Ocular Toxoplasmosis (outline)

Uveitis course, SOIE, Vilnius, Lituania

Friday, September 23-24, 2011

Carl P. Herbort1,3 MD, PD, fMER, FEBOphth

1

Centre for Ophthalmic Specialised Care (COS), Lausanne, Switzerland

University of Lausanne, Lausanne, Switzerland

Carl.herb@bluewin.ch

Toxoplasma Gondii is an obligate intracellular pathogen that replicates within a

parasitophorous vacuole. Infections are initiated by digestion of parasites deposited in cat
faeces or in undercooked meat and probably many more infection routes (1). Parasites then
disseminate to target tissues such as all neuronal tissues including the retina where they then
develop into long-lived asymptomatic tissue cysts (2). Occasionally, cysts reactivate and
growth of newly emerged parasites occurs when the control of cysts by the host's immune
system is escaped (3).
There is a substantial variation between patients in the severity of intraocular inflammation
associated with ocular toxoplasmosis, attributable to multiple host- and disease-related
factors. Results suggest that disease characteristics also vary in different areas of the world
tributary to different virulence of strains (4). The mechanisms that regulate the inflammatory
process in recurrent TRC are poorly understood and also the dynamics of the humoral

response are still to be fully explained (5,6,7).

The immune response in TRC, triggered by the presence of newly emerged parasites that
originate from the rupture of the cysts, is crucial for the control of the infection and is activated
towards the causing agent and therefore high titres of Ig can be found in the active phase of
recurrence (8).
Clinical presentation, diagnosis and treatment of toxoplasmic retinochoroiditis
Unlike written in textbooks, the great majority of intraocular toxoplasmic episodes
(retinochoroiditis) is not occurring following congenital toxoplasmosis but is the result of
acquired (often silent) toxoplasmic infection. Therefore retinochoroiditis is presenting in the
classical way of a retinal focus in the vicinity of a previous scar in less than 60% of cases.
Symptoms
Most often patients complain of floaters and blurred vision. Sometimes the brow is painful
when a hypertensive uveitis is present.
Clinical signs
Clinical presentation consists usually of a solitary focus of a whitish-yellow retinitis next to a
pre-existing scar or without a scar. The disease is usually unilateral. Vitritis is usually severe
taking the aspect of the often described headlight in the fog feature. Sometimes an
associated granulomatous hypertensive anterior uveitis can be present.
Sometimes the toxoplasmic focus can be located just beside or adjacent to the optic disc and
this is termed juxtapapillary toxoplasmosis or Jensens juxtapapillary chorioretinitis, or it
can even involve the optic disc directly. In this situation therapeutic intervention is an
emergency.

Invetigations
Fundus imaging is necessary to be able to monitor the evolution of the lesion. If possible
dual fluorescein and indocyanine green angiography should be performed, showing the
extent of retinal vasculitis, the importance of associated papillitis and the extent of choroiditis.
[9} Optical coherence tomography (OCT) gives details of the retinitis and information on the
macula indicating the presence or not of cystoid macular oedema (CMO). Visual field testing
is indicating the effect of the retinitis focus on the nerve fibre layer in the area involved
showing a sectorial scotoma. Visual field testing is also important to monitor evolution of the
disease and response to treatment.
In immunocompromised patients the extension of the retinitis can be very large, there can be
more than one focus and there can be bilateral involvement.
Differential diagnosis
Any granulomatous posterior uveitis has to be considered, including infectious etiologies such
as acute retinal necrosis (necrotic herpetic retinopathies), cytomegalovirus retinitis (in
immunocompromised patientrs), syphilitic chorioretinitis and tuberculous chorioretinitis. Non
infectious causes such as sarcoidosis should also be considered being however less likely as
a differential diagnosis.
Treatment
Retinal foci in the vicinity of the optic disc or the macula or within the vascular arcades should
absolutely be treated. Large lesions with severe vitritis outside these areas should probably
also be treated. The aim of the treatment is to limit the tissue damaging inflammatory reaction
and for this corticosteroids should be given, usually systemically (50 to 70 mg to begin with).
In order to be able to give corticosteroids and to avoid proliferation of the parasite

concomitant anti-toxoplasmic antibiotics should also be given systemically. Several antibiotics

can be used such as sulfadiazine (4g) and pyrimethamine (25mg) per day together with folinic
acid, or clindamycin (4X600 mg/day), both for 4-6 weeks, or azithromycin (250 mg / day for 5
weeks) [10] to cite only a few possibilities.
Role of serologic testing in toxoplasmic retinochoroiditis
So far, in the literature and in uveitis conferences the role for toxoplasmic serology in
toxoplasmic retinochoroiditis has been downplayed and even considered as irrelevant. This
comes from the fact that general serology laboratories where samples from ocular patients
are sent, do not understand what is the exact purpose for asking a serology in a patient with
ocular toxoplasmosis. They invariably respond that the serology shows an old toxoplasmic
infection and is negative for an acute infection (no IgM). This is an adequate response for
internal medicine patients where an acute infection is usually searched for and motivates the
serology quest. In ocular patients where, in an overwhelming majority of cases, the disease is
the result of a recurrence, we want to know whether a clinical picture compatible with ocular
toxoplasmosis is actually due to Toxoplasma Gondii and we therefore only ask to serology
whether the patient has once been in contact with the agent which is confirmed by the
presence even of low levels of IgGs. In summary, serology is useful in all active cases of
suspected toxoplasmic retinochoroiditis. Very high titres are specific for toxoplasmic disease,
thus confirming the suspected diagnosis. This is very important, especially in atypical cases.
Aim of this lecture is to summarize the pathophysiology of Toxoplasmic retinochoroiditis and
give a hint on latest treatment options.

References
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presenting in an outbreak. Ophthalmology. 1998;105:1032-7.
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9. Auer C, Bernasconi O, Herbort CP. Indocyanine green angiography features in toxoplasmic retino
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Ophthalmol 1998; 82:1306-8.