Our results suggest that concentrations of glucose, BOHB and cortisol in plasma may provide a precocious diagnosis of subclinical OPT, using values of 1.59 (SD 0.24) mmol/L, 2.26 (SD 1.03) mmol/L and 15.09 (SD 7.75) nmol/L, respectively. The identification of a potentially harmful metabolic imbalance could lead to the improvement of treatment success.

The histological changes of the liver in ewes with pregnancy toxemia were characterized. Ten ewes were fed on grass ad libitum, and another ten were starved from day 130 of pregnancy for up to four days. Liver puncture biopsies were performed at days 70, 100, 130, and 140 of pregnancy, and at day 45 in postpartum. Seric hydroxybutyrate (HB), non-esterified fatty acids (NEFA), aspartate aminotransferase, and alkaline phosphatase were dosed. Histological preparations revealed similar incidence and intensity of mild liver steatosis in both groups at day 130. Starved ewes become toxemic (as indicated by HB), and at day 140 exhibited more severe injury in a higher proportion (9/9 vs. 4/10; P<0.01). Almost all of them (7/9) had large amounts of small lipid droplets in almost every hepatocyte over the whole liver acinus, and higher NEFA values. At day 45 in postpartum, both groups had mild steatotic changes as initially. A positive correlation between severity of liver damage seric and only aspartate aminotransferase was observed at day 140 in starved animals (P<0.05). This enzyme could be used to assess liver damage, but not alkaline phosphatase. All samples with degeneration corresponded to the microvesicular type. A short starvation period during late pregnancy in ewes produced reversible liver degeneration. (9/9 vs. 4/10; P<0,01)

BackgroundOvine pregnancy toxaemia is a common metabolic disorder of ewes due to increased foetal energy requirements in late pregnancy. This pathology is a metabolic condition characterized by hypoglycaemia and hyperketonaemia resulting in the inability of the animal to maintain an adequate energy balance. The response to treatment is effective, if it is started in the early stages of the disease, when irreversible neurological injuries have not yet been established. The aim was to evaluate three therapeutic alternatives to effectively reverse the disease process in its early stages.For this, thirty adult Corriedale ewes, pregnant with a single lamb, were randomly separated in three groups of ten animals each, at day 130 of gestation. From that day onwards, ewes were locked up for forage fasting until glycaemia reached clinical values defining sub-clinical pregnancy toxaemia (1.59 ± 0.24 mmol/L). After fasting, ewes grazed and received a treatment for 4 days: 50 ml i.v. infusions of hypertonic glucose and 20 UI insulin/ewe/day s.c. or 100 ml/sheep/12 h of glycerol together with propylene glycol oral solution or fed with pasture supplemented with two daily intakes 300 g/sheep of cracked corn. Glycaemia and ß-hydroxybutyrate were determined in all the animals from the beginning of fasting until the completion of the treatment.ResultsFasting caused a decline in blood glucose in the 3 groups. This decline continued until fasting was withdrawn and treatment began. Thereafter blood glucose increased in all three groups, although in the group supplemented with glycerol and propylene glycol it started to increase significantly after 12 h. The values of ß-hydroxybutyrate decreased in the 3 groups at the start of treatment, and this decline was more pronounced earlier on and in the group supplemented with glycerol and propylene glycol. We found no significant differences between all experimental groups. No animal showed clinical signs of pregnancy toxaemia throughout the research.ConclusionsThe three treatments administered to sheep affected by sub-clinical pregnancy toxaemia were able to restore normal concentration of glucose and ß-hydroxybutyrate in blood, although per os administration of 100 ml/sheep/12 h of glycerol with propylene glycol, was the most successful treatment, normalizing the aforementioned biochemical parameters in a shorter time.

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