"Brain Worm" (Meningeal Worm) Infestation in Llamas and Alpacas
(March 21, 2013 Knoxville, TN)
David E Anderson, DVM, MS, DACVS
Department of Large Animal Clinical Sciences
College of Veterinary Medicine
University of Tennessee
The meningeal worm (Parelaphostrongylus tenuis), also known as the deer worm or meningeal deer worm, frequently infects llamas and alpacas. Aberrant migration of the meningeal worm 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 whitetailed deer (Odocoileus virginianus) prevalent throughout much of eastern North America.1 Adult meningeal worms reside in the meninges of whitetailed deer and rarely cause clinical signs of disease.1,2
Adult worms lay eggs in the meninges of whitetailed deer. The eggs then pass into the venous circulation and travel to the lungs where they hatch into firststage 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 34 weeks.13 Infected snails or slugs are then ingested by susceptible aberrant hosts such as llamas, alpacas, goats, sheep, moose, wapiti, caribou, blacktailed deer, and red deer1, and the L3 are released in the digestive tract. Infective third stage larvae migrate to the spinal cord and continue to migrate aimlessly within the central nervous system causing neurologic disease.13
In the definitive host, the whitetailed 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 2030 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 8292 days.2,4
Many snails and slugs prefer a moist or wet environment for survival. Consequently, lowlying 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 shortlived 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 dryheat or deep freezes.
Once the aberrant host is infected, clinical disease begins 4553 days later as demonstrated by experimental inoculation. 4 Clinical 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,1,2 muscular 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,2 apparent 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 whitetailed deer.2,9 However, in many areas of the United States, it is not feasible to separate the two populations.
Tools to minimizing risk and minimize use of drugs:
- Placing a deerproof 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.
- 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.
- Thick ground cover can be removed to expose the environment to fluctuations in temperature, and vegetationfree buffer zones (i.e. gravel, limestone) can be placed around fence lines to reduce migration of snails and slugs into the pasture.
- 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 can not be used in heavy amounts or frequently without creating a build-up 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.
- The slugs and snail that transmit meningeal worm larvae include a large array of arboreal slugs not aquatics. Thus, pastures with leaf piles, etc are equally at risk as pasture with ponds or streams.
- 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 Sept-Dec 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 by administration of ivermectin (0.3 mg/kg) every 30 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 in llamas and alpacas.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 are studying the use of a vaccine developed against meningeal worm. Hopefully this will enable us to protect the animals, but limit use of drugs such as ivermectin. The constant use of ivermectin over the past 20 years is leading to build up of extremely dangerous intestinal parasites in herds and will eventually be more dangerous that meningeal worms.
1. Fowler, ME: Medicine and Surgery of South American Camelids. Ames, Iowa:Iowa State University Press 161162; 1989.
2. Pugh, DG et al: Clinical parelaphostrongylosis in llamas. Compendium on Cont. Ed. for Pract. Vet. 17:600606;1995.
3. Smith, MC et al: Goat Medicine. Philadelphia:Lea & Febiger 150; 1994.
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 25:390402; 1994.
5. Foreyt, WI et al: Experimental infections of two llamas with the meningeal worm (Parelaphostrongylus tenuis ). J Zoo Wildl Med 23:339344;1991.
6. Baumgartner, W et al: Parelaphostrongylosis in llamas. J Am Vet Med Assoc 187:12431245;1985.
7. Welles, EG et al: Composition of cerebrospinal fluid in healthy adult llamas. Am J Vet Res 55:10751079;1994.
8. Dew, TL et al: Parasitespecific immunoglobulin in the serum and cerebrospinal fluid of whitetailed deer (Odocoileus virginianus) and goats (Capra hircus) with experimentally induced parelaphostrongylosis. J Zoo Wildl Med 23:281287;1992.
9. Rickard, LG. Parasites. Vet Clin North Am Food Anim Pract 10:239247;1994.
10. MacDiarmid, SC. Clinical pharmacology of the female reproductive tract: manipulation of parturition, its sequeslae and infections. Clinical Pharmacology and Therapeutics Proceedings 71:21-45;1984.
11. Kopcha, M et al: Cerebrospinal nematodiasis in a goat herd. J Am Vet Med Assoc 194:14391442;1989.
Posted: 03-21-13 Viewed: 33806 times
Media RelationsSandra Harbison
College of Veterinary Medicine
University of Tennessee
2407 River Drive
Knoxville, TN 37996