Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.     

Toxicology of selected pesticides, drugs, and chemicals. Zinc

Zinc poisoning in small animals has been described in dogs, cats, birds, and ferrets, but the dog appears to be the species most often affected. Ingestion of zinc-containing metallic objects, including pennies, and zinc oxide ointments has been associated with the majority of the toxicoses. Clinical signs include anorexia, vomiting, diarrhea, hemolytic anemia, kidney dysfunction, and possible liver and pancreatic abnormalities. Treatments that have proven efficacious include fluid diuresis, blood transfusions as needed, general supportive care, and removal of the source of zinc. Further evaluation of the benefit of chelation therapy is urgently needed.     

Bee sting envenomation resulting in secondary immune-mediated hemolytic anemia in two dogs

Immune-mediated hemolytic anemia secondary to bee envenomation developed in 2 dogs. Clinical signs included lethargy, hematuria, ataxia, and seizures; 1 dog died. Clinicopathologic data included nonregenerative anemia, spherocytosis, positive results for Coombs' test, and occult hematuria. Treatment included oral administration of corticosteroids at immunosuppressive dosages and supportive care. The surviving dog initially responded to corticosteroids, but hemolysis recurred as the dosage was tapered. Hemolysis resolved with prolonged administration of corticosteroids. Bee venom contains hyaluronidase, histamines, and hemolysins that cause toxic and hemolytic effects. Envenomation should be considered in any dog with hemolytic anemia in which other causes are ruled out and exposure to bees is known.     

Surface ultrastructure of pyruvate kinase-deficient erythrocytes in the Basenji dog.

The scanning electron microscope was used to study the surface morphologic features of erythrocytes from a Basenji dog with hereditary hemolytic anemia due to a pyruvate kinase-deficient erythrocytes (RBC). Cells from this dog were compared with RBC from normal dogs and from dogs with regenerative anemias unrelated to pyruvate kinase deficiency. Demonstration of spherical RBC with uniform spicules on their surface (spheroechinocytes) may provide a morphologic explanation for the shortened erythrocytic life-span previously reported in congenital hemolytic anemia of Basenji dogs. Spherical, spiculated RBC were not found in blood from normal dogs or from anemic dogs with reticulocytoses. The surface of reticulocytes from all dogs with regenerative anemia was roughened, with pronounced folding of the cell membrane.     

Hypocellular marrow and extramedullary hematopoiesis in a dog: hematologic recovery after splenectomy

Nonregenerative anemia, poikilocytosis, thrombocytopenia, and splenomegaly were found in a 6-year-old dog. Marrow aspiration did not yield marrow particles, and microscopic examination of a marrow-core biopsy indicated hypocellular marrow. Marked extramedullary hematopoiesis was found in liver and spleen biopsy specimens. After splenectomy, the clinical and hematologic abnormalities resolved. The dog subsequently developed hemolytic anemia caused by Haemobartonella canis, which was resolved with oral tetracycline treatment. The dog remained healthy without recurrence of cytopenias or hypocellular marrow for 2 years after splenectomy. The clinical, hematologic, and microscopic findings in this dog were compatible with hypersplenism.     

Hemolytic Uremic Syndrome in Dogs

A disease syndrome similar to the hemolytic uremic syndrome of people is described in three dogs with acute renal failure. In each dog, hemorrhagic gastroenteritis preceded the onset of anuric acute renal failure. Evidence of microangiopathic hemolytic anemia (schizocytes, thrombocytopenia, and increased concentrations of fibrin split products) was present in the three dogs. Serum chemistry results showed increased concentrations of blood urea nitrogen, creatinine, and phosphorus. Ultrasound examination performed in one dog revealed increased echogenicity of the renal cortices. Treatment for anuric acute renal failure using a continuous dopamine and furosemide infusion established urine production in one of three dogs. Microscopic examination of tissue from the two dogs that underwent necropsy showed occlusion of the renal vasculature by fibrin thrombi consistent with microangiopathic arteriolar thrombosis. The pathophysiology and current knowledge of human hemolytic uremic syndrome is compared with hemolytic uremic syndrome in these dogs. (Journal of Veterinary Internal Medicine 1993; 7:220–227. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Lupus-Type "Anticoagulant" in a Dog With Hemolysis and Thrombosis

A circulating anticoagulant was detected in a 2-year-old Chesapeake Bay Retriever with hemolytic anemia, nephrotic syndrome, thrombocytopenia, polyarthropathy, and pulmonary thromboembolism. A persistent prolongation of the activated partial thromboplastin time (aPTT) was detected, and it did not correct with repeated administration of fresh frozen plasma. The aPTT was still prolonged, with a 1:1 mixture of patient's plasma and normal dog plasma in vitro, suggesting the presence of a circulating inhibitor. Results of assays to characterize the inhibitor were compatible with those described for the lupus anticoagulant in human patients with systemic lupus erythematosus. Paradoxically, patients having the lupus anticoagulant are at increased risk for thrombosis. Pulmonary thromboembolism has been described as a frequent complication of immune-mediated hemolytic anemia in the dog, and the presence of a circulating anticoagulant should be considered as a potential mechanism.     

Progressive polysystemic immune-mediated disease in a dog

A dog with polyarthritis, angular joint deformities, and a high serum antinucleolar antibody titer was treated over a period of 20 months. During the clinical course, leukopenia, thrombocytopenia, Coombs' positive hemolytic anemia, and a pemphigus-type skin disorder developed, all of which responded to immunosuppressive therapy. It is not known whether the polysystemic disease in this dog represents a pleomorphic manifestation of canine systemic lupus erythematosus or multiple autoimmune disorders occurring in the same animal.     

Zinc-associated acute pancreatitis in a dog

Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.     

Intravenous Human Immunoglobulin for the Treatment of Immune-Mediated Hemolytic Anemia in 13 Dogs

Intravenous immunoglobulin (IVGG) was administered to 13 of 37 dogs with immune-mediated hemolytic anemia. All dogs received concurrent prednisone therapy, 14 dogs also received cyclophosphamide; and a single dog each received cyclosporine, azathioprines, and danazol. Dogs that responded to prednisone therapy without IVGG generally did so within 7 days (mean ± standard deviation = 5.6 ± 2.9 days). Intravenous immunoglobulin was administered after 10.4 ± 6.6 days of prednisone therapy as an intravenous infusion of 0.5 g/kg (range 0.25 to 0.73 g/kg). Eleven dogs received a single treatment, 2 dogs each received 2 treatments. No relevant adverse effects were noted. Eleven dogs had an increase in PCV of at least 4% 2.2 ±1.5 days after IVGG infusion. In 10 of these dogs, the PCV continued to increase until the time of hospital discharge. One responder died 1 hour after the increase in PCV, 1 dog was euthanized within 24 hours of IVGG administration, and 1 dog had no response over a period of 13 days. Results of this study suggest that IVGG therapy may be of value in dogs with immune-mediated hemolytic anemia that do not respond within 7 days of appropriate corticosteroid therapy.     

Inherited phosphofructokinase deficiency in an American cocker spaniel.

A 3-year-old female American Cocker Spaniel with a chronic hemolytic disorder and hemolytic crises was found to have M-type phosphofructokinase deficiency. This inherited erythroenzymopathy and myopathy is commonly diagnosed in English Springer Spaniels, but the family study of this Cocker Spaniel, although supporting an autosomal recessive mode of inheritance, did not reveal any English Springer Spaniel ancestors. Molecular genetic studies did, however, identify the same mutation in this dog as we previously reported in the English Springer Spaniel breed, suggesting that this mutation originated prior to the separation of these 2 breeds.     

Autoantibodies and red blood cell membrane proteins in a case of canine autoimmune hemolytic anemia.

Autoantibodies and erythrocyte membrane proteins were analyzed in a case of a dog with autoimmune hemolytic anemia (AIHA). In crisis phase, antiglobulin test was positive. The eluate from the erythrocytes of the dog with AIHA gave agglutination against autologus erythrocytes. Immunoglobulin subclasses in the eluate were revealed to be IgG and IgA by the double diffusion test. Comparing the SDS polyacrylamide gel electrophoretic patterns of erythrocyte membrane proteins between the crisis and remission phases, there was a change in the protein on protein 4.1 region. However, there were no changes in blood group typings in two phases.     

Acute zinc poisoning in a dog

Zinc-induced haemolytic anaemia was diagnosed in a young dog. The origin of the zinc intoxication was the ingestion of a toy material which contained a high percentage of zinc. The level of zinc in the liver and kidneys was resp. 1050 and 1320 ppm.     

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.     

Babesia vulpes in a dog from Prince Edward Island,Canada

A 12-year-old neutered male American Staffordshire terrier dog was referred to the Atlantic Veterinary College, Prince Edward Island, Canada, for suspected immune-mediated hemolytic anemia. Babesiosis (Babesia vulpes) was confirmed using polymerase chain reaction testing. The dog was successfully treated with a 10-day protocol of atovaquone/proguanil (TEVA Pharmaceutical Industries, Toronto, Ontario), 13.5 mg/kg BW, PO, q8h and azithromycin (Pharmascience, Montreal, Quebec), 10 mg/kg BW, PO, q24h. To the authors’ knowledge, this report is the first documented case of babesiosis caused by Babesia vulpes in a dog from Canada.     

Clinical and pathological findings of acute zinc intoxication in a puppy

This report describes the clinical and pathological findings in a case of acute zinc poisoning in a young dog. The puppy suffered four days of progressively more severe vomiting and diarrhoea. Jaundice and pale mucous membranes, severe haematemesis and haemoglobinuria were other findings. Despite intensive therapy, the dog died a few hours after hospitalisation. Postmortem examination revealed a metallic foreign body in the stomach, catarrhal gastritis, hepatomegaly and enlarged, dark kidneys. Histology showed hepatic centrilobular vacuolar degeneration, haemoglobinuric nephrosis with early tubular necrosis, haemosiderosis and extramedullary haematopoiesis, as well as neuronal damage. The foreign body was mainly composed of zinc. Plasma zinc values were markedly raised (34.5 microg/ml; normal range 0.8 to 1.0 microg/ml). Pathophysiological mechanisms of zinc poisoning are discussed.     

Heinz body haemolytic anaemia in a dog secondary to ingestion of a zinc toy: a case report

A 6-year-old Labrador retriever was referred for investigation of severe lethargy and suspected immune-mediated haemolytic anaemia. Clinical examination revealed pale mucous membranes and jaundice. Haematology demonstrated large numbers of Heinz bodies and a marked anaemia, which was strongly regenerative. Serum zinc concentrations were markedly elevated. Analysis of a metal toy vomited by the dog 3 days prior to presentation revealed it to be composed of almost pure zinc. A diagnosis of haemolytic anaemia secondary to acute zinc toxicity was made and supportive therapy instigated. There was a subsequent decrease in numbers of Heinz bodies and a rise in the haematocrit, and the dog made an uneventful recovery. Acute zinc toxicity resulting in haemolytic anaemia is rarely observed, and this case was also unusual in that the main clinicopathological finding was the presence of numerous Heinz bodies without other evidence of oxidative damage to red blood cells.     

Tritrichomonas foetus: a scanning electron microscopy study of erythrocyte adhesion associated with hemolytic activity

The in vitro hemolytic activity of Tritrichomonas foetus was investigated. The parasite was tested against human erythrocytes of groups A, B, AB, and O, and against erythrocytes of nine adult animals of different species (the rabbit, rat, chicken, cat, dog, swine, horse, bovine, and sheep). The results showed that T. foetus strains (ATCC KV1, K, PAL, 5022, RJ, 90) did not present any hemolytic activity against any human erythrocyte group nor against rabbit, rat, chicken, cat, dog and swine erythrocytes. T. foetus strains, however, lysed horse, bovine, and sheep erythrocytes. No hemolysin released by the parasites could be identified. Hemolysis did not occur with trichomonad culture supernatants, with sonicated extracts of T. foetus, nor with killed organisms. Scanning electron microscopy (SEM) showed that human erythrocytes did not adhere to the trophozoites, in contrast horse erythrocytes adhered to the surface of the parasites and were phagocytosed for up to 90 min. The parasites are able to exert their cytopathic effects through: (a) physical contact established between the two cell surfaces, (b) toxins released from parasites into the interaction media, or (c) the association of both mechanisms. Further studies are necessary to clarify the importance of the hemolytic activity in the biology of T. foetus.     

Mushroom Poisoning in a Dog

The false morel (Gyromitra esculenta), a mushroom responsible for occasional fatalities in man, caused a fatal hemolytic episode in a ten week old dog. The clinical symptoms observed and the gross and histopathological findings, are discussed.