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The within-pond epidemiology of amphibian ranavirus

The within-pond epidemiology of amphibian ranavirus



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Brunner Brunner Presentation Transcript

  • • The within-pond epidemiology of an amphibian ranavirus A synthetic modeling approach Jesse Brunner Washington State University
  • Questions • What which feature(s) of host or pathogen biology are required to reproduce the broad features of ranaviral outbreaks in pond-breeding amphibians (i.e., Wood frogs, Rana sylvatica)? • Initially low prevalence • Sudden onset of mortality event in mid-to-late summer (even though Rv introduced at the beginning of or early in the larval period) • Some metamorphs leave the pond infected • How important is water-borne transmission vs direct transmission? • How important is the heterogeneity in susceptibility we have seen in laboratory experiments?
  • Model assumptions / conditions • Large population (40–400 tadpoles / m2) • Medium-sized pond (600 m2 x 1m deep) • Only one species: Rana• Only one species: Rana sylvatica • Epidemic starts from a single infected tadpole • Transmission is (quickly) saturating function of density (Brunner et al. in prep)
  • Initial model • SIS model with recovery to susceptible state (no immunity) • No exposed class (immediately infectious) • Epidemic is far too early
  • Initial model • SIS model with recovery to susceptible state (no immunity) • No exposed class (immediately infectious) • Epidemic is far too early
  • Initial model • Does a lower rate of transmission help? • Only if we lower transmission rate by an order of magnitude! • Then the epidemic is too slow
  • water-borne transmission • Add term for concentration-specific transmission from water • Probability of infection from LD50 study in Warne et al. 2011 • Add terms for accumulation and loss of virus in water • Viral shedding: rough estimates range from 102 to 104 pfu/day in lab experiments with Ambystoma nebulosum (Storfer et al. in prep, Brunner unpublished data) Half-life of ranaviruses ranges from• Half-life of ranaviruses ranges from • 9.65 days in “unsterile” pond water at 20°C (Nazir et al. 2011) • 0.57 days in pond water at 20–24°C (Johnson & Brunner in prep; see poster)
  • water-borne transmission • Very few tadpoles infected from the water (even with lower transmission)
  • water-borne transmission • Does a longer half-life of Rv in water help? • Even with very long persistence times, water-borne transmission contributes very few infections
  • water-borne transmission • What about a greater shedding rate? Even with a • low rate of direct transmission, • long persistence time, & • high shedding rate water-borne transmission is still minor source of infection compared to direct contacts
  • Metamorphs & Developmental stages • Add terms for metamorphosing tadpoles (susceptible & infected) • Rate of metamorphosis is 1/duration of larval period (60- 80d) • Explicitly model development from Gosner (1960) stages 20 – 40 • Rate of development is # stages / duration of larval period
  • Metamorphs & Developmental stages • Does not change the timing or shape of epidemics
  • • Probability of ranavirus infection and death changes dramatically with stage • Modified the transmission terms by multiplying by the stage-specific odds- ratio as predicted logistic-regression Warne et al. 2011 STAGE-SPECIFIC SUSCEPTIBILITY ratio as predicted logistic-regression
  • STAGE-SPECIFIC SUSCEPTIBILITY • Timing of the epidemic is right with estimated transmission rate • See the sharp increase in cases
  • Conclusions • Water-borne transmission is minor relative to direct transmission (and negligible under more realistic assumptions) • Environmental heterogeneity may slow transmission• Environmental heterogeneity may slow transmission • Epidemics appear later • More gradual onset of mortality • Smaller epidemic • Stage-specific susceptibility may be key in timing, dynamics, and outcome of ranaviral outbreaks in Wood frogs
  • Open questions • How important is transmission from carcasses? • An important role for scavengers and decomposers? • Does the stage-specific susceptibility hypothesis hold for other species? • Are multihost communities radically different? • Can these models match real epidemics?