No abstract

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.

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.

SUMMARY: In a controlled experiment, term lambs born of caesarean sacrifice, normal or artificially prolonged birth were examined at autopsy to determine the role of vaginal birth in the pathogenesis of presumed birth injury to the fetal CNS characterised by subdural and extradural haemorrhage, subarachnoid haemorrhage and congestion, and blood‐stained cerebrospinal fluid in and around the cranial and spinal meninges of lambs dying during or within 7 days of birth. Additional material, comprising near‐term fetuses, was examined at an abattoir to determine the prevalence of meningeal lesions in unborn fetuses. Mean durations of parturition in the caesarean‐born controls, natural and artifically‐delayed vaginal deliveries were 0 min., 56 min., and 185 min. respectively. The experimental treatments influenced the frequency of cranial lesions only. Single lambs were more prone to injury than twin lambs. The incidence of affected lambs in delayed births was 8.9 times higher than that in caesarean births and 1.7 times higher than that in normal births. Within the delayed group the incidence of affected single lambs in the subgroups was similar despite wide differences in the nature of parturition. It was concluded that the induced lesions resembled those associated with the perinatal mortality of livestock and infants and that pathogenetic variables included interactions between the duration and the vigour of the birth process. Repeated stretching and relaxation of the rostral fetal cranio‐vertebral skeleton during Stage 2 labour may be involved in pathogenesis. At that stage of delivery, the fetus is relatively fixed because the chest and shoulders have firmly engaged the pelvic inlet, while the head and neck are exposed to the lower pressure of the vagina and atmosphere. Intrafetal pressure is hydrostatically continuous with intrauterine pressure which is higher than atmospheric pressure. Rises in intrauterine pressure due to labour are probably transmitted hydraululically to the fetal cranio‐vertebral canal leading to stretching of the head and neck. Because the fetal CNS is firmly anchored to the cranio‐vertebral skeleton such movement may set up the shearing action necessary to rupture small vessels in the cranial and cervical meninges.