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American Trypanosomiasis (Chagas' disease), a zoonotic infection by the
protozoan Trypanosoma cruzi, causes acute, subacute and chronic
parasitemia, with dissemination to many organs, specially the heart,
brain, esophagus and colon.
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African Trypanosomiasis
Trypanosoma
cruzi occurs in blood as a trypomastigote and in reticuloendothelial
and other tissue cells typically as a leishmanial form, the amastigote.
The amastigote form lacks flagella but retains the kinetoplast,
which permits its differentiation from other intracellular organisms
such as
Toxoplasma and
Histoplasma.
The disease
occurs in North and South America, mostly in the area from Mexico to
Argentina(Image). It has never been reported outside the Western Hemisphere,
though the vectors and animal reservoirs are common to many parts of
the world.
The vectors
are large biting insects of the genus Triatoma. These insects are
found in areas where there are unhygienic conditions associated with
poverty. They bite only at night. During the day they hide in cracks
in the walls of primitive country dwellings.
The organism
is sucked up by the
Reduviids, the
kissing bugs(Image) as a free flagellate or as an
intracellular leishmanial form within a macrophage. In the midgut of
the insect the organism becomes flagellated, and binary multiplication
occurs. It migrates to the hindgut, where it is transformed into the
metacyclic trypanosome form infective for the vertebrate host.
Since the
triatoma defaecates at the time of biting, the infection is usually
acquired by rubbing the faeces containing the metacyclic trypanosome
stage of the parasite into the tiny skin puncture or into other
abrasions of the skin in the area.
Infections through the intact
mucous membranes occur most frequently in the lips or in the
conjunctivae, when the eyes are rubbed with fingers soiled with the
insect faeces.
T. cruzi
enters macrophages by parasite-specified phagocytosis. Phagocytosis is
partially dependent on macrophage cell surface receptors. The
protozoon does not remain within phagocytic vacuole but escapes into
the cytoplasm where it multiplies. By leaving the parasitophorous
vacuole, the organism escapes the action of microbicidal lysosomal
enzymes.
The
circulating forms are susceptible to the trypanosomal activity of the
lysosomal enzymes and major basic protein of eosinophils.
Specific
diagnosis of America trypanosomiasis may be accomplished by the
finding of the typical trypanosome stage of T. cruzi in the blood
during febrile episodes.
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Aspiration of spleen, liver, lymph nodes, or
bone marrow will frequently reveal the leishmanial form of the
organism in fixed macrophages.
In reticuloendothelial cells T. cruzi
cannot be easily distinguished from species of leishmania, but only T.
cruzi invades myocardial and neuroglial cells as a leishmanial type of
organism.
Serologic
methods include complement fixation, indirect immuno-fluorescence,
hemagglutination, enzyme-linked immunosorbent assay and thin layer
immunoassay.
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myocardiTIS
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CARDIOMYOPATHY ;
SUDDEN CARDIAC DEATH
ACUTE CHAGAS'
DISEASE :
The acute form
is the more common of the two types of Chagas' disease. It occurs
predominantly in small children and is characterized by moderate
hepatosplenomegaly, facial edema, tachycardia, and the presence of
T. cruzi in peripheral blood.
In 50% of
cases the primary site is the outer canthus of one eye, with
unilateral palpebral edema and satellite preauricular lymph node
enlargement (Romana's sign)-
Image .
In 25% of cases the portal of entry
is
represented by a nodular or ulcerative skin lesion (chagoma),
accompanied by enlargement of regional lymph nodes.
Histologically,
the primary lesion is characterized by numerous histiocytes, chronic
inflammatory cells, and areas of fat necrosis throughout which
numerous leishmanial forms are identified.
Multiplication
of the organisms that have been engulfed by nearby macrophages is soon
followed by the invasion of other structures such as smooth and
striated muscle (including cardiac muscle), glial and nervous cells
and fat cells.
Parasites are
found in almost all organs, and their presence is accompanied by
mononuclear cell infiltration, congestion, and edema, and occasionally
by granulomatous areas.
Reticuloendothelial
activity and increase in the number of fixed macrophage cells cause
splenomegaly, hepatomegaly, adenopathy and hyperplasia of bone marrow.
The process is then a reticulopathy similar to
kala-azar and
histoplasmosis.
Death during
acute phase is caused by
acute myocarditis with
congestive cardiac failure,
meningoencephalitis, or complications such as
bronchopneumonia. A recent study
showed that T. cruzi readily enters the central nervous system during
the acute infection. Cerebrospinal fluid findings include pleocytosis
and high protein levels.
The heart is
enlarged and flabby with pronounced dilatation of the left ventricle.
The myocardium is pink and shows yellowish gray streaks.
Microscopically, the myocardium is diffusely involved but reveals only
spotty cell destruction.
The myocardial fibers are separated by
intense edema, proliferation of histiocytes, and infiltration with
chronic inflammatory cells and few polymorphonuclar cells.
Within the
muscle fibers are leishmanial forms either arranged in rows or in
cystlike dilatations.
Cardiac fibers
show degenerative changes , the most important of which is hyaline
necrosis of isolated fibers. Inflammatory changes in the myocardium
also may involve the bundle of His and its ramifications.
CHRONIC
CHAGAS' DISEASE:
The dominant
factor in the chronic stages of Chagas' disease is almost always some
degree of myocardial fibrosis. Many patients report a previous acute
attack. However, in a number of cases there is no history of a
previous attack. The chronic cardiac form of Chagas' disease is a
leading cause of cardiac failure and sudden death in endemic areas.
The heart is
enlarged with generalized hypertrophy and dilatation. Mural
endocardial thromboses are usually present, most frequently in the
right auricle and at the apex of the left ventricle. Apical
thrombosis, with focal endomyocardial fibrosis at the base, represents
the most important single gross finding suggestive of Chagas'
myocarditis.
In the absence
of thrombosis the myocardium at the apex frequently appears
distended and thinned, sometimes even to the point of aneurysmal
formation.
Embolic
phenomena, both pulmonary and systemic are present in about 75% of
autopsied cases. The main source of emboli are intracardiac
thrombi which are also found at autopsy in approximately 75% of cases.
Microscopically the myocardium shows chronic, non-specific,
mononuclear inflammation. Hypertrophy of cardiac fibers, small focal
areas of necrosis and granular degeneration of cardiac fibers, focal
and diffuse fibrosis, vascular dilatation and congestion, and
interstitial and interfibrillary edema are other common microscopic
features. Parasites (leishmanial forms in pseudocysts) are identified
with difficulty in a very limited percentage of cases. Thus the
pathogenesis of myocardial fiber damage in chronic Chagas' disease is
still unclear. Autoimmunity and intravascular platelet aggregation
have both been proposed as having a pathogenetic role.
DIGESTIVE
FORM OF CHAGAS' DISEASE:
Megaesophagus
and megacolon are manifestations of chronic Chagas' disease. Fibrosis
and degeneration of autonomic ganglia in the heart have been
demonstrated in persons with megaesophagus, as well as considerable
diminution in the number of ganglionic cells in the Auerbach plexus of
the esophagus and intestine.
CONGENITAL
CHAGAS' DISEASE:
The
transplacental transmission of T. cruzi infection has been well
documented in humans. Congenital Chagas' disease can lead to premature
birth birth and fetal death. A chronic placentitis, similar in some
respects to the syphilitic placenta, with bulky and ischemic villi,
has been described. Leishmanial forms are found within the cytoplasm
of macrophages in variable numbers. Interstitial pneumonitis with a
prominent mononuclear histiocytic infiltrate can develop in infants.
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