|Year : 1981 | Volume
| Issue : 4 | Page : 463-466
Protein deficiency and cornea
Department of pathology, M.R. Medical College, Gulbarga, India
K S Ratnakar
Department of Pathology, M.R. Medical College, Gulbarga-585105
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Ratnakar K S. Protein deficiency and cornea. Indian J Ophthalmol 1981;29:463-6
The two main factors invoked in keratomalaeia have been suggested as protein deficiency and local infection "(W.H.O. 1976) There is conflicting evidence on the inter-relationship of protein calorie malnutrition and vitamin A. deficiency. Clinical and epidermiological studies revealed increased incidence of ocular signs in Kwashiorkor children with vitamin A deficiency. However, rats fed on diet deficient in both protein and vitamin A failed to develop any ocular lesions. It is, therefore, proposed to conduct a study to evaluate the corneal changes, if any, in protein deficiency.
| Materials and methods|| |
The study was conducted on weaning albino rats and young rabbits obtained from central animal House, A.I.I.M.S. The animals were divided into two groups. Group I and II received low protein and high protein diets respectively. The diet was otherwise adequate in all other vitamins and minerals. The methods and dietary schedules of protein deficient and control were according to Deo et a1. The animals were weighed for every week and the detailed general and ocular examination were made at frequent intervals. The total serum protein was estimated by Biuret method and differential by electropropheresis. The rabbits at the end of six weeks dietary regime received coagulase positive staph. aureus 1 X 10 6, 1 X 10 7 and 1 X 10 8 both by intrastromal and by surface inoculations. The eye was examined at regular intervals and one eye was removed for histological studies. The animals were sacrificed and the ocular tissues and internal viscera were removed. These were subjected to histopathological examinations after staining the sections by haematoxylin and eosin, Alcian blue PAS, and Toluidine Blue. The rat cornea subjected to electronmicroscopy was fixed in glutaraldehyde followed by osmium tetroxide. The tissues were embedded in epoxyresin and serial sections were studied.
| Observations|| |
Rats (Low Proiein)
The animals showed retardation of growth [Table - 1] and were lethargic. The hair was brownish and sparse. On light microscopic examination, the corneal thickness was normal. The basal cells showed paucity of mitosis, and were vacuolated [Figure - 1]. Vascularisation and leucocytic infiltration was seen in the subepithelial area of the stroma. The Descemet's membrane and the endothelium did not show any abnormality. Ultrastructurally, there was loss of villous pattern with attenuation of layers in epithelium. The stroma showed vascular channels and perikeratocytic oedema [Figure - 2].
All animals were active, and showed steady growth but the increments of weight were not marked as the animals were pair fed with test group [Table - 1]. The ocular structures, both clinically and microscopically were normal.
(1) Corneal abrasion and inoculation of Staph. Aureus:
A remarkable difference in the reaction of cornea to the injury was seen in the two groups. In high protein animals, the abrasion healed rapidly with mucoid discharge only. By 5th day, all the abrasions completely healed, leaving nebular to macular corneal opacities. In low protein rabbits, evidence of infection soon appeared, with ciliary and conjunctiva.l congestion and mucoporulent discharge. The intensity of reaction was uniform with 3 doses. The course followed a definite pattern. Infiltration and corneal oedema was evident on 3rd day. The epithelium broke down resulting in purulent ulcer. The signs were at peak on 7th day. Majority showed resolution by 10th day. The oedema and infiltration slowly diminished in another 10 days, resulting in macular vascularised corneal scars. Histologically, the lesions were corroborative to clinical findings.
(2) Intrastromal injection of Staph. aureus :
Lesions were more effectively and definitely produced by this procedure. All the animals of either series showed a corneal ulcer. In the well fed group, epithelium over the white mound of intrastromal injection broke by 3 or 4 days. The ulcer had sodden sloaping edges with purulent slough on the floor. Mucopurulent discharge was present. Lids were not affected. The signs were at peak on 7th day. In undernourished animals, the epithelium gave way in 2 or 3 days of the course and was more virulent and prolonged. Lids also showed signs of infection. The ulcers healed by 20th day resulting in dense vascularised scars. In both groups of the series, the intensity of lesion was dose related. Histological examination at various intervals revealed severe ulceration, poor cellular infiltration with varying degrees of vascularisation, proportional to the dose in undernoureshed animals compared to controls.
| Discussion|| |
The results of the present study indicate that protein deficiency alone failed to produce any clinically discernible lesions other than vascularisation. However, microscopic studies, both light and electron, revealed epithelial vocuolations with attenuation of layers and loss of surface projections with stromal oedema and hydropic degeneration of endothelium. In addition, the cornea of protein deficient rabbits, has been found to be susceptible to infection even after surface abrasion and inoculation of infecive agents.
Protein malnutrition either directly or indirectly has been linked with development of Xerophthalmia and Keratomalacia in vitamin A deficient subjects. There is very little experimental evidence to indicate that protein energy malnutrition per se is associated with any ocular lesion. Clinical and epidemiological studies, however, suggest that Xerophthalmia complicates protein calorie malnutrition Interference to absorption, metabolism and utilisation or vitamin A in protein deficiency have been suggested. But recent studies, using labeled vitamin A, showed normal absorption of vitamin A. in protein deficient children. As the retinal binding protein (RBP) levels are low, it is likely that protein deficiency affects the synthesis of this carrier protein (W.H.O. 1976). McLaren reported keratinisation of corne, following protein deficiency. In the present study, protein deficient rats have not shown keratinisation. This is possibly because of lack of 'building blocks' for the synthesis of filamentous protein, keratin.
Animals fed on a variety of deficient diets including protein, vitamin A, riboflavin, developed vascularisation. The reaction is, therefore, nonspecific. But the pathogenesis appears to be imperfectly understood. Recently, it has been shown that irrespective of the insult, nutritional, chemical, or infective, vascularsation is preceded by infiltration of leukocytes. The histological sections in protein deficient groups, vascularisation is noticed alongwith leukocytic infiltration. It is not clear what factors are responsible for this leukocytic migration.
Epithelial collagenase enzyme appears to have an affect on the stroma which shows some disturbances in ground substance Acid mucopolysaccharides). In the protein deficient state, mucopolysaccharides appear to be lowered as observed in the present study.
Corneal abrasion and inoculation of even concentrated suspension of Staph. aureus failed to produce bacterial ulcers in healthy rabbits. Several authors,,, reported similar experience. They can however be produced readily in protein deficient animals. Protein deficiency has a definite role in the enhanecment of bacterial corneal ulcers, making the eye more susceptible for bacterial invasion.
We have demonstrated that neonatal under nutrition followed by dietary protein deficiency in rats results in atrophy of lacrimal glands and reduction in the number of goblet cells and size of the meibomian glands Protein deficiency alone depresses the reticulo endothelial function and interferes with the antibody formation(12). Non-specific protective substances of serum have been reported to be lowered in Kwashiorkar children. Similarly both humoral and cell mediated immune responses are depressed in vitamin A deficiency Conversely intercurrent infections may also precipitate deficiency of either protein or vitamin A. Against the complexities of these factors the clinical syndrome develops. Singular deficiencies experimentally, however, fail to show severe ocular lesions like keratomalacia. It is, therefore, considered that disturbances in both internal mileu and environmental factors are involved in the genesis of severe ocular lesions in nutritional deficiencies.
| Summary|| |
The experimental study presented indicate that the cornea in vit A and protein deficiency is mere prone to infections. No pathology could be produced simulating keratomalacia by either Vit A or protein deficiency.
| References|| |
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[Figure - 1], [Figure - 2]
[Table - 1]