Hypothyroidism in the foal

Hypothyroidism in the foal occurs as two entities because of the separate actions of thyroid hormones in regulation of metabolic rate and in cell differentiation. The hypometabolic state which results in inadequate thermogenesis and lethargy, occurs concurrently with a period when thyroid hormone secretion is inadequate. Also the severity of the concurrent symptoms is related to the degree of hormone inadequacy as measured by plasma concentrations of free T4 and T3. By contrast, the developmental lesions caused by hypothyroidism are often observed during periods when plasma thyroid hormone concentrations are normal. This is because during the development of most tissues there is a period during which deprivation of thyroid hormones leads to developmental defects which may first appear weeks or months later, by which time thyroid hormone levels may have returned to normal. In the foal the critical period for some developmental processes, eg, myelination, is before birth so it is difficult to confirm a pre-natal hypothyroid state as the cause of neonatal neuromuscular incompetence. Post natal developmental lesions of the epiphyses or ossification centres, for example, may also manifest themselves some weeks subsequent to the period during which hypothyroidism existed. Because confirmation of diagnosis using plasma hormone measurements is very difficult in the foal, and because the symptoms of hypothyroidism are not specific, the incidence of confirmed hypothyroidism in foals is low. However there is suggestive evidence that where awareness of the condition exists it is diagnosed frequently. The aetiology is obscure although diet has been implicated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Recent advances in reproductive endocrinology of the mare

The recent development of radioimmunoassay techniques to determine changes in blood hormone levels has increased our understanding of the endocrinology of the oestrous cycle and pregnancy in the mare. This review describes recent findings concerning the endocrine basis and treatment of some common types of infertility.

Further evidence supporting the concept that prostaglandin F2∝ is the uterine luteolysin in the mare is discussed. Persistent corpus luteum is now recognized as an important cause of infertility, which may be treated by uterine distension or prostaglandin; recommendations for avoiding treatment failures are presented.

The clinical significance of recent findings on the effectiveness of HCG in hastening ovulation, and on the increase in anti-HCG antibodies after repeated injections of this hormone are also discussed.

Although antibiotics successfully control the specific pathogen causing contagious equine metritis, the treatment of common opportunistic organisms with antibiotics appears to give indifferent results. The increased understanding of the role of sex steroids in susceptibility to uterine infection seems likely to lead to improved methods of control.

Although stimulation of folliculogenesis and ovulation in seasonally acyclic mares is possible using extracts of equine pituitary glands, this treatment is impractical on a clinical scale. Gonadotrophin-releasing-hormone provides a more physiological method of stimulation, and results of recent experiments using this hormone are reviewed.

In the pregnant mare, recent studies have shown that the “pregnancy signal” to the mare may be the production of oestrogens from the developing blastocyst from Day 14. Measurement of PMSG as an aid to pregnancy diagnosis is evaluated, and the use of progesterone supplementation to prevent abortion is discussed.     

The effect of large doses of thiamine on the horse

Extract

In conjunction with a trial to determine the effect of nematode infestation upon the liveweight gain and wool production of young sheep (Brunsdon, unpublished), information was sought on the seasonal succession and availability on pasture of infective larvae of the principal trichostrongyle genera parasitic in sheep. Data were collected in the form of nematode populations found at postmortem examination of Romney lambs, previously maintained worm-free, which were exposed to risk of parasitism in the field. A series of these lambs ran with the flock in the above-mentioned trial and served as indicators of the abundance of infective larvae on the pasture.     

The molecular basis for recognition of bacterial ligands at equine TLR2, TLR1 and TLR6

TLR2 recognises bacterial lipopeptides and lipoteichoic acid, and forms heterodimers with TLR1 or TLR6. TLR2 is relatively well characterised in mice and humans, with published crystal structures of human TLR2/1/Pam3CSK4 and murine TLR2/6/Pam2CSK4. Equine TLR4 is activated by a different panel of ligands to human and murine TLR4, but less is known about species differences at TLR2. We therefore cloned equine TLR2, TLR1 and TLR6, which showed over 80% sequence identity with these receptors from other mammals, and performed a structure-function analysis. TLR2/1 and TLR2/6 from both horses and humans dose-dependently responded to lipoteichoic acid from Staphylococcus aureus, with no significant species difference in EC50 at either receptor pair. The EC50 of Pam2CSK4 was the same for equine and human TLR2/6, indicating amino acid differences between the two species’ TLRs do not significantly affect ligand recognition. Species differences were seen between the responses to Pam2CSK4 and Pam3CSK4 at TLR2/1. Human TLR2/1, as expected, responded to Pam3CSK4 with greater potency and efficacy than Pam2CSK4. At equine TLR2/1, however, Pam3CSK4 was less potent than Pam2CSK4, with both ligands having similar efficacies. Molecular modelling indicates that the majority of non-conserved ligand-interacting residues are at the periphery of the TLR2 binding pocket and in the ligand peptide-interacting regions, which may cause subtle effects on ligand positioning. These results suggest that there are potentially important species differences in recognition of lipopeptides by TLR2/1, which may affect how the horse deals with bacterial infections.