Classic symptoms of vitamin C deficiency, or scurvy, are marked deterioration of mucosal integrity and health and subsequent loss of disease resistance. Because ruminants possess the metabolic pathway to synthesize ascorbic acid, they are only likely to experience outright deficiency symptoms in the neonatal period, before synthesis reaches full capacity. Cummins (1992) cites several published reports of vitamin C deficiency signs in young calves. The signs included lesions of the oral cavity and skin, low plasma ascorbate levels, increased susceptibility to disease and evidence of muscle pain and subcutaneous hemorrhage. In other species, vitamin C deficiency results in impaired neutrophil and macrophage chemotaxis and depressed T-lymphocyte response to respiratory disease (Beisel, 1982; Sauberlich, 1994; Hemila and Douglas, 1999).
Stress caused by housing, disease, weather changes, transport or other factors is the most likely cause of marginal vitamin C deficiency in ruminants (Cummins and Brunner, 1991; Mackenzie et al., 1997). However, studies to date have not established a clear basis for the level of vitamin C that may be required for optimal health and performance of calves, lambs or goat kids. Supplementation of milk replacer with vitamin C at levels similar to whole milk would appear advisable.
Death of cows and calves due to scurvy was characterized by changes in the oral cavity mucosa, muzzle and skin, accompanied by weight loss and general unthriftiness (Cole et al., 1944; Duncan, 1944). In calves, extensive dermatosis, accompanied by hair loss and thickening of skin, was observed in animals receiving insufficient milk. Blood ascorbic acid was low, and the condition was successfully treated with parenteral vitamin C administration. Martynjuk (1952) reported the incidence of scurvy and reduced blood ascorbic acid content in weaned calves. Studies of blood vitamin C concentrations in calves fed a common diet revealed large individual differences, with variations related to genetic background (Palludan and Wegger, 1984).
Positive effects of ascorbic acid supplementation on milk yield and milk quality were reported by Kucmyj (1955). Studies with bulls indicated reduced vitamin C status during cold stress (Hidiroglou et al., 1977). Hypovitaminosis C has been observed primarily in winter and early spring, and most commonly in calves (Soldatenkov and Suganova, 1966). Jagos et al. (1977) found considerably lower plasma vitamin C content in calves with bronchopneumonia than in healthy animals. A relationship has been reported between hypovitaminosis C and skeletal muscle pain and subcutaneous hemorrhages in calves (Pribyl, 1963). Dobsinska et al. (1981) studied the relationship between ascorbic acid status and body weight gain of calves in a large commercial facility and found a negative correlation between the two parameters in two- to 22-week-old bull calves. Calves from herds characterized by poor health status generally had reduced ascorbic acid status during the critical period from birth to two weeks of age. Supplementation with 1.25 to 2.5 g of vitamin C per day reportedly reduced the incidence of respiratory disease (Itze, 1984; Palludan and Wegger, 1984; Hemingway, 1991).
In conclusion, it appears that the basic vitamin C requirement of mature, healthy ruminant animals is met by endogenous synthesis. However, young ruminants are susceptible to deficiency during the first few weeks of life, particularly when subjected to stress, disease exposure or limited colostrum intake.
