Parasitic disease in amphibians: control by the regulation of worm burdens

Abstract

This review considers three case studies based on macroparasites of anurans: (a) natural infections in the permanently-aquatic Xenopus laevis which represent the worm burdens acquired, and the implications for pathology, when hosts are exposed to continuous, year-round, transmission; (b) the desert toad, Scaphiopus couchii, which experiences invasion very briefly each year and provides a simplified system involving only a single significant infection (Pseudodiplorchis americanus); (c) the mesic Bufo bufo which has been the subject of experimental laboratory studies designed to measure the effects of Rhabdias bufonis infection on host growth, physical performance and survival. Experimental manipulation of both Scaphiopus and Bufo provide quantitative data on disease effects of macroparasites, including precise measurements of parasite-induced host mortality. Field data for Xenopus and Scaphiopus show that, despite high initial worm burdens from efficient transmission, infection levels at parasite maturity are modulated below those leading to significant disease. Experimental data for Scaphiopus and Bufo have documented the time-course and magnitude of this decline in intensities, and there is circumstantial evidence for Scaphiopus that this regulation is host-mediated. Immunological studies on Xenopus show that disease effects of the pathogenic Pseudocapillaroides xenopodis are exacerbated in thymectomised hosts and reversed by implantation of thymuses from MHC-compatible donors. Thus, whilst factorial experiments can demonstrate the potential of helminths to cause significant disease and mortality in anuran host-macroparasite interactions, powerful post-invasion regulation of worm burdens appears to exert a strong control of parasite-induced disease in natural host populations.

Exposure of leopard frogs to a pesticide mixture affects life history characteristics of the lungworm Rhabdias ranae

“…For example, parasites are more fecund in immunodeficient animals (Viney 2002b). These generalizations are supported by observations in amphibians, whereby regulation of worm abundance occurs after infection due either to density-dependent effects or immune responses of the host (Tinsley 1995). In our study, the total number of worms recovered in frog tissues at the end of the experiment corresponded to 75% of the initial dose and was similar among treatment groups, showing that the skin of naïve leopard frogs is very susceptible to R. ranae larvae as observed in other anurans (Goater and Ward 1992) and that pesticide exposure did not influence host recognition and penetration components of the transmission process.…”

Infection Dynamics of the Lungworm Rhabdias Pseudosphaerocephala in Its Natural Host, the Cane Toad (Bufo Marinus), and in Novel Hosts (Native Australian Frogs)

“…However, this lack of pathology could be due to the early stage of infection, and inflammation could intensify with continued damage to the lung via hematophagous feeding by the parasite and irritation to the lung as gravid females release eggs/larvae into the lumen. In Rhabdias bufonis infecting B. marinus, the primary damage inflicted by the parasite comes from worms penetrating the skin and migrating, rather than effects of adults in the lungs (Tinsley, 1995). Larval migratory pathways and inflammatory responses to parasite exposure differed among the frog species, and between frogs and toads.…”

Life history specializations of monogenean flatworms: A review of experimental and microscopical studies

“…Maximum ingestion rates by adult P. americanus are 1.9-5.3 µl of blood/parasite/week at 25°C. Such precise measurements are rare for blood-feeding platyhelminths and enable calculation of pathogenic effects on the host under different environmental conditions Tinsley, 1992, 1994;Tinsley, 1993Tinsley, , 1995.…”