How Parasitic Chytrids Could Facilitate the Dominance of Host Phytoplankton

Like other pathogens, parasitic fungal chytrids contribute to the collapse of phytoplankton blooms. When a bloom crashes, limiting nutrients become more freely available, facilitating subsequent blooms dominated by different species. Although this disease‐mediated control can enhance overall phytoplankton diversity, some studies suggest that parasites can increase host density at short timescales; some at long (equilibrium) timescales; still others report negative effects of parasites on host density.

This article collates such theoretical and empirical studies, illustrates the mechanisms underlying the positive effects of chytrids on host density, and explores the conditions under which these effects occur. Lastly, I propose a hypothesis by which parasitic infections may increase host density and how these positive effects contribute to seasonal plankton bloom dynamics.

At short timescales, chytrid exploitation of hosts reduces their fitness and can leave more nutrients available for uninfected phytoplankton (a cascading effect on nutrient availability). The parasites take 2–19 days to kill infected hosts—indicating their interaction durability—and release free‐living infectious zoospores that enable new infections. This lag delays death of the infected host and parasite attacks on susceptible hosts, and thus prolongs the period of growth for susceptible hosts on the available nutrients. A combination of the cascading effect and interaction durability can increase total host density relative to uninfected phytoplankton, leading to a phenomenon called the “hydra effect”. Here, I show that such an effect on host phytoplankton is possible when their maximum growth rate is sufficiently high and the parasite infection rate is sufficiently low. At longer timescales, with host death, chytrids release zoospores that are edible and nutritious for zooplankton. Predation of zoospores (the mycoloop) can boost zooplankton growth, then increase predation pressure on edible nonhost phytoplankton (apparent competition). A mycoloop therefore positively affects host density by reducing zoospore and host competitor densities.

A mini‐review shows that parasitic chytrids can enhance the dominance of host phytoplankton under certain host–parasite trait combinations modulated by environmental conditions, even in the absence of the mycoloop. However, infections that turn inedible hosts into edible prey for zooplankton should reduce these positive effects.

In conclusion, parasites of phytoplankton can play significant roles in host bloom initiation and termination, potentially controlling bloom timing and magnitude. This should be especially true in temperate regions, where the prevalence of parasitic fungi is predicted to increase over time with warming.