Host Susceptibility to Parasites: ‘Vicious Circles’

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:

1. 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.
2. 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:

1. 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.
2. 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.

References:

1. Beldomenico, P. M., and M. Begon. 2010. Disease spread, susceptibility and infection intensity: vicious circles? Trends Ecology Evolution 25(1): 21–27.
2. Loot, G., F. Thomas, and S. Blanchet. 2010. “Vicious circles” and disease spread: elements of discussion. Trends in ecology & evolution 25(3): 131.
3. Beldomenico, P., and M. Begon. 2010. Response to comment by Loot et al. Trends in Ecology & Evolution 25(3): 32.