Effects of experimental Schistocephalus solidus infections on growth, morphology and sexual development of female three-spined sticklebacks, Gasterosteus aculeatus

Abstract

The use of naturally infected hosts in studies attempting to identify parasite-induced changes in host biology is problematical because it does not eliminate the possibility that infection may be a consequence, rather than a cause, of host trait variation. In addition, uncontrolled concomitant infections may confound results. In this study we experimentally infected individual laboratory-bred female three-spined sticklebacks Gasterosteus aculeatus L. with the pseudophyllidean cestode Schistocephalus solidus [Müller], and compared the morphology and growth patterns of infected females with sham-exposed controls over a 16-week period. Fish were fed a ration of 8% body weight per day. Non-invasive image analysis techniques allowed the growth of individual plerocercoids to be tracked in vivo throughout the course of infection, and patterns of host and parasite growth were determined. Females that developed infections diverged morphometrically from unexposed control females and exposed-uninfected females at 6 weeks post-infection, with the width of the body at the pectoral fins giving the earliest indication of infection success. When including the plerocercoid, infected females gained weight more quickly than controls, but when plerocercoid weight was removed this trend was reversed. There was no effect of infection on the increase in fish length. Plerocercoids grew at different rates in individual hosts, and exhibited measurable sustained weight increases of up to 10% per day. Final estimates of plerocercoid weight from morphometric analysis prior to autopsy were accurate to within +/- 17% of actual plerocercoid weight. At autopsy, infected female sticklebacks had significantly lower perivisceral fat reserves but had developed significantly larger ovaries than controls. The results are discussed in relation to previous studies examining natural infections, and the value of utilizing experimental infections to examine ecological aspects of host-parasite interactions is discussed.

Why do parasitized hosts look different? Resolving the “chicken-egg” dilemma

“…Similarly, it seems evident that some phenotypic traits make some individuals more susceptible to parasitic infections. Currently, the diVerential susceptibility between hosts and parasite is rarely considered, principally because most studies on the eVects of parasites on host phenotype experimentally infect hosts using individual exposure to parasites (e.g., Barber and Svensson 2003;Blair and Webster 2007). Such a design should be altered to exploit any natural pre-existing diVerences in the susceptibility of hosts and for disentangling causes and consequences in host-parasite interactions (Poulin 1998;Barber et al 2000).…”

“…Currently, most studies assume that observed variation in the host phenotype population is a consequence of parasite infection (e.g., Lello et al 2005;Holmstad et al 2006;Wood et al 2007). Otherwise, the possibility that the host phenotype can cause diVerent patterns of parasite infection is reduced by experimentally infecting the hosts or by removing parasites from infected hosts (e.g., Albon et al 2002;Barber and Svensson 2003;Seivwright et al 2005;Schultz et al 2006;Blair and Webster 2007). Very few tests have yet been developed to explore the possibility that both causes and consequences may intervene, having reciprocal eVects in underlying the relationship between parasite infection and phenotypic variation within the host population (but see Barber 2005;Bourque et al 2006).…”

Compensatory growth in threespine sticklebacks (Gasterosteus aculeatus) inhibited by experimental Schistocephalus infections

“…Because the proportion of S. solidus successfully establishing in host fish after experimental infection is often low (e.g., Arnott et al 2000), the size of the S. solidus-exposed group was increased relative to the number of placebo-exposed controls, and exposed fish were fed multiple infective parasites. At a size of~20 mm (~0.15 g), 20 sticklebacks were each fed copepods (Cyclops strenuus) containing a total of five infective (i.e., cercomer-bearing; Smyth 1994) S. solidus procercoids (see Smyth 1994 andBarber andSvensson 2003 for details of in vitro parasite culture and exposure protocols). Sixteen placebo-exposed control sticklebacks were fed noninfected copepods.…”

“…All fish were then fed to satiation for a further 6 weeks to allow any compensatory response in weight, length, and condition of the previously food-deprived fish to occur. At weekly intervals, each fish was weighed (to 0.001 g) and digitally photographed from above to allow length measurements (to 0.1 mm) to be made using computerised image analysis (Barber and Svensson 2003). Fish were not anaesthetized prior to being weighed because of concerns over behavioural and appetite effects of repeated anaesthesia and the potential for an interaction with infection status.…”

“…Most intuitively, because host-derived energy used by parasites for growth and development is not available to the host, infections with energy-demanding parasites can be associated with reduced host growth (Barber and Svensson 2003;Finley and Forrester 2003). Parasites that have behavioural effects also have the potential to reduce host growth indirectly by altering the competitive foraging success of their hosts (Milinski 1990; Barber and Ruxton 1998).…”