The curious
pathway exploited by fungi is quite accidental although the effect certainly is
not. It also seems that such an
infection must remain invisible unless the immune system gets wiped out in a
manner similar to AIDS. Reading this one
is clearly reminded of AIDS.
At least the
pathway is now clearly identified. What
we need however is some form of effective yet gentle cocktail to search out and
flush out fungal processes generally. I
suspect many ailments could be traced back to such agencies and simply learning
how to help the body solve the problem.
In any event we
now have opened up a new valuable research endeavor.
Accident of
Evolution Allows Fungi to Thrive in Our Bodies
Cryptococcal fungi have evolved mechanisms for
eluding their protist predators, giving them an inadvertent advantage over
look-alike immune cells in humans, porpoises and other mammals
Sudden fungal outbreaks have long been routine
among plants,
and more recently, animals.
A recent outbreak among humans in the Pacific Northwest raises the disturbing
prospect that we are not immune either. The mystery of this outbreak’s origins
is detailed in “Strange Fungi Now Stalk Healthy People” in the December issue of Scientific American.
The outbreak is ongoing but, in spite of
appearances, Cryptococcus gattii doesn't exist to plague us. The
fungus prefers to live in soil and on trees, where it subsists quite
happily on decaying matter. So how can an organism that seems to enjoy a full
and rich life on plants and dirt possibly find itself suited to living inside
humans? The answer, it turns out, may be an accident of evolution.
Life in the wild is not all sunshine and rotting
roses for C. gattii. “Microorganisms are in a constant fight for
territory, for food sources, for their place in that microbial community,” says
Karen Bartlett of the University of British Columbia, an expert in the behavior
of biological aerosols. Yeasts have many predators, and formidable among them
are amoebas. These protists ooze their way through the soil and water of
the world, engulfing and digesting tiny prey. To prevent amoebic annihilation, Cryptococcus
species have evolved mechanisms to elude their would-be predators, such as a
drying- and digestion-resistant coat, UV-protective pigments and the ability to
survive being swallowed by predators.
Those same mechanisms allow yeast to evade a type of
human immune cell that looks and acts just like an amoeba (similar cells are
also found in other animals). We call them macrophages. Macrophages, which may
share evolutionary roots with free-living amoebas, do virtually the same job in humans that amoebas do
in the environment: they crawl around eating things. In our case, those things
are bits of junk and microbes, which they ingest and kill with digestive
enzymes—just like wild amoebas. “If you didn't know the difference, you'd
think that they were amoebas,” Bartlett says.
And apparently, neither does Cryptococcus. In our lungs macrophages scour the surface, mopping
up the many foreign objects that land but don’t belong there. In susceptible
people and animals Cryptococcus species are just as skillful in
duping macrophages as they are their soil attackers. And they use the same
methods, at least in the lab.
C. gattii not only can kill macrophages, they
can also hide inside them. If ingested,
the fungal cells resist digestion while hiding from antibodies, T cells, and
other immune system components, effectively converting a macrophage into a
microbial Trojan horse. Macrophages travel extensively through the body and can
cross the blood–brain barrier. If a yeast cells finds its way from the lung to
the brain via a phage or other routes, “that's very bad news,” Bartlett says,
“because once it gets into the central nervous system it's in heaven. It has
all of the sugars it wants to be able to rapidly proliferate.” When Cryptococcus kills
it's generally because such a brain infection has happened.
There are other reasons Cryptococcus has
an easy job when it infects us. Unlike the vast majority of fungi, it can
survive at 37 degrees Celsius—human body temperature. And it has a tough
polysaccharide coat that helps prevent it from drying out in the environment
but also helps protect it from macrophages. Finally, its exterior contains
melanin, the same pigment that colors human skin, which both protects it from
UV radiation as well as inhibits the digestive action of macrophages. “All of
these things are protective mechanisms that have allowed it to become
established in the environment,” Bartlett says, “and unfortunately those same
protective mechanisms make it a pathogen for us.”
Amazingly, this is not an isolated
phenomenon. Legionella pneumophila, the bacterial cause of Legionnaires'
disease, lives symbiotically inside wild aquatic amoebas and similarly
mistakenly infects human macrophages when victims inhale it. Arturo Casadevall,
chair of the Department of Microbiology and
Immunology and director of the Center for Immunological Sciences at the Albert
Einstein College of Medicine, who has been studying Cryptococcus for
over 20 years, has compared the phenomenon with a card game where soil microbes
are playing for survival, but by chance, a few hands confer “accidental
virulence” on other hosts.
“Virulence is not their business,” Casadevall says.
“Their business is survival. But the same pressures that are allowing them to
survive results in traits that gives them capacity to survive in mammals.”
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