Grants and Contributions:

Title:
Host-Parasite Interactions in Experimental Populations
Agreement Number:
RGPIN
Agreement Value:
$200,000.00
Agreement Date:
May 10, 2017 -
Organization:
Natural Sciences and Engineering Research Council of Canada
Location:
Quebec, CA
Reference Number:
GC-2017-Q1-02076
Agreement Type:
Grant
Report Type:
Grants and Contributions
Additional Information:

Grant or Award spanning more than one fiscal year. (2017-2018 to 2022-2023)

Recipient's Legal Name:
Scott, Marilyn (McGill University)
Program:
Discovery Grants Program - Individual
Program Purpose:

My LONG-TERM GOAL is to identify factors that impact host-parasite population dynamics using two MODEL SYSTEMS: a fish ectoparasite and a mouse intestinal nematode. Parasites directly impact host health through reduced growth, reproduction and survival with implications that extend to the host population. What is less understood, but possibly of equal importance, is whether the infected host is able to SIGNAL OTHERS OF THE RISK OF INFECTION. Recent results suggest this is possible both in fish and mice, with implications for host-parasite population dynamics and for pathways of host-parasite co-evolution.

In tracking the epidemic dynamics of infection on guppies, my students found that the negative impact on guppy mass was due to presence of infection in the POPULATION but not on the affected INDIVIDUAL. Also infection spread more rapidly when introduced on a guppy of high relative condition. Similar to chemical alarms released in response to predation, epidermal club cells of infected fish (especially those of poor condition) may release chemical alarms that reduce susceptibility of other fish and dampen spread of infection. If so, our findings will extend understanding of the chemical ecology of fear.  

My students have also shown that infected pregnant mice transfer signals to their fetus and newborn that impair linear growth and that alter gene expression in the placenta and fetal brain. This may involve alterations to the microbiome in the pup gut and subsequent gut-brain cross talk. As changes to the neonatal microbiome persist, altered brain gene expression may also persist. The brain regulates behaviors, some of which are related to parasite transmission, and the brain influences innate immunity which may alter susceptibility should the pups be exposed to the parasite. Altered transmission dynamics or susceptibility will impact transmission of infection through the F1 population.

The consequences of communicating risk of infection on host-parasite population dynamics will be explored in host populations and supported by individual-based research to document that infected fish release chemical alarms and that infected mouse dams alter the pup microbiome and brain gene expression. At an applied level, our findings may be helpful in controlling infections in aquaculture facilities in Canada and internationally and may demonstrate that maternal infection increases the resilience of offspring to a future risk of infection.