Adult P. tenuis nematodes reside in the subdural space of the central nervous system and in the associated blood vessels and sinuses.  The life cycle begins when adult females lay their eggs in the venous  vessels and the eggs hatch in the capillaries of the lungs.  First stage larvae (L1) enter the alveolar sacs and are coughed up and swallowed.  L1 larvae leave the host in the mucus covering of fecal pellets, then actively penetrate gastropods residing in the pasture.  The larvae molt twice in their intermediate host.  Accidental ingestion of the snails containing infective L3 larvae continues the life cycle.  L3 larvae leave the gastrointestinal tract of the host and enter the central nervous system in approximately ten days.  Larvae develop in gray matter of the dorsal horn of the spinal cord and migrate to the subdural space 40 days later.   In aberrant hosts, the parasite persists in the parenchyma of the central nervous system instead of  migrating to the subdural space.  Disease is caused by physical trauma to the parenchyma of the  central  nervous system by developing and migrating worms.

White-tailed deer are the natural host of P. tenuis;   however, other wild and domestic ungulates have been identified as aberrant hosts and may develop severe neurologic disease.  In response to infection, clinical signs usually reflect focal, asymmetrical spinal cord lesions and include ataxia, stiffness, muscular  weakness, hypermetria, posterior paresis, paralysis, head tilt, arching neck, circling, blindness, gradual weight loss, depression, seizures, and death.  Clinical signs generally begin in the hind limbs and progress to the front limbs.  The disease may be acute or chronic, with death within days to ataxia that lasts months to years.

Microscopic lesions include scattered foci of hemorrhagic necrosis.  Acute lesions are characterized by focal parenchymal loss with hemorrhage in and around the area of injury.  Most chronic lesions have no

hemorrhage, but varying numbers of large, foamy macrophages, some containing gold pigment  consistent with hemosiderin.  Around some necrotic foci there can be swollen axons.  The microscopic   lesions seen are most compatible with lesions caused by a migrating parasite.

The use of cerebrospinal fluid for diagnosis of P. tenuis infection is valuable, especially since    hematologic abnormalities are often not found with meningeal worm infection  Eosinophilia in the cerebrospinal fluid is a  common, although inconsistent, finding in aberrant hosts..  Leukocytosis and vacuolated     monocytoid cells are often found.  CSF eosinophilic pleocytosis is not always associated with cerebrospinal parelaphostrongylosis, and other parasites can cause eosinophilic meningitis in South American camelids.

The only antemortem test for diagnosing P. tenuis is the Baerman technique, which relies on the detection of L1 larvae in the feces of infected animals by microscopic examination.  Aberrant hosts rarely shed larvae within their feces, thus this test is unreliable even when repeated.  Experimental ELISA-based   antigen-antibody tests in goats and elk have shown promise but this test is not currently available. Additionally, an antigen-capture ELISA has been    developed that can detect antigens of P. tenuis in  cerebrospinal fluid, but this test is not commercially available.

The definitive diagnosis of meningeal worm currently requires demonstration of larval or adult P. tenuis in the brain or spinal cord of an affected animal at necropsy.  Nematodes are identified on the basis of their size and the following features: lateral cord cells broader at the base than at the apex, multinucleated intestinal cells, with no more than two cells per cross section, and  polymyarian coelomyarian musculature. A presumptive diagnosis may be based on clinical signs, exposure, and response to treatment.

Recommendations for the prevention of meningeal worm infections include the exclusion of white-tailed deer from llama and alpaca pastures in endemic areas and clearing thick ground cover to discourage  establishment of snail intermediate hosts.  Prophylactic treatment with ivermectin is more effective against early larval stages because the drug does not cross the blood brain barrier.  Anti-inflammatory drugs are also important for reduction of the inflammation associated with migrating larvae and the subsequent inflammatory response to killed larvae.  Use of anti-inflammatory drugs is especially important to prevent the clinical signs from worsening after treatment.

The prognosis of suspected meningeal worm infection is guarded.  Some clinicians suggest that animals that are only able to stand with support have a much poorer prognosis than those who are able to stand without assistance.  Some animals suffer permanent    neurologic damage but remain otherwise healthy  members of the herd.

Meningeal worm infection may be severely debilitating and potentially fatal, but can be effectively prevented.  Simple steps such as routine deworming every 4-6 weeks, minimizing cohabitation with white-tailed deer, 4-6 weeks, minimizing cohabitation with white-tail deer,

and a clean, dry environment unfavorable for the growth of snails and slugs will considerably reduce the herd's risk of infection with meningeal worm.

-by Abby Durkes, Class of 2008

-edited by Dr. Grant Burcham, ADDL Graduate Student

References:

1. Anderson DE: Parelaphostrongylus tenuis (Meningeal Worm): Infection in Llamas and  Alpacas-Ohio State University.  http://www.vet.ohio-state.edu/378.htm. Accessed  September, 2007.

2. Anderson RC: 1992.  Nematode parasites of     vertebrates: their development and transmission. CAB International, Oxon, United Kingdom.  p. 151-208.

3.  Baumgartner W: 1985.  Parelaphostrongylosis in llamas. JAVMA 185 (11): 1243-1245.

4. Brown T, H Jordan, and C Demorest: 1978.   Cerebrospinal Parelaphostrongylosis in llamas.  Journal of Wildlife Diseases 14(4): 441-444.

5. Duffy MS, TA Greaves, NJ Keppie, and MD Burt: 2002.  Meningeal worm is a long-lived parasitic nematode in white-tailed deer.  Journal of Wildlife Diseases 38:448-452.

6. Leguia G: 1991.  The epidemiology and economic impact of llama parasites.  Parasitology Today 7: 54-56.

7. Nagy, DW: 2004.  Parelaphostrongylus tenuis and other parasitic diseases of the ruminant nervous system.  Veterinary Clinics-Food Animal 20: 393-412.

8. Ogunremi O: 2001.  Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk.  The Canadian Journal of Veterinary Research 66(1): 1-7.

9. Pugh DG: 1995.  clinical parelaphostrongylosis in llamas.  Compendium on Continuing Education for the Practicing Veterinarian 17: 600-606.

10. Welles EG et al: 1994.  Composition of cerebro-spinal fluid in healthy adult llamas.  American  Journal of Veterinary Research 55 (*): 1075-1079.