Department of Natural Resources
The adult brainworm (Parelaphostrongylus tenuis) is a roundworm or nematode normally found in the venous sinuses and subdural space of the brain of white-tailed deer in eastern North America. Moose, wapiti (elk), caribou, reindeer, mule deer, black-tailed deer, sheep, goats, and guinea pigs are susceptible to infection. However, they are abnormal hosts, and in them the worm frequently causes cerebrospinal nematodiasis, a disease of the nervous system, often resulting in death.
Brainworm is found in most places in eastern North America where white-tailed deer exist in abundance. It has been reported from deer in several states and provinces. It is generally absent, however, in deer from the coastal plains of the southeastern United States (coastal North Carolina, South Carolina, southern Georgia, Florida and southern Alabama) and St. Croix of the Virgin Islands. The incidence in deer herds can be extremely high.
Naturally occurring cerebrospinal nematodiasis is found fairly often in moose on the southern fringe of its distribution in eastern and central North America where white-tailed deer are abundant (Nova Scotia, New Brunswick, Quebec, Ontario, Maine, Minnesota and Michigan). It also occurs in elk (wapiti), caribou and reindeer introduced into areas in eastern North America where there are white-tailed deer.
In Michigan, brainworm is a very common parasite in white-tailed deer. The disease has been diagnosed in elk throughout their range in the northern portion of the Lower Peninsula. It was first noticed in 1938; since then, a few affected animals have been seen nearly every year. Males and females seem to be involved in equal proportions and approximately 80 percent of affected animals are subadults. It has not been diagnosed in calves.
Brainworm has been diagnosed in moose in Michigan since their reintroduction in 1985. It has been found in adult and subadult age groups, but not in calves.
The adult worm living in the subdural space of the brain, deposits eggs on the dura mater surrounding the brain, or in adjacent small blood vessels. The eggs hatch on the dura mater and young larvae emerge. The larvae penetrate small blood vessels and are swept into the lungs. Eggs deposited in blood vessels are carried directly to the lungs where they lodge in the smallest capillaries. The eggs hatch and young larvae emerge. Once larvae are in the lungs, they enter bronchioles and move up the respiratory tract until they reach the throat. They are swallowed and carried through the gastrointestinal tract, and eventually leave the deer in the mucus coat surrounding the fecal pellets. The mucus is fed upon by numerous species of snails or slugs and the mollusks thereby become infected. Species of gastropods that can be infected are Anguispira alternata, Arion circumscriptus, Discus cronkhitei, Deroceras laeve, D. reticulatum, Haplotrema concavum, Mesodon thyroidus, Stenotrema fraternum, Triodopsis albolabris, T. notata, Zonitoides arboreus, and Z. nitidus. The most likely species to be infected are D. laeve, Z. nitidus, and Z. arboreus. After a period of development, the larvae become infective for deer. An infected snail or slug is ingested by a deer, probably accidentally, while browsing or grazing. The tiny larvae penetrate the wall of the small intestine and enter the body cavity. From there, they migrate along nerves to the spinal cord. Once in the spinal cord, they begin to grow. They remain there only a short time before they migrate to the space surrounding the cord. They then migrate along the outside of the cord to the subdural space surrounding the brain. Here they grow to maturity, thus completing their life cycle. From the time a deer is infected, 82-91 days are required before the worm matures and larvae start appearing in the feces.
The infection is largely silent in white-tailed deer, although temporary lameness and spasms of one front limb have been noted in fawns which were experimentally infected. There have been a few reports of neurologic signs in naturally infected adult white-tailed deer.
In naturally infected elk, an individual tends to leave its herd and remains near a road, field, or woodland clearing, and becomes less wary. In some instances, vision seems impaired. In advanced cases, the animal often walks aimlessly or in circles, and may carry its head in a tilted position. The disease is generally progressive and terminates in death, although there may be short periods of remission when the animal appears quite normal.
Severe neurologic disease terminating in paralysis has been produced experimentally in the young of moose, elk, mule deer, caribou, black-tailed deer, goats, sheep, and guinea pigs, all of which may be regarded as unfavorable hosts. Signs of illness in these animals consisted of ataxia, lameness, stiffness, general and lumbar weakness, circling associated with blindness, abnormal positioning of the head and neck, and finally, paraplegia. Signs were variable in onset and character. Moose, elk and mule deer
appeared listless and showed slight ataxia 10-60 days after infection. Signs appeared 5-7 days after infection in young caribou. In all the experimental cases, there were remissions of a short duration.
The lack of lesions is consistent with the absence or slightness of neurologic signs in infected deer. The neural parenchyma rather quickly assumes a normal appearance after the departure of worms, between 25 and 40 days. Lesions in the central nervous system are usually not visible grossly. In general, the lesions in elk, moose, caribou, and other abnormal hosts consists of cellular responses consistent with a migration of a parasite through the brain tissue.
In deer, a tentative diagnosis can usually be made by finding larvae in the feces of infected animals. However, muscle worm (P. andersoni) larvae are indistinguishable from those of the brainworm. Therefore, in deer, a positive diagnosis can be made only by recovering and identifying the adult worms. In animals which develop clinical signs, worms are oftentimes difficult to find and diagnosis must often be based only on signs of illness and histopathological lesions.
Control of deer populations is obviously desirable, especially in areas where priority should be given to moose, elk or caribou. Control of mollusk populations is probably neither feasible nor desirable. Medical treatment of infected animals has not been reported.
It has been suggested, but not proven, that cerebrospinal nematodiasis caused by P. tenuis is responsible for the decline of moose in some areas of the United States and Canada and is a major factor preventing the establishment of moose, elk and caribou in areas where white-tailed deer are abundant. The worm is of no public health significance since it is not infective to humans, and meat of infected animals is safe for human consumption. The parasite may be of some importance to veterinarians since sheep and goats are susceptible.