Veterinary Pathology最新文献

Amyloidosis is a group of diseases in which proteins become amyloid, an insoluble fibrillar aggregate, resulting in organ dysfunction. Amyloid deposition has been reported in various animal species. To diagnose and understand the pathogenesis of amyloidosis, it is important to identify the amyloid precursor protein involved in each disease. Although 42 amyloid precursor proteins have been reported in humans, little is known about amyloidosis in animals, except for a few well-described amyloid proteins, including amyloid A (AA), amyloid light chain (AL), amyloid β (Aβ), and islet amyloid polypeptide-derived amyloid. Recently, several types of novel amyloidosis have been identified in animals using immunohistochemistry and mass spectrometry-based proteomic analysis. Certain species are predisposed to specific types of amyloidosis, suggesting a genetic background for its pathogenesis. Age-related amyloidosis has also emerged due to the increased longevity of captive animals. In addition, experimental studies have shown that some amyloids may be transmissible. Accurate diagnosis and understanding of animal amyloidosis are necessary for appropriate therapeutic intervention and comparative pathological studies. This review provides an updated classification of animal amyloidosis, including associated protein misfolding disorders of the central nervous system, and the current understanding of their pathogenesis. Pathologic features are presented together with state-of-the-art diagnostic methods that can be applied for routine diagnosis and identification of novel amyloid proteins in animals.

Pigment-containing and light-reflecting cell neoplasms, generically termed chromatophoromas, affect fish, reptiles, and amphibians. Chromatophoromas of light-reflecting cells are named iridophoromas. In this study, we aimed to describe the gross, histologic, and ultrastructural findings of 71 cases of iridophoromas in farmed Siamese fighting fish (Betta splendens). Macroscopically, iridophoromas appeared as whitish, gray, or black friable masses or plaques in the fin, trunk/tail, or head of the fish. Forty-five tumors (63%) were malignant and invaded the adjacent skeletal muscle and/or metastasized to other organs, whereas 26 (37%) tumors were restricted only to the skin, but due to the cytologic similarity to the malignant counterpart, we were not able to classify them as malignant or benign. Sixty-five (91%) tumors were classified as iridophoromas, whereas 6 (8%) were diagnosed as mixed chromatophoromas. Despite immunolabeling for PNL-2, melan A, or S-100 failing to demonstrate antigen expression, ultrastructural analysis identified light-reflecting neoplastic cells, unequivocally confirming iridophoromas as the predominant tumor. The high incidence of iridophoromas in Siamese fighting fish from the same breeding facility, coupled with a higher occurrence in royal blue and fancy copper color patterns and in young males, suggests a potential genetic/hereditary factor in the tumorigenesis of these neoplasms.

Insulinoma-associated protein 1 (INSM1), a recently identified neuroendocrine marker, is a transcriptional regulator with highly conserved INSM1 homologues in various species. This study investigated the immunohistochemical reactivity of the INSM1 antibody in 20 normal canine neuroendocrine tissues from various anatomical locations, 87 hyperplastic or neoplastic tissues of neuroendocrine origin, and 62 non-neuroendocrine neoplasms and compared the results with those of chromogranin A and synaptophysin in neuroendocrine neoplasms. Western blot was performed on fresh canine pituitary glands and canine parathyroid glands to confirm the specificity of the anti-INSM1 antibody. The results showed that the anti-INSM1 antibody could detect nuclear expression in normal canine neuroendocrine tissues, except for the parathyroid glands. INSM1 was detectable in 79/87 (91%) of the hyperplastic and neoplastic neuroendocrine lesions, but all parathyroid carcinomas and parathyroid adenomas (three samples each) were negative for INSM1. In contrast, INSM1 was detected in only one of 62 (2%) non-neuroendocrine neoplasms. The overall percentage of neuroendocrine neoplasms that immunolabeled positively for all three markers was 89%. In addition, the nuclear expression of INSM1 was easier to interpret than that of chromogranin A or synaptophysin. These findings confirm that INSM1 is a useful immunohistochemical marker for diagnosing canine neuroendocrine neoplasms, except for parathyroid neoplasms, and should be considered as part of immunohistochemistry panels to improve diagnostic capability.

This report describes subacute and chronic toxic hepatopathy in cattle due to Crotalaria spectabilis poisoning. A total of 200 male Nellore cattle were introduced into a paddock contaminated with C. spectabilis. After spending 20 days grazing in this area, 6 cattle became ill and died. The remaining 194 cattle were moved to non-contaminated pasture in a nearby farm and, 45 days after arrival, 15 cattle became ill and died. Three affected cattle were necropsied. The main clinical changes consisted of anorexia, isolation from the herd, weight loss, jaundice, recumbency, and death. The primary lesions were observed in the liver. Subacutely poisoned cattle had slightly firm livers with an accentuated lobular pattern. Histologically, hepatocyte loss with dilated sinusoids, hepatomegalocytosis, and fibrosis was observed. Cattle with chronic disease had small, pale, firm livers with an irregular hepatic capsular surface. Microscopic changes included hepatocyte loss, hepatomegalocytosis, bile duct proliferation, and fibrosis.

Feline eosinophilic sclerosing fibroplasia (FESF) is a proliferative, inflammatory disease of the gastrointestinal tract and other sites, uncommonly diagnosed in the cat. This entity of uncertain etiology typically presents as a progressive mass lesion, mimicking a neoplastic process. In this case series, we present 17 cases of FESF associated with intralesional lymphoma. Histologic and immunohistochemical characterization of this unique lymphoma revealed that the neoplastic lymphocytes were immunopositive for CD56 and/ or CD3, suggesting a natural killer cell, natural killer T-cell, or T-cell origin. This case series represents the first description of this lymphoma subtype, for which the term eosinophilic sclerosing lymphoma is proposed.

Sarcoma samples from 33 dogs, 25 subcutaneous and 8 articular, were submitted for cytokeratin immunohistochemistry. Eight of the 25 subcutaneous sarcomas (32%) expressed cytokeratin in 1% to 50% of the neoplastic cells. Of the 7 articular sarcomas evaluated, 1 (14%) expressed cytokeratin in 10% of neoplastic cells. The Kaplan-Meier survival analysis showed that the mean overall survival of dogs with subcutaneous sarcomas (28.1 months [confidence interval [CI]:17.8, 38.4]) did not significantly differ from those with articular sarcomas (24.8 months [CI = 0.5, 29.0]). Overall survival of dogs with sarcomas (both locations combined) immunoreactive for cytokeratin (31.2 months [CI = 17.8, 44.6]) did not differ from those not immunoreactive for cytokeratin (22.0 months [CI = 8.4, 35.6]). Therefore, cytokeratin expression does not indicate synovial origin (P = .64) and neither sarcoma location (P = .76) nor cytokeratin expression (P = .53) affects patient overall survival in this small study. The use of cytokeratin immunohistochemistry is not helpful to determine synovial origin of sarcomas in dogs.

Increased proliferation is a driver of tumorigenesis, and quantification of mitotic activity is a standard task for prognostication. This systematic review is an analysis of all available references on mitotic activity in feline tumors to provide an overview of the assessment methods and prognostic value. A systematic literature search in PubMed and Scopus and a nonsystematic search in Google Scholar were conducted. All articles on feline tumors that correlated mitotic activity with patient outcome were identified. Data analysis revealed that of the 42 eligible articles, mitotic count (MC, mitotic figures/tumor area) was evaluated in 39 studies, and mitotic index (MI, mitotic figures/tumor cells) in 3 studies. The risk of bias was considered high for most studies (26/42, 62%) based on small study populations, insufficient details of the MC/MI methods, and lack of statistical measures for diagnostic accuracy or effect on outcome. The MC/MI methods varied between studies. A significant association of MC with survival was determined in 20 of 28 (71%) studies (10 studies evaluated other outcome metrics or provided individual patient data), while 1 study found an inverse effect. Three tumor types had at least 4 studies, and a prognostic association with survival was found in 5 of 6 studies on mast cell tumors, 5 of 5 on mammary tumors, and 3 of 4 on soft-tissue sarcomas. MI was shown to correlate with survival for mammary tumors by 2 research groups; however, comparisons to MC were not conducted. Further studies with standardized mitotic activity methods and appropriate statistical analysis for discriminant ability of patient outcome are needed to infer the prognostic value of MC and MI.