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Moose in Minnesota have been seen exhibiting abnormal behavior and physical disabilities, not caused by injury, since at least 1912. Perhaps the most common and oldest reported observations were of moose walking in endless circles in the snow on frozen lakes. Other sightings often were that of the head tilted and turned to one side, stumbling, poor coordination, leg paralysis, lameness, and lack of fear. This became known as “moose sickness”. I might add that I have seen them running and swimming in circles. Do not get too bold with sick moose; I have seen some that had considerable trouble walking, suddenly regain full coordination. I can assure you sometimes they can be just as dangerous as any other moose. An additional danger is that they are traffic hazards when they spend considerable time on roads. I have known some sick moose to be hit by vehicles and now regret not having the heads of a number of others examined.
Biologists examined many dead moose trying to determine what caused these abnormal actions. In 1964, Canadian biologist Dr. Roy Anderson demonstrated that the causative agent was the meningeal worm (now better known as the brain worm) by infecting two young moose calves with third stage larvae of the parasite. The calves then developed the classic signs exhibited by the sick wild moose. The adult worm is about 1/100 of an inch in diameter and two to three inches long.
The brain worm is a common parasite of white-tailed deer (where it does no harm). However, the parasite causes a debilitating, and often fatal, neurologic disease in moose, caribou, mule deer, elk, pronghorn antelope, bighorn sheep, domestic sheep and goats, and llamas. A number of moose declines have been attributed to this parasite when white-tailed deer populations become too high (once considered to be 12 to 13 deer per square mile, but accuracy of population density estimates from those days are suspect). However, moose declines did not always occur under those conditions. Obviously other factors can play a role. Separation of habitat use by white-tails and moose whether by time of year, predominant vegetation type preference or vegetation age class distribution could be involved in some areas.
The life cycle of this parasite is rather complex. The adult worms are found on, or near, the brain near a venous blood vessel (especially in the sub-dural venous sinuses below the brain). Eggs are deposited in these vessels and carried to the heart, then pumped to the lungs. The eggs hatch into first stage larvae while on the way to the lungs where they pass from the blood stream into the lungs, at the same locations where the blood exchanges carbon dioxide for oxygen.
As larvae accumulate in the lungs, they are brought up to the mouth (much as we “clear our throat”) and are swallowed. They pass through the digestive tract unharmed and are excreted in the mucus covering on the fecal pellets. They then infect a number of terrestrial gastropod (snails and slugs) species which either crawl over the pellets or come in contact with the larvae after they have been washed off the pellets by rain or other means.
While in the gastropods they become second stage and then third stage larvae (this is the infective stage). When a deer (or other suitable host) ingests the infected gastropod while feeding on vegetation, the larvae are freed while in the digestive tract and burrow into the body cavity. They then travel upwards until they encounter a nerve and follow it to the spinal cord. Then they follow the spinal cord to the brain (going through two more larval stages and then becoming adult worms on the way).
Some may feel that depending on snails and slugs to become infected and then for deer to accidentally ingest them to be a rather unreliable way to reproduce. However, this and a number of other closely related parasites use this method and nearly all of the normal host species for each parasite eventually becomes infected. I and Dr. Murray Lankester (parasitologist at Lakehead Univ. in Thunder Bay) conducted a number of studies involving brain worm here in Cook and Lake Counties which yielded some very interesting information that has been published in peer-reviewed scientific journals.
One study looked at the percentage of deer fawns that become infected with the parasite during their first year of life. Overall, 68 percent of fawn heads examined had adult worms in the head. However, it takes time for the larvae to travel to the brain (about 40 days from ingesting the gastropod to the larvae reaching the spinal cord, and additional time to reach the brain). Therefore, some fawns examined in summer and fall may have been infected, but adult worms had not yet reached the brain. Only 43 percent of fawn heads examined in fall had adult worms in the head, 68 percent of those examined during winter, and 79 percent of those examined in spring.
Prevalence of adult worms in the heads of older deer increased with age of the deer. In the age group of 7-to-15 year old deer, 96 percent had worms in the head. Obviously, the vast majority of deer here eventually become infected with the parasite. How many worms did the heads contain? In this study the overall average was 3.2 adult worms per head with a maximum of 13 in one deer. Not all infected deer pass larvae on their pellets. Of 311 heads containing adult worms, 92 (29 percent) had only one sex of the worm and there must be at least one worm of both sexes in order to produce eggs.
Part two will cover the number of larvae on deer pellets, infection of gastropods, their ingestion by deer or other hosts, and immune system responses to infection.
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