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ARTICLES |
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Year : 1974 | Volume
: 22
| Issue : 1 | Page : 8-14 |
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Diagnosis of ocular toxoplasmosis
S.R.K Malik, DK Gupta, S Choudhary
Department of Ophthalmology, Maulana Azad Medical College and associated Irwin and G.B. Pant hospitals, New Delhi, India
Correspondence Address: S.R.K Malik Department of Ophthalmology, Maulana Azad Medical College and associated Irwin and G.B. Pant hospitals, New Delhi India
Source of Support: None, Conflict of Interest: None | Check |
PMID: 4448538
How to cite this article: Malik S, Gupta D K, Choudhary S. Diagnosis of ocular toxoplasmosis. Indian J Ophthalmol 1974;22:8-14 |
Toxoplasmosis is caused by a protozoa 'Toxoplasma Gondii.' It is an obligatory intracellular parasite with a special affinity for the tissues of the nervous system including the retina. It appears from the study of Wood [37] that in 1941 tuberculosis was responsible for 80% cases of chorioretinitis and there was no reference to toxoplasmosis. Some of the recent studies by the same author showed a 20% incidence of tuberculosis against a 36% incidence of toxoplasmosis in cases of uveitis.
The incidence of toxoplasmosis in the normal population has been given as 14.3% among Arabs and 15.8% in Cairo [23] . In Rome, toxoplasmosis accounts for 27% of cases of uveitis [23] . In India Santokh Singh [35] reported the first case. Kalra [17] reported an incidence of 4% in a study of 400 army recruits on the basis of a positive complement fixation test. Prakash [29] studied 327 uveitis patients by the haemagglutination test. He got positive results in 14% of the cases. Batta et al [4] studied 309 uveitis cases by the htemagglutination test getting positive results in 12.6% of the cases.
This study was undertaken in order to find out the incidence of toxoplasmosis among cases of uveitis.
Methods and Material | | |
258 cases of endogenous uveitis referred to the uveitis clinic of the Irwin Hospital have been taken up for this study. The cases were classified into anterior, posterior and generalised uveitis. Thorough systemic and local clinical examinations were conducted in each case.
The cases of uveitis were subjected to complete blood, urine and stool examinations including serological tests for syphilis and an estimation of the antistreptolysin titre. A radiological survey of the chest, paranasal sinuses, sacroiliac joints, wrist and ankle joints was done. The cases were referred to the E.N.T., dental, and gynaecological departments to exclude any focus of infection. Tests for toxoplasmosis were done in collaboration with the parasitology department of the A.I.I.M.S. The skin test was done by injecting the toxoplasma antigen into the forearm. Induration of 10mm or more after 48 hours was considered positive. The methylene blue dye test was done by the Sabin and Feldman method [33] with the modification of Jacob while htemagglutination test was done by the method of Jacob [16] . Serum dilution of 1/16 or above was taken as positive in these two tests. In the complement fixation test a serum dilution of 1/4 or above was considered significant.
Observations and Discussion | | |
A total of 258 cases of endogenous uveitis were fully investigated for all causes of uveitis. The observations are discussed under different investigating procedures:
A. Toxoplasmin Skin Test : This was done in 137 non-uveitis cases and 258 patients having uveitis. This test was positive in 5.8% of non-uveitis cases and 12.4% of uveitis cases [Figure - 1]. The maximum positive results were obtained in posterior uveitis, i.e., in 21.4% of the cases. The results of the skin test as obtained by other workers are indicated in [Table - 1].
B. Dye Test : Out of 88 cases having uveitis, 27.2% showed a positive dye test as compared to 15.9% positive test obtained in 44 non-uveitis cases [Figure - 2]. A positive dye test was found most common in posterior uveitis [Figure - 2]. This agrees with the findings of mist of the workers (Keller & Vivell [18] , Hogan et al [12] , Jacob et al [15] , Beverley [3] and Perkins et al[26],[27]).
C. Haemagglutination Test : This test was done in 77 cases of uveitis. 10 cases i.e. 13%, gave positive haemagglutination test [Figure - 3]. The incidence was more in posterior uveitis (16.6%). Park and Neville [28] in 1963 found a positive haemagglutination test in 51% off his uveitis cases. Our results are more comparable to those of Prakash [29] and Battar [4] . The hxmagglutination test is easier to perform as compared with the dye test and employs non-living antigen which can be stored for a long time.
D. Complement Fixation Test : The complement fixation test was performed in 21 cases. In 14.3% cases the test was positive [Figure - 4]. The complement fixation test titre was much less as compared with the dye test and with hxmagglutination test titres. No definite comments can be made about this test as the number of patients studied is too small. The incidence of positive results as reported in the overseas literature is much more (Siegert [34] 26°G in posterior uveitis; Davenport [6] 8%, in non-uveitis and 19% in uveitis cases).
E. Isolation of Toxoplasma : T oxoplasma gondii was isolated from the cervical lymph node of a patient with central acquired choroiditis. This patient had a positive skin test and positive serological tests for toxoplasmosis with enlarged cervical lymph nodes. The first report of isolation of toxoplasma came from Pinkerten Weimman in 1940. Reports of .isolation have also come from Sabin [32] in 1941. Jacob [14] isolated toxoplasma gondii from an enucleated blind eye in 1954. Armstrong' isolated the organism from an axillary lymph node.
Correlation between the various tests used for diagnosis of Toxoplasmosis | | |
This is shown in [Table - 2]
Usually there is no agreement in the intensity of one reaction with another in an individual as the antibodies of each test appear at different time, attain different concentrations and last for variable periods. This is evident from [Figure - 5]. The dye test antibodies appear within 3 weeks and are detectable upto 8 years after the infection. H emagglutination antibodies appear a few days after dye test antibodies and closely follow the dye test pattern. The complement fixation antibodies appear later and disappear by about 2 years. Immunoglobulins appear early and completely disappear by about a year [Figure - 5]. The skin reaction usually becomes positive a year after infection and shows an increasing concentration with the age of the patient. It can be detected throughout the span of the patient's life. As the dye test and haemagglutination antibodies remain elevated for many years after infection they have a limited diagnostic value in active infections. Recently more emphasis is being placed on immunoglobulin and gel diffusion antibodies for detection of early infection [22] .
From the antibody titre pattern, it is expected that there should be a strong correlation between one test and another at particular time in the disease evolution. We found 87.5% agreement between the dye test and the skin test. A majority of other workers in the field have also found a high percentage of agreement between these two tests.
We found 93% correlation between the dye test and haemagglutination test. This agrees with the findings of most of the worker [2],[20],[21],[24] . As there is a good correlation between these two tests, the haemagglutination test, which is the simpler of the two, can be regarded as a good substitute for the dye test.
Relation of various tests for Toxoplasmosis with site of lesion | | |
From [Figure - 1],[Figure - 2],[Figure - 3],[Figure - 4] it is evident that positive results of toxoplasmosis are more common in cases of posterior uveitis as compared with anterior uveitis. This has been found to be statistically significant. This can be expected as toxoplasma has a predilection for the retina. These findings are in agreement with those of Keller et al[18], Hogan [12] , van Metre [36], Prakash [29] and Batta et al[4].
From [Table - 3] it is evident that the incidence of positive dye and hxmagglutination tests was highest in iuxtapapillary and central choroiditis. These findings correlate with the work of Goneperts [10] , Garin [11] and van Metre et al[36]. In our series a high incidence of positive dye test (37.8%) and positive haemagglutination test (14.2%) was also obtained in disseminated chorio-retinitis.
It can be explained on the basis that most of these cases also had central involvement. Perkins [27] believes that disseminated chorioretinitis is unlikely to be due to toxoplasmosis.
Relationship of dye test and haemagglutination test with acute and chronic uveitis | | |
It is evident that the serological tests for toxoplasmosis are more often positive in acute uveitis than in chronic uveitis. These results agree with those of Jacob et al [14] and Perkins [27] . This is expected because most of the acute cases appear soon after the onset of the disease when most of the tests for toxoplasmosis are positive. The chronic cases, on the other hand, remain asymptomatic and are detected only during routine examination years after the infection when the dye test and haemagglutination test antibodies are on the ebb [Figure - 5]. The dye test and haemagglutination antibodies are detectable for a period of 6-7 years whereas complement fixation antibodies can be detected within 3 years of an infection with Toxoplasma gondii. The skin test however, is likely to remain positive in these cases.
Incidence of Toxoplasmosis | | |
The diagnosis of ocular toxoplasmosis is presumptive because subclinical infection is common. In the present study 22 cases (8.4%) were attributed to toxoplasmosis. The diagnosis was based on (a) a positive serological test for toxoplasmosis in high titres, (b) positive toxoplasmin skin test, (c) clinical picture, and (d) absence of other causes. Out of the 22 cases, 4 had anterior uveitis while 18 cases had posterior uveitis. There is a marked difference in the incidence of toxoplasmosis throughout the world. This is attributed to unequal prevalence of the diseases. In India, no authentic report regarding the incidence of the disease is available but it seems that the condition is less prevalent as compared to the Western countries.
References | | |
1. | Armstrong, C. and Mx Murray, F.G., 1953, JAMA, 151, 1103. |
2. | Angelillo, B. and Mandras, A., Cited by Lunde, M.N.. 1963, A.M.A. Arch. Ophtha!. 69, 10. |
3. | Beverley, J.K.A.; and Watson, W.A., 1959, Nature, London 184 Suppl., 26, 2041. |
4. | Batta, R.K., Sharma, O.P., Agarwal, L.P., Choudhry, P. and Om Prakash, 1968, Orient. Arch. Opgtgal., 6, 51. |
5. | Correspondence: Trans. Roy, 1969, Soc. Trop. Med. & Hyg., 63, 675. |
6. | Devenpcrt, R.C., 1955, Proc. Roy. Soc. Med. 49, 19. |
7. | .Darrell, R.W., Pieper, S.. Kurland, L.T. and Jacobs, L., 1964, A.M.A. Arch. Opgtgal.71, 63. |
8. | Frenkel, J.K., 1949, JAMA, 140, 369. |
9. | Ibid, Acta, XVII, Cong. Ophthal. 3, 1965, (quoted). |
10. | Goneperts, C.E., 1950, Opqtqalmologica, 120, 178. |
11. | Garin, J.P., 1953, Thesis, Lyous (quoted from Trop. Dis. Bull.). |
12. | Hogan, M.J., Thygesm, P. and Kimura, S. 1952, Traits. Amer. Acad. Ophthal. 56, 863. |
13. | Hogan, M.J., 1958, Amer. J. Ophthal, 46, 467. |
14. | Jacobs, L. and Cook, M.K., 1954, Anner. J. Trop. Med., 3, 860. |
15. | Jacobs, L., Naquin, H., Hoover, R. and Woods, A.C., 1956, Bull. John hopkins Hosp., 99, 1. |
16. | Jacobs, L. and Lunde, M.N., 1957, Science, 125, 1035. |
17. | Kalra, S.L., 1957, AFMJ (India), 13, 181. |
18. | Keller, W. and Vivell, 0., 1952, Cited 1958, A.MA. Arch. Ophthal. 59, 260. |
19. | Kessell, J.F., 1958, Arch. Ophthal, 59, 861. |
20. | 20, Lunde, M.N. and Jacobs, L., 1958, Amer. J. Trop. Med. c& Hvg., 7, 523. |
21. | Lunde, M.N., Jacobs, L. and Woods, R.M., 1963, A.M.A. Arch. Ophthal. 69, 10. |
22. | Lunde, M.N., Gelderman, A.H., Sherrard, Hayes, L. and Vogal, C.C., 1970, Cancer, 25, 657. |
23. | Moschini, G.B., 1969, Ctin. Oculist., 48, 340. |
24. | Oniki, S., 1963, Cited, 1963, Arch. Ophthal, 73, 420. |
25. | Puckerton, H. and Handerson, R.G., 1941, JAMA, 116, 807. |
26. | Perkins, E.S., 1958, Trans. Ophth. Soc. U.K., 78, 123-511. |
27. | Perkins, E. S., 1961, Ureitis in Toxoplasmosis. Churchill Ltd., London. |
28. | Park, H.K. and Neville, M.A., 1963, Amer. J. Ophthal, 56, 235. |
29. | Prakash, O., 1966, Ind. J. Med. Res., 54, 5. |
30. | Riffa.t, M.A., 1962, J. Egypt. Publ. HIM. Ass., 37, 121. |
31. | Riffat, M.A., 1963, Trans. Roy. Soc. Trop. Med. & Hyg. 57, 134. |
32. | Sabin, A.B., 1941, JAMA, 116, 801. |
33. | Sabin, A.B. and Feldman, H.A., 1948, Science, 108, 660. |
34. | Siegert, P., 1953, Quoted 1960, Arch. Ophthal, 59, 260. |
35. | Singh, S., 1952, Indian Physician, 11, 209. |
36. | Van Metre, T.E., Knox, D.L. and Maumanee, A.F., 1964, Amer. J. Ophthal, 58, 6. |
37. | Woods, A.C., 1960, Amer. J. Ophthal, 50, 1170. |
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5]
[Table - 1], [Table - 2], [Table - 3], [Table - 4]
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