Patterns of prevalence and intensity: How helminth burdens are distributed across mammalian hosts

Background/Question/Methods

How parasite burdens are distributed across populations can have significant impacts on hosts. Disease measures such as parasite prevalence and intensity capture distinct aspects of those distributions and can influence individual fitness and population stability. Prevalence represents the fraction of the host population infected and intensity the individual parasite burdens. In Anderson and May’s macroparasite model prevalence and intensity were positively linked by a scaling parameter (aggregation). If we consider host individuals as colonizable habitat patches we create a link to macroecological theory (abundance-occupancy). Prevalence becomes analogous to occupancy and infection intensity to local abundance. Investigations of prevalence-intensity relationships have resulted in the proposal of multiple responsible mechanisms, but often these studies focus either on the role of parasites or their hosts. Here, we reexamine the prevalence-intensity relationship for helminth parasites of mammalian hosts in the Global Mammal Parasite Database and consider how hosts/parasites differentially shape these patterns. First, we investigate if and how prevalence and intensity are related. Second, we examine how variability in prevalence and intensity differs between host and helminth species. Lastly, we explore how an alternative measure of parasite burden (parasite volume) might impact our interpretations of the relationships of prevalence and intensity.

Results/Conclusions

In agreement with theoretical expectations, we observe a positive relationship between infection prevalence and log mean infection intensity for helminth parasites of mammalian hosts. When we parse the associated variability in prevalence and intensity between host and parasite species we observe statistically distinct means between hosts and parasites, and in both cases parasites exhibit lower mean values of intraspecific variability. However, the variability of prevalence values within parasite species appears more evenly distributed than that of hosts. Finally, when we consider an alternate measure of infection burden –log(parasite volume)—rather than log(parasite count), the relationship between prevalence and individual infection generally remains positive, indicating that the burden of infection, not just parasite count, also tends to increase with prevalence. Together, our results support the positive relationship between prevalence and intensity, demonstrate that these measures may be more driven by parasite species than their hosts, and lastly, extend measures of infection to assess the relationship to impacts on hosts.