COMPANION ANIMALS
Myelodysplastic syndrome progressing to acute myelogenous leukemia in a dog
Felipe Reggeti, Emily Brouwer
A 6-y-old Shetland Sheepdog was presented to the OVC with history of pancytopenia (Table 1). There were no atypical cells noted in the blood smear. SNAP 4Dx and direct Coomb’s were negative. Coagulation profile was unremarkable. Considering multi-lineage unexplained cytopenias, bone marrow (BM) examination was performed.
BM smears showed predominance of erythroid cells (Fig. 1), with a markedly decreased granulocytic-to-erythroid ratio (1:10). There was an increased proportion of rubriblasts, whereas metarubricytes and polychromatophils were observed in very low numbers. Binucleate rubricytes, mitoses, and irregular nuclear shapes were present. A BM core biopsy was > 95% cellular (Fig. 1, inset). These findings indicated erythroid hyperplasia, dysplasia and ineffective erythropoiesis (dyserythropoiesis), compatible with myelodysplastic syndrome (refractory anemia with excess blasts) or precursor-targeted immune-mediated anemia.
The patient improved after 2 wk on cyclosporine and prednisone (Hct 0.17 L/L; platelets 113 x 109/L; neutrophils 11.3 x 109/L; reticulocytes 306 x 109/L). Unfortunately, 2 mo after initial presentation, the dog became very sick, with severe non-regenerative anemia (Hct 0.10 L/L), leukopenia, and thrombocytopenia. Given progressive deterioration and inconsistent response to treatment, euthanasia was elected.
On postmortem examination, there was hepatomegaly, splenomegaly, and discolored red bone marrow in humeri and femurs. Microscopically, 80% of the cells in the BM were large myeloblasts with 44 mitoses/10 hpf and myeloid-to-erythroid ratio 8:1; ~ 90% of the splenic parenchyma was effaced by neoplastic myeloblasts (Fig. 2), and similar cells were noted within the hepatic sinusoids (Fig. 3). Histopathology was diagnostic for acute myeloid leukemia.
Myelodysplastic syndrome progressed in this dog to acute myeloid leukemia. In humans, myelodysplastic syndrome consists of a heterogeneous group of myeloid neoplasms characterized by cytopenias, ineffective hematopoiesis, morphologic abnormalities, and genetic instability leading to acute myeloid leukemia in ~ 30% of patients. AHL
Table 1. Hemogram of a Shetland Sheepdog with myelodysplastic syndrome, on presentation.
Figure 1. Very cellular marrow smear, with predominance of erythroid cells. Inset: Very cellular bone marrow core biopsy.
Figure 2. Splenic parenchyma effaced by neoplastic myeloblasts.
Figure 3. Hepatic sinusoids contain neoplastic myeloblasts.
Baylisascaris procyonis encephalitis in a dog
Murray Hazlett, Hugh Cai
Baylisascaris procyonis - the raccoon round worm - is found very commonly in raccoons in southern Ontario. The larval form of B. procyonis is well recognized as a cause of visceral larval migrans in humans and dogs. A recent submission of a 14-wk-old puppy from the metropolitan Toronto area was diagnosed with encephalitis as a result of migration of B. procyonis larvae1 (Fig 1). The dog had suffered from a 1-wk period of tremors and hypermetria followed by increasing neurologic deficit and uncontrolled paddling, and had eosinophilia. Diagnosis was confirmed by the morphology of the parasite as well as PCR testing (which is now an available test at the AHL. Baylisascaris procyonis - PCR. Code = bpropcr).
We suspect that visceral larval migrans caused by this parasite is underdiagnosed, with some cases being non-fatal, depending on the number of larvae involved. It is important to realize that eggs are found in large numbers in areas where raccoons defecate (“raccoon latrines”) and can survive for years in the environment2. Most human cases are in young children due to play habits and poor hand/mouth hygiene. Both adult and juvenile raccoons can shed eggs, in one study shedding up to 23,600 and 228,000 eggs per gram of feces respectively.3 AHL
References
1. Hazlett M, et al. Neurologic Baylisascaris procyonis infection in a young dog. Can Vet J 2018;59:1325-1328.
2. Kazacos KR. Baylisascaris procyonis and related species. In: Samuel WM,et al., eds. Parasitic Diseases of Wild Mammals. 2nd ed. Ames, Iowa: Iowa State Univ Pr, 2001:301–341.
3. Snyder DE, Fiktzgerald PR. Contaminative potential, egg prevalence, and intensity of Baylisascaris procyonis-infected raccoons (Procyon lotor) from Illinois, with a comparison to worm intensity. Proc Helminthol Soc Wash 1987;54:141–145.
Figure 1. Baylisascaris procyonis larvae (arrows) migrating in cerebral cortical white matter. H&E.