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ARTICLE
Year : 1964  |  Volume : 12  |  Issue : 4  |  Page : 147-153

Viral uveitis- a review of 11 cases


Muslim University Institute of Ophthalmology and The Gandhi Eye Hospital, Aligarh, India

Date of Web Publication13-Feb-2008

Correspondence Address:
S D Paul
Muslim University Institute of Ophthalmology and The Gandhi Eye Hospital, Aligarh
India
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How to cite this article:
Paul S D, Ahuja O P, Shukla B R. Viral uveitis- a review of 11 cases. Indian J Ophthalmol 1964;12:147-53

How to cite this URL:
Paul S D, Ahuja O P, Shukla B R. Viral uveitis- a review of 11 cases. Indian J Ophthalmol [serial online] 1964 [cited 2020 Oct 20];12:147-53. Available from: https://www.ijo.in/text.asp?1964/12/4/147/39091

Table 1

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Table 1

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Interest in the subject of viral uveitis has been renewed since the attempts in recent years to correlate Vogt-Koyanagi disease, Harada's disease, Behcets' dis­ease and sympathetic ophthalmia.

In a review of 140 cases of endoge­nous uveitis carried out in our depart­ment in the last four years, uveitis was attributed to a probable viral source in 11 cases. An analysis of the clinical aspects of these cases is undertaken here to study their resemblances and differences in correlating these dis­eases. Their typical clinical features stand them out distinctly from other causative factors of endogenous uveitis. No virus studies have been carried out in these cases and only clinical and certain laboratory findings have been depended upon.

In the present series were noted four cases of Vogt-Koyanagi-Harda's syn­drome, three cases of Behcet's disease and four of sympathetic ophthalmia.

A detailed history and comprehen­sive examination was made and re­corded in each case. The main labora­tory investigations carried out were total and differential white blood cell count, erythrocyte sedimentation rate, V.D.R.L. and Kahn's tests, Mantaux's test and examination of cerebrospinal fluid.

The cases were put on treatment and their progress was regularly observed and recorded. The cases have beer followed up for a period of 2-4 years.

Vogt-Koya Nagi-Harada's Syndrome

Under this head there were four cases, 2 males and 2 females of ages between 12-49 years.

The disease process was clinically manifested with meningeal symptoms and poliosis in all the four cases while vitiligo was present in 3 cases, dysa­cousia in 2 and alopecia in one case only. In none of these cases the fundus condition could be ascertained due to hazy media.

It may be of interest to note that in one case, vitiligo and poliosis and in a second one vitiligo were present be­fore the onset of ocular disease, whereas deafness in the other two cases developed after the onset of ocular disease and was only temporary. It disappeared after a couple of days.

Amongst the laboratory investiga­tions a pleocytosis in cerebro-spinal fluid was seen in 3 cases while a raised erythrocyte sedimentation rate was present in 2 cases.

All the cases were given prolonged, systemic corticosteroid therapy and considerable improvement of the clini­cal picture and the visual function was seen in 3 out of 4 cases. The improve­ment was as much as from 2/60 to 6/24 in one case, whereas in the left eye of case No. 3 where there was no light perception, no improvement was possible.

Sympathetic Ophthalmia

Out of the 4 cases of sympathetic ophthalmia, three were males and l female, with ages varying from 11-40 years.

The period which elapsed between the dates of injury and development of the disease in the uninjured eye varied from 12 days to 2 months.

In two cases the sympathetic disease started as anterior uveitis while in the other two cases the process started as neuro-retinitis.

All the cases were treated mainly with prolonged systemic corticosteroids and locally with mydriatics and corti­costeroid preparations. In 3 cases a satisfactory improvement was noted which has been maintained up to the end of the follow-up period, i.e. 2-3 years whereas in I case the eye did not improve and became atrophic.

Behcet's Disease

The three cases of Behect's disease were 2 males and 1 female, the ages varying from 24-32.

Hypopyon iritis and aphthous ulcers in the mouth were seen in all the three cases while polyarthritis was seen in two cases and ulcers on genitalia in one case. In one case the onset of the ocular disease was accompanied by fever. The same case also suffered from pyodermia.

In another case, optic nerve involve­ment was observed. First, a marked bilateral constriction of retinal blood vessels was seen. This was followed by a complete bilateral optic atrophy.

All the cases were treated with sys­temic broad spectrum antibiotics, corticosteroids, salicylates and irgapy­rin. No relief was seen in any of the eyes and all the eyes were ultimately lost.


  Discussion Top


Vogt-Koyanagi-Harada's Disease

Vogt (1906) described elaborately a form of uveitis associated with poliosis. Koyanagi (1929) amplified these ob­servations and added, in the clinical picture, the accompaniment of dysa­cousia, vitiligo and alopecia in addi­tion to poliosis as described by Vogt, and the syndrome began to be known as Vogt-Koyanagi syndrome.

Harada (1926) described a condition in young adults accompanied by mark­ed accumulation of subretinal fluid leading to retinal detachment. Pleocy­tosis in cerebrospinal fluid was a con­stant finding.

Bruno and McPherson (1939) cor­related the two conditions and found many a feature which were common to both Vogt-Koyanagi syndrome and Harda's disease. This has been agreed to by a number of other workers and now the condition is generally termed as Vogt-Koyanagi-Harada's syndrome. (Woods 1961).

From time to time certain more un­usual features have been added to the classical description of Vogt-Koyanagi­ Harada's syndrome, e.g. bilateral papil­loedema-Gregory (1959) and bilateral scleritis Cowper (1951).

A probable hereditary factor is in­troduced by Benedict and Benedict (1951) who reported Vogt-Koyanagi­ Harada's syndrome in siblings, and Flyn (1952) described a case of the same syndrome, whose paternal rela­tions exhibited the same picture.

Recent work on isolation of the virus has confirmed the viral nature of Vogt-­Koyanagi Harada's disease.

Sugiera and his associates (1953) re­ported the actual isolation of a virus from the eyes of patients suffering from this syndrome. After four to eight blind passages, the authors isolated a specific virus strain. They further re­ported that the blood serum of another patient, suffering from the same dis­ease, gave a positive neutralisation test against this virus with an index of 100.

Erbaken (1962) also has been able to isolate a virus from the spinal fluid of a patient suffering from Vogt­-Koyanagi-Harada's syndrome. The type of virus, however, remained un­determined.

In all cases of Vogt-Koyanagi­-Harada's syndrome the presence of meningeal symptoms was a noticeable feature.

Cowper (1951) in his review of the cases of Vogt-Koyanagi-Harada's synd­rome reported the incidence of menin­geal symptoms of one kind or the other in 90%, of his cases. The severity of these symptoms varied from case to case. Cordes (1955) also, reported meningeal symptoms in the initial stages of the disease in his case.

It appears, therefore, that some kind of intra-cranial affection leading to the signs of meningeal irritation forms a definite component of the disease pro­cess. The precise mechanism of this phenomomenon is obscure. However, keeping in mind the widespread mani­festations of the disease, it may be presumed that the virus of Vogt­-Koyanagi-Harada's syndrome probably affects the ocular and intracranial structures simultaneously causing a sort of meningitis or meningo-encepha­litis.

In this context, Hague (1944) also, suggested that the disease process starts as an encephalitis and the clinical manifestations of the syndrome are the results of involvement of the hypotha­lamus.

Although all the cases in our series of Vogt-Koyanagi-Harada syndrome had meningeal symptoms, all the other classical systemic signs, viz.-alopecia, poliosis, vitiligo and dysacousia were not present together in every case. They need not be so. Similar varying incidence of these signs have been noted by Parker (1940) and Rosen (1945).

Further, it was observed that the ocular and extra-ocular signs of the syndrome did not develop simultane­ously, either group of signs preceding the other in different cases.

The clinical diagnosis of Vogt­-Koyanagi-Harada's syndrome becomes evident in a case where the ocular and extra-ocular signs are present together. On the other hand, if the extra ocular signs do not develop until late in the course of the ocular disease, it becomes difficult to make the diagnosis of Vogt-Koyanagi-Harada's syndrome in its early stages.

For an early diagnosis of such cases, where the extra-ocular signs appear late, it is suggested that a cerebro-spinal fluid examination be carried out in all cases of granulomatous uveitis where other etiologic factors have been ruled out. This statement is borne out by the observation that a pleocytosis in cerbro-spinal fluid can be found in most cases of Vogt-Koyanagi-Harada's syndrome. This was observed in 3 out of our 4 cases.

Therapeutic response to the systemic administration of corticosteroids was fairly encouraging in our cases of Vogt­-Koyanagi-Harada's syndrome. A con­siderable clinical and functional im­provement was seen in 3 out of 4 cases. Similar results of systemic cor­ticosteroid therapy have been reported by Lamberto (1955) and Bronstein (1957).

Some patches of vitiligo of several years standing, were seen in the mother of case No. 1 of Vogt-Koyanagi­-Harada's syndrome. These patches were, however, not associated with any ocular signs of the syndrome. There­fore, no conclusion could be drawn re­garding the hereditary character of the disease as reported by Benedict and Benedict (1951) and Flyn (1952).

Sympathetic Ophthalmia

Woods (1961) describes the com­mencement of the sympathetic reaction in the posterior segment in some cases of sympathetic ophthalmia. He states that the process is usually present in the anterior choroid. No mention has been made about the development of neuro-retinitis.

In the present series, however, 2 out of 4 cases of sympathetic ophthalmia exhibited a significant feature of neuro­retinitis as the reaction of sympathising with the injured eye. In the other two cases the sympathetic reaction con­formed to the classical description of a plastic iridocyclitis.

Levatin (1958) reported the develop­ment of neuro-retinitis during the course of disease in a case of sympa­thetic ophthalmia.

The review of recent literature of sympathetic ophthalmia thus reflects a great paucity of reports about this rare manifestation of the disease process. The authors, in the present report, contribute two such cases where the dis­ease process in the sympathising eye started as a neuro-retinitis.

The condition of sympathetic oph­thalmia has always presented many problems regarding the determination of its etiology. Many factors notably allergy (Elschnig 1911) saprophytic in­fection (Redslob 1956), and others have been put forward as to the causa­tive factor of sympathetic ophthalmia.

Recently many workers have tried to establish a correlation between auto­immune diseases and sympathetic ophthalmia. Aronson and co-workers (1963) tried to sensitise the animals to complete adjuvant and uveal tissue but all they could find was a uveitis of a shorter duration which was histologi­cally dissimilar to that in sympathetic ophthalmia. Perkins and Wood (1964) tried to establish a correlation of syn­pathetic ophthalmia with auto-immune disease. They were able to demon­strate staining of fluorescein in the choroid. The over all results were how­ever not specific.

In this context, it is interesting to note various similarities between sym­pathetic ophthalmia and Vogt­-Koyanagi-Harada's syndrome as re­ported from time to time. Hutchinson (1892-1893) in a report of historical in­terest described an incomplete case of Vogt-Koyanagi-Harada's syndrome as "non-traumatic sympathetic ophthal­mia".

Laje-Weskamp (1932) has pointed out that the sporadic association of symptoms like dysacousia, alopecia, vitiligo and poliosis in both these con­ditions have engaged the attention of many clinicians Soriano (1929), Ta­kahashi (1930), whereas demonstration of uveal pigment sensitivity-Rones (1932) and histological similarity­-Hager (1957), in both these conditions have been instrumental in forcing an etiological identity between the two.

This has eventually led Ikui and Associates (1958) to the view that pro­bably sympathetic ophthalmia and Vogt-Koyanagi-Harada's syndrome are merely stages of a local manifestation of a systemic involvement. The etio­logic factor probably acts specifically on the pigment-bearing structures of the body and uvea, the factor possibly being a choromato-tropic virus.

Behcet's Disease

It is another important condition which has been attributed to be caused by a virus.

Behcet (1937) described it as a con­dition of recurrent uveitis with hypopyon and aphthous ulcers on the mucous membrane of the mouth, tongue and genitalia. Occasionally other manifestations, notably acute in­flammatory poly-arthritis, various skin lesions, orchitis, phlebitis with a febrile onset have been described (Woods 1961).

Martin (1954) reported a case of Behcet's disease in which an eye was enucleated. Histological examination revealed a round-cell perivascular in­filtration which he believed was the fundamental lesion in the disease.

Several workers have been able to isolate a virus from patients suffering from Behcet's disease.

Sezer (1953, 1956) reported the iso­lation of a filter passing agent from the ocular fluids of three patients suffering from Behcet's disease. He cultured this agent on chick embryos and pro­duced a typical encephalitis in mice by intracerebral inoculation of this mate­rial. Later he has been able to isolate the virus from the blood of 20 addi­tional cases and from the urine of some of them. Similarly Evans and asso­ciates (1957) have isolated a filter pass­ing agent from the aqueous and Naka­gowa and Shingu (1959) from vitreous and aphthous ulcers in the mouth and genitalia of patients suffering from Behcet's disease.

In this disease the extra-ocular signs, are again different and distinctive. As regards the intraocular signs, the uveitis is usually so severe that hypopyon is a regular feature.

In our Behcet series the optic nerve involvement in one case perhaps lends support to the suggestion of Sezer (1956) and Zeavin et al (1956) that the disease probably begins in the optic nerve, spreads to the retina and se­condarily involves the uveal tract.

An experimental evaluation in ani­mals has recently been carried out by Mortada and Imam (1964). The au­thors have conclusively proved the viral etiology of Behcet's disease by isolating the virus from hypopyon and also from ulcers of the membrane. They have shown that the virus primarily in­volves the neuro-epithelium of the iris, the ciliary body and the retina, causing secondary vasculitis of the uvea and the retina.

As regards therapeusis the response to cortico-steroids is discouraging, in contrast to that in Vogt-Koyanagi­-Harada and sympathetic ophthalmia. In this series all the eyes were ulti­mately lost in spite of rigorous treat­ment.

Comparing the clinical manifesta­tions of all the three, [Table - 1] they all had ocular and extra-ocular mani­festations. True it is that in sympathe­tic ophthalmia no extra-ocular manifestations have been recorded. In this con­dition the ocular manifestation always comes first in contrast with the other two conditions, where extra-ocular manifestations may precede the ocular ones. In our reported series, favour­able response to cortico-steroids com­mented upon, did not allow the later extra-ocular manifestations to develop in sympathetic ophhalmia. However, one can always recall to memory cases of sympathetic ophthalmia with deaf­ness and vitiligo often found in pre­cortison days. (See Table on p. 148.)

Thus, as regards extraocular mani­festations, Vogt-Koyanagi-Harada and sympathetic ophthalmia are inti­mately related and probably may be having an identical viral etiology (Chromotropic virus) whereas it may be quite different in the case of Rehcet's, where exposed mucous­membranes are involved and no dis­turbance of the pigment-bearing struc­tures have been reported.

Comparing the ocular manifesta­tions, again one is impressed by the similarity of the granulomatous type of iritis in Volt-Koyanagi-Harada and sympathetic ophthalmic whereas that of Behcet's is quite different - hypopyon iritis, where there is a strong cyclitic element.

Comparison of the fundus condition offers a faint degree of similarity, a neuro-retinitis being found even in Behcet's disease. though only in 1 case.

As examination of the cerebro-spinal fluid was done only in the case of Vogt-Koyanagi-Harada, and so does not offer itself for comparison.

Thus, the clinical and virological studies offer support to the similarity of the nature of the lesion in sympa­thetic ophthalmia and Vogt-Koyanagi-Harada, but does not offer the same degree of support to Behect's as a re­lated condition, although the latter can also be classed among VIRAL UVEITIS.[37]


  Summary Top


Out of 140 cases of endogenous uveitis, eleven cases with a probable viral etiology are described and com­pared. Of these 11, 4 were cases of Vogt-Koyanagi syndrome, 4 of sym­pathetic ophthalmia and 3 of Behcet's disease.

Clinical comparison and study of literature on the subjects suggest a close relationship between Vogt-Koya­nagi-Harada disease and sympathetic ophthalmia but not so with Behcet's, although all the three can be grouped under viral uveitis.

Of special interest are two cases of sympathetic ophthalmia, which are re­corded, in which the sympathising re­action began as an optic neuritis in the sympathising eye.

 
  References Top

1.
Aronson, S. B.; Hegan, M. J. and Weigart, P.: (1963) A.M.A. Arch. Ophthal. 69: 105. 203-219, 370-388.  Back to cited text no. 1
    
2.
Behcet. H. (1937): Derm, Wschr., 105: 1152. As quoted in 36 p. 263.  Back to cited text no. 2
    
3.
Benedict. W. H. and Benedict. W. R. (1951): A.M.A. Arch. of Ophthal. 46: 510-512.  Back to cited text no. 3
    
4.
Bronstein. M. (1957): A.M.A. Arch. Ophthal. 57: 303.  Back to cited text no. 4
    
5.
Bruno, M. and McPherson. S. D. Jr. (1949): Am. J. Ophthal. 32: 513.  Back to cited text no. 5
    
6.
Cordes, F.C. (1955): Am. J. Ophth. 39: 499.  Back to cited text no. 6
    
7.
Cowper, A.R. (1951): A.M.A. Arch. Ophthal. 45: 367-376.  Back to cited text no. 7
    
8.
Elschning, A. (1911): Graefe, Arch. Ophthal. 79: 428. As quoted in 36. p. 39.  Back to cited text no. 8
    
9.
Erbakan, S. (1962): Amer. J. Ophth. 53: 308-371.  Back to cited text no. 9
    
10.
Evans, A. D.; Pallis, C. A. and Spillane, J. D. (1957): Lancet 2: 349.  Back to cited text no. 10
    
11.
Flyn, G. E. (1952): Amer. J. Ophthal. 35: 568-572.  Back to cited text no. 11
    
12.
Gregory Irene, D. R. (1959): Brit. J. Ophth. 43: 113.  Back to cited text no. 12
    
13.
Hager, G. (1957): Am. J. Ophth. 44: 716.  Back to cited text no. 13
    
14.
Hague, E. B. (1944): Arch. Ophthal. 31­:520.  Back to cited text no. 14
    
15.
Harada, Y. (1926): Nipp. Zauk. Xass, 30: 357. As quoted in 36, p. 267.  Back to cited text no. 15
    
16.
Hutchinson (1892-1893): Arch. Surgi­cal London, 4: 357.  Back to cited text no. 16
    
17.
Ikui, H.; Kimura, K.; Iwaki, S.; Furu­yoshi, Y (1958): Acta XVIII Internat. Congr. Ophthal. 2: 1285.  Back to cited text no. 17
    
18.
Koyanagi, Y. (1929): Klin. MIN. Augen­heilk, 82: 194. As Quoted in 36. p. 267.  Back to cited text no. 18
    
19.
Laje Weskamp (1932): Rev. Asoc. Med. Argent. 46: 1451.  Back to cited text no. 19
    
20.
Lamberto, M. (1955): Amer. J. Ophth. 40: 148.  Back to cited text no. 20
    
21.
Levatin, P. (1958): Ophth. Lit. 12: 583.  Back to cited text no. 21
    
22.
Martin, J. D. (1954): A.M.A. Arch. Ophth, 52: 272.  Back to cited text no. 22
    
23.
Mortada, A.: Imam. Z.E.I.: (1964): Brit. J. Ophthal. 48: 250-259.  Back to cited text no. 23
    
24.
Nakagawa, Y. and Shingu. M. (1959): Excerpta Medica (XII) 13: 131.  Back to cited text no. 24
    
25.
Parker, W. R. (1940): A.M.A. Arch. Ophth. 24: 499.  Back to cited text no. 25
    
26.
Perkins, E. S.: Wood, R. NI. (1964): Brit. J. Ophthal. 48: 61,  Back to cited text no. 26
    
27.
Redslob. E. (1956): Ann. d'Ocul. 189: 53.  Back to cited text no. 27
    
28.
Rones, B. (1932): A.M.A. Arch. Ophth. 7: 847.  Back to cited text no. 28
    
29.
Rosen, E. (1945): A.M.A. Arch. Ophth. 33: 281.  Back to cited text no. 29
    
30.
Sezer. F. N. (1953): Amer. J. Ophth. 36: 301.  Back to cited text no. 30
    
31.
(1956): Amer. J. Ophth. 41: 41.   Back to cited text no. 31
    
32.
Soriano (1929): Quoted by Hague 18.  Back to cited text no. 32
    
33.
Sugeirra, S., Fukunda, M., and Eda, K. (1953): Acta. Soc. Ophthal. Jap. 57: 117. As quoted in 36 p. 268.  Back to cited text no. 33
    
34.
Takahashi, M. (1930) Acta Soc. Ophthal. Jap. 34: 506 as quoted in 36. p. 268.  Back to cited text no. 34
    
35.
Vogt, A. (1906) Kim, Mbl. Augenheilk, 44: (Part 1), 228 as quoted in 36, p. 267.  Back to cited text no. 35
    
36.
Woods, A. C. (1961). Endogenous In­flammations of the Uveal Tract. The Williams & Wilkins Co. Baltimore.  Back to cited text no. 36
    
37.
Zeavin, B. H.. King, M. J. and Gohd. R. S. (1956) Amer. J. Ophthal. 41: 55.  Back to cited text no. 37
    



 
 
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