goats (Jul 20, 2008)

:hug: I am sorry too.


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