Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017536 (giardiasis)
 1,714 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data are presented on scanning electron microscopy (SEM) on small intestinal biopsies of children with chronic diarrhea. In particular, there were 230 patients aged 3 months to 13 years with the following diagnoses: chronic nonspecific diarrhea, cow's milk protein intolerance, soy protein intolerance, giardiasis, cystic fibrosis, gluten-sensitive enteropathy, isolated lactase deficiency, isolated sucrase-isomaltase lactase deficiency, microvillus inclusion disease, rotavirus enteritis, protracted diarrhea of infancy, chylomicron retention disease, visceral myopathy and villous asthenia. Examination of biopsied intestinal mucosa by SEM has yielded important new information and insights on structural pathology and ultrastructural topography. Many of the observed changes helped to better understand the pathophysiology of some of the diarrheal disorders. SEM was also able to detect new features such as mycoplasma-like microorganisms and the absence of the glycocalyx. To adequately assess small bowel mucosal pathology at the ultrastructural level, scanning electron microscopy is an indispensable tool.
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PMID:The scanning electron microscope: how valuable in the evaluation of small bowel mucosal pathology in chronic childhood diarrhea? 182 28

The aim of this study was to assess and correlate changes in weight gain, food intake, small intestinal disaccharidase activities and microvillous border surface area over the course of a primary Giardia duodenalis infection in weanling Mongolian gerbils (Meriones unguiculatus). Weight gain in infected animals was significantly impaired between days 8 and 20 postinoculation when compared to age- and weight-matched controls. No difference in food intake was observed between groups. Trophozoite population in the small intestine was maximal on day 4 and 6 of infection, and colonization persisted in the duodenum throughout the experiment (30 days). In infected gerbils, mucosal sucrase and maltase activities were significantly depressed in the duodenum and jejunum on day 4 and in all areas of the small intestine by day 6. Eight and 25 days postinoculation, disaccharidase activities had recovered in the jejunum and distal small intestine but remained depressed in the duodenum, the area where trophozoite colonization persisted. Diffuse loss of microvillous border surface area was observed in the duodenum and jejunum after 6 days of infection. Eight days postinoculation, microvillus surface area had returned to normal in the jejunum, but not in the duodenum. Our findings demonstrate that acute giardiasis in weanling gerbils impairs weight gain, depresses disaccharidase activities, and diffusely reduces mucosal microvillous border surface area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth, activities of enzymes in the small intestine, and ultrastructure of microvillous border in gerbils infected with Giardia duodenalis. 202 78

In a retrospective study, jejunal mucosal disaccharidase and alkaline phosphatase activities have been investigated in 40 controls and patients with proven celiac sprue (n = 26), lactase deficiency (n = 26), osteoporosis or osteomalacia (n = 16), chronic pancreatitis (n = 12), giardiasis (n = 7), or Crohn's disease (n = 7). Apart from a nonselective reduction of mucosal enzyme activities in the sprue syndrome and a selective reduction of lactase activity in the patients with primary lactase deficiency, assays of mucosal disaccharidases revealed only inconstant or slight deviations from the control group and were not of diagnostic significance for any of the above-mentioned disorders. Isolated forms of enzyme deficiencies other than lactase deficiency, such as sucrase-isomaltase or trehalase deficiency were not present among 168 investigations carried out from 1972-1982. It is concluded that assay of small intestinal disaccharidase or alkaline phosphatase activities does not expand the diagnostic impact of morphological examination of small bowel biopsy specimens and modern noninvasive methods for the detection of carbohydrate malabsorption. Thus, the method does not appear a necessary or relevant investigation in routine clinical practice.
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PMID:Is the assay of disaccharidase activity in small bowel mucosal biopsy relevant for clinical gastroenterologists? 274 34

We report results on determinations of small intestinal brush-border enzyme activities in 22 children (aged 11 months to 14 years) with giardiasis. In particular, activities of disaccharidases (lactase, sucrase, maltase) and of alkaline phosphatase were investigated. Forty-one percent of the patients, irrespective of age, had a demonstrable depression of disaccharidase activities, usually in a combination involving two or more enzymes. A depression of intestinal alkaline phosphatase activity was present in 33% of patients, and only in those who demonstrated disaccharidase deficiencies. Mild villus atrophy was present in two mucosal specimens, whereas all others showed normal villus morphology by light microscopy. The results obtained in this study suggest that giardiasis in otherwise healthy children does not cause marked structural damage to the small bowel mucosa, as seen by the light microscope. However, some form of damage to the brush border does occur frequently, as evidenced by a depression of brush-border enzymes. This damage most likely contributes to the diarrhea and also to the carbohydrate intolerance in these patients.
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PMID:Intestinal disaccharidase and alkaline phosphatase activity in giardiasis. 642 May 34

Investigations of the small bowel mucosa by scanning and transmission electron microscopy are reported in two coetaneous children with giardiasis. Serum immunoglobulins and mucosal architecture by light microscopy were normal in both, as well as activities of lactase, sucrase, and maltase. One of the children had suggestive evidence of malabsorption. Scanning and transmission electron microscopic examination of biopsied mucosa of the child with malabsorption suggested the following: increased secretory activity in crypts and increased cell damage, producing excess mucus containing extruded cytoplasm. It is hypothesized that the physicochemical properties of the mucoid material permitted ready interaction with the mucosal surface, the biochemical qualities of which could have been altered by the presence of the parasites. Close adherence of this mucoid layer to the surface gave it the aspect of a pseudomembrane which, by covering wide areas of the mucosal surface, probably functioned as an effective luminal barrier for nutrients. This pseudomembrane was not seen by light microscopy. Excessive secretion of mucus, its physicochemical and immunologic properties, and mucus-mucosal surface interaction could have been engendered by genetic and environmental factors, which need further study. Although some mucus was present in the mucosa of the other child, it was confined to the base of the villi, and did not cover the mucosal surface. The presence of a luminal barrier (mucoid pseudomembrane) may be added to the list of mechanisms implicated in causing malabsorption in giardiasis.
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PMID:Malabsorption in giardiasis: presence of a luminal barrier (mucoid pseudomembrane). A scanning and transmission electron microscopic study. 718 28

To elucidate the contribution of host and parasite factors in induction of small-intestinal disaccharidase deficiency in giardiasis, we determined the activity of four enzymes in male and female C57BL/6 mice infected with Giardia muris. Both male and female mice exhibited significant disaccharidase deficiency as shown by decreases in the activities of lactase, sucrase, trehalase and maltase on day 10 after infection. However, by 20 days after infection the females had normal enzyme activities, whereas those in males remained significantly reduced. Prolonged disaccharidase deficiency in the males was related to the course of the primary infection where males had higher parasite loads in the small intestine than did females on day 20 after infection. By day 40 after the primary infection the enzyme activities had returned to normal levels and were similar in male and female mice. Secondary exposure of mice to either the infective cysts or a crude extract of the trophozoites caused disaccharidase deficiency. The females had lower activities of sucrase and trehalase as compared with males after the challenge. Thus, during the primary infection, disaccharidase deficiency was strongly associated with parasite number, whereas after challenge infections the more resistant females had lower enzyme activities in the small intestine than did males.
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PMID:Disaccharidase activity in male and female C57BL/6 mice infected with Giardia muris. 773 22

Intestinal colonization with the protozoan Giardia causes diffuse brush border microvillous alterations and disaccharidase deficiencies, which in turn are responsible for intestinal malabsorption and maldigestion. The role of T cells and/or cytokines in the pathogenesis of Giardia-induced microvillous injury remains unclear. The aim of this study was to assess the role of T cells and interleukin-6 (IL-6) in the brush border pathophysiology of acute murine giardiasis in vivo. Athymic nude (nu(-)/nu(-)) CD-1 mice and isogenic immunocompetent (nu(+)/nu(+)) CD-1 mice (4 weeks old) received an axenic Giardia muris trophozoite inoculum or vehicle (control) via orogastric gavage. Weight gain and food intake were assessed daily. On day 6, segments of jejunum were assessed for parasite load, brush border ultrastructure, IL-6 content, maltase and sucrase activities, villus-crypt architecture, and intraepithelial lymphocyte (IEL) infiltration. Despite similar parasitic loads on day 6, infected immunocompetent animals, but not infected nude mice, showed a diffuse loss of brush border microvillous surface area, which was correlated with a significant reduction in maltase and sucrase activities and a decrease in jejunal IL-6 concentration. In both athymic control and infected mice, jejunal brush border surface area and disaccharidases were high, but levels of tissue IL-6 were low and comparable to the concentration measured in immunocompetent infected animals. In both immunocompetent and nude mice, infection caused a small but significant increase in the numbers of IELs. These findings suggest that the enterocyte brush border injury and malfunction seen in giardiasis is, at least in part, mediated by thymus-derived T lymphocytes and that suppressed jejunal IL-6 does not necessarily accompany microvillous shortening.
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PMID:Jejunal brush border microvillous alterations in Giardia muris-infected mice: role of T lymphocytes and interleukin-6. 1081 92

The study was conducted to detect the effect of giardiasis on human disaccharidase levels. Forty patients attending the medical outpatient department of PGIMER, Chandigarh were enrolled. Twenty patients, positive for Giardia lamblia comprised the study group while 20 patients negative for Giardia lamblia were taken as controls. Upper gastrointestinal endoscopy was performed in all patients. Estimation of lactase, sucrase, maltase and trehalase was done in biopsies. Histopathological investigation was carried out in all biopsy specimens after Haematoxylin and Eosin staining. Complaints of pain abdomen and bloating occurred commonly in giardiasis. Four biopsy samples in study group showed mild increase in lymphomononuclear infiltrate. Giardia lamblia was detected in 7 biopsies. Lactase levels were decreased significantly (p < 0.05) in giardiasis. Rest of the enzymes were comparable to the controls. No differences in the enzyme activities were observed between males and females in either group and with the duration of symptoms.
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PMID:Effect of Giardia lamblia on duodenal disaccharidase levels in humans. 1119 77

T-cell-mediated pathogenesis has been documented in various idiopathic and microbially induced intestinal disorders. Diffuse microvillous shortening seen in giardiasis is responsible for disaccharidase insufficiencies and malabsorption of electrolytes, nutrients, and water. Other mucosal changes include crypt hyperplasia and increased numbers of intraepithelial lymphocytes (IEL). A recent report using an athymic mouse model of infection showed that these epithelial injuries were dependent on T cells. The aim of the present study was to identify which subset of superior mesenteric lymph node (SMLN) T cells were responsible for mucosal alterations in giardiasis. CD4+ and CD8+ T cells, as well as whole lymphocyte populations, were isolated from SMLN of Giardia muris-infected mice for adoptive transfer. Jejunal segments of recipient mice were assessed for brush border ultrastructure, sucrase activity, crypt/villus ratio, and IEL numbers. Mice that received enriched CD8+ and whole SMLN lymphocytes, but not CD4+ T cells, from infected donors showed diffuse shortening of microvilli, loss of brush border surface area, impaired sucrase activity, and increased crypt/villus ratios compared to respective controls. Transfer of whole SMLN lymphocytes, as well as enriched CD4+ or CD8+ T cells, from infected donors led to increased IEL numbers in the recipient jejunum. The findings indicate that loss of intestinal brush border surface area, reduced disaccharidase activities, and increased crypt/villus ratios in giardiasis are mediated by CD8+ T cells, whereas both CD8+ and CD4+ SMLN T cells regulate the influx of IEL.
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PMID:Role of CD8+ and CD4+ T lymphocytes in jejunal mucosal injury during murine giardiasis. 1515 62

Gardia intestinalis, the aetiological agent of giardiasis, one of the most common intestinal diseases in both developing and developed countries, induces a loss of epithelial barrier function and functional injuries of the enterocyte by mechanisms that remain unknown. Three possible mechanisms have been proposed: (i) Giardia may directly alter the epithelial barrier after a close interaction between the trophozoite and polarized intestinal cells, (ii) intestinal functions may be altered by factors secreted by Giardia including an 'enterotoxin', proteinases and lectins, and (iii) based on mouse studies, a mechanism involving the intervention of activated T lymphocytes. We used fully differentiated cultured human intestinal Caco-2/TC7 cells forming a monolayer and expressing several polarized functions of enterocytes of small intestine to investigate the mechanisms by which G. intestinalis induces structural and functional alterations in the host intestinal epithelium. We first report that adhesion of G. intestinalis at the brush border of enterocyte-like cells involves the lipid raft membrane microdomains of the trophozoite. We report an adhesion-dependent disorganization of the apical F-actin cytoskeleton that, in turn, results in a dramatic loss of distribution of functional brush border-associated proteins, including sucrase-isomaltase (SI), dipeptidylpeptidase IV (DPP IV) and fructose transporter, GLUT5, and a decrease in sucrose enzyme activity in G. intestinalis-infected enterocyte-like cells. We observed that the G. intestinalis trophozoite promotes an adhesion-dependent decrease in transepithelial electrical resistance (TER) accompanied by a rearrangement of functional tight junction (TJ)-associated occludin, and delocalization of claudin-1. Finally, we found that whereas the occludin rearrangement induced by G. intestinalis was related to apical F-actin disorganization, the delocalization of claudin-1 was not.
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PMID:Lipid raft-dependent adhesion of Giardia intestinalis trophozoites to a cultured human enterocyte-like Caco-2/TC7 cell monolayer leads to cytoskeleton-dependent functional injuries. 2179 Sep 40


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