Pure white cell aplasia in a dog

A 3‐year‐old Irish Wolfhound was evaluated because of acute onset of lethargy and fever. Severe neutropenia (0/μL; reference interval 2500–11,200/μL) was associated with granulocyte aplasia in the bone marrow (myeloid:erythroid ratio, 0.009:1). Antineutrophil antibodies were assessed by an indirect immunofluorescence assay using flow cytometry. When normal canine leukocytes were incubated with the patient's serum and anti‐IgG, a marked shift was observed in the forward‐angle light scatter of the neutrophil population, and the monocyte cluster disappeared, possibly the result of fragmentation or lysis. Both neutrophil fluorescence intensity (309 ± 11 median channel units (MCU), control values 107–152 MCU) and the percentage of neutrophils with increased fluorescence intensity (61 ± 5%, control values 3.8–13.7%) were increased in the patient's serum, consistent with the presence of antineutrophil antibodies. Repeated episodes of neutropenia occurred while treatment with steroidal and nonsteroidal immunosuppressive therapy was initiated and modified. The neutrophil count eventually stabilized in the low‐normal range, and the dog was maintained for the next 15 months on prednisone (0.4 mg/kg PO q 48 h) and azathioprine (2 mg/kg daily). During this period, the dog developed immune‐mediated hemolytic anemia and thrombocytopenia, decubital ulcers, nasal aspergillosis, and eventually, multi‐organ septicemia, which led to euthanasia on day 784. A diagnosis of pure white cell aplasia was made in this dog, based on the many similarities to human patients with pure white cell aplasia, including severe neutropenia with selective granulocyte aplasia, serum antineutrophil antibodies, remission dependent on treatment with immunosuppressive therapy, and recurrent bacterial infections.