Evolution 101: Host-Parasite Interactions: Of Mice and Cheese and Men and Zombies

This week’s Evolution 101 Post is by MSU graduate student Alita Burmeister.

Hollywood loves a good parasite story—from zombies and vampires to Alien and Star Trek II — nothing creeps audiences out like a parasitic infection that controls its host’s actions.  Though notorious in sci-fi films, the parasite control strategy is not unknown in the natural world. For example, the parasite Toxoplasma gondii infects both rats and cats, but it can only reproduce within cats. While we know that normal rats avoid cats, T. gondii-infected rats seem drawn to the scent of cat urine. The parasite manipulates its rodent host by reversing the normal aversion to cat scent, thereby increasing the chances of its host being eaten, and consequently, its own reproductive success in the belly of Felix.

Mind-control is not a defining characteristic of a parasite, which is simply an organism that lives in or on a host, deriving benefit at the host’s expense. But like in the movies, the most abundant earthling parasites do indeed replicate by controlling their hosts. These parasites are the bacteriophage. Bacteriophage (“phage” for short) are predators-and-parasites in one that live off of their single celled bacterial hosts. Like other viruses, phages are simple critters—a small genome surrounded by a bit of protein—and reproduce only within a host cell.

Phage parasitize bacteria by binding to the outside of a host cell and injecting their genomes. Once inside the cell, the phage DNA goes to work, co-opting the host machinery and reprogramming the cell into a phage assembly line. If it is unable to stop the infection, the bacterial host cell does the work to replicate the phage—the cell provides building blocks, energy, and a protected environment. The cell replicates the phage genome, turning one copy into a hundred copies. The cell replicates the body of the phage, again producing hundreds of copies. And in a last, self-defeating step, the cell’s own machinery stamps out a protein that eats the cell from the inside-out. The cell dies in a burst of a hundred new infectious phage. Take that, Shark Week. (For more, Radiolab’s lively telling of marine phage cycling is worth a listen.)

The cutthroat simplicity of lytic phage infection makes it a great way to study how interacting hosts and parasites evolve. When bacteria and phage are grown together in the lab, the bacterial population evolves resistance to phage infection, and the phage population evolves new infection mechanisms. This process is an example of coevolution— an interaction in which one organism’s evolution responds to another organism’s evolution. The evolutionary interactions of hosts and parasites are part of a general class of interactions called exploiter-victim interactions, which also includes interactions between predators and prey.

Outside of the lab, we see the implications of hosts and parasites in health, agriculture, and industry. A quirky example comes from Wisconsin, where the (un)official State Microbe is Lactococcus lactis—the bacterium that makes cheese. L. lactis produces an acid that turns white gold into curds and whey and produces cheddar’s distinctive flavor. However, when bacteriophage hang out in cheese factories, reproducing as they kill L. lactis, the cheesemaking process is disrupted. The dairy industry has developed a small arsenal of approaches to deal with phage, saving cheesemakers money and strife. 

Many parasites, however, are not so easy to defeat. The World Health Organization estimates that the parasitic disease malaria caused 665,000 deaths in 2010. The number of people killed by malaria each year would fill Spartan Stadium eight times over.

Malaria presents a double evolutionary challenge. Plasmodium falciparum—the malaria-causing parasite—is evolving resistance to anti-malarial drugs including artemisinin. Artemisinin-based combination therapies (ACTs) are the first-line of defense against malaria, but resistance to artemisinin has already been observed in four countries—all since 2009—making drug resistance an emergent threat to eradication efforts. Another major evolutionary challenge is the emergence of insecticide resistance in mosquito populations. Mosquitoes are the primary way malaria spreads from person to person, and with forty-five countries reporting insecticide resistance, this problem is even more widespread than artemisinin resistance.

Malaria demonstrates a general problem encountered in fighting diseases. The effectiveness of vaccines and drugs can change as their targets evolve. However, an understanding of the evolutionary processes that shape a disease will help us devise prevention and treatment strategies.  That’s good news for us, bad news for the zombies.

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