Abstract. Feline infectious peritonitis (FIP) is a fatal, coronavirus (CoV)-induced systemic disease in cats, characterized by granulomas in organs and granulomatous vasculitis. This study describes the morphologic features of granulomatous vasculitis in FIP as well as its development in the course of monocyte-associated feline CoV (FCoV) viremia in five naturally infected Domestic Shorthair cats with FIP. Monocyte-associated FCoV viremia was demonstrated by immunohistology, RNA in situ hybridization, and electron micropscopy. Granulomatous phlebitis at different stages of development was observed. Vasculitic processes ranged from attachment and emigration of FCoV-infected monocytes to vascular/perivascular granulomatous infiltrates with destruction of the vascular basal lamina. Monocytes as well as perivascular macrophages were activated because they were strongly positive for CD18 and expressed cytokines (tumor necrosis factor-␣ and interleukin-1␤) and matrix metalloproteinase-9. In addition, general activation of endothelial cells, represented by major histocompatibility complex II upregulation, was observed in all cases. These results confirm FIP as a monocyte-triggered systemic disease and demonstrate the central role of activated monocytes in FIP vasculitis.Key words: Cats; feline coronavirus; feline infectious peritonitis; granulomatous vasculitis; monocyte-associated viremia; phlebitis.Feline infectious peritonitis (FIP) is a well-known and widely distributed coronavirus (CoV)-induced systemic disease in cats, characterized by fibrinous to granulomatous serositis with protein-rich effusions in body cavities and granulomatous inflammatory lesions in several organs. 24,45 Not the most obvious finding, but one of its morphologic hallmarks is a granulomatous to necrotizing phlebitis and periphlebitis. 8,16,24,43 Up till now, the pathogenesis of FIP is largely undetermined.Feline CoV (FCoV) is transmitted via the fecal-oral route and primarily infects enterocytes. 28 Despite the generally high prevalence of FCoV infection among the cat population, especially in multicat facilities, FIP morbidity is low and rarely surpasses 5%. 1,7,28 FIP seems to develop in the individual infected animal when FCoV acquires virulence by deletions in open reading frames 3 and 7, coding for nonstructural proteins of unknown function, which occur as mutations primarily during replication in the infected host. 39 Most infected cats develop an FCoV viremia that can be detected by reverse transcriptase-polymerase chain reaction (RT-PCR) on isolated (and cultivated) monocytes regardless of the development of FIP. 7,15 FCoV-1 Present address: Department of Veterinary Pathology, Faculty of Veterinary Science, University of Liverpool, Liverpool, UK infected circulating monocytes are considered as responsible for viral dissemination within the host. 10,11,28,44 Furthermore, the demonstration of FCoV antigen within intravascular leukocytes and among cells in the lesions of vasculitis in a previous experimental study suggested that the inf...

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Hepatic and renal electron microscopic investigations were carried out in 10 chickens that had experimental intraduodenal infection with Clostridium perfringens Type A. Fourteen days postinfection, there were ultrastructural changes in hepatocytes and renal tubular epithelial cells; these included mitochondrial lesions (swelling, cristolysis, rarefication of the matrix, myelin figures), glycogen loss, and capillary endothelial cell swelling in both organs, as well as thickening of glomerular basement membrane. The findings are discussed with particular reference to the pathogenesis of Clostridium perfringens Type A enterotoxemia.

Summary Experimental studies on effects of chronic aerogenous toxic gas stress on unweaned piglets with ammonia of varying concentrations 3. Light‐ and electronmicroscopic studies on the pathology and pathogenesis of chronic aerogenous ammonia damage to the respiratory apparatus of the piglet Tistopathological and EM studies on the respiratory tract of sucking piglets after chronic aerogenous NH3‐exposure (50 and 100 ppm for 4.5–6 weeks) showed, in comparison with controls without NH3 exposure, the following changes: 1. Proliferation and hypersecretion of goblet cells in the tracheobronchial mucosa, with production of an acid mucus in the upper trachea after 100 ppm compared with reduction and death of goblet cells. 2. Occurrence of necrobiotic changes in ciliary cells (vesicular widening of microvilli; cytoplasmic protruberances with and without inclusion of cilia; nodular swelling of cilia; local or extended loss of cilia etc.). 3. Destruction of pneumocyte‐1 extensions, in part with exposure of the alveolar membrane; partial or complete alveolar collapse; proliferation of pneumocytes‐II; freeing of lamellar bodies and uptake of these by alveolar macrophages. 4. Reactive inflammatory processes in the tracheobronchial mucosa (massive cellular infiltration) and in lung parenchyma (slight to medium grade interstitial pneumonia). The changes are discussed in relation to the pathogenesis of NH3 effects on the respiratory tract of the sucking pig. Zusammenfassung Pathohistologische und transmissionselektronenmikroskopische Untersuchungen am Atmungsapparat von Saugferkeln nach chronischer aerogener NH3‐Exposition (50 und 100ppm; Exposition 4,5–6 Wochen) ergaben im Vergleich mit Kontrolltieren ohne NH3‐Einwirkung folgende Veränderungen: 1. Vermehrung und Hypersekretion von Becherzellen in der Tracheobronchialschleimhaut mit Produktion eines sauren Schleims, in der oberen Trachea nach 100 ppm dagegen Verringerung und Untergang von Becherzellen. 2. Auftreten degenerativ‐nekrobiotischer Veränderungen an den Zilienzellen (blasige Auftreibung von Mikrovilli; zytoplasmatische Protuberanzen ohne und mit Einschluß von Zilien; kolbenartige Anschwellung von Zilien; umschriebener oder ausgedehnter Zilienverlust…). 3. Destruktion von Pneumozyten‐I‐Ausläufern z.T. mit Freilegung der alveolären Basalmembran; partieller oder vollständiger Alveolenkollaps; Vermehrung von Pneumozyten‐II; Abgabe von Lamellarkörperchen und Aufnahme derselben durch Alveolarmakrophagen. 4. Reaktiv‐entzündliche Prozesse an der Tracheobronchialschleimhaut (mäßige zellige Infiltration) und am Lungenparenchym (gering‐ bis mittelgradige interstitielle Pneumonie). Die Veränderungen werden unter dem Gesichtspunkt der Pathogenese der NH3‐Wirkung auf den Atmungsapparat des Saugferkels diskutiert.