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what two groups are essential dietary minerals split into?
macro minerals (major elements) - g/d
micro minerals (trace elements) - mg/d
why is knowledge of minerals important?
some deficiency states occur commonly
all are treatable (by provision of the mineral in the appropriate form
all are preventable (by correction of dietary or physiological imbalances
some can induce toxicity states if given in excess quantities
why are both calcium and phosphorus important?
most important mineral constituents of bone and teeth:
bone = 46% ash
ash = 36% calcium and 17% phosphorus (2:1)
physiological regulation of Ca and P uptake, storage, function and excretion are interrelated
what are the functions of calcium?
structural component of skeleton
controls cell excitability (nerve and muscle)
regulates muscle contraction
regulates blood coagulation
many enzyme actions
there is rigid homeostatic control of plasma calcium ion concentrations via vitamin D and hormones
what are the different sources of calcium?
must take Ca:P ratio into account (ideally 1:1 to 2:1)
leafy greens
hay/silage
animal products (milk, meat, eggs)
some food contain more P than Ca and require artificial ration balancing:
bran
cereals
roots
legume and oil seeds
what are some corrective sources of calcium?
limestone flour
in poultry: soluble grit (e.g. limestone/oyster shell)
what factors affect calcium absorption?
much plant Ca is bound as phytates (prevents absorption in monogastrics but rumen microflora can release (phytases))
oxalates: bind to Ca to form insoluble salts so Ca can’t be absorbed by animals - significant quantities in spinach, sugar beet tops etc
total absorption of dietary Ca and P decreases as dietary conc. becomes excessive
high fat diets: excess dietary free fatty acids bind to Ca (and Mg) to form insoluble salts
enteritis: inflamed mucosa will not absorb Ca
what are signs of calcium deficiency?
hypocalcaemia:
occurs if sudden decrease in blood calcium concentration - homeostatic control sluggish to correct
acute form:
can occur in female mammals at onset or peak of lactation as high demands of mammary gland for calcium to synthesise milk
can occur in laying hens due to high calcium demands for eggshell production
when does hypocalcaemia often occur in dairy cows?
also called milk fever:
commonly from 1 day before calving to 3 days post-partum - high demand for Ca from lactation
high-yielding cows in their third and subsequent lactations
slow homeostatic adaptation in combination with increased Ca demand - mechanisms unable to prevent a sudden decrease in blood Ca level
what are signs of hypocalcaemia in dairy cows?
flaccid paralysis (progressive)
general uneasiness
dullness
paddling/shifting of hind legs
dry muzzle
constipation
inability to stand
coma
death
recumbency (‘downer cow’)
rumen stasis
pupil dilation
what are signs of hypocalcaemia in bitch, sow, and beef cattle?
eclampsia (lactation tetany - involuntary, sustained muscle spasms)
what are symptoms of hypocalcaemia in growing animals?
high rate of skeletal growth (high Ca and P demand)
beware of breeds/species with high growth rates
osteodystrophy = abnormal bone growth
deficiencies of Ca, P, and vitamin D
nearly always accompanied by osteoporosis: loss of Ca and P from bones making them thinner and weaker, increasing incidence of fractures
rockets = failure of bone to ossify
vitamin D deficiency (classically)
in ruminants a deficiency of either vitamin D or P can cause rickets
what are the causes of osteodystrophy in different species?
puppies/kittens: excessive P (secondary Ca deficiency)
foals: poor artificial rearing, gut parasites, low hay and high cereal diets (secondary deficiency)
calves and lambs: unsupplemented high cereal/straw diet
piglets: failure to supplement dietary Ca, P, vitamin D
treatment = correct dietary Ca:P balance
what are the symptoms of chronic hypocalcaemia in adult animals?
skeletal Ca and P reserves are high and can be withdrawn upon if temporary imbalance (except in late pregnancy and early lactation)
mobilisation of skeletal Ca and P long term leads to osteomalacia (due to lack of provision of Ca and P):
weakened, thin bones = easily fractured
increased incidence of osteoarthritis
decreased milk yields
urethral caliculi in entire and castrated male lambs fed high concentrate diet
in horses, goats, and pigs: demineralisation of bones of skull and compensatory collagen deposition causing thickening of the bones (bran disease - excessive P)
what factors affect phosphorus absorption?
oxalates and phytates: much plant P is organically bound as salts of phytic acid - in simple stomached animals little of the phytate is available
excess dietary Ca or P inhibit the absorption of P or Ca
what are signs of phosphorus deficiency?
hypophosphataemia:
abnormal bone growth and osteomalacia
reduced growth rate
‘pica’ (abnormal appetites) e.g. bone/wood chewing
infertility
what are the functions of magnesium?
no body reserves and no homeostatic regulation - dependent on dietary intake to maintain function
around 70% total body magnesium is present in bone
most common enzyme activator
muscle contraction
propagation of nerve impulses
what are the different sources of magnesium?
all green plants (chlorophyll)
meat and bone
colostrum
magnesite and calcined magnesite
how much magnesium do animals absorb from diet?
20-30%
decreased by high copper and high phytate P intakes
what is hypomagnesia?
lack of/not enough magnesium
what are the 4 major presentations of hypomagnesia?
calves fed unsupplemented all-milk diets are at risk (2-3 months)
milk is a poor source of Mg
Mg absorption decreases with age
beef cattle and sheep fed on low quality roughage (straw) or fodder crops (kale, beet)
symptoms may occur over several days
dullness, hyperaesthesia, convulsions, death
lactating cattle and sheep
grass staggers = emergency
signs:
hyperaesthesia (hyper-sensitive to stimuli)
incoordination
muscle tremor
recumbency
convulsions
death
frequent cause of sudden deaths - treatable by giving magnesium
sub-clinical hypomagnesaemia
possibly a cause of reduced fertility and milk production in dairy cattle
what are predisposing factors for grass staggers?
in spring:
rapid grass growth = Mg uptake by plant
grass diarrhoea = faster passage of digesta through the gut decreases Mg uptake
bad weather = grass intake reduced as cows shelter
fertilisers:
nitrogen fertilisers - increase rumen NH3 which depresses Mg uptake
potassium fertilisers - increase Mg excretion
liming - decrease grass Mg concentration
in autumn:
gradual decrease in grass Mg
year round:
stresses which decrease food intake (e.g. bad weather/dog worry)
how is hypomagnesaemia controlled or prevented?
provide shelter
introduce to spring grass slowly (prevents diarrhoea)
use fertilisers with care and avoid potassium fertiliser in spring
provide mineral (Mg) licks
top dress pastures (calcinated magnesite)
increase clover in swards
supplement diet or water with Mg
Mg rumen boluses
avoid stress
what are the major/macro minerals?
calcium
phosphorus
magnesium
sodium
potassium
chloride
sulphur
generally deficiency is uncommon or rare
what are the trace/micro elements?
copper
molybdenum
iron
zinc
selenium
iodine
manganese
cobalt
what are the functions of copper?
important in formation of some plasma proteins (e.g. ceruloplasmin)
component of other blood proteins and plays a role in oxygen metabolism
vital role in many enzyme systems e.g. component of cytochrome oxidase in oxidative phosphorylation
essential for normal hair, wool, and feather pigmentation and crimp in wool
essential for immune function
how well is copper absorbed?
CuSO4 is the most readily absorbed copper salt
metallic copper is poorly absorbed
how is copper transported and used in tissues?
loosely bound to albumen in the plasma
stored and released from the liver to meet body requirements
if too much is stored, the liver explodes
what are signs of copper deficiency?
in all species:
anaemia (impaired RBC formation)
abnormal bone growth
abnormal hair, feather, and wool growth
loss of hair pigmentation
cardiovascular disease
in practice:
most common in sheep and cattle
what are signs of copper deficiency in sheep?
swayback:
affects lambs born to Cu2+ deficient ewes
failure or degeneration of normal neural development in the lamb
congenital (from birth)
stillborn, weak - ataxia, paresis, unable to stand, death
irreversible
delayed onset (few weeks old)
normal at birth
depressed growth rate, rapid onset hind limb weakness, ataxia then paresis and death
can be prevented/reduced in Cu deficient lambs by parenteral injection of small doses of Cu complexes
how does copper deficiency in cattle present?
common 3-9 months of age
especially in suckler calves where the dam may not be Cu deficient
failure to thrive
poor growth
stiff gait/lameness
loss of hair pigment
what is copper thiomolybdate?
rumen microbes form sulphides which combine with Mo to thiomolybdate
thiomolybdate binds to copper to form copper thiomolybdate
it decreases Cu absorption and causes signs of Cu deficiency despite adequate dietary Cu provision
how does tolerance to copper toxicity vary by species?
pigs > horses > cattle > sheep
what does copper accumulation in the liver cause?
cell necrosis
what are signs of copper toxicity?
jaundice
appetite loss
hepatic come and death
what is important about copper toxicity in sheep?
tolerance varies between breeds e.g. north ronaldsay sheep are less tolerant to copper toxicity than the scottish blackface breed (would only show copper deficiency)