Molybdenum

Question 1

What can the syndrome manifest as a what is important to figure out?

Answer 1

can manifest as Cu deficiency

important to see whether the syndrome is primary Cu def or secondary problem related to excess Mo

Question 2

What terms are used to describe the syndrome?

Answer 2

teart, peat scours, swayback or enzootic ataxia

Question 3

What is a source of Mo toxicity?

Answer 3

high Mo in the soil, industry, mines, fertilizers

Question 4

Which animals are susceptable?

Answer 4

cattle are more susceptable to Cu/Mo problems
ruminants
young animals

Question 5

What animals are more resistant?

Answer 5

pigs

storage of Cu is not affected by Mo in pigs

Question 6

What is the pathogenesis? three things Mo interferes with?

Answer 6

Mo interferes with Cu storage by reducing absorption and enhancing excretion
Mo also competes with Cu in many Cu dependent enzymes

Mo interefers with P absorption and mineral metabolism in the bone (faulty bone development in young animals)

Mo interferes with synthesis of phospholipids by the mitochondria and ATP syn (reduced bone and maintenance of myeline)

Question 7

What are the clinical manifestations in sheep?

Answer 7

swayback (enzootic ataxia)
incoordination, ataxia
occasionally blind
depigmented, stringy wool (black wool tinged red)
usually young animals

Question 8

What are the clinical signs in cattle?

Answer 8

“poor dooer”

- emaciation, diarrhea, anemia, achromotrichia, enlarged joints, osteoporosis, reduced fertility and milk production

Question 9

what is the Dx?

Answer 9

clinical appearance
forage levels (Cu:Mo 2:1)
tissue levels (Cu:Mo)
reponse to Cu therapy

Question 10

what is the treatment?

Answer 10

shot of Cu and boom
copper sulfate as mineral mix
copper oxide needles
scintered glass boluses
chelated mineral mix/injectable