Bacterial resistance to antibiotics – short-term evolution of virulence

In all of this website other posts we deal mainly with features of human biology established by long-term historical processes. In the present post we will discuss evolutionary changes that can occur within the next year, or perhaps maybe even next week. Because pathogens reproduce so rapidly, they also evolve rapidly.

Some of our defenses against disease, such as sickle cell hemoglobin, have evolved markedly in the last ten thousand years, during which we have had perhaps three hundred generations. The species as a whole has evolved significantly higher resistance to a few epidemic diseases such as smallpox and tuberculosis in the last few centuries, perhaps a dozen generations. Compare this to a bacterium’s three hundred generations in a week or two and the even faster reproduction of a virus. Bacteria can evolve as much in a day as we can in a thousand years, and this gives us a grossly unfair handicap in the arms race. We cannot evolve fast enough to escape from microorganisms. Instead, an individual must counter a pathogen’s evolutionary changes by altering the ratios of its various kinds of antibody-producing cells. Fortunately, the number and diversity of these chemical weapons factories are enormous and at least partly compensate for our pathogens’ great evolutionary advantage.

From an immunological perspective, an epidemic may change a human population dramatically. Those individuals who have contracted a disease and recovered will likely be immune to reinfection because they harbor vastly increased concentrations of the lymphocytes that make the antibodies that are most destructive of that particular pathogen. Adult immunity to childhood diseases such as mumps depends not on changing human gene pools but on changing the concentrations of different kinds of antibodies within each individual.

Small size gives our pathogens another advantage: their enormous numbers. Each of us carries around (mostly in our digestive and respiratory systems) more bacterial cells than there are people on Earth. These enormous numbers mean that even improbable sorts of mutations will occur with appreciable frequency and that any mutant bacterial strain with even the most minute advantage over the others will soon prevail numerically. We can expect our pathogens’ quantitative characteristics to evolve rapidly to whatever values are optimal for present circumstances.

In some catastrophic epidemics, a human population can evolve a higher level of resistance to an infectious disease in mere months. When Europeans first arrived in the New World, for example, some European diseases quickly killed as much as 90 percent of a Native American community in a short time. If the Native Americans’ vulnerability had had any genetic basis, the genes of the lucky few who survived the epidemic would have become proportionately more frequent, and we could say that the population, in this limited sense, evolved a higher resistance. This is an extreme example. More often, a human gene pool will be little changed by an epidemic, while the pathogen’s features may evolve dramatically.