Indian Journal of Ophthalmology

ARTICLES
Year
: 1983  |  Volume : 31  |  Issue : 7  |  Page : 869--871

Aetiopathogenesis of lepromatous ititis


SP Garg, VK Kalra, N Verma 
 Dr. Rajendra Prasad Centre for Ophthalmic Sciences A.I.I.MS. New Delhi, India

Correspondence Address:
S P Garg
Dr. Rajendra Prasad Centre for Ophthalmic Sciences A.I.I.M.S., New Delhi-110 029
India




How to cite this article:
Garg S P, Kalra V K, Verma N. Aetiopathogenesis of lepromatous ititis.Indian J Ophthalmol 1983;31:869-871


How to cite this URL:
Garg S P, Kalra V K, Verma N. Aetiopathogenesis of lepromatous ititis. Indian J Ophthalmol [serial online] 1983 [cited 2021 Sep 16 ];31:869-871
Available from: https://www.ijo.in/text.asp?1983/31/7/869/29689


Full Text

 INTRODUCTION



As per 1971 estimates there are 3.2 million patients of leprosy in India. One of the com­mon disability in leprosy is blindness as com­plications due to leprosy frequently terminate to blindness. Ocular complications in leprosy mainly occur by involvement of anterior seg­ment. A chronic iridocyclitis is a frequent complication of lepromatous leprosy. Dif­ferent opinions have been presented in litera­ture regarding the genesis of iritis in leprosy. Cameron 1961, Choyce 1969, Weekeroon 1969 are of the opinion that it is infective in origin. Asymptomatic nature, relative lack of signs and absence of organisms lead others to hypothesize a neuroparalytic basis to explain the iritis.

The present study was undertaken at Lep­rosy Home Shahdra, Delhi, by us to under­stand the genesis of uveitis in lepromatous leprosy.

 MATERIAL AND METHODS



A total of 982 inmates of Leprosy Home were surveyed. Detailed ophthalmic exami­nation including slit lamp examination was done. The findings were recorded in a profor­ma. 48 intraocular operations were done (cataract extraction & optical iridectomy).

In each case aqueous tap was done before entering the anterior chamber. Aqueous was centrifuged and sediment stained by Gram's stain and Z.N. Stain. Complete iridectomy was performed as a routine. The iris tissue was fixed in formaldehyde and processed for his­topathology by Haematoxylin and Eosin and special staining for acid fast bacilli.

 OBSERVATIONS



Results: The incidence of uveitis and its varied manifestations are highlighted in [Table 1][Table 2][Table 3][Table 4].

None of the 15 samples of iris removed at complete iridectomy showed presence of A.F.B. None of the 15 samples of aqueous of lepromatous iritis was positive for A.F.B. when the smears were made from the sedi­ment of centrifuged samples.

Histopathology showed presence of chronic inflammatory cells in majority of irides. In 3 cases no histopathological anomaly was seen. Diffuse atrophy of the muscle involving both the sphincter as well as dilator muscle was seen in 4 cases.

Discussion: The manifestations and later effects of acute iritis which occur as a part of lepra reactions is a well known entity and of granulomatous nature. By contrast chronic iritis of lepromatous leprosy offers a different nature as it lacks symptoms, has minimal ocular signs and is non responsive to topical steroids.

The absence of organisms in aqueous and iris in all the cases of lepromatous leprosy along with chronic, low grade uveitis noted in our study also goes in favour of a non organis­mal basis.

Evidences for neuroparalytic iritis are:

1) Organismal: (a) Preferential attach­ment of leprabacilli to nerves in various organs, a similar affliction might occur in iris.

(b) Preferential lodgement of organism to cooler parts of body (testes, nose, ear).

As iris temperature is 3.5°C less than that of body temperature (Schwartz 1962) it can be a preferential site.

2) Clinical: (a) Sluggishly reacting pupils with anisocoria without overt signs of uveitis goes in favour of neproparalytic basis.

(b) Corneal nerve involvement is a well known clinical entity in leprosy. A parallel situation might occur in iris.

3) Pharmacological: (a) Early autonomic denervation hypersensitivity has been des­cribed by Bauschard and Swift (1972) in which pupils of lepromatous patients respon­ded positively to epinephrine in an abnor­mal way.

(b) Poor response to anticholinergic drugs like atropine as the basic fault lies in adrener­gic nerve fibres.

4) Histopathological: Lack of organisms in aqueous or iris and functional changes much more marked as compared to organic iris changes.

The presumed pathogenesis -sub of chronic lepromatous iritis is that during primary bac­teremia, bacilli lodge in. autonomic nerve fib­res of iris and cause a'slow degeneration of nerves which causes a secondary muscular atrophy. Due to the atrophy of muscle, toxins are released which cause a low grade chronic uveitis with mild flare, KPs. and cells with eyes remaining essentially white and asymp­tomatic.

Further studies to demonstrate selective muscle atrophy, electron microscopic studies for demonstrating organisms in the auto­nomic nerves are needed along with phar­macological studies to come to a definite conclusion regarding the exact genesis.[6]

References

1Cameron, A.N. Leprosy and its ocular mani­festations. Trans. Ophthalmol. Sec. U.K 1961, 81: 637­47.
2Choyce, D.P. The diagnosis and management of ocular leprosy.
3Duke Elder, S. -System of Ophthalmology, (1977) Uveal diseases, Page 298.
4Ffytche, T.J, Role of iris changes as a cause of blindness in lepromatous leprosy. Brit. Jt. Ophthalmol. 1981, 65: 231-39.
5Swift, T.R and Bauschard, F.B. Pupillary reactions in lepromatous leprosy. In. J. Leprosy 1972, 40: 142-48.
6Weekeroon, L. Ocular leprosy in Ceylon. Brit. J Ophthal. 1969,53: 457-65.