Localization of Ascaridia galli larvae in the jejunum of chickens 3 days post infection

The normal habitat of the parasitic stages of Ascaridia galli is in the small intestine of poultry but the exact localization is poorly understood. Therefore, a histological study was conducted in order to localize the larvae during the early phase of infection. Six layer pullets seven-week old were infected orally with 20,000 embryonated A. galli eggs each, whereas four chickens were left as un-infected controls. At necropsy 3 days after infection the first half of jejunum/ileum was divided into two equally sized sections (J1 and J2). After taking samples for histology from the middle of J1 and J2 and the junction between these determined JX, the two sections were subjected to parasitological examination. A higher number of A. galli larvae were recovered from section J2 than J1 and the majority of larvae were recovered from the most profound layers. Based on histology 144 larvae were identified and their location was noted. The highest number of larvae was observed in the JX sample as compared to J1 and J2 (P<0.001). Most of them were located in the profound crypt zone of the mucosa (51%) as compared to the other zones (P<0.05). The number of larvae was higher in the lumen (63%) compared to the epithelium (32%) and lamina propria (5%) (P<0.001). A significantly higher number of eosinophils were found in lamina propria of the infected group compared to the control group (P<0.001). This experiment clearly showed that only few larvae had penetrated the epithelium and were positioned in the lamina propria at 3 days post infection. It was far more common that the larvae were localized within the epithelium or in the lumen of the crypts. It is therefore suggested that at least in this early phase "mucosal phase" is a more appropriate term to be used for the A. galli larval localization as compared to the term "histotrophic phase" currently used in many textbooks.     

Plasma pepsinogen,inhibited larval development,and abomasal lesions in experimental infections of calves with Ostertagia ostertagi

Single doses of Ostertagia ostertagi, followed in 42 days by multiple increasing doses in calves, were monitored by fecal egg counts and plasma pepsinogen. The level of plasma pepsinogen increase was related to the increase in graded levels of inoculation and to the fecal egg counts. Plasma pepsinogen in uninfected controls remained below 1 IU/L. Plasma pepsinogen in all calves reached levels greater than 5 IU/L at 48 days of the extended inoculation period, although fecal egg counts remained low in the previously inoculated calves. The previously infected calves had a higher proportion of early fourth-stage larvae, while larger adult worm burdens were found in the previously uninfected calves. Early fourth-stage larvae were observed in extra-glandular sites, notably between the glandular epithelium and basement membrane or within the lamina propria. An immunological response of the host was suggested by the lymphoid cell infiltration in the mucosa. This host immune response may account for the greater larval inhibition exhibited by the previously infected calves.     

The pathological changes caused by Eimeria falciformis var pragensis in mice.

Groups of Swiss white mice weighing 25-28 grams were infected orally with 500, 2,000, 5,000 or 20,000 oocysts of Eimeria falciformis var pragensis. Depression, anorexia, weight loss, diarrhea or dysentery, and dehydration were most pronounced at eight to ten days postinfection. The highest mortality, 31%, occurred in mice infected with 20,000 oocysts. None of the mice infected with 500 oocysts died. The pathological findings were equally severe in mice infected with 5,000 and 20,000 oocysts. The enteric lesions, most pronounced at eight to ten days postinfection, were restricted mainly to the large intestine and consisted initially of both cryptal and absorptive epithelial cell destruction and submucosal edema. These changes were followed in 12 to 24 hours by a transient influx of neutrophils into the lamina propria followed by mononuclear cell infiltration which lasted for five to ten days. As the infective dose decreased, the inflammatory response occurred later and was less extensive. When seen, hemorrhage occurred seven to 11 days postinfection. In 50% of the mice infected with 5,000 and 20,000 oocysts, varying degrees of a nonselective mucosal necrosis were seen at eight to 12 days postinfection. In mice infected with 500 oocysts, mucosal destruction was restricted to the epithelium. Neutrophils predominated when necrosis was extensive, otherwise, mononuclear cells were the main inflammatory cells. Two to three days following necrosis, crypt hyperplasia was marked and mucosal integrity was restored. Ulcers, some of which extended into the submucosa, healed by days 14 to 20. Localized granulomatous colitis, induced by trapped oocysts within the lamina propria, was seen until the experiment was terminated at 25 days postinfection. Infection was followed by lymphoid hyperplasia in the lymph nodes and the spleen.     

Gastrointestinal zygomycosis in suckling pigs

Gastrointestinal zygomycosis was diagnosed in 3 suckling pigs (10, 14, and 28 days old) with diarrhea that was unresponsive to treatment with broad-spectrum antibiotics. The 3 pigs were from separate farms, and littermates of the 3 pigs with similar clinical signs had died. At necropsy, 2 of the 3 pigs had catarrhal to fibrinonecrotic gastroenteritis, and the third pig had hemorrhagic gastritis without intestinal lesions. Microscopically, transmural necrosis of the stomach and intestines was associated with marked inflammatory cell infiltration and thrombosis and vasculitis of vessels of the lamina propria and submucosa. Numerous broad, irregularly branching, nonseptate, mucoraceous fungi were seen in the lumens of blood vessels and in the necrotic mucosa and submucosa.     

Electron microscopic changes in colon in experimental swine dysentery.

Colonic lesions in experimental swine dysentery were studied electron microscopically. Changes indicative of stasis were commonly observed in the microcirculatory vessels of lamina propria. Early lesions in epithelial cells included sparse, short and irregular microvilli, swollen and degenerated mitochondria, and swelling and vesiculation of endoplasmatic reticulum. Numerous large spirochaetes were observed in these locations: a) in the crypts, b) free (i.e. not membrane bound) in cytoplasm of damaged epithelial cells, and c) in cavities, around vessels of lamina propria. It is suggested that stasis, and resultant disturbances in microcirculation in early developmental stages of swine dysentery, may play a pathogenetic role in the development of the necrotic colonic lesions. Finally, it is discussed whether a mechanism related to Sanarelli-Shwartzman reaction is implicated in the development of colonic lesions in swine dysentery.     

Die Mikroangioarchitektur der Mukosa des Antrum pyloricum des Magens beim Kaninchen 1

Microangioarchitecture of the mucosa of the Antrum pyloricum in rabbit was studied by optical and scanning electron microscopy. Passing the lamina muscularis mucosae, arteries of the submucosa reach the lamina propria and branch in to the terminal arteries forming a subglandular network. From these vessels, two capillary nets arise. The first forms a capillary skein around the base of the glands, while the second ascends along the tubuli, moving upwards to the surface along the glandular tubuli. These ascending capillaries also arise directly from the subglandular arterioles of the lamina propria, as well as from capillaries of the basal parts of the glandular tubuli. Subepithelial capillaries form arcuate loops with 2-3 venules or collecting venules, which run into the venous net in the basal region of the lamina propria. Numerous horizontal interconnections exist between the collecting venules but arteriovenous anastomosis in the mucosa was not observed.     

Inter-relationship between Gasterophilus larvae and the horse's gastric and duodenal wall with special reference to penetration.

The degree of penetration into the stomach and duodenum of the horse by bot fly larvae, Gasterophilus intestinalis (De Geer) and G. nasalis (Linnaeus) (Diptera : Gasterophilidae) was evaluated. Evidence of larval perforation of the stomach or duodenum was not found on gross inspection. Palpation of the intact stomach and duodenum was not effective in establishing the existence of Gasterophilus larvae within the organs. Findings suggest that larvae of both species produce an ulcer of similar depth within the gastrointestinal wall. The ulcer depth produced by larvae did not correlate with the normal, unaffected thickness of the particular stomach or duodenum. Tissue proliferation beneath ulcers of the stomach and duodenum was not correlated with the depth of the ulcer. Proliferation of the tissue beneath the ulcers of the stomach generally exceeded that found under duodenal ulcers. Gastric wall beneath the G. intestinalis ulcer frequently attained a thickness equal to or greater than the normal stomach wall. Histopathological examinations below the ulcer revealed intense fibrosis. Duodenal thickness below the G. nasalis ulcer was typically less than normal and resulted in an attenuated wall. Histopathological analysis of the affected duodenum revealed severe loss of submucosal glands in a sharply demarcated area below and surrounding the lesion. Fibrosis of the underlying lamina propria mucosae and tunica submucosa was appreciable but failed to restore the original thickness of the duodenal wall. Host tissue response and moderation of the parasite' s behavior reduce the chances of direct perforation of the gastrointestinal tissue.     

Small strongyle infection: consequences of larvicidal treatment of horses with fenbendazole and moxidectin

The study was undertaken to evaluate adverse effects of larvicidal treatment in horses naturally infected with cyathostomins. Out of 24 ponies kept on pasture, four animals were housed in September and anthelmintically cured to serve as worm-free controls (group C-0). The others were housed in December. Eight animals each were treated 8 weeks later with 5 x 7.5mg/kg fenbendazole (FBZ) or 1 x 0.4 mg/kg moxidectin (MOX). Four animals remained untreated (group C-i). Two, 4, 6 and 14 days after the end of treatment two animals of each of the treated groups were necropsied together with group C-0 and C-i animals. Infected animals before treatment showed weight loss, eosinophilia, increased plasma protein and globulin contents. Treatment was followed by weight gain and temporal plasma protein and globulin increase. Proportions of CD4+ and CD8+ T lymphocytes in the peripheral blood did not differ between the groups before treatment but dropped significantly temporally after FBZ treatment. Group C-0 was worm-free at necropsy. Group C-i animals contained variable numbers of luminal and tissue cyathostomins. Histological sections showed larval stages in the lamina propria und submucosa surrounded by macrophages. Either treatment was effective against luminal parasites and reduced the number of larvae in the bowel wall beginning 4-6 days after FBZ and 6-14 days after MOX treatment. Histologically, as a first reaction after FBZ application T lymphocytes accumulated around morphologically intact L4 in the submucosa. Subsequently T lymphocytes associated with eosinophils infiltrated the submucosa. Parasites became enclosed by granulomas with eosinophils adhering to and invading the larvae which started to disintegrate on day 4. Later on, particularly on day 14 inflammation extended into the mucosa and was frequently associated with ulcerations. Third stage larvae in general and L4 in the lamina propria, however, seemed not to be affected until day 14 and even then, parasites did usually not generate extensive inflammation. After MOX treatment severe morphologically detectable alterations of tissue larvae could not be observed earlier than day 14. Different from FBZ treatment, larvae disintegrated and were obviously resorbed without causing severe inflammation in the gut wall. In conclusion treatment with either drug was efficacious against tissue larvae of cyathostomins but there may be different clinical consequences: in contrast to MOX effects, killing of larvae due to FBZ was associated with severe tissue damage, which clinically may correspond to reactions caused by synchronous mass emergence of fourth stage larvae, i.e., may mimic larval cyathostominosis.     

An immunohistochemical study of S-100 protein in the intestinal tract of Chinese soft-shelled turtle, Pelodiscus sinensis

The present work describes the distribution of S-100 protein in the intestinal tract of a Chinese soft-shelled turtle specimen (Pelodiscus sinensis). S-100 protein positive cells were located in the intestinal tract, from the proximal small to distal large intestine. S-100 protein positive dendritic cells had irregular shape and were positive in both cytoplasm and nucleus. Most of them were located both lamina propria and submucosa in the small intestine, while few were found in the large intestine. S-100 protein, C-kit positive ICCs and Silver staining glial cells were predominantly observed in three locations: (1) in the interspace between the submucosa and circular muscle layer; (2) in the circular muscle layer; and (3) between the circular and longitudinal muscle layers of the intestine. Fewer were found in the large intestinal lamina propria and submucosa. Three types of positive cells (S-100 protein positive cells, C-kit positive ICCs and Silver staining glial cells) with 1–2 long or 2–3 short processes were distributed as lace-like or surrounding blood vessels in the different locations mentioned above. In the lamina propria, all the positive cells with irregular processes were connected with each other and formed a network. In the submucosa, all the positive cells were found surrounding the blood vessels.     

Prevalence, lesions, and differential diagnosis of Ollulanus tricuspis infection in cats

Ollulanus tricuspis were found in the stomachs of 26 of 201 cats which were mainly from Washington and Idaho. Twenty-four of the cats were from research or commercial breeding colonies (catteries) and two were pets. Twenty-seven percent of colony cats were infected with O. tricuspis, whereas only 2% of the pet cats were infected. No consistent clinical signs were seen. Histologically there was a significant increase in fibrous connective tissue in the lamina propria and in the number of lymphoid follicles and globule leukocytes in the gastric mucosa of infected cats. Histologic examination revealed no parasites in 13 of the 26 infected cats. The 26 infected cats were identified by examination of stomach washings. An additional 21 cats had larvae of other nematodes in their stomachs. These nematode larvae need to be differentiated from O. tricuspis.     

An immunohistochemical study of S-100 protein in the intestinal tract of Chinese soft-shelled turtle,Pelodiscus sinensis

The present work describes the distribution of S-100 protein in the intestinal tract of a Chinese soft-shelled turtle specimen (Pelodiscus sinensis). S-100 protein positive cells were located in the intestinal tract, from the proximal small to distal large intestine. S-100 protein positive dendritic cells had irregular shape and were positive in both cytoplasm and nucleus. Most of them were located both lamina propria and submucosa in the small intestine, while few were found in the large intestine. S-100 protein, C-kit positive ICCs and Silver staining glial cells were predominantly observed in three locations: (1) in the interspace between the submucosa and circular muscle layer; (2) in the circular muscle layer; and (3) between the circular and longitudinal muscle layers of the intestine. Fewer were found in the large intestinal lamina propria and submucosa. Three types of positive cells (S-100 protein positive cells, C-kit positive ICCs and Silver staining glial cells) with 1–2 long or 2–3 short processes were distributed as lace-like or surrounding blood vessels in the different locations mentioned above. In the lamina propria, all the positive cells with irregular processes were connected with each other and formed a network. In the submucosa, all the positive cells were found surrounding the blood vessels.     

Gizzard nematodiasis in Japanese mountain hawk eagle (Spizaetus nipalensis)

In this paper, we report spontaneous gizzard nematodiasis in an adult Japanese mountain hawk eagle (Spizaetus nipalensis). Grossly, the gizzard had a black mucoid substance attached to the surface mucous membrane, and the heart was dilated. Histologically, immature larvae with yellow pigments invaded crypts of the mucous membrane. More developed larvae invaded the lamina propria and muscular layers and serosa of the gizzard, with pressure atrophy and cellular reaction (infiltration of heterophils and macrophages and proliferation of fibrous connective tissue). Moderate bronchopneumonia due to larvae invasion was also seen in the lung. The morphology suggests that the parasites may be nematodes, but the species of nematode could not be confirmed. The bird may have died from malabsorption and respiratory damage as a result of the gizzard and lung lesions.     

Small strongyles. Recent advances

The recent increased interest in cyathostomes can be traced to simplification of their taxonomy, improved knowledge of pathogenicity, and failures of practical control due to anthelmintic resistance. Cyathostome ova develop to infective third-stage larvae (L3) at a rate that is directly proportional to environmental temperature. Equine feces serve as a reservoir for L3, which are liberated by moderate amounts of rainfall. Third-stage larvae persist for longer periods at low temperatures, easily surviving over-winter on pastures to provide a source of infection during the following grazing season. Third-stage larvae exsheath within the host and enter the mucosa and submucosa of the cecum and large colon. Larvae develop within mucosal cysts, molt to the fourth stage, and may persist within the tissues for up to 2 1/2 years. Larvae ultimately emerge from the mucosa to become adults in the lumen. Adult populations are replenished by recently ingested larvae and by immature worms newly emerged from arrested development. The magnitude of larval and adult populations within the host displays seasonal variations, with peak numbers occurring in early spring and autumn in the United States. In typical natural infections, a small number of species comprise the majority of the cyathostome populations. Cyathostome infection may result in anorexia, weight loss, diarrhea, colic, and death. Cyathostome ova are easily detected in feces, but ova may not be present during larval cyathostomiasis. Increased concentrations of beta-globulins, hypoalbuminemia, anemia, and leukocytosis occur inconsistently. Two major problems in the treatment of cyathostome infections are anthelmintic resistance and the insusceptibility of encysted larvae to recommended dosages of most anthelmintics. The major goal of cyathostome control is prevention of environmental contamination with nematode ova. Host resistance appears to protect against cyathostome disease rather than cyathostome infection, and one manifestation of this resistance appears to be prolongation of the prepatent period.     

Bovine ileal dome lymphoepithelial cells: endocytosis and transport of Brucella abortus strain 19

Ligated ileal loops of calves were inoculated with Brucella abortus and examined at 2, 4, 6, 10, and 24 hours post-inoculation. B. abortus was identified by light and electron microscopy using immunoperoxidase and antibody-coated colloidal gold techniques. B. abortus was detected in vesicles, phagolysosomes, and large vacuoles of lymphoepithelial cells. Numbers of intracellular bacteria decreased with time after inoculation. B. abortus was also seen between and below lymphoepithelial cells and free in the dome interstitium and intestinal lymph vessels. Neutrophils and macrophages in both epithelium and lamina propria contained intact or degraded bacteria within phagosomes, phagolysosomes, and multivesicular bodies. These studies showed that (1) transepithelial migration of B. abortus occurred principally by dome lymphoepithelial cell endocytosis and transport, and (2) B. abortus was degraded by macrophages and neutrophils of the gut-associated lymphoid tissue.     

Experimentally induced porcine proliferative enteritis in specific-pathogen-free pigs

Thirty-three, 10-week-old, specific-pathogen-free pigs were randomly allotted to 3 treatment groups: group 1--intragastrically given homogenized intestinal mucosa (crude inoculum) from pigs with naturally occurring proliferative enteritis; group 2--given cultures of Campylobacter sputorum subsp mucosalis; and group 3--controls. One pig from each group was killed 4, 7, 10, 14, 18, 21, 24, 28, 31, 36, and 38 days after inoculation. The earliest intestinal lesion observed in groups 1 and 2 was leukocytic exudate within crypt lumina and focal inflammation of the surrounding lamina propria. The lesions occurred primarily over ileal aggregated lymphoid nodules (Peyer's patches). These changes were followed by focal proliferation of immature crypt epithelial cells and infiltration of increasing numbers of macrophages into the lamina propria. Campylobacter sp-like organisms were observed within the cytoplasm of affected epithelial cells by light and electron microscopies. Lesions progressed to diffuse crypt cell proliferation, elongation of crypts, and loss of villi. Mucosal necrosis was not a prominent feature.     

Normal and abnormal xylose absorption in the horse.

The D-xylose absorption test was applied to clinically normal horses and to horses with signs of gastrointestinal disease. A dosage of 0.5 grams of xylose per kilogram of bodyweight was useful in detecting horses that absorbed the pentose abnormally. The clinical findings were correlated with gross and microscopic findings by biopsy and at necropsy. Gastrointestinal lesions associated with abnormal xylose absorption were classified as: 1) villous atrophy; 2) edema of the lamina propria or 3) necrosis of the lamina propria.     

Morphology of the non-sensory tissue components in rat aging vomeronasal organ

With 30 figures, 3 histograms and 3 tables SUMMARY: The vomeronasal organ (VNO) is a chemosensory organ that detects environmental pheromones. The morphology of the 'non-sensory' epithelium (NSE) of the VNO and its lamina propria, as well as how it relates to ageing has received little attention. Histological, histochemical, morphometric and ultrastructural techniques were used to study the morphological structure of the rat NSE in five adult (3 months old) and five aged (2-2.5 years old) male albino rats. In adult rats, the NSE contained dark and light columnar cells with predominance of the latter. The surface of the epithelial cells was covered with microvilli and/or cilia. The lamina propria contained serous vomeronasal glands (VNGs), smooth muscles with numerous variable-sized mitochondria, vessels including lymphatic capillaries and nerve bundles. The following changes were detected in aged rats. The NSE exhibited an increase in number of dark columnar cells. Some cells revealed a prominent cell coat, dense aggregation of filaments in the luminal cytoplasm and appearance of multinucleated cells. Their surface revealed malformed configuration. Large mitochondria (2 μm), formed by fusion, were frequently observed in the smooth muscle cells of the lamina propria. Lipid droplets were frequently detected both in the VNGs acini and in the lymphatic endothelium. Ageing affected both the cells of the tissues and the extracellular matrix.     

The development of the lesions caused by second generation schizonts of Eimeria necatrix.

First generation merozoites of Eimeria necatrix were found in epithelial cells of the crypts of Lieberkühn of chicks cells appeared to migrate into the lamina propria, forming nests of second generation schizonts that extended from the external muscularis to the lamina propria of the mid-villus. On the fourth and fifth days the mature schizonts, usually still within the infected cells were dishcarged into adjacent crypts. The muscularis mucosa appeared to be repaired by the formation of new, smooth muscle cells that spliced the broken ends of the ruptured muscle. 'Ghosts' of schizonts were found in the lamina propria on the sixth day after infection.     

Cell mediated responses in a porcine enterovirus infection in piglets.

Sixteen pathogen-free piglets were infected orally with procine enterovirus strain T80 and the cell mediated response to the virus was measured at intervals after infection. Five uninfected piglets were used as controls. Indirect macrophage migration inhibition tests were performed with lymphocytes from blood, ileal lamina propria and mesenteric lymph node. Blood lymphocyte culture supernatants showed no consistent T80 specific on macrophage migration, suggesting the absence of a systemic cell-mediated response. Ileal lamina propria lymphocyte culture supernatants showed irregular migration stimulation. The mesenteric lymph node lymphocyte culture supernatants produced migration inhibition at seven days postinfection, followed by stimulation of migration from ten to 22 days postinfection. Subsequently, migration was again inhibited from 24 to 31 days postinfection. Mesenteric lymph node lymphocyte culture supernatants contained only trace amounts of interferon activity at 28 and 31 days postinfection. It was concluded that the cell mediated responses in this infection were weak and localized and not associated with significant antiviral activity.     

Mycotoxicosis caused by aerosolized T-2 toxin administered to female mice

Thymus, spleen, adrenal glands, and small intestine of female mice exposed to aerosolized T-2 mycotoxin were examined at postexposure hours (PEH) 0.25, 1, 2, 4, 6, 9, 12, and 24. Lymphocyte necrosis was observed at PEH 1 in the thymus, spleen, and lamina propria and Peyer patches of the small intestine. Necrosis of small intestinal crypt epithelial cells was observed at PEH 2, and necrosis of parenchymal cells and increased number of neutrophils were seen in sinusoids of the adrenal cortex at PEH 4. These results indicated that the earliest microscopic evidence of T-2 mycotoxicosis after aerosol exposure was necrosis of lymphocytes in the thymus, spleen, and lamina propria and Peyer patches of the small intestine.