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Methods of investigating perinatal loss in grazing sheep flocks are reviewed and evaluated. The "wet-dry" method is the simplest method for assessing minimal prevalence, whereas the differences between the numbers of single and twin foetuses present at ultrasonic determination of litter size during pregnancy, and the numbers of single and twin lambs present at lamb-marking, is the most precise. The veterinary investigation of field mortality involves full autopsy of a representative sample of dead lambs, a history of prenatal nutrition, disease and husbandry, as well as a qualitative estimate of weather conditions over the period of lamb collection. Pathological processes may be identified in over 95% of deaths and the specific cause determined in about 75% of deaths. The identification of the specific causes in the remainder of deaths, all classified as the starvation-mismothering-exposure (SME) complex, requires intensive, costly, on-site observation, and physiological and biochemical assessment. The probable causes of these deaths include prenatal physiological handicaps resulting from placental insufficiency, aberrant parent-offspring behaviour, management-induced mismothering, misadventure, inadequate milk supply or teat and udder abnormalities, and cold-induced starvation. The gross pathology and pathophysiology of birth stress and the SME complex, which are associated with at least 80% of mortality, are summarised. Birth injury to the foetal central nervous system, characterised by cranial and spinal meningeal haemorrhage is exclusive to parturient deaths and the SME complex. Observed flock prevalences range from 81% to 100% in parturient deaths, and 20% to 57% in the SME complex. The high total prevalence and experimental evidence, indicate the major causal role of birth stress in the pathogenesis of these entities. Lethal congenital malformations, infections (both congenital and acquired after birth), trace element deficiencies and predation are reviewed as minor causes. The new understanding of the pathogenesis of perinatal lamb mortality, recognises the heritable nature of birth mass, maternal pelvic dimensions, parent-offspring behaviour, and the resistance of neonates to cold. Control measures need to incorporate selection for maternal rearing ability, further refinement of prenatal nutritional management of twin-bearing ewes, disease control, provision of shelter for lambing flocks, and avoidance of husbandry practices which frustrate innate parent-offspring behaviour. A selection programme is summarised.

Investigations into ovine pelvic size and its relationship to repetitive rearing failure require accurate estimation of pelvic dimensions in live animals. Radiographic pelvimetry was used to estimate pelvic dimensions of 84 Merino, 21 Dormer and 20 S A Mutton Merino ewes. Transverse diameter and conjugate diameter were estimated; the area of the pelvic inlet was defined as the product of transverse and conjugate diameters. Dissected measurements obtained from all ewes after slaughter were regressed on estimated dimensions to obtain prediction equations for the correction of radiographic estimates. Prediction equations for the estimation of dissected pelvic dimensions from radiographs were accurate (r greater than or equal to 0.87), irrespective of dimension estimated or breed. Derived equations for estimation of dissected pelvic dimensions for the 3 breeds were not statistically different. It was concluded that pelvic dimensions of ewes could accurately be predicted by radiographic pelvimetry.

Lamb mortality to weaning age was compared in Merino flocks selectively bred from maternal ancestors with high or low lifetime rearing ability. The High Efficiency (HE) flock comprised the descendants of ewes that had reared lambs on 3 or all occasions from 4 rearing opportunities. The Low Efficiency (LE) flock comprised descendants of ewes that had failed to rear any progeny on 2, 3 or all occasions from 4 rearing opportunities. During the first 3 years of testing the response to selection the mean mortality to weaning among HE single lambs was 19.5% of lambs born compared with 32.3% in the LE flock (p less than 0.001). Mean mortality of twin lambs in the HE flock was 21.5% compared to 36.3% in the LE flock (p less than 0.01). In the HE flock significantly fewer single lambs died during and within 3h of birth and significantly fewer twins died during birth and shortly thereafter, and between 3h and 2 days of age. The viability of LE singles and twins may have been lower overall as the mortality rate in most periods was higher than that of their HE counterparts. The results highlighted the major impact of intrinsic maternal and, or foetal defects on lamb survival. It was concluded that rearing ability was heritable, and that selection for rearing ability offers excellent prospects for alleviating the hitherto intractable problem of high perinatal lamb mortality.

The changes in plasma cortisol levels in response to intravenous infusions of prostaglandin E2 (PGE2), prostacyclin and 1-24 ACTH have been studied in chronically catheterized fetal sheep during the last third of gestation. All three drugs increased plasma cortisol levels with prostacyclin being sigificantly more potent than either PGE2 or 1-24 ACTH. No interaction between the steroidogenic actions of 1-24 ACTH and either PGE2 or prostacyclin could be demonstrated. The steroidogenic action of PGE2 was not significantly modified by fetal hypophysectomy. It is concluded that neither PGE2 nor prostacyclin is likely to be involved in the enhanced adrenal responsiveness to 1-24 ACTH observed in fetal sheep in the period immediately before birth.

A high frequency of meningeal lesions was found at autopsy in foals dying perinatally. Such lesions are considered an index of injury to the fetal central nervous system, from trauma and/or hypoxia during birth. Their incidence in the sample examined (26 foals) is similar to that observed in the perinatal mortality of lambs and calves.

Thirty Angus, Hereford and Shorthorn term calves dying before, during or within 7 days of birth in a large beef herd were autopsied. Selected specimens were examined histologically. Two carcasses were classified in the category of ante-parturient death, 24 as parturient, and 4 were classified in the post-parturient death category. Three of the latter showed evidence of starvation. Eight of the calves in the parturient death category were assisted during delivery, and 16 were not assisted. The incidence of nulliparous dams among assisted parturient deaths was significantly higher than among the unassisted group. A high incidence of meningeal haemorrhages and congestion were observed at single or multiple sites, within and around the cranial and spinal meninges. The lesions comprised subdural and epidural haemorrhages, bloodstained cerebrospinal fluid and leptomeningeal haemorrhage and congestion. They were seen in calves in both parturient and post-parturient death categories but not in the ante-parturient group. All calves classified in the parturient death category which were assisted during delivery showed haemorrhages involving the cranial and/or spinal meninges. Additional birth injuries, including separation of the costo-chondral junctions, fractured ribs, haemorrhage into the hip joints, inter-vertebral fibrocartilages and axillae, and rupture of the liver, were frequently present. Ten of the calves in the parturient death category which were unassisted during delivery showed meningeal haemorrhage and congestion. Two of the 4 calves in the post-parturient death category showed similar lesions and both showed evidence of starvation. The meningeal haemorrhages and congestion were similar to those observed in perinatal lamb mortality. They are considered manifestations of injury to the CNS arising from trauma and/or hypoxia during birth. Gross or microscopic evidence of infection was present in 2 calves in the post-parturient death category. Calves which had starved showed subcutaneous oedema of the distal limbs, congestion and focal haemorrhage of the adrenal cortex and red-brown fat depots. It is suggested that these changes are evidence of cold injury, and that fat in newborn calves responds to cold and starvation in a manner similar to the brown fat of newborn lambs.