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PubMed2003

Immunohistochemical localization of Clostridium perfringens beta2-toxin in the gastrointestinal tract of horses.

Clostridia-associated intestinal disease in horses was generally reported to be due to infection with Clostridium perfringens type A, which harbors the cpa-encoded alpha-toxin. A recent study demonstrated a high incidence of beta2-toxigenic C. perfringens in horses suffering or dying from typhlocolitis, suggesting that this novel type of C. perfringens might play an important role in typhlocolitis and possibly other equine intestinal diseases. A retrospective study was conducted to assess the presence of the beta2-toxin in tissues of the equine gastrointestinal tract. Monospecific polyclonal antibodies against recombinant beta2-toxin were produced in rabbits and used to demonstrate the beta2-toxin in sections of the gastrointestinal tract by immunohistochemical methods. Sections from 69 horses were stained and beta2-toxin was observed immunohistochemically in 40 animals. Sections from the stomach, small intestine, and large intestine were positive. Immunopositivity for beta2-toxin was significantly associated with presence of beta2-toxigenic bacteria. This investigation demonstrates local production of beta2-toxin and suggests that immunohistochemistry using antitoxin antibodies represents a useful diagnostic method in those cases where isolation of bacteria and polymerase chain reaction typing is not feasible. Although the association between the presence of beta2-toxin and development of gastrointestinal disease in horses remains uncertain, the findings of this study indicate that the potential causal relationship warrants further investigation.

Animals↗
PubMedDate not supplied

[Experience with peroral biopsy of the small intestine at the University Hospital--Federal University of Rio de Janeiro].

The experience with 103 jejunal biopsies in the Rio de Janeiro University Hospital--UFRJ, from January 1983 to June 1985 is presented. It is reported the effectiveness of the method and the low number of complications. The importance as a valuable complementary method of diagnosis and the usefulness in the small intestine disease's scientific investigation is emphasized.

Adolescent↗
PubMed1998

Molecular mechanisms of enteroendocrine differentiation.

Passing through a complex series of developmental steps, the visceral endoderm differentiates into four intestinal epithelial lineages comprising enterocytes, goblet cells, paneth cells, and enteroendocrine cells. The intestinal enteroendocrine system consists of at least 15 different cell types, which can be classified on the basis of morphological criteria, expression of secretory products, and abundance of specific marker molecules. During intestinal development and in the adult gut, neuroendocrine subpopulations display strictly controlled differences in their geographical distribution that go along with dramatic differences in cell type-specific gene expression. Identification to transcription factors and regulatory DNA elements responsible for cell-specific gene expression in different neuroendocrine cell types as well as various transgenic and "knock-out" mouse models have largely added to our understanding of mechanisms controlling appropriate special and temporal activation of enteroendocrine differentiation programs. This article reviews current in vitro and in vivo studies analyzing different molecular aspects of enteroendocrine differentiation. In addition, the influence of intestinal diseases including malignant transformation on enteroendocrine differentiation and the underlying mechanisms will be discussed.

Animals↗
PubMed1996

Sonde enteroscopy. Technique, depth of insertion, and yield of lesions.

Sonde enteroscopy provides the only opportunity to directly view the contents and mucosa of potentially the entire small intestine. Although the instrumentation and technique are less than ideal, sonde enteroscopy can be a useful adjunct to the evaluation of small intestinal disease. A comprehensive review of this labor-intensive procedure from patient selection to its outcome is provided in this article.

Diagnosis, Differential↗
PubMed1981

Human intestinal mononuclear cells. II. Demonstration of a naturally occurring subclass of T cells which respond in the allogeneic mixed leukocyte reaction but do not effect cell-mediated lympholysis.

We have examined the T-cell functional capabilities of human intestinal mononuclear cells isolated from surgically obtained normal and inflammatory bowel disease intestinal specimens. Intestinal mononuclear cells have T cells present which respond to the mitogenic lectins E-PHA, Con A, and PWM and to foreign cell-surface antigens in the allogeneic-mixed leukocyte reaction. Intestinal mononuclear cells from ulcerative colitis patients exhibit a significantly decreased responsiveness in comparison to normal intestinal mononuclear cells with regard to both mitogenesis and the allogeneic-mixed leukocyte reaction; however, these defects may be secondary to the severity of the disease process that led to intestinal resection or the therapy which patients had received. Although both normal and inflammatory bowel disease intestinal mononuclear cells exhibit responsiveness in the allogeneic-mixed leukocyte reaction, thus indicating recognition of and sensitization by foreign cell-surface determinants, intestinal mononuclear cells do not subsequently kill the sensitizing cells in cell-mediated lympholysis. Therefore, the subclass of T cells which mediates cell-mediated lympholysis may either be absent from intestinal mononuclear cells or nonfunctional, while the subclass of T cells which responds in the allogeneic-mixed leukocyte reaction is both present and functional. This observation adds to the evidence of major functional differences between intestinal and peripheral blood mononuclear cells. Therefore, it will be necessary to better understand the factors regulating the effector capabilities of intestinal mononuclear cells before delineation of immunopathologic events in these tissues.

Adult↗
PubMed2005

Pattern recognition and feature extraction of canine celiac and cranial mesenteric arterial waveforms: normal versus chronic enteropathy--a pilot study.

In this pilot study, we hypothesize that waveform patterns of the celiac and cranial mesenteric arteries differ pre- and post-prandially in normal dogs compared to those with chronic enteropathy. We further suggest that it is possible to classify these findings according to the type of disease present. Eleven dogs with chronic enteropathy and eight normal dogs were examined. Doppler examinations were performed at times 0 (fasted), and at 20, 40, 60 and 90 min post-prandially. The waveform shapes were described and the following features were extracted: resistive and pulsatility index, mean maximum velocity, mean diastolic velocity, peak systolic velocity, early diastolic notch ratio and the deceleration time interval. Dogs with inflammatory bowel disease had either lower or absent flow at fasting in early diastole compared to the other groups. Resistive and pulsatility indices decreased during digestion in all groups except those with protein losing enteropathy. The increase in mean diastolic flow during digestion in affected dogs was either lacking (protein-losing enteropathy) or significantly lower (inflammatory bowel disease, P<0.05) compared to normal dogs. Dogs with chronic enteropathies had abnormal arterial waveform shapes and suboptimal increases in diastolic blood flow during digestion and these findings worsened with the severity of the histological lesions present. Doppler ultrasound of the celiac and mesenteric arteries has great potential to enhance our understanding of intestinal disease in conscious dogs.

Animals↗
PubMed1991

Blastocystis hominis--past and future.

The history of B. hominis is unique. Few infectious agents have provoked the many misconceptions that plague this enigmatic parasitic ameba. Conflicting descriptions of its nature and pathogenesis have continued throughout the 20th century. As seen by the greatly expanded number of reports in recent years, B. hominis is now a major subject of study, particularly for evidence of disease causation. Physicians are treating patients with intestinal disease caused by B. hominis. Many mild cases resolve in about 3 days without treatment, but others are acute and chronic disease is common. As with E. histolytica, the carrier state is often seen without symptoms. Treatment is usually with metronidazole, but emetine (for refractory infections), trimethoprim-sulfamethoxazole, and pentamidine are also effective. In fecal samples, this complex protozoan appears in a variety of cell forms which makes microscopic diagnosis difficult. As yet, no specific fluorescent-antibody test is available for diagnosis. A culture method to demonstrate the more easily recognized CB form is available, but probably not feasible for most diagnostic laboratories. The common cell forms are the CB form, the granular (mitochondria) form, and the ameba form. The unexpected size range of these forms in clinical material, from yeast size (ca. 7 microns) to giant cells of 20 to 40 microns, makes diagnosis difficult Pseudopodia may be demonstrated by the ameba form in heated microscope stage culture chambers. The anaerobic B. hominis has no cyst form. Its mitochondria are uniquely anaerobic and have no cytochrome protein or oxidative mitochondrial enzymes. Because of its many cell forms and anaerobic mitochondria, B. hominis is an organism of great interest for morphologic and biochemical study. Reproduction is asexual, usually by binary fission. Shizogony occurs in cultured cells. The CB appears to be an organelle whose specific purpose is for reproduction by shizogony. From 2 to 30 progeny are derived from schizogony. The ameba form reproduces by plasmotomy; it has no CB. The pathology of B. hominis infections has been studied in gnotobiotic guinea pigs in which inflammation of the intestinal mucosa and invasion of the superficial layers were seen. Only limited studies of human pathology are available. Those who have studied mucosal histopathology report inflammation and cellular changes that resolve after treatment. More study in this area is strongly indicated (32, 44, 57, 62, 67, 75). Ultrastructural details of B. hominis major forms, except for the schizont, are complete. The organism has no cell wall. The concentric CB takes up as much as 95% of the cell. The major organelles, which include multiple nuclei, Golgi apparatus, mitochondria, endoplasmic reticulum, fat, and other inclusions, are confined in two or four opposed pods in a thin band of peripheral cytoplasm between the spherical entire plasma membrane and the CB membrane. The pods buldge the CB membrane inward. There is evidence of a bacteroid endosymbiont. Education about B. hominis is needed. Entry of recent findings into new textbooks is imperative for its understanding among medical practitioners. Laboratory workers need to be aware of it for many reasons. The College of American Pathologists includes B. hominis in its proficiency testing samples and requires that it be reported from clinical samples.

Animals↗