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Joint International Conference on Long-term Experiments ...

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As in any other cyclic, infectious, self-limiting disease, there can be observed a period<br />

of incubati<strong>on</strong> of 10-21 days, after c<strong>on</strong>sumpti<strong>on</strong> of infested meat, or even shorter, 5-18<br />

days, after ingesti<strong>on</strong> of oocysts.<br />

The state period comprises the acute infecti<strong>on</strong>, which in 80-90% of cases in<br />

asymptomatic. Thus can be explained the de<strong>term</strong>inati<strong>on</strong> in populati<strong>on</strong>al studies from<br />

many European countries (e.g. France) of an 80% of IgG antitoxoplasma antibodies<br />

possessors, indicators of them having previously acquired the infecti<strong>on</strong>.<br />

In 10-20% of cases, even in immunocompetents, the acute infecti<strong>on</strong> can manifest<br />

symptomatically, with lymphogangli<strong>on</strong>ic, febrile or m<strong>on</strong><strong>on</strong>ucleosic syndrome<br />

(adenopathy, fever, asthenia, myalgia, fugitive exanthema, hepatosplenomegaly without<br />

angina, lymphocytosis persistent for days or weeks). During this stage of acute<br />

symptomatic disease, clinical c<strong>on</strong>fusi<strong>on</strong>s can be made with other diseases that develop<br />

the so-called „m<strong>on</strong><strong>on</strong>ucleosis-like syndrome” (rubella, HIV infecti<strong>on</strong>, Epstein-Barr<br />

infecti<strong>on</strong>). Extremely rarely, immunocompetents develop myocarditis, pericarditis,<br />

hepatitis, encephalitis or meningoencephalitis. The presence of acute infecti<strong>on</strong>, either<br />

asymptomatic or symptomatic is proven by the IgM antitoxoplasma antibodies.<br />

Chr<strong>on</strong>ic (or latent) infecti<strong>on</strong> exists in all infested pers<strong>on</strong>s after the resoluti<strong>on</strong> of<br />

acute phase, for a shorter or l<strong>on</strong>ger period of time (weeks-years), sometimes generating<br />

ocular manifestati<strong>on</strong>s of recidivating chorioretinitis, at other times chr<strong>on</strong>ic toxoplasmic<br />

endometritis. The appearance probability of clinical symptomatology of chr<strong>on</strong>ic<br />

infecti<strong>on</strong> in immunocompetents is also owing to external or internal factors which<br />

generate a degree of immunodepressi<strong>on</strong>. Acutizati<strong>on</strong> of chr<strong>on</strong>ic infecti<strong>on</strong> is marked by<br />

the presence of IgM antitoxoplasma, together with elevated titers of IgG<br />

antitoxoplasma.<br />

The producti<strong>on</strong> mechanism of ocular toxoplasmosis in immunocompetents is the<br />

reactivati<strong>on</strong> of c<strong>on</strong>genital infecti<strong>on</strong> or acquired acute infecti<strong>on</strong> which eventually<br />

cr<strong>on</strong>icizes. The forms of manifestati<strong>on</strong> can be: chorioretinitis or focal necrotic retinitis<br />

(visi<strong>on</strong> disorders, scotomas, local pains, photophobia, epiphora), glaucoma with visi<strong>on</strong><br />

loss, posterior uveitis or panuveitis, papilitis with optic atrophy.<br />

Endometrial toxoplasmosis resulted after chr<strong>on</strong>icized acute infecti<strong>on</strong>, can<br />

generate sterility, aborti<strong>on</strong>, premature birth and infecti<strong>on</strong> transmissi<strong>on</strong> to the c<strong>on</strong>cepti<strong>on</strong><br />

product, resulting in c<strong>on</strong>genital malformati<strong>on</strong>s compatible or incompatible with life.<br />

Fig. No.1 – Toxoplasmic Encephalitis Fig. No.2 – Toxoplasmic Chorioretinitis<br />

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