Historically, a new disease of dogs was reported in the United States and Europe during the late 1800s and early 1900s. In the southern United States, the disease was known as "sore mouth" or "black tongue." Signs similar to those of the naturally occurring disease could be produced experimentally by using a diet of whole corn, boiled cowpeas, casein, sucrose, cottonseed oil, cod liver oil, salt and calcium carbonate (Goldberger and Wheeler, 1928). The similarity of niacin deficiency signs between dogs and the devastating human disease pellagra in the southern United States was important; the dog became the laboratory animal used to identify the vitamin deficiency. The black tongue (canine pellagra) had naturally occurred in dogs fed a diet primarily of flaked corn (maize) with little materials of animal origin.
The onset of clinical signs for black tongue was acute, with anorexia and weight loss appearing first. The initial lesions were described as a reddening of the mucosa of the lips and later that of the cheeks and floor of the buccal cavity. Patches of superficial necrosis of these areas occurred, as well as necrosis of the tongue, soft palate, and gums. With the necrosis was drooling of thick ropy saliva accompanied by a fetid odor.
The inflammatory changes may extend to the esophagus and eventually to the large intestine. There was bloody diarrhea, inflammation and hemorrhagic necrosis of duodenum and jejunum with shortening and clubbing of villi, and inflammation and degeneration of the mucosa of the large intestine. Occasionally dogs with canine pellagra exhibited pruritic dermatitis of the hind legs and ventral abdomen (Scott et al., 1995). Uncorrected deficiencies lead to dehydration, emaciation, and death (NRC, 1985). Because of a burning or itching sensation, animals would scratch or bite the skin, producing a traumatic dermatitis. Death generally occurred within 10 days of the onset of clinical signs (Ralston Purina, 1987).
On autopsy, gross lesions of niacin deficiency included emaciation and congested, necrotic buccal mucosa. The rugae of the duodenum and jejunum were moderately atrophic, and in some segments a thick layer of mucus and bile streaked with blood covered the mucous membrane (Madhavan et al., 1968).
