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)

Fourteen patients between the ages of 9 months and 5 years with chronic diarrhea and giardiasis were studied. Ten were eutrophic and 4 undernourished. The parasitological diagnosis was based on stool examination, a trophozoite search in duodenal aspiration, mucus adhered to mucosa and parasite identification in the intestinal biopsy material. Functional intestinal absorption studies, IgA determination in intestinal secretions and immunofluorescence studies were made. After the tests, tinidazole in suspension was administered at 60-70 mg/kg in one single oral dose. Patients were clinically re-evaluated and tests were done again after 30 days. The purpose of this paper was to evaluate the changes in the functional morphologic and immunologic studies and the therapeutic efficacy of the drug in a single dose. Nine patients had good clinical results, 2 fair and 3 were not evaluated due to celiac disease. All had negative results on the parasitological tests after treatment. There was no relationship between the number of parasites and the severity of symptoms. There was no significant difference between stool fat and d-xylose at the time of diagnosis and 30 days after the administration of tinidazole. The lactose tolerance test presented a significant difference (p less than 0.05) in the disaccharide absorption after treatment. The secretory IgA revealed significantly lower value (p less than 0.01) with respect to the normal values. The immunofluorescence showed productive IgA cells in all cases. The histologic changes were: mild enteropathy (grade I) in 6 patients; moderate (grade II) in 5; and severe (grade III-IV) in 3. Improvement of the mucosa was seen in 6 patients.
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PMID:Giardiasis. Functional, immunological and histological study of the small bowel. Therapeutic trial with a single dose of tinidazole. 333 25

We investigated the ability of patients with AIDS to develop antibody responses to a naturally encountered antigenic stimulus, Giardia lamblia. Using an enzyme-linked immunosorbent assay to detect IgG, IgM, and IgA to G. lamblia trophozoites, we tested sera from 29 patients with AIDS (15 without and 14 with G. lamblia infection); 20 healthy homosexual men; and 91 immunocompetent heterosexual subjects, 25 of whom were infected with G. lamblia. Heterosexual subjects infected with G. lamblia had significantly higher levels of all three classes of specific antibody than did the uninfected subjects (P less than .0001). Patients with AIDS who had acute symptomatic giardiasis had significantly lower levels of all antibodies than did the heterosexual subjects who had giardiasis; specific IgM was absent in all but one patient with AIDS. The symptomatically infected patients with AIDS had low levels of G. lamblia-specific antibodies that were similar to those of the uninfected patients with AIDS. Patients with AIDS do not have to suffer from prolonged symptomatic G. lamblia infections, however, because available therapy is effective against the parasite, independent of a patient's immune status.
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PMID:Acute antibody responses to Giardia lamblia are depressed in patients with AIDS. 334 71

Fifteen healthy volunteers were inoculated enterally with trophozoites of two distinct human isolates of Giardia lamblia, GS/M and Isr. Each of two groups of five volunteers were inoculated with 50,000 (GS/M or Isr) trophozoites. All of the volunteers inoculated with GS/M and none of the volunteers inoculated with Isr became infected. Three of five volunteers infected with GS/M became ill, including two who had diarrhea and typical symptoms of giardiasis. In the second study, three patients who were previously infected with GS/M and treated were rechallenged 12 weeks after the first inoculation, together with five new control volunteers. All of the latter group became infected, and two developed loose stools; two rechallenged volunteers became reinfected but were asymptomatic, and a third was retrospectively found to be infected at the time of challenge. Serum IgM, IgG, and IgA antibody responses to Giardia and intestinal fluid IgA antibody responses to Giardia occurred in 100%, 70%, 60%, and 50%, respectively, of infected volunteers. These studies fulfill Koch's postulates and demonstrate strain variation in the pathogenicity of Giardia infections in humans.
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PMID:Experimental human infections with Giardia lamblia. 368 Sep 97

The role of specific serum and milk anti-Giardia muris antibodies in mediation of host-effector responses to this enteric pathogen is unknown. We have investigated antibody-dependent cell-parasite interactions, potentially important as mediators of protection against infection at the mucosal surface. Elicited mouse peritoneal neutrophils and macrophages were incubated with G. muris trophozoites in the presence of either serum or milk antibodies, and their adherence and phagocytosis of the parasites were assessed. The percentage of trophozoites with adherent neutrophils increased significantly in the presence of heat-inactivated immune rabbit serum (93.5% +/- 6.5) and immune mouse milk (54.4% +/- 11.3) and their purified IgG (35.2% +/- 9.7) and secretory IgA fractions (48.0% +/- 12.3) when compared with incubation in RPMI-10% FCS (21.7% +/- 13.9). Similarly, macrophage adherence to trophozoites increased from 49.7% +/- 14.3 in medium alone to respective values of 92.8% +/- 7.1 in immune rabbit serum and 77.3% +/- 11.0 in immune milk. Phagocytosis of parasites by macrophages also was enhanced after incubation in immune rabbit serum (48.0% +/- 4.0) and immune mouse milk (35.0% +/- 5.0) when compared with the percentage of trophozoites ingested when cells and parasites were incubated in RPMI-10% FCS (3.3% +/- 3.0). Transmission electron microscopy showed ingestion of parasites by neutrophils or macrophages after 15 min of incubation. Morphologic evidence of intracellular parasite injury was observed at 6 hr. A decrease in parasite infectivity also resulted when trophozoites were incubated with neutrophils or macrophages and a source of antibodies, and intragastrically fed to weanling mice. These observations show that both antitrophozoite IgG, secretory IgA, and mouse phagocytic cells interact in vitro to promote parasite clearance. Because both the humoral and cellular components of this system are found intraluminally in the small intestine and in milk, they may represent a biologically relevant protective response against giardiasis.
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PMID:Effector mechanism of host resistance in murine giardiasis: specific IgG and IgA cell-mediated toxicity. 396 37

Ten pediatric patients investigated for chronic diarrhea, chronic weight loss, or failure to thrive were found on intestinal biopsy and/or in a duodenal aspirate to have Giardia lamblia. Serum immunoglobulin levels were normal or elevated in all patients. Three children had increased excretion of fecal fat and three other children had low D-xylose absorption. Jejunal biopsy specimens showed two severe, three moderate, and two mild morphological abnormalities, and three were normal. Except for lactase deficiency, disaccharidase activities correlated poorly with the severity of mucosal damage on biopsy. Steatorrhea was seen only with the more normal biopsies. Immunofluorescent staining of the biopsies for IgG, IgM, IgA, and secretory piece revealed no immune defects. Thus, there was no single malabsorption defect associated with giardiasis, and the specific defects did not necessarily correlate with morphological changes.
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PMID:Giardiasis in childhood: poor clinical and histological correlations. 635 23

The clinical course of giardiasis is variable, and serum antibodies do not appear to be protective. We propose that natural factors either produced by intestinal tissue, transported into the intestine, or ingested (ie, by breast-fed babies) might promote resistance to this disease. Human milk is very rich in secretory IgA (S-IgA) antibodies, as well as nonspecific antibacterial factors (eg, lactoferrin, lysozyme). Previous studies showed that Giardia lamblia trophozoites were killed by nonimmune human milk (NHM) in a time- and concentration-dependent manner. Removal of greater than 99% of the S-IgA from NHM did not decrease its Giardia-cidal activity. Thus, the killing was not antibody dependent. This is the first demonstration of nonimmune antiparasitic defenses in human milk. The present studies show that in the presence of NHM, trophozoites lost motility, swelled, and lysed. The Giardia-cidal activity (GCA) may be specific to human milk, since unheated cow's and goat's milk were virtually devoid of activity. Much, but not all, of the GCA was lost when NHM was heated or reacted with diisopropylfluorophosphate (DIFP), a specific esterase inhibitor. Activity of the major human milk lipase (BSL, bile salt-stimulated lipase, a fatty acid esterase) was lost after heat or DIFP treatment and was absent from cow's or goat's milk. The parasites were also killed by pure BSL. These studies suggest that BSL may be a heat-labile Giardia-cidal component of NHM.
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PMID:Killing of Giardia lamblia trophozoites by normal human milk. 667 55

Biopsy of the liver revealed granulomas in portal tracts and cholangitis in a woman with chronic diarrhea, weight loss, fever, hypoalbuminemia, and anemia attributed to giardiasis. Eradication of Giardia resulted in rapid improvement of symptoms and resolution of histologic changes on a second biopsy of the liver after 3 mo. The patient had serum immunoglobulin levels that were either normal (IgG, IgM) or elevated (IgA), detectable levels in serum of anti-Giardia antibody, and an HLA phenotype (B12, B27) known to be associated with prolonged giardiasis.
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PMID:Granulomatous hepatitis and cholangitis associated with giardiasis. 708 26

Three cases of selective IgA deficit with chronic diarrhea associated to Turner's syndrome are reported. The first patient presented gluten intolerance (celiac disease), confirmed by intestinal biopsy. The second patient turned out to suffer from cow's milk and gluten intolerance, and in the third an intestinal lambliasis was detected as well as gluten intolerance. Cytogenetic studies revealed in two patients a Turner's syndrome variant with isochromosome X, and the third presented Turner's syndrome associated with chromosome breakage. In all of the patients a history of repetitive upper respiratory infections and otitis was reported. The low incidence found in the literature of this rare association is also remarked, speculating about the role played by chromosome X in IgA synthesis.
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PMID:[Chronic diarrhea with selective IgA deficit associated with Turner's syndrome]. 712 99

We have studied three cases of patients with lymphoid nodular duodenal hyperplasia, two of them being in the child group. We observed giardiasis in one of the cases of this child group. Also vague dyspeptical complaints in all cases were noticed. The diagnostics were based on the results obtained with endoscopy, later confirmed by hystological tests. We found two cases with absence of IgA without alterations in IgG and IgM when using immunoeletrophoresis.
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PMID:[Nodular lymphoid hyperplasia of the duodenum: study of 3 cases]. 721 29

Selective serum IgA deficiency and follicular lymphatic hyperplasia of the terminal ileum were observed in a 30-year-old patient. Due to the relative ileal stenosis he complained of colicky abdominal pains particularly after flatulant food. There was no malabsorption syndrome or lambliasis. Although immunohistochemically IgA producing plasma cells were demonstrated in the intestinal wall, no immunoglobulin could be demonstrated in the intestinal juice, suggesting a secretory defect. The very high percentage of IgE producing plasma cells was noteworthy, these cells having led to the macroscopical picture of follicular hyperplasia. Due to the relative frequency of IgA deficiency (about 1 : 700) and the known increased incidence of malignant disease regular surveillance of these patients is indicated.
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PMID:[Follicular lymphatic hyperplasia of the small intestine in antibody deficiency syndrome (author's transl)]. 723 22


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