Hepatic fungal infection in a young beagle with unrecognised hereditary cobalamin deficiency (Imerslund‐Gräsbeck syndrome)

A 12‐month‐old beagle presented for anorexia, pyrexia and vomiting. The dog had been treated intermittently with antibiotics and corticosteroids for inappetence and lethargy since five months of age. Previous laboratory abnormalities included macrocytosis and neutropenia. At presentation, the dog was lethargic, febrile and thin. Laboratory examination findings included anaemia, a left shift, thrombocytopenia, hypoglycaemia and hyperbilirubinaemia. Multiple, small, hypoechoic, round hepatic lesions were observed on abdominal ultrasound. Cytological examination of hepatic fine needle aspirates revealed a fungal infection and associated pyogranulomatous inflammation. The dog's general condition deteriorated despite supportive measures and treatment with fluconazole, and owners opted for euthanasia before hypocobalaminaemia was identified. Subsequent genomic analysis revealed a CUBN:c.786delC mutation in a homozygous state, confirming hereditary cobalamin malabsorption (Imerslund‐Gräsbeck syndrome). Similar to human infants, dogs with Imerslund‐Gräsbeck syndrome may rarely be presented for infectious diseases, distracting focus from the underlying primary disorder.     

Basset Hound thrombopathia in a 4‐month‐old female Ba‐Shar (Sharp Asset)

A 3‐month‐old female Basset Hound‐Shar Pei mix puppy (Ba‐Shar or Sharp Asset) presented with oral bleeding due to a cracked molar. On physical exam, an aural hematoma was also noted that the owner indicated was chronic. The puppy was hospitalized for over 24 h until the bleeding was brought under control. At 4 months of age, the puppy again presented with oral bleeding due to loss of deciduous teeth and was hospitalized until bleeding was controlled. Coagulation screening tests, platelet numbers, and von Willebrand Factor antigen levels were within reference limits. Based on the presence of platelet‐type bleeding in the face of normal screening test results, samples were submitted for DNA testing for Basset Hound thrombopathia. The puppy tested as affected for the calcium and diacylglycerol regulated guanine nucleotide exchange factor I (CalDAG‐GEFI) mutation causing this disorder. This is the first time thrombopathia has been diagnosed in a “designer” breed.     

True cementomas (cementoblastomas) associated with a nonvital left maxillary second premolar in an 11‐year‐old miniature horse

An 11‐year‐old miniature horse gelding presented for a left maxillary facial swelling and surgical removal of 2 ovoid mineralised masses located near the tooth roots of the left maxillary second and third premolars. Preoperative radiographs were performed to triangulate the location of the calcified masses for removal, and an oral examination revealed that the left maxillary second premolar was nonvital with multiple feed‐packed pulp exposures. Both the radiographs and oral examination indicated that the mineralised masses were associated with the nonvital second premolar. Therefore, the tooth was extracted intraorally, and the masses were removed via a maxillary trephine dorsal to the extracted tooth. Both masses were submitted for histopathology, which diagnosed the masses as true cementomas (cementoblastomas) with adenomatous hyperplasia of the surrounding nasal glandular tissue.