The animal was a 3-year old male koi carp (Cyprinus carpio), 28-cm long. The first two years (2006-2008) the animal was kept in a farm with natural reproduction in a backyard pond in Italy. Afterwards the koi was kept for one year with other koi in a pet-shop in a 1.500 liter tank with a water recirculation system and standard filtration system. The fish was fed a commercial pellet diet and had not been treated with chemicals during the maintenance in the tank. On May 2008, the animal started showing lethargy of one month duration. One week before death the koi presented with anorexia and abdominal enlargement. Shortly after death the animal was send to the Dipartimento di Sanità Pubblica Veterinaria e Patologia Animale, Bologna for further investigation. Macroscopically, the koi showed epaxial muscle atrophy, especially in the caudal part of the body, and a symmetric abdominal enlargement. The skin overlaying the enlargement was thinned and missed scales. At necropsy, a multinodular, 7x5x3,5 cm, ventral to the kidney and to the swim bladder, white-yellowish, firm mass, filling the celomatic cavity, was identified. The mass was in strict connection with the liver and some parts of the intestine. The kidney, gall bladder, swim bladder and parts of the intestine were not involved. Gonads were not recognizable (Fig.1). Histologically, the neoplasm was non-encapsulated, poorly demarcated, multilobulated, highly cellular, with invasive growing and was characterized by a lobular architecture with abundant fibro-connective septa and large necrotic and calcified areas. Lobules were composed of solidly, cellular sheets of neoplastic polygonal cells, supported by fine fibrovascular stroma (Fig.2). Within some normal residual seminiferous tubules, small aggregates of 3-5 μm, round basophilic cells referred to spermatids were present (Fig.3). The neoplastic cells were 10-15 μm large, with not well-demarcated cytoplasmic boundaries; the cytoplasm presented numerous and thin granulations; the nucleus was large, round, hypochromatic and centrally located, with scattered chromatin and a single nucleolus (Fig.4). There was moderate anisocytosis and anisokaryosis. The mitotic rate was low (<1/ high power field). In the stroma scattered clusters of lymphocytes and melanomacrophages were present. Neoplastic cells massively infiltrated the intestinal wall and the liver (Fig.5, 6). Moreover, neoplastic lobules compressed the hepatic parenchyma causing atrophy (Fig.7). Neoplastic cells were PAS-negative. Immunohistochemically, normal seminiferous cells displayed an immunoreactivity to PLAP, vimentin and catalase, while the stromal component cross-reacted with cytokeratin AE1/AE3. The signal was not detected concerning the remaining antibodies tested (alpha feto protein, estrogen receptor, NSE, calretinin). Based on the macroscopic findings and the morphological features, the tumor was diagnosed as seminoma with a diffuse pattern. The evident malignancy was supported by the neoplastic cells invasion through the intestinal wall and the liver.

Celomatic neoplasm in a Cyprinid

SIRRI, RUBINA;MANDRIOLI, LUCIANA
2009

Abstract

The animal was a 3-year old male koi carp (Cyprinus carpio), 28-cm long. The first two years (2006-2008) the animal was kept in a farm with natural reproduction in a backyard pond in Italy. Afterwards the koi was kept for one year with other koi in a pet-shop in a 1.500 liter tank with a water recirculation system and standard filtration system. The fish was fed a commercial pellet diet and had not been treated with chemicals during the maintenance in the tank. On May 2008, the animal started showing lethargy of one month duration. One week before death the koi presented with anorexia and abdominal enlargement. Shortly after death the animal was send to the Dipartimento di Sanità Pubblica Veterinaria e Patologia Animale, Bologna for further investigation. Macroscopically, the koi showed epaxial muscle atrophy, especially in the caudal part of the body, and a symmetric abdominal enlargement. The skin overlaying the enlargement was thinned and missed scales. At necropsy, a multinodular, 7x5x3,5 cm, ventral to the kidney and to the swim bladder, white-yellowish, firm mass, filling the celomatic cavity, was identified. The mass was in strict connection with the liver and some parts of the intestine. The kidney, gall bladder, swim bladder and parts of the intestine were not involved. Gonads were not recognizable (Fig.1). Histologically, the neoplasm was non-encapsulated, poorly demarcated, multilobulated, highly cellular, with invasive growing and was characterized by a lobular architecture with abundant fibro-connective septa and large necrotic and calcified areas. Lobules were composed of solidly, cellular sheets of neoplastic polygonal cells, supported by fine fibrovascular stroma (Fig.2). Within some normal residual seminiferous tubules, small aggregates of 3-5 μm, round basophilic cells referred to spermatids were present (Fig.3). The neoplastic cells were 10-15 μm large, with not well-demarcated cytoplasmic boundaries; the cytoplasm presented numerous and thin granulations; the nucleus was large, round, hypochromatic and centrally located, with scattered chromatin and a single nucleolus (Fig.4). There was moderate anisocytosis and anisokaryosis. The mitotic rate was low (<1/ high power field). In the stroma scattered clusters of lymphocytes and melanomacrophages were present. Neoplastic cells massively infiltrated the intestinal wall and the liver (Fig.5, 6). Moreover, neoplastic lobules compressed the hepatic parenchyma causing atrophy (Fig.7). Neoplastic cells were PAS-negative. Immunohistochemically, normal seminiferous cells displayed an immunoreactivity to PLAP, vimentin and catalase, while the stromal component cross-reacted with cytokeratin AE1/AE3. The signal was not detected concerning the remaining antibodies tested (alpha feto protein, estrogen receptor, NSE, calretinin). Based on the macroscopic findings and the morphological features, the tumor was diagnosed as seminoma with a diffuse pattern. The evident malignancy was supported by the neoplastic cells invasion through the intestinal wall and the liver.
2009 Histopathology workshop
1
2
R. Sirri; L. Mandrioli
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11585/84470
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