Pathogens can cause substantial mortality of amphibian eggs. If the timing
of hatching is phenotypically plastic, embryos could escape from otherwise
lethal infections by hatching early. We tested this with the arboreal eggs
of red-eyed treefrogs, Agalychnis callidryas. A filamentous ascomycete (Dot
hideales: Phaeosphaeriaceae) was present on similar to7% of egg clutches co
llected from a pond in the rain forest in Panama and, when present, killed
40% of the eggs, on average. Inoculation experiments confirmed that the fun
gus attacked and killed healthy embryos, establishing that this fungus is a
pathogen of A. callidryas eggs. As predicted from life history theory, emb
ryos hatched earlier from both naturally infected and inoculated clutches t
han from fungus-free control clutches. Within infected clutches, live embry
os in contact with fungal hyphae hatched before those embryos not in contac
t with the fungus. Accelerated hatching allowed embryos to survive that oth
erwise would have been killed, and tadpoles hatched from infected clutches
were themselves uninfected. Red-eyed treefrog embryos also hatch early if a
ttacked by predators, apparently in response to vibratory cues. Because fun
gal infection provides no vibratory stimuli, embryos must respond to differ
ent cues in fungus-induced hatching than in predator-induced hatching. The
behavioral decision of when to hatch is complex and merits further investig
ation. Our study indicates that pathogens can influence the timing of life
history transitions, as do other stage-specific risks.