An unlikely partnership: parasites, concomitant immunity and host defence

DOI: 10.1098/rspb.2001.1821



For certain systems, hosts are only able to mount a successful immune defense during the larval stage of the attacking parasite. In disease ecology, this is known as concomitant immunity with a well-studied example being schistosomiasis. Evidence suggests that infection from adult worms is the important driver for any host development of resistance when subsequently exposed to larval worms. Additionally, larval immunity can be stimulated from hosts exposure to larval worms themselves. The present two potential routes leading to one type of immune response. These forms of immunity can be broken down even further where one represents passive immunity and another active (or adaptive) immunity. Passive immunity can be defined as a response from the host by the presence of either adult or larval. While active (adaptive) immunity is a result of increased adult behavior leading to increased production of larval antigens. Variation in the individual contribution of larval immunity from adults has a potential for evolutionary trade-offs between adult and larval worms. Where adult worms benefit by suppressing worm burden for the host, decreasing the costs of infection. At the risk of decreased fitness through reproduction. This paper presents a simulated approach that investigates the ecological-evolutionary trade-offs for this system.


Foundations for the modeling framework are referenced to Brown 1999, Cooperation and conflict in host-manipulating parasites. Brown provides a model that analytically addresses the problem of cooperation among host-manipulating parasites. This model was adapted to include concomitant immunity. However, strangely the full simulation model isn’t presented in the methods section.

To incorporate adaptive CI. Authors present a fitness term w for adaptive CI that allows for contributing larval immunity to result in a negative fitness impact on the adult-larval represented by I (through lower fecundity), but an increase in group fitness represented by G.

Simulations include a fixed number of hosts each with a worm carrying capacity. Hosts will accumulate more worms over each generation through density dependence of infected adult worms. When each host generation arrives at an equilibrium, a set of naive hosts is generated for the next host generation. Naive hosts are then infected with the offspring of parasites from the previous generation. New parasites inherit a value from their parents that control the secretion of larval suppressing antigens.

Results show favorability for the evolution of adaptive CI over time when density-dependence is present.

Key figure: