Many strategies don’t require declining virulence.

A second theory, developed by evolutionary epidemiologist Paul Ewald, which he calls the "theory of virulence,” suggests that, as a rule, the deadlier the germ, the less likely it is to spread. The reason: If victims are quickly immobilized (think of Ebola, for example), then they can’t readily spread the infection. By this thinking, if a germ requires a mobile host to spread, its virulence will, of necessity, decline. Like the older conventional wisdom, the theory of virulence recognizes that many germs will evolve less virulence as they circulate and adapt to the human population. But Ewald’s theory also proposes that germs all have their own strategies to spread, and some of those strategies allow the germ to maintain high virulence and transmissibility.

Durability, Ewald says, is one such strategy. Variola virus, which causes smallpox, is very durable in the external environment, and it can have a high death rate of 10 to 40 percent. Ewald calls it and other durable germs “sit-and-wait” pathogens. Some deadly infections are spread from very sick hosts by vectors: fleas, lice, mosquitos, or ticks. Others, such as cholera, are spread in water. Still others, such as hospital-acquired staph infections, are spread by people taking care of the sick or dying. This is what happened in the women’s hospitals of the 19th century, when doctors spread puerperal or “childbed” fever from one postpartum woman to another.

All of these strategies, according to Ewald, may prevent a germ’s otherwise inevitable slide to lower virulence.