Back in the 1880’s, before tuberculosis had a known cause,
experts attributed it to a combination of risk factors –
things like depression, bad ventilation, insufficient food and
"family predisposition." One standard textbook noted
expansively that "the idea of infection being a cause still
prevails in the South of Europe." Fast-forward to the 1980’s,
and you hear similar accounts of peptic ulcers. The highly
touted risk factors were stress, smoking, alcohol and, of
course, "genetic predisposition." Never mind that an
Australian researcher named Barry Marshall was successfully
giving himself ulcers by swilling beakers of bacteria – and
curing them with antibiotics. The textbooks didn’t even
mention his work.
We now know that TB and ulcers are infectious conditions,
caused by specific microbes and treatable with anti-microbial
drugs. Yet we’re still laboring to explain most of our leading
scourges – cancer, heart disease, mental illness, Alzheimer’s
– with long lists of risk factors. In a compelling new book
titled "Plague Time" (282 pages, Free Press. $25).
Amherst College biologist Paul Ewald argues that were missing
an obvious lesson here. Roughly translated: It’s the germs,
stupid. Though genes and lifestyle are no doubt important,
Ewald says, the primary causes of today’s "slow burning
plagues" are parasites –viruses, bacteria and other infectious
microbes – whose long tem effects we have simply failed to
recognize.
Ewald is not a virologist but a bold minded evolutionist
who, in past work, has created a whole new framework for
thinking about infectious disease. To understand why microbes
behave as they do, he considers their ecological incentives.
Cold viruses can’t afford to be too virulent because they
require mobile hosts. (A dying cold sufferer wouldn’t get
around enough to infect other people.) But parasites that can
survive outside their hosts don’t have to be so considerate –
especially if they can travel from host to host via mosquitoes
or drinking water. A dying malaria suffer is, if anything,
preferable to a healthy one from the parasite’s perspective.
All the person has to do to spread infection is lie still and
get bit.
In "Plague Time," he takes a similar approach. By his
reasoning, our genes shouldn’t cause much heart disease,
mental illness, cancer or autoimmune disease. Genes that
impede our survival tend to die out over time, at their owners
fail to reproduce. By contrast, the parasites with the best
tricks for exploiting us are the most likely to stay in
the game. There is no question that the viruses and bacteria
can take up long-term residence in our bodies. Some hide
deep within our cells to avoid detection by the immune system,
while others disguise themselves to resemble our own tissues.
And we know the consequences can be serious. Suppose the
immune system catches sight of a streptococcal bug that
normally evades detection by making itself as a heart cell. As
the body attacks the invader, it may demolish the organ as
well.
The question is whether these chronic infections are as
pervasive as Ewald suspects. Some experts would scoff at the
notion, but the recent findings are impressive. "Until the
1980’s," he writes, "it was generally not appreciated that
women who were suffering and dying from cervical cancer were
the victims of a venereal disease epidemic." Today it’s
undeniable. Epidemiologists have puzzled for more than a
century over the link between sexual promiscuity and cervical
cancer. But over the past 15 years, studies have revealed that
human pillomaviruses. America’s most common sexually
transmitted pathogens, are present in some 93 percent of
cervical tumors. Scientists have even identified the proteins
that HPV’s use to release the brakes on normal cell division.
Cervical cancer may be the tip of an iceberg. Less
definitive studies have linked childhood strep infection to
obsessive-compulsive disorder and Tourette’s syndrome. Traces
of a virus that causes mammary cancer in mice have been
recovered from human breast tumors. Researchers in Japan and
Germany have linked borna virus – a brain infection seen in
horses, sheep and cats – to schizophrenia and bipolar disorder
in people. And a growing body of evidence suggests that
Chlamydia pneumoniae, a common respiratory bug, may play a key
role in coronary artery disease, the leading cause of death
throughout the Western world. Since 1988, researchers have
consistently found the bacterium in clogged vessels but not in
health ones. They’ve caused arterial lesions in rabbits by
infecting them with the germ. They have even found hints that
antibiotics can slow the progression of heart disease in
infected patients.
As these connections are borne out, they could change
medicine as profoundly during the 21st century as
germ theory did in the 20th. The question is
whether they’ll get the attention they deserve. As Ewald
observes, "Those who control access to funding and the
channels of scientific communication tend to be believers in
the established views." When Edward Jenner hit upon the notion
of a small pox vaccine in 1797, the Royal Society of London
scolded him for risking his reputation of something "so much
as variance with established knowledge, and withal so
incredible."
When the Hungarian physician Ignaz Semmelweis figured out
that physicians’ unwashed hands were causing fatal infections
among new mothers at the University of Vienna in the 1850’s,
he lost his own position there. And though Barry Marshall
first reported his finding on the infectious cause of ulcers
in 1983, his peers ignored the discovery until 1990,