Molybdenum is an essential element associated with a variety of metalloenzymes and corresponding metabolic functions. Excessive dietary intake of molybdenum produces secondary copper deficiency. The resultant toxicosis in ruminants is seen worldwide. Cattle and sheep are approximately 10-fold more susceptible than other species. Acute toxicosis associated with massive intake of molybdenum is rarely encountered.
Etiology of Molybdenum Toxicity in Animals
Metabolic interactions related to the utilization, bioavailability, and kinetics of copper, molybdenum and sulfate are highly important; albeit complex and incompletely understood. In ruminants, various molybdates react with sulfides to produce thiomolybdate compounds, which combine with copper to form an insoluble complex that is poorly absorbed. This reduced bioavailability of copper impairs copper utilization and the synthesis of a variety of copper-dependent proteins, ultimately inducing secondary copper deficiency. Excessive dietary molybdenum intake also enhances the excretion of copper.
The limited bacterial formation of thiomolybdates in monogastric animals is primarily responsible for the tolerance of dietary molybdenum in these species. Hence, molybdenum toxicity is uncommon in horses.
The susceptibility to molybdenum toxicity in ruminants depends on several factors, including:
dietary copper content—susceptibility increases as the copper content decreases
dietary sulfate content—susceptibility increases with high sulfate content via impairment of copper utilization; whereas low sulfate content enhances susceptibility by reducing molybdenum excretion
the chemical form of molybdenum—water-soluble forms found in fresh feed are more toxic
sulfur-containing amino acids may alter copper utilization or molybdenum excretion
animal species—cattle are more susceptible
age—young animals are more susceptible, and excretion of molybdenum into milk may produce toxicoses in nursing calves
season of year—molybdenum concentrations in plants increase in the fall
plant species—legumes bioaccumulate more molybdenum
breed differences—seen in sheep and goats
Molybdenum toxicity has been encountered in geographic areas with peat, muck, or shale soil types that naturally contain molybdenum. Environmental contamination associated with mining or metal production or areas in which molybdenum-contaminated fertilizers are used can result in enhanced uptake of molybdenum by plants used as feed sources.
Clinical Findings for Molybdenum Toxicity in Animals
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 typically characterized by severe, persistent diarrhea with the presence of green, liquid feces containing gas bubbles, often referred to as peatscours. 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, and joint pain characterized by lameness. Because molybdenum competes with phosphorus utilization, bone mineralization is reduced, causing osteoporosis, often manifest as pathologic fractures.
Delayed puberty, decreased weight at puberty, delayed fertility, poor conception rates, and decreased milk production are common. Reduced libido has been reported in bulls. In sheep, particularly in lambs <30 days old, affected animals exhibit stiffness of the back and legs and have difficulty rising. The syndrome in sheep is known as enzootic ataxia, or swayback. Abnormal development of connective tissue and growth plates are apparent in affected animals. Clinical signs typically appear within 1–2 weeks.
Occasionally, acute toxicosis may be encountered in cattle or sheep. Anorexia and lethargy may be evident within 3 days. Deaths begin within 1 week of exposure and may continue for many months. Neonates frequently exhibit hindlimb ataxia that often progresses to the forelimbs. Salivation and scant mucoid feces are common.
Excessive molybdenum exposure may also impair a variety of enzymes involved in collagen and elastin production and maintenance, which has been associated with cardiovascular disorders. Molybdenum exposure may also affect phospholipid synthesis in nervous system tissues, resulting in demyelination and various neurologic manifestations.
At post-mortem examination, hemosiderosis, periacinar to severe hepatic necrosis, and nephrosis are evident histopathologically. In affected sheep, neuronal degeneration, demyelination, and lysis of white matter are evident in neurologic tissues.
Diagnosis of Molybdenum Poisoning in Animals
Characteristic clinical signs (eg, greenish diarrhea, lameness, poor weight gain, breeding problems), particularly when a herd is affected
Analysis of feed samples for determination of copper:molybdenum ratio
Analysis of liver and plasma samples for determination of copper and molybdenum concentrations
The diagnosis of molybdenum toxicosis, a herd-related problem with typically high morbidity, may be confirmed by analysis of feed samples to measure the copper:molybdenum ratio (normal ratio, 6:1 to 10:1). A ratio of 2:1 is consistent with a diagnosis of molybdenum toxicosis. Post-mortem analysis of liver specimens (preferred) as well as testing of plasma samples for copper and molybdenum concentrations also provides valuable diagnostic information.
Distinguishing between primary 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. In the early stages of the chronic toxicosis, vague clinical manifestations such as infertility may be difficult to confirm by means of analysis of tissue samples. Plasma copper concentrations may be within reference limits. Assessment of ceruloplasmin activity, a copper-containing ferroxidase enzyme, may be more informative diagnostically. Clinical improvement after copper sulfate administration provides valuable support for the diagnosis.
Analysis of the feed samples for copper and molybdenum concentrations is recommended. In cattle feed, a copper:molybdenum ratio of 6:1 is optimal. If the ratio is less than 2:1, molybdenum toxicosis will occur. Ratios exceeding 15:1 may cause chronic copper toxicosis. Absolute molybdenum concentrations in the diet >10 mg/kg will result in toxicosis independent of copper intake. Massive molybdenum exposure via the feed (ie,>2,000 mg/kg) will result in acute toxicosis and death.
Analysis of liver and plasma samples to determine molybdenum concentrations provides useful insight to confirm a diagnosis; however, results must be interpreted in association with results for 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 toxicity in the presence of a low tissue copper concentration. Livestock guidelines for water concentration range from 0.3 to 0.5 ppm. Species susceptibility and effects of copper interaction metabolically, impact disease development.
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Treatment and Prevention of Molybdenum Poisoning in Animals
Dietary supplementation with appropriate, breed-specific copper mineral mixes
Administration of injectable or chelated copper products
Molybdenum toxicity manifests primarily as a copper deficiency syndrome. In many instances, simple dietary supplementation with copper mineral mixes is insufficient to restore the optimal mineral imbalance created by the biologically key interaction between copper and molybdenum. Injectable or chelated copper products may be required to restore normal productivity and animal health.
Dietary supplementation with copper sulfate will reduce the bioavailability of molybdenum in the gastrointestinal tract, thus reducing absorption and enhancing excretion. In feed containing molybdenum at >5 mg/kg, supplementation with 1% copper sulfate in salt will help control development of toxicosis in herds. In animals housed on recovered mining areas, the supplementation may need to be increased to as much as 5% copper sulfate in the salt supplement. If the source of dietary 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.
When the feeding of mineral supplements is impractical, treatment may be administered as a weekly liquid drench administered orally. Injectable products such as copper glycinate or copper edetate (Cu-EDTA) may be administered at a dose of 120 mg/cow. Practitioners should note that these products are legally approved only in some jurisdictions. Chelated mineral products, although more expensive, are often more successful as a treatment option in animal populations refractive to other treatments. The strong copper-molybdenum interaction may require a prolonged treatment period, potentially several months. It should be noted that many mineral feeding guidelines for production animals fail to recognize the importance of this key metabolic interaction on performance and disease.
Molybdenum toxicosis typically affects ruminants (cattle, sheep) as a herd diagnosis.
Clinical signs include characteristic chronic greenish diarrhea, poor production, and lameness, with morbidity up to 80%.
Molybdenum-copper imbalance in feed is a common cause; treatment is via dietary copper supplementation.
For More Information
Diagnostic information concerning molybdenum toxicity is summarized in: Puls R. Mineral Levels in Animal Health: Diagnostic Data, 2nd ed. Sherpa International Clearbrook; 1994:192–198.
Agriculture and Agri-Food Canada: Livestock Water Quality: A Field Guide for Cattle, Horses, Poultry and Swine