Congenital hypothyroidism and dysmaturity syndrome in foals: First reported cases in Europe

Congenital hypothyroidism and dysmaturity syndrome (CHD) in neonatal foals was first described in western Canada in 1981 and remains an important problem for the western Canadian horse industry. This syndrome is characterised by hyperplasia of the thyroid gland, increased gestational length and multiple congenital musculoskeletal abnormalities. This case series describes the first confirmed cases of CHD in Europe and challenges contemporary opinion which suggests that this syndrome is distinct from congenital hypothyroidism associated with visible goitre.     

Congenital malignant melanoma in two foals

Two cases of congenital malignant melanomas in horses are described in this report. In each case, wide surgical excision of the mass was performed; no recurrence or metastasis was detected after a minimum of 15 months' follow-up. Melanomas are among the most common neoplasms of horses, but they typically develop in gray horses greater than 6 years old.     

Congenital hypothyroidism in Scottish Deerhound puppies

Two Scottish Deerhound puppies had clinical and pathological features consistent with the diagnosis of congenital non-goitrous hypothyroidism. They were from separate litters, but were the progeny of the same sire and dam. The puppies were smaller, had shorter limbs and shorter, broader heads than their littermates. They also had histories of weakness, difficulty in walking and somnolence. A characteristic radiographic feature was the absence of epiphyseal growth centres. Both had depressed serum thyroxine (T4) levels and one did not respond to exogenous thyroid stimulating hormone. On necropsy, the thyroid glands were small, the follicles varied in size and contained little or no colloid. The adenohypophysis contained many cells with markedly vacuolated cytoplasm. It is suggested that the clinicopathological pattern is the result of a primary thyroid abnormality. Possible mechanisms include either primary thyroid hypoplasia or an unresponsiveness to thyroid stimulating hormone.     

Congenital hypothyroidism in a boxer dog

Congenital central hypothyroidism was diagnosed in a one-year-old boxer dog. The dog was presented for investigation of lameness, lethargy and obesity. Survey skeletal radiographs revealed delayed bone maturation and epiphyseal dysgenesis. A diagnosis of hypothyroidism was confirmed on the basis of a low basal serum thyroxine (T₄) concentration that failed to increase following bovine thyroid stimulating hormone (TSH) administration. However, repeated administration of TSH resulted in reactivation of the thyroid gland suggesting a central rather than a primary problem. Consistently low basal plasma Cortisol concentrations were suggestive of a concurrent secondary or tertiary hypoadrenocorticism. Surprisingly, plasma growth hormone concentrations were elevated before treatment but decreased once thyroid replacement therapy had commenced.     

A case-control study of the congenital hypothyroidism and dysmaturity syndrome of foals.

A case-control study was conducted to identify risk factors for the congenital hypothyroidism and dysmaturity syndrome of foals. A questionnaire was used during personal interviews of foal owners and farm managers to collect information on animal signalment, farm environment, and mare management. Information on 39 foals with the congenital hypothyroidism and dysmaturity syndrome were compared with 39 control foals. Foals with the syndrome had a significantly (P < 0.0001) longer gestation (357.6 d) than control foals (338.9 d). Pregnant mares that were fed greenfeed, did not receive any supplemental mineral, left their "home farm" during gestation, or grazed irrigated pasture had 13.1 (P = 0.0068), 5.6 (P = 0.0472), 4.3 (P = 0.0076), and approximately 15.3 (P = 0.0245), respectively, greater odds of producing an affected foal than mares not experiencing these events. Greenfeed often contains high levels of nitrate (NO3-), which is known to impair thyroid gland function. In light of this, forage samples from participating farms were analyzed for nitrate levels. The odds of one or more congenitally hypothyroid and dysmature foals being born on a farm feeding forage with at least a trace of nitrate was 8.0 times greater (P = 0.0873) than the odds of the disease occurring on a farm that fed forage free of nitrate. Further, the odds of a mare producing an affected foal when fed forage containing at least a trace of nitrate were 5.9 times greater (P = 0.0007) than those of a mare fed nitrate free forage. This study suggests that congenital hypothyroidism and dysmaturity syndrome in foals may be the result of diets that contain nitrate or that are low in iodine being fed to pregnant mares.     

Congenital hypothyroidism with goiter in toy fox terriers

Congenital hypothyroidism with goiter was observed to segregate as a simple autosomal recessive trait in Toy Fox Terriers (TFTs). Neonatal affected pups exhibited inactivity, abnormal hair coat, stenotic ear canals, and delayed eye opening. Palpable ventrolateral cervical swellings were evident by 1 week of age. Serum thyroid hormone and thyroid-stimulating hormone concentrations were low and high, respectively. Histologic examination of the cervical masses disclosed cuboidal to columnar follicular epithelial cell hyperplasia with widely varying follicular size, shape, and amount of colloid. Oral thyroid hormone replacement therapy restored near-normal growth and development. At 8 weeks of age, radioiodine uptake and perchlorate discharge testing indicated an iodine organification defect. Biochemical analysis of thyroid tissue from affected dogs demonstrated enzymatic iodine oxidation deficiency and lack of sodium dodecyl sulfate-resistant thyroglobulin dimers, suggesting thyroid peroxidase deficiency. A nonsense mutation in the thyroid peroxidase gene of affected dogs was discovered and demonstrated to segregate with the disease. A DNA-based carrier test was developed and currently is used by TFT breeders to prevent this disorder.     

Enterotoxemia in two foals.

Two Quarter Horse foals from different premises died from enterotoxemia. Clostridium perfringens toxins alpha and beta were demonstrated in the foal's intestines by mouse protection tests. Clostridium perfringens type C was isolated from the intestines of each foal. Histologic examination revealed hemorrhage, necrosis, and massive numbers of C perfringens.     

Congenital hypothyroidism of dogs and cats: a review

Congenital hypothyroidism is a rare and underdiagnosed congenital endocrine disorder in dogs and cats and the true incidence is unknown. The disorder may cause a range of clinical signs depending on the primary defect, which affect production of thyroid hormones; some cases present when adult. Hallmark clinical signs of congenital hypothyroidism are mental impairment and skeletal developmental abnormalities, resulting in disproportionate dwarfism; goitre may or may not be present. Documented causes of congenital hypothyroidism in dogs include deficiency of, or unresponsiveness to, thyrotropin-releasing hormone (TRH) or thyroid-stimulating hormone (TSH), thyroid dysgenesis, dyshormonogenesis and iodine deficiency. In cats, TSH unresponsiveness, thyroid dysgenesis, dyshormonogenesis and iodine deficiency have been confirmed. Adequate replacement therapy results in a successful outcome in the majority of cases, especially when started early in life, as permanent developmental abnormalities can be prevented. This review describes reported cases in dogs and cats, diagnostic investigation, and recommendations for treatment.     

Sepsis in adults and foals.

Sepsis develops in horses when the host response to the invading pathogens is not properly balanced according to the severity of the insult. Several clinical conditions frequently encountered in equine practice may be associated with the development of sepsis and have the potential to progress to more severe forms, such as severe sepsis, MODS, and septic shock. Consequently, it is important for equine practitioners to be aware of the manifestations,pathophysiology, and treatment of sepsis. Although enormous progress has been made in recent years in our understanding of the pathophysiology of sepsis. more work remains to be done in improving basic critical care guidelines and basic monitoring in equine intensive care units and in critically evaluating potential equine sepsis therapy. Fortunately, we can learn from the important advances made recently in the treatment of human sepsis patients;hence, rapid progress may be expected in a near future, especially as more and more veterinarians show interest in the discipline of equine critical care. With the completion of several genome projects and the availability of high-throughput genetic techniques, one hopes that we will further refine our understanding of the events underlying the development of severe sepsis and septic shock, which could lead to more appropriate therapeutic intervention targeted to each individual according to the state of the immune response in that horse.     

Immunologic disorders in neonatal foals.

Foals live in an environment heavily populated by bacteria, many of which are capable of causing disease. Development of infection,however, is the exception rather than the rule. The ability of the foal to prevent infection by most pathogens is the result of a sophisticated set of defense mechanisms. These defense mechanisms can be divided into adaptive and innate immunity. Innate immunity encompasses defense mechanisms that pre-exist or are rapidly induced within hours of exposure to a pathogen. Conversely, adaptive or acquired immunity represents host defenses mediated by T and B lymphocytes, each expressing a highly specific antigen receptor and exhibiting memory during a second encounter with a given antigen. Immunologic disorders are relatively common in foals compared with their occurrence in adult horses. This article summarizes the current understanding of the equine fetal and neonatal immune system and reviews common immunodeficiency disorders as well as disorders resulting from allogenic incompatibilities.