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ARTICLES
Year : 1979  |  Volume : 27  |  Issue : 4  |  Page : 32-33

Ocular and laboratory diagnosis of toxoplasmic uveitis and its treatment


S.M.S. Medical College, Jaipur, India

Correspondence Address:
O P Kulshrestha
S.M.S. Medical College, Jaipur
India
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How to cite this article:
Kulshrestha O P. Ocular and laboratory diagnosis of toxoplasmic uveitis and its treatment. Indian J Ophthalmol 1979;27:32-3

How to cite this URL:
Kulshrestha O P. Ocular and laboratory diagnosis of toxoplasmic uveitis and its treatment. Indian J Ophthalmol [serial online] 1979 [cited 2019 Oct 20];27:32-3. Available from: http://www.ijo.in/text.asp?1979/27/4/32/32567

The role of toxoplasma in causing uveitis, specially retino-choroiditis is now well accepted. It was established by: statistical analysis of the high frequency of positive toxoplasma reactions and serological (dye) tests in patients with ocular lesions, by the discovery of parasites in mor­phologically identical with toxoplasma in sections of enucleated eyes, and by isolation of the organisms from ocular tissues.

The diagnosis of each patient with retino­choroiditis remains difficult however, as tests based on serum antibody only do not provide definite answers to the following reasons:

1. Asymptomatic infections are frequent in the normal population.

2. Retinal lesions, toxoplasmic or other wise may appear in a patient who had a low antibody titre.


  Clinical features Top


1 Bilateral focal retino-choroiditis (in 85%) with heavy, atrophic scarring in central or between central and equatorial areas. Unilateral case may be seen in early stage.

2. C.N.S.: Hydrocephalus or cerebral calcification (not common).

Laboratory Diagnosis

Any combination of previous clinical signs or symptoms in the new born infant, child or even adult suggest the diagnosis. Serological data and positive intradermal skin tests lend support to the presumptive diagnosis. But absolute diagnosis can be made only when toxoplasma itself is isolated from infected tissues or body fluids.

In acute stages infected lymph nodes can be excised, minced and subjected to animal inoculation (in labora­tory mice) studied or examined directly for toxoplasma gondii.

The methylene blue (dye) test is the main stay of diagnosis although replaced by haemagglutination tests or fluorescent antibody test in many laboratories. The dye test may become positive as early as 4 days after infection.

The question may be asked: What is a significant titre? The answer is that any positive titre is significant if the patient has one or more of the accepted physical signs of congenital toxoplasmosis.

It should be emphasised that dye test, haemagglutination test and fluorescent antibody test, all give comparative results.

Skin tests: Intradermal or skin test is of value in routine surveys of population for determining evidence of infection. This is comparable to tuberculin skin test producing hypersensitivity 4-6 months after infection. This test is therefore not useful for indicating early infection.

There is an added value in diagnosis if serological test can be carried out in the mother and found positive.

Treatment

The sulphonamide (sulphadiazine, suiphamethazine and sulphamerazine) are active against the infection. In addition Pyrimethamine (Daraprim) a potent anti­malarial has significant antitoxoplasma activity. Since sulphonamides and pyrimethamine are believed to affect different parts of the metabolic cycle of the parasite, both should be given simultaneously. Chemotherapeutic agents are assumed to be effective against those organisms which are extracellular in position. In no case are they believed to affect the encysted form of the parasite.

Initial dose of Daraprim is 150 mg. followed by 25 to 50 mg. daily for four to six weeks. Concomitant therapy with triple sulpha is recommended-8 tablets daily (4.0 gms) for the same period.

Blood picture should be studied at weekly intervals for any suppression of white cell count. To prevent this, folinic acid injections are given routinely with chemotherapy.

Aureomycin can be used as a substitute for pyrimethamine where there is persistent nausea with the latter drug. The dose is 4 capsules daily for 4 to 6 weeks.

Oral corticosteroids can also be combined in acute stages of the disease for obvious beneficial results.




 

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