This fact sheet was published 11/8/2020.
This fact sheet was published 11/8/2020.
Parelaphostrongylus tenuis, commonly known as brain worm, is a nematode (roundworm) parasite of several species of hooved mammals, both wild and domesticated. The white-tail deer is the definitive or natural host. The long, threadlike worms can be found in spaces and veins surrounding the brain. Adult male worms are greenish-yellow to brown in color and up to 6.2 cm (2.4 in) long and 0.2 mm (0.008 in) wide. Females are darker brown to red to black in color and up to 9 cm (3.5 in) long and 0.25 wide (0.01 in).
P. tenuis is common in white-tailed deer in eastern North America; around 80% of the population are estimated to be infected. The brain worm rarely causes illness in this species but, white-tailed deer can introduce the parasite to other susceptible species such as moose, elk, and caribou, in which it can cause deadly disease.
The brain worm seems to play a significant role in preventing the establishment of mule, elk, and caribou populations in areas with high densities of white-tailed deer. P. tenuis may have contributed to the decline of moose in some areas of the United States and Canada because of increased interactions with white-tailed deer. P.tenius infections have also been implicated in the failure of several elk restoration attempts in eastern United States.
White-tailed deer can also introduce the parasite to livestock such as sheep, goats, alpacas, and llamas. Humans cannot become infected with this worm, and properly cooked meat of infected animals is safe to eat.
White-tailed deer are the normal definitive host for this brain worm. P. tenuis can also infect moose, black-tailed deer, elk, caribou, mule deer, fallow deer, bighorn sheep, pronghorns, domestic sheep, goats, llamas, alpacas, camels, guinea pigs, and rarely, domestic cattle and horses. These are all aberrant or dead-end hosts of P. tenius.
Compared to caribou and moose, elk are more tolerant of P.tenuis.
P. tenuis is common in white-tailed deer populations throughout eastern North America. It is rare in the Southeastern United States and is not known to occur in western North America.
The life cycle of the brain worm is indirect and requires both a definitive host, the white tail deer, and an intermediate host, a snail or slug. It typically takes 82-137 days before clinical signs of P. tenuis are evident in the host after infection.
Adult worms inhabit veins and venous sinuses on the surface of the brain in white-tailed deer. Females lay eggs that develop into first stage larvae (L1), which migrate through the bloodstream and become lodged in the small capillaries of the lungs. L1’s then move into the air space of the lungs. From the lungs, the larvae are coughed up and swallowed. The L1s move through the digestive tract unchanged and are passed in the feces. The larvae must then penetrate the intermediate host, snail or slug, or be eaten by it, in order to develop into second (L2) and third (L3) stage larvae. L3’s infect new white-tailed deer hosts when the slug or snail is accidentally consumed along with vegetation. Once ingested, the L3’s penetrate the stomach or intestinal wall and migrate through the body cavity to the spinal cord and to the brain. During this final migration to the brain, the larvae develop into adult worms. Most white-tailed deer become infected during the first or second summer of life. Some deer are infected with only male or only female worms, so they do not shed larvae. Worms acquired by fawns likely stay with the deer for life, but deer probably do not acquire any more worms after the initial infection. While brain worms can infect many species, larvae are generally only produced and released in the feces of white-tailed deer, and occasionally moose and elk. In other aberrant hosts, the larvae often die when migrating through nervous tissue before reaching the brain and maturing into reproductive adults.
White-tailed deer typically do not show clinical signs of P. tenuis infection. When deer are infected with a large burden of worms, temporary swelling of the forelimbs and lameness (especially in fawns), circling, or other neurological signs may be observed.
When non-definitive hosts such as moose and elk are infected they may exhibit severe neurological signs such as weakness, loss of coordination, head tilt, apparent blindness, circling, loss of fear, depression, weight loss, progressive loss of function, and death. These clinical signs, which usually begin 30-60 days after infection, are due to tissue destruction and inflammation caused by the migrating larvae.
On post-mortem examination, gross lesions are often obscure or absent but are restricted to the central nervous system. Many affected animals have lesions that are only visible microscopically.
Definitive diagnosis in white tailed deer can be reached by recovering and identifying adult P. tenuis worms. Finding larvae on fecal examination using a modified Baermann’s technique is not sufficient because these larvae are identical to the muscle worm (P. andersoni) larvae. The suspected larvae must be confirmed by PCR.
Currently, a serological ELISA test has recently been developed for rapid screening of live cervids for P. tenuis infection.
In aberrant host species, P. tenuis infections can only be diagnosed post-mortem by identification of adult worms in the nervous system.
Clinical disease in wild species are typically observed when the disease is advanced so treatment and prevention is not feasible for free-ranging wild populations.
This disease can be controlled by reducing white-tailed deer populations in regions where they share habitat with susceptible species. White-tailed deer can be prevented from interacting with susceptible captive animals (building fences or other barriers), and snails as well as slugs should be kept out of enclosures (controlling drainage etc.). It is important that wildlife managers work to prevent the spread of P. tenuis into western North America by ensuring that infected animals are not translocated or introduced.