Goats, Sheep And Deer Worm

Goats, Sheep And Deer Worm

By Gail Damerow

During 30-plus years of raising dairy goats, I had never heard of meningeal deer worm until December of 2013, when I lost that season’s best young doe and my senior breeding buck to a mysterious disease — mysterious because the two goats were housed in separate barns and grazed in separate pastures, and none of the other goats in their respective herds came down with the illness.

In Amber’s case, the first sign I noticed was that her back legs seemed stiff, and she had difficulty walking. Since she was reluctant to come into the barn to join the rest of the goats at mealtime, I thought she might have incurred a butting injury. Accordingly, I moved her into a private stall for a little R&R. She ate and drank as usual, but the back leg stiffness worsened into paralysis. The day she went down and could no longer get up, even with help, I knew it was time to let her go.

Meanwhile, as soon as it had become apparent that this was no ordinary injury, I began researching causes of back leg stiffness and paralysis. One possibility that kept coming up was a hair-like nematode known as meningeal deer worm, although I was repeatedly assured this parasite rarely affects goats. But the more I learned, the more convinced I became that Amber had been afflicted by deer worm.

Two weeks later, while I was still reeling from the loss of Amber and trying to learn how to prevent a repeat occurrence, our senior buck Jaxon appeared reluctant to come in for his morning snack. I went into the pasture to fetch him and saw that his back legs were stiff and he was having trouble walking. I began the best deer worm treatment plan I had learned to date, but to no avail — the next day he was gone.

Terrified of the possibility of losing more of my Nubians, and convinced that deer worm was the cause, I sought out the most recently recommended treatment protocol along with the necessary arsenal of medications recommended by veterinarians who specialize in treating goats. For nearly a year I had no use for them.

Then, in November of 2014, Amber’s mother Candy didn’t want to come in for her evening meal. When I saw that one back leg looked a little draggy, I immediately began deer worm treatment. In short order Candy was back to her old sweet self. A few months later she delivered triplets. In April 2015 Jaxon’s son Red Baron, our current herd sire, became unusually quiet. He moved only tentatively and appeared not to know where to put down his back feet. Again I immediately began treatment and his condition improved, though gradually. He still walks stiffly and we don’t know yet if he will eventually be able to resume breeding.

I can’t prove that Candy and Baron were or were not infected with meningeal deer worm, but neither did they die the same horrible deaths as Amber and Jaxon. Given the facts of these events, two of the veterinarians  I consulted agreed that deer worm is the most likely cause.

Why so much speculation about the cause and treatment of this horrible disease? Because no method has been found to definitively diagnose meningeal deer worm infection in a living goat, and no controlled studies have been done to determine the best treatment for infected goats. Here is what is currently known about this devastating parasite:


The deer worm (Parelaphostrongylus Tenuis) parasitizes white-tail deer, but rarely causes illness in them. Mature worms live in the membranes that enclose the deer’s brain and spinal cord. Collectively these membranes are called meninges, hence the term meningeal deer worm.

The worms lay eggs in the deer’s blood vessels. Through the blood stream the eggs migrate to the lungs, where they hatch into larvae. The infected deer coughs up larvae, swallows them, and passes them in the mucus that coats its droppings.

Gastropods (slugs and snails) crawling over the droppings take in larvae, which become infective within three to four months while living inside the gastropod. Infective larvae may remain inside the gastropod, or may be excreted in its slime trail.

While grazing, the same (or another) white-tail deer may ingest the infected slug or snail, or eat vegetation coated with infected slime. In the deer’s abomasum, or fourth stomach compartment, the gastropod releases infective larvae that migrate to the deer’s spinal cord and brain, where they develop into mature egg-laying worms. At some point the infected deer develops immunity against invasion by additional larvae, limiting the number of worms in carries.

The reason meningeal deer worms don’t sicken white-tail deer is because the worms need healthy deer in order to complete their life cycle. A problem occurs, however, when a grazing animal such as a goat or sheep accidentally eats an infected slug or snail. The infective larvae are released in the digestive system, the same as in white-tail deer, but now they are in unfamiliar and confusing territory.

The larvae don’t develop in the normal way, don’t follow their usual path through the central nervous system, and don’t mature into egg-laying worms. Instead they wander around within the spinal cord, destroying tissue and causing inflammation. Because they can damage different locations within the central nervous system, or more than one location, the resulting signs of illness may vary from one infected animal to the next.

Susceptible animals include deer other than white-tails — black-tail deer, fallow deer, mule deer, and red deer — as well as caribou, elk, moose, alpacas, llamas, goats, and sheep. Compared to infected goats and sheep, more research has been done with alpacas and llamas because of their greater susceptibility to deer worm and their higher monetary value.

The two medical terms for this disease are both tongue-twisters: cerebrospinal nematodiasis and parelaphostrongylosis. No wonder the condition is commonly known as meningeal deer worm infection, or simply deer worm infection.


Like any disease affecting the brain or spinal cord, deer worm infection results in a lack of coordination and other neurologic disorders. The first signs can appear between 11 days and 9 weeks after a goat or sheep ingests an infective larva. Initial signs often occur at the animal’s back end, where the muscles seem to weaken or become stiff, causing the animal to walk unsteadily.

Other signs may include head tilting, arched or twisted neck, circling, rapid eye movements, blindness, gradual weight loss, lethargy, and seizures. Some infected animals prefer to be alone. Itchiness resulting from worms migrating along nerve roots can cause an animal to scratch vertical raw sores along its shoulders and neck.

Because of the variable nature of this illness, signs may appear in any order or combination and may or may not grow progressively worse. Unlike some diseases, which cause an affected animal to become lethargic and lose interest in eating and drinking, deer worms typically do not affect an animal’s alertness or its interest in eating and drinking. Even when Amber had trouble standing up, she remained alert and eager to eat.

A chronic case of deer worm infection can result in incoordination and unsteadiness that goes on for months or even years. An acute infection can cause rapid death, as happened to our Jaxon. One day he looked fine, the next day he was gone.

Deer Worms
Deer worms — spread by slugs and snails —
cycle through white-tail deer without causing
harm, but can result in serious illness or death in
goats and other grazers. artwork by bethany caskey


Since deer worm do not complete their life cycle in aberrant hosts (defined as any infected animal other than a white-tail deer), parasite eggs or larvae will not be found in the animal’s droppings, as would occur with stomach or intestinal parasites. This factor rules out using fecal testing as a diagnostic tool.

So far no method has been found to diagnose deer worm in a living animal. The only way to identify the infection for certain is to find worms or larvae on the animal’s brain or spinal cord during necropsy, meaning the animal must either die from the infection or be euthanized.

A presumptive diagnosis—an educated guess as to the most probable cause of illness—involves answering several pertinent questions. Although the answer to each individual question does not provide a definite diagnosis, considered together they offer a pretty good indication as to whether or not deer worm is the likely offender. These questions are as follows:

• Did the infected animal graze in or near white-tail habitat?

• Does the grazing area harbor terrestrial slugs or snails?

• Are the signs of illness consistent with deer worm infection?

• Could the same signs be the result of some other disease?

• How well does the infected animal respond to treatment?

The first question is easy to answer, because white-tail deer are easy to see. Traditionally they have been concentrated in the eastern states, but are now found just about anywhere in the United States and Canada, so much so that in some areas they are considered pests (“rats with antlers”).

In my case, our farm is surrounded by forests that are teeming with white-tails, which routinely cross our hayfields and wander through our orchard. We rarely see them in our goat pastures, but that doesn’t mean they don’t occasionally pass through.

As for slugs and snails, they are typically abundant in low-lying, damp, and poorly drained fields. But they also occur in other areas when the weather is persistently damp over long periods and in fields where vegetation is overgrown.

Our farm is at the top of a welldrained ridge; we don’t have the abundance of large snails and giant slugs that plague gardeners in Pacific states; and our usually droughty warm-weather conditions are not conducive to large populations of the tiny gastropods we do have. However, in the past couple of years we’ve had unusually long periods of rain during spring and fall, and we’ve seen large numbers of slugs crawling out of the grass onto our concrete sidewalk and gravel driveway. Plus all that rain has prevented timely mowing of our pastures, so instead of the exposure slugs usually get to debilitating sunlight and heat, lately they have enjoyed plenty of damp cover.

Determining if signs are consistent with deer worm may not be so easy, because the signs are not always the same. In our case, though, all four of our infected goats initially appeared to have stiff back legs and sought to separate themselves from the rest of the herd—two of the many signs of deer worm infection.

Could these signs result from some other disease? Janice E. Kritchevsky, VMD, MS, of Purdue University’s College of Veterinary Medicine, cautions that, although deer worm is common in alpacas and llamas, it is quite rare in goats. She suggests first considering three much more common causes of neurologic illness in goats—polioenceophalomalcia (polio), listeriosis (listeria), and caprine arthritis encephalitis.

Polio is a nutritionally related illness caused by thiamine deficiency. It primarily affects intensively managed goats that are fed large amounts of concentrates (commercially bagged rations) to make up for a lack of quality roughage, to promote rapid growth in meat kids, or to increase milk production in dairy goats. We limit the amount of concentrates we feed our goats because we want to encourage them to graze the several pastures in which they are regularly rotated. We feel that grass is more natural and better for grazers than formulated concentrate, and it makes the milk more healthful.

Dr. Kritchevsky points out that goats with polio are blind, and often the pupils of their eyes are oriented vertically like a cat’s, not horizontally like a normal goat’s. Left untreated, a goat with polio will die within about three days of the appearance of the first signs. The only effective treatment is thiamine (vitamin B1) injections. Except for Jaxon’s rapid death, this scenario does not match our goats’ illness.

Listeriosis is another neurologic disease that affects primarily intensively managed goats. According to Dr. Kritchevsky, it usually affects individual goats, but can be a herdwide problem. It is caused by the bacteria Listeria monocytogenes and usually results in severe head tilting. Two common signs are depressed appetite and circling in one direction. Treatment involves the use of antibiotics. Our affected goats maintained healthy appetites, did not experience the typical head tilting and circling, and have not been treated with any antibiotics.

Caprine arthritis encephalitis is a virus to which our closed herd has not been exposed. We ruled out other possible neurologic disorders, including copper deficiency (our goats have free-choice access to a loose trace mineral salt that includes copper), brain abscess (which would likely not affect more than one animal), rabies (extremely rare and results in death within five days), scrapie (usually affects goats age 2 years or older; Amber and Baron were both younger), white muscle disease (a nutritional condition of young kids).

I hasten to point out that we reviewed each possibility more throughly than indicated by the above brief descriptions. A veterinarian could have run tests to rule out all these possibilities, but our county has no vet, and subjecting an ailing goat to a long trailer haul for tests to confirm what we already know seems inhumane.

At any rate, had we transported each sick goat to the nearest vet, the best she could have done toward diagnosing deer worm would have been to take a spinal tap. A possible, but not definite, indication of deer worm infection is cerebrospinal fluid with higher than usual levels of white blood cells (primarily eosinophils, which are disease-fighting white blood cells that attack parasites and can result from inflammation caused by parasites) and protein (due to leakage from damaged blood vessels).

So that leaves us with the final factor — how well affected goats respond to treatment. Candy and Red Baron were both treated with the latest recommended protocol. Candy recovered and shows no lasting signs of infection. Baron is still shaky on his legs, but his condition appears to have stabilized.


More has been written about meningeal deer worm in camelids—llamas and alpacas—than in sheep or goats. Therefore, the treatment protocol recommended for sheep and goats has been derived mainly from studying and treating camelids.

According to the latest best information, as verified by several veterinarians specializing in treating goats, the current recommended treatment for deer worm infection is as follows:

• Fenbendazole (Panacur or Safeguard) given by mouth once a day at the rate of 25 ml per 100 pound body weight for five days, to kill deer worm in the spinal cord

• Vitamin E, given by mouth at the rate of 500 to 1000 units once a day for 14 days, to help restore normal neuromuscular function

• Dexamethasone (a corticosteroid requiring a prescription), given as directed by the prescribing veterinarian, to reduce inflammation in the central nervous system

Since migration of deer worm larvae into the central nervous system causes inflammation, as does the presence of dead larvae killed during treatment, an anti-inflammatory is important to reduce pain and to prevent the animal’s condition from getting worse. However, dexamethasone may induce abortion in pregnant does or ewes. An alternative for pregnant females is the non-steroidal anti-inflammatory prescription drug flunixin (Banamine).

Additional to treatment with drugs, the affected animal may also require physical therapy to help restore muscle function. Therapy might include muscle massages, flexing of the limbs to improve flexibility, encouraging the animal to remain mobile, and making sure it doesn’t rest in one position for long periods. Although our Candy recovered rapidly without physical therapy, Red Baron tends to walk on his knees and must be encouraged to stand and walk normally to exercise his leg muscles.

Despite this recommended regimen, treatment doesn’t always work. Whether or not an infected animal recovers, or survives at all, depends on how many larvae it ingested and the severity of its condition before treatment begins. Success is most likely when treatment is started early in the course of the infection — and an animal that can stand on its own when treatment begins has a much better chance to recover. Once the disease progresses to the point that the animal can no longer stand, it has little chance for survival.

Seriously affected animals may take weeks or months to recover, requiring a great deal of patience and perseverance. Although a survivor may have permanent neurologic issues, it may still remain otherwise healthy and productive.

Because of the long meat withdrawal periods for the drugs involved, with no certainty that the infected animal will improve, treatment is not recommended for meat goats and sheep. Provided a veterinarian has ascertained that the animal’s condition is limited to spinal cord injury and that no other diseases are involved, and the withdrawal period has been observed for any medications used, such animals may be safely slaughtered for home use, according to Mary C. Smith, DVM, at Cornell University’s College of Veterinary Medicine.


At the top of the list of usual suggestions for preventing deer worm infection in goats and sheep is to control both white-tail deer and gastropods. That’s pretty much like asking you to herd cats.

If you feed your local deer, a good starting place is to avoid placing feeders near where goats or sheep graze. A guardian dog may also discourage deer from hanging around.

An often repeated deer-control suggestion is to avoid grazing goats or sheep in pastures adjoining woodland where deer abound. Since our entire farm, like many in our area, is surrounded by deer-infested forest, we don’t have much choice about grazing locations. But where deer favor certain grazing areas over others, an option is to make hay from the fields the deer prefer.

Even if deer don’t graze in the same pasture as goats, they will pass nearby and leave their calling cards. Gastropods don’t respect fences and can easily crawl from a deer grazing area to a goat grazing area.

Suggestions for controlling slugs and snails sometimes include using massive amounts of molluscicides, which are so dangerous their use requires a permit. It’s much safer, and easier, to maintain a flock of poultry— chickens or guinea fowl—along with the goats. We have large flocks of both, which may account for why we haven’t had a deer worm issue until a couple of years ago when our spring and fall weather got wetter and the slugs got more numerous.

Ducks are much better at controlling slugs and snails, but they also like to play in water, which only attracts more gastropods. Because slugs and snails prefer moist areas, keep goats or sheep from grazing in poorly drained pasture, or improve drainage so puddles don’t accumulate. Also keep pastures clear of gastropods’ favorite hiding places, such as stacks of lumber, piles of rocks, and mounds of discarded waste hay.

Slugs and snails may be further discouraged by plowing around the outside  of the pasture fence and by regularly mowing pasture grass to open the land to sunlight’s warm rays. Sunlight and drying will kill larvae clinging to deer pellets, and will also cleanse the pasture of the nasty stomach and intestinal worms that plague goats and sheep. In addition to destroying worm larvae, hot dry weather reduces slug and snail activity.

Guinea Fowl & Goats
Guinea Fowl and other poultry are helpful in controlling slugs and snails in pastures where goats or sheep graze. Photo by Gail

Unfortunately, winter freezing doesn’t much affect deer worm larvae. But cold weather does hinder gastropod activity, and at freezing temperatures they hibernate.

So in areas that experience winter freezes and warm summer dry spells, slugs and snails are most active during spring and fall, when temperatures are mild and the weather tends to be damp. In Tennessee, the periods of greatest gastropod activity are the rainy seasons of early fall and late winter. In Texas the peak season is spring. In states farther north, the peak period is late summer to early fall.

One recommended option for such areas is to remove goats and sheep from pasture when gastropod activity is greatest. For us here in Tennessee, as in much of the Midwest, that would mean keeping the animals off pasture when grazing is optimum. In other words, we’d basically have to keep the herd in a barn or on a dry lot.

So much for minimizing grain rations to keep our goats healthier. And so much for enjoying the benefits of drinking grass-fed milk.

Camelid owners have been controlling meningeal worm by regularly deworming their alpacas and llamas. Where the weather is mild year round, deworming must be done every 4 to 6 weeks. Because deer worm don’t reproduce in animals other than whitetails, they cannot become resistant to dewormers. However, camelids now suffer from large burdens of other parasites that have become resistant to dewormers. The treatment intended to prevent one problem has resulted in an even bigger problem.

Temperate-climate goat and sheep owners are therefore between a rock and a hard place with respect to using dewormers to control deer worm. But those of us who live in areas that enjoy seasonal temperature extremes have an option other than year-around deworming. Since the risk of exposure to deer worm is lowest during prolonged periods of dry heat or deep freezes, we can opt to skip deworming during those periods of low or no slug and snail activity.

For my goats, that means deworming toward the end of winter (January/ February) and again at the end of summer (September/October), adjusting the dates as determined by each year’s temperatures and rainfall. Such a plan does not offer 100% protection against deer worm, but it does help prevent the much worse problem of creating drug resistance in other killer parasites.

As a dewormer, the macrocyclic lactone ivermectin (Ivomec) is considered to be the most effective against deer worm larvae that haven’t yet crossed the bloodbrain barrier (see “Blood-Brain Barrier” below). The late Cliff Monahan, DVM, PhD, of the Ohio State University’s College of Veterinary Medicine, suggested that instead of ivermectin, using a longer-acting macrocyclic lactone would reduce the overall number of treatments, thus delaying or avoiding the development of drug resistance. These long-acting dewormers require a prescription, so should be discussed with your veterinarian.

Since goats and sheep are largely resistant to deer worm, another potential course of action is to cull susceptible individuals from your herd. That would be a difficult choice for those of us with a small herd in which every individual has a name and seems like family. So we are left with these options for reducing the risk of deer worm infection in our goats and sheep:

• Do not actively encourage deer to hang around.

• Keep the pasture environment unfriendly to slugs and snails.

• Deworm following peak seasons for slug and snail activity.

• Know the signs of deer worm infection and begin treatment at the first signs.

Above all, remember these important points: Deer worms do not spread from one goat or sheep to another, and the survivor of a deer worm infection cannot infect other animals in your herd.

Gail Damerow raises Nubian dairy goats in Tennessee’s Upper Cumberland. She is the author of “Raising Milk Goats Successfully” and “Your Goats — A Kid’s Guide.”


Fenbendazole (SafeGuard or Panacur) is the dewormer of choice for deer worm treatment, but a macrocyclic lactone such as ivermectin (Ivomec) is preferred as a preventive to kill worm larvae before they enter the spinal cord. Although ivermectin destroys deer worm larvae better than fenbendazole, it does not penetrate the blood-brain barrier as readily.

The blood-brain barrier is an important factor in the course and treatment of deer worm infection. It consists of a layer of cells separating blood circulating in the body from brain fluid in the central nervous system. The blood-brain barrier performs these important functions:

1. It protects the brain from bacteria and other harmful substances in the blood.

2. It protects the brain from the body’s normal hormones and neurotransmitters.

3. It provides a steady environment that allows the brain to function effectively.

The blood-brain barrier is selectively permeable, meaning it prevents some substances (such as certain drugs, including ivermectin) from entering brain tissue, while allowing other substances (including fenbendazole) to enter freely. Because inflammation makes the blood-brain barrier more permeable than usual, deer worm infection may break down the barrier, thus allowing penetration by ivermectin, a potential toxin to the mammalian nervous system. Therefore fenbendazole is used for treatment, ivermectin for prevention.

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