June 23rd 2001

By Dr. John Mee, Teagasc, Moorepark Research Centre

Outbreaks of dwarfism can devastate suckler herds. An increasing number of cases have been reported this year, particularly in the midlands, west and north of the country.

What is it?

This type of deformity is called congenital joint laxity and dwarfism (CJLD). Calves are abnormal at birth (congenital). They have excessive movement of the lower limb joints, particularly the hock, giving rise to sickle hocks (joint laxity) and have disproportionately short legs for the size of their body (dwarfism).

Associated defects may include skull shortening, bowing or rotation of the front legs and sloped pasterns.

The damage is done from mid pregnancy onward and is irreversible after the sixth month. Because of the relatively short bones, the calves often appear double-muscled. This can cause calving problems and difficulty in standing and sucking.

All calves are not affected to the same degree and so the survivors vary in stature.

How common is it?

A survey of Irish veterinary laboratories revealed that they had picked up this condition as early as the 1980s.

In the early years it is likely that many cases went un-reported. There can be considerable year-to-year variation in the incidence.

This may be related to an early start to silage feeding because of bad weather or grazing conditions in the autumn with either out-wintered or housed cows.

The reported incidence of the condition has increased in the past decade both here and worldwide. Signs of CJLD have been seen in Australia, Canada, England, France, North America, Northern Ireland, Scotland, South Africa and Sweden.

The condition is more common in beef herds, but has been reported in dairy heifers fed similar to beef cows. It can also occur in purchased pregnant stock if they are fed the same as the homebred cows.

Three times as many cases may occur in heifers compared to cows. In an individual herd, two out of every three calves born can be affected to varying degrees.

In some years losses can be high both from mortality and the reduced value of the survivors. Dwarfed calves never attain full size.

What causes it?

Suggested causes include: infection with BVD virus, lack of Vit. D, manganese deficiency, iodine deficiency, a genetic defect, mouldy fodder (mycotoxins) and an unidentified grass silage-associated toxin.

This particular defect can be distinguished from similar defects by veterinary clinical and laboratory examination. Attempts to definitively identify the cause have been hampered by lack of research funds to carry out controlled experiments.

Research workers who published the early reports have now moved on to other work and left the cause unanswered.

Silage

While all of these factors can cause abnormal calves, evidence to date points to a silage-associated toxin as the cause of this particular defect.

Silage with a high leaf content has been implicated. Early cases were associated with feeding silage without an additive.

There is an apparent higher incidence in the north of Scotland where cows are on silage for a longer period pre-calving and where affected calves are generally born in late spring.

In Canada the condition has been reproduced by silage feeding alone during pregnancy in a split-herd experiment on a farm that had not experienced the problem before.

Fungal toxin?

As silage feeding alone is commonly practised on Irish suckler farms without the problem, something different must occur in the years that these farms have the problem.

One of these possible differences is the presence of a fungal toxin in the silage. Fusarium is a possible source.

Mycotoxins have been linked to congenital defects of the long bones and spine in both calves and in poultry.

Cases seen worldwide have been associated with feeds prone to spoilage or mould growth such as grass silage, fruit pulp and straw.

In one outbreak, preventing aerobic deterioration by covering the silage pack solved the problem. In another, applying a silage additive appeared effective.

Genetics?

A predisposition in certain continental breeds has been suggested. But cases may occur in all breeds and with different bulls, whether natural service or AI. Changing the bull has not altered the incidence. Inbreeding is not the cause.

Manganese deficiency?

Considerable interest has been generated by the similarity of CJLD and skeletal defects associated with manganese deficiency.

Whereas manganese levels are similar in silage and hay, silage-fed cows have lower blood manganese levels. This suggests a lower bio-availability of manganese in silage compared to hay. This may cause secondary manganese deficiency.

High ash levels in silage due to iron may cause this from soil contamination.

Naturally high soil pH or overliming is associated with reduced manganese absorption as is high calcium, phosphorous and protein levels in the diet.

Blood phosphorus levels are higher in silage-fed compared to hay-fed cattle and also in affected calves compared to normal calves.

In Scotland, low manganese levels were found in bone and liver samples from dwarf calves, but also in unaffected calves.

The authors concluded that manganese deficiency alone was unlikely to cause the problem but it could be a factor. This condition has occurred on farms where trace element supplementation was routinely practised.

No one has yet proven that it can be prevented by manganese supplementation. Clinically, simple manganese deficiency is not recognised as a problem in Irish cattle.

What can you do about it?

1. Define the problem.

Seek veterinary confirmation that this particular defect is involved as there are numerous other similar defects with different causes and, hence, different remedial measures.

2. Accept your losses.

If you have a compact calving pattern you probably will not be able to affect the outcome of the outbreak for this year, irrespective of what precautions you take.

3. Plan for next winter.

(a) Alter the diet of the pregnant cows and heifers during the critical period of the latter half of pregnancy next autumn/winter.

Specifically, attempt to replace up to 20 per cent of the silage dry matter allowance with other fodder (eg. hay, straw), barley or compound ration.

This practise may work by diluting the amount of toxin ingested or by altering the rumen micro-environment sufficiently to prevent absorption/production of a toxin or increase absorption of trace elements.

Increased intake of long-stem fibre may be important in this regard.

(b) Avoid feeding mouldy parts of the silage pit/bag as this may also cause abortions and is associated with increased risk of listeriosis.

(c ) Supplementation with a range of trace elements or with specific trace elements may be advisable for pregnant stock.

This may be particularly important in suckler herds where Teagasc surveys show lower trace element status than in dairy herds.

Adoption of some or all of these guidelines has resulted in a dramatic reduction in the incidence of the condition. But, as the winter diet is usually group-fed, some cows will consume proportionately more silage and so a few cases may continue to occur.