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Meningeal worm - deer worm - brain worm

What is it?
The meningeal worm is an internal parasite (Paralaphostrongylus tenius) of the white-tailed deer that usually completes its life cycle in the deer without causing significant problems. However, when unnatural hosts, such as sheep, goats, and camelids become infested with meningeal worm, the parasite moves into the brain and/or spinal cord and causes neurological problems that can be fatal.

Llamas and alpacas seem to be particularly susceptible to meningeal worm infection. Cattle are not known to be affected. While not as common in horses, meningeal worm infection is possible in horses. Meningeal worm is not a health concern to humans.


The life cycle of the meningeal worm requires terrestrial snails or slugs to serve as intermediate hosts. White-tailed deer become infected with P. tenius by eating snails or slugs that contain the infective stage of the larvae. The larvae migrate through the deer's gut and eventually move into the central nervous system where they mature into adults, produce eggs, and the life cycle begins again when they excrete the eggs in their feces. However, when P. tenius-infected snails and slugs are ingested by aberrant hosts, such as small ruminants, the larvae migrate into the brain and/or spinal cord and cause various neurological problems.

In an abnormal host, the larvae do not mature into adults, but rather wander through the central nervous system causing inflammation and swelling which damages sensitive nervous tissue producing a variety of neurologic symptoms. Experimental evidence suggests that it takes approximatley 10 to 14 days for the parasite to reach the brain and/or spinal cord after the animal eats the infected snail or slug.

The neurologic signs observed in infected animals depend upon the number of larvae present in the nervous tissue and the portion of the brain or spinal cord that has been affected. A mild infection may produce a slight limp or weakness in one or more legs, while a more severe infection may cause an animal to be partially or completely paralyzed. When larvae migrate to the brain, they may cause blindness, a head tilt, circling, disinterest in or inability to eat, or other signs that mimic brain diseases.


Affected animals may get progressively worse, remain static, or in some cases improve without therapeutic involvement. In most cases, infected animals remain alert and continue to eat and drink normally.

Meningeal worm infection cannot be diagnosed in the live animal. A fecal examination is not useful since sheep and goats are “dead end” hosts for the parasite and the larvae do not produce eggs or pass larvae into the feces. The parasites cannot be detected by blood testing. The only way to confirm diagnosis is to find the parasite in the nervous system, which requires a necropsy examination. Testing the cerebrospinal fluid, which requires the animal to be tranquilized or anesthetized for extraction, may help to support suspicions of brain worm infection. A definitive diagnosis depends on identifying the parasite in the nervous itissue at the time of necropsy (3).


Thus, diagnosis of meningeal worm in the live animal is based on symptoms and clinical history. Usually animals have been grazing for at least two months and there is a history of deer in the area. Diseases which look similar to meningeal worm infection include: listeriosis, CAE, scrapie, rabies, trauma, copper deficiency, vitamin E/selenium deficiency, spinal cord or brain abscesses, or polioencephalomalacia.

Treatment regimes usually involve high, repetitive doses of anthelmintics, along with steroids, and other supportive therapies. Many different anthelmintics (levamisol, ivermectin, albendazole, fenbendazole, thiabendazole) have been used to treat meningeal worm infection (8). It is believed that some anthelmintics can kill the larvae before it enters the central nervous system, while others may be able to cross the blood-brain barrier and kill the larvae regardless of its location in the body (8). Steroid therapy may have some value in reducing inflammation of nervous tissue (3).

However, it is important to note that no controlled studies have confirmed or refuted the efficacy of different treatment regimes. Nor does treatment repair damaged nervous tissue. Producers who suspect meningeal worm should contact their veterinarian for treament recommendations.

As with other disease conditions, prevention is usually more satisfying than treatment. Unfortunately, the meningeal worm is a hard one to prevent. Reducing deer populations is usually impractical. A single deer can shed thousands of eggs per gram of feces, and the larvae are highly resistant to environmental forces. However if feasible, sheep and goats should not be pastured in areas which receive high deer utilization or removed from these pastures before the weather turns wet and cool. It may be helpful to limit sheep and goat pasturing to fields without contiguous woodlands and to pastures that are on high ground and well-drained.

Controlling the intermediate hosts may be a more effective means of prevention. Sheep and goats can be fenced away from likely snail and slug habitats: ponds, swamps, wetlands, low-lying, poorly-drained fields, and woodlands. Some veterinarians advocate strategic deworming as a means of preventing infection. However, it is important to realize that regular use of anthelmintics (e.g. monthly treatments) rapidly leads to anthelmintic resistance, so while regular treatments may help to control the meningeal worm, eventually those drugs will lose their efficacy against ordinary stomach worms, which may be an even greater problem on most sheep and goat farms.

This article was originally written in 2004 by Susan Schoenian.

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