Dogs diagnosed with sudden acquired retinal degeneration syndrome (SARDS) commonly are presented with concurrent clinical, physical, and historical findings consistent with hyperadreno-corticism (HAC) at the time of vision loss. Thirteen dogs diagnosed with SARDS on the basis of complete ophthalmic examination and extinguished bright-flash electroretinogram were evaluated for steroid hormonal abnormalities. Signalment, case history, physical examination, and clinicopathological findings were recorded. Serum cortisol and sex-hormone concentrations were measured before and after adrenocorticotropic hormone (ACTH) stimulation. Clinical signs of HAC, systemic hypertension, and proteinuria were commonly found in dogs with SARDS. Elevations in one or more sex hormones were found in 11 (85%) of 13 dogs (95% confidence interval [CI] 65% to 100%); cortisol was elevated in nine (69%) of 13 dogs (95% CI 44% to 94%). A minority of dogs (three [23%] of 13; 95% CI 0.2% to 46%) exhibited only an increase in adrenal sex hormones. Only one dog had completely normal ACTH stimulation test results. Symptoms of HAC were associated with abnormal ACTH stimulation results. Routine ACTH stimulation testing to evaluate cortisol and sex hormones, blood pressure screening, and urinalysis are recommended in these animals.

Fourteen cats received either daily prednisolone (4.4 mg/kg per os [PO]) or dexamethasone (0.55 mg/kg PO) for 56 days. These doses were clinically equipotent. Serum fructosamine and urine glucose were measured on days 0, 28, and 56. Insulin sensitivity, glucose tolerance, and peak insulin secretion were measured in each group prior to and at the end of the courses of glucocorticoid administration. On day 56, the prevalence of glucosuria was significantly greater (P=0.027), and a trend was seen toward greater fructosamine concentrations (P=0.083) in dexamethasone-treated cats compared to prednisolone-treated cats. The results of this pilot study also showed a trend toward a greater decrease in insulin sensitivity (P=0.061) and a significantly lower compensatory increase in insulin secretion (P=0.081) in the dexamethasone-treated cats than in cats administered prednisolone. These preliminary data suggest that dexamethasone exhibits greater diabetogenic effects in cats than equipotent doses of prednisolone. Further study is justified to support this hypothesis.

Encephalitozoon (E.) cuniculi has been occasionally identified as a cause of neurological or renal disease in dogs, but cases are not well documented in the United States. The medical records from a state veterinary diagnostic laboratory for 19 cases of fatal encephalitozoonosis in puppies were reviewed. Clinical histories included depression, inappetence, and progressive neurological signs of short duration. Histopathological evaluation showed brain and renal lesions typical of encephalitis and nephritis, respectively. Molecular analyses of parasites from 13 cases confirmed the identity of the organisms as E. cuniculi strain III. This parasite may be an underdiagnosed cause of fatal canine neurological or renal disease.

Granulocytic anaplasmosis is an emerging infectious disease affecting dogs and humans in the United States and other regions of the world. Relatively few cases have been described in pregnant women, and perinatal transmission appears to occur infrequently in humans. Infection in pregnant dogs has not been reported. Diagnosis of infection during pregnancy poses therapeutic challenges, because doxycycline, the treatment of choice, is teratogenic. Also, infection during pregnancy may result in more severe disease. When infection is diagnosed after parturition, knowledge of the risk of perinatal transmission to offspring is important, because prophylactic therapy in neonates is also not without risk. In this report, we describe relatively severe clinical manifestations of Anaplasma phagocytophilum infection in a postpartum bitch and a lack of perinatal transmission to her puppies.

A 4-year-old, spayed female, mixed-breed dog was presented for evaluation of chronic left hind-limb lameness. Lytic lesions were observed in the left patella on radiographs of the stifle. A biopsy of the patella led to a histopathological diagnosis of blastomycosis. Surgical debridement followed by a 90-day course of itraconazole and physical rehabilitation resolved the clinical signs and stopped the progression of radiographic lesions. Blastomycosis should be considered as a differential diagnosis for stifle joint lameness with lytic lesions in the patella.

Situs inversus totalis is a rare, congenital condition that is characterized by the development of the thoracic and abdominal viscera in a mirror image to their normal orientation. This case report describes the condition in a 4-year-old, spayed female Doberman pinscher that was evaluated for dyspnea following sedation. Radiography confirmed a diaphragmatic hernia. Situs inversus was discovered during surgical correction. The diaphragmatic rent was repaired, and the dog was clinically normal at recheck 13 months after surgery.

A 13-month-old, male bichon frise was examined for the investigation of intermittent seizures, ataxia, abnormal behavior, polyuria, and polydipsia. At presentation, clinical and neurological examinations were unremarkable with the exception of mild truncal ataxia and a domed skull. Severe hyponatremia and hypoosmolality were identified, and following diagnostic testing a diagnosis of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was made. Magnetic resonance imaging revealed changes consistent with severe hydrocephalus. Water restriction resulted in increased serum osmolality and a reduction in severity of clinical signs. The current case report documents SIADH associated with hydrocephalus in a dog. Structural brain disease should be excluded before a diagnosis of idiopathic SIADH is made.

A 13-year-old, spayed female golden retriever was referred for further evaluation of ascites, characterized as a modified transudate, detected after an episode of acute collapse. Prior to referral, the dog was treated for suspected right-sided heart failure and developed ventricular tachycardia. On referral, echocardiography ruled out cardiac causes for the effusion, and following stabilization the dog was taken to surgery for abdominal exploration. Surgery revealed entrapment of the left lateral liver lobe within the falciform ligament. Surgical removal of the entrapped liver lobe and falciform fat resulted in resolution of the Budd-Chiari-like syndrome. No abdominal effusion was seen on follow-up ultrasound examination. This is the first reported case of Budd-Chiari-like syndrome caused by liver lobe entrapment within falciform fat that was successfully corrected with surgery.