ABSTRACT
In the past 20 years in Switzerland, dogs with suspect acute leptospirosis frequently showed severe glomerular changes that had not been previously reported. These features were characterized by abundant extravasated erythrocytes and fewer neutrophils accompanied by marked fibrin exudation into the urinary space that was interpreted as an exudative glomerulonephritis (GN). This retrospective study describes this significant glomerular pathological change and investigates the association with leptospirosis. Tissues from 50 dogs with exudative GN, retrieved from 2 pathology archives in Switzerland were reviewed using hematoxylin and eosin, periodic acid-Schiff, phosphotungstic acid-hematoxylin, and Warthin and Starry stains. Clinical and postmortem data were collected for each case. Immunohistochemistry (IHC) and/or polymerase chain reactions were used as confirmatory tests for leptospirosis. While all 50 cases had clinical and pathological features supporting a diagnosis of leptospirosis, 37 cases were confirmed for the disease. Using a LipL32 antibody in addition to the OMV2177 antibody raised against the lipopolysaccharide of Leptospira interrogans serovar Copenhageni increased the detection rate of Leptospira by IHC in exudative GN from 24% to 62%. Signalment, seasonality, clinical signs, blood results, and pathological changes in dogs with exudative GN were similar to those reported for dogs without GN and confirmed infection by Leptospira spp.. Exudative GN was common among Swiss dogs with leptospirosis where it caused acute severe disease. Leptospirosis should be considered as a cause of this new pathologic feature by the pathologist. The pathogenesis remains unclear, but involvement of a geographic-specific serovar with unique virulence factors is suspected and warrants further investigation.
ABSTRACT
In collaboration with the American College of Veterinary Pathologists.
Subject(s)
Pathology, Veterinary , Veterinarians , Animals , Humans , United StatesABSTRACT
A 2.5-year-old cat presented with progressive ataxia and lethargy. Magnetic resonance imaging (MRI) showed enlargement of the cerebellum and herniation of cerebellar vermis. Postmortem examination confirmed the MRI findings, and histopathology showed numerous large dysplastic neurons populating and displacing the Purkinje cell layer and extending into the molecular and granular layers of the cerebellum. The lesion was diagnosed as dysplastic gangliocytoma of the cerebellum. In humans, this tumor is often associated with Cowden syndrome, a genetic disorder characterized by multiple hamartomas and an increased risk of developing certain neoplasms, known to be linked to a germline mutation of the phosphatase and tensin homolog (PTEN) gene. Reduction in PTEN nuclear and cytoplasmic immunohistochemical labeling of dysplastic neurons in this case suggested a possible PTEN mutation involved in the tumorigenesis. This report provides a detailed pathology description of the tumor and the use of neuronal and PTEN markers which will help guide pathologists presented with this rare condition in the future.
Subject(s)
Cat Diseases , Cerebellar Neoplasms , Ganglioneuroma , Hamartoma Syndrome, Multiple , Hamartoma , Animals , Cat Diseases/diagnosis , Cat Diseases/pathology , Cats , Cerebellar Neoplasms/diagnosis , Cerebellar Neoplasms/genetics , Cerebellar Neoplasms/veterinary , Cerebellum/pathology , Ganglioneuroma/complications , Ganglioneuroma/diagnosis , Ganglioneuroma/veterinary , Hamartoma/pathology , Hamartoma/veterinary , Hamartoma Syndrome, Multiple/complications , Hamartoma Syndrome, Multiple/diagnosis , Hamartoma Syndrome, Multiple/veterinary , Hyperplasia/pathology , Hyperplasia/veterinary , Magnetic Resonance Imaging/veterinaryABSTRACT
Toxoplasma gondii is a cosmopolitan zoonotic parasite and nowadays considered as an emerging neozoan pathogen in the marine environment. Cetacean innate immune reactions against T. gondii stages have not yet been investigated. Thus, T. gondii tachyzoites were utilized to trigger neutrophil extracellular traps (NETs) in bottlenose dolphin (Tursiops truncatus) polymorphonuclear neutrophils (PMN). Scanning electron microscopy unveiled T. gondii tachyzoites as potent and rapid inducers of cetacean-derived NETosis. Co-localization of extracellular chromatin with global histones, granulocytic myeloperoxidase and neutrophil elastase confirmed classical characteristics of NETosis. Interestingly, different phenotypes of NETs were induced by tachyzoites resulting in spread, diffuse and aggregated NET formation and moreover, 'anchored' and 'cell free' NETosis was also detected. Current data indicate that cetacean-derived NETosis might represent an early, ancient and well-conserved host innate defense mechanism that not only acts against T. gondii but might also occur in response to other closely related emerging apicomplexan parasites affecting marine cetaceans.
