Treatment, Diagnosis, and Prevention of Parelaphostrongylus tenuis Infection in Elk

Parelaphostrongylus tenuis Treatment

Parelaphostrongylus tenuis (brain worm) is common in white-tailed deer and occasionally causes disease in moose, caribou, mule deer, bighorn sheep, goats, llamas, and domestic sheep. This parasite has contributed to moose population declines in areas of high deer densities.

Elk do not consistently excrete nematode larvae in feces, making field diagnosis of a brain-worm infection difficult. ELISA testing using excretory-secretory (ES) products of L3 and somatic antigens of adult worms provides diagnostic options.


Although natural infections are asymptomatic in white-tailed deer, P. tenuis migrates more extensively in the central nervous system of incidental definitive hosts, such as elk and domestic ungulates, causing severe, disabling neurologic disease that can cause death. Anthelmintic drugs do not cure the disease because the drugs cannot get to high enough levels in the nervous system.

The current method of diagnosing field-infected elk requires demonstration of larval Parelaphostrongylus tenuis in the feces at necropsy. A serologic diagnosis would be more useful but currently requires a reliable test to detect anti-P. tenuis antibodies. To develop such a test, we used ES products and somatic antigens from adult P. tenuis in ELISAs with sera from elk experimentally infected with 6, 20, or 30 infective L3 larvae of P. tenuis, judiciously chosen to mimic the conditions of natural infections. We found that the ES product Pt-API-1 is specifically recognized by antibody from infected elk. The presence of this inhibitor in ES products and sonicated adult worms suggests that this life stage secretes the enzyme for interaction with the host.


The normal definitive host of Parelaphostrongylus tenuis is white-tailed deer, and infection normally causes a subclinical neurologic disease in these animals. However, other wild and ranched cervids, such as moose, wapiti (elk), caribou, reindeer, black-tailed deer, mule deer, fallow deer, antelope, bighorn sheep, stag, grizzly bears, llamas, alpacas, and domestic goats, can become aberrant hosts and develop severe neurologic disease that leads to paralysis and death.

Once a nematode reaches the adult stage, it becomes infective and is shed in the slime trail by the host. Once ingested, infective larvae migrate through the spinal cord and into the brain where they cause cerebrospinal nematodiasis, or “brain worm disease.” Unfortunately, diagnostic methods for P. tenuis are limited to a Baermann method and recovery of dorsal-spined larvae in feces, which is challenging for elk because of the low number of larvae excreted, intermittent shedding of larvae, and difficulty distinguishing them from muscle worm (P. andersoni) larvae (9). There are also barriers that prevent anthelminthics, such as ivermectin, from reaching high drug levels within the nervous system (10). Nonetheless, recent research suggests that this treatment may be possible for P. tenuis in elk (12).


There are lots of barriers to substances getting into and staying in the nervous system. This evolved as a protective mechanism, but it makes it difficult to treat infections caused by nematodes like P. tenuis.

The only definitive diagnosis is demonstration of larval or adult worms at necropsy. This is challenging as only a few cross sections are required for identification. However, a recent study has shown that a peptide from the aspartyl protease inhibitor of the infective L3 stage of P. tenuis (Pt-API-1) shares 19% identity with a peptide from the aspartyl protein of A. suum and that the peptide is detectable in excretory-secretory (ES) products from P. tenuis-infected white-tailed deer.

The nematode enters the central nervous system (CNS) of white-tailed deer by ingestion of the intermediate host, terrestrial gastropods such as snails and slugs, which ingest live L1 larvae in feces. After maturing to the infective L3 stage, these worms migrate through the intestinal tract and intestine to arachnids and then to the peripheral nervous system. Symptoms of neuroangiostrongylosis vary depending on the site within the CNS where migration occurs; common symptoms include weakness, loss of coordination, head tilt, circling and inability to stand.


Elk are atypical hosts for P. tenuis, which usually causes a neurologic disease that is fatal in cervids and other wild and domestic ungulates. This disease is characterized by focal, asymmetrical spinal cord lesions that result in ataxia, muscle weakness, head tilt, arching of the neck, circling, trembling and other twitching movements, paralysis, loss of the use of the front limbs, difficulty breathing, depression, weight loss, emaciation, seizures and death.

Currently, the only available antemortem test for P. tenuis infection relies on the detection of larvae in feces by microscopic examination. However, elk excrete few larvae and intermittently shed them in their feces; thus the sensitivity of the Baermann technique is low even when tested twice weekly.

Vaccination of red deer with Pt-API-1 produced robust serum antibodies against crude L3 antigens and inhibited neurologic disease in experimentally infected animals. The strong response to immunization and the presence of antibodies in atypical hosts prior to onset of neurologic disease suggest that a serologic test for P. tenuis could be useful in atypical host management programs.

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