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Trypanosoma
cruzi
Trypanosoma
cruzi belongs to the subkingdom Protozoa. They are
flagellar organisms that have one nucleus and an organelle,
the kinetoplast, that gives rise to one mitochondrion
and mitochondrial DNA. T. cruzi reproduce asexually
by binary fission. Like all other trypanosomes, T.
cruzi live one stage of their lives in the blood
and/or tissues of vertebrate hosts and during other
stages they live in the digestive tracts of invertebrate
vectors (temporary hosts). T. cruzi's vectors,
Triatoma infectans (vinchucas) are triatomine
insects, with over 100 species that carry the parasite.
(For other endemic and dangerous species see Kiss
of Death: Chagas Disease in the Americas, pages
186 through 193.)
The
subspecies Stercorian
T. cruzi
belong to the subspecies A. stercoria, because
the parasite develops its infectious stage in the insect's
digestive tract. When the vector defecates, the parasite
travels in the feces. The parasite enters the bite wound
or through abrasions on the skin caused by the victim
scratching the sore bite. As one prevention, not scratching
the bite and morning washing of the wound may help to
decrease chagas. The vector's effectiveness in spreading
the infectious T. cruzi is related to infestation
of houses by T. infectans, and the proximity
and short time between blood feeding and defecation,
and a lack of personal hygiene.
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Trypomastigotic
T. cruzi
T.
cruzi changes forms in its life cycle as it travels
from insects to humans. The general forms are trypomastigote
(tryps), amastigote, sluggish trypomastigote, and epimastigote.
Because it undergoes different forms, it easily adapts
to different/hostile environments and renders itself
a difficult and evasive target for attack by the immune
system and immunization because it changes its surface
area. Metacyclic trypomastigotes are effective forms
of T. cruzi that pass from the insect's hindgut
in the fecal matter and burrow into the skin, either
through the bite site or skin abrasions. Metacyclic
tryps have a nuclei near the posterior of their bodies.
They have a free flagellum (tail) attached to an undulating
membrane on the body. The flagella whip them along in
the person's blood and attaches to the insect's intestinal
wall. Infinitesimally small, these tryps are 20 microns
(0.20 mm) long and 3 microns wide. (More than a million
can fit in a pixel, so Bill Gates beware!) After metacyclic
tryps pass through the skin, they briefly travel in
the blood stream (and area of quick attack from the
immune system) and then colonize muscle and neuron tissue,
areas less vulnerable to attack, where they encyst and
form amastigotes
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Amastigotic T. cruzi
After
they have entered muscle tissue, metacyclic form amastigotes.
Amastigotes are intracellular, round and oval in shape,
and without flagella. They are 1.5 to 5 microns long.
Amastigotes cluster into cysts - bundles of evolving
forms that erupt amastigotes into the bloodstream where
they move on to other tissue cells. This provides for
rapid proliferation. Amastigote also provide stumpy
trypomastigotes that are ingested by vinchucas
during bloodfeeding. This sustains the parasite's life
cycle.
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Epimastigotic
T. cruzi
When
vinchucas blood feed upon an infected animal
or human, they ingest stumpy trypomastigotes from chagas
victims. The vinchucas become carriers of T.
cruzi for life, as the parasite reproduces and transforms.
These trypomastigotes travel to the insect's midgut
and transform into epimastigotes, which are more adaptable
to survive the insect's intestines. Epimastigotes have
flagellum attached near the center of the body, which
differ from tryps whose flagellum starts near the rear
end of the body. Epimastigotes have a central nucleus
and kinetoplast. They multiply by binary fission. Epimastigotes
are 10 to 20 microns long at first, but grow another
10 microns as they travel to the insect's hindgut, where
they transform into metacyclic trypomastigotes. The
insect stage of T. cruzi takes from six to sixteen
days, and the parasite apparently does no damage to
the vinchucas.
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This complicated
and delicate relationship between T. cruzi and
triatomines is the result of millions of years of selective
pressure, natural selection, and adaptive strategies
that provide T. cruzi with excellent defenses
against human and animal immune systems. T.cruzi
employ an adaptive strategy common to many parasites
in maintaining their population levels within hosts.
It is not to their advantage to destroy the host organism
too quickly because this would destroy their home. This
leads to relatively low levels of parasitemia for those
already with acute phase chagas. After the acute phase,
sufferers from chagas rarely suffer another acute phase
of the disease because this is adverse to the survival
of T.cruzi.
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