Studies on a-Avitaminosis in Chickens

Abstract

1. The principal tissue changes in the respiratory tract of chickens caused by a vitamin A deficiency in the food are, first, an atrophy and degeneration of the lining mucous membrane epithelium as well as of the epithelium of the mucous membrane glands. This process is followed or accompanied by a replacement or substitution of the degenerating original epithelium of these parts by a squamous stratified keratinizing epithelium. This newly formed epithelium develops from the primitive columnar epithelium and divides and grows very rapidly. The process appears to be one of substitution rather than a metaplasia, and resembles the normal keratinization of the skin or even more closely the incomplete keratinization of the mucous membranes (e.g., the esophagus or certain parts of the tongue of chickens). In this connection findings have been described which not only afford an interesting insight into the complicated mechanism of keratinization, but also show probable relations between keratinization and the development of Guarnieri's inclusion bodies. Balloon and reticular degeneration of the upper layers of the new stratified epithelium has been frequently observed. All parts of the respiratory tract are about equally involved in the process; and the olfactory region as well, so that the sense of smell may be lost. The lesions, which first take place on the surface epithelium and then in the glands, show only minor differences. 2. The protective mechanism inherent in the mucous membranes of the entire respiratory tract is seriously damaged or even entirely destroyed by the degeneration of the ciliated cells at the surface and the lack of secretion with bactericidal. properties. Secondary infections are frequently found, and nasal discharge and various kinds of inflammatory processes are common, including purulent ones, especially in the upper respiratory tract, communicating sinuses, eyes and trachea. The development of the characteristic histological process is not dependent upon the presence of these infections, since it also takes place in the absence of infection. 3. The specific histological lesions make it possible to differentiate between A-avitaminosis and some infectious diseases of the respiratory tract. These studies we hope will serve as a basis for further investigations on the relationship between A-avitaminosis and infection in general.

Vitamin a Deficiency in Turkey Poults

“…2,7 Gross lesions are initially confined to the mucous glands and ducts of the pharynx and esophagus and appear as white to yellowish caseous, coalescing nodules. 11,18,19 Microscopically, squamous metaplasia is the hallmark of vitamin A deficiency (VAD), affecting the cuboidal and columnar epithelia of the mucosal glands of the digestive, respiratory, and urinary tracts and the eye. 3,8,10,18,19 Natural and experimental VAD are well documented in chickens but a natural occurrence and histopathological description of this condition has not been reported in commercial turkeys.…”

“…11,18,19 Microscopically, squamous metaplasia is the hallmark of vitamin A deficiency (VAD), affecting the cuboidal and columnar epithelia of the mucosal glands of the digestive, respiratory, and urinary tracts and the eye. 3,8,10,18,19 Natural and experimental VAD are well documented in chickens but a natural occurrence and histopathological description of this condition has not been reported in commercial turkeys. This report is an account of the gross and histopathological changes caused by VAD in commercial turkeys.…”

“…The clinical signs and the gross and microscopic lesions provide evidence of the similarities of signs and lesions in humans and birds affected either experimentally or naturally with VAD. 3,5,8,18,19 Experimental VAD in turkeys is characterized by squamous metaplasia in the esophagus, oropharynx, paraocular glands, sinuses, proventriculus, and bursa of Fabricius. 3,7 The length of time that these poults received the vitamin A-deficient diet is unknown, but based on previous experimental studies, 3,4,8 it might have been about 3 weeks before the onset of signs.…”

Histopathology of Infectious Laryngotracheitis in Chickens

“…It is a striking fact that in many instances the affected nuclei underwent dissolution. We have not observed similar changes of epithelial cells in other diseases involving the same structures, such as A-avitaminosis, coryza contagiosa, and fowlpox (12,13). Since the same type of intranuclear inclusions and nuclear changes are present in other virus diseases, we feel justified in considering them a result of virus activity in the epithelial cells of the trachea and larynx.…”

Vitamin A Storage by Chickens

“…On the other hand, Sugiura and Benedict (1923) state that the fat-soluble vitamin is not essential in any stage of avian nutrition. However, this view is not supported by other investigators, for Emmett and Peacock (1923), Hart, Steenbock, Lepkovsky, and Halpin (1924), Hughes, Lienhardt, andAubel (1929), Capper, McKibbin, andPrentice (1931), Elvehjem and Neu (1932), Seifried (1930), Hauge, Carrick, and Prange (1927), Frohring and Wyeno (1934), and others have shown that vitamin A is essential for the proper development of young chicks and that growing chicks which are limited for any length of time to rations that are inadequate or lacking in vitamin A develop characteristic symptoms of A-avitaminosis.…”