Juliana Sousa Terada Nascimento, Átila Bezerra de Mira, Kelly Cristina de Araujo Barbosa, Sara Preato de Oliveira, Maria de Lurdes Silva Ardição, Sandro de Vargas Schons
{"title":"猫科动物全脑畸形伴突眼和鼻炎:病例报告","authors":"Juliana Sousa Terada Nascimento, Átila Bezerra de Mira, Kelly Cristina de Araujo Barbosa, Sara Preato de Oliveira, Maria de Lurdes Silva Ardição, Sandro de Vargas Schons","doi":"10.21708/avb.2023.17.3.11602","DOIUrl":null,"url":null,"abstract":"The aim of this study was to describe the macroscopic and histological lesions observed in domestic newborn felines with facial lesions characterized by holoprosencephaly associated with synophthalmia and arhinia. A feline with multiple craniofacial congenital anomalies was necropsied, and the brain was collected, followed by photodocumentation and histopathological processing with H&E. The diagnosis of alobar holoprosencephaly with grade (I) morphological lesions of the face was made through the anatomopathological changes observed during the clinical and necroscopic examination, characterized by deformation of the cerebral hemispheres, shown failure in the forebrain vesicle development, located in the cranial neural tube part, associated with craniofacial dysmorphisms. In the microscopic study of the CNS, lesions characterized by abnormal lamination of the cerebral hemisphere's outermost cell layers and multiple areas of vacuolization of the cortex and in the cerebellum low cell density of the granular layer, with the presence of large intracytoplasmic vacuoles and absence of Purkinje cells were observed. It was not possible to determine the deformation cause, since laboratory tests were not performed, as well as the association with the FeLV virus.","PeriodicalId":38626,"journal":{"name":"Acta Veterinaria Brasilica","volume":"57 7","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Holoprosencephaly associated with synophthalmia and arrhinia in feline (Felis catus): a case report\",\"authors\":\"Juliana Sousa Terada Nascimento, Átila Bezerra de Mira, Kelly Cristina de Araujo Barbosa, Sara Preato de Oliveira, Maria de Lurdes Silva Ardição, Sandro de Vargas Schons\",\"doi\":\"10.21708/avb.2023.17.3.11602\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The aim of this study was to describe the macroscopic and histological lesions observed in domestic newborn felines with facial lesions characterized by holoprosencephaly associated with synophthalmia and arhinia. A feline with multiple craniofacial congenital anomalies was necropsied, and the brain was collected, followed by photodocumentation and histopathological processing with H&E. The diagnosis of alobar holoprosencephaly with grade (I) morphological lesions of the face was made through the anatomopathological changes observed during the clinical and necroscopic examination, characterized by deformation of the cerebral hemispheres, shown failure in the forebrain vesicle development, located in the cranial neural tube part, associated with craniofacial dysmorphisms. In the microscopic study of the CNS, lesions characterized by abnormal lamination of the cerebral hemisphere's outermost cell layers and multiple areas of vacuolization of the cortex and in the cerebellum low cell density of the granular layer, with the presence of large intracytoplasmic vacuoles and absence of Purkinje cells were observed. It was not possible to determine the deformation cause, since laboratory tests were not performed, as well as the association with the FeLV virus.\",\"PeriodicalId\":38626,\"journal\":{\"name\":\"Acta Veterinaria Brasilica\",\"volume\":\"57 7\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-01-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta Veterinaria Brasilica\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.21708/avb.2023.17.3.11602\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Veterinary\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Veterinaria Brasilica","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21708/avb.2023.17.3.11602","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Veterinary","Score":null,"Total":0}
Holoprosencephaly associated with synophthalmia and arrhinia in feline (Felis catus): a case report
The aim of this study was to describe the macroscopic and histological lesions observed in domestic newborn felines with facial lesions characterized by holoprosencephaly associated with synophthalmia and arhinia. A feline with multiple craniofacial congenital anomalies was necropsied, and the brain was collected, followed by photodocumentation and histopathological processing with H&E. The diagnosis of alobar holoprosencephaly with grade (I) morphological lesions of the face was made through the anatomopathological changes observed during the clinical and necroscopic examination, characterized by deformation of the cerebral hemispheres, shown failure in the forebrain vesicle development, located in the cranial neural tube part, associated with craniofacial dysmorphisms. In the microscopic study of the CNS, lesions characterized by abnormal lamination of the cerebral hemisphere's outermost cell layers and multiple areas of vacuolization of the cortex and in the cerebellum low cell density of the granular layer, with the presence of large intracytoplasmic vacuoles and absence of Purkinje cells were observed. It was not possible to determine the deformation cause, since laboratory tests were not performed, as well as the association with the FeLV virus.