Hypomagnesaemia (Grass Staggers)
The NADIS data shows that in previous years the number of cases of
hypomagnesaemia (grass staggers, grass tetany) increases each spring
after turn out reaching a peak incidence in May, with another peak in
October.





What is Hypomagnesaemia?
Hypomagnesaemia occurs when the intake of magnesium is exceeded by its
output. The clinical signs can occur very quickly because the cow
does not store magnesium, and is thus reliant on its daily dietary
intake. Hypomagnesaemia is most commonly a disease of lactating cows
at grass, because grass can be very low in magnesium and the output in
milk is high. When the losses in the milk exceed the dietary intake,
clinical hypomagnesaemia occurs. Like most nutritional diseases, the
animals showing clinical signs are just the tip of the iceberg, for
every cow with obvious disease many more will be affected sub
clinically.

The increase in disease in spring occurs because rapidly growing
grasses, particularly ryegrasses, are very low in magnesium. This low
concentration of magnesium can be further reduced by the application
of fertiliser, partly because of the increase in growth rate, but also
because application of potassium directly inhibits uptake of magnesium
by the grass. Slower growing forages, particularly clovers and other
broad-leaved plants contain much higher levels of magnesium.

The significant increase in late autumn, may be partly due to the
increase in forage growth that occurs at this time, particularly after
a dry summer, and also to the feeding silage produced from spring
grass that was low in magnesium.



Clinical Signs

The signs of hypomagnesaemia are vary variable ranging from mild
apprehension and tremor to sudden death. Hypomagnesaemia is probably
the major cause of sudden death in lactating cows at grass The signs
of hypomagesaemia are probably best visualised by detailing the
changes in an untreated animal with mild hypomagnesaemia.

I) The animal appears apprehensive with the head held high and a mild
tremor.

2) The gait stiffens, and the animal begins to stagger and frequently
falls over

3) The animal becomes recumbent (lies on its side unable to get up),
with marked convulsions Other signs, which may be seen at any of these
stages, include watery diarrhoea, skin that is cold to the touch and a
low body temperature

4) Death

Often there are signs of struggling evident on the ground around the
cow



For every cow obviously affected with hypomagnesaemia, there are many
more with marginal magnesium levels. Some of these animals mild show
very subtle behavioural changes but the most common effect is a small
reduction in milk yield.



Diagnosis


? Clinical signs



? Blood magnesium

Individual cows

For most animals treatment will have to begin before a diagnosis is
confirmed as there are no rapid cow-side tests available, but
individual measurements can be useful retrospectively in animals where
treatment has been unsuccessful

Herd
As hypomagnesaemia is primarily a herd disease, in most cases it is
important to assess the extent and severity of the hypomagnesaemia in
the rest of the herd, This is best done by testing six cows at the
same stage of lactation as those clinically affected. Care must be
taken when handling such animals as stress could initiate clinical
hypomagnesaemia.



?Aqueous humour magnesium concentration.

Samples can be taken by a veterinarian in animals suspected to have
died of hypomagnesaemia, however results must be interpreted with
caution

Treatment
I) All animals that are suspected of having hypomagnesaemia
should be immediately treated with 400ml of 25% magnesium sulphate
given subcutaneously. A 25% solution of magnesium should never be
given intravenously as it can cause a heart attack. No further action
is necessary for mild cases that respond to treatment, but if mild
cases do not respond to treatment or if the animal is recumbent a
veterinarian should be called.

2) Veterinary treatment usually involves further infusion of
magnesium, often intravenously diluted a calcium solution. For
severely affected animals a sedative may be given. As both of these
treatments are unlicensed they should only be given by a veterinarian.

Following treatment it is important to prevent stimulation for 10-15
minutes to prevent further convulsions. For recumbent animals they
should be put on their breastbone and left to get up.

Oral administration of magnesium bullets is recommended to prevent
relapses as is moving affected groups to fields with slower-growing
pastures.



Prognosis

Animals treated at an early stage have a very good prognosis. For
recumbent animals, the prognosis is very poor if they do not rise
within two hours of treatment and casualty slaughter should be
considered.

Prevention


I) Feeding magnesium in the concentrates to the cows.



2) Giving magnesium bullets at turn out to cover the period when the
animals are most at risk. For some farms, several bullets per cow are
needed to prevent hypomagnesaemia.



3) Buffer feed silage with magnesium added



4) Supplement the water supply (this is only effective if the cows
have no access to natural water supplies, and may depress water
intake)



5) Avoid potassium fertilisers if possible.



6) Adjust grazing sward to a clover/grass mixture



Richard Laven BVetMed MRCVS



"As I was walkin' - I saw a sign there
And that sign said - no tress passin'
But on the other side .... it didn't say nothin!
Now that side was made for you and me!"
Woody Guthrie

A prophet is only despised in his own country....
..........among his own relations...
............and in his own house