Immunology of infective preterm delivery in the mare

Placentitis is reported to be the cause of 9.8–33.5% of abortions, stillbirths and perinatal losses in horses. Bacterial infections are responsible for 53% of placentitis cases with Streptococcus equi ssp. zooepidemicus being isolated in 28% of these cases. Clinically, mares may have a vaginal discharge, show udder development, lactate prenatally and deliver a premature or dead foal. Major aspects of the pathogenesis of infectious preterm delivery that may require more effective therapeutic targeting are myometrial contraction, immunological aspects of preterm delivery, and the effects of proinflammatory cytokine signalling on activation of the fetal hypothalamic–pituitary–adrenal axis. This article focuses on current knowledge of inflammatory signalling secondary to equine placentitis, and the interplay among inflammation, loss of myometrial quiescence and activation of the fetal hypothalamic–pituitary–adrenal axis.     

Equine placenta – A clinician's perspective. Part 2: Abnormalities

Any insufficiency of the equine placenta has dramatic effects on the developing equine fetus. Placental abnormalities, such as the separation of the chorioallantois from the maternal endometrium or torsion of the umbilical cord, lead to fetal demise, premature labour or abortion. These conditions are each associated with characteristic lesions on the equine placenta, which can be found during a detailed examination. These findings can be very helpful for diagnosing problems and implementing appropriate treatments for mares and affected newborn foals. Furthermore, the retention of the entire placenta or any small fragment thereof can cause metritis, laminitis and sepsis. The prompt diagnosis and aggressive treatment of this condition is necessary to save the mare from becoming seriously ill. Therefore, a thorough evaluation of the equine placenta is a crucial element of the post partum evaluation of every brood mare.     

Influence of litter size and breed on variation in length of gestation in the dog

Summary

The variation in the length of gestation, the period from mating until parturition, was studied in 77 dogs of different breeds; the time for mating was determined by measuring peripheral blood progesterone levels. The mean length of gestation was 62.1 ± 0.2 (S.E.M.) days, with a variation of 11 days. The number of pups appeared to influence the length of gestation. Length of gestation was negatively correlated (r = ‐0.96, P < 0.001, n = 44) with litter size in litters with 7 or fewer pups. The intra‐breed variation in length of gestation in the five breeds represented by five or more bitches was 3 ‐ 6 days. The mean gestation of Alsatians (60.1 ± 0.5, n = 9) was shorter (P < 0.005) than that of the other breeds combined (62.3 ± 0.3, n = 68). The primiparous/multiparous status of the bitch did not influence the length of gestation.     

Spurious hypercreatininemia: 28 neonatal foals (2000–2008)

Objectives – To (1) determine the occurrence of spurious hypercreatininemia in a population of hospitalized foals <2 days old, (2) assess the resolution of the hypercreatininemia, and (3) determine its association with survival in these foals. Design – Retrospective case series. Setting – 2 Referral hospitals. Animals – Foals <2 days old with an admission creatinine >442 μmol/L (>5.0 mg/dL) from 2 referral hospitals. Interventions – None. Measurements and Main Results – The medical records of 33 foals were reviewed. Twenty‐eight had spurious hypercreatininemia and 5 had acute renal failure. Admission creatinine was not significantly different between the 2 groups (mean [standard deviation]). The creatinine was 1,202 μmol/L (663 μmol/L) (13.6 mg/dL [7.5 mg/dL]) versus 1,185 μmol/L (787 μmol/L) (13.4 mg/dL [8.9 mg/d]) (P=0.96) in each group, respectively, though BUN at the time of hospital admission was significantly higher for acute renal failure foals (P=0.009). In the spurious group, serum creatinine at admission decreased to 504 μmol/L (380 μmol/L) (5.7 mg/dL [4.3 mg/dL]) by 24 hours, and to 159 μmol/L (80 μmol/L) (1.8 mg/dL [0.9 mg/dL]) at 48 hours, and to 115 μmol/L (44 μmol/L) (1.3 mg/dL [0.5 mg/dL]) at 72 hours. Twenty‐three of 28 foals with spurious hypercreatininemia survived to hospital discharge and there was no difference in mean admission creatinine between survivors (1176 μmol/L [628 μmol/L]) (13.3 mg/dL [7.1 mg/dL]) and nonsurvivors (1308 μmol/L [857 μmol/L]) (14.8 mg/dL [9.7 mg/dL]) (P=0.67). Twenty of 28 foals had clinical signs suggestive of neonatal encephalopathy. Conclusion – Creatinine decreased by >50% within the initial 24 hours of standard neonatal therapy and was within the reference interval in all but 1 foal within 72 hours of hospitalization. The diagnosis of neonatal encephalopathy was common in these foals.