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Focal Segmental Glomerulosclerosis in Dogs
J. Comp. Path. 2016, Vol. 154, 58e123
ESVP, ECVP and NSVP Proceedings 2015
FOCAL SEGMENTAL GLOMERULOSCLEROSIS IN DOGS J.J. van der Lugt *,y, L. Aresu y,z, S. Benali z and A.M. van Dongeny,x *IDEXX Europe, BV, Hoofddorp, The Netherlands, yEuropean Veterinary Renal Pathology Service, zDepartment of Comparative Biomedicine and Food Science, Universita di Padova, Italy and xDepartment of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, The Netherlands Introduction: Focal and segmental glomerulosclerosis (FSGS) is a common disease in people with nephrotic syndrome that was reported in dogs for the first time in 2010. The aim of this study was to determine the prevalence of FSGS in canine renal biopsies submitted to the Utrecht Veterinary Nephropathology Service between January 1, 2010 and December 31, 2014, and to review the clinicopathological features of the condition. Materials and Methods: Renal biopsies that were examined by light microscopy (LM), transmission electron microscopy (TEM) and immunofluorescence were included. Results: Of 118 cases, 21 (17.7%) revealed histological lesions of FSGS characterized by segmental solidification of the glomerular tuft by deposition of mesangial matrix leading to obliteration of capillary lumens. All dogs with FSGS presented with proteinuria prior to biopsy, documented as a urine protein:creatinine ratio 2 and/or persistent renal proteinuria. In all affected dogs, effacement of podocyte foot processes and moderate to severe podocyte damage associated with increased mesangial matrix was evident with TEM. However, in eight cases, dense deposits consistent with immune complexes (ICs) were detected in the mesangium, supporting an immune-mediated origin of the disease. Conclusions: FSGS is a common glomerular disease in proteinuric dogs with two possible origins: primary, likely genetic, and secondary to IC deposition. The use of TEM in conjunction with LM is mandatory for identification of this condition.
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SPREAD OF FELINE HERPESVIRUS TYPE-1 ALONG THE RESPIRATORY TRACT TO THE LUNG: ASSESSMENT OF ASSOCIATED CHANGES IN NATURAL CASES AND AN INVITRO MODEL J.M. Monn e Rodriguez *, G. Leeming *, K. K€ ohler y and A. Kipar*,z *Division of Pathology, School of Veterinary Science, University of Liverpool, UK, yInstitute of Veterinary Pathology, Faculty of Veterinary Medicine, University of Giessen, Germany and zInstitute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, Switzerland Introduction: Feline herpesvirus type 1 (FHV-1) is an important cause of feline infectious respiratory disease. FHV-1 is an epitheliotropic, cytopathic virus that usually induces self-limiting necrotizing inflammation of the upper respiratory tract; however, this progresses occasionally to necrotizing pneumonia. The aim of this study was to determine the effects of FHV-1 on the epithelium and its mode of spread to the lungs. Materials and Methods: Eighteen naturally occurring cases with FHV-1 pneumonia (confirmed by viral culture, PCR and/or immunohistology) and in-vitro FHV-1-infected tracheal cultures were examined. Immunohistology for relevant markers and TEM were used to examine viral spread and effects on airway epithelial cells. Results: All animals showed multifocal necrotizing to necrosuppurative bronchitis, bronchiolitis and alveolitis. Respiratory and alveolar epithelial cells were infected and cell-to-cell spread of the virus from the upper respiratory tract to the lungs was suggested. FHV-1induced cell death was via apoptosis, after initial cell contraction and rearrangement, then loss of intercellular junctions. Epithelial cell infection was often associated with marked neutrophilic influx. In naturally occurring cases, severe necrotic changes extended to the underlying bone and cartilage, where cell-free viral antigen was found together with inflammatory cells. Macrophages in the infiltrates and type II pneumocytes were found to express matrix metalloproteinase-9. Conclusions: Airway epithelial cells are the sole target of FHV-1, which enters the lungs via cell-to-cell spread rather than by aerosol. Infected cells die via apoptosis, but recruit (and activate) macrophages and neutrophils, leading to further tissue damage.
ESVP, ECVP and NSVP Proceedings 2015
FOCAL SEGMENTAL GLOMERULOSCLEROSIS IN DOGS J.J. van der Lugt *,y, L. Aresu y,z, S. Benali z and A.M. van Dongeny,x *IDEXX Europe, BV, Hoofddorp, The Netherlands, yEuropean Veterinary Renal Pathology Service, zDepartment of Comparative Biomedicine and Food Science, Universita di Padova, Italy and xDepartment of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, The Netherlands Introduction: Focal and segmental glomerulosclerosis (FSGS) is a common disease in people with nephrotic syndrome that was reported in dogs for the first time in 2010. The aim of this study was to determine the prevalence of FSGS in canine renal biopsies submitted to the Utrecht Veterinary Nephropathology Service between January 1, 2010 and December 31, 2014, and to review the clinicopathological features of the condition. Materials and Methods: Renal biopsies that were examined by light microscopy (LM), transmission electron microscopy (TEM) and immunofluorescence were included. Results: Of 118 cases, 21 (17.7%) revealed histological lesions of FSGS characterized by segmental solidification of the glomerular tuft by deposition of mesangial matrix leading to obliteration of capillary lumens. All dogs with FSGS presented with proteinuria prior to biopsy, documented as a urine protein:creatinine ratio 2 and/or persistent renal proteinuria. In all affected dogs, effacement of podocyte foot processes and moderate to severe podocyte damage associated with increased mesangial matrix was evident with TEM. However, in eight cases, dense deposits consistent with immune complexes (ICs) were detected in the mesangium, supporting an immune-mediated origin of the disease. Conclusions: FSGS is a common glomerular disease in proteinuric dogs with two possible origins: primary, likely genetic, and secondary to IC deposition. The use of TEM in conjunction with LM is mandatory for identification of this condition.
59
SPREAD OF FELINE HERPESVIRUS TYPE-1 ALONG THE RESPIRATORY TRACT TO THE LUNG: ASSESSMENT OF ASSOCIATED CHANGES IN NATURAL CASES AND AN INVITRO MODEL J.M. Monn e Rodriguez *, G. Leeming *, K. K€ ohler y and A. Kipar*,z *Division of Pathology, School of Veterinary Science, University of Liverpool, UK, yInstitute of Veterinary Pathology, Faculty of Veterinary Medicine, University of Giessen, Germany and zInstitute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, Switzerland Introduction: Feline herpesvirus type 1 (FHV-1) is an important cause of feline infectious respiratory disease. FHV-1 is an epitheliotropic, cytopathic virus that usually induces self-limiting necrotizing inflammation of the upper respiratory tract; however, this progresses occasionally to necrotizing pneumonia. The aim of this study was to determine the effects of FHV-1 on the epithelium and its mode of spread to the lungs. Materials and Methods: Eighteen naturally occurring cases with FHV-1 pneumonia (confirmed by viral culture, PCR and/or immunohistology) and in-vitro FHV-1-infected tracheal cultures were examined. Immunohistology for relevant markers and TEM were used to examine viral spread and effects on airway epithelial cells. Results: All animals showed multifocal necrotizing to necrosuppurative bronchitis, bronchiolitis and alveolitis. Respiratory and alveolar epithelial cells were infected and cell-to-cell spread of the virus from the upper respiratory tract to the lungs was suggested. FHV-1induced cell death was via apoptosis, after initial cell contraction and rearrangement, then loss of intercellular junctions. Epithelial cell infection was often associated with marked neutrophilic influx. In naturally occurring cases, severe necrotic changes extended to the underlying bone and cartilage, where cell-free viral antigen was found together with inflammatory cells. Macrophages in the infiltrates and type II pneumocytes were found to express matrix metalloproteinase-9. Conclusions: Airway epithelial cells are the sole target of FHV-1, which enters the lungs via cell-to-cell spread rather than by aerosol. Infected cells die via apoptosis, but recruit (and activate) macrophages and neutrophils, leading to further tissue damage.