Ghost Plant


Ghost Plant

Monotropa uniflora, or ghost plant, does not photosynthesize. Instead, it steals sugars and other compounds from fungi (mycorrhizae) in the soil. It’s a parasitic plant – like mistletoe, but the methods of parasitism are different in the two plants. (I took this picture from Wikipedia; sadly, I don’t have my own)


Transmission and Disease

When people ask me about my research interests, I generally tell them “Disease Ecology,” because I feel that that term will be more familiar than “Parasite Ecology.” But the two terms are different. For example, a person could have dementia, inflammatory bowel syndrome, atherosclerosis, or diabetes – just to name a few – and not have any parasites. But each is considered a disease. Disease is just a general term for a disorder; it does not tell us about the cause. Disease ecology, then, broadly refers to the study of these various disorders and their distinct causes. Parasite ecology, on the other hand, specifically entails the study of parasites, which may or may not cause disease.

Speaking of which, when I think of parasites, disturbing images of dramatic symptoms come to mind (like Elephantiasis). But as I said, parasites may or may not cause systems, i.e., disease, in their hosts. Why is that? Many possible reasons exist, and most of them are still being elucidated. For now, I think I’ll focus on just one: transmission intensity.

Transmission intensity refers to the extent of parasite transmission within a population. Let’s play with a hypothetical example for a second: Assume we have a number of separate populations, each consisting of 10,000 individuals, and each is exposed to a parasite. Initially, 50 members of each population become infected. In one population, the infection rapidly spreads to 80% of the entire group. In another, the infection does not spread at all. In a third, the infection spreads less quickly than in the first and infects roughly 30% of the population. These factors, the speed and percentage of parasite transmission, are what I’m referring to when I speak of transmission intensity.

Anyway, how does transmission intensity affect whether parasites induce symptoms in their hosts? Well, AW Park et al. (2013) argue that intermediate transmission intensity results in highest disease prevalence (for white-tailed deer and viruses in the Orbivirus genus). They demonstrate that at high parasite transmission, more individuals in the population become infected with the parasite multiple times. As a result, they develop immunity which – while it does not prevent infection – mitigates symptoms, i.e., the disease. At lower transmission, on the other hand, so few individuals become infected that overall disease presence in the population is small. Thus, disease prevalence in the population is maximized at moderate transmission intensities because at intermediate levels more individuals are infected than at low transmission levels, and few individuals are infected multiple times in quick succession, preventing the population from developing immunity that mitigates symptoms of the infection.

However, a number of complications exist for this scenario. The immunity generated must allay symptoms, and not prevent the disease. Such a situation is possible, but it does not apply to every  parasite. Furthermore, the symptoms that the parasite induces must not significantly affect parasite transmission. If, for example, the symptoms harm parasite transmission, one would expect an ever-declining disease burden among the hosts. Because the symptoms harm transmission, the parasites would experience selective pressure to moderate symptoms and parasites in previously-infected hosts would gain a fitness advantage. On the other hand, if the symptoms display after parasite transmission, the selective pressure on parasites to minimize disease would be little, and the disease burden could actually increase with parasite transmission intensity. I could go on. The point here is that the connection between parasite transmission intensity and host disease burden varies markedly among host-parasite systems, depending on multiple factors, such as the nature of the host immune response, timing of parasite-induced symptoms, timing of host-induced symptoms, timing of parasite transmission, host symptoms’ affects on transmission success, and competition among and within parasite species within an individual host. I’m planning on getting to that stuff in later blogs.

1.    Park, A.W., et al., When more transmission equals less disease: reconciling the disconnect between disease hotspots and parasite transmission. PLoS One, 2013. 8(4): p. e61501.