Resistance to chytridiomycosis varies among amphibian species and is correlated with skin peptide defenses

Abstract

Innate immune mechanisms of defense are especially important to ectothermic vertebrates in which adaptive immune responses may be slow to develop. One innate defense in amphibian skin is the release of abundant quantities of antimicrobial peptides. Chytridiomycosis is an emerging infectious disease of amphibians caused by the skin fungus, Batrachochytrium dendrobatidis. Susceptibility to chytridiomycosis varies among species, and mechanisms of disease resistance are not well understood. Previously, we have shown that Australian and Panamanian amphibian species that possess skin peptides that effectively inhibit the growth of B. dendrobatidis in vitro tend to survive better in the wild or are predicted to survive the first encounter with this lethal pathogen. For most species, it has been difficult to experimentally infect individuals with B. dendrobatidis and directly evaluate both survival and antimicrobial peptide defenses. Here, we demonstrate differences in susceptibility to chytridiomycosis among four Australian species (Litoria caerulea, Litoria chloris, Mixophyes fasciolatus and Limnodynastes tasmaniensis) after experimental infection with B. dendrobatidis, and show that the survival rate increases with the in vitro effectiveness of the skin peptides. We also observed that circulating granulocyte, but not lymphocyte, counts differed between infected and uninfected Lit. chloris. This suggests that innate granulocyte defenses may be activated by pathogen exposure. Taken together, our data suggest that multiple innate defense mechanisms are involved in resistance to chytridiomycosis, and the efficacy of these defenses varies by amphibian species.

Profile of cortisol, glycaemia, and blood parameters of American Bullfrog tadpoles Lithobates catesbeianus exposed to density and hypoxia stressors

“…However, in the present study, the stressor mechanisms promoted an increase in the percentage of lymphocytes. Reductions in neutrophils counts in amphibians were observed in some studies corroborating the present one that show a decrease in eosinophils numbers and percentage (Woodhams et al 2007, Belden & Kiesecker 2005.…”

Skin microbes on frogs prevent morbidity and mortality caused by a lethal skin fungus

“…It is becoming clear that to understand disease dynamics, the interactions between the host, its resident microbes and colonizing pathogens need to be characterized. In this experiment, we exposed juvenile frogs to a low concentration of Bd zoospores relative to most other investigators (Rachowicz et al, 2006;Retallick and Miera, 2007;Woodhams et al, 2007a). However, the concentration of zoospores we used was higher than that estimated from pond water in nature (Kirshtein et al, 2007;Walker et al, 2007).…”

“…Caused by the chytrid species Batrachochytrium dendrobatidis (Bd), this skin disease is linked to population declines and extinctions of over 200 amphibian species in areas unaffected by habitat loss (Longcore et al, 1999;Skerratt et al, 2007). Since its description in 1999, we have learned a considerable amount about the pathogen's life history, physiology, population genetics, its responses to host immunity and how it causes death (Morehouse et al, 2003;Piotrowski et al, 2004;Berger et al, 2005;Rollins-Smith and Conlon, 2005;Morgan et al, 2007;Voyles et al, 2007;Woodhams et al, 2007aWoodhams et al, , b, 2008. Much less is known about how to control or manage the disease in nature.…”

Molecular toolkit unlocks life cycle of the panzootic amphibian pathogen Batrachochytrium dendrobatidis

“…wrote the paper. shown that a key host-defense mechanism is the production of secreted skin peptides with antimicrobial properties; research has found that amphibian species that produce peptides with anti-Bd activity show increased survival (7). The current study shows that serine-type peptidases constitute a large gene family in the Bd genome and show differential expression between the two Bd life stages, with a bias toward expression in the sporangia.…”