2l8 INANITION AND MALNUTRITION 



of xerophthalmia. Bulley ('19) concluded that the xerophthalmia is due to 

 infection, rather than to specific food deficiency, although admitting that the 

 latter may cause a lack of resistance to the infection. Stephenson and Clark 

 ('20) found an invasion of leukocytes to be the earliest change in the cornea of the 

 rat, followed by edema, vascularisation, etc., which may lead to complete 

 corneal degeneration with protrusion of the lens. They obtained various 

 bacteria in cultures from the conjunctival sac, and concluded that "the condi- 

 tion directly attributable to dietetic deficiency is a predisposition to bacterial 

 infection," leading to the characteristic lesions. 



On the other hand, observations and conclusions are presented supporting 

 the theory that the absence of vitamin A is the primary factor in experimental 

 ophthalmia in young rats by Mendel ('20), Emmett ('20), and Emmett and 

 Sturtevant ('20), Wason ('21), Osborne and Mendel ('21 ; also observed by them 

 as early as 1913), Hess, McCann and Pappenheimer ('21), Mori ('22), Walker 

 ('22), Yudkin and Lambert ('22, '22a) and Holm ('22); though not found 

 (in adults ?) by Emmett and Allen ('20). Ophthalmia with similar lesions has 

 been produced, by diets deficient in vitamin A, in the chick by Guerrero and 

 Conception ('20) (on polished rice diet), and by Emmett and Peacock ('22) and 

 Beach ('23); in the young rabbit by Nelson and Lamb ('20), and Nelson, Lamb 

 and Heller ('22); in the dog by Steenbock, Nelson, and Hart ('21); in the duck 

 by Rumbaur ('22); and in the pigeon by McCarrison ('23). There is found, 

 however, much difference in the susceptibility to this disorder, varying accord- 

 ing to species, individuals and diets used. 



The extent of recovery upon adequate refeeding varies according to the 

 degree of the ocular lesions. In most cases in rats complete recovery is possible, 

 according to Stephenson and Clark ('20), but where degeneration is advanced 

 the cornea may remain opaque. "In some cases the cornea has so far degener- 

 ated before cure is begun that the lens is forced through the aperture during 

 life, and cure consists in the disappearance of pus and the healing over of the 

 injured tissues." 



Wason ('21) found that in rats the anatomic lesions (Fig. 69) in experimental 

 xerophthalmia include hyalinization or necrosis of the outer layer of corneal 

 epithelium, exudation of serum and cells into epithelium and stroma, a prolifera- 

 tion of blood vessels and fibroblasts, and, in advanced cases, an invasion of the 

 anterior or (occasionally) the posterior chamber. The degree of restoration 

 possible upon proper diet depends upon the extent of the secondary injury. The 

 manner in which the deficiency of vitamin A renders the cornea susceptible to 

 bacterial invasion is unknown. Walker ('22) also found a staphylococcus-like 

 organism present, but he (like other investigators) was unable to prevent or cure 

 the disorder by external antiseptics. He concludes that there may be some 

 other (possibly hereditary) factor concerned. 



Mori ('22) concludes that the xerosis (dryness) of the conjunctiva and cornea 

 is the essential change produced in the eyes of rats by the deficiency in vitamin 

 A, and that the corneal ulcers (keratomalacia) are produced by the secondary 

 infection. He finds that the two characteristic initial changes are (1) a cornifi- 

 cation of the outer layer of epithelial cells of the conjunctiva bulbi and cornea; 



