Paper accepted for publication in Functional Ecology!

I recently wrote a review article that has now been accepted for publication in Functional Ecology on how eutrophication influences host-parasite interactions (link). Here is also a link to read the lay summary, available on the webpage of the journal.

Better fed host does not necessarily imply more resources for parasites

Increases in phytoplankton biomass following nutrient enrichment can impact host-parasite interactions by altering the amount of resources that parasites can acquire during an infection. As parasite fitness is primarily affected by the quality of the host as a resource (i.e. the nutritional quality of the host and, by extension, host body condition), a positive relationship between host body condition and parasite fitness was evidenced in a number of systems impacted by anthropogenic eutrophication such as parasite-induced malformations in amphibians (Johnson et al. 2007), whirling disease and proliferative kidney disease in salmonids (Hartikainen etal. 2009) and swimmer’s itch (Soldánová etal. 2013).

Male threespine stickleback in eutrophied waters during breeding season

However, it should be noted that better fed host does not necessarily imply more resources for parasites because higher food resources for hosts as a result of eutrophication can also limit parasite proliferation by promoting host resistance to infection (Aalto, Decaestecker & Pulkkinen 2015). Such a negative influence of nutrient enrichment on parasite transmission is poorly documented in the literature. An exception is the study by Anaya‐Rojas et al.(2016). Using mesocosms, the authors investigated the connections between nutrient loading, parasitism and host condition using the monogenean parasite Gyrodactylus spp. and the threespine stickleback Gasterosteus aculeatus. The parasite reproduces on the host skill and gills and transmission is directly connected to host density (Bakke, Cable & Harris 2007). By controlling fish density in mesocosms and by manipulating nitrogenous nutrient (NaNO₃ and HNa₂PO₄) loading and exposure to parasites, the authors found fish assigned the low nutrient treatment to be in worse condition, with lower stomach fullness compared to fish assigned to high nutrient treatment (Anaya‐Rojas et al. 2016). For sticklebacks originating from the lake ecotype, where Gyrodactylus spp. load is high, nutrient enrichment was negatively correlated to parasite load, but this was not true for fish originating from the stream ecotype, where prevalence is lower. Additionally, more sticklebacks from the lake ecotype died after being exposure to parasites during the experiment, indicating a higher sensitivity to Gyrodactylus infection compared to fish from the stream ecotype. This led the authors to hypothesize that lake sticklebacks might alter their diet or feeding rate in order to better cope with Gyrodactylus spp. (Anaya‐Rojas et al. 2016). 

Communication between phages alters infection spread in bacterial populations

A growing amount of research evidences how co-infections can alter infection likelihood in a wide range of organisms. Most of this work has focused on how weakened host defences can facilitate new infections, hence contributing to the spread of directly-transmitted parasites in a population. This situation can lead to vicious circles and trigger disease outbreaks (reviewed in Beldomenico & Begon 2010). The work by Erez et al. (2017) presents new perspectives on how infections can disease spread in host populations.

This work focuses on phages infecting bacteria (Bacillus subtilis). These pathogens can enter lytic or lysogenic life-cycle when invading the host. While the lytic cycle allows high replication from the phage, its strong virulence also leads to the death of the host. Phage lysogeny implies the phage to integrate the host DNA, providing it resistance against further infection from the same pathogen, and replicates with the host cellular division without killing the host. Lytic life-cycle is thought to be advantageous when hosts are abundant in the environment while lysogeny is seen as an advantage when the probability of infecting new host cells is low (see Chibani-Chennoufi et al. 2004). However, the mechanisms inducing lytic over lysogenic transmission are still poorly known (Davidson 2017). 

source for picture: http://www.nature.com/nature/journal/vaop/ncurrent/images_article/nature21118-f1.jpg

The study by Erez et al. evidences that communication between phages can influence life-cycle determination in phages. By infecting B. Subtilis bacteria with four different phages, the authors found one of the phages, phi3T, to protect hosts from infections by the same pathogen by promoting phage lysogeny. The authors suggested that the phage protein AimP triggers the release of a peptid fragment they called Arbitrium from infected cells. When this compound is taken up by neighbouring cells, high concentrations would favour lysogeny while low concentrations would favour lytic infections by phages. This study is the first to evidence such a quorum sensing mechanism in phage and could change our perception of life-cycle determination.