TREMATODE INFECTION OF AN INTERMEDIATE FISH HOST: IMPLICATIONS FOR HOST ENERGETICS AND VISUALLY-MEDIATED ESCAPE RESPONSES

Abstract

Trophically-transmitted multiple host parasites have been known to have significant effects on their intermediate hosts through factors such as histopathology related to parasite development, as well as the well-known host behavioural alterations which are associated with increased transmission to the next host in the parasite life cycle. Ornithodiplostomum ptychocheilus is a multihost parasite which is trophically-transmitted from its intermediate fathead minnow (Pimephales promelas) host to their definitive hosts, piscivorous birds. Within fathead minnows, this parasite causes histological damage of host tissue at its infection site – the superficial layers of the optic tectum and cerebellum – and is associated with the disruption of visually-mediated behaviours. Similar to many multihost parasites, the degree of host physiological and behavioural alterations during O. ptychocheilus infection has been found to be dependent upon parasite developmental stage and parasite burden. The described pathologies suggest that infection represents a direct cost to host energy budgets as well as survival costs related to host antipredator responses to visual stimuli. Therefore, I investigated the influence of O. ptychocheilus infection on host metabolic rates as well as during visually-mediated escape responses – an antipredator behaviour which requires rapid visual processing. First, I compared standard metabolic rate of uninfected and infected fish during the obligate growth period – a parasite developmental stage associated with significant O. ptychocheilus growth as well as host histopathology. I found that infection significantly increased metabolic rates at very low parasite loads, but standard metabolic rate gradually decreased with parasite numbers until it was comparable to that of uninfected fish. The following year, I measured fast-start response latencies of both newly infected hosts and minnows infected from the previous year to fast-moving visual looming stimuli approaching from above and the front (vertical and horizontal planes) across parasite developmental stages. I found that infection significantly reduced host abilities to respond to the stimulus, but this was dependent upon parasite load as well as the direction of stimulus approach. Surprisingly, the influence of infection was similar regardless of days post parasite exposure indicating that parasite development did not alter visual capabilities. Overall, my results suggest that, while infection-induced pathologies are costly for hosts and may persist overtime, there appears to be significant host compensation to mitigate the pathologies associated with the obligate growth period.