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What determines how damaging a given strain of pathogen will be
is still something of a mystery. Some of the nastiest infectious
agents in humans aren’t even full-time pathogens. They cause few
problems in their animal host—like E. coli in cattle or
Salmonella in reptiles—or they are free living, with no host
at all—like Listeria, a food-borne pathogen in humans.
Doug Call uses molecular techniques to try to figure out what
makes some strains of Salmonella and Listeria
infective. He suspects it takes more than a single gene to turn a
bug into a killer; it’s more likely that a strain needs a suite of
dozens of genes in order to be virulent. Call says that when his
recent graduate student, Min-Su Kang, began his research, he was
certain there had to be a unique gene or small group of genes that
allows one strain of Salmonella to be nastier than others.
After much fruitless searching, the student concluded there was no
such “virulence gene.”
“He did a very good job,” says Call. “If anyone was going to
find it, he was.”
Ecologist Andrew Storfer is exploring the possibility that
pathogens can become more deadly when something in the environment
lowers our natural defenses.
He’s working to understand why amphibian populations worldwide
have gone into freefall in the last few decades. Nearly half of the
6,000-plus species of amphibians on earth are declining. Ten
percent have gone extinct or nearly extinct in recent decades.
“This is unparalleled, unprecedented, by other vertebrates,”
says Storfer.
Along with loss of habitat and competition from invasive
species, amphibians have been getting hammered by diseases they
once fought off with some success, such as an iridovirus and a
fungal skin infection. Storfer began to wonder if their immune
systems might have been compromised by something in their
environment. Because they breathe through their skin and are
exposed to contaminants both in the water and on land, amphibians
might be peculiarly vulnerable to pollution. Could toxins in the
water be affecting their ability to fight infection?
Storfer and his research team exposed tiger salamander larvae to
atrazine, a widely used herbicide, and iridovirus, starting when
they were 12 weeks old. At that age, the salamanders are entirely
aquatic, and their immune systems are fully functional. The
atrazine was applied at levels found in ponds across the U.S. in
springtime, the result of run-off from farm fields. The larvae were
monitored for three months, until they were ready to metamorphose
and become adults.
The results were striking. Atrazine decreased white-blood-cell
counts in the salamanders and doubled their infection rate. And
since the salamanders were housed individually, the experiment
probably low-balled the incidence of disease; in a crowded natural
pond, the virus would likely spread even more.
“The dynamics of this disease are what is called density
dependent,” says Storfer. “The more animals [that are]
infected, the more get infected.” If atrazine causes the
same effects in nature that it did in his experiment, he says, the
difference in infection level could mean the difference between a
population surviving or going extinct.
Those results offer a clear warning, says Storfer. Amphibians
have many of the same disease-fighting tools we have. Their immune
systems are more primitive than ours, but have the same basic
components.
“If these guys are the first to go and they’re sort of a litmus
test of environmental quality, then that means as it gets worse,
it’s going to start affecting other vertebrates—like us,” says
Storfer. “If their immunity is being compromised at certain
levels of pesticides or other things in the environment, we have to
worry about what’s going to happen to us.”
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