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Clinical Findings of Molybdenum Poisoning

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.

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