A dog with myelodysplastic syndrome: chronic myelomonocytic leukemia

An eleven-year-old female pug was referred to Yamaguchi University Animal Hospital for evaluation of anemia and thrombocytopenia. The cytological examination of the peripheral blood showed some giant monocytic lineage blast cells. A few granulocytes and platelets had dysplastic features. On day 7, in addition to increasing the monocytic lineage cells, the dysplastic features of the blood had also increased compared to the initial examination. We performed bone marrow aspiration upon her death. The bone marrow revealed dysplastic features in all three hematopoietic cell lines, and an increase in the monocytic cell line. Based on the features of the bone marrow and the peripheral blood, this case was confirmed to be myelodysplastic syndrome--Chronic myelomonocytic leukaemia (MDS-CMML).     

A severe hepatic disorder with myelodysplastic syndrome, treated with cytarabine ocfosfate, in a dog

An 8-year-old female Shih Tzu was presented with weight loss and vomiting. Alanine aminotransferase was high and abdominal radiographs revealed hepato- and splenomegaly. Mild anaemia, neutrophilia with left shift, eosinophilia, a thrombocytosis with dysplastic features of eosinophils and platelets, were detected. The animal was initially considered to have hepatitis and was treated accordingly, but clinical signs persisted. Histological examination of liver biopsy samples showed disruption of the hepatic lobule, with extensive infiltration by haemopoietic cells. Further investigation of the bone marrow suggested a diagnosis of myelodysplastic syndrome. The animal was treated with cytarabine ocfosfate, a prodrug of cytosine arabinoside, and appeared to recover.     

Malabsorption syndrome in the dog: a study of thirty-eight cases

The clinical findings and results of an investigational procedure on thirty-eight confirmed cases of canine malabsorption are described in detail. Exocrine pancreatic insufficiency was frequently responsible for the syndrome, but on occasions small intestinal disorders, liver disease and alactasia were diagnosed. Possible methods of treatment are suggested and their value in the present series of cases discussed briefly. Résumé. Les résultats cliniques et les résultats d'un procédé d'investigation concernant trente-huit cas confirmés de malabsorption canine, sont décrits en détail. L'insuffisance sécrétoire du pancréas en exocrine était fréquemment la cause responsable du syndrome, mais en certaines occasions, on a diagnostiqué de légers troubles intestinaux, une maladie de foie et une alactasie. On suggère des méthodes possibles de traitement et leur valeur dans la présente série des cas est brièvement discutée. Zusammenfassung. Die Abhandlung gibt eine eingehende Beschreibung der klinischen Befunde und die Ergebnisse einer Forschungsmethode an 38 nachgewiesenen Fällen von Malabsorption bei Hunden. Exokrine Pankreasinsuffizienz war dabei häufig für die Entstehung des Syndroms verantwortlich; jedoch wurden in einigen Fällen auch kleine Darmstörungen, Lebererkrankungen und Alaktasie diagnostiziert. Auf einige mögliche Behandlungsmethoden wird hingewiesen und deren Wirksamkeit im Rahmen der vorliegenden Serie wird kurz besprochen.     

Nephrotic syndrome in a dog

The occurrence of the nephrotic syndrome in a dog is reported. The outstanding clinical feature was oedema; profuse proteinuria and hypo-proteinaemia were also observed. Steroid therapy, use of a high protein diet and administration of diuretics failed to halt the course of the disease. The renal lesions were morphologically similar to those of membranous glomerulonephritis in man.
Résumé. Les auteurs décrivent un cas de syndrome néphrotique chez un chien; le signe le plus important était l'oedème, et on a également noté une albuminurie considérable et une hypo-protéinémie. Le traitement par les stéroïdes et les diurétiques ainsi qu'un régime riche en protéines n'ont pas empêché la progression de la maladie. Les lésions morphologiques du rein étaient semblables à celles que l'on observe dans la glomérulonéphrite membraneuse de l'homme.
Zusammenfassung. Es wird über das Auftreten des nephrotischen Syndroms bei einem Hund berichtet. Das auffällige klinische Merkmal war Ödem; es wurden auch profuse Proteinurie und Hypoproteinaemie beobachtet. Steroidtherapie, die Verabreichung proteinreichen Futters und die Anwendung von Diuretica konnten den Verlauf der Krankheit nicht beeinflussen. Die ren-alen Läsionen waren morphologisch ähnlich denen bei membranöser Glomerulonephritis beim Menschen.     

Haemolytic-uraemic syndrome in a dog

An 11-year-old female German Shepherd dog presented with lethargy and anorexia, which progressed to haemorrhagic vomiting, diarrhoea and seizures. Serum biochemistry and haematology results showed azotaemia and mild thrombocytopaenia. Euthanasia was elected and the dog was submitted for necropsy examination. There were widespread serosal and mucosal petechial and ecchymotic haemorrhages within the abdomen, with ascites and multiple renal infarcts. The renal infarcts were associated with fibrinoid necrosis and thrombosis of inter-lobular arteries and arterioles. These arterial lesions and clinical signs are consistent with haemolytic-uraemic syndrome, which has not previously been reported in dogs in Europe.     

Hemolytic-uremic syndrome in a dog

A 3-year-old, spayed, female Boxer was presented because of acute onset of anorexia, vomiting, and hemorrhagic diarrhea. Microangiopathic hemolytic anemia with intravascular hemolysis, thrombocytopenia, and acute renal failure were detected. The dog was treated with fluids, antiemetics, antibiotics, and diuretics. Despite supportive therapy, the dog's condition worsened, and the owners elected euthanasia. Necropsy revealed disseminated petechiae on the parietal peritoneum and serosal surfaces of the intestinal tract. The histologic lesions were consistent with severe arteritis and microvascular thrombosis involving only the renal and intestinal arterioles. The final diagnosis was hemolytic-uremic syndrome (HUS), a rarely described disorder in dogs. The clinical presentation of primarily gastrointestinal clinical signs was similar to that of typical or diarrhea-associated HUS (D+ HUS) in humans (mainly children), which is caused by gastrointestinal proliferation of verocytotoxin-producing Escherichia coli. Bacterial toxins can be adsorbed and cause endothelial injury, activation of hemostasis, and thrombosis, with lesions confined primarily to the kidneys. Although rare, HUS should be considered in the differential diagnosis of dogs with microangiopathic hemolytic anemia.     

Malignant hyperthermia in a dog: case report and review of the syndrome

Malignant hyperthermia occurred in an adult Greyhound 24 hours after narcotic anesthesia and surgery. Stress was considered the most likely cause. Treatment with dantrolene, in conjunction with cooling techniques and other symptomatic and supportive therapy, was successful.     

A case of hemophagocytic syndrome progressing into large granular lymphoma in a dog

A 12‐year‐old castrated male mixed breed dog was presented with anorexia, lethargy, intermittent vomiting, diarrhea, and weight loss. Clinicopathologic and imaging abnormalities included pancytopenia, icterus, and splenomegaly with multiple minute hypoechogenic nodules. Bone marrow (BM) smears revealed 2.5% hemophagocytic macrophages. In addition, an increased number of small to intermediate lymphocytes (16.3%) and plasma cells (3.2%) were recognized in the BM smears. More than 80% of the lymphocytes contained multiple small intracytoplasmic magenta granules. Histopathologic findings of the spleen revealed hemophagocytosis. Large granular lymphocytes (LGLs) were not found on the liver cytology or splenic histopathology at this time. PCR for antigen receptor rearrangement (PARR) analysis showed a clonal reaction in the T‐cell receptor ? (TCR?) gene in the BM sample. The dog was diagnosed with hemophagocytic syndrome (HPS). The dog was maintained in good condition with immunosuppressive therapy. However, the dog developed hepatic LGL lymphoma 7 months later. At this time, PARR analysis showed a clonal TCR? gene rearrangement in the hepatic LGL lymphoma samples. The BM and liver sample clonal rearrangements showed 100% homology, indicating that the small to intermediate granular lymphocytes in the BM at the HPS stage had progressed to hepatic LGL lymphoma. To our knowledge, this is the first report of canine secondary HPS caused by the occurrence of a BM LGL lymphoma clone that progressed to hepatic LGL lymphoma.     

Imerslund-Grasbeck syndrome in a cross-breed dog

Imerslund-Gräsbeck syndrome is an autosomal recessive disease reported only in certain pure-breed dogs. An 18-month-old, male neutered beagle cross-breed was presented for evaluation of severe lethargy, progressive weakness and anorexia. Main clinicopathological findings included low body condition score (2.5/9), severe muscle atrophy, several neurological abnormalities, mild normochromic, normocytic, non-regenerative anaemia, severe hypocobalaminemia and mild proteinuria. Extensive diagnostic tests ruled out most of differential diagnoses for the aforementioned clinicopathological abnormalities and genetic evaluation showed that the dog was heterozygous for two previously described mutations affecting the CUBN gene, the beagle and the border collie variants. The dog showed an excellent clinical response to oral cobalamin supplementation with no relapse after 4 months. In conclusion, this case creates awareness that Imerslund-Gräsbeck syndrome should be considered even in mixed-breed dogs with compatible clinical signs and that two different pathogenic CUBN mutations in compound heterozygosity can lead to a typical Imerslund-Gräsbeck syndrome phenotype.     

Limy bile syndrome in a dog

A 11-year-old spayed female golden retriever was examined because of lethargy, anorexia, vomiting and abdominal pain. Plain abdominal radiography showed a uniform radiopacity of the gallbladder. Ultrasonography demonstrated hyperechoic material in the gallbladder lumen associated with an acoustic shadow and findings consistent with acute pancreatitis. Fine-needle aspiration of the bile revealed bacterial cholecystitis. Following cholecystectomy, it was apparent that the gallbladder was filled with a semi-solid, pasty-like greenish-brown material composed of 80% calcium carbonate, consistent with a diagnosis of ‘limy bile’. After surgery and medical treatment, the dog's condition improved. Two months after discharge, the dog had fully recovered a good appetite and no relapse has been observed after 11 months of follow-up. To our knowledge, this is the first report of limy bile syndrome in a dog.     

A hematological study on thirteen cats with myelodysplastic syndrome

Hematological abnormalities were investigated in 13 cats with myelodysplastic syndrome (MDS). Examination of the peripheral blood samples from the 13 cats revealed anemia in 11 cats, leukopenia in 9 cats, and thrombocytopenia in 9 cats. Four cats had pancytopenia (30.8%) and 9 cats had bicytopenia (69.2%). Dysplastic changes of erythrocytes, neutrophils, and platelets in the peripheral blood were found in 5, 10 and 8 cats, respectively. Bone marrow examination of the 13 cats revealed that ratios of blast cells to all nucleated cells (ANC) ranged from 0 to 20%. Ratios of erythroid progenitor cells to ANC were more than 50% in 3 cats and less than 50% in 10 cats. Eosinophils accounted for more than 5% of non-erythroid cells in 10 cats. Dysplastic changes in the granurocytic, erythrocytic, and megakaryocytic cells in the bone marrow were found in 11, 7 and 5 cats, respectively. Dysplastic changes in these cats included giant neutrophils, ring-nucleated neutrophils, binuclear myelocytes, hypersegmented and hyposegmented neutrophils, megaloblastoid erythroblasts, multinucleated erythroblasts, micromegakaryocytes, and segmented multinucleated megakaryocytes. Virological examination indicated the presence of feline leukemia virus antigen in the peripheral blood from all of the 13 cats with MDS. The peripheral blood cytopenias and dysplastic changes in each blood cell lineage in the bone marrow were shown to be important for the diagnosis of MDS in cats.     

Long-term survival of a dog with Alexander disease

A 1-year- and 11-month-old spayed female toy poodle had showed progressive ataxia and paresis in the hindlimbs since 11 months old. Magnetic resonance imaging revealed high signal intensity on T2-weighted and fluid-attenuated inversion recovery images at the thoracic and lumbar spinal cord. The dog’s neurological condition slowly deteriorated and flaccid tetraparesis was exhibited. At 4 years and 11 months old, the dog died of respiratory failure. On postmortem examination, eosinophilic corkscrew bundles (Rosenthal fibers) were observed mainly in the thoracic and lumbar spinal cord. Histological features were comparable to previously reported cases with Alexander disease. This is a first case report to describe the clinical course and long-term prognosis of a dog with Alexander disease.