wroteknowynick
28.12.06, 23:59
Coughs and sneezes spread mind diseases
06 November 2004, Janet Ginsburg, Newscientist.com, Magazine issue 2472
(filelink)
IT WAS hell on earth. "I was in a concentration camp. I could smell the
burning bodies," recalls Stephanie Diers. But it was 1975, the second world
war was long over, and Diers was in Martinez, California, thousands of miles
from Auschwitz. The 19-year-old was locked up, but in a mental ward.
Diers's psychotic break was just the latest in a string of illnesses that had
plagued her and puzzled her parents for the better part of a decade. No one
could figure out what had happened to the bright little girl who loved riding
horses and playing in the woods. Her list of ailments was as baffling as it
was extensive: headaches, dizziness, fatigue, pain in her teeth, tingling in
her toes, sore throats, flu-like illnesses, chest pains, pains in her spleen
and liver, poor balance, sensitivity to light and sound, memory lapses. And
now psychosis.
After six months in hospital, Diers was released and struggled on with her
life, eventually earning a college degree and working as a teacher. But it
would take another 14 years of serial illness before any of her doctors
thought to test for Lyme disease, a tick-borne illness identified in the late
1970s.
Like its distant cousin syphilis, Lyme is caused by corkscrew-shaped bacteria
called spirochaetes that are able to burrow into tissue, including the brain.
There they can lie dormant and harmless for months, even years. But once
active, they can stir up a devil's brew of symptoms, including conditions
that match the clinical diagnoses for schizophrenia, bipolar disorder and
depression.
Diers, of course, tested positive, and was put on a long course of
antibiotics. "I had so many psychiatrists and psychologists tell me it was
all in my head," she says. They just didn't know how right they were.
Borrelia burgdorferi, the Lyme bacterium, is now widely accepted as a cause
of psychiatric disease. And in recent years several other bugs have come to
light that are able to trigger symptoms of mental illness, ranging from
behavioural problems to depression and full-blown psychosis. In fact, so many
potential "mind germs" have now been unearthed that some researchers are
ready to challenge the conventional wisdom about the principal causes of
mental illness.
When it comes to causes, genes have always been the prime suspects, with
environmental triggers poorly understood and infectious disease an
afterthought. Infectious disease is "maybe 5 per cent as important as genes",
claims Richard Straub of the Genes, Cognition, and Psychosis Program at the
US National Institute of Mental Health in Bethesda, Maryland. Straub, who has
identified several genes tentatively associated with schizophrenia, thinks
that among environmental causes, peer groups, drug experiences and other
social factors are far more significant targets for research.
But according to evolutionary biologist Paul Ewald of the University of
Louisville in Kentucky, that ignores some obvious facts. "The biggest
breakthrough in the history of psychiatry was recognising that syphilis
causes insanity and that it can be prevented with antibiotics," he says. The
same mistake is being repeated today with Lyme disease and other infectious
agents, Ewald believes.
If diagnosed quickly, before the bacterium gets a foothold, Lyme disease can
be cured with a round of antibiotics. But spotting it can be tricky. Not
everyone gets the telltale "bull's eye" rash and antibody tests can be
unreliable, especially early on. That presents a dilemma for doctors
concerned about overprescribing antibiotics. If they wait too long - as
little as a few months after infection - the spirochaetes begin to attack the
central nervous system with devastating consequences. This "late stage" Lyme
is very hard to cure, often requiring months or years of antibiotics.
At Columbia University in New York, neuropsychiatrist Brian Fallon is in the
middle of a series of studies designed to see what actually goes on inside
the brains of chronic Lyme patients. One finding so far is that patients show
significant reduction in blood flow in brain regions associated with memory
and visuospatial organisation. Fallon has also looked at children, who are
especially at risk because they tend to play outside, where the ticks are. He
found significant cognitive and psychiatric problems in children who had been
diagnosed late, on average a year after infection. They scored low on memory
and perception tests and were also depressed, with some having suicidal
thoughts.
In 2003, more than 21,000 cases of Lyme disease were reported to the Centers
for Disease Control in Atlanta, Georgia, making it the most common vector-
borne disease in the US. Yet as few as 1 in 10 cases are documented, so the
true tally might be more than 200,000. And in 1996, another bacterium,
Borrelia lonestari, which is carried by the lone star tick common throughout
the American south, was linked to Lyme-like symptoms. So far there are no
tests for it, so no case statistics.
Lyme isn't just a problem in the US. "You really have a pandemic," says
Raphael Stricker, a San Francisco physician specialising in chronic
Lyme. "It's all over the US. It's all over Europe. It's in parts of Asia.
It's everywhere."
Beyond Lyme disease, the evidence linking infections to psychiatric disorders
becomes a little more hazy. Ironically, though, some of the most tantalising
clues are found in the very same data used to prove the case for genetic
links: twin studies.
Identical twins, who have 100 per cent of their genes in common, are much
more likely to both develop schizophrenia than are fraternal twins or full
siblings, who share just 50 per cent of their genes. Clearly, then, genes are
important. But the data is more complicated, explains Ewald. "People saw
these associations without thinking about alternative explanations," he says.
For example, when one identical twin develops schizophrenia, half the time
the other does not. If schizophrenia were strictly genetic, concordance
(meaning both twins get sick) should be 100 per cent. This holds true even if
many genes are involved in the disorder, as geneticists now believe.
But when the environment inside the womb is taken into account, the story
begins to shift. Fetuses develop inside two porous sacs, the inner chorion
and the outer amnion. Nearly 70 per cent of identical twins share a chorion,
a feature that can be determined after birth by the presence of subtle
physical traits such as mirror-image fingerprints. Those twin pairs are
nearly six times as likely to be concordant for schizophrenia as identical
twins with separate chorions.
Meanwhile, the concordance rate for non-identical twins is nearly twice that
of full siblings, even though the genetic relationship is the same: 50 per
cent. Fraternal twins rarely share sacs, but they do share a womb. That, says
Ewald, points to an environmental factor - though not necessarily an
infection.
Influenza's legacy
To look for evidence that a prenatal infection could be linked to the
development of schizophrenia years later, a team of Columbia University
epidemiologists led by Ezra Susser and Alan Brown sifted through the medical
records of 20,000 women who were pregnant in Alameda county, California,
between 1959 and 1966. The women, all patients at Kaiser-Permanente, the
largest healthcare provider in the region, were part of a massive child
health and development study. But the real stroke of luck was that most of
their children have remained in the Kaiser-Permanente system. "We could
follow them right up to age 40," says Susser.
The researchers first determined which children had been diagnosed with
schizophreni
