A RARE CASE OF BILATERAL TOXOPLASMOSIS

ABSTRACT
TOXOPLASMOSIS THOUGH IT IS AN ENDEMIC, BENIGN DISEASE , MOST OF THEM ARE
ASYMPTOMATIC. UNILATERAL TOXOPLASMOSIS IS A COMMON ENTITY. BILATERAL
TOXOPLASMOSIS IS A RARE CONDITION EVEN WITH IMMUNOCOMPROMISED AND ELDERLY
PATIENTS WHO MAY PRESENT WITH ATYPICAL RETINOCHOROIDITIS. HERE WE PRESENT A 17
YEAR OLD BOY WHO CAME WITH COMPLAINTS OF DEFECTIVE VISON IN BOTH EYES. HIS
VISION WAS 6/60 NIG , NIP IN BOTH EYES. ON FUNDUS EXAMINATION OLD CHORIORETINAL
SCAR WITH REACTIVATION SEEN IN BOTH EYES. A DIAGNOSIS OF BILATERAL TOXOPLASMOSIS
IS MADE. THE PATIENT WAS TREATED WITH ORAL ANTIHELMINTHICS, ANTIBIOTICS, STEROIDS
AND TOPICAL STEROID AND CYCLOPLEGIC EYE DROPS. THE PATIENTS VISION IMPROVED
FROM BE 6/60 TO 6/36 IN RE,6/18 IN LE.

KEY WORDS : TOXOPLASMOSIS , IMMUNOCOMPROMISED.

INTRODUCTION
TOXOPLASMOSIS IS CAUSED BY TOXOPLASMA GONDI . IT IS AN OBLIGATE INTRACELLULAR
PROTOZOAN . IT IS ESTIMATED TO INFEST AT LEAST 10 % OF ADULTS IN NORTHERN
TEMPERATE COUNTRIES AND MORE THAN HALF OF THE ADULTS IN MEDITERRANEAN AND
TROPICAL COUNTRIES. THE CAT IS THE DEFINITIVE HOST. INTERMEDIATE HOSTS INCLUDING
MICE , LIVESTOCK, BIRDS AND HUMANS. OOCYSTS ARE EXCRETED IN CAT FECES AND THEN
INJESTED BY INTERMEDIATE HOSTS INCLUDING via CONTAMINATED WATER SUPPLIES. CAT
LITTER DISPOSAL WITH SUBSEQUENT TRANSFER TO FOOD IS A WELL KNOWN POTENTIAL
MODE OF INFECTION IN HUMANS. TREATMENT IS NOT INDICATED IN EVERY CASE.
INDICATIONS INCLUDE SIGHT THREATENING LESION INVOLVING THE MACULA ,
PAPILLOMACULAR BUNDLE , OPTIC NERVE HEAD OR A MAJOR BLOOD VESSEL, SEVERE
VITRITIS AND IN IMMUNOCOMPROMISED.TOXOPLASMOSIS CONSTITUTES 20 – 60 % OF ALL
POSTERIOR UVEITIS CASES.

CASE REPORT :

A 17 YEAR OLD YOUNG MALE CAME WITH COMPLAINTS OF DEFECTIVE VISION IN BOTH EYES
4 DAYS DURATION WHICH HE NOTICED WHILE HE WAKE UP FROM BED IN THE MORNING.
VISUAL ACUITY IN BOTH EYES WERE 6/60 NIG NIP. INTRA OCULAR PRESSURE IN BOTH EYES
WERE 14 mmHg. VISUAL FIELDS IN BOTH EYES WERE NORMAL. NO H/O SYSTEMIC ILLNES OR
OCULAR COMPLAINTS OR CONTACT WITH PET ANIMALS IN THE PAST.

O/E FUNDUS RE (fig : 1a) : MEDIA CLEAR , DISC NORMAL , VESSELS NORMAL , OLD
CHORIORETINAL SCAR WITH PIGMENTATION SEEN OVER THE MACULA AND THE SUPERO
TEMPORAL ARCADE . SEROUS ELEVATION WITH CYSTOID MACULAR EDEMA TEMPORAL TO
MACULA.

Fig 1a : FUNDUS PHOTO OF RIGHT EYE SHOWING OLD CHORIORETINAL SCAR fig 1b : FUNDUS PHOTO
OF LEFT EYE SHOWING ACTIVE LESION

FUNDUS LE (fig 1b) : MEDIA CLEAR , DISC HYPEREMIC , MACULA SEROUS DETACHMENT
PRESENT EXTENDING AROUND THE DISC. VASCULAR INFILTRATION PRESENT INFERIORLY.
MULTIPLE INFILTRATION ALONG THE VESSEL WALL. OLD CHORIORETINAL SCAR PRESENT
INFERIORLY WITH INFILTRATION ALONG THE SUPERIOR MARGIN OF THE LESION . VASCULAR
AND RETINAL INFILTRATION ALONG THE SUPERO NASAL QUADRANT AND SUPERIOR
PERIPHERY. SUPERFICIAL HEMORRHAGES WITH VESSEL WALL INFILTRATION SUPERO
TEMPORALLY. SUPERFICIAL HEMORRHAGES NASAL TO MACULA.

INVESTIGATIONS

OCT

Fig 2 : OCT BE

RE (Fig 2): CENTRAL FOVEAL THICKNESS 614 um. FOVEAL COUNTOUR ALTERED. SEROUS
ELEVATION NOTED IN THE NEURO SENSORY RETINA. HYPER REFLECTIVE ECHOES IN
SUBFOVEAL REGION.

LE (Fig 2): CENTRAL FOVEAL THICKNESS 938 um. FOVEAL COUNTOUR ALTERED . LARGE
SUBFOVEAL SEROUS DETACHMENT PRESENT.

OTHER INVESTIGATIONS :

BLOOD SUGAR 96 mgs / dl ,UREA 22 mgs / dl , CREATININE 0.9 mgs / dl , Hb 13.2 mg / dl ,TC
7250 cells , DC P56 %, L40% , Eo 4%, ESR 5mm/15mm , MANTOUX - NEGATIVE, HIV
NEGATIVE , VDRL NEGATIVE.

CHEST PHYSICIAN OPINION: CHEST X RAY Normal study, NIL ACTIVE INTERVENTION.

TORCH SCREENING :

Anti RUBELLA IgG POSITIVE 141.32 IU / ml

Anti CMV IgG POSITIVE 138.59 RU / ml

Anti HSV IgG POSITIVE 212.70 RU / ml

DIAGNOSIS : RE – OLD TOXOPLASMOSIS SCAR WITH CNVM

LE – OLD TOXOPLASMOSIS WITH REACTIVATION

TREATMENT :

PATIENT WAS TREATED WITH ORAL ANTIBIOTICS, STEROIDS AND TOPICAL STEROID AND
CYCLOPLEGIC EYE DROPS.

PATIENT AFTER A WEEK OF TREATMENT SHOWED IMPROVEMENT IN VISION FROM 6/60 TO

6/36 IN RIGHT EYE, 6/60 TO 6/18 IN LEFT EYE. OCT SHOWED DECREASE IN THE SEROUS
ELEVATION IN THE LE (fig 3).

fig 3 : OCT BE AFTER TREATMENT

fig 4 : OCT RE : OLD CHORIRETINAL SCAR LE : SHOWING REDUCED SEROUS ELEVATION IN

AND AROUND THE MACULA.

DISCUSSION :
Individuals with ocular toxoplasmosis may present with myriad signs and
symptoms. These include decreased vision, floaters, pain or ocular redness. The
hallmark clinical finding of ocular toxoplasmosis is a retinochoroiditis.
Characteristically, it appears as a fluffy, white or yellowish fundus lesion with
overlying vitreous cells . The lesion initiates within the inner layers of the retina,
while the choroid and sclera may become sites of contiguous inflammation and
subsequent necrosis. The inflammation may lead to a posterior vitreous
detachment and/or the formation of vitreous “snowball” precipitates.
In addition, patients may have a granulomatous or non-granulomatous anterior
uveitis. Severe inflammation may lead to posterior synechiae. Further, it is
common to note increased intraocular pressure in patients who exhibit an
accompanying anterior uveitis.
Inactive ocular toxoplasmosis fundus lesions appear as “punched-out”
chorioretinal scarring. Upon reactivation of the initial infection, satellite areas of
newly affected retinal tissue typically present adjacent to existing lesions.
Other posterior segment findings have been associated with ocular
toxoplasmosis. Retinal vascular changes may include periphlebitis/arteritis,
perivascular sheathing, branch retinal artery or vein occlusion and choroidal
anastomosis.
Punctate outer retinal toxoplasmosis—characterized by multifocal punctate
outer retinal lesions—is a less commonly reported finding that may be
associated with a low-grade vitritis. Its appearance is similar to that of the white
dot syndromes and histoplasmosis. (However, histoplasmosis does not present
with an associated vitritis.)
Complications from ocular toxoplasmosis may pose further diagnostic
challenges as well as threaten the eye’s visual function. One such challenge is
neovascularization secondary to retinal ischemia. Severe retinal vasculitis
and/or inflammation, for example, may predispose a patient to
neovascularization.The inflammatory response may extend to the optic nerve
head, manifesting as an optic neuritis or papillitis.
Also, patients with ocular toxoplasmosis are at increased risk for
retinochoroiditis juxtapapillaris (Jensen disease). Jensen disease has been
described as an active retinal lesion with concomittant optic nerve involvement.
Neuroretinitis in toxoplasmosis is associated with optic nerve head edema and
macular exudate that presents in a stellate pattern (similar to the presentation
exhibited by patients with cat scratch disease).
CONCLUSION

BILATERAL TOXOPLASMOSIS IS A RARE CASE SCENARIO. THE MAINSTAY OF TREATMENT

INCLUDES ANTIBIOTICS, STEROIDS AND TOPICAL STEROID EYE DROPS. DRAMATIC PATIENT
OUTCOME WITH IN FEW DAYS OF STARTING TREATMENT WILL BE NOTED.

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