Molybdenum is an essential micronutrient that forms molybdenoenzymes, which are necessary for the health of all animals. In ruminants, the dietary intake of excessive molybdenum causes, in part, a secondary hypocuprosis. Toxicosis due to massive doses of molybdenum is rare. Domestic ruminants are much more susceptible to molybdenum toxicity than nonruminants. The resistance of other species is at least 10 times that of cattle and sheep.
The metabolism of copper, molybdenum, and inorganic sulfate is a complex and misunderstood interrelationship. It appears that the ruminal interaction of molybdates and sulfides gives rise to thiomolybdates (mono-, di-, tri-, and tetrathiomolybdates). Copper reacts with thiomolybdates (primarily tri-and tetrathiomolybdates) in the rumen to form an insoluble complex that is poorly absorbed. In addition, systemic thiomolybdates chelate copper, making it not bioavailable and causing a copper deficiency. On this basis, tetrathiomolybdate is used in treating and preventing copper toxicity (see Copper Poisoning) in sheep. Molybdenum also appears to be directly toxic to tissue reductive enzymes, which may explain the poor response to copper therapy in severely affected animals. The lack of bacterial formation of thiomolybdates in monogastric animals partially explains the relative tolerance of these animals to molybdenum toxicity.
The susceptibility of ruminants to molybdenum toxicity depends on a number of factors: 1) copper content of the diet and intake of the animal—tolerance to molybdenum toxicity decreases as the content and intake of copper decrease; 2) the inorganic sulfate content of the diet—high dietary sulfate with low copper exacerbates the condition, while low dietary sulfate causes high blood molybdenum levels due to decreased excretion; 3) chemical form of the molybdenum—water-soluble molybdenum in growing herbage is most toxic, while curing herbage decreases toxicity; 4) presence of certain sulfur-containing amino acids; 5) species of animal—cattle are less tolerant than sheep; 6) age—young animals are more susceptible; 7) season of year—plants concentrate molybdenum beginning in spring (maximum level reached in fall); and 8) botanic composition of the pasture—legumes take up more of the element than other plant species.
Molybdenum toxicity associated with copper deficiency has been seen in areas with peat or muck soils, where plants grow in alkaline sloughs (eg, western USA), as a result of industrial contamination (mining and metal alloy production), where excess molybdenum-containing fertilizer has been applied, and where applications of lime appeared to increase plant molybdenum uptake.
In the diet of cattle, copper:molybdenum ratios of 6:1 are considered ideal; 2:1–3:1, borderline; and <2:1, toxic. Dietary molybdenum of >10 mg/kg can cause toxicity regardless of copper intake; as little as 1 mg/kg may be hazardous if copper content is <5 mg/kg (dry-weight basis). Mixing errors may occur; concentrations above 1,000 mg/kg (as sodium molybdate) cause growth retardation while concentrations of 2,000–4,000 mg/kg cause death within 40 days.
Most of the clinical signs attributed to molybdenum toxicity arise from impaired copper metabolism and are the same as those produced by simple copper deficiency. Molybdenum toxicity in cattle is characterized by persistent, severe scouring with passage of liquid feces full of gas bubbles (peat or teart scours). Depigmentation, resulting in fading of the hair coat, is most noticeable in black animals and especially around the eyes, which gives a spectacled appearance. Other signs include unthriftiness, anemia, emaciation, joint pain (lameness), osteoporosis, and decreased fertility. Effects on reproduction, particularly in heifers, include delayed puberty, decreased weight at puberty, and reduced conception rates. It appears that fertility is uniquely vulnerable to the effects of molybdenum or thiomolybdates and alone responds indirectly to copper acting as an antidote. Some studies have suggested that relatively low levels of molybdenum may exert these direct effects on certain metabolic processes, particularly reproduction, independent of alterations in copper metabolism. Sheep, and young animals in particular, show stiffness of the back and legs with a reluctance to rise (called enzootic ataxia in Australia). Joint and skeletal lesions appear to be due to defects in development of connective tissue and growth plates. Clinical signs appear within 1–2 wk of grazing affected pasture.
Effects in cattle and sheep acutely poisoned with massive concentrations of molybdenum are unlike the chronic induced copper deficiency described above. Cattle lose appetite within 3 days. Deaths begin to occur within 1 wk and continue for months after exposure ends. Animals are lethargic, display hindlimb ataxia that progresses to involve the front limbs, salivate profusely, and produce scant, mucoid feces. The molybdenum is toxic to hepatocytes and renal tubular epithelial cells, producing periacinar to massive hepatic necrosis and nephrosis.
Primary copper deficiency must always be ruled out. In molybdenum toxicity, low copper levels in blood and tissue and the occurrence of clinical signs of copper deficiency in cattle are poorly correlated. In areas with high levels of molybdenum, a provisional diagnosis of molybdenosis can be made if the diarrhea stops within a few days of oral dosing with copper sulfate. The diagnosis is further supported if other causes of diarrhea and unthriftiness (including GI parasites) are ruled out. Diagnosis is confirmed by demonstrating abnormal concentrations of molybdenum and copper in blood or liver and by a high dietary intake of molybdenum relative to copper.
Prevention and Treatment
Molybdenum is excreted in the milk; the concentration depends on levels in the feed. When animals are removed from the source, molybdenum is rapidly excreted. Because there is minimal tissue retention, products from exposed animals are soon safe for consumption. Signs of severe acute toxicosis are reversed by providing copper sulfate in the diet. The copper-thiomolybdate complexes reduce bioavailability, while sulfate competes with molybdenum in the gut and kidneys, reducing molybdenum absorption and enhancing its excretion. In areas where the molybdenum content of the forage is <5 mg/kg, the use of 1% copper sulfate (CuSO4•5H2O) in salt has provided satisfactory control of molybdenosis. With higher levels of molybdenum, 2% copper sulfate has been successful; up to 5% has been used in a few regions where the molybdenum levels are very high. In areas where, for various reasons, cattle do not consume mineral supplements, the required copper may be supplied as a drench given weekly, as parenterally administered repository copper preparations, or as a top-dressing to the pasture. Copper glycinate injectable has been used successfully as an adjunct to therapy.
Last full review/revision March 2012 by Herman J. Boermans, DVM, MSc, PhD