This article presents the results of pathomorphological research on the spleen and mesenteric lymph nodes of 23 dead cats aged from 3 months to 7 years, which in their lifetimes (according to anamnesis, clinical signs, laboratory-instrumental methods of examination and VetExpert FCoV Ab express test) had been diagnosed with infectious peritonitis. All the animals were domestic. Blood was drawn from the subcutaneous vein of the forelimb of the diseased cats. We determined ESR, morphological parameters of blood and content of hemoglobin. For histological and histochemical examinations, we selected samples of spleen and mesenteric lymph nodes, which were fixated in 10% aqueous solution of neutral formalin, Carnoy’s and Bouin’s solutions. The prepared histological sections were stained using haematoxylin and eosin, Van Gieson’s stain, methyl green-pironin stain (Brashe), PAS-reaction (McManus), alcian blue and Congo red. Hematological parameters during 3 weeks of clinical progression of the disease among the cats demonstrated a decrease in the hemoglobin content and in the number of erythrocytes and leukocytes. Possible decrease in the number of lymphocytes indicated the development of an immune-deficiency state. Also, during the development of disease, the animals had possible increase in ESR, which indicated the development of an inflammatory process in the organism and decrease in the number of thrombocytes, which conditioned development of disseminated intravascular coagulation. The anatomical pathology autopsy showed that in most animals the spleen was diminished in size, the surface of the organ was tuberous, the capsule was wrinkled and mat, the edges were sharpened. The histostructural change was accompanied by a sharp depletion of the lymph nodes and reduction in the number of micro- and macrophages, which indicated the reduction of white pulp, rapid inhibition of the activity of T- and B-lymphocytes, plasmacytic and macrophage reaction and manifested in development of immune-deficient condition of the organism. In this process, the reticular carcass of the lymph nodes saturated with PAS-positive and eosinophilic masses was clearly manifested, which indicated formation of fibrinoid. In the spleen of 5 individuals, during staining using Congo red, we found deposition of amyloid masses both in the intima of the blood vessels and along the reticulary fibers of the lymph nodes. In the cytoplasm of macrophages, we found pyroninophilic formations. In two cases, we observed blood accumulation of red pulp and bleeding following the reduction of white pulp, and in one case fibrinogenous perisplenitis. In the mesenteric lymph nodes of most of the cats which had suffered from infectious peritonitis, we determined that edema, exposure of the reticular soft skeleton (stroma) of adrenal and paracortical zones, dilation of the border and central sinuses and thrombosis of vessels were followed by steep decrease in the number of T- and B-lymphocytes, plasma cells, micro- and macrophages, which indicated the development of atrophic processes of lympoid tissue and immune-suppression. In three cases, in mesenteric lymph nodes of cats, we determined development of sinus histiocytosis. The changes determined in the spleen and lymph nodes of the cats which had suffered from FIP indicate immune-suppressed condition and steep decrease in the functional ability of the organs and organism in general.
The article presents the results of pathoanatomical, pathohistological and histochemical researches of the lung tissue for exudative form of the spontaneous infectious peritonitis of cats. The results of researches allow us to analyze pathoanatomical, microstructural changes in lung tissue of cats in various forms of peritonitis infectious and to define the mechanism of the pathological process that cause lethal consequence.The pathoanatomical research of dead bodies of 4 cats has been carried out: a 3 year–old cat and 1 year and 2 month–old cat and 1 year and 5 month–old with symptoms of exudative pleurisy; a 2 year–old cat with clear signs of exudative peritonitis and pleurisy. Peritoneal fluid and lung tissue fragments for cytological and pathohistological examination were selected. At pathoanatomical autopsy accumulation in the thoracal, abdominal cavities and pericardial space fluid with the flakes of fibrin were revealed, thickening of the serous membranes, layering them fibrin. At the pathohistological research in lung tissue noted the consequences of hemodynamic disturbances in the form of multiple perivascular hemorrhage, interstitial pneumonia, atelectasis and emphysematous cells and signs of fibrinous pleurisy in the state organization have been noted. The hardest changes were developed in the structures of the vascular system and are characterized by the damage of vascular endothelium, the development of productive meso– and periarteritis, syndrome of disseminated intravascular coagulation, stasis and hemolysis of erythrocytes in small vessels of interalveolar septum leading to the oppression of hemocirculation. In lungs, the mononuclear–macrophage infiltration prevailed, especially in periarteritis zone, indicating the presence of productively–necrotic vasculitis.The development of the syndrome disseminated intravascular coagulation led to the formation of multiple micro–blood clots, aggregated cells in vascular channel, the presence of which has led to the development of thrombi and then hemorrhages. The blockade microcirculation, in their turn, led to tissue hypoxia, acidosis and, as a result, distrophic changes in the past. The discovered processes in the vascular system of the lung tissue caused the insufficient flow of blood, irreversible changes of homeostasis and a sharp decline in adaptive capacity.
The article presents the results of macroscopic and microscopic examinations of myocardial cats in wet and mixed forms of FIP. A pathoanatomical study of 19 cat carcasses, aged from 3 months to 7 years, was diagnosed with infectious peritonitis during life (on the basis of anamnesis, clinical features, morphological and biochemical blood test, ultrasound, Rivalt test and FCVetx rapid test VetE.) All animals were kept at home. For the microstructural study, samples of cats' hearts were selected, which were fixed in 10% aqueous formalin neutral solution, Carnua, Buen solutions and 96 ° ethyl alcohol. Histogram sections were stained with hematoxylin and eosin staining, picrofuxin (Van Gizon), PAS reaction (McManus), methyl green pyronin (Brache), Malory, and examined under a microscope. Histological examination of the cardiac muscle of cats in various forms of infectious peritonitis revealed changes of non-inflammatory and inflammatory nature. In the exudative form, non-inflammatory processes prevailed. In the myocardium, the most severe changes occurred in the capillaries, the walls of the arterial vessels and the stroma, which were characterized by diapedic hemorrhage, mucoid and fibrinoid swelling and necrosis of the walls of the arterioles. Disorganization of connective tissue was accompanied by stratification of connective tissue fibers and impregnation of weakly oxyphilic, PAS-positive compounds of the intermuscular lumen, which was combined with dystrophic changes in cardiomyocytes. In the mixed form, proliferative-destructive vasculitis, diffuse or focal lymphoid-histiocytic infiltrates in the myocardium prevail. The revealed optical changes in the structural elements of the heart indicated a sharp weakening of the contractile function of cardiomyocytes and heart failure. In addition, it should be noted that the characteristic morphological manifestation for immunocomplex diseases is the development of vasculitis, which is preceded by fibrinoid necrosis of the walls of the arterial vessels and intensive infiltration of their circulatory elements, and these changes occurred in infectious peritonitis of cats.
Наведено результати патологоанатомічного розтину 20 трупів котів, віком від 3 місяців до 7 років, у яких прижиттєво (на основі анамнезу, клінічних ознак, лабораторно-інструментальних методів дослідження та експрес-тесту VetExpert FCoV Ab) було діагностовано інфекційний перитоніт. Усі тварини утримувалися в домашніх умовах. Для гістологічного та гістохімічного дослідження були відібрані зразки нирок, які фіксували у 10% водному розчині нейтрального формаліну, рідині Карнуа та Буена. Виготовлені гістозрізи фарбували гематоксиліном та еозином, за методами Браше, Стідмена та Мак-Манусом. Зразки нирок після фіксації в 10% водному розчині нейтрального формаліну промивали в проточній воді та за допомогою заморожуючого мікротома ТОС-2 виготовляли гістозрізи, які в подальшому фарбували суданом-ІІІ. За патологоанатомічного розтину виявлено в більшості випадків помірну нефромегалію, застійну гіперемію, де в одних котів - превалювали дрібні крапкові крововиливи, в інших – сіруваті осередки. За гістологічного дослідження нирок котів, хворих на інфекційний перитоніт, структурні зміни були не однотипними, що, ймовірно, зумовлено тривалістю перебігу хвороби. У паренхімі нирок одних котів спостерігали кровонаповнення капілярів клубочків, мікросудин строми, гломерулярні та тубулоінтерстиціальні зміни. Структурні зміни в клубочках характеризувались розширенням капсули Шумлянського-Боумена та нагромадженням у просвіті гомогенної білкової або пінистої фуксинофільної маси, потовщення капілярних мембран сплетінь клубочків з помірним розширенням мезангіального матриксу, а в епітелії дистальних та проксимальних відділів канальців – білково-жирову дистрофію, що вказувало на розвиток серозного гломерулонефриту і білково-жирової дистрофії епітелію канальців. У нирках інших котів превалювало інтерстиціальне запалення. Інтерстиція просочена глікозаміногліканами, глікопропротеідами та інфільтрована клітинними елементами. В осередках запалення відзначали лімфогістіоцитарну інфільтрацію з домішками нейтрофілів і плазматичних клітин. Навколо клубочків, судин та між канальцями формувались клітинні інфільтрати. У ниркових клубочках простежували розширення перикапілярного просвіту з набубнявінням капілярних стінок і нагромадженням між ними гомогенної білкової еозинофільної маси. В епітелії звивистих канальців кіркової і мозкової речовини нирок виражені різного ступеня дистрофічно-некробіотичні зміни. Виявлені світлооптичні зміни вказували на розвиток гострого тубулоінтерстиціального нефриту.
The article presents the results of histological studies of the frontal area of the cerebral cortexб taken from 10 corpses of cats aged from 3 months to 5.5 years, in which infectious peritonitis (based on anamnesis, clinical signs, morphological and biochemical blood analysis , ultrasound diagnostics, Rivalt test and express diagnosis) was diagnosed during their life. A pathoanatomical study was conducted; samples of the frontal area of the cerebral cortex of cats, which were fixed in a 12% aqueous solution of neutral formalin, a solution of Carnoua and 96° ethyl alcohol, were selected. The histocuts were made, which were stained with hematoxylin and eosin, thionine for Nisslem. In order to detect the astrocytic glory, a fraction of the cerebral cortex was fixed by the Golgi-Clatzo method with a fresh mixture of chloral hydrate-formalin-bichromate and produced histocuts on a freezing microtome. For histological examination of the cerebral cortex of cats, changes in the non-inflammatory character were observed, which were characterized by disorders of hemomycrocycle circulation, edema and degenerative processes of the neuroglial complex and neurons. Violations of the structural organization of endothelial cells, basal membranes of capillaries and venules should be considered as an important indicator of functional changes in tone, permeability of the microcirculatory channel, which contributed to the development of perivascular and pericellular edema, which in its turn led to regressive changes of glial elements; acute swelling of neurons with the formation of microcavities in nuclei; a sharp decrease in the content of the chromatophilic substance in pyramidal and stellate cells; the development of gidropic dystrophy in star cells and creatures; rise of shadow cells. Circulatory disorders caused the violation of the trophic transport systems, which caused hypoxia, accumulation of acidic metabolism products, and formed the basis for the pathogenesis of the development of dyscirculatory dystrophy of neuroglial cells and neurons, i.e. neurotrophic disorders of the cerebral cortex of cats for FIR.
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