Reproductive compensation in female Palaemonetes argentinus (Decapoda: Natantia) due to Microphallus szidati (Trematoda) infection

Abstract

Parasites may affect host demographic characteristics because they can directly or indirectly cause the death of their hosts and/or influence their reproduction. Parasitism is therefore recognized as a factor that influences the composition and structure of populations and communities. One of these behaviours is the compensatory response: the host can compensate for the parasite losses effect, modifying the reproductive effort to enhance fitness. Ovigerus female Palaemonetes argentinus was collected and sorted into two groups according to the degree of development of their embryos: newly spawned embryos and embryos ready to hatch. The number of embryos and their dry weight for each female were determined. All parts of the female body were checked for parasites. The females of P. argentinus were parasitized by Microphalus szidati. We found that parasitized females produce more embryos but had more egg loss during development and the percentage of embryonic loss was higher in the parasitized females than in non-parasitized. Parasitized females produced lighter eggs than those from uninfected females. This supports the compensatory reproduction hypothesis suggested for this species. Parasitism can change life history traits in a way that fecundity can be compensated; this co-evolution between host and parasites will be population or context dependent. Parasites are a functional part of any ecosystem and as our results show, deleting parasites in life history traits and reproduction studies in free living organisms could lead to an incomplete picture of the true processes that happen in nature.

Host-parasite dialogue: fecundity compensation mechanisms of Fissurella crassa

“…Although it is unknown whether this decrease in spawning is a widespread phenomenon in Chile, its association with the increase in parasite intensity, which according to our results is positively related to the level of progesterone (Figure 6D), suggests a compensatory response of parasitized F. crassa against the oocyte losses during spawning. In this sense, increased fecundity would reflect a trade-off between the number and size of eggs (Einum and Fleming, 2000;Rollingson and Hutchings, 2013), with eggs from infected females having a smaller area, as has been observed in other host-parasite systems (Heins, 2012;Parietti et al, 2020). Previous studies have shown that parasitized limpets F. crassa have more parasite intensity in sites where the GSI is also higher, suggesting that the increase in gonadal biomass could provide more space for the accumulation of metacercariae (Aldana et al, 2014;Aldana et al, 2020;Garcıá-Huidobro et al, 2020).…”

“…The increase in the percentage of reproductively active host females, at low infection levels, was considered as a mechanism that could compensate for the subsequent reduction in snail fecundity, as a result of the increase in trematode intensity (Serbina, 2014). Studies carried out on the shrimp Palaemonetes argentinus, the second intermediate host for the digenean Microphalus szidati, demonstrated that parasitized females produced more embryos, but had more egg loss throughout embryonic development than non-parasitized females (Merlo et al, 2016;Parietti et al, 2020). In this sense, female shrimp should produce a greater number of offspring at the early season to compensate for egg losses as a result of being parasitized.…”

“…Hosts, in response to the fitness loss, may evolve nonimmunological defenses such as fecundity compensation, by adjusting their reproductive traits (Agnew et al, 2000;Hurd, 2009;Parker et al, 2011). However, the impact of trematodes on the reproduction of second intermediate hosts, as well as the existence of this type of non-immunological defenses, remains understudied (but see Fostera, 1958;Serbina, 2014;Parietti et al, 2020). The mechanisms underlying fecundity compensation are not fully understood, but previous research suggests that nonimmunological defenses against parasites involve energetic, hormonal, and physiological pathways that involve a molecular dialogue between hosts and parasites (Hall et al, 2007;Pike et al, 2019;Gomez de Leon et al, 2021).…”