|Year : 1965 | Volume
| Issue : 2 | Page : 65-67
Etiology of phlyctenulosis
AM Gokhale, SR Limaye
Department of Ophthalmology, Bai Yamunabai Nair Charitable Hospital, Bombay-8, India
|Date of Web Publication||21-Feb-2008|
A M Gokhale
Department of Ophthalmology, Bai Yamunabai Nair Charitable Hospital, Bombay-8
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gokhale A M, Limaye S R. Etiology of phlyctenulosis. Indian J Ophthalmol 1965;13:65-7
Phlyctenular kerato-conjunctivitis or phlyctenulosis is one of the most common ocular manifestations. A large amount of literature is available on the subject because of two reasons: (1) the incidence of phlyctenulosis is high even today: (2) its causative factors are variable. In many instances one is not able to point out a single etiological factor.
Description of nodules in the conjunctiva and cornea probably of a phlyctenular nature, may be found in the works of Paul Aegina of Ancient Greece and of Ali ben Isa of the Golden Age of Arabian Medicine. With the advent of the bacterial era almost every type of microorganism has been blamed for this condition. Out of these, the staphylococcus has been blamed the most. Many workers have concentrated on the micobacterium tuberculosis as the causative organism. Histological studies of phlyctenular nodules have not shown any caseation or the presence of the micobacterium tuberculosis in them. So the phlyctenular nodule cannot be a direct result of a tuberculous infection of the conjunctiva. Experimentally Weekers (1909) was able to produce phlyctenular nodules in rabbits which were sensitised to bovine tuberculin, by instilling the antigen namely tubercular protein into the conjunctival sac. Further it was shown that the lesion could be produced not only in tuberculin sensitized eyes but also in eyes sensitized to Staphylococci, horse serum, chemicals, cocain and calcium caseinate provided that the same antigen was instilled later in the conjunctival sac.
It is our common experience that many cases of phlyctenulosis are tuberculin positive but still there are other cases which do not show any hypersensitivity to tubercular proteins. In the latter group a variety of causative factors have been discussed. On the other hand it is also well known that all the persons sensitive to tubercular proteins (a positive Mantoux) do not develop phlyctene. It is suggested that there should be some other factor also responsible for this lesion.
Thus we find many reports caused by different agents in the case of phlyc-tenulosis. For example, Heerfordt (1909) associates it with metastatic endogenous gonococcal conjunctivitis, Peters (1925) with diplobacillus and Schelbe with diphtheritic antitoxin. Parasites have also been brought into the picture. Thus Moro (1909) attributes phlyctenulosis to pediculosis, Laurel( (1926) to helminthiasis, especially ascariasis and oxuriasis and Jeffrey (1955) has reported two cases of phlyctenulosis due to nematode infestation in the Nilgiris.
Thygeson believes that phlyctenular ophthalmia is always due to bacterial allergy and never is a result of non bacterial proteins e.g. hayfever, urticaria. He has never observed development of phlyctenulosis in vernal catarrh or in simple allergic conjunctivitis.
The purpose of this study was to investigate the probable etiology of phlyctenulosis in patients attending our out patient department and to compare the same with the incidence found in the literature on the subject.
| Material and Method|| |
All the information was collected from patients attending ophthalmic out patients department of this hospital. The study covers a period of three years during which 208 cases of phlyctenulosis were encountered.
Once the phlyctenular ophthalmia (conjunctiva or cornea or both) was diagnosed all the clinical information and further investigations were recorded on a separate case sheet. Majority of the cases were followed upto 2-3 weeks and some of them even longer. Following points were specially recorded:
- History of tuberculosis in the patient or in his family.
- History of recurrences.
- Unilateral or bilateral.
- Cervical adenitis.
- Septic foci-like carious tooth, tonsilitis, sinusitis, ear discharge, etc.
- Any obvious vitamin deficiency.
All the patients were subjected to the following investigations.
- Screening of the chest.
- Intradermal tuberculin test-first 0.1 cc. of a 1 in 100,000 dilution. If negative 0.1 cc. of 1 in 10,000 dilution.
- Examination of the stool.
Special investigations like X-Ray examination of the chest and E.S.R. were carried out in certain patients where any active tuberculosis was suspected. Total and differential cell counts were done for any evidence of eosinophilia or lymphobytosis. Certain cases were classified depending upon the therapeutic response, e.g. in the Case of helminthiasis to antihelminthic drugs only, which were given no other medication except oculentum sulphacetamida locally as a placebo. Where tuberculin sensitivity was suspected only desensitisation with tuberculin was done and the condition was classified according to the response.
| Analysis of the Cases|| |
Following worms and parasites were detected
- Ascaris lumbricoidis.
- Ancylostoma Duodenale.
- E. Histolytica.
- Tricuris Trichiura.
- G. Lamblia.
Out of these ascaris lumbricoids were found in 26 out of 41 cases who showed helminthiasis-if not alone, associated with other worms.
| Conclusions|| |
- Both males and females are equally affected.
- Maximum cases are found between the age of 5 to 20 years.
- Most common cause appears to be "allergy to tuberculo protein".
- Intestinal worms feature conspiculously as a causative factor.
- In 7 adult females either pregnancy or lactation were associated. Estimation of serum calcium may be interesting in these cases.
- Between the age of 0-2 years only one case was recorded. This shows definitely that phlyctenulosis has no relation with the primary complex.
- There were a considerable number of cases where we were not able to attribute any specific cause. Malnourishment and Vitamin deficiency were the commonest findings in such cases.
| Discussion|| |
Phlyctenulosis has many etiological factors. In some of the cases more than one factor exists while in others one chief contributing cause could be found. In the latter groups patients markedly improved without any recurrence when the cause was treated adequately which was the criterion for putting them under one or the other group. There is strong evidence that in our country hypersensitivity to tuberculin from a healed, undetectable tuberculous focus may well be the cause of phlyctenulosis in many cases -(52/208). Its presence in 13 cases which also had worms also suggests a contributing element. In 37 out of 208 cases a tuberculous focus was detected. This shows the strong influence played by tuberculosis direct or indirect, in phlyctenulosis in our country where the incidence of tuberculosis is high. It was noticed that a good number of cases having phlyctenulosis showed some worms on examination of the stools. These cases were treated only with antihelminthic drugs and they showed remarkable improvement. Just as Laurell and Jeffery have reported cases of phlyctenulosis associated with helminthiasis, we also feel that phlyctene may be often associated with intestinal worms.
The question may be asked why is the incidence of phlyctenulosis associated with worms not greater when so many patients attending the O.P.D. are found to be having worms in their stools. It may be that there is certain individual susceptibility and some unknown precipitating or initiating factor. It may be compared with those cases which show a positive Mantoux test but do not develop phlyctenes. Production of phlyctenes in experimental animals sensitised to an antigen prepared from intestinal worms would be interesting.
In many cases some nutritional or vitamin deficiency was observed. Even though it may not be the cause of phlycten it may act as a contributing factor and may cause delay in recovery. Hence treatment of the deficiency in addition is necessary.
| References|| |
Heerfordt (1909) quoted in 7, p. 292.
Jeffrey M.P. (1955) Amer. J. Ophthal. 40, 41.
Laurell (1926) quoted in 7. p. 294.
Moro (1909) quoted in 7, p. 292.
Peters (1925) quoted in 7. p. 292.
Schelbi (1915) quoted in 7, p. 294.
Theodore F. H. and Schlossman (1958) Ocular Allergy. The Williams and Wilkins Co., Baltimore.
Thygeson P. (1942) Amer. J. Ophthal. 26, 159. 189.
[Table - 1], [Table - 2]