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During the BP Deepwater Horizon (DWH) oil spill in 2010, 319 live oiled sea turtles were rescued and admitted to rehabilitation centers for decontamination and veterinary care. Most turtles were small, surface-pelagic juveniles that were collected from oiled habitat distant from shore. Serial hematology, plasma biochemistry, and blood gas analyses were reviewed to characterize abnormalities relative to observed degree of oiling. Clinicopathological abnormalities upon admission indicated acute, nonspecific metabolic and osmoregulatory derangements that were attributable to a combination of events including stress, exertion, physical exhaustion, and dehydration related to oiling, capture, and transport. Specific toxicological effects reported in other taxa were not observed. Initial point-of-care blood data from one rescue center were evaluated using clinical assessment of physiological status for all turtles of all species with available data for pH, pCO 2 , sodium, and potassium. In addition, a prognostic model that was specifically developed for cold-stunned Kemp's ridley sea turtles Lepidochelys kempii was applied to oiled Kemp's ridley turtles from one center. Thirty-six percent of oiled turtles were identified as physiologically de ranged based on a clinical assessment of their physiological status, and 25% of oiled Kemp's ridley sea turtles exceeded the mortality risk threshold of the prognostic model. These results indicate that the physiological derangements in these animals were relatively severe and clinically relevant. Based on observations during the DWH spill, adverse physiological effects in sea turtles may be an important consequence of stress, exertion, physical exhaustion, and dehydration secondary to oiling, capture, and transport.

Two young adult dogs with gastrointestinal signs were each found to have an intra-abdominal mass based on physical examination and diagnostic imaging. On exploratory laparotomy, small intestinal masses and mesenteric lymphadenopathy were found in both dogs; a liver mass was also found in dog 1. Cytologic and histologic examination of intestinal and liver masses and mesenteric lymph nodes revealed 2 distinct lymphoid cell populations: lymphoblasts and atypical Mott cells. With Romanowsky stains, the atypical Mott cells contained many discrete, clear to pale blue cytoplasmic inclusions consistent with Russell bodies that were positive by immunohistochemistry for IgM and CD79a in both dogs and for IgG in dog 2. The Mott cells and occasional lymphoblasts stained strongly positive with periodic acid-Schiff. Using flow cytometric immunophenotyping in dog 1, 60% of peripheral blood mononuclear cells and 85% of cells in an affected lymph node were positive for CD21, CD79a, IgM, and MCH II, indicative of B-cells. With electron microscopy, disorganized and dilated endoplasmic reticulum was seen in Mott cells in tumors from both dogs. Antigen receptor gene rearrangement analysis of lymph node and intestinal masses indicated a clonal B-cell population. Based on cell morphology, tissue involvement, and evidence for clonal B-cell proliferation, we diagnosed neoplasms involving Mott cells. To the authors' knowledge, this is the second report of Mott cell tumors or, more appropriately, B-cell lymphoma with Mott cell differentiation, in dogs. More complete characterization of this neoplasm requires further investigation of additional cases. This lymphoproliferative disease should be considered as a differential diagnosis for canine gastrointestinal tumors.