Toxoplasmosis, caused by the protozoan Toxoplasma gondii, is a widely distributed parasite infecting up to 60–80% of the elderly worldwide and poses significant risks for immunocompromised individuals. The disease can be acquired through ingestion of contaminated food or through maternal transmission to the fetus, with symptoms ranging from mild to severe, including lymphadenopathy and ocular or neurological infections. Diagnosis involves serological tests for antibodies, and prevention strategies include avoiding contact with cat feces and undercooked meat, especially for vulnerable populations such as pregnant women.

1. TOXOPLASMOSIS
TOXOPLASMA GONDII
By : Ali A. Al-Rubaiye
MUC - Babil Iraq

2. NAME
Greek – toxon = bended, plasma = masses, structure.
The genus name has its origin in the Latin name of the
rodent species (Ctenodactylus gundi),
where the agent of disease was detected by the French
scientists Nicolle and Manceaux in the year 1907.

3. GEOGRAPHIC DISTRIBUTION/EPIDEMIOLOGY
T. gondii are protozoans belonging to Alveolata(Sporozoa)
and is distributed worldwide, reaching enormous infection
rates in humans which increase during ageing .
Thus this probably most common human parasite is found
in 60–80% of elder people worldwide. For HIV-infected
persons as well as for other immunocompromised people,
this parasite acts as “killer” number 3.
Besides humans practically all warm blooded animals may
become infected, too.

4. BIOLOGY, MORPHOLOGY
The life cycle of this protozoan parasite runs facultatively.
Final hosts are cats (house cats and species such as lions,
tigers, etc.), which excrete unsporulated oocysts measuring
1210 μm . During sporulation outside of the body, the
oocysts develop inside two sporocysts, each finally
containing four sporozoites. These stages are infectious for
intermediate hosts, which get in contact with feces of
felines. In humans and in many slaughter animals, the
parasites (sporozoites) enter first into the cells of the
reticuloendothelial system (RES), where they start to be
surrounded and thus protected inside parasitophorous
vacuoles and undergo repeated binary fissions
(endodyogeny). During this process two daughter cells are
de novo developed inside a mother cell . ( figure a )

5. CONTINUE :
These daughter cells are also described as tachyzoites
(Greek: tachys=quick), since they develop very quickly and
enter other host cells ( figure B ) . During this phase of very
quick reproduction, the tachyzoites are found in many
organs but also inside lymph nodes and in the fluid
cerebrospinalis. Finally they enter muscle and brain cells
and are now called bradyzoites (Greek: bradys= slow).
In this stage the host cells develop themselves into socalled
tissue cysts, which reach a size of 50–300 μm in diameter(
figure c,d ) If cats ingest such cysts within raw meat, they
start again the production of infectious oocysts .

6. STAGES OF TOXOPLASMA GONDII.

7. LIFE CYCLE OF TOXOPLASMA GONDII

8. SYMPTOMS OF THE DISEASE
(TOXOPLASMOSIS)
In most cases, i.e. in healthy persons, toxoplasmosis is
mostly not noted, since the symptoms are unspecific and of
low grade (e.g. weakness, pain in arms and legs, etc.).
However, serologic investigations show that with the
increasing age of persons, the rate of infections increases.
Besides these common, unspectacular symptoms under
special conditions, Toxoplasma gondii infections may
become harmful reaching the status of a severe disease:

9. (A) ACQUIRED POSTNATAL INFECTION
This disease is acquired by ingestion of sporulated oocysts
excreted by cats or by ingestion of undercooked raw meat
of infected vertebrates. After an incubation period of about
2–3 weeks, the following symptoms can be observed:
– Swellings of lymph nodes (adenitis)
– Infections of the eyes (iridocyclitis, chorioretinitis)
– Infections of the brain (meningoencephalitis),
– Infection of visceral organs (e.g. leading to intestinal
pneumonia, hepatitis, myocarditis, enterocolitis, myositis,
oedema of the skin)

10. (B) CONGENITAL TOXOPLASMOSIS
If the fetus inside a woman becomes infected for the first
time, it is highly endangered. In Germany about 6000–7000
of such cases occur per year. In about 50% of these cases,
the parasites enter the fetus so that about 1500 fetuses per
year suffer from slight to severe symptoms of a
toxoplasmosis. In such cases the above-listed organs may
be affected, so that severe fetopathias may be introduced.
Also early birth or aportus may occur. Toxoplasmosis
obtained as a baby may even induce 20 years later severe
symptoms such as loss of eye functions

11. PATHWAY OF INFECTION
With respect to the complicated life cycle of this species, several
possibilities exist to get infected with Toxoplasma gondii.
Infections may occur:
(a) By ingestion of sporulated oocysts originating from cat feces,
cat fur or contaminated food
(b) By oral uptake of stages in tissue cysts within muscles of
infected animals in case the meat is eaten raw or undercooked
(c) By intrauterine passage from mother to foetus (often in
several regions, 1% of the newborn babies are already infected)
(d) By blood transfusions (this pathway occurs in rather few
cases due to the fact that tachyzoites occur only in very low
numbers in blood)

12.  Incubation period: Hours up to 2 days in cases of acute
toxoplasmosis.
 Prepatent period: Depending on the pathogenicity and
virulence of the Toxoplasma strain: 1–2 days up to
several weeks.
 Patency: Years, tissue cysts may exist for years within
tissue cells without any symptoms. In cases of ruptures
of these cysts, new phases of infections of other cells
may occur (see chronic toxoplasmosis).

13. DIAGNOSIS:
Acute Toxoplasma infections may be diagnosed by detection of
parasites (tachyzoites) in blood, lymph node punctions, in fluid or
in biopsies of tissues. For the determination of the age of an
infection, serological tests are used, which can be done by
examination of the presence of the different antibody classes.
Fresh infections are indicated by the early presence of the IgM
class. If these antibodies are lacking or occur in lower numbers
than those of the IgG class, an older infection is present.
IgM antibodies can be diagnosed by the following tests:
– Double-sandwich IgM-ELISA (DSIgM-ELISA)
– Reverse-enzyme immunoassay (REIA)
– Immunosorbent agglutination assay (ISAGA)
– Enzyme immunoassay (EIA)

14. DETERMINATION OF A FIRST INFECTION OF A PREGNANT WOMAN
The seroconversion is the essential marker. Thus it is
needed to control monthly the blood status of a
Toxoplasma-seronegative pregnant women, since fresh first
infections need treatment. Within this context it is needed to
evaluate and interpret the antibody reactions:
– Toxoplasma antibodies are noted with the help of the IIFT-
test system already 11 days after the infection and reach
their highest levels after 3–4 weeks (like those in SAF-
tests).
– Significant IgG levels, absence of IgM antibodies and
KBR-titers of >1:10 indicate an acute toxoplasmosis.

15. PROPHYLAXIS:
Very young children, pregnant women (in case they are still
seronegative for Toxoplasma) and immunosuppressed persons
should avoid contact to cats and cat feces and should not eat raw
or undercooked meat. Deep freezing of meat at - 20 C for at least
24 h and preparation of meat at at least 54 C will potentially kill
Toxoplasma stages inside the meat. Cats in own
household should not be fed with raw meat.
Important: Pregnant women should be tested for Toxoplasma
antibodies at the very beginning of the pregnancy. In case there
are no existing Toxoplasma antibodies, this test must (!) be
repeated at each of the following monthly investigations.

16. REFERENCES
• Pittman KJ, Knoll LJ (2015) Long-term relationships: the
complicated interplay between host and the developmental
stages of Toxoplasma gondii during acute chronic infections.
Microbiol Mol Biol Rev 79:387–399.
• Wei HX et al. (2015) A systematic review and meta-analysis of
the efficacy of anti-Toxoplasma gondii medicines in humans.
PLoS One. doi:10.1371/journal.pone.0138204.
• Wyrosdick HM, Schaefer JJ (2015) Toxoplasma gondii history
and diagnostic test development. Anim Health Res Rev.
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• Hakimi MA, Bougdour A (2015) Toxoplasma’s way of
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Opin Microbiol 26:24–31.
• Blader IJ et al. (2015) Lytic cycle of Toxoplasma gondii 15
years later. Annu Rev Microbiol 69:463–485.