title: Inhibition of gametogenesis by the cestode Ligula intestinalis in roach (Rutilus rutilus) is attenuated under laboratory conditions.
abstract: Reproductive parameters of Ligula intestinalis-infected roach (Rutilus rutilus) which were held under long-tem laboratory conditions with unlimited food supply were investigated. Although uninfected and infected roach showed no difference in condition factor and both groups deposited perivisceral fat, the gonadosomatic-index was significantly lower in infected female and male roach. Quantitative histological analysis revealed that gonad development was retarded upon parasitization in both genders. In contrast to the phenotype described in the field, infected females were able to recruit follicles into secondary growth, but a high percentage of secondary growth follicles underwent atresia. In both genders, the histological data corresponded well with reduced expression of pituitary gonadotropins and lowered plasma concentrations of sex steroids, as revealed by real-time RT-PCR and ELISA, respectively. Furthermore, a reduction of vitellogenin mRNA and modulated expression of sex steroid receptors in the liver was demonstrated. Like in the field, there was a significant adverse impact of L. intestinalis on host reproductive physiology which could not be related to parasite burden. Our results show, for the first time, that maintenance under laboratory conditions can not abolish the deleterious effect of L. intestinalis on gametogenesis in roach, and indicate a specific inhibition of host reproduction by endocrine disruption.
authors.affiliation: Department of Ecophysiology and Aquaculture, Leibniz-Institute of Freshwater Ecology and Inland Fisheries, Mueggelseedamm 310, D-12587 Berlin, Germany. trubiroha@igb-berlin.de
authors.forename: Achim
authors.initials: A
authors.lastname: Trubiroha
authors.forename: Hana
authors.initials: H
authors.lastname: Kroupova
authors.forename: Sabrina N
authors.initials: SN
authors.lastname: Frank
authors.forename: Bernd
authors.initials: B
authors.lastname: Sures
authors.forename: Werner
authors.initials: W
authors.lastname: Kloas
mesh_terms: D000818:Animals; D002589:Cestoda / Q000472:pathogenicity / Q000502:physiology*; D002590:Cestode Infections / Q000469:parasitology / Q000503:physiopathology / Q000662:veterinary*; D003530:Cyprinidae / Q000469:parasitology* / Q000502:physiology; D052244:Endocrine Disruptors / Q000494:pharmacology; D004780:Environment, Controlled; D005260:Female; D005393:Fish Diseases / Q000469:parasitology* / Q000503:physiopathology; D005718:Gametogenesis / Q000502:physiology*; D012739:Gonadal Steroid Hormones / Q000097:blood; D006062:Gonadotropins / Q000235:genetics / Q000378:metabolism; D006066:Gonads / Q000033:anatomy & histology / Q000254:growth & development; D006790:Host-Parasite Interactions; D008099:Liver / Q000378:metabolism; D008297:Male; D010902:Pituitary Gland / Q000378:metabolism; D011944:Receptors, Androgen / Q000235:genetics; D011960:Receptors, Estrogen / Q000235:genetics; D012098:Reproduction / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014819:Vitellogenins / Q000235:genetics
chemical_list: D052244:Endocrine Disruptors; D012739:Gonadal Steroid Hormones; D006062:Gonadotropins; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D014819:Vitellogenins