Taurine deficiency is a relatively rare disease of cats resulting in acquired heart diseases and eye diseases. Until the end of the 1980s, dilated cardiomyopathy (DCM) was more common than HCM in the feline population. Improved knowledge of the taurine requirements of cats has since reduced its incidence considerably.
Blood taurine levels and dietary intake
A study conducted by Heinze et al (2009) attempted to establish comprehensive reference ranges for plasma amino acid and whole body taurine concentrations in healthy adult cats eating commercial diets. Additionally, the researchers wanted to study the relationships of age, gender, body weight, body condition score (BCS), dietary protein concentration, and dietary ingredients with plasma amino acid and whole body taurine concentrations. Samples were taken and a complete health and diet history were obtained from 120 healthy adult cats. The study population consisted of cats belonging to students and faculty as well as a lesser number of university-owned cats housed in colony facilities. The investigators hypothesized that there would be associations between plasma amino acid concentrations and dietary protein concentrations and ingredients. The study did provide data on plasma amino acid and whole body taurine concentrations for a large population of adult cats fed commercial diets. Whole body taurine concentration is considered to be a more accurate measure of taurine status than plasma taurine concentration in cats and reflects the skeletal muscle concentrations more accurately. Gender and neuter status had an affect on plasma amino acid and whole body taurine concentrations where age, body weight, and BCS did not. Dietary protein concentration and dietary ingredients were not directly associated with plasma amino acid or whole blood taurine concentrations in this study.
Taurine was discovered in 1827 as a constituent of ox bile (Bos taurus), which is where the name is derived from. It is a sulfur-containing amino acid. Taurine cannot be linked by peptide bonds and thus cannot be part of a protein. In its free form, it is mainly found in the striated muscles (including the myocardium), the central nervous system, the retina and the liver. Taurine plays a membrane protection role in the myocardium and regulates contractile function. An inadequate taurine intake can thus cause myocardial dysfunction, which in turn may be complicated by congestive heart failure.
Taurine is primarily synthesized in the liver from sulfur-containing amino acids, methionine and cysteine, and the action of several enzymes, including cysteine dioxygenase and cysteine sulphinic acid decarboxylase. In cats, the biosynthesis of taurine from its precursors is inadequate to cover the needs, as the activity of the hepatic enzymes is very low (especially compared with dogs). A dietary intake of taurine is therefore essential.
Moreover cats waste large amounts of taurine. Indeed, as dogs, they use only taurine for the conjugation of bile acids, whereas humans and rats can also use glycine (Morris et al., 1987). This represents a continual loss of taurine, as a substantial part is not recovered by the entero-hepatic circulation and is lost in the feces.
Why has the cat lost its ability to synthesize a nutrient as essential as taurine? Taurine is one of the most abundant amino acids in animal tissues, so cats are not at risk of taurine deficiency when on their natural diet. Under those circumstances producing taurine is a waste of energy whereas the deamination and desulfurization of cysteine is an alternative metabolic pathway that allows cats to produce energy rather than taurine from sulfur amino acid catabolism.
Clinical signs vary widely depending on the individual. Experimental taurine deficiency often produces the simultaneous appearance of irreversible central retinal degeneration (see below) (within six months and inducing total blindness within less than two years) and DCM of varying degrees within two to four years. Not all cats fed taurine deficient diets will develop ultrasonographic or clinical signs of DCM during this time frame. When taurine-deficiency DCM develops, owners are often alerted by the sudden appearance of dyspnea caused by the development of congestive heart failure. Echocardiography shows a reduced shortening fraction as well as an increased systolic diameter of the left ventricle. Later on a left ventricular dilatation that is both systolic and diastolic, associated with thinning of the cardiac walls occurs. In well-developed forms, all four heart chambers are dilated.
In healthy cats, the plasma taurine concentration is greater than 50 nmol/mL but the plasma concentration reflects recent taurine intake only. It is affected by fasting and does not provide any information on the body’s reserves. The result may be artificially high in cats with systemic thromboembolism. As white blood cells and platelets contains high levels of taurine, plasma concentration will be affected by hemolysis or poor separation of the buffy coat.
Establishing a conclusive diagnosis of taurine deficiency requires measurement of the whole blood taurine level because it better reflects taurine concentrations in the myocardium and skeletal muscles. In healthy cats, the whole blood taurine concentration should be higher than 250 nmol/mL (Pacioretty et al., 2001). If lower, taurine deficiency is confirmed.
A feline central retinal degeneration was first reported in 1970 in New York. The aetiology of this feline eye disease was unknown but it was not originally considered to be a nutritional retinopathy.
Taurine deficiency retinopathy (TCRD) is a bilateral, usually symmetrical, progressive condition that occurs in both sexes. The retinal changes are typical, unusual and highly specific for this condition, particularly in the early stages. The first lesion appears at the area centralis, level with and temporal (lateral) to the optic disc in a region devoid of visible blood vessels. A zone of granularity has been described but the first obvious change is the presence of a horizontally oval, focal and well-demarcated millet-seed like spot of increased reflectivity. Hyperreflectivity in a tapetal region always indicates retinal thinning, i.e. retinal degeneration, whatever the cause. The affected area increases in size but remains clearly defined and horizontal and oval in shape. Ophthalmoscopically, the appearance may suggest a pigmented border particularly along the upper and lower edges. A second and similar area appears next on the nasal (medial) side of the disc. These two areas spread toward one another, meet, and fuse in a bridge immediately superior to the optic disc. Further progression occurs but until this time there has been no apparent loss of vision noticed clinically. The whole of the fundus is then affected with a generalised retinal degeneration which appears ophthalmoscopically as hyperreflectivity in the tapetal region; previously no change would have been noted except in the areas described. Finally, attenuation of blood vessels and blindness occurs.
Histopathologically, there are no inflammatory changes; the outer retinal layers are most severely affected with loss of photoreceptors and associated nuclear layer and the inner layers remaining more normal; no changes by light microscopy have been described in the retinal pigment epithelium despite the apparently pigmented borders visible ophthalmoscopy.
The amino-sulphonic acid taurine is now recognised as essential for the cat and approximately 10mg/kg has been shown to be the daily requirement for an adult cat. However, occasional cases of naturally occurring taurine deficiency retinopathy still occur in household cats which are sometimes kept indoors and fed unusual diets including entirely dog foods (dogs are able to synthesise their own taurine).
1. Barnett, KC & Crispin, SM Feline Ophthalmology (2002) Saunders
2. Heinze CR, Larsen JA, Kass PH et al: Plasma amino acid and whole blood taurine concentrations in cats eating commercially prepared diets, Am J Vet Res 70:1374, 2009.