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Meningeal Worms

The meningeal worm (Parelaphostrongylus tenuis)

represents a significantly different problem to llamas. Also known as the deer worm or meningeal deer worm, it frequently infects llamas and alpacas. These worm larvae are passed through the feces of deer (natural reservoir), are consumed by snails, and then are consumed by llamas and alpacas. Llamas are not the normal host for these worms and they perform “aberrant migration.” Aberrant migration of the meningeal worm to the spinal cord in susceptible hosts such as llamas and alpacas causes damage to the central nervous system and may result in death.

Identification and Life Cycle

The meningeal worm is a nematode parasite belonging to the family Protostrongylidae. The definitive host is the white-tailed deer (Odocoileus virginianus) prevalent throughout much of eastern North America.1 Adult meningeal worms reside in the meninges of white-tailed deer and rarely cause clinical signs of disease.1,2

Adult worms lay eggs in the meninges of white-tailed deer. The eggs then pass into the venous circulation and travel to the lungs where they hatch into first-stage larvae (L1). The L1 are coughed up, swallowed, and passed in the feces of infected deer. Larvae then invade or are ingested by snails or slugs (terrestrial gastropods). Snails and slugs serve as intermediate hosts in which the first stage larvae develop into infective third stage larvae (L3) over a period of 3 to 4 weeks.1-3

Infected snails or slugs are then ingested by susceptible aberrant hosts such as llamas, alpacas, goats, sheep, moose, wapiti, caribou, black-tailed deer, and red deer1 , and the L3 are released in the digestive tract. Infective L3 migrate to the spinal cord and continue to migrate aimlessly within the central nervous system causing neurologic disease.1-3

In the definitive host, the white-tailed deer, the infected snails or slugs are ingested and the L3 are released in the abomasum. The L3 then migrate to the spinal cord via the spinal nerves over the next 10 days. The larvae mature in the dorsal horns of the gray matter of the spinal cord for 20 to 30 days. Adult meningeal worms migrate to the subdural space, then to the brain through the dura mater and cranial venous sinuses.2 The prepatent period in deer is 82 to 92 days.2,4

Many snails and slugs prefer a moist or wet environment for survival. Consequently, low-lying and wet, poorly drained fields provide an increased risk of exposure to snails and slugs.3 However, exposure risk is not limited to wet climates since dry-land snails and slugs may serve as intermediate hosts. Snails and slugs feed on organic matter, leaf litter, and vegetation. Survival of L3 outside the intermediate host is believed to be short-lived unless water is available. Repeated freezing or desiccation has been shown to decrease survival of the infective L3.2 Therefore, the risk of exposure to llamas and alpacas is lowest when there are prolonged periods of dry heat or deep freezes.


Clinical Disease

Once the aberrant host is infected, clinical disease begins 45 to 53 days later as demonstrated by experimental inoculation.4Clinical neurologic disease is the result of tissue destruction and inflammation caused by randomly migrating larvae. Thus, the clinical signs observed depend upon the location of the migrating larvae.3

Most commonly, clinical signs reflect asymmetrical, focal spinal cord lesions.4 These include hypermetria, 2,5 ataxia,1,2,5,6 stiffness, 1,2muscular weakness,2,5,6 posterior paresis, 2,6 paralysis, 1,2 head tilt,2 arching neck,2 circling, 1,2 blindness, 1,2 gradual weight loss,2apparent depression, seizures, and death.2 Clinical signs generally begin in the hind limbs and progress to the front limbs. 2,4 The course of disease may be acute to chronic, ranging from death within days to ataxia which lasts months to years.2 In our experience, clinical sings of meningeal worm infection are exacerbated during summer months because heat stress develops with prolonged periods of recumbency.



Prevention of meningeal worm infection may be difficult. Ideally, llamas should not graze the same pasture as white-tailed deer. 2,9However, in many areas of the United States, it is not feasible to separate the two populations. Fencing deer out of the pasture is not enough and chemicals to kill snails cause environmental residues that may be harmful and are of limited efficacy. Therefore, most prevention against meningeal worm larval infection is aimed at killing the larvae during their migration, but prior to entry into the spinal cord. This requires a deworming frequency of at least every 4 to 6 weeks at least during the high risk periods of the year (e.g., April-May through November-December in Ohio). The most efficacious anthelmintic for protection against meningeal worm has been ivermectin (1.5 to 2 cc of 1% ivermectin per 100 pounds body weight, injected under the skin, every 4 weeks).


Tools to Minimizing Risk and Minimize Use of Drugs:

1. Placing a deer-proof fence may offer some protection, but many fences do not present a sufficient barrier to prevent movement of deer. A true “deer proof” fence is 12 feet high and of woven wire – not high tensile fencing.

2. Eliminate organic matter. Snails and slugs prefer dark, damp areas. Thus, these pests will accumulate around leaves, buildings, wood piles, compost, etc. Keep areas around pasture and barns clear.

3. Thick ground cover can be removed to expose the environment to fluctuations in temperature, and vegetation-free buffer zones (i.e., gravel, limestone) can be placed around fence lines to reduce migration of snails and slugs into the pasture.

4. Fowl (e.g., Guinea hens) may be used to help decrease pasture contamination with snails and slugs. Molluscicides may be considered to destroy snails and slugs which serve as intermediate hosts, thereby interrupting the life cycle of the meningeal worm and preventing infection in aberrant hosts. However, molluscicides cannot be used in heavy amounts or frequently without creating a buildup of toxins in the environment. Drainage should be established in low lying areas and access to swampy areas may be restricted by fencing off these areas. These compounds present a potential environmental risk from contamination of ground water and may be toxic if consumed by camelids or other animals.

5. The slugs and snail that transmit meningeal worm larvae include a large array of arboreal slugs – not aquatics. Thus, pastures with leaf piles and so forth are equally at risk as pasture with ponds or streams.

6. Geography: If you live in an area where hard freezes (Ohio from Dec–March) and dry summers are severe, transmission is at a minimal risk during those periods. In spring, slug and snail contamination is minimal as the “over wintering” is harsh. In these geographic areas, more than 85% of transmission occurs during September through December and we can selectively target long-acting avermectin drug prevention during those times. In geographic areas of high deer density and established meningeal worm in the populations, these seasonal effects are unlikely to be relevant.


Using Drugs to Plug the Holes

Based on 30 years of field experiences and our clinical and pharmacologic research, prophylactic treatment against migrating larvae may be achieved administration of ivermectin (0.2 mg/kg) every 30 days or doramectin (0.3 mg/kg) every 45 days during the high-risk periods or throughout the year in regions which have mild summers and winters. Anthelmintic resistance is unlikely to become a problem in the meningeal worm because these infections do not become patent.However, meningeal worm infection has occurred in some herds that maintain vigilant prophylaxis. These "breaks" in prevention of the larval migration may have been caused by insufficient dosing of anthelmintic, accidental failure to administer the anthelmintic, or extremely high environmental contamination. Employing environmental management tools will reduce risk and help maintain a healthy meningeal worm free herd.


On the Horizon

Researchers at Cornell University are studying the use of a vaccine developed against meningeal worm. Hopefully this will enable us to protect animals, but limit use of drugs such as ivermectin. The constant use of ivermectin over the past 20 years is leading to buildup of extremely dangerous intestinal parasites in herds and will eventually be more dangerous that the meningeal worms themselves. An effective vaccine may give protection and peace of mind!


1. Fowler ME. Medicine and Surgery of South American Camelids. Ames, IA: Iowa State University Press, 1989, pp 161-162.

2. Pugh DG et al. Clinical parelaphostrongylosis in llamas. Compendium Contin Educ Pract Vet. 1995; 17:600-606.

3. Smith MC et al. Goat Medicine. Philadelphia: Lea & Febiger, 1994, p 150.

4. Rickard LG et al. Experimentally induced meningeal worm (Parelaphostrongylus tenuis) infection in the llama (Lama glama): Clinical evaluation and implications for parasite translocation. J Zoo Wildl Med. 1994;25:390-402.

5. Foreyt WI et al. Experimental infections of two llamas with the meningeal worm (Parelaphostrongylus tenuis). J Zoo Wildl Med. 1991;23:339-344.

6. Baumgartner W et al. Parelaphostrongylosis in llamas. JAVMA. 1985;187:1243-1245.

7. Welles EG et al. Composition of cerebrospinal fluid in healthy adult llamas. Am J Vet Res. 1994;55:1075-1079.

8. Dew TL et al. Parasite-specific immunoglobulin in the serum and cerebrospinal fluid of white-tailed deer (Odocoileus virginianus) and goats (Capra hircus) with experimentally induced parelophostrongylosis. J Zoo Wildl Med 1992; 23:281-287.

9. Rickard LG. Parasites. Vet Clin North Am Food Anim Pract. 1994;10:239-247.

10. MacDiarmid SC. Clinical pharmacology of the female reproductive tract: manipulation of parturition, its sequeslae and infections. Clinical Pharmacology and Therapeutics Proceedings. 1984;71:21-45.

11. Kopcha, M et al: Cerebrospinal nematodiasis in a goat herd. JAVMA. 1989;194:1439-1442.

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