A 23-year-old castrated male California sea lion (Z. californianus) presented with acute anorexia. Blood work revealed a leukocytosis (19900) with a profound lymphocytosis (absolute lymphocytes = 19502) and neutropenia (absolute neutrophils = 199). All lymphocytes observed on the peripheral blood smear were mature in appearance. RBC indices were low normal and platelet counts were adequate. This presentation was suggestive of a lymphoproliferative disorder such as chronic lymphocytic leukemia (CLL) or small cell lymphocytic leukemia (SLL) with possible neoplastic suppression of the other cell lines in the bone marrow.
While lymphoid neoplastic disorders are relatively common in mammals, they have rarely been described in California sea lions. T and B cell lymphoma have been reported and in both cases the cell types were described as immature or lymphoblastic.1,2 In the present case a small B cell leukemia was confirmed using cytology and immunocytochemistry. Ninety-three percent of the nucleated cells present were identified as small lymphocytes that were positive for Pax5. A bone marrow biopsy was obtained from the left femoral head and microscopic interpretation indicated panhypoplasia. No normal marrow constituents were noted. Adipocytes were the primary cell population and a focal accumulation of small lymphocytes was seen. This pattern was most suggestive for a lymphocytic neoplasm.
A 92% reduction in the lymphocyte count was observed 12 days after starting a 0.6 mg/kg daily dose of prednisone. Although his lymphocyte count was drastically reduced, the neutropenia persisted and he developed a progressively severe anemia. He died 6 weeks after the initial diagnosis.
Histopathology revealed changes in the bone marrow, spleen and lymph nodes that were compatible with CLL with a significant population of neoplastic small lymphocytes in the spleen and lymph nodes. Immunohistochemistry confirmed these small lymphocytes were Pax5+/CD3- at both sites. Bone marrow from flat bones (sternum and rib) was up to 99% composed of sheets of neoplastic lymphoid cells. In contrast, a section of bone marrow from the proximal femur was composed primarily of mature adipocytes with a few small aggregates and widely scattered individual neoplastic lymphoid cells. These findings suggest that in an animal of his age obtaining a marrow biopsy from the sternum or iliac crest may have provided a better diagnostic sample.
Three blood samples were obtained from this animal several months apart within 5–19 months before diagnosis. Lymphocytosis was not observed in any of these samples indicating a short timeline in this case, a fact inconsistent with the chronic nature of CLL seen in most other species. This may suggest that either CLL progresses more rapidly in California sea lions or perhaps he had another type of B cell neoplasia that is characterized by small cells, but is very aggressive.
The authors would like to acknowledge and thank the following: Gennifer Brookshire and the Sea Life Park Hawaii Animal Care staff for their dedicated care and training with this animal, Dr. Ann Avery and Dr. Douglas Thamm (Colorado State University), Dr. Jenny Meegan (National Marine Mammal Foundation), Dr. Shawn Johnson (The Marine Mammal Center) and Dr. Judy St. Leger (Sea World) for consulting on this case.
* Presenting author
1. Colegrove KM, Wellehan JF, Rivera R, Moore PF, Gulland FM, Lowenstine LJ, Nordhousen RW, Nollens HH. Polyomavirus infection in a free-ranging California sea lion (Zalophus californianus) with intestinal T-cell lymphoma. J Vet Diagn Invest. 2010;22:628–632.
2. Venn-Watson S, Benham C, Gulland FM, Smith CR, St. Leger J, Yochem P, Nollens HH, Blas-Machado U, Saliki J, Colegrove KM, Wellahan JF, Rivera R. Clinical relevance of novel Otarine herpesvirus-3 in California sea lions (Zalophus californianus): lymphoma, esophageal ulcers, and strandings. Vet Res. 2012;43:85.