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Pathology of gastrointestinal helminthiasis in the brown pelican (Pelecanus occidentalis).

Lesions caused by experimentally produced mixed infections (two flukes, Phagicola longa and Mesostephanus appendiculatoides, and an ascarid, Contracaecum sp.) were studied in 40 brown pelicans. The flukes occurred throughout the intestines and caused mild villus atrophy, lengthening of the crypts, increased goblet cell population, and lymphoplasmacytic infiltration. Contracaecum caused small ulcers where they attached to the esophagus and proventriculus. Microscopically, these ulcers had an eosinophilic, hyaline lining surrounded by focal necrosis, cellular infiltration, and fibrosis. Changes in several biochemical constituents of the blood were seen. These gastrointestinal parasitisms had low virulence, and they probably play a secondary role as a factor influencing population fluctuations in brown pelicans.

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Distribution and ultrastructure of mast cells in the duck.

The distribution and ultrastructure of mast cells in the duck were studied. Carnoy's fluid was found to be the best fixative, and Padawer's method was found to be useful in demonstrating the metachromasia. Mast cells were seen in many of the organs and were most numerous in the proventriculus. Perivascular location was frequently seen. The ultrastructure resembled that of the chicken mast cell. The cell contained different types of membrane-bound granules, some of which were electron-dense and mottled.

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Ultrastructural analysis of peritrophic membrane formation of Drosophila auraria larvae.

The cells of the external layer of the proventriculus of Drosophila auraria larvae, which produce the peritrophic membrane are characterized by bears microvilli, polytenic nuclei, large quantities of ribosomes, very well developed rough endoplasmic reticulum and many Golgi complexes. The examined cells present one of the rare exceptions of insect intestinal cells, that form a prominent secretory product. The material of the peritrophic membrane, that gives a positive neutral polysaccharide reaction, is synthesized by the Golgi complex and is transported to the apex of the cells via secretory granules which discharge their contents in the space between adjacent microvilli and in that way they contribute to the peritrophic membrane formation.

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Lead poisoning in Canada geese: a case report.

A case report of lead poisoning in Canada geese at Cheyenne Bottom Wildlife Management Area in Kansas is presented. Seventy-nine dead geese and 10 geese too weak too fly were found by management personnel. Clinical signs in the live geese were weakness, lethargy, anorexia, emaciation and bile stained diarrhea. Seventeen geese were necropsied. Lesions were impacted roots and fibrous stalks in the esophagus and proventriculus and numerous lead shot in the gizzard. One to 44 lead shot (mean 13) were found in the 17 gizzards examined. The concentration of lead in liver and kidney was 9.21 to 102.56 ug/g (wet weight). The presence of lead shot in the gizzard, characteristic clinical signs, and the concentration of lead in the liver and kidney confirmed the diagnosis of lead poisoning.

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[Effect of the digestive process on the survival of the plague agent in Xenopsylla gerbilli Minax fleas].

Hystological investigations of experimentally infected X. gerbilli minax have shown that at the early stages of the digestion, while in the intestine compact clots of non-digested blood, are preserved, proceeds the reproduction of the plague agent. With the decay of the alimentary clot it changes into the dying off of the microbe population and after the ceasing of digestion the accumulation of bacteria renews again. Simultaneously with the changes in the number of microbes their morphology varies. At the initial stage of blood digestion bacilli typical for the agent are dominant. With the decay of the alimentary clot they are replaced by ovoid and spheroid forms. After the ceasing of the digestion cycle the microbe mass is represented by small coccobacteria. During the decrease in the plague agent abundance bacteria are absent mostly often from the midgut and posterior parts of the alimentary canal. Most favourable conditions for their preservation exist in this period in the proventriculus and in adjoining to it oesophagus part.

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Subtotal pancreatectomy in the chicken: evidence of a diabetic state and effect on the somatostatin cells of the digestive tract.

The effect of subtotal pancreatectomy on the regulation of plasma glucose was studied in the chicken. The eventual appearance of an extra-pancreatic source of insulin and the effect of pancreatectomy on somatostatin containing cells of the intestine were also investigated. Over a period of 3-5 weeks, pancreatectomy decreased body weight gain, greatly impaired glucose tolerance and hindered the regulation of plasma glucose levels after a meal. A large deficit in the insulin release induced by a meal was noticed after pancreatectomy. Therefore, in the fed chicken, pancreatectomy results in the typical signs of diabetes. No extrapancreatic source of insulin could be found either by radioimmunoassay of extracts of proventriculus, gizzard, gizzard-duodenum junction and duodenum from controls or depancreatized chickens, or by immunohistological studies in the same organs plus pancreatic ducts. No glucagon producing cells could be found by immunohistological studies in the gastrointestinal tract. The size of the somatostatin cells from the gizzard-duodenum junction was negatively related to the magnitude of the glucose-induced insulin release, which suggests an increase in somatostatin cell activity in true insulin-deficient depancreatized chickens as observed in insulin deficient diabetic mammals.

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The development of peptidergic neurons in the foregut of the chick.

We have used antisera specifically directed against Met-enkephalin (met-ENK), somatostatin (SOM), substance P (SP), and vasoactive intestinal peptide (VIP), to study the development of neurons containing these peptides in the foregut of the chick. All four peptides were detected early in ontogeny, at 4 to 9 days of incubation (d.i.), and were localized primarily to cell bodies in the primitive myenteric plexus. There were differences in the times at which they were first detected and in the sequence of their appearance in the proventriculus, gizzard, and duodenum. The differentiation of these peptidergic neurons in the duodenum was examined in some detail. Cell bodies containing these peptides were first detected in the primitive myenteric plexus at 5 to 7 d.i. and increased in number from 7 to 11 d.i. Processes containing varicosities became prominent between 11 and 13 d.i. VIP was the first of the peptides to appear in the submucosal plexus and was found in more proximal regions of the duodenum at 5 d.i. Shortly thereafter, SOM- and SP-containing cell bodies were seen; met-ENK-containing cell bodies were never detected in the submucosal plexus. At 13 d.i., the circular smooth muscle contained a number of VIP-immunoreactive and a smaller number of SOM-immunoreactive processes. met-ENK- and SP-immunoreactive processes appeared in the circular smooth muscle between 17 and 21 d.i.; VIP- and SP-immunoreactive processes appeared in the mucosal plexus at 17 to 21 d.i. Our results suggest that neuropeptides appear very early in the ontogeny of enteric neurons, at the same time or even before cholinergic and serotonergic neurons express their phenotypes. These findings argue against a sequential developmental order in which peptidergic neurons appear after those containing acetylcholine and serotonin.

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[Epizootiological importance of Frontopsylla hetera (Siphonaptera) fleas in the Gorno-Altai natural plague focus].

Experiments conducted during all seasons have established that F. hetera, one of the mass species of fleas in Mountain Altai, can be infected both by the strain of selective virulence typical to this nidus and by the non-typical non-virulent mountain-altai strain of plague agent. The non-virulent strain does not form in fleas the block of proventriculus and within 1.5-2 months they become free from the microbe. At the infection with the typical strain of the altai subspecies rare transmissions of the agent to Pallas' pika can take place as well as its long preservation in fleas.

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Invasion of avian encephalomyelitis virus from the gastrointestinal tract to the central nervous system in young chickens.

Invasion sites of avian encephalomyelitis virus in the internal organs of orally infected chicks were determined by the immunofluorescent method. The invasion began when the epithelium tunica mucosae of the duodenum (together with the proventriculus, jejunum, or cecum in certain birds killed at postinoculation day 1) became test-positive. Viremia persisted for more than 5 days in the early stage of infection, then the pancreas was rapidly infected, followed by the liver, kidney, and spleen. Subsequently, the virus spread to the CNS. Rapid infection of the duodenum and pancreas was clearly observable.

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Cytochemical characterization of mucosubstances in the chick glandular stomach during embryonary and postnatal development.

The chick stomach is composed of two parts: glandular or proventriculus and muscular or gizzard which are morphological and functionally different. Since characterization of the mucosubstances in the adult stomach and its comparison with the embryonary stomach have not been made, we performed the study of the cytochemical characteristics of mucosubstances in the chick glandular stomach during the embryonic and post-natal periods, to obtain information on changes produced in these components during functional differentiation. In this work we established that during development, the epithelial cells of the superficial layer content predominantly glycoproteins and the glycosaminoglycans of the glands decrease when they begin to secrete other compounds, such as proteolytic enzymes necessary for digestion. This sequence of mucosubstances appearance is concordant with the increase of carbonic anhydrase, which reaches its highest specific activity from 15 to 20 days of incubation. In this period hydrochloric acid secretion increases and therefore, glycoprotein secretion becomes necessary to protect the mucous membranes.

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Cryptosporidiosis in domestic birds.

From March to June 1982, three cases of avian cryptosporidiosis were encountered in chickens, ducklings, and canaries. The bursa of Fabricius of chickens and ducklings were the main target organs and the agents were found to attach the microvillus border of the plical epithelium. In canaries, the parasites adhered to the microvillus border of mucosal epithelium of the proventriculus. Diagnoses were based on the microscopic pathology, the morphology of the parasites, and the type of attachment to epithelium. This represents the first authenticated evidence of cryptosporidial infection in Taiwan.

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Chronological observations on hemato-pathological changes in chicks inoculated with chicken anemia agent.

Chicks were inoculated with the Gifu-1 strain of the chicken anemia agent (CAA) on the day of hatching. They manifested distinct anemia accompanied with pancytopenia 8--20 days after inoculation. Discoloration of the bone marrow and atrophy of the thymus began to be seen 6 days after inoculation. Histologically, hematopoietic cells began to decrease and large blastic cells to appear in the bone marrow 4--6 days after inoculation. Hypoplasia and subsequently aplasia occurred to all over the bone marrow 8 days after inoculation. In the bone marrow erythrocytopoiesis was noticed first 16--18 days after inoculation, granulocytopoiesis later, and transient hyperplasia finally. At last, the bone marrow returned to a normal condition 32 days after inoculation or later. In the thymus the depletion of cortical lymphocytes became distinct 4--6 days after inoculation, and lobular atrophy 8 days after inoculation or later. The depletion of lymphocytes in the other lymphatic tissues and hemorrhage in the lamina propria of the proventriculus were observed only in the anemic phase. The results mentioned above indicated that the anemia induced by CAA was caused by the disorder of hematopoietic cell formation in the bone marrow. It was also noteworthy that cortical lymphocytes in the thymus began to decrease remarkably soon after inoculation.

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Pathology of ochratoxicosis A in young broiler chicks.

Ochratoxin A (OA), a potent nephrotoxin, was fed in the diet in sublethal concentrations (2 and 4 ppm) to broiler chicks for 20 days from hatch. Its effects on growth, relative organ size and histology of the liver, kidney and lymphoid organs were investigated. In young broiler chicks, OA caused a significant enlargement of the kidney, liver and proventriculus, whereas the thymus and bursa of Fabricius were reduced in size. It principally affected the proximal convoluted tubules of the kidney causing severe distension, enlargement and hypertrophy, and it also resulted in thickening of the glomerular basement membrane. In the liver, vacuolation and glycogen accumulation in the hepatocytes were seen. The toxin also caused regression of and a drastic reduction in the lymphoid cell population in the immunological organs. The toxicity of OA was found to be dose related.

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Pleuritis and peritonitis in a golden eagle.

A female Golden Eagle died despite intensive treatment after being struck by a vehicle. Necropsy revealed poor body condition, with no fat stores. The proventriculus and ventriculus contained a pellet of fur and bone fragments, at the center of which was the leg of a Red-Tailed Hawk. A talon on the leg had punctured the ventriculus, resulting in fatal pleuritis and peritonitis.

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Experimentally induced fatty liver and kidney syndrome in the young turkey.

Turkeys were fed up to four weeks of age on diets of low biotin content and then fasted for 18 hours. Three birds developed clinical signs of fatty liver and kidney syndrome (FLKS) and on autopsy had pale and swollen livers and kidneys. Morphological studies showed fatty accumulations in liver, kidney, heart and proventriculus but no signs of inflammatory or degenerative changes. The infiltrated lipid had an abnormal fatty acid composition, with an increased proportion of monounsaturated fatty acids. Affected birds suffered from severe hypoglycaemia and hepatic glycogen was depleted. These findings demonstrate that FLKS can be induced experimentally in turkeys.

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Pathology of experimental erysipelas in turkeys.

Gross and histopathologic lesions were studied in 10 Broad-Breasted White turkeys with acute erysipelas induced experimentally. The gross pathologic features of the disease conformed very closely with descriptions in the literature (7). Histopathologic evaluation was concentrated on the inoculation site (skin), proventriculus, ileocecal area of the intestine, liver, spleen, kidney, lung, and heart. In all organs examined the dominant histopathologic alteration was vascular damage as evidenced by: generalized congestion, edema, focal hemorrhage, disseminated fibrin thrombi, and numerous bacterial aggregates either within fibrin thrombi or engulfed by cells of the reticuloendothelial system. Degenerative changes or overt necrosis of parenchymal cells were evident in liver, spleen, and kidney. The cellular inflammatory component of acute lesions was minimal. Heterophil and mononuclear leukocytic infiltrates were observed in scarified skin and, in turkeys surviving several days, in livers and hearts.

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Oosporein-toxicosis in the turkey poult.

Turkey poults were fed diets containing oosporein at concentrations of 0, 500, 1,000, and 1,500 micrograms/g from hatching until three weeks of age. Low feed consumption resulted in poor growth rates at every dietary level of oosporein; however, a dose-related increase in water consumption was observed. The most significant effect of dietary oosporein was severe visceral and articular gout, with death ensuing in 24 and 52% of the poults at the 1,000 and 1,500 micrograms/g levels, respectively. Gout and mortality were absent at 0 and 500 micrograms/g. In addition to tissue urate deposition, necropsies revealed dehydration, swollen pale kidneys, hemorrhagic proventriculitis with mucosal necrosis, gizzard enlargement and lining discoloration, an increase in gall bladder size, and focal hepatic necrosis. The relative weights of the kidney, liver, proventriculus, gizzard, and pancreas were increased in a dose-related fashion; spleen and bursa weights were unaffected. Among plasma constituents, uric acid, urea, and the activities of glutamic-oxalacetic transaminase and lactic dehydrogenase were elevated in response to dietary oosporein; albumin, potassium, phosphorus, and calcium were decreased. The toxin had no effect on plasma total protein, sodium, glucose, cholesterol, triglycerides, alkaline phosphatase, or creatine phosphokinase. These data substantiate the original classification of oosporein as a nephrotoxin and etiologic agent of gout in avian species.

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Malabsorption syndrome in broiler chickens.

A disease syndrome of broiler chickens is described. Affected birds exhibited poor pigmentation of the shanks, decreased weight gains, elevated feed conversions, poor feathering, enlargement of the proventriculus, and a decrease in the size of the gizzard. Reoviruses were isolated from affected chickens from several farms. Signs and lesions similar to those seen in chickens with the field syndrome were reproduced when these isolates were inoculated into day-old chicks with low levels of maternal antibody against viral arthritis. The pathogenicity of the viral isolates was variable. The incidence of lameness was much higher in those groups of chicks injected with these viruses than in the control groups.

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