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Overview of Molybdenum Poisoning


Molybdenum is an essential element associated with a variety of metalloenzymes and corresponding metabolic functions. Excessive dietary intake of molybdenum induces a secondary copper deficiency. The syndrome, predominately reported in ruminants (versus nonruminant species) is seen worldwide. Cattle and sheep are ~10-fold more susceptible than other species. Acute toxicity associated with massive doses is rarely encountered.

The interactions associated with copper, molybdenum, and sulfate metabolism related to the utilization, bioavailability, and kinetics of copper are among the most biologically significant interrelationships in veterinary medicine. The complexity of the interactions is not fully understood. In ruminants, various molybdates react with sulfides to produce thiomolybdate compounds, which react with copper to form an insoluble complex that is poorly absorbed. The reduced copper absorption impairs copper utilization and the synthesis of a variety of copper-dependent proteins. The reduced bioavailability of copper ultimately induces secondary copper deficiency. Excessive molybdenum intake also enhances the excretion of copper. Based on this observation, the administration of tetrathiomolybdates may be a useful treatment for chronic copper poisoning (see Copper Poisoning). The limited bacterial formation of thiomolybdates in monogastric animals is primarily responsible for the tolerance to molybdenum encountered in these species. Excessive molybdenum exposure may also impair a variety of enzymes involved in collagen and elastin maintenance and stability, which has been associated with cardiovascular disorders. Molybdenum exposure may reduce phospholipid synthesis in nervous tissue, resulting in demyelination and neurologic disorders clinically.

The susceptibility to molybdenum toxicity in ruminants depends on a number of factors, including 1) dietary copper content—susceptibility increases as the copper content decreases; 2) dietary sulfate content—susceptibility increases with high sulfate levels by impairing copper utilization, whereas low sulfate content enhances susceptibility by reducing molybdenum excretion; 3) the chemical form of molybdenum—water-soluble forms found in fresh feed are more toxic; 4) sulfur-containing amino acids may alter copper utilization or molybdenum excretion; 5) animal species—cattle are more susceptible; 6) age—young animals are more susceptible, and excretion of molybdenum into milk may produce toxicoses in nursing calves; 7) season of year—molybdenum concentrations in plants increase in the fall; 8) plant species—legumes bioaccumulate more molybdenum; and 9) breed differences—seen in sheep and goats.

Molybdenum toxicity has been encountered in regions of the world containing peat, muck, or shale soil types that are naturally contaminated with molybdenum. Industrial contamination associated with mining or metal production or areas using molybdenum-contaminated fertilizers result in enhanced uptake of molybdenum by plants used as a feed source.

The manifestations of molybdenum toxicity are related primarily to impaired copper metabolism and utilization, resulting in secondary copper deficiency. Typically, the syndrome is a herd problem, with morbidity as high as 80%. In cattle, clinical disease is characterized by severe, persistent diarrhea with the presence of green, liquid feces containing gas bubbles, often referred to as peat or teart scours. Depigmentation, resulting in fading achromotrichia of the hair coat is evident in black animals associated with impaired tyrosinase activity and reduced melanin synthesis. Pica, unthriftiness, microcytic hypochromic anemia, emaciation, joint pain characterized by lameness, and osteoporosis often manifested by bone fractures are seen. Molybdenum competes with phosphorus utilization, resulting in reduced mineralization of bone. In heifers, fertility is reduced. Delayed puberty, poor conception rates, decreased weight at puberty, and decreased milk production are common. Reduced libido has been reported in bulls. In sheep, particularly in lambs <30 days old, the animals exhibit stiffness of the back and legs and have difficulty rising. The syndrome in sheep is known as enzootic ataxia, or sway back. Abnormal development of connective tissue and growth plates are apparent in affected animals. Manifestations appear within 1–2 wk if molybdenum levels are excessive.

Occasionally, acute toxicity may be encountered in cattle or sheep. Anorexia and lethargy may be evident within 3 days. Deaths begin within 1 wk and may continue for many months. Neonates frequently exhibit hindlimb ataxia that often progresses to the forelimbs. Salivation and scant mucoid feces are common.

At necropsy, hemosiderosis, periacinar to severe hepatic necrosis, and nephrosis are evident. In affected sheep, neuronal degeneration, demyelination, and lysis of white matter are seen in nervous tissue.

Distinguishing between primary copper deficiency and secondary copper deficiency related to excessive molybdenum exposure is important. Often with molybdenum toxicity, there is a poor correlation between tissue concentrations of copper and clinical disease. Clinical improvement after copper sulfate administration provides valuable support for the diagnosis. Analysis of the ration for copper and molybdenum concentrations is recommended. In cattle rations, a copper:molybdenum ratio of 6:1 is optimal. If the ratio is less than 2:1, molybdenum toxicity will occur. Ratios exceeding 15:1 may cause chronic copper poisoning. Absolute molybdenum concentrations in the diet >10 mg/kg will cause poisoning independent of copper consumption. Massive molybdenum exposure in the ration >2,000 mg/kg will result in death. Analysis of the liver and plasma for molybdenum provides useful insight to confirm the diagnosis, but the concentrations must be interpreted in association with the comparable tissue concentrations of copper. In cattle, liver concentrations >2 ppm (wet weight) and plasma concentrations >0.1 ppm are consistent with a diagnosis of molybdenum poisoning in the presence of a low copper status. Other disease syndromes characterized by emaciation or unthriftiness (parasite infections, selenosis, fluorosis, ergotism), diarrhea (metal poisonings, GI infections), and lameness or bone abnormalities (fluorosis, selenosis, ergotism, lead poisoning) may resemble molybdenum poisoning and should be investigated as possible etiologies.

Most treatment options are associated with the biological interactions associated with copper, molybdenum, and sulfate. Under circumstances in which dietary exposure is difficult to eliminate, simple treatment with copper products may be futile. If the source of molybdenum can be removed, excess molybdenum is rapidly eliminated and food products are safe for consumption within a relatively short time. If the dietary exposure cannot be reduced, elimination of molybdenum in the milk may produce toxicosis in nursing calves. Dietary supplementation with copper sulfate will reduce the bioavailability of molybdenum in the GI tract, ultimately reducing absorption and enhancing excretion. In feed containing molybdenum at >5 mg/kg, supplementation with 1% copper sulfate in salt will control development of the syndrome. In recovered mining areas, the supplementation may need to be increased to as much as 5% copper sulfate in the salt. When the consumption of mineral supplements is impractical, the treatment may be administered as a weekly drench. Injectable products such as copper glycinate or copper edetate (Cu-EDTA) may be given at a dose of 120 mg/cow. These products are approved only in some jurisdictions.

Last full review/revision December 2013 by Barry R. Blakley, DVM, PhD

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