Most parasites that I deal with on the farm are your run-of-the-mill roundworms, commonly causing diarrhea and weight loss in cattle and horses, and severe anemia in sheep and goats. However, there’s an insidious threat in the field that goes beyond the usual gastrointestinal upset. This one hits the central nervous system. It’s commonly called the meningeal worm.
Taxonomically speaking, this parasite is called Parelaphostrongylus tenuis (pronounced para-laugh-ah-stron-gilus). The definitive host of this parasite is the white-tailed deer. This means the meningeal worm is supposed to infect the deer; think of the deer as their natural habitat. Adult meningeal worms live in the lining of the brain (called the meninges) and spinal cord of the deer. When this parasite sheds eggs, other animals can become infected through ingestion of the eggs. Sheep, goats, llamas, and alpacas are prone to infection by meningeal worm and are called aberrant hosts.
But let’s back up a second. If the worms are surrounding the brain, how are their eggs making it out to the environment? This is where it gets cool. When the adult female meningeal worm lays eggs, these eggs are washed out of the nervous system via venous circulation. Now in the bloodstream, they get filtered to the lungs where they hatch into larvae. These larvae are then coughed up, swallowed, and then there you go: delivery into the gastrointestinal tract where they get passed in the feces.
OK. The cool stuff isn’t finished just yet. The larvae passed in feces are still too immature; they are not infective to the deer or alpaca or sheep yet. First, snails and slugs, known as intermediate hosts, ingest these tiny larvae. Inside these invertebrates, the larvae continue to develop to a point where they become infective to our farm animals. At this point, if a deer or llama ingests an infected snail or slug, the larvae are ready to migrate from the intermediate host to the definitive (or aberrant) host for completion of the life cycle.
After the snail or slug is ingested — and we’re talking tiny snails and slugs that are accidentally ingested while grazing, not the giant slugs you see on the sidewalk after rain — who’d want to eat those? — the larvae migrate from the digestive system into the spinal canal where they develop into adults and the lifecycle beings again.
When this occurs in a white-tailed deer, there usually aren’t any problems. When this migration into the spinal canal occurs in an aberrant host, the nervous tissue becomes severely inflamed and damaged. This is when we see clinical signs of infection.
The clinical signs of a small ruminant or camelid infected with meningeal worm most often include weakness in the hind limbs that progresses to the front limbs. Affected animals frequently appear uncoordinated or stiff. Since this migration through the nervous system is at the whimsy of the worm, signs and severity of disease vary greatly from one animal to the next. Although the worms commonly destroy spinal tissue, they can also migrate to the brain, potentially causing blindness, change in personality, and seizures.
The course of the disease can vary. Some animals are acutely affected and succumb within days while others are only mildly affected for months.
Frustratingly, there is no test to definitively diagnose meningeal worm infection in a living animal. I say living because the only way to officially diagnose meningeal worm infection is on necropsy, when you observe damage to the spinal cord under the microscope.
Meningeal worm can be a diagnostic challenge because the neurological signs mentioned above can also be indicators of other diseases, such as brain abscesses, bacterial meningitis, certain mineral deficiencies, even rabies. However, usually in the case of a spinal cord infection with meningeal worm, the animal is not running a fever, and still has an appetite. In the field we make what’s called a presumptive diagnosis, begin treatment, and literally hope for the best.
Treatment of meningeal worm infection involves deworming to kill the parasite and supportive treatment to aid in the recovery of the nervous tissue. Here we’re talking about anti-inflammatories and neuro-friendly supplements that help repair oxidative damage like vitamin E and selenium, as well as vitamin B complex and thiamin. Supportive care in the form of physical therapy is also warranted.
The fact of the matter is, though, that nervous tissue, once damaged, does not regenerate. Once damage is done, it’s done. This means that if you’re faced with a badly affected animal, there might not be much you can do and sometimes euthanasia is the most humane option, particularly if the animal cannot walk.
Prevention isn’t a simple option, either. Deer-proofing a pasture sounds good in theory, but difficult in practice. The same with slug- and snail-proofing. Many alpaca owners prophylactically administer dewormer at regular intervals to their herd to kill any potential larvae in the digestive tract that are getting ready to make their break into the central nervous system. However, this gives rise to the concern of the development of antiparasitic resistance, since the same dewormers are used to treat parasites like common roundworms.
So what’s a poor small ruminant or camelid owner to do? Really, education is key. If a farmer knows what signs to look for and can call me out ASAP before severe damage is done, there’s hope.
Dr. Anna O’Brien