Age affected: Piglets pre-weaning.
Causes: Infections; mismanagement.
Effects: >10% mortality of pigs born alive.
Pre-weaning mortality occurs in all herds and is caused by congenital factors resulting in weak piglets, environmental factors, disease in the sow or piglet and failure to manage these factors correctly. Congenital factors include weakness and poor viability resulting from incomplete lung expansion, congenital malformations, severe splay leg, congenital tremor, congenital infection with Leptospira or PRRS, navel bleeding, low birth weight and high numbers born.
All can lead to failure of the piglet to reach a teat to suck colostrum or milk and to compete with the remainder of the litter for food. The piglet then dies of hypoglycaemia or is crushed. Environmental factors include poor creep heating and poor arrangement of heaters so that piglets become chilled, bedding which traps piglets and allows crushing, lack of piglet drinkers and flooring which predisposes to foot lesions and arthritis.
Disease in the sow consists of systemic disease, death, agalactia or mastitis and acts largely through loss of milk, but may affect temperament and result in savaging. Disease in the piglet includes neonatal septicaemia, neonatal diarrhoea, septicaemia, arthritis and meningitis caused by Streptococcus suis or Haemophilus parasuis, greasy pig disease, coccidiosis and diseases such as TGE with high mortality in this age group.
Mode of transmission
Only the infectious conditions contributing to the overall problem are transmissible, and the mode of transmission is specific to each condition present. Management and congenital causes of pre-weaning mortality will recur in successive batches of animals reared under the same conditions.
Dead pigs are present in farrowing and nursing accommodation. To be considered part of pre-weaning mortality as opposed to born dead or intrapartum deaths, they must have cleared the foetal membranes and to have walked. Piglets may be seen in life with one of the contributory conditions such as splay leg, congenital tremor, neonatal septicaemia or diarrhoea, and can be identified as ill by their bodily condition, inability to leave the creep, presence of diarrhoea, lameness or by the presence of special features as in greasy pig disease. The sow may be dead, may have systemic illness, mastitis or agalactia, all of which can be established by examination.
Pre-weaning mortality occurs on every farm, so it is important to consider whether the level present is abnormal. Pre-weaning mortality rates of 4% or less are possible, but the target is 8% and interference levels are 10-12%. It is important to establish the extent of the mortality by accurate recording of numbers born alive and numbers weaned. Where mortality rates justify interference, a clinical inspection of the affected unit should be carried out and the causes of illness identified where possible. Clinical inspection should include inspection of piglets and the sows at all stages of production, an assessment of the environmental factors which might be involved such as creep lighting and temperature. An assessment should be made of whether the management practices in place contribute to pre-weaning mortality for example when iron injection is given too early in PRRS-infected piglets.
Post-mortem examination of the dead piglets is required to establish accurately and objectively the stage at which piglets die and the causes of death. This is particularly important in the perinatal period, when failure of piglets to suck in cool conditions results in death from hypoglycaemia, and failure to take colostrum predisposes to disease for much of the pre-weaning period.
Enteritis, pneumonia, arthritis and septicaemia can also be recorded. It reveals the contribution made by euthanasia to the mortalities, as crushed skulls are frequently found in animals which have been destroyed for undersize, arthritis or other chronic conditions.
Treatment and prevention
Diseased piglets may be treated as with E. coli neonatal diarrhoea or the litter at risk treated as in clostridial diarrhoea and streptococcal infection. Disease in the sow can be treated and agalactia and mastitis managed by treating the sow and supporting the litter by supplementary feeding with milk substitute or creep feed according to age or by fostering. Management practices such as early induction of farrowing to prevent the birth of weak piglets, attending farrowings to ensure that all piglets clear membranes and suck colostrum and rescheduling interferences like iron injection during PRRS outbreaks, can be corrected rapidly.
Environmental factors such as chilling should be capable of rapid correction by placing creep lights correctly and boxing creeps. Prevention on a longer term may be required. Reduction of death from coccidiosis may require longer term hygiene and management. Protection of the piglet from disease requiring maternal vaccination such as E. coli and clostridial diarrhoeas on a more permanent basis may take 2 to 4 weeks. Prevention from crushing may require new or modified crates or the installation of blowaway units.
Other building alterations, such as permanent piglet water supplies or improvements to floor quality, may take longer to correct. The success of these control measures can be determined within weeks by improvements in the mortality rates in the pre-weaning period.
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