224 VITAMIN D GROUP 



but the low calcium type of rickets with either moderate or low levels of 

 phosphorus also has been studied in the rat." Experimental rickets has also 

 been produced in mice/^ hamsters/^ foxes/'' and sheep. '^ In the last two 

 cases the diets contained ample calcium and phosphorus. 



One of the first investigators to study experimental rickets in animals 

 was Findlay,^^ who worked with pups. Mellanby likewise used pups in his 

 early work on rickets. ^^ From this work he concluded that rickets was due 

 to a deficiency of a specific dietary factor. These results aroused considerable 

 interest and led to a very large number of investigations in this field during 

 the following decade. 



The signs of rickets in animals are not particularly different from those 

 in humans, and those of spontaneous rickets are essentially the same as in 

 experimental rickets. In the latter case, however, the condition may be 

 allowed to go to a more advanced state than in spontaneous rickets. Below 

 are discussed the various signs of rickets in animals. Most of the cases 

 discussed are experimental in type. 



1. External Appearance 



Numerous investigators have described (either by photographs or words) 

 the outward signs of rickets in various animals. The signs in the calf have 

 been described very well by Bechtel et al^ as follows: "... the skeletal 

 changes included bowing of the forelegs either forward or to the side, 

 swelling of the knee and hock joints, straightening of the pasterns, occa- 

 sional ring-like swellings on the pasterns, and humping of the back. Poste- 

 rior paralysis occurred in cases of fractured vertebrae. Fractured femora 

 sometimes occurred. Other symptoms frequently observed were stiffness 

 of gait, dragging of the rear feet, standing with the rear legs crossed, ir- 

 ritability, tetany, rapid respiration, bloat, anorexia for grain and roughages 

 but not for milk, weakness and inability to stand for any length of time, 

 and finally the retardation or complete cessation of growth in body weight." 



Similar signs are seen in other types of animals but with some variations, 

 depending on the anatomy of the animal and on the severity of the disease. 

 Bowing of the forelegs, enlargement of the hock and the knee joints, and a 

 tendency to drag the hind legs are very characteristic of all animals suffering 

 from severe rickets. Another common sign is the enlargement of the costo- 

 chondral junctions or beading of the ribs. Deformities of the thorax are 



11 A. T. Shohl, J. Nutrition 11, 275 (1936). 



1^ C. Foster, J. H. Jones, W. Henle, and S. A. Brenner, /. Infectious Diseases 85, 



173 (1949). 

 13 J. H. Jones, J. Nutrition 30, 143 (1945). 



1* L. E. Harris, C. F. Bassett, and C. F. Wilke, /. Nutrition 43, 163 (1951). 

 IS J. Duckworth, W. Godden, and W. Thomson, J. Agr. Sci. 33, 190 (1943). 

 i«L. Findlay, Brit. Med. J. II, 13 (1908). 

 " E. Mellanby, Lancet I, 407 (1919). 



