Systemic granulomatous disease in dairy cattle during a dicyandiamide feeding trial.

CASE HISTORY: Mature, in-calf, non-lactating, Friesian or Friesian-cross cows were fed dicyandiamide (DCD) at daily doses of 0.15 g/kg (Group 1; n=31), 0.45 g/kg (Group 2; n=21) and 0.75 g/kg (Group 3; n=12), as part of a safety trial, which also included a control group (n=15). Daily health observations were carried out on each cow until Day 86 of the study. On Day 28 one cow from Group 3 was observed with signs of disease, and subsequently disease was noted in other cows. CLINICAL FINDINGS: Clinical signs in the first case included depression, pyrexia (40.9°C), salivation and dehydration, in addition to progressive weight loss, followed by death on Day 32. Other cows from all treatment groups developed clinical signs of disease resulting in euthanasia of seven animals. Disease occurred in 10/12 (83%) cows in Group 3, 11/21 (52%) cows in Group 2, and 7/31 (23%) cows in Group 1. Clinical signs were variable and included dermatitis and pruritus of the head and neck, petechial haemorrhages, pyrexia, weight loss, thrombocytopenia, neutropenia, and regenerative anaemia. PATHOLOGICAL FINDINGS: Gross findings included generalised lymphadenopathy, subcutaneous oedema, petechiation of mucosal and serosal surfaces, and gastrointestinal haemorrhage. Histologically, multiple organs and tissues contained inflammatory foci characterised by infiltrates of lymphocytes, plasma cells, macrophages and occasionally prominent multinucleated giant cells and eosinophils. DIAGNOSIS: Multisystemic granulomatous and haemorrhagic syndrome resembling cell-mediated hypersensitivity, associated with DCD ingestion. CLINICAL RELEVANCE: This is the first report of toxicity in cattle associated with ingestion of DCD. The proportion of affected cows increased with increasing dose of DCD, but not all cattle in the high dose group developed disease, therefore additional factors may determine whether or not an individual cow will develop DCD-associated disease.

Canine hyperadrenocorticism.

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.

IgA multiple myeloma in a dog.

Multiple myeloma was diagnosed in a lo-year-old female Labrador which showed signs of weight loss, lethargy and skeletal pain. Radiography revealed well circumscribed osteolytic lesions in vertebrae, sternebrae, and the left humerus and radius along with generalised osteoporosis. The number of plasma cells in the bone marrow was increased and the serum gamma globulin concentration was elevated. Treatment with cyclophosphamide, mephalan and prednisone successfully controlled the malignancy but also resulted in suppression of the bone marrow. There was a remission time of 21.5 months.

Adrenal adenoma in a cross-bred terrier.

An adrenal tumour was diagnosed in a 12-year-old female cross-bred terrier. The dog was presented to the veterinary clinic because she had been gaining weight and had started urinating in the owners' house. Clinical findings included obesity, abdominal enlargement, thinning of the hair coat, seborrhoea sicca, and polydipsia and polyuria. The diagnosis was made by clinical pathology, endocrine function tests and abdominal radiography. Surgical removal of the neoplastic right adrenal gland resulted in resolution of the clinical signs, including regrowth of the hair coat.

Radio-iodine treatment of hyperthyroid cats.

Thirty-two elderly domestic shorthaired cats (mean age 12.9 years) were treated with radioiodine (131I). The dose of 131I administered ranged from 39 mBq to 134 mBq. Twenty-eight cats became euthyroid after treatment, one became hypothyroid and three remained hyperthyroxaemic. Two of the hyperthyroxaemic cats were successfully re-treated with 131I. Five cats died from concurrent diseases within one year of treatment. The administration of a dose of 131I selected by assessing the severity of the clinical signs, the size of the thyroid gland(s) and the serum level of thyroxine was an effective treatment for hyperthyroidism.