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The macroscopic and microscopic appearance of villous atrophy in weaned pigs orally infected with Salmonella cholerae-suis is described. The other intestinal diseases of pigs in which villous atrophy occurs are discussed.
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Intestinal disease in cystic fibrosis (CF) mice closely mirrors aspects of obstructive syndromes in CF patients. The pathogenesis involves accumulation of mucoid debris in the crypts that fuse with intestinal content to form obstructing mucofeculant impactions. Treatment involves modalities that increase the fluidity of the luminal content, such as osmotic laxatives and liquid diets. We investigated the effects of talniflumate (Lomucin, Genaera Corporation, Plymouth Meeting, PA), a compound that may be beneficial to treatment of CF intestinal disease based on three mechanisms of action: mucus synthesis inhibition by blockade of the murine calcium-activated chloride channel 3 (mCLCA3), nonsteroidal anti-inflammatory effects, and inhibition of Cl(-)/HCO (-)(3) exchanger(s) involved in intestinal NaCl absorption. Cohorts of CF mice were fed control diet or diets containing either talniflumate (0.4 mg/g chow) or ibuprofen (0.4 mg/g chow) for 21 days to assess survival. Talniflumate significantly increased CF mouse survival from 26 to 77%, whereas ibuprofen had no effect (22% survival). Oral talniflumate did not alter crypt goblet cell numbers or change intestinal expression of mCLCA3 but tended to decrease crypt mucoid impaction. Ussing chamber studies indicated that talniflumate slightly increased the basal short-circuit current of CF intestine, but the change was not sensitive to secretagogue stimulation or bumetanide inhibition. In contrast, intracellular pH measurements of intact intestinal villous epithelium indicated that talniflumate significantly inhibited apical membrane Cl(-)/HCO (-)(3) exchange by >50%. We conclude that oral talniflumate increases the survival of CF mice, possibly by the beneficial effects of decreasing small intestinal NaCl absorption through the inhibition of apical membrane Cl(-)/HCO (-)(3) exchanger(s).
Small intestinal bacterial overgrowth (SIBO) has been reported to occur commonly in dogs with signs of chronic intestinal disease. There are usually few intestinal histological changes, and it is uncertain to what extent bacteria cause mucosal damage. The aim of this study was to apply a differential sugar absorption test for intestinal permeability and function to the objective assessment of intestinal damage in dogs with SIBO. Studies were performed on 63 dogs with signs of chronic small and, or, large bowel disease, in which SIBO (greater than 10(5) total or greater than 10(4) anaerobic colony forming units/ml) was diagnosed by quantitative culture of duodenal juice obtained endoscopically. None of the dogs had evidence of intestinal pathogens, parasites, systemic disease or pancreatic insufficiency. differential sugar absorption was performed by determining the ratios of urinary recoveries of lactulose/rhamnose (L/R ratio, which reflects permeability) and D-xylose/3-O-methylglucose (X/G ratio, which reflects intestinal absorptive function) following oral administration. Dogs with SIBO comprised 28 different breeds, including 13 German shepherd dogs. SIBO was aerobic in 18/63 dogs (29 per cent), and anaerobic in 45/63 (71 per cent). Histological examination of duodenal biopsies showed no abnormalities in 75 per cent, and mild to moderate lymphocytic infiltrates in 25 per cent of the dogs. The L/R ratio was increased (greater than 0.12) in 52 per cent, and the X/G ratio reduced (less than 0.60) in 33 per cent of the dogs. Differential sugar absorption was repeated in 11 dogs after their four weeks of oral antibiotic therapy. The L/R ratio declined in all 11 dogs (mean +/- SD pre: 0.24 +/- 0.14; post: 0.16 +/- 0.11; P < 0.05), but changes in the X/G ratio were more variable. These findings show that SIBO is commonly associated with mucosal damage not detected on histological examination of intestinal biopsies, and that changes in intestinal permeability following oral antibiotics may be used to monitor response to treatment.
A 35-year-old man, who had spent 10 1/2 out of 18 months in hospital, has required repeated courses of intravenous nutrition (IVN) because of nutritional failure due to severe inflammatory bowel disease. He has been maintained on a nocturnal pump-fed liquid diet supplementing his day-time oral diet for five months, four of which have been at home. The cost of such therapy is less than with an elemental diet and there are other advantages. This regime has been shown to be nutritionally adequate. The need to assess other cheaper liquid diets in patients with intestinal failure is recognised.
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UNLABELLED: The understanding of mechanisms responsible for alterations in mucin synthesis and secretions is essential in elucidating the aetiology of intestinal disorders. The existence of distinct mucins and M-cell transport mechanisms, and their beneficial effects, have long been recognised. Since nutritional and bacterial factors alter the mucin characteristics and are relevant to planning preventative strategies for intestinal diseases, the studies described in this monograph were designed to test the hypothesis that mucin composition and endocrine status of the intestinal tract are altered by dietary constituents and microbial flora. A study of gut-associated lymphoid tissue (GALT) was undertaken to test the hypothesis that lymphocyte-epithelial interactions influence the glycosylation of cells overlying Peyer's patches. The effects of diet and microbial flora were analysed by comparing the data from male Wistar germ-free rats, with conventional or human flora. Such rats were fed either a commercial diet, containing crude fibre, or a purified diet. Bone marrow transfers from syngeneic Balb/c mice to severe combined immunodeficient (SCID) mice were made to induce the formation of GALT. A comparison was made of the glycoconjugate profile of Peyer's patches in the guts of mice and humans. The results of the study showed that feeding a fibre-rich diet to germ-free rats resulted in increased villus-crypt lengths, decreased carboxylated mucin content of goblet cells, increased N-acetylglucosamine and sialic acid residues in the surface goblet cells, and a reduction in the number of endocrine cells in the small intestine. The lectin markers revealed M-cell development in the dome epithelium of the reconstituted SCID mice. Mouse M cells were labelled by fucose-specific lectins but in human Peyer's patches no distinct M-cell-staining pattern was observed. CONCLUSIONS: (1) the interactions between diet and flora alter the mucosal architecture and the activity of endocrine cells; (2) the dietary changes are influential in modifying the epithelial mucin predominantly in the small intestine while the microbial flora influences the mucosal architecture predominantly in the large intestine; (3) the use of bone marrow transplantation from syngeneic mice into SCID mice along with lectin markers for M cells can be used to study the histogenesis of Peyer's patches; (4) the distinct differences between mouse and human Peyer's patches suggest that when considering cell surface glycoconjugates as target molecules appropriate lectin should be used for each species. A future challenge in intestinal epithelial cell biology is identifying the nature and distribution of cell surface receptors for specific dietary components and bacteria.
Crohn's disease is an inflammatory intestinal disease of unknown etiology. The disease primarily affects whites, with both sexes being affected equally. A genetic predisposition exists. Symptoms frequently present in the second to third decades of life, although they may present in the pediatric and/or geriatric populations. Oral lesions are significant as they are frequently reported to precede intestinal symptoms. Treatment of Crohn's disease is palliative, with a focus on remission. Pediatric and general dentists play a critical role in the early diagnosis of Crohn's disease. Evaluation of a pediatric patient with complaints of oral ulcerations, as well as gastrointestinal symptoms, fatigue, and/or weight loss requires prompt referral to a gastroenterologist for further evaluation for Crohn's disease.
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REASONS FOR PERFORMING STUDY: Epiploic foramen entrapment (EFE) has been associated with a particularly poor post operative prognosis for equine colic cases, but the reasons for this are unknown. OBJECTIVES: To identify variables associated with post operative survival following surgery for small intestinal disease; develop a model describing long-term post operative survival; and identify reasons for the poor prognosis associated with EFE. METHODS: Data from 382 horses undergoing surgery were used to identify variables associated with survival. A multivariable Cox proportional hazards model for post operative survival was developed and model fit evaluated. RESULTS: The final model included the variables total plasma protein (TP) and packed cell volume (PCV) at admission, duration of surgery and the dichotomous variable relaparotomy (yes/no). Risk of death was positively associated with increasing PCV, but negatively associated with increasing TP (which decreased the probability of death). In a univariable model, EFE cases had a significantly higher death rate than other types of small intestinal disease (hazard ratio = 1.7, P = 0.035). Multivariable modelling indicated that some of the increased risk associated with EFE cases was due to lower TP values and longer duration of surgery. CONCLUSIONS: Preoperative TP is associated negatively with the risk of post operative death in horses recovering from small intestinal surgery. Other variables associated with the probability of survival are preoperative PCV, duration of surgery and relaparotomy. The increased post operative death rate of EFE cases can be explained in part by lower TP and longer surgery times of these cases. POTENTIAL RELEVANCE: Total plasma protein may be not simply a measure of hydration status in small intestinal colic cases, but an important determinant of survival. Further investigation of this relationship is warranted. Our model for post operative survival highlights the importance of preoperative TP, PCV and duration of surgery as prognostic indicators. This information should allow a more accurate post operative prognosis following small intestinal surgery.
The human intestine is colonized by a large number of microorganisms, collectively termed microbiota, which support a variety of physiological functions. As the major part of the microbiota has not yet been cultured, molecular methods are required to determine microbial composition and the impact of specific dietary components including probiotics. Probiotics are viable microbial food supplements, which have a beneficial impact on human health. Health-promoting properties have been demonstrated for specific probiotic products. The most significant demonstrations for probiotic efficacy include prevention and treatment of antibiotic associated diarrhea, rotavirus diarrhea and allergy prevention. Lactobacillus rhamnosus GG (=ATCC 53103) and Bifidobacterium lactis Bb12 are the among the best-characterized and most studied probiotic strains with demonstrated impact on human health. New complex targets for probiotics include irritable bowel syndrome and Helicobacter pylori infection. For future probiotics the most important target is a demonstrated clinical benefit supported by knowledge on the mechanistic actions in the microbiota of the target population. Molecular and genomics-based knowledge of the composition and functions of the microbiota, as well as deviations from the balanced microbiota, will advance the selection of new and specific probiotics. Potential combinations of specific probiotics may prove to be the next step to reduce the risk on intestinal diseases and reconstruct specific microbial deviations.
Intestinal ulcers in Behçet's disease (BD) tend to cause perforation with significant morbidity. The optimal surgical procedure in such cases is controversial and the postoperative period can be eventful with an unpredictable course. We report three cases of perforations with varying locations in three patients with long-standing Behçet's disease. Two patients required two and one patient required four operations. It is emphasized that the clinician must be alert in a patient with BD when abdominal symptoms accompany the clinical picture. As soon as the diagnosis is reached, surgical intervention with limited resection must be performed. Endoscopic examination and careful medication play major roles in the follow-up.
Data from the surveillance scheme of general outbreaks of infectious intestinal disease in England and Wales were used to describe the epidemiology of outbreaks of salmonellosis in hospitals from 1992-1994. Outbreaks of infectious intestinal disease in hospitals accounted for 15% (189/1275) of all outbreaks. A salmonella was the implicated pathogen in 12% (22/189). The mode of transmission was described as mainly person to person in 12 outbreaks, mainly foodborne in eight and equal or unknown proportions of foodborne and person to person in two. The most common strain involved was Salmonella enteritidis PT4 (11 outbreaks). The mean duration of outbreaks was 16 days. The mean attack rate in patients was 25% but varied from 2-67%. Illness was reported in 260 patients, of whom 130 had a laboratory confirmed infection. Eight hundred and twenty-six asymptomatic patients were tested, 31 of whom were positive. The salmonella infection was believed to have contributed to the deaths of five patients. Ill staff (115) were tested and 68 were positive; 1508 well staff were tested and 33 were positive. Outbreaks of salmonellosis in hospitals are preventable. Attack rates can be high and outbreaks are often prolonged, with high morbidity and associated disruption of hospital services. There is need for effective infection control policies, appropriate training of staff, simple surveillance systems and readily available expert advice to ensure outbreaks are rapidly controlled.
Few studies have been published on peptide hydrolase activities of human small intestine mucosa. We developed methods to screen tissue extracts for such enzymes and to quantitate hydrolase activities for dipeptides containing the aromatic amino acid L-phenylalanine. The screening procedure indicated glycyl-L-proline hydrolase activity was reduced in biopsy specimens from patients with flattened intestinal mucosa. To explore this further, we established optimal assay conditions for hydrolase activities (a) glycyl-L-proline, (b) L-phenylalanyl-L-proline, (c) L-alanyl-L-phenylalanine, and (d) L-phenylalanylglycine. Biopsy specimens from patients with various intestinal disorders, but without flattened mucosa, and from three patients with flattened mucosa, showed a disproportionate reduction in activities (a) and (b), with the reduction being significantly more marked in the latter patients. We suggest that intestinal imidopeptide hydrolase activities, such as (a) and (b), are sensitive to changes in intestinal disease generally, particularly to the altered physiology associated with flattening of the mucosa, and are secondary to, rather than a cause of, the intestinal pathology. Our finding that intestinal alkaline phosphatase activity tended to parallel imidopeptide hydrolase activity, and that activity (a) was partially localized to the particulate fraction of mucosal homogenate, suggested that imidopeptide hydrolase activities may be located in the microvilli of the intestinal epithelium and that, like alkaline phosphatase activity, they may be reduced in flattened mucosae, in part at least because of the pathologic changes in the microvilli. In our studies of control subjects we did not detect peptide hydrolase activity deficiency analogous to asymptomatic disaccharidase deficiency.
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Pancreatic polypeptide (PP) islet cell tumors are usually not associated with a distinct clinical syndrome, although some reports suggest that they can cause a watery diarrhea syndrome similar to vasoactive intestinal polypeptide (VIP) cell tumors. We report the case of a young woman with an unusual presentation of a pancreatic neuroendocrine tumor mainly secreting PP. The patient developed a reversible hypokalemic rhabdomyolysis very likely secondary to the presence of the tumor. The myopathy resolved following the restoration of normokaliemia using potassium supplementation and a partial laparoscopic pancreasectomy. Isolated cases of hypokalemic rhabdomyolysis induced by intestinal diseases have been described in literature but these did not include gastroenteropancreatic neoplasms. We suggest that pancreatic neuroendocrine tumors should be added to the list of intestinal diseases capable of producing hypokalemic myopathy.
BACKGROUND/PURPOSE: Probiotic and prebiotic therapies are potent new strategies to treat various intestinal diseases, including inflammatory bowel disease and viral and bacterial infections. Synbiotics is defined as the combined use of probiotics and prebiotics and is expected to have a stronger effect on intestinal diseases than probiotics or prebiotics alone, but there has been no report of its clinical application. The authors designed a protocol for synbiotic therapy composed of Bifidobacterium breve, Lactobacillus casei, and galactooligosaccharides and preliminarily ascertained its clinical effects in humans. METHODS: This protocol of synbiotic therapy was applied for more than 1 year to 7 malnourished patients with short bowels who suffered from refractory enterocolitis. RESULTS: The therapeutic protocol improved the intestinal bacterial flora (inducing the domination by anaerobic bacteria and suppressing the residence of pathogenic bacteria) and increased short chain fatty acids in the feces (from 27.8 to 65.09 micromol/g wet feces). All patients but 1 accelerated their body weight gain, and 5 patients showed increased serum rapid turnover proteins. CONCLUSIONS: This protocol for synbiotic therapy might be a potent modulator of intestinal flora and a promising strategy to treat short bowel patients with refractory enterocolitis.
By analyzing the morphology of a focal lesion or the distribution, location, and morphology of the intestinal folds, the radiologist can come to a specific diagnosis or construct a graded differential diagnosis. This article presents a simplified approach to the differential diagnosis of small intestinal diseases by combining this roentgen analysis with the clinical history.