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Toxoplasmosis is a
severe, world-wide generalised or central nervous
system disease by the Protozoan toxoplasma
gondii. This protozoan parasite is found in
man and many species of birds and animals. T
gondii has recently been shown to be a
coccidian that exists in 3 infectious forms:
1. The tachyzoite (or
endozoite), the proliferative form, is present in
large numbers in blood, excreta and secretions in
acute disseminated infections;
2. The cystozite (or bradyzoite), the resting
form, is present within encapsulated cysts,
particularly in muscle and nerve tissue, in
chronic infections;
3. The oocyst is the form passed only in the
faeces of cats following their infection by the
coccidian intestinal epithelial stages
characteristic only of feline toxoplasmosis. The
coccidian stages in cats appear to be crucial to
the maintenance of T. gondii in nature.
However the relative importance of several sources
of infection for man remains to be determined,
including, particularly, accidental ingestion of
oocysts denied from cat faeces or the ingestion of
encapsulated cysts in raw or under-cooked meat.
In human terms the clinical patterns of
Toxoplasmosis can be divided into four patterns;
acquired toxoplasmosis, congenital infection,
retinochoroiditis and disease in the altered host.
In the latter, toxoplasmosis may present as a
disseminated disease. In patients treated with
immuno suppressive drugs or in patients with
neoplasms of the lymphatic system. Patients
with acquired toxoplasmosis are often
asymptomatic, but may present with fever, general
malaise, enlarged glands, splenomegaly, headaches
and a macropapular rash. Rarely, severe cases
include myocarditis (inflammation of the heart
muscle) and retinochoroiditis (eye problems).
Congenital transmission occurs only during
acute infection – which has been detected in 1% of
pregnant women. Approximately 20-40% of such adult
infections are transmitted to the
foetus, resulting in some abortions and still
births. Signs of congenital toxoplasmosis are
present at birth or progress during the first
months of life: seizures, mental retardation,
enlarged spleen and/or liver, pneumonitis, rash,
fever, retinochoroiditis and cerebral
calcification. The retinochoroiditis is usually
a late manifestation of asymptomatic congenital
infection, with symptoms being first noted in the
second or third decade of life.
The congenital disease is often fatal and if the
infant survives the acute infection, he is likely
to be handicapped with severe Central Nervous
System and ocular lesions. The acquired disease
is usually symptomatic or mild, but acute
infections in adults have been known to be fatal.
Asymptomatic infections are common, serological
surveys indicate that 20-80% of various
populations (human and animals) are infected!
Diagnosis is based on
the presence of changing or elevated titers of
toxoplasmosis antibodies (which are very specific)
and on the isolation of the parasite from infected
tissues.
Toxoplasmosis organisms may be directly identified
in smears of blood, bone marrow, spinal fluid or
wound exudates.
Human treatment of symptomatic acute infections is
pyrimethamine, trisulfapyrimidines, and folic acid
for one month. Recently trimethoprim has been
found effective. Steroids may also be used. Blood
tests should be done weekly. Congenital
toxoplasmosis should be treated whether
symptomatic or asymptomatic. Pregnant women
should have their serum examined for the
toxoplasmosis antibody. Those with negative titers
should take precautionary measures to prevent the
infection, preferably having no further contact
with cats, and eating no undercooked meats or
unwashed/undercooked vegetables.
Reference: Current Medical Diagnosis and
Treatment, 1980. Marcus A Krupp, M.D. Milton J
Chatton, M.D.
A
Hunt
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