Introduction

Sow longevity is a key component of an efficient and profitable pig farming enterprise. However, the sow culling rate is steadily increasing at a rate of between 0.7 per cent and 1.0 per cent per annum and currently stands at 50 per cent, indicating that the longevity of Irish sows is declining. Efforts to improve sow longevity should be aimed at the replacement animals which are undervalued on many units. They need to be managed, housed and fed appropriately during the developmental phase to ensure that they are at a high level of health and are both physiologically and behaviourally mature on entry to the breeding herd.

This will become even more important once the national herd switches to group housing next year as this will place greater stress on the young replacement animal.

In individual housed systems, lameness is one of the main reasons for the loss of young sows from the herd. However, preliminary findings from an ongoing Teagasc survey of lameness in pigs indicate that the problem is greater in group systems. Lameness reduces the productivity of a unit by; increasing the involuntary culling rate of sows, the higher cost incurred in replacing sows and reducing the number of pigs produced per sow per year. However, there are also indirect costs associated with the negative effects of lameness on sow reproductive performance. This is mediated both by poor lactation feed intake of lame sows but also by the physiological changes associated with infection and inflammation. It can result in energy for growth and litter development being diverted to the energy requirements of the immune response and interference with reproduction hormones. Lame sows produce fewer litters per lifetime and also have higher piglet mortality rate when compared with non-lame sows.

Lameness

Lameness presents as an abnormal gait as a result of physical injury or infection in the limbs or back. The main causes of lameness include: osteochrondrosis, infectious arthritis, arthrosis, trauma and lesions to the limb and claw. In group systems claw lesions are a major cause of lameness. Almost all lame sows on farms and 90 per cent of culled sows have claw lesions. A survey on UK units observed abnormal gait in 45 per cent of pregnant sows housed on partially slatted flooring. Similarly in Ireland early indications are that almost 50 per cent of pregnant sows are either in the early or recovery stages of lameness or are clinically lame.

Claw health

Trace minerals such as zinc, manganese and copper are crucial to hoof health. Zinc is important as it has an essential role in cellular repair and replacement and therefore the rate of wound healing is increased. Copper is essential in the development of antibodies and the replication of lymphocytes, while manganese is vital for the formation and maintenance of cartilage and bone. Copper deficiency is associated with joint stiffness and enlargement, and weak or short bones.

The dietary supplement Availa Sow® (Zinpro) contains trace amounts of organic zinc, copper and manganese in a structure that makes the minerals more bioavailable than other forms, thus easier to absorb and utilise. The inclusion of this in the diet of breeding sows reduced heel erosion, heel overgrowth and white line lesions in sows and in one study reduced the removal rate of young sows from the herd (up to parity 3) by 20 per cent.

Osteochondrosis

Osteochondrosis is a non-infectious disease of the joint surface; it results in deterioration of cartilage quality and underlying bone. It causes increased pressure on the surface of an affected joint in developing animals. It is most common and severe in the elbow joint of pigs. The main risk factors for osteochondrosis are genetics, high growth rate and joint stress. It is the primary contributor to leg weakness in pigs, increases lameness and reduces longevity.

Nutrition

Another factor contributing to lameness in young gilts is inappropriate nutrition during the developmental phase. Many producers feed their replacement gilts one of two feeding regimes; a finisher diet to service or a gestation sow diet from 100kg until service. Such regimes may not be optimum for the developing gilt; finisher diets are formulated for fast growth rates and high lean meat deposition and a gestating sow diet is formulated for a sow that has finished growing.

In contrast, diets specifically formulated for the developing gilt take into account the nutritional requirement for bone development and fat deposition. High growth rates are linked with several pig welfare issues including osteochondrosis, leg weakness, postural defects, cardiovascular issues, increased skeletal injuries, modification of the release of various hormones and behavioural modifications. Replacement gilts require higher levels of calcium and phosphorus for bone mineralisation to prevent bone weaknesses and as a back-up source of calcium and phosphorus for the litter requirement if needed during gestation and lactation.

Increased calcium and phosphorus in developing females improves longevity and reproductive performance. It is important to implement a gilt feeding strategy early (at 60- 70kg) before bone formation is complete and to facilitate gradual weight gain.

The objectives of this study were to investigate the effects of feeding a finisher diet, a gestating sow diet and a gilt developer diet (including Availa Sow) on lameness indicators in replacement gilts.

Methods

Thirty six Large White × Landrace gilts were selected from finisher stock at Moorepark at approximately 55kg and transferred to individual pens where they were provided with ad-libitum access to a first-stage finisher diet until around 65kg. Gilts were then switched to one of following dietary treatments; finisher, gestating sow and developer (Table 1). The experiment lasted 12 weeks and the gilts were slaughtered at about 140kg, which was the target weight that corresponded to service.

Feeding

Gilts on the finisher dietary treatment were ad-libitum fed throughout (Table 1). Their diet was formulated as a second-stage finisher diet (Table 2). Gilts on the gestating sow and developer dietary treatments were switched from limited to ad-libitum feeding of their appropriate experimental diet between 130 and 140kg or for 2 weeks before service to replicate flushing.

Measurements

Feed intake was measured daily. Locomotory ability was scored weekly on a scale of 0 (normal) to 5 (most abnormal/indicative of lameness) according to severity. The gilts were weighed at day 0 (start of the experiment around 65kg), week 4 (around 100kg), week 10 (prior to flushing/around 130kg) and week 12 (prior to slaughter/around 140kg). Eight types of lesions on the hind claws and soles of feet were scored from 0 to 3 according to severity at day 0, week 6 and week 12 by raising the pig 0.75m off the ground using a pig chute to allow for inspection of claw and sole lesions.

The front right leg of each pig was removed after slaughter and dual-energy xray absorptiometry (DXA) analysis was used to measure bone mineral density (BMD; g/cm²). Surface lesions (SL) on the cartilage of the elbow joints were scored from 1 (normal) to 5 (severe) on the humeral condyle and 1 (present) or 2 (absent) on the anconeal process (Fig.1). Severe corresponded to osteochondrosis dessicalciumns [OCD].

Figure 1. Diagram of the pig elbow joint

Results

Lameness

None of the gilts on the developer treatment were scored as lame (i.e. none received scores >1) at any stage during the experiment (Table 3). From the fifth week of the trial, there were significantly more lame gilts on the finisher and gestating sow dietary treatments than on the developer treatment.

Claw lesions

Claw lesions were present in 100 per cent (n=12) of gilts on the finisher treatment by week 12 (Table 4). The lowest percentage of gilts with claw lesions was in the developer treatment (81.8 per cent). All gilts on the finisher and gestating sow treatments had uneven claws by week 12. In the developer treatment, the proportion of gilts with uneven claws reduced as the trial progressed (Table 4).

Joint lesions

Gilts in the developer treatment had lower surface lesion scores on the elbow joint than gilts in the gestating sow and finisher treatments (Table 5). Gilts on the Finisher treatment had the highest incidence of OCD (score 5).

Bone mineral density

Bone mineral density levels did not significantly differ between the 3 treatments. However gilts on the developer treatment had numerically higher bone mineral density (1.04g per square cm) than gilts on the finisher (1.01g per square cm) and gestating sow treatments (0.99g per square cm).

Body weight

At weeks 4, 10 and 12 (trial end/slaughter) gilts on the developer treatment weighed less than gilts on the finisher and gestating sow treatments (Figure 2).

Figure 2. Average body weight of gilts on three treatments at day 0, week 4, week 1 and week 12

Conclusions

Limit feeding a diet specifically formulated for developing gilts from 65kg reduced lameness, claw abnormalities and joint surface lesions of the cartilage in the elbow joint compared to the two most commonly practised feeding regimes for replacement gilts on Irish farms. Such improvements would be expected to translate into improved welfare, longevity and productivity of the breeding herd. The results from an experiment carried out in Moorepark on the effect of ad-lib feeding a developer, finisher and gestating sow diet on group-housed gilts may provide further information on the effects on limb health in a more on farm representative setting.

Further Reading You can view other papers presented at the conference by clicking here.