While parasites are fantastically well-adapted to life in their specific hosts, that usually means they are somewhat lacking in the “living literally anywhere else” department. Thus, when natural selection has nixed the ability to read a map and a parasite finds itself in unfamiliar territory, it is rarely very good at improvising.
Years of co-evolution with their hosts have helped many parasites find a happy medium between harming its host and causing just enough damage to happily feed, reproduce, and spread to a new host. After all, it’s ill-advised to destroy your meal ticket. However, if a parasite finds itself in a host that is not a usual part of its lifecycle – an incidental infection – the usual rules no longer apply.
As a parasite’s attempts to MacGyver its way out of an incidental host to a more familiar one often aren’t pretty, incidental infections can be more severe, or simply more bizarre, than the normal course of infection.
Take, for example, the case of cutaneous larval migrans. Cutaneous larval migrans, also known by the appetizing names “creeping eruption” and “sandworm,” occurs when a human becomes infected with canine hookworm larvae. These parasites have evolved to infect the intestines of dogs and other canids, and so become very confused when they find themselves in a two-legged, hairless ape instead of a loveably dopey quadruped.
Rather than stopping to ask for directions, the now very lost larvae short-circuit and meander in the upper layers of the skin, trying to find their way to the gut. This aimless rambling gives the disease its name – though it uses more SAT words than necessary to say so, “cutaneous larval migrans” just means “worm larvae that wander in the skin.”
The result of the larvae’s migration through the skin is an angry, red, very itchy rash. The little worms actually leave behind tiny, visible trails on the skin in their search for a familiar environment (someone call Kevin Bacon.)
On the bright side, since the parasites are not well-adapted to life in a human host, they cannot complete their life cycle and survive in people. As a result, the larvae die within a few weeks and the rash clears up on its own, though treatment with standard anthelmintic drugs can speed up the process.
Sometimes meeting a familiar host at an unfamiliar time can be equally as disastrous for the parasite and the host.
The pork tapeworm, Taenia solium, is a very common human intestinal worm. If a person eats undercooked pork that is infected with hard, spherical cysticerci – encysted T. solium larvae – the digestive proteins in the intestines propel the worm into the next stage of its lifecycle.
During this stage, the worm latches onto the intestinal lining, feeds itself on the nutrients in its surroundings, and sheds eggs in the feces of their human host. Pigs, who are not particularly known for their discerning palates, become infected upon eating these eggs, completing the worm’s lifecycle.
While not pretty, a normal Taenia infection is not severe; if any symptoms show up at all, the worst of them include indigestion and mild anemia. However, when it comes to parasites, timing is everything. Even a relatively harmless parasite can be thrown for a loop if a host enters the mix at the wrong stage of its lifecycle.
If a human ingests T. solium eggs instead of its larvae, that person effectively takes the place of the pig in the lifecycle. This means that cysticerci form in the tissues of the human instead of the pig.
This isn’t ideal for the parasite; as cannibalism is typically frowned upon in polite society, a human host at this stage of the lifecycle is a dead-end for the worm. As a result, pork tapeworms haven’t had a chance to evolve to become as good at forming cysticerci in humans as they are in pigs.
These misplaced, inexperienced tapeworms have a penchant for forming cysts in brain tissue in people, as opposed to muscle tissue in pigs. The resulting disease – called neurocysticercosis – causes severe neurological problems.
Though neurocysticercosis is preventable through proper sanitation and hygiene practices, the lack of basic sanitation infrastructure and sufficient medical care has allowed this disease to persist as one of the leading causes of epileptic seizures in the developing world.
STRANGER IN A STRANGE LAND
West Nile Virus is an arbovirus of simple tastes – give it a warm environment populated by birds and mosquitoes, and it will be happy to cycle back and forth between those two hosts. It doesn’t feel the need to make life difficult with an overly complex lifecycle like some pathogens (…we’re looking at you, Dicrocoelium dendriticum.)
Sadly, you know what they say about the best-laid plans of mice and Flaviviridae. If a West Nile Virus-infected mosquito takes a blood meal from a human instead of a bird, the virus enters this strange host and finds itself trapped.
Though it passes into this new host easily enough, it cannot reproduce efficiently in it, and so only achieves low levels of virus in the bloodstream. This means that even if another mosquito feeds on one of these incidental hosts, it cannot pick up enough of the virus to become infected.
Despite the fact that West Nile Virus does not replicate well in people, the virus still causes disease in about 20% of infected human hosts. Most people who develop West Nile fever experience mild symptoms that soon resolve themselves, such as headache and fever.
However, in some rare cases the virus causes encephalitis – inflammation of the brain – or meningitis – inflammation of the brain, spinal cord, and surrounding tissues. Encephalitis and meningitis cause serious neurological problems, including paralysis in the limbs or, worse, the muscles needed to breathe.
A PARASITE WITHIN THEE, HAPPIER FAR.
In the end, things rarely go well for a parasite that has been cast out of its intended host and into unfamiliar territory. Whether they end up in the right place at the wrong time, or simply go where they never should have gone in the first place, parasites that have lost their way are far from paradise.