Effect of increasing taurine and methionine supplementation on urinary taurine excretion in a model insectivore, the giant anteater (Myrmecophaga tridactyla)
Giant anteaters are specialized insectivores; in the wild, they mainly consume ants and termites (Nowak, 1999; Valdes & Brenes‐Soto, 2012). Providing them with a diet that adequately meets their nutritional requirements is often challenging when they are under human care because their nutrient requirements have not been empirically determined (Clark, Silva‐Fletcher, Fox, Kreuzer, & Clauss, 2016; Valdes & Brenes‐Soto, 2012). A study documenting clinical information on a population of 88 giant anteaters and 15 lesser anteaters (Tamandua tetradactyla) over a period of 23 years at the Sao Paulo Zoo in Brazil reported that 26% of the observed clinical disorders were of digestive origin, while 20% were attributed directly to nutritional causes (Diniz, Costa, & Oliveira, 1995). A later healthcare survey of captive giant anteaters at 24 institutions in the United States and Europe reported that “heart problems” identified at necropsy were recorded for 8% of animals (Morford & Meyers, 2003). Cardiomyopathy is among the conditions that may have nutritional causes in giant anteaters (Liu, Dolensek, & Tappe, 1985). Aguilar, Dunker, and Garner (2002), Coke, Carpenter, Aboellail, Armbrust, and Isaza (2002) and Wilson, Dunker, Garner, and Aguilar (2003) reported cases of cardiomyopathy in this species. Aetiologies include pre‐existing heart disease, electrolyte imbalance, hypoxia, parasitic invasion of cardiac tissue, nutritional deficiencies and unspecified stress (Coke et al., 2002). Among nutritional causes, Aguilar et al. (2002) pointed specifically to taurine (TAU) deficiency. In other species, nutritional causes of myocardial disease also include deficiencies of vitamin E, selenium, potassium, copper, iron, thiamine, magnesium, tryptophan, L ‐carnitine and choline (Van Vleet & Ferrans, 1986). Other non‐nutritional causes of cardiomyopathy in animals include infectious disease, toxic, genetic, traumatic, metabolic and idiopathic conditions (Van Vleet & Ferrans, 1986).
Vitamin E and TAU deficiencies as causal factors in the development of cardiomyopathy have been reported for several species. In a case of cardiomyopathy in flying foxes (Pteropus spp.) under human care, plasma vitamin E levels were reported to be unmeasurable in bats clinically diagnosed with cardiomyopathy, and critically low to unmeasurable in bats in the same group without a cardiomyopathy diagnosis (Heard, Buergelt, Snyder, Voges, & Dierenfeld, 1996). In this case, TAU plasma levels were reported as above 20 nmol/ml, concentrations not commonly associated with TAU‐deficiency cardiomyopathy in domestic cats (Pion, Kittleson, Rogers, & Morris, 1987). Both vitamin E and TAU deficiency have been established as causes of cardiomyopathy in several species of carnivores (Aguilar et al., 2002; Wilson et al., 2003), American opossums (Didelphis spp.; Miller, Garner, & Terrell, 2011), nine species of non‐domestic ruminants, six non‐domestic avian species and gelada baboons (Theropithecus gelada; Liu et al., 1985).
Although in many species TAU is a byproduct of cysteine degradation, cats, some dogs, foxes and some primate species may lack the capacity to synthesize sufficient amounts of TAU to maintain adequate levels (reviewed in Schaffer, Ito, & Azuma, 2014).