Reference interval for thrombin-antithrombin complex (TAT) level was determined using an in-house TAT measurement device, and its validity for diagnosis of disseminated intravascular coagulation (DIC) was evaluated in dogs. One hundred and two clinically healthy dogs and 247 diseased dogs with conditions that potentially caused DIC were recruited in the study. Six diagnostic testing for DIC were evaluated in diseased dogs and the diseased dogs were categorized into five groups depending on abnormal findings. TAT was measured in all study animals and between-group differences were evaluated. TAT level was positively associated with severity of DIC. There were no significant differences in TAT levels among clinically healthy dogs, diseased dogs without any abnormal finding and diseased dogs with one abnormal finding in the DIC diagnostic testing. TAT levels in groups with two or more abnormal findings were significantly higher than clinically healthy dogs. Reference interval of TAT level for clinically healthy dogs was ≤ 0.25 ng/ml. Validity of using TAT for early detection of DIC was evaluated. In-house TAT measurement was suggested to be a clinically relevant and useful tool for early detection of canine DIC.

To clarify the prevalence of canine intracranial tumors in Japan, a retrospective study was performed using data on 186 canine intracranial tumors. Of 186 cases, 159 cases (85.5%) were primary and 27 cases (14.5%) were secondary intracranial tumors. Among primary intracranial tumors, meningioma (50.9%) was the most common, followed by glial tumors (21.4%) and primary intracranial histiocytic sarcoma (12.6%). These 3 tumors were most frequently found in middle-aged to elderly dogs without any sex predilection. Regarding glial tumors, the incidence of oligodendroglial tumors (79.4%) was higher than that of astrocytic tumors (17.6%). A significant breed predisposition (P<0.05) was observed for meningioma in Rough Collie, Golden Retriever, Miniature Schnauzer, and Scottish Terrier; for glial tumors in Bouvier de Flandres, French Bulldog, Newfoundland, Bulldog, and Boxer; for primary intracranial histiocytic sarcoma in Pembroke Welsh Corgi, Siberian Husky, and Miniature Schnauzer. The high incidence of oligodendroglial tumors in dogs and the breed predisposition for primary intracranial histiocytic sarcoma in Pembroke Welsh Corgi have not been reported in previous epidemiological studies on canine tumors. Since the incidence of intracranial tumors was vary among dog breeds, the present results demonstrate the uniqueness of the canine breed population in Japan.KEY WORDS: brain tumor, dog, epidemiology, histopathology, intracranial tumor Intracranial tumors include a large group of different benign and malignant tumors arising from the brain parenchyma and its surrounding structures [11]. These tumors are an important cause of morbidity and mortality in companion animals, particularly dogs. The increased use of computed tomography (CT) and magnetic resonance imaging (MRI), along with pathological examinations of biopsy samples, have increased the accuracy of antemortem diagnoses of canine intracranial tumors in recent years. However, the epidemiology of these tumors in dogs remains unclear, and few studies have investigated the incidence of canine intracranial tumors in the United States and United Kingdom [5,6,[21][22][23]. Previous reports revealed that the incidence of canine intracranial tumors varied between 0.01% [21] and 4.5% [8,23].According to the World Health Organization (WHO) classification of tumors in domestic animals, intracranial tumors are divided into neuroepithelial, meningothelial, hematopoietic, and other tumors based on the anatomical location and tissue type [11]. Among these tumors, meningioma is the most common primary intracranial tumor in dogs, followed by glial tumors, including astrocytoma, oligodendroglioma, and oligoastrocytoma [8,22]. Certain breeds are predisposed to specific types of intracranial tumors: meningioma in dolichocephalic breeds, such as German Shepherd dog and Rough Collie, and glial tumors in brachycephalic breeds, including Boxer and Boston Terrier [4,8,17,23].There are large differences in the popularity of dog breeds and breeding systems among countries, which may poten...

Case summary A 7-year-old mixed-breed cat presented with subcutaneous oedema and erythema extending from the right axilla to the abdomen. Fine-needle aspiration of the subcutaneous lesion revealed large, atypical, round cells. A clonality analysis for the T-cell receptor-gamma and immunoglobulin heavy chain genes showed no clonal rearrangement. The presumed diagnosis was lymphoma and the cat was treated with prednisolone and L-asparaginase but died 78 days after initial treatment. At necropsy, an oedematous subcutaneous mass in the right axilla, hepatomegaly, splenomegaly and lymphadenopathy of the mediastinum and left axilla were observed. Histopathological examination revealed diffuse infiltration of large atypical round cells in the subcutaneous mass, liver, spleen, lymph nodes and bone marrow. Immunohistochemically, the tumour cells were strongly positive for CD56, and negative for CD3, CD20, CD79a, CD57, granzyme B and perforin. Based on these findings, the cat was diagnosed with blastic natural killer (NK) cell lymphoma/leukaemia. Relevance and novel information Here, we report the pathological and clinical findings of NK cell lymphoma/leukaemia in a cat. The antibody for human CD56, a diagnostic marker for human NK cell neoplasms, showed cross-reactivity with feline CD56 by immunohistochemistry and Western blotting analysis. The antibody could be a useful diagnostic marker for feline NK cell neoplasms.

Histiocytic proliferative diseases are rare in cats, and their pathogenesis is poorly understood. In the present study, 25 cases of histiocytic sarcoma (HS) and 6 of feline progressive histiocytosis (FPH) were examined, and survival times were recorded in 19 cases. The immunophenotypes of tumor cells in these cases as well as of nonneoplastic feline histiocytes were characterized using formalin-fixed, paraffin-embedded tissues. An FPH cell line (AS-FPH01) and xenotransplant mouse model of FPH were also established. The median survival time of HS (150 days) was significantly shorter than that of FPH (470 days). Immunohistochemically, nonneoplastic histiocytes were immunopositive for various combinations of Iba-1, HLA-DR, E-cadherin, CD204, CD163, CD208, and MAC387. By immunohistochemistry, dermal interstitial dendritic cells (iDCs) and macrophages were CD204+/E-cadherin−, while epidermal Langerhans cells (LCs) were CD204−/E-cadherin+. Neoplastic cells of 4 FPH and 18 HS were CD204+/E-cadherin− (iDC/macrophage immunophenotype), while 2 FPH and 2 HS were CD204−/E-cadherin+ (LC immunophenotype), and 5 HS were CD204+/E-cadherin+ (LC-like cell immunophenotype). Furthermore, immunohistochemical and western blot analyses of AS-FPH01 cells derived from E-cadherin-negative FPH revealed that cultured cells were immunopositive for both CD204 and E-cadherin in vitro and in vivo. These results indicate that the neoplastic cells of feline HS and FPH were variably positive for iDC/macrophage and LC markers, and their immunophenotype changed in different microenvironments. The novel cell line established in the present study may serve as an experimental model of FPH that will enable further molecular and therapeutic studies on this disease.

The present study describes the association between inflammatory cell types and feline infectious peritonitis virus (FIPV) antigen in the brain of 4 cats diagnosed as feline infectious peritonitis (FIP). Immunohistochemically, FIPV antigens were detected in the inflammatory foci of the leptomeninges, choroid plexus and ventricles in 3 of the 4 cats. In 3 cases, inflammatory foci mainly consisted of CD204- and Iba1-positive macrophages, and the FIPV antigens were found in the macrophages. In the other case which was negative for FIPV antigen, severe inflammation predominantly consisting of CD20-positive B lymphocytes was observed in the leptomeninges and subventricles, accompanied with diffuse proliferation of gemistocytic astrocytes. The difference in histopathology may reflect the inflammatory process or the strain variation of FIP virus.