Equine Multisystemic Eosinophilic Epitheliotropic Disease (EMEED) is an uncommon syndrome that affects horses characterized by eosinophilic infiltration of multiple organs of ectodermic origin such as skin, gastrointestinal tract, liver, pancreas, lungs, lymphnodes, etc (1). Clinical signs include weight loss, diarrhea, exfoliative dermatitis and, less frequently, respiratory distress (2). The aetiology of EMEED is unknown, although parasitic, allergic, toxic and viral causes have been suggested. Case 1 was a 2 y.o. Standardbred colt with anorexia, multiple oral ulcerations, ventral and limb edema and weight loss. Laboratory findings showed eosinophilia, increased ALP, GGT and LDH, hypoalbuminaemia, hypergammaglobulinaemia and hyperfibrinogenaemia. Oral glucose tolerance test revealed total malabsorption. Bone marrow aspirate demonstrated increased maturative stages of the eosinophilic series. Abdominal ultrasonography showed enlargement of the liver with hyperechoic parenchyma, dilated bile ducts, increased peritoneal fluid and fibrin deposition. Liver biopsy indicated an eosinophilic hepatitis with fibrosis and cholestasis. Post mortem examination revealed marked enlargement of mesenteric lymphnodes, liver and pancreas, with a severe infiltration of eosinophils. Case 2 was a 13 y.o. Pony gelding referred for labored breathing. Clinical examination showed the presence of nasal discharge, cough, prolonged expiration and inspiratory crackles on auscultation. Laboratory findings showed leukocytosis with marked eosinophilia and increased PLT, PT and aPTT. Blood gas analysis revealed hypoxaemia and hypercapnia. Thoracic ultrasonography showed disseminated comet tail artifacts, and abdominal ultrasonography showed several renal and hepatic small hyperechoic nodules. Thoracic radiography revealed a markedly increased interstitial pattern. Endoscopy of the upper airways demonstrated the presence of small white nodules on the mucosal surface; cytological examination of bronchoalveolar lavage showed eosinophilic inflammation. Biopsy of the liver and the of the airway nodules showed eosinophilic infiltration. Post mortem examination showed the presence of small calcific nodules on the liver, lymphnodes, lung and kidney, that were largely infiltrated with eosinophils. According to these findings, the diagnosis of EMEED was confirmed for both cases. This paper contributes to increase the low number of EMEED cases reported worldwide. Interestingly, in case 2 the pulmonary involvement is described, which represents a quite uncommon feature. Amongst possible different aetiologies, neoplasia should be considered, because of several common features with human clonal hypereosinophilic syndromes (3).
Equine multisystemic eosinophilic epitheliotropic disease (EMEED) : two case reports / L. Stucchi, E. Zucca, G. Stancari, S. Ceriotti, B. Conturba, E. Ferro, F. Ferrucci. ((Intervento presentato al 68. convegno Convegno nazionale S.I.S.Vet tenutosi a Pisa nel 2014.
Equine multisystemic eosinophilic epitheliotropic disease (EMEED) : two case reports
L. StucchiPrimo
;E. ZuccaSecondo
;G. Stancari;S. Ceriotti;B. Conturba;E. FerroPenultimo
;F. FerrucciUltimo
2014
Abstract
Equine Multisystemic Eosinophilic Epitheliotropic Disease (EMEED) is an uncommon syndrome that affects horses characterized by eosinophilic infiltration of multiple organs of ectodermic origin such as skin, gastrointestinal tract, liver, pancreas, lungs, lymphnodes, etc (1). Clinical signs include weight loss, diarrhea, exfoliative dermatitis and, less frequently, respiratory distress (2). The aetiology of EMEED is unknown, although parasitic, allergic, toxic and viral causes have been suggested. Case 1 was a 2 y.o. Standardbred colt with anorexia, multiple oral ulcerations, ventral and limb edema and weight loss. Laboratory findings showed eosinophilia, increased ALP, GGT and LDH, hypoalbuminaemia, hypergammaglobulinaemia and hyperfibrinogenaemia. Oral glucose tolerance test revealed total malabsorption. Bone marrow aspirate demonstrated increased maturative stages of the eosinophilic series. Abdominal ultrasonography showed enlargement of the liver with hyperechoic parenchyma, dilated bile ducts, increased peritoneal fluid and fibrin deposition. Liver biopsy indicated an eosinophilic hepatitis with fibrosis and cholestasis. Post mortem examination revealed marked enlargement of mesenteric lymphnodes, liver and pancreas, with a severe infiltration of eosinophils. Case 2 was a 13 y.o. Pony gelding referred for labored breathing. Clinical examination showed the presence of nasal discharge, cough, prolonged expiration and inspiratory crackles on auscultation. Laboratory findings showed leukocytosis with marked eosinophilia and increased PLT, PT and aPTT. Blood gas analysis revealed hypoxaemia and hypercapnia. Thoracic ultrasonography showed disseminated comet tail artifacts, and abdominal ultrasonography showed several renal and hepatic small hyperechoic nodules. Thoracic radiography revealed a markedly increased interstitial pattern. Endoscopy of the upper airways demonstrated the presence of small white nodules on the mucosal surface; cytological examination of bronchoalveolar lavage showed eosinophilic inflammation. Biopsy of the liver and the of the airway nodules showed eosinophilic infiltration. Post mortem examination showed the presence of small calcific nodules on the liver, lymphnodes, lung and kidney, that were largely infiltrated with eosinophils. According to these findings, the diagnosis of EMEED was confirmed for both cases. This paper contributes to increase the low number of EMEED cases reported worldwide. Interestingly, in case 2 the pulmonary involvement is described, which represents a quite uncommon feature. Amongst possible different aetiologies, neoplasia should be considered, because of several common features with human clonal hypereosinophilic syndromes (3).Pubblicazioni consigliate
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