Research on riboflavin deficiency in dogs developed when animals were fed semi-purified diets. The first signs of deficiency were seen after three to nine weeks and were characterized by loss of appetite, weight loss, ocular lesions and flaky dermatitis with marked erythema on the hind legs, chest and abdomen. Conjunctivitis with or without corneal vascularization and opacities was also seen (Potter et al., 1942). The ocular lesions are generally bilateral, and progress from a discharge accompanied by conjunctivitis to opacity and vascularization of the cornea (Street et al., 1941a; Potter et al., 1942; Heywood and Partington, 1971; Noel et al., 1972).
In the final stages of the deficiency disease, muscular weakness develops and progresses within a few days to ataxia, followed by collapse, coma, and death. Dogs also exhibit a unique phenomenon, the collapse syndrome (Street and Cowgill, 1939). Street and Cowgill (1939) used the collapse syndrome as an indicator of deficiency. They reported loss of appetite and muscular weakness before collapse. During the collapse syndrome, the animals were unable to stand and had elevated heart rates (140 to 190 beats per minute), along with vomiting and diarrhea (Potter et al., 1942).
Street et al. (1941a) reported degeneration of the myelin sheath of the posterior spinal cord and the peripheral nerves when adult dogs were fed 8 µg of riboflavin per day for more than 400 days. They suggested this as the basis for the incoordination and loss of deep muscle reflex in the hind limbs observed in the deficient dogs.