Kill the Killer of the Winner: protozoan predators grabbing a piece of the KW action

Viruses and bacteria are the most abundant microorganisms in aquatic ecosystems, with respective abundances around 1010 and 109 l–1. The interactions between the two are vital for the continued function of processes such as the viral and microbial loops and are an important link in the microbial food web. These regulate the amount of food available at higher trophic levels as well as maintaining bacterial biodiversity through the ‘kill the winner’ (KW) hypothesis. The KW hypothesis functions through viruses with high host specificity more frequently killing hosts with higher growth rates, thus preventing competitive exclusion and maintaining bacterial species richness (BSR). Many experiments have shown BSR to be influenced by the abundance of viruses, however the experiments fail to include protozoan grazers as a factor. Protozoan grazers have been shown to kill viruses through intraguild predation (IGP) either by digestion of host cells (coincidental) or free-living progeny (omnivorous). IGP is the process of killing a competitor which is after the same resource. As viruses and protozoan grazers both require bacteria to survive, albeit in different ways, there is the possibility for IGP to be a major factor.

Miki and Yamamura (2005) set out to test, through the use of a theoretical model, whether IGP by protozoan grazers could affect the viral abundance of the ‘killer of the winner’ thus changing the bacterial community structure by a process they call ‘kill the killer of the winner’ KKW.  They used a chemostat model and made assumptions based on experimental observations or for simplicity, such as one protozoan predator with a non-selective attack rate on all bacterial species with one host specific virus. Although these assumptions are needed, it is possible for either a wrong observation or a simplistic factor to provide inaccurate results.

From this model they found when the viral latent period is short (10min and 1hr) then BSR was not affected by IGP, however, when the latent period was long (6 and 12hrs) BSR decreased as IGP increased. This means, in certain situations the KKW hypothesis could potentially explain the growth and competitive dominance of bacterial blooms if their ‘killer’ has itself been ‘killed’, or brought to a negligible level. Further supporting this idea they found BSR to be more negatively affected by eutrophication under the influence of the KKW hypothesis. This also suggests that viruses have much more impact on nutrient cycling in oligotrophic waters.

This model provides us great insight into a relatively new process of controlling BSR and may allow us to further explore the viral-bacterial-protozoan relationship with the cycling and release of nutrients into different systems and trophic levels. However, as mentioned before the model relies on the use of assumptions which may not fully hold up such changes in viral and protozoan host and prey selectivity. It also does not consider the effect of bacteria viral resistance which is believed to diminish the KW hypothesis and may also be another example of KKW. For these reasons, field and laboratory studies are imperative to our understanding of the KKW and IGP processes. The use of experiments combined with theoretical studies will allow a greater understanding of environmental and biological processes and provide further reliability and accuracy to expected and predicted outcomes.

Miki, T., & Yamamura, N. (2005). Intraguild predation reduces bacterial species richness and loosens the viral loop in aquatic systems:kill the killer of the winner' hypothesis. Aquatic microbial ecology, 40(1), 1-12.

http://www.chikyu.ac.jp/yamamura-pro/yamamura/PDF/05Intraguild.pdf