(Meningeal Worm)

Description
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.
Distribution
The brainworm is
found in most places in eastern North America where white-tailed deer exist in
abundance. It has been reported from deer in Nova Scotia, New Brunswick,
Ontario, Minnesota, New York, Maine, Pennsylvania, Michigan, Alabama, Arkansas,
Georgia, Kentucky, Louisiana, Maryland, Mississippi, North Carolina, South
Carolina, Tennessee, Virginia, and West Virginia. 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 state. 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 their
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.
Transmission and Development
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.
Clinical Signs and Pathology
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 are similar to those in white-tailed deer, but
much more severe.
Diagnosis
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, a positive diagnosis can be made only by recovering and
identifying the adult worms. In animals which develop clinical signs, worms are
hard to find and diagnosis must often be based only on signs of illness and
microscopic lesions.
Treatment and Control
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.
Significance
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.
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For questions about wildlife diseases, please contact the Michigan DNR Wildlife Disease Laboratory.