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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven-day-old mice were infected orally with murine rotavirus (EDIM) and regions of the gut examined at 24 h intervals up to 7 days by electron microscopy. Structural changes were correlated with data on viral antigen production, thymidine kinase activity, and clinical signs of diarrhea. No pathological changes were detected in the colon. Infection and structural damage were confined to the small intestine, with middle regions showing the most pronounced changes. Constriction of villus bases, edema of the lamina propria, and vacuolation of enterocytes occurred at 24 h postinfection (PI), i.e., before evidence of major virus replication. Transient villus atrophy occurred at 48 h PI. Recovery of villus length was evident by 72 h PI accompanied by evidence of marked enterocyte replication at villus bases. Many enterocytes were damaged with little evidence for the presence of virus particles. By 96 h PI, villi had almost recovered from infection although some enterocytes were still damaged; no virus particles were detected in these cells. A second phase of villus damage and edema of the lamina propria occurred at 120 h PI; the pathology resembled that at 24-48 h PI. By 144 to 168 h PI, recovery of the mucosa from infection was virtually complete. We suggest that many of the pathological features following rotavirus infection result from rotavirus-induced ischemia of villi and that diarrhea results from malabsorption of fluid by damaged villi and hypersecretion of ions released from increased numbers of dividing cells at villus-crypt borders.
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PMID:An electron microscopic investigation of time-related changes in the intestine of neonatal mice infected with murine rotavirus. 283 83

We studied the effects of oral taurine supplementation on bile acids conjugation and duodenal bile salt concentrations in infants. Seventeen infants receiving enteral artificial nutrition were investigated. At the beginning of the study they were 6 to 14 weeks old, in good nutritional state, without malabsorption, protein-losing enteropathy and liver or infectious diseases. After at least 8 days of a stable, taurine-free regimen the infants received oral taurine supplementation (36-45 micromol/kg.24 h) for 8 days. Bile acids were measured before and after each supplementation period in bile samples obtained by duodenal tubing, using enzymatic methods and colorimetry. According to the initial plasma taurine levels before supplementation, the infants were divided into two groups: I) plasma taurine levels less than 60 mumol/l (mean 47 +/-5 mumol/l, n = 8); II) plasma taurine levels greater than 70 mumol/l (mean 77 +/- 2 mumol/l, = 9). After 8 days of taurine supplementation a significant increase of plasma and urinary taurine (P less than 0.01),total duodenal bile salt concentrations (P less than 0.05), total duodenal tauroconjugates (P less than 0.05),taurocholate (P less than 0.01), taurochenodeoxycholate (P less than 0.05), and glycocholate (P less than 0.01), duodenal concentrations, and a significant decrease of the glycoconjugate/tauroconjugate ratio (P less than 0.05), were observed, but only in group I. in group II infants we only noted a significant increase of urinary taurine (P less than 0.01), and of duodenal total tauroconjugates (P less than 0.05). This study shows that the biliary effects of an oral taurine supplementation depends on taurine status and that in taurine-depleted infants intakes of exogenous taurine higher than 45 mumol/kg. 24 h are perhaps necessary for optimal bile salt effects.
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PMID:[Influence of oral taurine supplementation on the intraduodenal concentration and conjugation of bile acids in full-term newborn infants]. 297 13

In young broiler chicks inoculated with 2 x 10(6) sporulated oocysts of Eimeria acervulina per bird, total plasma lipids were significantly depressed compared with controls in the first week after inoculation. The lowest level observed was at 5 days post-inoculation (d.p.i.), at which time the chick host is known to experience malabsorption in the chick host (Ruff and Wilkins, 1980). Analysis of plasma components of infected chicks at 4 and 7 d.p.i. showed that triglycerides, total cholesterol, free fatty acids, pigments and total protein were significantly decreased compared with controls. At 7 d.p.i., reduction of total cholesterol reflected mainly reduction in high density lipoprotein (HDL) cholesterol. However, the ratio of HDL cholesterol/total plasma cholesterol was not significantly different from the control ratio. Density gradient ultracentrifugation of chick plasma separated lipoproteins into three main fractions: portomicrons plus very low density lipoproteins (PM + VLDL), low density lipoproteins (LDL) and HDL. These fractions were analyzed for lipid content. Infection with E. acervulina caused (1) significant reduction in the triglyceride and cholesterol contents of the PM + VLDL fraction at 3 and 5 d.p.i., (2) significant reduction of LDL cholesterol at 9 d.p.i. and LDL phospholipid at 5-9 d.p.i., and (3) significant reduction of HDL cholesterol at 3-9 d.p.i. and HDL phospholipid at 5-9 d.p.i. Starvation of uninfected chicks for 48 h caused significant reduction in plasma triglycerides and phospholipids, but an increase in total cholesterol. Density gradient ultracentrifugation showed that the changes in these components reflected mainly reduction of the lipids in the PM + VLDL fraction. The LDL fractions, however, appeared more intense than those of the controls and contained more cholesterol and phospholipids. These results suggest that changes at 3 and 5 d.p.i. in the plasma lipoprotein pattern of chicks infected with E. acervulina most closely resemble changes seen in chicks starved for 48 h as far as PM + VLDL fraction is concerned. However, changes seen from 7 to 9 d.p.i. involve the LDL and HDL fractions and may reflect alterations in lipid and/or lipoprotein synthesis in the liver and intestine.
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PMID:The effect of Eimeria acervulina infection on plasma lipids and lipoproteins in young broiler chicks. 321 27

A better understanding of the physiologic response to and nutritional consequences of acute diarrhea can facilitate an improved outcome for this and other infectious diseases. Acute diarrhea causes the host to undergo a sequence of hormonal, metabolic, and immunologic responses, all of which have nutritional consequences. Its most profound effect is on the malabsorption of water and electrolytes by the intestinal epithelial cell, the electrolyte, leading to dehydration. Diarrhea is defined as any alteration of fluid and electrolyte movement that results in increased fecal water due to an excessive amount of solute in the stool. Infectious agents that damage the enteric mucosa cause villous atrophy, which is accompanied by increased proliferation, migration, and extrusion of epithelial cells; this results in alterations of fluid and electrolyte movement and is the final common pathway to the development of diarrhea. During the acute stages of diarrhea, there are increased losses of fecal weight and volume as well as sodium and chloride and the level of disaccharidase enzymes is depressed. Different bacteria affect different parts of the gastrointestinal tract. After bacterial adherence and surface colonization of the intestinal epithelium, diarrhea can result from any of 3 major mechanisms: 1) production and release of enterotoxins, 2) direct invasion of the mucosa or submucosa, and 3) adhesion and cytotoxic disruption of the microvilli of the enterocyte. There is evidence of diarrhea-associated changes in the plasma concentration of certain gastrointestinal hormones and indications that calcium plays a key role in the intracellular regulation of electrolyte transport. The impact of diarrhea will be more significant in the debilitated or marginally nourished child. To improve the host response to infection, nutrients that are essential for optimal immune function and are rapidly being metabolized should be selectively replaced, while nutrients needed by the offending organism can be withheld.
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PMID:Nutritional implications and physiologic response to pediatric diarrhea. 394 85

Patients with acquired immunodeficiency syndrome (AIDS) frequently have diarrhea and weight loss. We prospectively examined the upper and lower gastrointestinal tracts in 22 AIDS patients, although severe medical problems often precluded full evaluation. Ninety-six percent (21 of 22) lost weight, and 55% (12 of 22) had diarrhea. The mean (+/- SD) weight loss was 34 +/- 19 lb. Steatorrhea was found in 4 of 14 patients, and D-xylose tests were abnormal in 8 of 14 patients. Mean serum albumin was 3.3 +/- 0.8 g/dl. A significantly diminished plasma selenium level, which can influence immune function, was noted in these AIDS patients. Gastrointestinal infections were identified in 45% of patients. Although diarrhea and malabsorption were more common in the infected group, weight loss and albumin were similar in those with and without demonstrated infections. Flexible sigmoidoscopy showed that of 15 patients, there were two with Kaposi's sarcoma, 10 normals, and three with nonspecific endoscopic changes of colitis. Infection was documented in all patients with colitis. Panendoscopy of the upper gastrointestinal tract was positive for AIDS-related pathology in five of 10 patients, including two with Kaposi's sarcoma, one with Candida esophagitis, one with herpetic esophagitis, and one with gastroduodenitis (biopsy positive for cryptosporidia); five patients had a normal-appearing tract. Small bowel or colonic biopsies frequently showed nonspecific inflammatory changes, although pathogens were identified in six patients (27% of all biopsies). We conclude that a wide variety of gastrointestinal pathology, which includes infectious agents, neoplasms, and inflammatory changes, may occur in AIDS patients. Therefore, AIDS patients, particularly those with diarrhea or weight loss, deserve an intensive evaluation for remediable lesions of their gastrointestinal tracts.
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PMID:Gastrointestinal manifestations of the acquired immunodeficiency syndrome: a review of 22 cases. 404 Nov 33

Giardia lamblia is the first protozoan to be identified and recognized as an important pathogen in human disease. We studied 8 pediatric patients with giardiasis in order to examine the clinical spectrum, the structural changes of the small intestinal mucosa and mainly the protozoan's ultrastructural features. The most common clinical manifestations were diarrhea, abdominal pain, anorexia, vomiting, failure to thrive. Infection was confirmed by excreted cysts in the stools in one patient, by the presence of trophozoites in duodenal aspirate and on jejunal mucosa. Giardiasis was not associated with hypogammaglobulinemia in our patients and no or only slight mucosal abnormalities were present in jejunal biopsies, except one which showed a flat mucosa. Specimens for transmissions and scanning electron microscopy were taken. We could establish the protozoan's features, its normal distribution, its relationship to intestinal mucosa and structural indications of the normal reaction of intestine with the use of ultrastructural techniques. The trophozoites colonized the proximal intestine, adhered to microvilli of columnar cells near the bases of villi, wedged or lodged in mucus. The sticky mucus producing an effective diffusion barrier to nutrients could explain malabsorption phenomena. Numerous intraluminal lymphocytes were seen, suggesting an immune response. These observations indicate that in giardiasis the clinical spectrum and structural changes of the small intestinal mucosa vary widely, suggesting a different reaction of immune system and/or a different degree of infection.
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PMID:[Giardiasis in children. Ultrastructural study of the parasite]. 664 80

Rotaviruses are now established as a major cause of neonatal enteritis and diarrhoea in calves. Laboratory diagnosis is usually based on detection of the virus or virus antigens in faeces by direct electron microscopy or tests such as ELISA and IEOP. Rotaviruses are resistant to inactivation and are normally present in large numbers in faeces, so that environmental contamination is both heavy and persistent. Infection is transmitted primarily by faecal-oral contact. Calves are usually protected from infection for the first few days of life by colostral antibody. When this disappears from the gut the calf is totally susceptible to infection and maximum virus excretion normally occurs around the end of the first week of life. The disease has a high morbidity, but clinically is of mild to moderate severity. Many infections are subclinical. The virus infects and destroys mature villous enterocytes in the small intestine, resulting in villous atrophy and replacement of mature epithelial cells by undifferentiated immature cells. Diarrhoea probably results from malabsorption and net water secretion. Control is based on management systems designed to decrease the amount of infection to which the calf is exposed and on increasing the specific resistance of the calf to infection e.g. by feeding immune colostrum or by vaccination. Vaccination of the dam with adjuvanted, inactivated vaccines has given promising results, but this work is still at an early stage.
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PMID:Rotavirus infections in calves. 667 80

A patient had common variable immunodeficiency, chronic malabsorption, and Campylobacter jejuni infection. Infection was diagnosed by jejunal aspiration. A follow-up jejunal aspirate was culture positive at the same time that a stool culture was negative. Infection resulted in worsening of chronic diarrhea, but it was not associated with clinical features of colitis or proctitis. The duration of infection was prolonged and initial antimicrobial therapy was ineffective. Single drug therapy with erythromycin ethylsuccinate and then chloramphenicol led to the emergence of resistant organisms. After five months of bacterial excretion, combination therapy with metronidazole and neomycin sulfate eliminated the organism. This case emphasizes that the clinical manifestations and response to therapy of C jejuni infection can be altered in immunodeficient patients.
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PMID:Jejunal infection with Campylobacter. 671 98

Routine data used to study infectious diseases may contain biases which obscure trends. A 16-year series (up to 1968) of routine laboratory data was used to study patterns of incidence of infective gastroenteritis for which no laboratory diagnosis could be made. An artificial pattern was detected. This arose because GPs tended to refer a greater proportion of their patients during dysentery epidemics. Multiple regression analysis was used to separate out this effect so that the underlying trends could be observed. The seasonal pattern of undiagnosed cases showed an autumn peak. There were also early-winter epidemics of disease with little or no excretion of red blood or pus cells in the diagnostic faeces specimen. Some of the winter communicable disease among older children and adults appeared to be associated with signs of a temporary fat malabsorption in pre-school age cases. Undiagnosed cases in older children and adults were not related to the E. coli serotypes causing disease in infants during this period. The statistical method applied increased the usefulness of these routine data. Although this series of laboratory records is now more than a decade old the results of the analysis can be compared with new observations as more is learned about the epidemiology of previously unrecognized pathogens, especially rotaviruses.
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PMID:Monitoring infectious diseases using routine microbiology data. II. An example of regression analysis used to study infectious gastroenteritis. 700 91

Infection with Mycobacterium intracellulare serotype 10 was diagnosed in 2 rhesus monkeys (Macaca mulatta) in a closed colony of 90 animals. The clinicopathologic presentation in 1 animal with advanced disease was characterized by a precipitous weight loss, therapeutically unresponsive diarrhea, anemia, weakness, prostration, refractory tuberculin tests (using mammalian old tuberculin and M bovis purified protein derivative tuberculin), and disseminated granulomas in the lungs, spleen, liver, kidneys, lymph nodes, salivary glands, and intestines. The lamina propria throughout the large and small intestines was infiltrated with mycobacteria-laden macrophages. Severe hypoproteinemia, hypoalbuminemia, hypoglobulinemia, mild hypocalcemia, and edema were compatible with a malabsorption-like syndrome. The 2nd animal was clinically normal, but a weak positive tuberculin reaction to M bovis purified protein derivative at 72 hours necessitated euthanasia. This animal's disease was characterized by microgranulomas in the lungs, bronchial lymph nodes, liver, and pancreas, without involvement of the gastrointestinal tract. There was no evidence of M intracellulare infection in the remaining 88 animals in the colony, as determined by mycobacterial cultures of tracheobronchial washings, additional tuberculin testing, thoracic radiography, and mycobacterial culture of the drinking water. Tuberculin testing and thoracic radiographs of personnel working with the nonhuman primates were also negative. These cases were considered to be important because both animals were infected with the same serotype and because there has been an increasing number of isolations of this organism in human infections throughout Massachusetts. Drug-sensitivity testing revealed the organism to be sensitive to cycloserine and resistant to isoniazid, rifampin, ethambutol, streptomycin, kanamycin, and pyrazinamide.
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PMID:Nontuberculous mycobacterial infection attributable to Mycobacterium intracellulare serotype 10 in two rhesus monkeys. 717 60


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