Congenital heart diseases of puppies and kittens.

Congenital heart disease (CHD) is defined as a morphologic defect of the heart or associated great vessels present at birth. Abnormalities are caused by alterations or arrests in particular phases of embryonic development of the fetal heart. The term congenital does not imply that the defect was inherited, and the defect may have occurred spontaneously or secondary to a drug or toxin. By studying families of animals with specific CHDs, many defects have also been shown to be heritable.Additionally, if the defect was caused by a spontaneous de novo mutation,that individual has the potential to transmit the mutation to offspring.The diagnosis of CHD is important not only to the health of the patient but to eliminate affected individuals from the breeding pool.     

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.     

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.     

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.     

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 adenohypophyseal hypoplasia associated with secondary hypothyroidism in a 2-week-old Portuguese water dog

This report describes the histomorphological changes of central hypothyroidism (pituitary dependent) in several target organs of thyroid hormones of a Portuguese water dog, and contrasts those with the reported features of central hypothyroidism in German shepherd dogs, in which central hypothyroidism is a part of a combined pituitary hormonal deficiency.     

弱胎仔犬浅议

弱胎是在犬的繁殖过程中经常遇到的问题。部分初生仔犬在体重、体质、哺乳能力和抗逆性等方面弱于正常仔犬,生活能力低下,死亡几率较高,我们把这部分仔犬称为弱胎仔犬。据不完全统计,弱胎仔犬占仔犬总数10%～20%左右。当同窝仔犬总数在5个以下时,弱胎现象表现得并不明显,同窝仔     

Brodifacoum toxicosis in two neonatal puppies

Eight out of a litter of 13 puppies were either born dead or died within 48 hours of birth. Three puppies that died shortly after birth were necropsied. Two puppies had hemorrhage in the thoracic and peritoneal cavities, intestinal serosa, and meninges. The third puppy was smaller than the other two puppies but did not have detectable hemorrhage. Brodifacoum, a second-generation coumarin anticoagulant, was detected in livers from the two puppies with hemorrhage. The dam did not have clinical signs of coagulopathy before or subsequent to whelping. The owners were confident that the dog had not been exposed to rodenticide for at least 4 weeks before whelping. A presumptive diagnosis of in utero brodifacoum toxicity was made. To the authors' knowledge this is the first time a second-generation coumarin anticoagulant has been detected in the liver of a newborn animal. This case is also unique because the dam was unaffected, suggesting that fetuses are more susceptible to brodifacoum toxicity than adult animals.     

Laryngeal collapse in seven brachycephalic puppies

OBJECTIVES: To document the histories, clinical findings, and management of seven puppies with laryngeal collapse occurring secondarily to brachycephalic airway syndrome. METHODS: Seven brachycephalic puppies aged between 4.5 and six months underwent surgery for management of brachycephalic airway syndrome following presentation for exercise intolerance and increased respiratory noise and effort. RESULTS: Stenotic nares of varying severity and an elongated soft palate were common to all dogs. All dogs had tracheal hypoplasia and this was severe in four dogs. Laryngeal collapse was present in all dogs. Two dogs had stage I, four dogs stage II, and one dog stage III laryngeal collapse. The dog with stage III laryngeal collapse and one dog with stage II laryngeal collapse died. There was no apparent association between the changes evident on thoracic radiographs or the degree of tracheal hypoplasia and postoperative outcome. CLINICAL SIGNIFICANCE: The development of severe secondary laryngeal changes in dogs aged six months or less supports the suggestion that immature brachycephalic dogs should undergo assessment and, if indicated, surgery as soon as any clinical signs of BAS are apparent.