Immunohistochemical Methods to Diagnose Atraumatic Spleen Rupture in Feline Infectious Peritonitis of Tiger (Panthera tigris)

http://www.revistadechimie.ro 1055 Feline infectious peritonitis (FIP) is viral, lethal disease caused by a feline coronavirus, with immune-mediated mechanism. The disease has been reported in a variety of species, mountain lion (Felis concolor), caracal (Caracal caracal), lion (Panthera Leo), tiger (Panthera tigris), jaguar (Panthera onca), sand cat (Margarita felis), shaving ( Lynx lynx) and cheetah (Acinonyx jubatus) [1, 2]. Feline coronaviruses are widespread in domestic and wild cats, being known two biotypes: enteric coronavirus (FECV), non-pathogenic and feline infectious peritonitis virus (FIPV) responsible for the lethal disease (Pedersen, 2009). Less than 10% of coronavirus carriers may develop FIP, as a result of FcoV mutagenic shifts in FIPV. Despite the low incidence, FIP is a major cause of mortality [3, 4]. In coronavirus infection lymphoid organs show T and B lymphocytes depletion, necrotic processes and often their complete involution. Splenic amyloidosis has been described in domestic cats suffering from FIV, associated with marked atrophy of lymphoid follicles [4]. In systemic AA amyloidosis, activated macrophages are producing IL-1 and IL-6 which stimulates hepatocytes to synthesize and secrete serum-A amiloid protein (SAA). During an inflammatory response SAA may increase more than 100 times. However, not all of systemic inflammatory reactions lead to AA-amyloid synthesis. Deposition of insoluble amyloid fibrils appear either due to faulty of enzymatic degradation of SAA or due to an abnormal synthesis of SAA resistant to enzymatic degradation [5]. At cheetahs and Siberian tigers amyloid deposits were found mainly in the medullary interstitium and seldom in glomerular corpuscle [6].