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Guy Palmer (’84 Ph.D.) and Terry McElwain (’86 Ph.D.) are on the
hunt. The Washington State University research veterinarians know
their quarry—Anaplasma and Babesia, the pathogens
that cause two of the world’s most debilitating diseases of
livestock—but they haven’t found the right weapon to bring them
down. What they need, what they have worked for years to find, are
vaccines that will stop the pathogens dead in their tracks.
Vaccines are such a routine part of health care for us that they
can seem like old news. Because of effective vaccines, those of us
who live in developed countries don’t have to worry about measles,
polio, or smallpox, diseases that inflicted grave harm on our
grandparents’ generation. Other than “new” diseases like next
year’s strain of influenza, we’re well protected. Yet, some of the
most common infectious diseases of people and animals have been
around just about forever—and we still don’t have vaccines against
them.
“The way I look at this is that we have vaccines for all the
ones that are easy to vaccinate against,” says McElwain. They’re
easy because of their biology, he says. When you get the disease,
it either kills you or your immune system fights it off and the
pathogen is cleared from your system. Vaccination gives you a head
start in the fight; it primes your immune system to recognize and
get rid of the pathogen before harm is done.
The “hard” diseases operate differently. If you get infected
with one of these pathogens, you will probably remain infected for
life. Your immune system can’t get rid of it. In humans the list of
such diseases includes malaria, sleeping sickness, and syphilis. In
cattle, it includes anaplasmosis and babesiosis, the diseases
Palmer and McElwain have targeted. Both are tick-borne blood
infections that cause severe anemia, often leading to death, and
both share an interesting MO.
“It’s an impressive disease to see,” says McElwain of
babesiosis. “Animals go from being fairly normal-looking one day to
just very, very sick the next.” Anaplasmosis is usually less
dramatic, but it is more widespread, affecting more than two-thirds
of the cattle in some regions. The economic costs of the diseases
are enormous—billions of dollars a year in lost animals and lowered
productivity—but the human costs are immeasurable. In sub-Saharan
Africa, for instance, smallholder farmers depend on their small
herds of cattle or goats for food, for cash income, for status, and
as beasts of burden.
“The loss of one animal can have a profound effect on the
family’s well-being,” says McElwain. “It may be the difference
between one of the children going to school or not.”
Palmer says most persistent pathogens are transmitted by vectors
(ticks, mosquitoes, tsetse flies) or by sexual contact. Since they
can’t spread to new hosts by casual contact, the pathogens have to
survive in one host until a transmission opportunity comes along.
Unfortunately for us, the strategies they’ve evolved to avoid the
host’s defenses also stymie our efforts to make a vaccine.
A vaccine works by showing the body’s immune system a pathogen
or part of a pathogen (usually a protein, in this context called an
antigen) so that it can develop cellular memory and antibodies that
will recognize and attack the pathogen in the future.
Many vaccines use the entire pathogen, which has been killed or
weakened so it won’t cause the full-blown disease. Such vaccines
work against persistent pathogens, but they are often expensive to
make and difficult to deploy. Live vaccines, for instance, need a
“cold chain”: they must be kept cold or frozen until just before
use, which is a tall order in poor countries in the tropics. A
subunit vaccine, based on just one or a few proteins, is usually
cheaper and hardier. Theoretically, any protein that sparks an
immune response and is a distinctive feature of the pathogen could
be the basis for a good vaccine. The problem is that no one’s been
able to make a subunit vaccine against Anaplasma,
Babesia, or any of the other persistent pathogens.
“Our challenge is to figure out why that is,” says McElwain.
“Biologically and immunologically, why is that the case? If we
could get a handle on that, I think we’d really have a significant
advance.”
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The M.O.
With both Anaplasma and Babesia, infection starts
with a bite from a tick that carries the pathogen. Within a couple
of weeks, the bitten cow becomes severely anemic. The pathogens
invade red blood cells, multiply inside them, then break apart the
cells and travel through the bloodstream to find new red blood
cells to invade. Infected cows may lose more than half their red
blood cells. Mortality can run as high as 70 percent.
Animals that survive the initial phase of illness recover and
are “just healthy as hounds,” says Guy Palmer. But they are not
free of the pathogen. Long after a cow recovers from acute
anaplasmosis, for instance, every milliliter of its blood—less than
a quarter teaspoonful—still carries a million Anaplasma
organisms. The number of pathogens peaks every four to six weeks,
then drops to very low numbers, then rises again. That ebb and flow
continues for the life of the cow. She remains healthy, but she
becomes a reservoir from which ticks can pick up the pathogen and
transmit it to other victims.
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