Penicillin-induced immune-mediated hemolytic anemia in a horse.

A 5-year-old female American Quarter Horse was determined to have immune-mediated hemolytic anemia after detection of a positive response to a direct Coombs' test. Penicillin-induced immune-mediated hemolytic anemia was confirmed via a direct antiglobulin test, using penicillin-coated RBC. The horse was clinically improved and the anemia resolved in response to supportive care and discontinuation of penicillin treatment. Penicillin should be considered a possible cause of immune-mediated hemolytic anemia in horses.     

Immune-mediated hemolytic anemia in a horse

An 18-year-old Quarter Horse gelding was determined to have immune-mediated hemolytic anemia after detection of autoagglutination of RBC spherocytosis as well as a positive direct Coombs test result. A lack of response to treatment with corticosteroids necessiated the administration of cyclophosphamide and azathioprine. The anemia resolved after treatment with chemotherapeutic drugs.     

Clostridium perfringens cellulitis and immune-mediated hemolytic anemia in a horse

A 10-year-old Quarter Horse mare was referred for evaluation and treatment of a large pectoral skin slough and hemoglobinuria. The skin slough was secondary to Clostridium perfringens cellulitis and associated gas gangrene. Cold hemagglutinin disease was diagnosed and was suspected to be secondary to C perfringens septicemia. The autoimmune hemolytic anemia, severe intravascular hemolysis, and hemoglobinuria were treated with dexamethasone and hydrocortisone. The infection was treated with 20 X 10(6) units of sodium penicillin, IV, 4 times daily, and the wound was debrided. When the mare relapsed, treatment was changed to 6 g of chloramphenicol sodium succinate, IV, 4 times daily. The mare died on day 11 of hospitalization, despite intensive therapy.     

Diet‐associated hepatic failure and immune‐mediated hemolytic anemia in a Weimaraner

Objective: To describe the medical and nutritional management of a 4‐year‐old Weimaraner with acute hepatic failure and immune‐mediated hemolytic anemia (IMHA) associated with consuming a commercial dog food. Case summary: A 4‐year‐old male castrated Weimaraner developed signs of IMHA, hepatic failure, disseminated intravascular coagulopathy, and malnutrition after consuming a commercial dog food. During the course of hospitalization, medical management included immunosuppressive therapy and supportive care. Nutritional support consisted of both enteral and parenteral nutrition. The dog was discharged after 19 days of hospitalization and fully recovered by 6 months. An investigation by the Food and Drug Administration was not able to determine the exact cause of the acute hepatic failure and IMHA. New information provided: This is the first case report documenting the medical and nutritional management of a critically ill animal associated with ingestion of this commercial dog food.     

Immune-mediated hemolytic anemia associated with trimethoprim-sulphamethoxazole administration in a horse.

A 10-year-old, thoroughbred gelding was administered sulphonamide drugs during surgical treatment of guttural pouch mycosis. The horse became anemic and a diagnosis of immune-mediated hemolytic anemia was made after other causes of anemia had been ruled out. The anemia resolved after the drugs were withdrawn.     

Zinc-induced hemolytic anemia in a dog

A dog ingested a zinc nut that was retained in the stomach and caused a life-threatening hemolytic crisis with renal, gastrointestinal, and hepatic dysfunction. The dog was stabilized by blood transfusion and was anesthetized, and the zinc nut was removed with a fiberoptic endoscope. With continued supportive care, the dog recovered. Metallic zinc is found in high concentrations in nuts, bolts, and pennies. Zinc toxicosis should be considered in cases of unexplained hemolytic anemia.     

Immune-mediated hemolytic anemia and thrombocytopenia in a foal

A one-month-old Quarter Horse filly had unilateral epistaxis, hyphema, icterus, petechial hemorrhages in the oral, nasal, conjunctival, and vulvar mucous membranes, anemia, thrombocytopenia, negative antinuclear test result, and a positive direct Coombs' test result. Megakaryocytes or cell-associated IgG (fluorescent antibody and immunoperoxidase stains) were not found in bone marrow biopsy specimens. Treatment consisted of glucocorticoids, antibiotics, and a single whole blood transfusion. The foal responded well to treatment, did not develop relapses of the disease, and was clinically normal one year after treatment.     

Suspected hepatic amyloidosis in a horse

A 9-year-old Saddlebred gelding was referred to the University of Wisconsin Veterinary Care for decreased energy levels, weight loss, persistently elevated liver enzymes, hyperglobulinaemia and leukocytosis. Abdominal ultrasonography showed a large volume of peritoneal fluid of mixed echogenicity, and the presence of focally distributed, circular to oval (approximately 1–2 cm), hyperechoic areas within the parenchyma of an enlarged liver. Cytological analysis of the peritoneal fluid revealed sterile neutrophilic/macrophagic inflammation, with haemosiderophages. A liver biopsy confirmed the presence of hepatic amyloidosis and focal fibrosis. Medical therapy with trimethoprim-sulfamethoxazole for 30 days and long-term dexamethasone was associated with both a clinical and biochemical response for 7 months, at which time the horse died from presumed hepatic rupture. To the authors’ knowledge, this is the first report describing potential successful management of hepatic amyloidosis in a horse.     

Idiopathic immune-mediated hemolytic anemia in a calf.

Severe anemia was found in a 4-month-old heifer, which was admitted with a 1-day history of anorexia, signs of depression, and recumbency. A diagnosis of immune-mediated hemolytic anemia (IHA) was made on the basis of a Coomb's titer of 1:128 and decreased resistance to osmotic stress, as determined by an RBC fragility test. Anaplasmosis and leptospirosis were ruled out as possible causes of the IHA. Other causes of hemolytic anemia, including intoxication by copper, water, Brassica spp, or drugs were ruled out. Therefore the IHA was considered idiopathic. Treatment consisted of supportive therapy, oxytetracycline, and dexamethasone. After 60 days of treatment, CBC, Coomb's test result, and RBC fragility were within normal limits.     

The kinetics of hematopoiesis in the light horse III. The hematological response to hemolytic anemia.

The hematological response to acetylphenylhydrazine hemolytic anemia was studied in three standardbred horses. The lifespan of erythrocytes produced during the most severe phase of the anemia were measured with 75-selenomethionine and found to be 144 days as compared to the 139 day lifespan in response to hemorrhagic anemia or 155 days in normal standardbred horses measured previously using the same technique. The erythrocyte counts returned to initial values in 42 days (37, 34 and 54 days) a mean erythrocyte production of 6.4 times 10-12 erythrocytes/day. The mean hemoglobin production was 0.31 gm/kg body weight/day as compared to 0.11 gm Hb/kg/day previously observed in response to hemorrhagic anemia. The mean increase in erythrocyte mean cell volume was 12 mu-3 during the acute response phase to hemolytic anemia in contrast to the absence of a significant increase in the mean cell volume as previously observed during response to hemorrhagic anemia. Free Heinz bodies separated from erythrocytes during the acute phase could not be differentiated from platelets on the hemocytometer counting chamber with standard techniques.