ESVP/ECVP Proceedings 2011
STRUCTURAL AND FUNCTIONAL CHANGES OF THE FELINE ENTERIC NERVOUS SYSTEM IN CATS WITH CHRONIC GASTROINTESTINAL DISEASES S. Kleinschmidt *, I. Nolte y and M. Hewicker-Trautwein* *Department of Pathology and ySmall Animal Clinic, University of Veterinary Medicine Hannover, Germany Introduction: Inflammatory Bowel Disease (IBD) is a complex of chronic gastrointestinal disorders of unknown aetiology and poorly understood pathogenesis. In this investigation, the possible involvement of the enteric nervous system (ENS) in cats with chronic gastrointestinal symptoms is described. Materials and Methods: Immunohistochemical examination of the submucosal and myenteric plexus was performed on intestinal biopsies of cats suffering from IBD (n 5 23) or intestinal lymphoma (n 5 10) by using antibodies directed against neuron-specific enolase (NSE), non-phosphorylated neurofilaments (NPN), phosphorylated neurofilaments (PN), vasoactive intestinal peptide (VIP) and glial fibrillary acidic protein (GFAP). Results: In lymphocytic-plasmacytic enterocolitis (LPE) a significant reduction of GFAP and VIP and mostly of NSE was present, while in eosinophilic gastroenterocolitis (EGEC) only PN was reduced. In fibrosing enteropathy (FE) reduced expression of NSE, NPN, PN and VIP was noted. Cases with intestinal lymphoma had only reduction of PN with increase of NPN. Conclusions: In LPE changes reflect alterations of enteric glial cells and neurons, while in EGEC disturbance in neuronal cytoskeleton is suggested. Only neuronal disturbance is present in FE, whereas lymphomas are associated with direct damage or interference of ENS. Structural and functional alterations of the ENS may contribute to clinically evident signs of vomiting and/or diarrhoea.
HEPATIC CIRRHOSIS IN TWELVE DOGS AFTER EXPOSURE TO INAPPROPRIATE COMMERCIAL DOG FOOD A.-L. Nagy, C. Cuc, F. Tabaran, A. Gal, M. Taulescu, P. Bolfa, G. Borza and C. Catoi University of Agricultural Sciences and Veterinary Medicine, Cluj-Napoca, Romania Introduction: Twelve dogs of different breeds and ages, from the same kennel, with a history of severe liver failure were presented to the Pathology Department of the Faculty. The aim of this study was to assess the lesions and determine the possible aetiology of this condition. Materials and Methods: Routine necropsy examination was performed and liver samples were taken, fixed in formalin, embedded in paraffin wax and examined using histochemical stains. Immunohistochemistry was performed to determine expression of a-smooth muscle actin (SMA) and vimentin. Food samples were sent for biochemical and toxicological analysis. Results: Macronodular hepatic cirrhosis with associated lesions such as ascites, jaundice and subcutaneous oedema were noted grossly. Microscopical examination revealed diffuse fibrosis with the presence of regenerative nodules, lipogranulomas and pigment-laden macrophages. SMA positive cells were present in the fibrous septa, in the periportal region and in some cases in the perisinusoidal region. Conclusions: Immunohistochemistry for SMA permited the identification of extracellular matrix components secreted by myofibroblasts. The number of these cells was correlated with the degree of hepatic fibrosis.
PATHOGENESIS OF FAILED CLOSURE OF OPTIC FISSURE IN FLS MICE WITH OCULAR COLOBOMA: ZYMOGRAPHIC ANALYSIS OF COLLAGENASE ACTIVITY N. Tsuji *, K. Ozaki *, I. Narama y and T. Matsuura* *Setsunan University, Osaka and yBiosafety Research Center for Foods, Drug and Pesticides, Shizuoka, Japan Introduction: Disturbed basement membrane disintegration at the optic fissure causes ocular coloboma in rodents. Previous studies clarified that almost all FLS fetuses developed ocular coloboma due to failure of optic fissure closure. This study was designed to explore the relationship between collagenase activity and disturbed basement membrane disintegration at the optic fissure in FLS mice. Materials and Methods: Serial coronal sections of eyes from FLS fetuses and F1 fetuses (crosses between FLS and CBA mice) were examined by in-situ FITC-conjugated zymography. Results: Positive collagenase activity was increased at GD 12.0e12.5 and it was undetectable at GD 13.5 around the fusing optic fissure in normal F1 fetuses, while collagenase activity was weakly positive or indistinguishable during GD 12.0e13.5 at unfused optic fissures in FLS fetuses. Conclusions: Decreased collagenase activity may cause disturbed basement membrane disintegration at the optic fissure, which is responsible for ocular coloboma.
SEASONAL CONGENITAL LESIONS OF THE CENTRAL NERVOUS SYSTEM IN CALVES L. Polledo, B. Martınez-Fern andez, J. Gonz alez, C. P erez-Martınez, Ma. J. Garcıa-Iglesias and J.F. Garcıa-Marın Juan University of Leon, Spain Introduction: Congenital anomalies in calves have been related to genetic factors, physical agents, vitamin A and copper deficiencies and infectious or toxic causes. In this study, an outbreak of congenital anomalies of the central nervous system in newborn cattle is described that occurred annually during FebruaryeMarch in a particular valley in the north of Spain. Materials and Methods: Necropsy examinations were performed on four animals from four different grazing herds and tissue samples were processed using routine histological and immunohistochemical techniques. Serum samples from these calves, their dams and other adult animals were collected for laboratory analysis. Results: The affected animals appeared annually at the same time of the year, but these outbreaks of disease only occurred in herds that grazed in a particular valley. Clinical signs were anaemia, weakness and ataxia, and other neurological signs such as blindness and recumbency were observed occasionally. Myelodysplasia with the presence of aberrant central canals and the absence of septa were the main histopathological findings found in all of the newborns. Conclusions: A viral aetiology or toxic plants are discussed as a possible origin of these outbreaks of disease. Nutritional deficiencies have been ruled out.