592 CHAPTER 22In Chapter 13 we described the conditions under which parasites (including
pathogenic microbes) are expected to evolve lower virulence (trade-off between
virulence and transmission, vertical transmission from parent hosts to offspring,
single-strain rather than multiple infections). Hosts suffer little mortality in some
old parasite-host associations, such as between some primates and their simian
immunodeficiency viruses (SIVs), due probably to evolution of both lower viru-
lence and enhanced host resistance [27].
Four perspectives from evolutionary biology bear special mention. First, phylo-
genetic methods are now a standard tool in tracing the time and region of a patho-
gen’s origin and its subsequent spread. For example, phylogenetic research showed
that the 2014–2015 Ebola virus outbreak originated from a natural reservoir in
Sierra Leone and was spread by human contact, undergoing rapid genetic diver-
sification in the process (see Chapter 1) [25, 51, 113]. Second, mutations in influ-
enza that change their antigenic phenotype enable such strains to increase rapidly
and cause outbreaks. The problem is to predict which of the many genotypes in
the virus population is likely to break out, so that vaccines can be constructed in
advance. Researchers have made progress toward this goal, using a combination of
fitness models and phylogenetic analysis [19, 71].
Third, progress is being made in using evolution to control the spread of infec-
tious diseases, such as dengue fever and malaria, by mosquitoes or other vectors.
One mode of selection at the level of the gene is segregation distortion by mecha-
nisms such as meiotic drive (see Chapter 12). The idea is to introduce into a mos-
quito population a driving genetic element that will increase in frequency by gene-
level selection, linked to a gene that will interfere with the ability of the mosquito
to transmit the pathogen. The aim is not to eliminate the mosquito vector (which is
nearly impossible in most situations) but to transform it so that it no longer carries
the pathogen. Several model systems have been developed, such as using Wolba-
chia, a bacterial parasite of many insects, as the driving agent [57]. Some strains of
Wolbachia spread rapidly through host populations by mechanisms that have the
same effect as meiotic drive. The best progress, so far, has been the creation of a
genetic construct with CRISPR-Cas9 that has been inserted into the genome of
experimental mosquitoes [47]. The construct makes the mosquitos unable to carry
malaria and is transmitted to 99.5 percent of their progeny.
Finally, and probably most important, is the evolution of antibiotic resistance, to
which we have referred repeatedly in this book. Public health officials have warned
that multidrug-resistant pathogens are a “nightmare” that poses a “catastrophic
threat” to humans throughout the world [73]. Some bacteria that are common in
hospitals have added resistance to carbapenems—drugs of last resort—to their
resistance repertoire. (This has occurred in Klebsiella pneumoniae, one of several
multidrug-resistant bacteria that are common in hospitals, which are environ-
ments that select for resistance. These bacteria caused about 90,000 deaths in the
United States in 2004 [108].) There is some hope that negative genetic correlations
in resistance to different drugs might be discovered; if so, selection for one might
cause resistance to the other(s) to be lost [10]. But the most urgent and important
priority must be to reduce the enormous, and often pointless, overuse of antibiotics
that create natural selection for resistance. Antibiotics, developed for controlling
bacteria, do not affect viruses, yet millions of antibiotic prescriptions are written
for viral ailments such as the common cold, by doctors who respond to pressure
from patients to “do something.” Worse, and completely inexcusable, is that as
much as half the antibiotic use in the United States is applied to farm animals—
and 80 percent of that usage is to promote growth, not to improve the animals’
health. There is powerful natural selection for mutations that provide resistance.
These mutations can easily spread among species of bacteria by horizontal gene
transfer (see Chapter 2) and end up in the worst human pathogens. (In December22_EVOL4E_CH22.indd 592 3/22/17 1:49 PM