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Host parasite interactions between freshwater phytoplankton and chytrid fungi (Chytridiomycota)

Journal

JOURNAL OF PHYCOLOGY
Volume 40, Issue 3, Pages 437-453

Publisher

WILEY
DOI: 10.1111/j.1529-8817.2004.03117.x

Keywords

chytrids; coevolution; diatoms; epidemics; food webs; hosts; parasites; phytoplankton; succession; zoospores

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Some chytrids are host-specific parasiticfungithat may have a considerable impact on phytoplankton dynamics. The phylum Chytridiomycota contains one class, the Chytridiomycetes, and is composed of five different orders. Molecular studies now firmly place the Chytridiomycota within the fungal kingdom. Chytrids are characterized by having zoospores, a motile stage in their life cycle. Zoospores are attracted to the host cell by specific signals. No single physical-chemical factor has been found that fully explains the dynamics of chytrid epidemics in the field. Fungal periodicity was primarily related to host cell density. The absence of aggregated distributions of chytrids on their hosts suggested that their hosts did not vary in their susceptibility to infection. A parasite can only become epidemic when it grows faster than the host. Therefore, it has been suggested that epidemics in phytoplankton populations arise when growth conditions for the host are unfavorable. No support for such a generalization was found, however. Growth of the parasitic fungus Rhizophydium planktonicum Canter emend, parasitic on the diatom Asterionella formosa Hassal, was reduced under stringent nutrient limitation,because production and infectivity of zoospores were affected negatively. A moderate phosphorous or light limitation favored epidemic development, however. Chytrid infections have been shown to affect competition between their algal hosts and in this way altered phytoplankton succession. There is potential for coevolution between Asterionella and the chytrid Zygorhizidium planktonicum Canter based on clear reciprocal fitness costs, absence of overall infective parasite strains, and possibly a genetic basis for host susceptibility and parasite infectivity.

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