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-α and interleukin-1β) 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.

A 4‐month‐old male British Blue cat with catarrhal to haemorrhagic enteritis showed massive colonization of the stomach, small intestine and caecum with spiral‐shaped bacilli. In the stomach, organisms were located in foveolae and gland lumina and within unaltered and degenerate epithelial cells. Inflammatory infiltration was moderate and T cell dominated. In the intestine, bacilli were found in the gut lumen, between villi, in crypt lumina and within epithelial cells. Degeneration of crypt epithelial cells as well as crypt dilation and moderate to massive macrophage‐dominated infiltration of the mucosa and submucosa were observed. Immunohistochemically, bacilli were positive with an antibody against Helicobacter. Ultrastructurally, the organisms strongly resembled ‘Flexispira rappini’, a spiral‐shaped Helicobacter species known as a normal intestinal colonizer in dogs and mice.

The morphology of endometrial blood vessels in uterine biopsy specimens from mares of varying age and reproductive status was examined by light (n = 117) and electron microscopy (n = 13), and additionally after elastase digestion (n = 86). Inflammatory vascular alterations were observed in 20.5% of the specimens. Smaller and larger arterial and venous vessels demonstrated mild to severe degenerative lesions. Unaltered vessels were detected only in maiden mares. Vessels in older maiden mares were frequently affected by angiosclerotic changes, characterized by mild to moderate perivascular and intimal sclerosis. The incidence and severity of angiosis increased with the number of previous pregnancies and with advancing age. Changes in multiparous mares resembled the so-called "pregnancy-sclerosis" of other species, with fraying and disruption of the membrana elastica interna, medial atrophy intimal, medial and adventitial elastosis and fibrosis, and calcification processes within the media. Ultrastructural studies revealed characteristic arterial changes in post-parturient mares, namely, disruption of the membrana elastica interna, as well as activated smooth muscle cells and immature elastic fibres within the intima and inner media, suggesting a pregnancy-induced pathogenesis. Haemodynamic and hormonal alterations during pregnancy and the puerperium possibly induce active vascular remodelling. Cycles of vascular growth during pregnancy and subsequent involution post partum are thought to result in progressive degenerative vascular changes, as seen in multiparous mares. Ageing processes, chronic inflammation and short foaling intervals have to be considered as additional pathogenetic factors. Furthermore, severe angiosis was frequently combined with phlebectasia and lymphangiectasia. This may indicate a reduced ability of the vessels to adapt to the varying demands of uterine circulation, with a decrease of uterine perfusion and lymph drainage. Angiosis in older, multiparous mares might therefore be intimately related to infertility.

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.

Chickens were inoculated intraduodenally with germs of Cl.perfringens Type A in 6 attempts (n = 146), spores (n = 6) and Cl.perfringens Type A toxin (n = 6). Birds, which had died spontanly or had been killed respectly were examined pathomorphologically and bacteriologically. The pathological-anatomical observations included: prestatic hyperemia of the parenchymatous organs; heavy injection of the mesenteric vessles: watery contents of the small intestine mixed with gas bubbles; lungs oedema; swollen and pale kidneys. Necrosis or hemorrhage of the intestinal mucous membranes wasn't observed. Histological investigations lead to the following findings: Colonisation and multiplication of Cl.perfringens in the intestinal lumen without adhesion onto the intestinal mucous membrane, cellular infiltration of the propria mucosae, intraepithelial accumulation of heterophiles, crypt abscesses of various degree; and occasionally desquamation of the epithel cells. The electron microscopical alterations concerned cristolyse of the mitochondria, destructions of the microvilli border, disolving of the terminal web, and detachment of isolated enterocyte groups. Cl.perfringens was isolated in 95.4% of the intestine samples and 1.2% from the liver samples.

It was reported about an outbreak of a massiv fibrinous Polyserositis by roaster chickens from 14 d old to the slaughter on the 40. d of age with a mortality rate of 20 % per flock. The pathological findings consisted in multifocal necrosis, macrophages infiltrates mainly into the portal triads, granuloms, basophilic intranuclear inclusions bodies, and hydropic swelling in the liver, intense infiltrations of lympho-histiocyts into the Lamina propria in good maintenance of the Lamina epithelialis in the bronchus, and the bronchioli, and pneumonia, fibrinous pericarditis, myocarditis perihepatitis, and perisplenitis. An adenovirus was detected by electron microscopical investigations. The epizootiological factors for the outbreak, and the role of the detected virus were discussed.

The following findings were obtained in some of 23 unweaned piglets from optical light and electron microscopy for studies into experimental intragastric Clostridium (Cl.) perfringens Type A intoxication (beta-toxin, 80-800 doses lethal to mouse, administered one to six hours from birth): moderate inflammatory reaction of intestinal mucosa with capillary hyperaemia, villous oedema, lymphatic congestion in chylous vessels as well as infiltration of neutrophilic granulocytes in villous stroma and intestinal lymph nodes. With most of the villous epithelia ultrastructurally intact, circumscribed alterations of enterocytes were occasionally recordable in the form of inflation, vesiculation, wasting of microvilli, softening or loss of terminal fibres, mitochondrial alteration, enlargement of endoplasmic reticulum as well as brigthening of basal plasma. No ultrastructural alterations were recordable from terminal blood and chylous vessels. The other organs and tissues were morphologically inconsicuous. These findings are discussed in some detail, with particular reference made to the pathogenesis of Cl. perfringens type A enterotoxaemia.

Liver bioptates taken 2 weeks post partum from 213 high-yielding cows (6000-8000 kg FCM per 305 days lactation) were investigated biochemically to liver lipid content (GL) and histologically to degree of lipid infiltration (GdL). Additional in 27 cases electron microscopic studies to liver cell morphology and clinico-chemical investigations (beta-OH-butyrate and acetacetate in blood; quantity of bilirubin, albumine, protein, activity of ASAT and GLDH in blood plasma) were carried out. 22.5 % of liver bioptates were histologically free of lipid infiltration (GL: 2.34 %; GdL: 0). 77.5 % of liver bioptates showed different lipid quantities (GL: 5.1-24 %; GdL: 0.3-5.7 %). 27 cases additionally investigated electron-microscopically and clinicochemically can be summarized in 3 groups (with regard to lipid contents): 1. < 5 %, n = 7; 2.5-10 %, n = 10; 3. 10-24 %, n = 10. Electron microscopic changes concerned occasional nucleus alterations, frequent RER dilation, mitochondria condensation or swelling, occurrence of secondary lysosomes and glycogen decrease. RER dilation and mitochondria swelling showed a statistical relation to liver lipid content. Ketone body (beta-OH-butyrate, acetacetate) and bilirubin concentration climed with increasing quantity of liver lipid. Activities of GLDH and ASAT failed any dependence to lipid quantity.The results are discussed under the aspect of pathogenesis and dignity of fatty degeneration of the liver post partum.

Liver biopsies taken 2 weeks post partum from 213 high-yielding cows (6000-8000 kg FCM per 305 days lactation) were investigated biochemically to liver lipid content (GL) and histologically to degree of lipid infiltration (GdL). Additional in 27 cases electron microscopic studies to liver cell morphology and clinico-chemical investigations (beta-OH-butyrate and acetate in blood; quantity of bilirubin, albumin, protein, activity of ASAT and GLDH in blood plasma) were carried out. 22.5% of liver biopsies were histologically free of lipid infiltration (GL: 2.34%; GdL: 0). 77.5% of liver biopsies showed different lipid quantities (GL: 5.1-24%; GdL: 0.3-5.7%). 27 cases additionally investigated electron-microscopically and clinico-chemically can be summarized in 3 groups (with regard to lipid contents): 1. < 5%, n = 7; 2.5-10%, n = 10; 3. 10-24%, n = 10. Electron microscopic changes concerned occasional nucleus alterations, frequent RER dilation, mitochondria condensation or swelling, occurrence of secondary lysosomes and glycogen decrease. RER dilation and mitochondria swelling showed a statistical relation to liver lipid content. Ketone body (beta-OH-butyrate, acetate) and bilirubin concentration climbed with increasing quantity of liver lipid. Activities of GLDH and ASAT failed any dependence to lipid quantity. The results are discussed under the aspect of pathogenesis and dignity of fatty degeneration of the liver post partum.

Optical light and electron microscopy were used in follow-up investigations of liver bioptates obtained from two groups of nonpregnant cows, including four individuals with delayed lactation (Group 1) and three without lactation (Group 2), which were all kept on restricted diet for four weeks (ten percent of maintenance rations). The findings recorded were related to selected clinical or biochemical parameters. The following evidence was found during the fasting period and was more strongly and regularly pronounced in Group 1 rather than in Group 2: fatty degeneration of the liver, glycogen drop, mitochondrial consolidation or condensation, dilatation and vesiculation of RER with partial detachment of ribosomes, increased occurrence of autolysosomes, occasional alterations to nuclei (condenstion of karyoplasm, karyopyknosis), hyperbilirubinaemia, increased activity of,two enzymes, GLDH and ASAT (the latter only in Group 1) as well as reduction of body weight, dorsal fat thickness and milk yield (the latter in Group 1). The morphological, ultrastructural as well as certain clinicochemical findings (bilirubin, GLDH and some ASAT behaviours) appeared to be indicative of impairement to various metabolic processes in the liver when the organism was experimentally exposed to fasting. These findings are described in some detail and are related to the degree and dynamics of incorporation of fat in hepatocytes and, finally, are discussed under the aspect of pathogenesis of fatty degeneration of the liver.

Electron microscopic investigations on the respiratory tract of piglets with and without Mycoplasma hyorhinis infection (10th day of life) partly combined with swim stress (15 degrees C water temperature) (n = 20/20) yielded the following results: colonization of Mycoplasma hyorhinis in the ciliary zone of trachea and bronchi in 15 out of 40 piglets (37.5%); the evidence rate of Mycoplasma hyorhinis in pneumonic lungs (8 out of 12 = 66.7%) was significantly higher than in nonpneumonic lungs (7 out of 28 = 25.0%) and highest in experimentally infected piglets with swim stress (9 out of 16 = 56.2%). Ultrastructural lesions: loss of cilia; bleb-formation; hydropic degeneration and desquamation of ciliary cells; the occurrence of cilia-free and immature epithelial cells; alveolar collapse; microatelectasis; oedematous swelling of pneumocyte I; accumulation of surfactant in the alveoli; hyperplasia of pneumocyte II; exudation of mononuclear macrophages and neutrophils with numerous digestion vacuoles; several lymphocytes and plasma cells, only a little lymphohistiocytic interstitial and peribronchial infiltration. Phagocytized mycoplasmas were found within the resorption vacuoles of neutrophils in the tracheobronchial area, for this once in alveoli, not (more) against in alveolar macrophages. The results were discussed with regard to etiology and pathogenicity of enzootic pneumonia in pigs.

Electron microscopic investigations on the respiratory tract of piglets with and without Mycoplasma hyorhinis infection (10th day of life) partly combined with swim stress (15 degrees C water temperature) (n = 20/20) yielded the following results: colonization of Mycoplasma hyorhinis in the ciliary zone of trachea and bronchi in 15 out of 40 piglets (37.5%); the evidence rate of Mycoplasma hyorhinis in pneumonic lungs (8 out of 12 = 66.7%) was significantly higher than in nonpneumonic lungs (7 out of 28 = 25.0%) and highest in experimentally infected piglets with swim stress (9 out of 16 = 56.2%). Ultrastructural lesions: loss of cilia; bleb-formation; hydropic degeneration and desquamation of ciliary cells; the occurrence of cilia-free and immature epithelial cells; alveolar collapse; microatelectasis; oedematous swelling of pneumocyte I; accumulation of surfactant in the alveoli; hyperplasia of pneumocyte II; exudation of mononuclear macrophages and neutrophils with numerous digestion vacuoles; several lymphocytes and plasma cells, only a little lymphohistiocytic interstitial and peribronchial infiltration. Phagocytized mycoplasmas were found within the resorption vacuoles of neutrophils in the tracheobronchial area, for this once in alveoli, not (more) against in alveolar macrophages. The results were discussed with regard to etiology and pathogenicity of enzootic pneumonia in pigs.