A study of the interaction between bromocresol green dye and bovine,ovine and equine serum globulins

In human medicine it has been shown that the bromocresol green (BCG) dye-binding method for the determination of serum albumin is not entirely specific, the dye reacting also with certain human serum globulins. This causes over-estimation of albumin when reaction times are prolonged beyond 30 seconds.In the present study, serum albumin values obtained from three animal species by the immediate, i.e. less than 30 seconds, BCG reaction were compared with those by the 10-minute BCG reaction. Albumin-depleted sera were prepared using an affinity chromatography technique and their reactions and those of purified gamma globulin preparations with the dye were studied.In cattle, sheep and horses, serum albumin values obtained by the 10-minute reaction were higher than those obtained by the immediate BCG reaction, the differences being statistically significant. Purified gamma globulin did not react with the BCG dye after 10 minutes, but other globulins did. There were differences between the species in the magnitude of the reaction of their globulins with BCG dye.     

Multiple cytopenias associated with monocytic proliferation in a dog

An unusual combination of blood cytopenias and monocytic proliferation was observed in a dog. Initial hematologic findings included severe thrombocytopenia, neutropenia, mild nonregenerative anemia and apparently normal bone marrow. Subsequently, a severe persistent monocytosis developed and the bone marrow became populated with monocytes and cytophagic macrophages. Splenomegaly was due to reticuloendothelial hyperplasia and extramedultary hematopoiesis. Treatment consisted of splenectomy and azathioprine but the response was poor and the dog was euthanized. Postmortem examination revealed a hypocellular bone marrow which contained moderate numbers of monocytes and plasma cells. Neoplastic proliferation was absent in visceral organs. No definite diagnosis was established; chronic blood cell consumption, perhaps immune-mediated, may have been responsible for the extensive reticuloendothelial hyperplasia and cytophagia.     

Congenital cardiac disease in dogs

Pulmonic stenosis is caused by a malformed pulmonic valve, stricture of the right ventricular outflow tract or stricture of the pulmonary artery. English Bulldogs, Beagles, Samoyeds, Fox Terriers and Chihuahuas are predisposed. Clinical signs in severely affected dogs include exercise intolerance, stunting, dyspnea, syncope and ascites. Auscultation reveals a high-frequency, crescendo-decrescendo murmur during systole, loudest over the left side of the thorax, near the sternal cardiac border. An ECG may reveal a right-axis deviation of greater than 120 degrees, S waves in leads I, II and III, deep S waves in CV6LL, CV6LU and V10, Q waves deeper than 0.5 mv in leads II, III and AVF, and positive T waves in lead V10. Plain film LAT thoracic radiographs reveal an elevated carina, increased sternal contact of the heart, loss of the cranial cardiac waist and a widened cardiac silhouette, with normal pulmonary vasculature. A DV projection reveals an inverted "D" shape of the right ventricle and a pulmonary artery bulge. A nonselective angiocardiogram reveals poststenotic dilation of the main pulmonary artery. Treatment involves surgical correction of the stenosis.