Physical Injury

Many of the cattle ailments we have to deal with are the result of physical trauma. The best example is lameness. Hoof and limb disorders are frequently associated with either trauma to the foot, for example, prolonged standing on a hard surface producing sole ulcers, or damage to the leg, for example resulting in dislocation of the joint or even fracture of a bone.

Examples of other physical injuries include:

• teat damage

• haematomas (blood blisters under the skin)

• skin cuts

• foreign bodies, e.g. barley awn or grass seed in the eye

• burns, either caused by fire or sunburn

• chemical injury, e.g. tank cleaner mistakenly used for teat dip

• abscesses (following penetration of the skin by thorns, nails, fragments of metal etc.)

Congenital Disorders

Congenital diseases are abnormalities which are present at birth. They may be caused by genetic factors or by ingestion of teratogens during pregnancy.

Genetic defects

The incidence of inherited genetic defects in cattle is said to be quite high (one in 500 births), but as at least half of the calves are stillborn, they do not represent a major problem to the cattle industry. Typical examples include cleft palate (Plate 1.2), harelip (Plate 1.3), spina bifida (Plate 1.4), a very small tail or no tail at all (hypoplastic tail, Plate 1.5), contracted tendons (Plate 1.6), hydrocephalus, brachygnathia (parrot mouth, Plate 1.7) and umbilical hernias. If it is found that a particular bull is throwing a high inci­dence of calves with genetic defects, he should be culled. Sometimes the defect is only seen when a bull mates with a particular cow. In this case the defect is said to be caused by a recessive gene, in that the defect will only appear if both the sire and dam are carrying the gene for that defect.

Plate 1.2.

Plate 1.4. Spina bifida. The tops of two lumbar vertebrae have not closed, leaving a hole into the lumbar spine, seen here as a red area. This calf was partially paralysed in the hind legs.

Plate 1.3. Harelip (also called cleft lip or primary cleft palate). This can also make suckling difficult, although this calf was able to drink from a bucket.

Plate 1.5. No anus and minimal tail (anal atresia and coccygeal hypoplasia). Calves with a totally blind anus rapidly develop abdominal distension, severe pain and colic. This calf was lucky and faeces were passed through the vagina. No tail or a shortened tail is commonly seen on its own without anal atresia.

Plate 1.6. Contracted tendons at the fetlock, as in this calf, are common, particularly in larger calves. They will correct in time without treatment.

Plate 1.7. Brachygnathia (parrot mouth or overshot upper jaw) is most commonly seen in stillborn calves.

Teratogenic defects

Teratogenic defects result from the ingestion of toxic agents during pregnancy. The most publicised example of this must be the effect of thalidomide in man, which resulted in the birth of deformed children. In cattle, ingestion of some species of the plant Lupinus can pro­duce crooked calf disease, where calves are born with malpositioned legs, either excess­ively flexed or excessively extended. Oral dosing of early pregnant cattle with the ring­worm treatment griseofulvin should be avoided, because of the risk of producing deformed, full-term calves.

Viral and other infections can also produce congenital defects. The best examples are BVD virus and Neospora caninum. Infection of mid to late pregnant cows with either agent can result in defects such as cerebellar hypoplasia. In this condition the part of the brain known as the cerebellum is far too small (hypoplasia, Plate 1.9) and the affected calf is unable to stand. The calf in Plate 1.8 is a typi­cal example. At birth it was unable to stand or suckle and when lifted it pushed its head back over its back (opisthotonos). Mid pregnancy infection with Akabane virus or BVD can cause arthrogryphosis (Plate 1.10), a condi­tion in which the hind limbs become fused or deformed.

Not all congenital abnormalities are immediately apparent at birth. Strabismus is a good example. Plate 1.11 shows a Hereford heifer with bilateral convergent strabismus,

Plate 1.8. Cerebellar hypoplasia. Although this calf appeared normal and healthy at rest, as soon as it tried to feed or stand it fell over and its head went into spasm over its back (opisthotonos). BVD and Neospora are possible causes.

Plate 1.9. Cerebellar hypoplasia. The cerebellum (C) is the part of the brain which controls balance.

that is both eyes (bilateral) point inwards (convergent) with a squint (strabismus). This condition gets progressively worse as the calf gets older and in some instances results in almost total blindness. In one unfortunate incident I dealt with, a dairy farmer purchased a freshly calved heifer with strabismus. A few weeks after purchase she had a bad fright and ran off. Because she could not see very well she became totally disoriented and finished up by drowning in the slurry pit. Fortu­nately, relatively few congenital defects have such a dramatic ending!

Other congenital defects causing blindness include cataracts (Plate 1.12) and microphthalmia or anophthalmia (very small or no eyes, Plate 1.13).

See Chapter 4 for other eye disorders.

Plate 1.10. Arthrogryposis. The hind legs are fixed in this extreme flexion position and cannot be moved. Often the pelvis is also involved (when a caesarean birth is necessary). This calf also had spina bifida. Arthrogryposis can be either teratogenic in origin or inherited.

Plate 1.11. Strabismus (squint). Note how the eyeball is protruding and pointing in towards the nose. Both eyes were affected. This is a progressive condition which can eventually lead to blindness.

Plate 1.12. Acataract is an opacity of the lens. The centre of the eye has a blue appearance, as in this calf.

Plate 1.13. Microphthalmia. This calf was born with the eye almost totally missing.

DEFENCES AGAINST DISEASE

Animals (and also man!) are continually exposed to a range of infectious agents and physical factors which could potentially cause disease, but fortunately disease occurs relatively rarely. This is because we all have a range of excellent defence mechanisms which afford a degree of protection against moderate challenge.

• Physical barriers

- skin

- respiratory passages

- digestive tract

- eye mechanisms

- commensal bacteria

• Chemical barriers

- acid in the stomach

- alkaline in the intestine

• Immunity

The body has an excellent ability to recognise materials which are ‘foreign’, that is materials which are not part of itself, and to control them. At the same time it has to recognise those tissues which are part of itself and leave them alone. The mechanism for dealing with ‘foreign invaders’ or ‘non-self’ materials has two components, namely:

- cellular mechanisms: certain cells are able to recognise and engulf infectious and other foreign agents

- humoral mechanisms: a system of ‘active’ proteins, most commonly known as antibodies, assist in the detection and destruction of non-self tissue

In addition, there are two categories of both cellular and humoral defence systems:

- innate systems: these exist in all animals and do not rely on previous exposure to an infection

- induced or acquired systems: these come into play after an animal has been exposed to an infection.

Following exposure, the precise characteristics of the invading organism are remembered and the body produces specific defences against it, using both cells and antibodies. These are then ready to attack the invader if it manages to gain entry into the body for a second time. This is the nature of vaccines. They give the unexposed animal a mild or dead form of the infection. The animal then manufactures huge quantities of specific defence materials (both antibodies and cells) and is able to repel an invasion by that infection. Different vaccines are needed for each disease.