Chapter 49 Hypocalcemia, Hypomagnesemia, and Rumenitis in Exotic Ruminants
As nutritional products provided to exotic ruminants have improved in quality to simulate those for domestic ruminants, an associated increase in the prevalence of subclinical and chronic disease states may be attributable to high-quality feeds and the feeding management of these species. An increased prevalence of hypomagnesemia and hypocalcemia, both subclinical and clinically associated with tetany, has been observed in multiple collections of exotic ruminants. Other manifestations of disease associated with systemic imbalances of calcium (Ca++) and magnesium (Mg++) are chronic laminitis and decreases in food consumption and body condition. Zoo practitioners have often observed inverse calcium/phosphorus (Ca/P) ratios in serum chemistry panels from captive ungulates receiving apparently balanced diets.
Because Mg++ is often not included in routine analysis, hypomagnesemia may be unrecognized. Persistent hypocalcemia paired with a sudden drop in serum Mg++ associated with fasting or decreased feed intake may lead to acute tetany. Chronic manifestations of hypocalcemia and hypomagnesemia, such as lameness and chronic laminitis, are often attributed to other causes, such as poor substrate or inadequate foot care.
The species in which this syndrome has been most often recognized are nyala (Tragelaphus angasii), kudu (Tragelaphus imberbis and T. strepsiceros), and eland (Taurotragus oryx), with bongo (Tragelaphus eurycerus) and giraffe (Giraffa camelopardalis) less frequently exhibiting acute manifestations. However, any ruminant species may be considered at risk.
From 60% to 70% of the body’s magnesium is found in bone and is not available to maintain serum Mg++ levels in adult animals.3 Magnesium is the second most common intracellular cation after potassium.6 Because the pool of available Mg++ is small, magnesium must be continuously ingested in the diet to maintain adequate systemic levels. There is minimal hormonal control over Mg++ homeostasis, and serum levels vary with dietary intake and renal excretion.14
Magnesium plays a role in muscle contraction, energy metabolism, and Ca++ metabolism. It is an essential mineral for enzyme activation, especially those reactions that use adenosine triphosphate (ATP).14 It is also important in the synthesis of ribonucleic acid (RNA), deoxyribonucleic acid (DNA), and proteins and as a modulator of synaptic transmission in skeletal muscles. Low Mg++ levels potentiate the release of acetylcholine (ACh) at neuromuscular junctions and may lead to tetany caused by increased ACh concentrations at motor end plates.14 Changes in ACh concentrations may also induce muscle weakness, cardiac arrhythmias, and ileus. Systemic inflammatory responses have been reported to be of increased severity in patients with subclinical hypomagnesemia.15
Typically a disease of pastured cattle, acute signs of hypomagnesemia are often seen after ruminants are put on lush pasture (“grass staggers”) and may manifest as severe tetany. Chronic hypomagnesemia may manifest as anorexia, abnormal gait, poor growth rate or body condition, hyperexcitability, twitching ears, kicking at the abdomen, bruxism, hypersalivation, tetany, seizures, and unexpected death. The development of clinical signs associated with hypomagnesemia is often associated with lactation, stress, transport, or anorexia.6,10 Stress may exacerbate previously subclinical hypomagnesemia because sympathetic nervous system activation causes epinephrine release, which results in decreased plasma Mg++.6
The majority of the body’s calcium is stored in the skeleton, with only 1% found in intracellular and extracellular fluids.11 Extraskeletal Ca++ plays a significant role in nerve and muscle function as well as numerous enzymatic processes. Hypocalcemia may be a result of a dietary deficiency or imbalance or a disruption of normal Ca++ homeostasis within the animal. Systemic Ca++ balance depends on interactions among parathyroid hormone (PTH), vitamin D, and calcitonin. PTH and vitamin D promote increases in serum Ca++, whereas calcitonin causes decreased intestinal absorption and increased renal excretion of Ca++. Hypomagnesemia in cattle may lead to decreased PTH secretion as well as decreased tissue responsiveness to PTH, resulting in impaired absorption and retention of Ca++.8
Acute signs of hypocalcemia may include muscle stiffness or tetany, decreased rumen motility, and death. Evidence of a chronic Ca++ deficiency may manifest as poor feed intake, slow growth, rickets or osteomalacia, and pathologic fractures.
Legumes generally are an excellent source of dietary calcium, whereas grains have lower concentrations of available calcium. Absorption of Ca++ from the diet is affected by multiple factors, including the presence of oxalates, concentrations of Ca++ and phosphorus in the feed, and relative balances of PTH, calcitonin, and vitamin D. Dietary Ca++ uptake is hormonally regulated in the small intestine.
Grains have higher levels of available Mg++ than most forages12; legumes also have relatively high Mg++ concentrations.3 Magnesium is both actively and passively absorbed in the rumenoreticulum in adult ruminants and the small intestine in preruminant calves.17 Interference with Mg++ absorption from the forestomach may lead to rapid development of hypomagnesemia both because substantial amounts of Mg++ are secreted into the saliva of ruminants3 and because body stores of Mg++ are not easily mobilized in times of deficiency. High forage potassium (K+) levels, such as those found in lush grasses, will interfere with rumen uptake of Mg++ by changing electrochemical gradients across the rumen epithelium.5 Other causes of impaired Mg++ absorption include sudden increases in rumen ammonia, high dietary Ca++ levels, and low dietary sodium (Na+) levels. Low Na+ results in an aldosterone-induced increase in K+ secretion into saliva and the rumen.7 The resulting high rumen K+ concentration results in decreased Mg++ absorption.