5 Sept 2016
Roger Blowey explains that changes occurring in heifers lead to increased lameness in cows later – and runs through practical prevention advice to offer farmers.
Roger Blowey
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Figure 1. Sole ulcers may lead to bony changes in the foot, as seen on the flexor tuberosity of the pedal bone on the right, thus predisposing to further lameness (Blowey, 2012).
The view “lameness is a problem of cows that starts in heifers” was first introduced by Bicalho et al (2009). An understanding of this important concept is vital if we are to fully appreciate the basics of lameness prevention.
Bicalho was referring to hoof lesions only, but other studies have since shown the principle also applies to digital dermatitis (DD) and other infectious causes.
In his paper, Bicalho compared the prevalence of sole ulcers and white disease in heifers with that in cows (Table 1), and showed although the prevalence of sole ulcers and white line lesions was not particularly high in first lactation heifers, it was the changes occurring in these heifers that led to increased lameness later in life.
We need to fully understand this concept ourselves and then use the information to explain the reasons for the various practical control measures to our clients. It is not the purpose of this article to discuss causation in detail, and those requiring further information should refer to other texts – for example, Blowey (2015) – although, of course, a detailed understanding of lesion development is essential when giving advice on prevention, and to persuade clients to implement early control. Preventive measures will vary with the type of lameness, although some measures – for example, reduced exposure to slurry – will be common to both.
Hoof lesions develop as a result of damage to the corium, the damage often being the result of trauma. This then leads to the production of defective horn, which, when it reaches the bearing surface of the foot, may allow infection to track back up through the damaged horn to reach the corium. Once the corium has been damaged it never fully heals, with some keratogenic cells being replaced by fibrous tissue, thus rendering the animal more susceptible to further lesions. Continual trauma can lead to bone overgrowth, as in the case of sole ulcers (Figure 1), thus, prevention is essential.
Longer-term changes to the corium – for example, a sole ulcer or white line lesion that becomes secondarily infected with digital dermatitis – may lead to further bony changes of the type seen in Figure 2. The corium will now be disrupted by both the treponeme infection in its substance and pressure from the bony exostoses above. An important link, therefore, exists between infectious and hoof lesions.
Previous articles have discussed the importance of a well-developed digital cushion in the prevention of lameness.
Increasing evidence shows the hypothesis of nutritional acidosis causing laminitis, and subsequent lameness, is no longer correct – or, if there is an association, it is that acidosis causes weight loss. The original theory was overfeeding of concentrates led to rumen acidosis and this, in turn, produced Inflammation and degradation of laminar suspension, sinking of the pedal bone and finally disruption of the corium. However, this has been difficult to induce experimentally and other studies show no adverse effect of severe overfeeding.
The effect of changes in body condition score (BCS) on lameness have been well summarised by Huxley (2015):
Gard et al (2015) have shown exercise on a hard surface increases the size of the digital cushion when compared to control animals left on grazing alone.
Calving is a critical period
It is well established the changes that occur around calving predispose to an increase in lameness, and that in the control of lameness, precalving feeding and management are vital. These changes are shown in Table 2 and include:
These changes apply especially to first lactation heifers where the digital cushion is much less well developed.
Recent studies have shown the sooner a lame cow is identified and treated, the higher is the probable recovery rate for that cow. This requires careful observation by farm staff, ideally by regular mobility scoring, accompanied by easily used equipment and well-trained staff.
Cows with chronic long-term lameness develop such extensive bony exostoses in the foot (Figure 2) they have no hope of a full recovery. Treatment must also be thorough; this involves modelling the foot to reduce weight-bearing at the sole ulcer site, frequent use of blocks to reduce weight-bearing on the affected claw, and NSAIDs to reduce the extent of the bony exostoses on P3.
It is well accepted weight-bearing should be on the wall, as the horn of the wall has a higher horn tubule density and is, as a result, stronger. Thus, I prefer the use of blocks (for example, cowslips) that transfer weight on to the wall.
The presence of DD in precalving cows and heifers has been shown to be a significant risk factor for lameness caused by DD post-calving (Laven and Logue, 2007). Similar results were reported by Gomez et al (2015), who found heifers with DD lesions precalving were four to five times more likely to go lame with DD post-calving.
Although attempts to find DD treponemes in slurry have not been successful, preliminary studies have shown DD can be identified in fresh footprints from infected cows, with a higher detection rate from rubber than concrete floors. Internal biosecurity measures, such as using different slurry and handling systems for youngstock, may, consequently, be beneficial.
Oliveira et al (2015) showed the importance of overall biosecurity in the control of DD. Attention to DD control in both youngstock and in pre-calving cows and heifers is, therefore, essential.
Unless both vet and farmer understand the reasons for adopting control measures, it is improbable they will be implemented correctly. Large herds in well-designed modern buildings, and managed by trained staff, have lower lameness levels (Chapinal et al, 2014).
My utopian regime to minimise lameness is given in the list on page 12. Many of the points refer especially to heifers; they are equally applicable to cows, but it is only by starting the implementation in heifers – thereby preventing the development of pedal bone changes and reducing the risk of chronic DD infections deep within the dermis – that the programme will be effective overall.
After calving, when there is increased laxity of the pedal bone, maximise lying comfort, preferably by using deep-bedded sand cubicles. Increasing evidence shows changing from mats and mattresses to sand cubicles will result in significant yield increases over the following 12 months. Putting heifers into a separate heifer group may further decrease standing times.
