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PubMed1994

[Clinical diagnosis of malaria and amoebiasis].

In all patients with fever after returning from tropical countries malaria must be excluded. Amebic liver abscess is an important differential diagnosis, especially in patients with pain in the right epigastrium. In all patients with diarrhea after returning from tropical countries amebic colitis is an important differential diagnosis. The diagnosis of malaria is based on microscopical demonstration of the parasite in blood slides. In patients with Plasmodium falciparum malaria the extent of organ complications has to be checked. The diagnosis of intestinal amebiasis rests on parasitological stool examination. Amebic liver abscess is diagnosed by demonstration of the liver abscess in imaging techniques and verification by finding specific antibodies.

Amebiasis↗
PubMed1997

Expression of costimulatory molecules B7-1 and B7-2 in macrophages and granulomas of Crohn's disease: demonstration of cell-to-cell contact with T lymphocytes.

The pathogenesis of Crohn's disease, an intractable inflammatory disease, involves impaired and/or excessive activation of mucosal macrophages and T lymphocytes. B7-1 (CD80) and B7-2 (CD86) molecules are costimulatory molecules that are indispensable to T-cell activation by antigen-presenting cells. To elucidate the roles and characteristics of these antigen-presenting cells in Crohn's disease, in situ localization of B7-1 and B7-2 (in relation to the distribution of T cells) was clarified by light and electron microscopic immunohistochemistry. The results were compared with those from a study of ulcerative colitis. Normal colonic tissue expressed B7-1 or B7-2 only sporadically. In active Crohn's disease, however, an increase in the number of B7-1/B7-2+ cells correlated with an increase in expression of HLA-DR and intercellular adhesion molecule-1. Most B7-1/B7-2+ cells were identified as noncaseating granulomas or as macrophages, which tended to form an aggregate especially in ulcer bases. In active ulcerative colitis, the increase of B7-1/B7-2+ cells was not as prominent as that in Crohn's disease. Double immunohistochemistry revealed a close cellular distribution between noncaseating granulomas and T cells. Immunoelectron microscopy confirmed the expression of B7-1/B7-2 along the plasma membranes of cytoplasmic processes of granuloma cells, where lymphocytes were closely attached. The present study suggested that granuloma formation in Crohn's disease is coupled with antigen presentation via a B7-1/B7-2-CD28 pathway, which may contribute to the pathogenesis of the disease.

Adult↗
PubMed2003

[Mechanism of the intestinal dysmotility in the inflammatory bowel diseases: possible involvement of muscularis resident macrophages].

We evaluated the changes in interstitial cells of Cajal (ICCs) and myenteric nerve system in relation to the activity and number of muscularis resident macrophage at a level of myenteric nerve plexus in the Crohn's disease model treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). In the TNBS-treated rat colon, ICCs network and also myenteric nerve system were damaged or disappeared in the inflamed region. The number of ED2-immunoreactive resident macrophage significantly increased where the ICCs or myenteric nerve systems changed. Although resident macrophage appeared morphologically ramified in control intestine, TNBS-treatment changed it to round shape, possibly an indication of functionally activated state. In fact, the round shape of macrophage expressed marked MHC class II comparing ramified macrophage in control intestine. Physiological study indicated that the motility index, the amplitude and frequency of spontaneous contractions were significantly decreased in the TNBS-induced colitis intestine. Moreover, the index of peristalsis observed in whole proximal colon tissue was inhibited by the treatment with TNBS. Electron microscopic analysis indicated that the contour of the myenteric ganglia became irregular in TNBS-treated rat colon, and numerous macrophages were observed around the ganglia. Similar results were obtained in the Hirschsprung's disease colitis model rats. In conclusion, the inhibition of spontaneous contractions and peristalsis in circular smooth muscle from TNBS-induced colitis rat colon may be attributable to the impairment of ICCs and myenteric nerve systems. Because of an indication of the macrophage activation and the close correlation between the degeneration and macrophage accumulation, it is suggested that the macrophages are involved in the degenerative pathology of intestinal motility.

Animals↗
PubMed1977

Colitis cystica profunda: report of a case in which differentiation from rectal cancer was difficult.

Colitis cystica profunda is a benign condition that has been confused with carcinoma. This rarely recognized condition is characterized by submucosal cysts. Macroscopically, the ulcerated character of the mass suggests carcinoma. Microscopically, attenuation of the innocuous-appearing cyst linings may give the false impression of a mucus-secreting carcinoma. A case of colitis cystica profunda in which the macroscopic appearance was so suggestive of malignancy that operation was carried out is reported.

Adenocarcinoma↗
PubMedDate not supplied

Ulcerative colitis and malignancy.

Ulcerative colitis is associated with an increased risk for colorectal cancer. The increase is approximately six to ten times the expected in the general population. Disease duration and extension are the major risk factors. Concomitant primary sclerosing cholangitis is an additional independent risk factor. The relative risk is approximately 14.8 for patients with pancolitis while it is 1.7 for patients with disease restricted to the rectum. The risk increases rapidly after 20 years of disease evolution. Active treatment might decrease the risk. The increased cancer risk is a major problem for longterm management of patients with ulcerative colitis. It is the rationale for various surveillance programs and the search for dysplasia. Two major types of dysplasia must be distinguished in ulcerative colitis: sporadic adenomas and ulcerative colitis-associated dysplasia. Sporadic adenomas can be treated by simple polypectomy. The diagnosis of dypsplasia relies mainly on microscopic analysis of biopsy samples. Additional techniques, including flow cytometry and the search for DNA abnormalities and immunohistochemistry or molecular techniques looking for genetic defects can help to improve the diagnostic yield.

Colitis, Ulcerative↗
PubMedDate not supplied

Contribution of immunofluorescence to the identification and characterization of anti-neutrophil cytoplasmic autoantibodies. The role of different fixatives.

OBJECTIVE: To study the sera from selected groups of antineutrophil cytoplasmic antibody (ANCA) positive patients by means of the indirect immunofluorescence test (ANCA-IIF) with different fixatives, in order to better discriminate among the various ANCAs (Ag-specificity and disease associations), especially those for which the antigen targets have not yet been identified. METHODS: Eighty pathological serum samples and 15 normal sera were evaluated. Pathological samples included sera from 30 ulcerative colitis (UC) ANCA positive patients, 30 P-ANCA/myeloperoxidase (MPO-ANCA) positive microscopic polyangiitis (MPA) patients, 10 C-ANCA/proteinase 3 (PR3-ANCA) positive Wegener's granulomatosis (WG) patients, and 10 antinuclear antibody (ANA) positive (ANCA negative) systemic lupus erythematosus (SLE) patients. ANCA were detected by IIF on ethanol, methanol and formalin-fixed granulocytes and by ELISAs specific for MPO, PR3, lactoferrin (LF) and bactericidal/permeability-increasing protein (BPI). Additionally, sera were tested for the presence of antinuclear antibodies on IIF. RESULTS: 96% of serum samples from UC patients, positive by IIF on ethanol-fixed granulocytes, became negative when tested on formalin-fixed neutrophil slides. On the contrary, 95% of sera from vasculitic patients showed a clear diffuse granular cytoplasmic pattern on the same substrate; sera from all 10 SLE patients did not show any reactivity when formalin was used as fixative. On methanol-fixed neutrophils, 100% of UC P-ANCA positive sera were positive with the same pattern versus only 20% of vasculitic P-ANCA positive (MPO positive). Methanol fixation had no effect on PR3-ANCA and ANA positive sera. CONCLUSION: The comparison of IIF patterns of sera tested on different fixed cells may be useful to distinguish vasculitis-related P-ANCA versus ANA and vasculitis-related P-ANCA versus UC-related P-ANCA.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1996

Crohn's disease in a 92-year-old male.

A case of Crohn's disease in an extremely elderly man (92-years-old) is reported. He was admitted for abdominal pain and was operated on under a diagnosis of ischemic colitis. At the mucosal surface, many linear and irregularly shaped shallow ulcers were found on the mesenteric side. Microscopically, transmural inflammatory cell infiltration, bead-like lymphoid aggregates around the propriate muscle, small epithelioid cell granulomas, fissure, and volcano-like streamers of inflammatory cells were found. Nerve fibers in Meissner's and Auerbach's plexi seemed to be increased in number, and some were hyperplastic. There was no feature of ischemic colitis or Yersinia enteritis. Serially sectioned tissue specimens did not show dysplastic mucosal change. Many cases of Crohn's disease in the elderly have been reported but an extremely elderly patient such as the present one is very rare, especially in Japan. Characteristics of elderly patients with Crohn's disease are discussed.

Age of Onset↗
PubMed2001

Dual effect of chronic nicotine administration: augmentation of jejunitis and amelioration of colitis induced by iodoacetamide in rats.

Smoking has a dichotomous effect on inflammatory bowel disease, ameliorating disease activity in ulcerative colitis but having a deleterious effect on Crohn's disease. This effect is thought to be due to nicotine. We investigated the effect of chronic nicotine administration on the small and large bowel in iodoacetamide-induced jejunitis and colitis. Jejunitis was induced in Sprague-Dawley rats by intrajejunal administration of 0.1 ml 2% iodoacetamide and colitis by intrarectal administration of 0.1 ml 3% iodoacetamide. Nicotine was dissolved in drinking water (12.5 or 250 micrograms/ml), rats drinking ad libitum. Nicotine administration started 10 days prior to damage induction and throughout the experiment and had no effect on weight gain or daily food intake of rats. Rats were killed 5 days after iodoacetamide-induced colitis and 7 days after induction of jejunitis. The jejunum and colon were resected, rinsed, weighed, damage assessed macroscopically and microscopically and tissue processed for myeloperoxidase and nitric oxide synthase (NOS) activities and prostaglandin E2 (PGE2) generation. Effects of nicotine on gut microcirculation were also assessed. Nicotine by itself caused no damage to the colon. Nicotine had a dichotomous effect on jejunitis and colitis. At a dose of 12.5 micrograms/ml nicotine improved the macroscopic damage of colitis from 252 +/- 66 to 70 +/- 31 mm2, and segmental weight also declined significantly in the colon (from 1.7 +/- 0.2 to 1.2 +/- 0.1 g/10 cm). In contrast, the same dose of nicotine had a deleterious effect on iodoacetamide-induced jejunitis, increasing the macroscopic damage from 368 +/- 38 to 460 +/- 97 mm2 in rats treated with injury escalating to 970 +/- 147 in rats treated with 250 micrograms/ml nicotine. Nicotine treatment also significantly increased jejunal segmental weight. By itself nicotine did not change NOS activity or PGE2 generation compared to control rats, but it enhanced microcirculation in the colon, whereas in the jejunum nicotine decreased PGE2 generation and increased NOS activity but not jejunal microcirculation. Nicotine has opposite effects on iodoacetamide-induced colitis and jejunitis, which may be partly explained by decreased PGE2 generation and increased NOS activity in the jejunum and an increase in the colonic microcirculation.

Animals↗
PubMed1999

Does microcirculation play a role in the pathogenesis of inflammatory bowel diseases? Answers from intravital microscopic studies in animal models.

The potential role of intestinal microcirculation for the development of inflammatory bowel diseases (IBD) has not been systematically investigated, mainly because of methodological problems. Using a well-established rodent model of IBD and intravital microscopy, the present study investigated whether (and when) gut microcirculation is disturbed in IBD, and whether microcirculatory disorders contribute to histological and functional alterations in the development of IBD. Colitis was induced by rectal injection of trinitrobenzene sulfonic acid. After 1, 3, and 15 days rats were laparotomized for intravital microscopic determination of mucosal colonic blood flow. In a second series it was examined whether enhancing colonic capillary blood flow by hemodilution therapy stabilizes colonic wall resistance and other electrophysiological parameters of gut permeability. Additional measurements involved hemodynamic monitoring and histological examinations. Colonic capillary blood flow was significantly decreased 3 days after colitis induction (1.8 +/- 0.05 vs. 2.6 +/- 0.04 nl/min in healthy control animals) when histology revealed signs of acute inflammation, and normal values after 15 days (2.4 +/- 0.06 nl/min) when chronic histological changes were evident. Hemodilution therapy enhanced colonic capillary blood flow in the initial stage (2.1 +/- 0.02 vs. 1.6 +/- 0.02 nl/min in saline-treated animals with trinitrobenzene sulfonic acid colitis) and improved gut resistance and electronic chloride secretion (73 +/- 15 vs. 33 +/- 8 microA cm2). Histological alterations were not significantly attenuated. Impaired colonic capillary blood flow in the initial stage of experimental colitis and improved mucosal microcirculation with stabilized gut permeability suggests that the early microcirculatory disturbances precede chronic histological changes and influence functional alterations in the course of the disease. Research should be continued in this field because important mechanisms in the pathogenesis of IBD and potentially therapeutic (vasoactive) substances may otherwise be overlooked.

Animals↗
PubMed1975

Intercurrent cytomegalovirus colitis in a patient with ulcerative colitis.

Acute intercurrent CMV colitis developed in a patient with UC who was receiving prednisone. CMV infection was suggested by light and electron microscopic study of a rectal biopsy taken during the acute episode and was confirmed by serology done nine months later. The microscopic studies of plastic-embedded tissues demonstrated that infected cells were concentrated in a subendothelial location and were presumably macrophages. Epithelial and endothelial cells were not involved. Steroid therapy and the inflammation and repair process (granulartion tissue) of active UC may have predisposed the present patient to CMV colitis. CMV infection has been reported to be more common in patients with UC than in the general population. Detection of CMV colitis in patients with UC could be of special importance since alteration of immunosuppressive therapy may be indicated.

Acute Disease↗
PubMed2005

Beneficial effects of N-acetylcysteine on acetic acid-induced colitis in rats.

Ulcerative colitis is a chronic recurrent inflammatory bowel disease in which oxidative stress has been implicated. The aim of the present study was to evaluate possible protective effects of N-acetylcysteine against acetic acid-induced colitis in a rat model. Rats were administered intrarectal saline (control group) or acetic acid (colitis model group). Rats with acetic acid-induced colitis were treated by intraperitoneal or intrarectal administration of N-acetylcysteine (500 mg/kg) (treated group). Another series of rats were pre-treated by intraperitoneal or intrarectal administration of N-acetylcysteine, then administered intrarectal acetic acid (pre-treated group). The degree of tissue injuries was assessed by macroscopical and histopathological scores of the colonic mucosa. Malondialdehyde, myeloperoxidase, reduced glutathione, superoxide dismutase, and catalase levels were measured in tissue extracts of the dissected colon. Administration of N-acetylcysteine intraperitoneally or intrarectally ameliorated macroscopic score alterations produced by acetic acid in treated groups. In addition, microscopical improvement was observed in all N-acetylcysteine-treated rats compared to untreated animals with colitis. In the colonic tissues of the acetic acid-induced colitis, myeloperoxidase activity and malondialdehyde levels were elevated, while the reduced glutathione levels and superoxide dismutase and catalase activities were decreased. However, intraperitoneal or intrarectal treatment with N-acetylcysteine reversed these parameters, compared to the untreated colitis group. Notably, intrarectal administration of N-acetylcysteine elevated the reduced glutathione levels more markedly compared to the other treatment groups. Superoxide dismutase levels were increased in intraperitoneally or intrarectally N-acetylcysteine-treated groups significantly compared to the control, colitis and pre-treated groups. But there was no significant increase in catalase activity. In conclusion, N-acetylcysteine could be beneficial as a complementary agent in treatment of ulcerative colitis.

Acetic Acid↗
PubMed1984

Evaluation of the 24-h API 20A anaerobe system for identification of Clostridium difficile.

Accurate identification of Clostridium difficile is important when antibiotic-associated diarrhea or pseudomembranous colitis is suspected. Presumptive identification of C. difficile was made on the basis of microscopic features and colony characteristics on cycloserine, cefoxitin, fructose, and egg yolk agar medium. We studied the reliability of the 24-h API 20A anaerobe system for definitive identification of C. difficile. This system showed low dependability after the recommended 24 h of incubation by confirming the identity of only 54% of the isolates presumptively identified as C. difficile. There was a marked improvement in the system's capability after 48 h of incubation, when the identity of 95% of the isolates was confirmed.

Anaerobiosis↗
PubMed2003

Hepatitis associated with a Sarcocystis canis-like protozoan in a Hawaiian monk seal (Monachus schauinslandi).

A Hawaiian monk seal (Monachus schauinslandi) died in captivity at the National Marine Fisheries Service, Kewalo Basin Facility in Honolulu, Hawaii. The animal was icteric, and the liver was friable. Microscopic lesions were detected in the colon and liver. Colonic lesions included multifocal, necrohemorrhagic colitis associated with gram-negative bacilli. The liver lesions included random hepatic necrosis and cholestasis. Asexual stages of a Sarcocystis canis-like apicomplexan were detected in hepatocytes. The parasite divided by endopolygeny. Merozoites occasionally formed rosettes around a central residual body. Ultrastructurally, merozoites lacked rhoptries. This is the first report of S. canis infection in M. schauinslandi, which is an endangered pinniped in U.S. waters.

Animals↗
PubMed1978

Equine myositis and septicemia caused by Acinetobacter calcoaceticus infection.

Myositis and septicemia caused by Acinetobacter calcoaceticus were diagnosed in a mare. The infection was characterized clinically by ventral swelling and edema, diarrhea, listlessness, and rectal temperature of 39.4 C. The mare was treated symptomatically for 2 days but died on the 3rd day. Conditions seen at necropsy were myositis, enteritis, typhlitis, colitis, and hepatitis. Lymph nodes were moderately enlarged throughout the body. Gross lesions in musculature were edema, scarring, petechiae, and an occasional exxhymosis. The enteritis was catarrhal, with excessive mucus and moderate hyperemia. The typhlitis and colitis were hemorrhagic. The swollen liver had a diffuse mottled pale and red pattern. Microscopic lesions in skeletal muscle consisted of petechiation, necrosis, scarring, and edema. Cardiac muscle was also scarred and necrotic, but edema was not prominent. Periacinal necrosis was found in the liver. Acinetobacter calcoaceticus was isolated from myocardium and liver.

Acinetobacter Infections↗
PubMed1981

[Pathogenesis of colon diverticular disease (author's transl)].

The longitudinal musculature of the taenia of the colon does play an important role in diverticular disease (DD), as can be found by comparing light and electron microscopic pictures of the colon from healthy persons and patients with diverticulitis and ulcerative colitis. Already in the early stages histological changes can be found, which have to be interpreted as being due to maximal contraction of the longitudinal musculature and to increased metabolism. These morphological changes are accompanied by increased electrical and mechanical activity. Disturbed function seems to be myogenic, as could be shown by studies with different drugs. These results seem to indicate that it might be preferable to incise the longitudinal musculature of the colon transversally during surgery because of diverticulosis.

Colitis, Ulcerative↗
PubMed1999

Bombesin ameliorates colonic damage in experimental colitis.

In the present study we investigated the possible therapeutic effects of bombesin on an experimentally induced colitis model in rats. Inflammation of the colon was induced by a single intracolonic administration of 30 mg of 2,4,6-trinitrobenzene sulfonic acid (TNBS) at 8 cm from the anus. Immediately after the induction of colitis, some rats were given bombesin (10 microg/kg; subcutaneously) three times a day for 14 days, while another group received vehicle treatment. On day 14, the rats were decapitated and plasma carbonyl content and tissue myeloperoxidase level, as an index of granulocyte infiltration into intestinal tissue, were determined in order to obtain an objective evaluation of colonic injury. In the colitis group, increased macroscopic damage score, elevated MPO level and high plasma carbonyl content, together with the microscopic appearance revealed severe inflammatory changes resembling IBD. Bombesin treatment attenuated the TNBS-induced colonic damage and stimulated histopathologically apparent mucosal proliferation, suggesting that bombesin may play a role in protecting gut integrity.

Animals↗
PubMed1999

Butyrate from bacterial fermentation of germinated barley foodstuff preserves intestinal barrier function in experimental colitis in the rat model.

BACKGROUND AND AIMS: The consumption of germinated barley foodstuff (GBF) prevents inflammation and diarrhoea in a colitis model. In this study we investigated the mechanism of the preventative effect of GBF on experimental colitis in rats, in view of production of bacterial butyrate and preservation of intestinal barrier function. METHODS: Sprague-Dawley rats administered with diets supplemented with 3.5% dextran sodium sulphate were used as an experimental colitis model. Butyrate was given to rats orally or intracaecally. Intestinal barrier function was estimated by light microscopic observation of the mucosa, intestinal permeability and bacterial translocation. RESULTS: Mucosal damage was reduced by intracaecal administration of butyrate, but not by oral administration. Bacterial butyrate production and reduction of mucosal damage depended on the dose of GBF in diets. The action of endogenous bacterial butyrate, including the reduction of intestinal permeability and bacterial translocation, was inhibited by administration of an inhibitor of beta-oxidation of short-chain fatty acids. CONCLUSIONS: The feeding of GBF promotes bacterial butyrate production and improves intestinal barrier function in rats, resulting in mitigation of experimental colitis.

Animals↗