Download Toxoplasma gondii

Toxoplasma gondii
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T.gondii causes Toxoplasmosis.
Recently, due to the emergence of several
outbreaks, prevalence of AIDS and the
improvement of diagnostic measures,
gradually it is realized to be an important
opportunistic protozoan, which may be
lethal.
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There are 5 morphologically different stages:
Trophozoite: or Tachyzoite is crescent or banana shaped
with a pointed end and a bluntly round end.
In the acute stage of the disease, trophozoites are
usually scattered in the blood, cerebrospinal fluid and
various pathological exudates arranged in pairs or singly.
The trophozoite community is within a host cell
parasitophorous vacuole not surrounded by a cystic wall.
Hence they are also known as a pseudocyst (usually a
swelling macrophage with a several parasites).
The trophozoites within a pseudocyst are Tachyzoites.
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Tissue cyst: is round and oval in
appearance and the cystic wall created by
the parasite is thin, but firm and elastic.
The protozoa multiply in the tissue cyst
slowly and repeatedly.
The trophozoites in the cyst are called
Bradyzoites, which are similar to the
Tachyzoites, but smaller than them.
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Schizont: can be found in the small intestinal
mucosa of the infected cat.
Schizonts contain about 4-40 merozoites.
Gametocytes are also found in the small
intestinal mucosa of the cat.
Male gametocytes produce 12-32 male gametes,
crescent in shape.
The female gametocyte develops into a female
gamete.
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Male and female gametes fertilize to form
a zygote that dvelops into an oocyst.
An oocyst is round or elleptic and covered
with a smooth transparent cystic wall
consisting of two layers.
Each mature oocyst contains two
sporocysts with each sporocyst containing
4 sporozoites.
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Two different kinds of host are needed in the sexual and
asexual generations present in the life cycle of T.gondii.
Sexual development or Gametogony and only the
schizogony of the asexual development occurs in the
epithelial cells of the small intestine of cats(intraintestinal phase).
The binary fission and endodyogeny ( process of internal
budding in which two daughter cells are formed within
the body of the mother cell that dies when the progeny
are released) of the asexual development takes place in
various nucleated cells outside the intestine of many spp.
Of mammals and birds.
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The extra-intestinal phase begins when the oocyst or the
meat or animal viscera containing cyst or pseudocyst are
ingested by an intermediate host (man, pig, cattle,
cheep. Mouse etc…), sporozoites bradyzoites or
tachyzoites are released in the host intestine.
Parasites penetrate the intestinal wall. They actively
invade or are ingested by the mononuclear phagocytes
and develop and inhabit them.
The ability and effeciency of the cell invasion is varied in
different strains of T.gondii with high or low virulence.
Binary fission and endodyogeny results in the production
of Tachyzoite bearing Trophozoites, encircled by the host
cell membrane called Pseudocysts.
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When Tachyzoites increase more than 10 per cell, the
host cell breaks and parasites released, that in turn
invade new cells , develop and multiply.
In an immuno competent host, these Tachyzoites
develop into cysts especially in the cells of the brain, eye
and skeletal muscles and can survive for several years.
Several hundred bradyzoites can be observed a cyst.
Under immuno suppressed conditions, cysts rupture,
deliver many bradyzoites which infect more cells.
The ability of invasion and multiplication of T.gondii and
the host immune status are in a dynamic equilibrium,
and as a result, tachyzoites can transform into
bradyzoites and vice versa.
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When food or water contaminated with T.gondii
oocyst or animal body containing cysts,
pseudocyst ingested by a feline, sporozoites,
bradyxoites or Tachyzoites are released in the
small intestine.
These parasites invade the epithelial cells, and
3-7 days later transform into multinucleated
schizont.
On maturation, merozoites are released, in turn
they invade new epithelial cells and repeat
schizogony.
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Several generations later, some merozoites
develop into micro and macro gametes .
Fertilization results into a zygote which develops
into an oocyst.
OOcyst leaves the host lumen, finally mixed with
feca and expelled.
Under favorable conditions, each oocyst devlops
into infectious stage with 2 sporocysts and each
containing 4 sporozoites.
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Pathogenesis:
Tachyzoite is the principle stage responsible for
the pathological changes.
After entering the host cell, trophozoites multiply,
break the cell and the released tachyzoites
invade new cells once again.
The process repeats itself and a foci of edema
and necrosis surrounded by lymphocytes
monocytes and plasma cells are formed.
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The pathological changes can be divided into 3 categories:
A) Necrotic foci result from cell destruction by the quickly
multiplying tachyzoites.
These foci, later form the fibrosis scars with the cysts present all
around.
B) Cysts normally do not induce inflammation, but if it breaks, the
released bradyzoites , although cleared by the host immune system,
some will survive and cause delayed hypersensitive reaction, which
results in the formation of granuloma and scar.
C) Secondary pathological changes initiated by focal damage can
result in blood vessel blockage induced by inflammation of these
vessels and further results in tissue infarction, usually in the brain.
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After infection of the intestinal epithelium,
the organisms can spread to other organs
like brain, lungs liver and eyes.
This spread controlled by cell-mediated
immunity, but circulating antibodies
enhance killing of the parasite.
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Congenital Toxoplasmosis:
Congenital infection occurs when mother is infected during
pregnancy.
Infection during First trimester, the outcome is often severe.
Second trimester infection, some babies will show symptoms
months or years after birth.
Third trimester infection is usually non-significant.
Congenital toxoplasmosis occurs only in babies of primigravida.
If mother infected before pregnancy, parasites will be in cyst form
and no trophozoites to cross the placenta.
If mother having previous infection, reinfected during pregnancy,
will have antibodies and will not transmit parasites to the child.
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Clinical findings:
Immuno competent adults asymptomatic, or may resemble
Infectious mononucleosis., but heterophil antibody test is negative.
Congenital infection can result in abortion, still birth or neonatal
disease with encephalitis, chorioretinitis and hepatosplenomegaly.
Fever, jaundice and intra-cranial calcifications are also seen.
Mental retardation may develop in children, months to years later.
Congenital infection is the leading cause of blindness in children.
Toxoplasmosis, is one of the most severe complications of AIDS,
leading primarily to encephalitis.
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Laboratory diagnosis:
Involves an Immunofluoroscens assay for IgM
antibody during acute and congenital infections.
High IgG antibody titres may be useful, but
could be of the mother.
Giemsa stained crescent shaped trophozoites in
acute infections. Cysts may be seen in tissue.
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Treatment:
For Congenital toxoplasmosis (symptomatic or
non-symptomatic and disseminated disease in
immuno- compromised individuals: Combination
of Sulfadiazine and pyrimethamine.
Prevention:
Cook meat thoroughly to kill the cysts.
Avoid proximity to cats.
References:
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