Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 7  |  Issue : 6  |  Page : 818-821  

Ocular toxoplasmosis: A case report with review of literature


1 Department of Ophthalmology, Dr. D.Y. Patil Medical College and Research Centre, Pimpri, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra; Lune Eye Clinic, Madhav Heritage, Pune, Maharashtra, India
2 Department of Ophthalmology, Dr. D.Y. Patil Medical College and Research Centre, Pimpri, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India
3 Lune Eye Clinic, Madhav Heritage, Pune, Maharashtra, India

Date of Web Publication18-Nov-2014

Correspondence Address:
Abhay A Lune
C/O Lune Eye Clinic, 1641, Madhav Heritage, Tilak Road, Pune - 411 030, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.144900

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  Abstract 

Ocular toxoplasmosis is a potentially blinding necrotizing retinitis with a progressive and relapsing course. It presents as a localized retinochoroidal lesion in most of the cases and is the most common cause of posterior uveitis, world-wide. The incidence of ocular infection is very high, most of which are subclinical. Hence to highlight this blinding disease, which may escape detection and to emphasize its preventive measures so as to prevent the visual disability arising from it. We report a case of a 35-year-old male who had diminution of vision in his right eye since 10 years. His best-corrected vision in that eye was three meters finger counting. Fundus examination showed a well-defined pigmented scar on the macula in the right eye and 2 small peripheral pigmented scars in the left eye. Since it is a potentially blinding disease with recurrences, preventive measures should be taken to avoid it. Proper washing of hands and strict food hygiene are important. Pica prevention is an important measure in children. Pregnant women should avoid contact with cats. Patients with a retinochoroidal scar harbor cysts and are to be periodically monitored due to the high risk of recurrence. Prophylactic treatment is recommended for these patients before undergoing cataract surgery. Immunocompromised patients with ocular toxoplasmosis should undergo a complete neurological evaluation due to the high risk of intracranial involvement.

Keywords: Intracranial calcification, posterior uveitis, retinochoroiditis, vitritis, zoonosis


How to cite this article:
Lune AA, Pujari SN, Lune SA. Ocular toxoplasmosis: A case report with review of literature. Med J DY Patil Univ 2014;7:818-21

How to cite this URL:
Lune AA, Pujari SN, Lune SA. Ocular toxoplasmosis: A case report with review of literature. Med J DY Patil Univ [serial online] 2014 [cited 2021 Oct 19];7:818-21. Available from: https://www.mjdrdypu.org/text.asp?2014/7/6/818/144900


  Introduction Top


Ocular toxoplasmosis is a potentially blinding necrotizing retinitis with a progressive and relapsing course. It presents as a localized retinochoroiditis in typical cases. [1] World-wide, it is the most common cause of posterior uveitis. [2] It is a zoonotic infection with cat as the definitive host and man and other animals as intermediate hosts.


  Case Report Top


A 35-year-old male patient reported to us with the complaints of diminution of vision in the right eye since 10 years. He did not give a history of ocular trauma, redness or pain in that eye, seizures or any treatment in the past. He is a non-vegetarian. There is no history of contact with cats. Clinically, the anterior segment examination of both the eyes were normal with a best-corrected vision of three meters finger counting in the right eye and 20/20 in the left eye. Fundus examination of the right eye revealed a well-demarcated circular atrophic pigmented scar about three disc diameters in size involving the macula [Figure 1]. The left eye revealed two small pigmented scars along the inferotemporal blood vessel beyond the macula [Figure 2]. The rest of the fundus and vitreous in both the eyes were normal. X-ray of skull was normal. Enzyme-linked immunosorbent assay (ELISA) of serum for anti-toxoplasma IgG antibodies showed high titers, more than 1.11. ELISA for human immunodeficiency virus was negative. He was advised a yearly follow-up.
Figure 1: Fundus photograph of the right eye showing a classical welldemarcated circular atrophic pigmented scar of inactive toxoplasmosis, about three disc diameters in size involving the macula

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Figure 2: Fundus photograph of the left eye showing two small pigmented scars of inactive toxoplasmosis along the inferotemporal blood vessel beyond the macula, which is uncommon

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  Discussion Top


There is no treatment for inactive toxoplasmosis. Thus no active treatment could be offered to our patient for the right eye macular scar as the visual loss is irreversible. The good vision in the left eye is due to the peripheral location of the scars. The patient was advised a regular six monthly follow-up to detect any recurrences.

Toxoplasma is an obligate intracellular parasite, affecting both humans and animals. Human infection can be congenital or acquired. The three forms of the parasite are trophozoites, the proliferating invasive form responsible for acute infection, bradyzoites, which is the encysted form found in tissue cysts with an affinity for neural and muscle tissue and the oocysts produced only in cats and excreted in their feces. Humans are infected by ingesting inadequately cooked meat or eggs infected with bradyzoites, ingestion of food and water contaminated with oocysts and infants eating soil (pica) or transplacental transmission of trophozoites from the mother. The host's immune response causes these trophozoites to transform into bradyzoites, which form tissue cysts that remain inactive and reactivate to cause acute infection.

Ocular toxoplasmosis can be congenital, acquired or recurrent. It may be active or inactive in the form of a scar. Most cases of retinochoroiditis are congenital. Recently, however, it has been shown that acquired infections occur more frequently than previously suspected. [3] Most of the active ocular toxoplasmosis represent reactivation. Clinically, congenital and acquired infections are usually asymptomatic and appear very similar.

Congenital toxoplasmosis occurs in about 1/1,000-1/10,000 live births. It develops in 30% to 50% of infants born to mothers who acquire toxoplasmosis during pregnancy. Transplacental transmission occurs only when the infection is acquired during pregnancy. Chronic maternal infection is not associated with congenital disease. The risk of transmission is lower in the first trimester (15-20%), but with severe fetal complications like stillbirth. Third trimester infection is more common (40%) and mostly subclinical.

The incidence of ocular infection in congenital toxoplasmosis is 80%, most of which are subclinical while 80% are bilateral. Other clinical manifestations are intracranial calcification (32%), hydrocephaly or microcephaly (26%), seizures, fever and rash. There is predilection for the posterior pole because of the end-artery anatomy of the fetal macular circulation. The classic triad of retinochoroiditis, intracranial calcification and seizures occur in a some cases of congenital infection. [4] In children with mild infection, the disease may become apparent only later in life when retinochoroidal scarring is detected on ophthalmoscopy.

Acquired toxoplasmosis in the immunocompetent patient occurs with an incidence of 2-20% and is often asymptomatic, with only 10-20% symptomatic with mild lymphadenopathy, flu-like symptoms or visual disturbance. The disease is benign and self-limiting but is life-threatening in immunocompromised cases due to the encephalitis, myocarditis and pneumonitis. Ocular toxoplasmosis in acquired immunodeficiency syndrome (AIDS) patients occurs in 1-2% cases and 30-50% of these patients have intracranial involvement. Hence, all AIDS patients with ocular toxoplasmosis must undergo a neurological evaluation including computed tomography or magnetic resonance imaging with contrast and lumbar puncture.

Recurrence in an old, healed, ocular lesion is the most common cause of active infection in healthy individuals and typically occurs adjacent to an old scar. The cysts remain inactive at the borders of the scar for years and may rupture causing recurrence. Toxoplasmic retinochoroiditis is a recurrent disease in two-thirds of patients. [5] The recurrences occur between the age of 10 and 35 years with an average age of 25 years. It is greater during the 1 st year after an acute infection than during subsequent years. [1]

The active lesions of ocular toxoplasmosis are classically adjacent to or at the border of an old inactive pigmented scar (satellite lesion). Typical symptoms are blurred vision, floaters and metamorphopsia. It typically affects the posterior fundus. It mostly presents as focal necrotizing retinitis involving the inner retinal layers appearing as a circular whitish fluffy lesion with surrounding retinal edema, localized or diffuse vitritis and a granulomatous anterior uveitis. The size varies from one-tenth to five disc diameters. The severe vitritis gives a "headlight in the fog" appearance. [6] The choroid and sclera may become involved secondarily. [2] Anterior uveitis is due to hypersensitivity reaction to the antigen. Sheathing of the retinal vasculature, vascular occlusions and periarterial exudates (kyrieleis arterialitis) at or away from the foci of retinitis may be seen. In healthy patients, the retinitis heals within 1-4 months of treatment and is replaced with a sharply demarcated atrophic scar with pigmented borders as seen in our case.

A large destructive lesion is the most common variant of active retinitis. Atypical variants are punctate inner retinal lesions, punctate outer retinal lesions, massive granuloma, multifocal punctate lesions and toxoplasmic papillitis. These are usually seen in elderly and immunocompromised individuals. Lesions in immunocompromised patients are multifocal, extensive, aggressive and bilateral with large areas of confluent retinal necrosis. [7]

Complications of ocular toxoplasmosis include cataract, secondary glaucoma, band keratopathy, vascular occlusions, scleritis, retinal gliosis, tractional retinal detachment, cystoid macular edema, macular pucker, optic atrophy and choroidal neovascular membrane. [4]

Nearly 40% cases suffer permanent unilateral visual loss of 20/100 or worse while small peripheral lesions are frequently self-limiting and innocuous as was seen in our case in the right and left eyes respectively. In adults active lesions are to be differentiated from tuberculosis, sarcoidosis, syphilis, viral and fungal infections while in the congenital form, from herpes simplex, cytomegalovirus and retinoblastoma.

The diagnosis of ocular toxoplasmosis is clinical, based on the characteristic lesion. The serologic laboratory tests are supportive. Various serological tests for diagnosing toxoplasmosis include Sabin-Feldman dye test, indirect fluorescent antibody test, immunosorbent agglutination assay and ELISA. ELISA detects IgM antibodies of active lesion or IgG antibodies of old lesion in serum or ocular fluid. The rising or high titer of antibodies in serum is diagnostic as was seen in our case. In humans, the prevalence of IgG antibodies to toxoplasma increases with increasing age. On an average 20-70% adults are seropositive. Anti-toxoplasma IgG antibodies can persist at high titers for years after acute infection and there is a high prevalence of such antibodies in the general population giving false positive results. [8] Polymerase chain reaction of ocular fluids is very sensitive in diagnosing the disease.

The classical "triple drug therapy" with pyrimethamine, sulphadiazine and prednisolone is reserved for lesions involving the macula and optic nerve head, in large destructive lesions, severe vitritis and in any lesion in AIDS patients. Some studies have shown that prophylactic treatment for ocular toxoplasmosis in immunocompetent patients reduces the chances of recurrence. [9] Prophylaxis with antibiotics are effective against disseminated toxoplasmosis in immunocompromised patients. Furthermore, prophylactic treatment is recommended in all patients with inactive toxoplasmic retinochoroiditis undergoing cataract surgery. [10]

Since ocular toxoplasmosis is a potentially blinding disease with recurrences, preventive measures should be taken to avoid it. Proper washing of hands and strict food hygiene are important. Pica prevention is an important measure. Pregnant women should avoid contact with cats. Patients with a retinochoroidal scar harbor cysts and are to be periodically monitored due to the high risk of recurrence. Prophylactic treatment is recommended for these patients before undergoing cataract surgery. Immunocompromised patients with ocular toxoplasmosis must undergo a complete neurological evaluation due to the high risk of intracranial involvement.

 
  References Top

1.
Holland GN. Ocular toxoplasmosis: A global reassessment. Part I: Epidemiology and course of disease. Am J Ophthalmol 2003;136:973-88.  Back to cited text no. 1
[PUBMED]    
2.
Smith JR, Cunningham ET Jr. Atypical presentations of ocular toxoplasmosis. Curr Opin Ophthalmol 2002;13:387-92.  Back to cited text no. 2
    
3.
Gilbert RE, Stanford MR. Is ocular toxoplasmosis caused by prenatal or postnatal infection? Br J Ophthalmol 2000;84:224-6.  Back to cited text no. 3
    
4.
Brady-McCreery KM, Hussein MA, Paysse EA. Congenital toxoplasmosis with unusual retinal findings. Arch Ophthalmol 2003;121:1200-1.  Back to cited text no. 4
    
5.
Araujo F, Slifer T, Kim S. Chronic infection with Toxoplasma gondii does not prevent acute disease or colonization of the brain with tissue cysts following reinfection with different strains of the parasite. J Parasitol 1997;83:521-2.  Back to cited text no. 5
    
6.
Rothova A. Ocular manifestations of toxoplasmosis. Curr Opin Ophthalmol 2003;14:384-8.  Back to cited text no. 6
[PUBMED]    
7.
Holland GN. Ocular toxoplasmosis in the immunocompromised host. Int Ophthalmol 1989;13:399-402.  Back to cited text no. 7
[PUBMED]    
8.
Ongkosuwito JV, Bosch-Driessen EH, Kijlstra A, Rothova A. Serologic evaluation of patients with primary and recurrent ocular toxoplasmosis for evidence of recent infection. Am J Ophthalmol 1999;128:407-12.  Back to cited text no. 8
    
9.
Silveira C, Belfort R Jr, Muccioli C, Holland GN, Victora CG, Horta BL, et al. The effect of long-term intermittent trimethoprim/sulfamethoxazole treatment on recurrences of toxoplasmic retinochoroiditis. Am J Ophthalmol 2002;134:41-6.  Back to cited text no. 9
    
10.
Bosch-Driessen LE, Berendschot TT, Ongkosuwito JV, Rothova A. Ocular toxoplasmosis: Clinical features and prognosis of 154 patients. Ophthalmology 2002;109:869-78.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2]


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