Pure white cell aplasia in a dog

Abstract

A 3-year-old Irish Wolfhound was evaluated because of acute onset of lethargy and fever. Severe neutropenia (0/microL; reference interval 2500-11,200/microL) 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.

Presumed primary immune‐mediated neutropenia in 35 dogs: a retrospective study

“…, Perkins et al . , Weiss , Weiss & Henson ). Identification of anti‐neutrophil antibodies might provide a more definitive means of confirming a diagnosis of IMN, although it cannot distinguish between primary and secondary disease (Weiss , Weiss & Henson ).…”

“…, Vargo et al . , Weiss & Henson ). Our study provides clinical, outcome, and relapse data on a cohort of 35 dogs with IMN, obtained from records at multiple institutions and practices.…”

“…, Vargo et al . , Weiss 2007a, 2007b, Weiss & Henson ). Indirect flow cytometry is considered the most sensitive test to detect membrane‐bound IgG and has been validated for use in dogs (Weiss 2007a, 2007b).…”

“…, Vargo et al . , Weiss & Henson , Schnelle & Barger ). Diagnosis of presumed primary IMN is made on the basis of a neutrophil concentration disproportionately low relative to clinical signs, exclusion of other causes of neutropenia, exclusion of secondary IMN and rapid response to immunosuppressive therapy (McManus et al .…”

“…, Vargo et al . , Weiss 2007a, 2007b, Weiss & Henson , Schnelle & Barger ). Neutrophil–antibody complexes trigger opsonisation of neutrophils in peripheral circulation and facilitate their removal by macrophages in the liver, spleen, lymph nodes and bone marrow.…”