Epidemics proceed with different dynamics. Sometimes they spike rapidly and disappear gradually; sometimes they ramp up slowly; sometimes they have multiple waves. What they all do at some point is end, usually with neither the pathogen nor the host going extinct. But we don’t usually understand how or why.

Chytridiomycosis is an epidemic that has been killing amphibians the world over for at least a decade. It is caused by a fungal pathogen called Batrachochytrium dendrobatidis (Bd), and it can cause limb deformities and skin abnormalities. Since amphibians absorb water and electrolytes through their skin rather than their mouths, such abnormalities can be fatal. But now we have some evidence that, as with past epidemics, Bd isn’t a one-way ticket to extinction.

Between 2004 and 2007, Bd decimated frog populations in Panama. About five years later, however, frog populations rebounded. Bd was still around, although it was not nearly as prevalent. Scientists collected frog and fungus samples from the start of the outbreak, in 2004, and after the recovery, in 2013, in order to figure out what factors went into making this particular epidemic subside. They hypothesized that either (a) the later Bd samples would be less pathogenic to the frogs; (b) the later frog samples would be more resistant to Bd; or (c) both.

The later Bd samples were not less pathogenic. They grew at the same rates, achieved the same sizes, and produced comparable numbers of spores. They had the same reactions to inhibitory factors in amphibian skin secretions and inhibited amphibian immune cells to the same degree. And when two different species of frogs were exposed to batches of 2004 Bd and 2013 Bd in the lab, all of the frogs got infected and died.

So the researchers looked at how well frog skin secretions could inhibit Bd. Inhibitory effectiveness differed among species and by location. But wild frogs collected in 2013—after the epidemic had abated—had more inhibitory material on their skin than frogs that had been in captivity since before the outbreak.

Since there was no difference in the fungus, the researchers concluded that “shifts in host resistance may be contributing to the recovery of some amphibian species.” But they did not do any genetic or biochemical studies to explore the basis of this shift.

The developing world is currently undergoing a resurgence in mumps, especially in vaccinated populations. The virus did not mutate to evade the vaccine, and the vaccine is still effective; its effect just wanes after about 27 years, so now we know that we need boosters in adulthood. Discoveries about the factors that influence the different trajectories that different epidemics can take—even amphibian epidemics—can arm us with information we will need to implement public health measures such as this one. It’s an added bonus to understanding how to preserve our amphibians.

Science, 2018. DOI: 10.1126/science.aao4806.1720692115 (About DOIs).

https://arstechnica.com/?p=1284665