I’m trying to do a better job of keeping up with parasite ecology and epidemiology related news this year. Here’s some recent work that might be of interest:
Tasmanian devils have TWO types of infectious cancer!
Romans were wormy, despite relatively good hygienic practices.
The West African Ebola outbreak is over.
It looks like the mosquito-borne Zika virus is the likely culprit of the rapid increase in microcephaly in infants born in Brazil.
Pertussis, also known as whooping cough, kills tens of thousands of children per year, despite high global vaccination coverage. Additionally, developed countries with high pertussis vaccine coverage – like the United States – have experienced bigger outbreaks in recent years. Many hypotheses have been suggested to explain the “resurgence” of pertussis: (1) there is waning immunity to the vaccines and adults act as bacterial reservoirs; (2) the new acellular vaccine isn’t as good as the previous whole-cell vaccine; (3) the vaccines protect against infection but not transmission; and (4) there isn’t really a resurgence; we’re just better at detecting pertussis now than we used to be. A recent paper argues that all of those commonly held views are wrong and proposes some new hypotheses. Cool stuff!
Antibiotic resistance is a huge challenge facing global medicine. We usually assume that when bacteria evolve resistance to a given antiobiotic, the mutation that provides resistance is costly. Because we assume that those resistance mutations are costly, we also assume that if we stop using an antibiotic, the bacteria populations will evolve back to their susceptible state by acquiring compensatory mutations that restore the function(s) lost by resistance mutations. But resistance mutations vary in how costly they are. Some aren’t costly at all. And there are only so many compensatory mutations that can restore a given function. So, we can’t necessarily expect a resistant population to revert to susceptibility, whether a compensatory mutation pops up in the population or not. Furthermore, there are many other possible mutations that can reduce or eliminate any cost of resistance just by increasing overall bacterial fitness, without actually returning lost functions. We might be overlooking the importance of those “generally beneficial mutations” in the evolution and subsequent loss of antibiotic resistance in bacterial populations. Check it out.
Today’s post is all about host susceptibility. In mathematical models, we usually assume that every host is equally susceptible to infection (i.e., constant success rate, v). That may be mostly true in laboratory settings, because laboratory hosts tend to 1) be maintained under optimal resource conditions and 2) have similar genotypes. However, in the field, both host genetics and resource availability vary widely, and we expect hosts to vary in their ability to resist infection by parasites. Specifically, we expect hosts in poor condition to be more susceptible to parasite infection.
As it turns out, variation in susceptibility among hosts is really important for two reasons:
- If there is variation in host susceptibility to infection among individuals (v), there must be variation in the per capita parasite transmission rates for each individual (β). Without variation in β, you cannot have aggregation of parasites among hosts. So, variation in host susceptibility is one potential cause of aggregation of parasites among hosts.
- Variation in host susceptibility to infection is one way to generate superspreader hosts. In this case, highly susceptible hosts end up being super infected hosts. (Seriously, I love that super host paper.)
So, what determines how susceptible an individual is? The answer is: many things. But those things mostly boil down to 1) genetics and 2) environment. Genetics example: some host genotypes may be more susceptible to a given parasite than others. Environment example: hosts in low resource environments may be in poor condition, and may not have enough energy to devote to mounting an immune response to parasites.
And that brings me to a series of cool TREE papers about “vicious circles” of host susceptibility and infection. The idea is that parasite infection is probably “both a cause and consequence of host condition.”1 That is, hosts might be in poor condition because they have many parasites, and/or hosts may have many parasites because they are in poor condition. This sets up a potential negative feedback loop, where host condition continuously degrades while parasite burdens increase: the host is in poor condition, the host gets more parasites, the host’s condition further declines, the host gets more parasites, etc.
These “vicious circles” may be important to parasite transmission at both the individual and population levels. At the individual level, ‘vicious circles’ may cause some individuals to have (increasingly) lower fitness and/or survival. It may also be one way to generate super infected hosts. At the population level, we might see population declines as individuals experience decreased fitness and/or survival. Therefore, we might expect that the effects of parasites/pathogens on populations will be stronger when populations are already experiencing some environmental stress that causes the individuals to be in poor condition.
Do we always expect to see vicious circles of infection? Nope! For instance:
- If predators tend to pick off super infected hosts, then there may be no chance for the vicious circles to perpetuate. Therefore, parasites/pathogens may have stronger effects on host populations where predators have been eliminated/reduced than in host populations regulated by healthy predator populations. COOL.
- If the parasite is trophically transmitted, we might not expect hosts in poor condition to be more likely to get infected. For instance, a definitive host might need to be in good condition to eat enough intermediate hosts to get infected. If that’s the case, then we might expect a stabilizing feedback loop, instead of a negative feedback loop.
Saddest cartoon ever.
- Beldomenico, P. M., and M. Begon. 2010. Disease spread, susceptibility and infection intensity: vicious circles? Trends Ecology Evolution 25(1): 21–27.
- Loot, G., F. Thomas, and S. Blanchet. 2010. “Vicious circles” and disease spread: elements of discussion. Trends in ecology & evolution 25(3): 131.
- Beldomenico, P., and M. Begon. 2010. Response to comment by Loot et al. Trends in Ecology & Evolution 25(3): 32.