Mortality of Cyclops bicuspidatus thomasi infected with the procercoid of Triaenophorus crassus was assessed and factors influencing the infectivity of the procercoid to the second intermediate host were evaluated. Over 80% of C. b. thomasi infected with T. crassus died after 28 days, and there was a bimodal pattern to cyclopid mortality. A decrease in the mean intensity over time indicated that this mortality was related to parasite numbers. The frequency of T. crassus in C. b. thomasi after 28 days fitted the negative binomial distribution. A higher proportion of lightly infected cyclopids at this time resulted from mortality of heavily infected hosts. Female cyclopids had larger procercoids than males, but the ratio of differentiated to undifferentiated procercoids did not vary between sexes. Procercoid size was smaller and the proportion of differentiated procercoids decreased with increasing intensities of infection. Exposure of laboratory-reared whitefish, Coregonus clupeaformis, and cisco, Coregonus artedii, to procercoids from crowded infections resulted in a low percent recovery of plerocercoids, while less crowded infections of procercoids produced a high percent recovery of plerocercoids in fish. The number of procercoids to which fish were exposed affected the percent recovery of plerocercoids.
The development, movement, and migration of the plerocercoid of Triaenophorus crassus in experimentally infected whitefish fry, Coregonus clupeaformis, were examined and the pathology of infection described. Plerocercoids penetrated through the stomach – pyloric caeca and anterior small intestine into the peritoneal cavity by 20 h postinfection (PI). Worms entered the muscle by day 5 PI and underwent a variety of migration patterns. Plerocercoid movement in muscle was aided by a series of peristaltic waves along the length of the worm. Plerocercoids underwent rapid growth during the first 2 months of infection and were wound extensively through the muscle by day 60 PI, at which time they occasionally penetrated into the peritoneal cavity or through the host integument. Migration of worms caused muscle necrosis resulting in formation of lesions by day 17 PI and granulomas by day 60 PI. Coincident with coiling of plerocercoids after day 60 PI was the formation of a host capsule around the worm and the initiation of plerocercoid hook development. Capsules and coiling of plerocercoids caused regional distortions in the body of the fish and displaced and (or) replaced large areas of muscle. Capsules containing live worms were recovered at 3 years PI. Mortality of infected whitefish was 21.7%, and 70.0% of this mortality occurred between days 48 and 59 PI. There was no difference in the rate of growth and the quantity of liver glycogen between infected and uninfected fish.
The furcocystocercous cercariae of the digenetic trematode, Proterometra macrostoma , possess a tail chamber into which their distome body withdraws prior to emergence from their snail intermediate host. The process of distome retraction and the conditions that trigger it in this species are not clear. The objectives of the present study were (1) to describe the retraction process in P. macrostoma; (2) to assess whether osmolality affects cercarial retraction; (3) to evaluate the effect of selected ions on retraction; and (4) to compare the swimming effectiveness of naturally ( = in vivo) retracted versus in vitro retracted cercariae. Retraction of the cercaria body into its tail chamber required only 2 min or less once initiated. The process began with the development of a chamber within the anterior end of the worm's tail. The chamber's lip advanced in a pulsating motion over the stationary distome. Retraction was completed with the constriction and fusion of the chamber lip once it passed over the anterior end of the distome, sealing the latter within the tail chamber. There was a significant difference in the proportions of cercariae with bodies retracted into tails, bodies not retracted, and bodies separated from tails in artificial pond water (APW) versus artificial snail water (ASW). A greater number of cercariae withdrew into their tail chambers in ASW (59/124; 47.6%) than in APW (21/124; 16.9%). In APW, more bodies separated from their tails (24/124; 19.4%) than in ASW (3/124; 2.4%). In both solutions (APW: 63.7% = 79/124; ASW: 50% = 62/124), a majority of cercariae never retracted. In APW, 76.2% of distomes retracting into their tails did so within the first 5 min compared to only 30.5% in ASW. There was no significant difference in the proportions of cercariae with bodies retracted into tails, bodies not retracted, and bodies separated from tails based on isosmotic replacement of individual ions, i.e., Na(+), K(+), Ca(++), or Mg(++), in ASW with Li(+). There was also no significant difference in the vertical swimming burst distance in cercariae whose bodies were initially retracted into their tails in vitro versus in vivo.
Richards growth curves were fitted to data from procercoids of Triaenophorus crassus (Pseudophyllidea) in experimentally infected Cyclops bicuspidatus thomasi (Copepoda). Average volume per procercoid varied inversely with intensity, and procercoids in female copepods were correspondingly larger than procercoids in males. The simple inverse relationship, which usually characterizes the crowding effect on cestode size, held for average procercoid growth rates, but the growth rates of differentiated and undifferentiated procercoids diverged at higher intensities. Three apparently intrinsic features of procercoid growth (initiation of differentiation at a fixed time, a minimum size threshold for differentiation, and an accelerated growth rate in procercoids following differentiation) provided a mechanism whereby natural variation in procercoid growth rates could be amplified to produce a parasite infrapopulation comprising large, differentiated procercoids and stunted, undifferentiated procercoids. Calculations using parameters of the fitted growth curves indicated that the hosts were probably under nutritional stress in low intensity infections during rapid growth of the differentiating and differentiated procercoids.
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