Age affected: Newborn.
Causes: Mismanagement of breeding; malnutrition; genetic; mycotoxins; viruses.
Effects: Average total born <10 for gilts, <11 for sows (these figures may be underestimates for hyperprolific sows).
Genetic, nutritional, management and infectious factors may all reduce the number of eggs shed, the number fertilised and the number implanting and surviving to term. Pure bred animals of certain breeds may have smaller litters. Nutrition is of major importance, especially energy. Anything less than condition score 3/4 or 6/10 (fat depth 16-20 mm at P2) may reduce the number of eggs produced.
Deficiency of vitamins A and E and of biotin may all reduce fertility and litter size. The oestrogenic mycotoxin zearalenone may also reduce both fertility and numbers born. Management factors are also important. Gilts produce fewer eggs at first oestrus than subsequently and fewer eggs than sows, so their litters are smaller. Adequate light levels, temperature, boar stimulation and management of the condition of the sow or gilt all contribute to the number of eggs shed. The timing of service may affect the numbers of embryos as may the ability of the boar to complete service and the quality of the semen produced.
Timing and semen quality is also critical for artificial insemination. Disease such as parvovirus, PRRS, leptospirosis, Japanese B encephalitis and Aujeszky’s disease may all reduce number of embryos and foetuses and cause small litters. Infection can affect numbers born by lowering body condition so fewer eggs are released or by destroying the products of conception at an early stage so that resorption occurs. The minimum number of foetuses required to maintain a pregnancy is 4, so lower numbers suggest foetal death after implantation.
Mode of transmission
Small litters caused by nutritional factors, mycotoxins, semen quality and management factors are not transmissible, but the problem may recur when successive batches of sows are subjected to the same conditions. Breed factors are hereditary. Infections are transmissible by the means specific for that disease, but affect numbers born after oronasal infection or by direct venereal infection.
Small litters are produced ranging in size from 4 (exceptionally 1 or 2) to 11.0 or more (depending on the target for the breed). They may all be viable or stillborn piglets and mummies may be present. In some cases there may be evidence of bacterial infection such as prolonged post-farrowing vulval discharge or of other diseases.
Recording numbers born allows the identification of a herd problem and records of age and service management allow investigation of the causes. Where mummies have been recorded, infection is likely and examination of mummies and stillborn piglets for the agent or antibody and the sow herd for serum antibody can confirm its identity. The absence of common infections from the sow herd should be confirmed where infection is suspected. Investigation of non-infectious causes should involve analysis of the breeding records to identify patterns. Small litters occurring in gilts suggest defects in gilt management or infection such as parvovirus, small litters in second litter sows suggest inadequate nutrition in pregnancy and lactation or weaning prior to 28 days and association with a particular boar may suggest poor mating technique or semen quality.
Timing of insemination in relation to ovulation should be investigated by observation of service management where small litters are not restricted to one boar and in artificially inseminated herds. The reproductive tracts of culled sows or gilts can confirm the number of eggs liberated and the presence of infection in the tract.
Post-mortem examinations are rarely performed to investigate this problem specifically. Only where ultrasound has confirmed the presence of a small litter in a problem herd will animals be slaughtered and investigations carried out. Information can, however, be gained from culled sows which have had small litters. If slaughtering is carried out before the first post-farrowing oestrus, the number of eggs released can be estimated from the number of corpora lutea present. Small numbers of corpora lutea suggest an egg number problem, many suggest that intrauterine embryonic death may have occurred. There may be evidence for persisting intrauterine infection.
Treatment and prevention
Where genetics are responsible for small litters, change to a more fertile sow line should be considered. Qualitative deficiencies in the ration (vitamin deficiencies, presence of mycotoxins) should be corrected. Sow condition should be restored to optimum by feeding high density rations during lactation, between weaning and farrowing and for 2-4 weeks afterwards where condition is still poor.
Worm burdens, disease and low environmental temperatures should be eliminated as causes of poor sow condition. Reproductive disease should be controlled by vaccination (parvovirus, PRSS, leptospirosis, Japanese B encephalitis and Aujeszky’s disease where relevant/possible) or treatment (leptospirosis, non-specific infections). Management changes should ensure that gilts are not served until the second obvious oestrus, that old sows should be culled after the seventh litter, that boars aged less than 9 months or aged boars should not be used and that service is supervised to ensure complete mating.
Matings should take place in the middle of standing oestrus (20 hours from its onset) and be repeated after 24 hours. Individual boars identified as the cause of small litters, those which cannot mate satisfactorily and those with poor semen quality should be culled immediately. Sows which produce small litters should also be culled. Quality in semen used for AI should also be checked and the techniques and timing used at insemination reviewed.