Leishmania life cycle |
ScienceDaily, December 21, 2011
Scientists of the
Institute of Tropical Medicine (ITG) discovered a parasite that not only had
developed resistance against a common medicine, but at the same time had become
better in withstanding the human immune system. With some exaggeration: medical
practice helped in developing a superbug. For it appears the battle against the
drug also armed the bug better against its host.
"To our
knowledge it is the first time such a doubly armed organism appears in
nature," says researcher Manu Vanaerschot, who obtained a PhD for his
detective work at ITG and Antwerp University. "It certainly makes you
think."
Vanaerschot studies
the Leishmania parasite, a unicellular organism that has amazed scientists
before. Leishmania is an expert in adaptation to different environments, and
the only known organism in nature disregarding a basic rule of biology: that
chromosomes ought to come in pairs. (The latter was also discovered by
ITG-scientists recently.) The parasite causes leishmaniasis, one of the most
important parasitic diseases after malaria. It hits some two million people, in
88 countries -- including European ones -- and yearly kills fifty thousand of
them. The parasite is transmitted by the bite of a sand fly. The combined
resistance against a medicine and the human immune system emerged in Leishmania
donovani, the species causing the deadly form of the disease.
On the Indian
subcontinent, where most cases occur, the disease was treated for decades with
antimony compounds. As was to be expected, the parasite adapted to the constant
drug pressure, and evolved into a form resisting the antimonials. In 2006 the treatment
was switched to another medicine, because two patients out of three did not
respond to the treatment. The antimonials closely work together with the human
immune system to kill the parasite. This probably has given Leishmania donovani
the opportunity to arm itself against both. It not only became resistant
against the drug, but also resists better to the macrophages of its host.
Macrophages are important cells of our immune system.
There is no
absolute proof yet (among other things, because one obviously cannot experiment
on humans) but everything suggests that resistant Leishmania not only survive
better in humans -- have a higher "fitness" -- but also are better at
making people ill -- have a higher "virulence" -- than their
non-resistant counterparts.
Superbug?
It is the first
time that science finds an organism that always benefits from its resistance.
Normally resistance is only useful when a pathogen is bombarded by drugs; the
rest of the time it is detrimental to the organism.
Resistant organisms
are a real problem to medicine. More and more pathogens become resistant to our
drugs and antibiotics -- to a large extend because you and I use them too
lavishly and improperly. For several microbes, the arsenal of available drugs
and antibiotics has so diminished that people may die again from pneumonia, or
even from ulcerating wounds. Luckily for us, resistance helps pathogens only in
a drug-filled environment. In the open field their resistance is a disadvantage
to them, because they have to invest energy and resources into a property with
no use there. Just like a suit of armour is quite useful on the battle field,
but a real nuisance the rest of the time.
So the propagation
of resistant organisms is substantially slowed down because they are at a
disadvantage outside of sick rooms. But this rule, too, is violated by
Leishmania: even in absence of the drug, the resistant parasite survives
better, instead of worse, and it is more virulent than a non-resistant
parasite.
Did
our medicines create a superbug? A legitimate question, and the phenomenon has
to be investigated, but this sole case doesn't imply we better stop developing
new medicines (as a matter of fact, the antimony-resistant Leishmania are still
susceptible to a more recent drug, miltefosine). On the contrary, we should
develop more new drugs, to give new answers to the adaptive strategies of
pathogens, and we should protect those drugs, for instance by using them in
combination therapies. In this never-ending arms race we should use our drugs
wisely, to minimise the chances for pathogens to develop resistance.
Story Source:
The above story is reprinted from materials provided by Institute of Tropical Medicine Antwerp.
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