GASTROENTERITIS  

January 2006

Some Selected Abstracts:

1.

Baker DE. Safety of balsalazide therapy in the treatment of inflammatory bowel disease. Rev Gastroenterol Disord. 2005 Summer;5(3):135-41

College of Pharmacy, Washington State University, Spokane, Washington, USA.

Balsalazide is a mesalamine prodrug that is generally well tolerated and useful in the treatment of inflammatory bowel disease (IBD). This review will focus on newer safety information regarding the use of balsalazide in the treatment of patients with IBD. In general, mesalamine compounds such as balsalazide are better tolerated than sulfasalazine. Balsalazide therapy should be avoided in patients with known hypersensitivity reaction to salicylates, mesalamine, other balsalazide metabolites, or the components of the Colazal (Salix Pharmaceuticals; Morrisville, NC) capsule (silicon dioxide, magnesium stearate) but may be tolerated in patients who were unable to tolerate other mesalamine compounds for non-hypersensitivity reasons. Overall, balsalazide is well tolerated and effective in the treatment of IBD.

2.

1.                      Hens DK, Niyogi SK, Kumar R.Epidemic strain Shigella dysenteriae Type 1 Dt66 encodes several drug resistances by chromosome. Arch Med Res. 2005 Jul-Aug;36(4):399-403

National Institute of Cholera and Enteric Diseases, Beliaghata Kolkata, India.

         BACKGROUND: Multiple antibiotic-resistant strains of Shigella dysenteriae type 1 were isolated from an epidemic in West Bengal, India (1984). During the past two decades, much attention was given to reevaluation of treatment recommendations. However, there are no useful data on drug resistance encoded by chromosome. METHODS: A total of 300 strains of Shigella dysenteriae type 1 were isolated from an epidemic. Strains were biochemically identified by API 20E system and further confirmed serologically. Antibiotic susceptibility was determined by disk diffusion method and plasmid DNA was prepared by alkaline lysis procedure. Elimination of plasmids was achieved by curing with acridine orange from a representative epidemic strain S. dysenteriae 1 Dt66. PFGE was performed for typing of wild-type and plasmid-cured strains. Southern blot of PFGE separated XbaI digested chromosomal DNA was done onto positively charged nylon membrane. For Southern hybridization, plasmid DNA was used as probe. RESULTS: All isolates showed identical drug resistance patterns and plasmid profiles. All these isolates contained six plasmids ranging in sizes from 3 to 145 kb. We have eliminated all the plasmids from a representative strain of S. dysenteriae 1 Dt66 by using acridine orange as curing agent. All epidemic Shigella isolates were resistant to amoxycillin, ampicillin, bacitracin, carbenicillin, cefixime, ceftazidime, chloramphenicol, clarithromycin, erythromycin, fusidic acid, methicillin, penicillin G, polymixin B, streptomycin, rifampicin, tetracycline and vancomycin, among 29 antibiotics used. Out of 17 resistant antibiotics, 12 were encoded by chromosome. Resistance to ampicillin, chloramphenicol, streptomycin, tetracycline and ceftazidime was plasmid encoded. Southern blot hybridization showed the recognition of two clear sites in the chromosome used plasmid DNA of Dt66 strain as probe, which reveled some sequential genetic homology between chromosome and plasmids. Pulsed-field gel electrophoresis (PFGE) was performed for typing of the chromosome of plasmidless strains of Dt66 and wild-type strain Dt66 (having plasmids) that remain unaltered. CONCLUSIONS: Seventy percent drug-resistant loci of Shigella dysenteriae 1 Dt66 are present in chromosome and the remaining are plasmid mediated.

3

Keyzer C, Zalcman M, De Maertelaer V, Coppens E, Bali MA, Gevenois PA, Van Gansbeke D.Comparison of US and unenhanced multi-detector row CT in patients suspected of having acute appendicitis. Radiology. 2005 Aug;236(2):527-34.

         Department of Radiology, Hopital Erasme, Universite Libre de Bruxelles, Route de Lennik 808, B-1070-Brussels, Belgium.

PURPOSE: To prospectively compare the diagnostic performance of ultrasonography (US) and unenhanced multi-detector row computed tomography (CT) in patients suspected of having acute appendicitis by using surgery or clinical follow-up as the reference standard. MATERIALS AND METHODS: The institutional review board approved the research protocol. Written informed consent was obtained from all patients or, for those who were adolescents, from their parents. Ninety-four patients (59 female and 35 male patients) aged 16-81 years (mean, 38 years) who were suspected of having acute appendicitis underwent both US and unenhanced multi-detector row CT of the entire abdomen. The examinations were performed within 1-2 hours of each other. US and CT images were obtained and prospectively interpreted by a different radiologist from a group of abdominal radiologists or a group of residents and general radiologists. Radiologists proposed an overall diagnosis and an alternative diagnosis. Data from US and CT were compared, and the definite diagnosis was established with surgical findings (n = 40) or results of clinical follow-up (n = 54) as the reference standard. Comparisons were made for each group of radiologists and the patient's age, body mass index (BMI), and sex. Proportion comparisons were made by using the Pearson chi2 test or the Fisher exact test. Continuous variables were compared between groups with the Mann-Whitney U test. RESULTS: Thirty patients had definite appendicitis. The sensitivity, specificity, positive and negative predictive values, and accuracy were not significantly different between US and CT or between groups of radiologists (P values ranged from .389 to >.99), regardless of the patient's BMI (P values ranged from .073 to >.99). Misclassifications were compared with the definite alternative diagnosis and were not significantly different between US and CT or between groups of radiologists (P = .061-.592), regardless of patient age (P = .875) or sex (P = .151 and >.99 for male and female patients, respectively). The frequency of inconclusive examinations, however, was significantly higher with US than with CT, regardless of radiologist experience (P = .020 and <.001, respectively). CONCLUSION: Although the diagnostic performances of US and multi-detector row CT are comparable, more inconclusive images were obtained with US.

4

1.                      Koopmans M.Outbreaks of viral gastroenteritis: what's new in 2004? Curr Opin Infect Dis. 2005 Aug;18(4):295-9.

         Diagnostic Laboratory for Infectious Diseases and Perinatal Screening, National Institute of Public Health and the Environment, Bilthoven, The Netherlands.

         Purpose of review: Descriptions of outbreaks of viral gastroenteritis have become a prominent feature in scientific journals and other media such as the electronic reporting service 'promed'. A review of outbreak reports was done to further our understanding of the burden of disease, common and rare modes of transmission, complications, and possibilities for control and prevention. RECENT FINDINGS: Viral gastroenteritis outbreaks occur worldwide. In 2004, besides outbreak reports and surveys, there was considerable attention paid to food and waterborne outbreaks and the difficulties in proving these modes of transmission. Costs of viral gastroenteritis outbreaks are high. Complications and unusual manifestations of viral gastroenteritis, such as convulsions, transplant rejection, and chronic infection, may have been underreported. SUMMARY: Viral gastroenteritis is a very common illness in health care settings that can cause significant disruption. Clinicians working in these settings should be familiar with the epidemiology and the possible modes of transmission of enteric viruses to be able to translate them into strategies for prevention or intervention. Research is needed to support these strategies.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:  

13275.  Chang F, Deere H, Vu C. Atypical forms of microscopic colitis: morphological features and review of the literature. Adv Anat Pathol. 2005 Jul;12(4):203-11. Review.

13276.  Cuffari C, Dubinsky M, Darbari A, Sena L, Baldassano R. Crohn's jejunoileitis: the pediatrician's perspective on diagnosis and management. Inflamm Bowel Dis. 2005 Jul;11(7):696-704. Review.

13277.  Dalby T, Strid MA, Beyer NH, Blom J, Molbak K, Krogfelt KA. Rapid decay of Salmonella flagella antibodies during human gastroenteritis: a follow up study. J Microbiol Methods. 2005 Aug;62(2):233-43.

13278.  Forbes A. Crohn's or abdominal tuberculosis? Gut. 2005 Aug;54(8):1156.

13279.  Fraquelli M, Colli A, Casazza G, Paggi S, Colucci A, Massironi S, Duca P, Conte D.  Role of US in detection of Crohn disease: meta-analysis.Radiology. 2005 Jul;236(1):95-101.

13280.  Kang G, Kelkar SD, Chitambar SD, Ray P, Naik T. Epidemiological profile of rotaviral infection in India: challenges for the 21st century. J Infect Dis. 2005 Sep 1;192 Suppl 1:S120-6. 

13281.  Keyzer C, Zalcman M, De Maertelaer V, Coppens E, Bali MA, Gevenois PA, Van Gansbeke D. Comparison of US and unenhanced multi-detector row CT in patients suspected of having acute appendicitis. Radiology. 2005 Aug;236(2):527-34.

13282.  Kratzer W, Schmidt SA, Mittrach C, Haenle MM, Mason RA, Von Tirpitz C, Pauls S.  Contrast-enhanced wideband harmonic imaging ultrasound (SonoVue): a new technique for quantifying bowel wall vascularity in Crohn's disease. Scand J Gastroenterol. 2005 Aug;40(8):985-91.

13283.  Lal M, Kaur H, Gupta LK. Y. Enterocolitica gastroenteritis a prospective study. Indian J med Microbiol 2003, 21(3), 186-8.

Pathogenesis:

13284.  Abir F, Alva S, Kaminski DL, Longo WE. The role of arachidonic acid regulatory enzymes in colorectal disease. Dis Colon Rectum. 2005 Jul;48(7):1471-83. Review. 

13285.  Becker C, Wirtz S, Neurath MF. Stepwise regulation of TH1 responses in autoimmunity: IL-12-related cytokines and their receptors. Inflamm Bowel Dis. 2005 Aug;11(8):755-64. Review.

13286.  Bon F, Ambert-Balay K, Giraudon H, Kaplon J, Le Guyader S, Pommepuy M, Gallay A, Vaillant V, de Valk H, Chikhi-Brachet R, Flahaut A, Pothier P, Kohli E.   Molecular epidemiology of caliciviruses detected in sporadic and outbreak cases of gastroenteritis in France from December 1998 to February 2004.J Clin Microbiol. 2005 Sep;43(9):4659-64.

13287.  Fischer TK, Ashley D, Kerin T, Reynolds-Hedmann E, Gentsch J, Widdowson MA, Westerman L, Puhr N, Turcios RM, Glass RI. Rotavirus antigenemia in patients with acute gastroenteritis. J Infect Dis. 2005 Sep 1;192(5):913-9.

13288.  Fitch BR, Sachen KL, Wilder SR, Burg MA, Lacher DW, Khalife WT, Whittam TS, Young VB. Genetic diversity of Campylobacter sp. isolates from retail chicken products and humans with gastroenteritis in Central Michigan. J Clin Microbiol. 2005 Aug;43(8):4221-4. 

13289.  Gallimore CI, Cheesbrough JS, Lamden K, Bingham C, Gray JJ. Multiple norovirus genotypes characterised from an oyster-associated outbreak of gastroenteritis. Int J Food Microbiol. 2005 Sep 15;103(3):323-30.

13290.  Gallimore CI, Taylor C, Gennery AR, Cant AJ, Galloway A, Lewis D, Gray JJ. Use of a heminested reverse transcriptase PCR assay for detection of astrovirus in environmental swabs from an outbreak of gastroenteritis in a pediatric primary immunodeficiency unit. J Clin Microbiol. 2005 Aug;43(8):3890-4.

13291.  Koopmans M. Outbreaks of viral gastroenteritis: what's new in 2004? Curr Opin Infect Dis. 2005 Aug;18(4):295-9. Review.

13292.  Matsushita M, Takakuwa H, Matsubayashi Y, Nishio A, Ikehara S, Okazaki K.  Appendix is a priming site in the development of ulcerative colitis. World J Gastroenterol. 2005 Aug 21;11(31):4869-74.

13293.   McGovern D, Ahmad T. New IBD genes? Gut. 2005 Aug;54(8):1060-1.

13294.   Medici MC, Martinelli M, Ruggeri FM, Abelli LA, Bosco S, Arcangeletti MC, Pinardi F, De Conto F, Calderaro A, Chezzi C, Dettori G. Broadly reactive nested reverse transcription-PCR using an internal RNA standard control for detection of noroviruses in stool samples. J Clin Microbiol. 2005 Aug;43(8):3772-8.

13295.  Metzger-Boddien C, Kehle J. Development and evaluation of a sensitive PCR-ELISA for detection of adenoviruses in feces. Intervirology. 2005 Sep-Oct;48(5):297-300.

13296.  Olesen B, Neimann J, Bottiger B, Ethelberg S, Schiellerup P, Jensen C, Helms M, Scheutz F, Olsen KE, Krogfelt K, Petersen E, Molbak K, Gerner-Smidt P. Etiology of diarrhea in young children in Denmark: a case-control study. J Clin Microbiol. 2005 Aug;43(8):3636-41.

13297.  Oshimoto H, Okamura S, Iida T, Ishikawa T, Hosaka K, Mori M. Diagnostic value of the serum platelet-activating factor acetylhydrolase activity in inflammatory bowel disease. Tohoku J Exp Med. 2005 Sep;207(1):65-71.

13298.  Rahman M, Banik S, Faruque AS, Taniguchi K, Sack DA, Van Ranst M, Azim T. Detection and characterization of human group C rotaviruses in Bangladesh. J Clin Microbiol. 2005 Sep;43(9):4460-5.

Vaccines:

13299.    Bresee JS, Hummelman E, Nelson EA, Glass RI. Rotavirus in Asia: the value of surveillance for informing decisions about the introduction of new vaccines. J Infect Dis. 2005 Sep 1;192 Suppl 1:S1-5. Review.

13300.    Heaton PM, Goveia MG, Miller JM, Offit P, Clark HF. Development of a pentavalent rotavirus vaccine against prevalent serotypes of rotavirus gastroenteritis. J Infect Dis. 2005 Sep 1;192 Suppl 1:S17-21.

13301.  Phua KB, Quak SH, Lee BW, Emmanuel SC, Goh P, Han HH, De Vos B, Bock HL.  Evaluation of RIX4414, a live, attenuated rotavirus vaccine, in a randomized, double-blind, placebo-controlled phase 2 trial involving 2464 Singaporean infants. J Infect Dis. 2005 Sep 1;192 Suppl 1:S6-S16.

Therapy:

13302.     Baker DE. Safety of balsalazide therapy in the treatment of inflammatory bowel disease. Rev Gastroenterol Disord. 2005 Summer;5(3):135-41. Review.

13303.  Engelhardt B, Briskin MJ. Therapeutic targeting of alpha 4-integrins in chronic inflammatory diseases: tipping the scales of risk towards benefit? Eur J Immunol. 2005 Aug;35(8):2268-73. Review.

13304.  Gibson PR, Muir JG. Reinforcing the mucus: a new therapeutic approach for ulcerative colitis? Gut. 2005 Jul;54(7):900-3. Review. 

13305.  Gordon JN, Di Sabatino A, Macdonald TT. The pathophysiologic rationale for biological therapies in inflammatory bowel disease. Curr Opin Gastroenterol. 2005 Jul;21(4):431-7. Review.

13306.  Hanauer SB. Infliximab: lifetime use for maintenance is appropriate in Crohn's Disease. A BALANCING VIEW: lifetime channeling of infliximab for crohn's disease. Am J Gastroenterol. 2005 Jul;100(7):1438-9.

13307.  Hens DK, Niyogi SK, Kumar R. Epidemic strain Shigella dysenteriae Type 1 Dt66 encodes several drug resistances by chromosome. Arch Med Res. 2005 Jul-Aug;36(4):399-403. 

13308.  Kesisoglou F, Zhou SY, Niemiec S, Lee JW, Zimmermann EM, Fleisher D.  Liposomal formulations of inflammatory bowel disease drugs: local versus systemic drug delivery in a rat model. Pharm Res. 2005 Aug;22(8):1320-30.

13309.  Siegel CA, Sands BE. Review article: practical management of inflammatory bowel disease patients taking immunomodulators. Aliment Pharmacol Ther. 2005 Jul 1;22(1):1-16. Review.

13310.   Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ. 2005 Sep 3;331(7515):498-501. Review.

13311.   Van Assche G, Vermeire S, Rutgeerts P.  Medical treatment of inflammatory bowel diseases. Curr Opin Gastroenterol. 2005 Jul;21(4):443-7. Review. 

Back

 

April 2006

Some Selected Abstracts:

1.

Doganci A, Neurath MF, Finotto S. Mucosal immunoregulation: transcription factors as possible therapeutic targets. Curr Drug Targets Inflamm Allergy. 2005 Oct;4(5):565-75. Review. Laboratory of Cellular and Molecular Lung Immunology and &Laboratory of Immunology, I Medical Clinic, University of Mainz, Germany.

Much progress has been recently made with regard to our understanding of the mucosal immune system in health and disease. In particular, it has been shown that uncontrolled mucosal immune responses driven by lymphocytes or non-lymphoid cells may lead to immunological diseases such as allergy, hypersensitivity and inflammation. Thus, a more detailed understanding of mucosal immune regulation and decision making at mucosal surfaces is essential for a better understanding of mucosal immune responses in health and disease. Antigen presenting cells and T lymphocytes play a key role in controlling mucosal immune responses. To deal with this key task, T helper cells differentiate into functionally distinct subsets: TH1 (CD4+ T Helper cells), TH2, TH3, Tr1, and CD4+CD25+ T (Treg) cells. This review summarizes the role of antigen presenting cells, eosinophils, mast cells and T-cell subsets in the pathogenesis of allergic inflammation and intestinal inflammation. Furthermore, we discuss novel immunological treatment modalities for allergic inflammation (e.g. allergic asthma) and chronic intestinal inflammation (e.g. inflammatory bowel diseases (IBD)) such as the control of the expression of transcription factors to redirect pathological immune responses.

2.

Du Pont HL. What's new in enteric infectious diseases at home and abroad. Curr Opin Infect Dis. 2005 Oct;18(5):407-12. Review.

School of Public Health, University of Texas-Houston, St. Luke's Episcopal Hospital, 6720 Bertner Avenue, MC 1-64, Houston, TX 77030, USA .

PURPOSE OF REVIEW: This review was designed to focus on the important research in the area of acute infectious diarrhea published within the past year. PubMed was reviewed for articles published in 2004 and 2005 relating to pathogen-specific diarrhea and for travelers' diarrhea to identify the newly published articles. RECENT FINDINGS: New studies continue to show the importance of the diarrheagenic Escherichia coli as causes of acute and persistent diarrhea. Enteroaggregative E. coli has recently been shown to be an unrecognized cause of community-acquired diarrhea in infants in the USA. Genetic factors explain an increased susceptibility to travelers' diarrhea among international travelers. Also, poorly non-absorbed rifaximin (< 0.4%) was shown to be an effective drug when used prophylactically to prevent bacterial diarrhea during high risk travel. SUMMARY: Studies will continue to define the etiology of diarrhea and to better understand the epidemiology and prevention of infectious diarrhea. Antibacterial resistance among enteric bacterial pathogens is a growing problem, leading to the search for newer antibacterial drugs. Diarrhea due to bacterial agents in international travelers can be prevented and treated successfully by antibacterial drugs. The nonabsorbed rifamycin drug, rifaximin, appears to be ideally suited to become the important new drug in prevention and treatment of travelers' diarrhea. Studies are underway to determine the value of the drug in preventing invasive forms of diarrhea during travel to Asia and in the prevention of the commonly occurring post-infectious irritable bowel syndrome.

3.

Jones NL, Wine E. Pediatric gastrointestinal diseases: are drugs the answer? Curr Opin Pharmacol. 2005 Dec;5(6):604-9.   Review.

Department of Paediatrics, Hospital for Sick Children, University of Toronto, Toronto, Canada. nicola.jones@sickkids.ca

Owing to the lack of large randomized controlled studies, which would produce level 1 evidence, to guide management of gastrointestinal disorders in children, data are often extrapolated from adult studies to aid in treatment strategies. However, there are unique aspects to the management of children and adolescents with these chronic diseases, including issues of growth, side effects, long-term outcomes and psychosocial factors that might not be considered in adult trials. There is a major need for increased research in this population. In the future, a better understanding of the pathophysiologic mechanisms of these diseases should guide the development of rational novel therapies with better safety profiles for children with gastrointestinal disorders.

4.

1.                   Mawdsley JE, Rampton DS. Psychological stress in IBD: new insights into pathogenic and therapeutic implications. Gut. 2005 Oct;54(10):1481-91. Review.

       Centre for Gastroenterology, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, UK.

Psychological stress has long been reported anecdotally to increase disease activity in inflammatory bowel disease (IBD), and recent well designed studies have confirmed that adverse life events, chronic stress, and depression increase the likelihood of relapse in patients with quiescent IBD. This evidence is increasingly supported by studies of experimental stress in animal models of colitis. With the evolving concept of psychoneuroimmunology, the mechanisms by which the nervous system can affect immune function at both systemic and gut mucosal levels are gradually becoming apparent. Recent data suggest that stress induced alterations in gastrointestinal inflammation may be mediated through changes in hypothalamic-pituitary-adrenal (HPA) axis function and alterations in bacterial-mucosal interactions, and via mucosal mast cells and mediators such as corticotrophin releasing factor (CRF). To date, the therapeutic opportunities offered by stress reduction therapy remain largely unexplored, in part because of methodological difficulties of such studies. This paper reviews recent advances in our understanding of the pathogenic role of psychological stress in IBD and emphasises the need for controlled studies of the therapeutic potential of stress reduction.

5.

1.                   Panaccione R, Ferraz JG, Beck P. Advances in medical therapy of inflammatory bowel disease. Curr Opin Pharmacol. 2005 Dec;5(6):566-72.   Review.

Division of Gastroenterology, University of Calgary, Calgary, Alberta, Canada. rpanacci@ucalgary.ca

The past few years have seen increased knowledge and optimism on the use of biological therapy in Crohn's disease. Important lessons have been learned from the expanding clinical experience with infliximab, fuelling belief that current treatment will continue to evolve as therapy is aimed at specific targets within the immune cascade. Several other studies of agents that target tumour necrosis factor-alpha revealed mixed and sometimes disappointing results. However, this was balanced by encouraging results with agents that inhibit lymphocyte trafficking, as well as with other biological agents. Previous disappointing results of biological therapy in ulcerative colitis have been overcome with recent positive clinical trials with infliximab and the anti-CD3 antibody visilizumab. There now appears to be an expanding array of treatment options available to clinicians; however, as the number of potential molecular targets expands, unanswered questions remain regarding optimal treatment strategies, the long-term safety of biologicals and the ability of these novel and often expensive therapies to alter the natural history of the disease.

6.

1.                   Penner R, Fedorak RN, Madsen KL. Probiotics and nutraceuticals: non-medicinal treatments of gastrointestinal diseases. Curr Opin Pharmacol. 2005 Dec;5(6):596-603.   Review.

Division of Gastroenterology, University of Alberta, 6146 Dentistry Pharmacy, Edmonton, Alberta T6G 2N8, Canada.

The demonstration that immune and epithelial cells can discriminate between different microbial and bioactive plant species has extended the known mechanism(s) of action of nutraceuticals and probiotics beyond simple nutrition and/or antimicrobial effects. The progressive unravelling of these plant and bacterial effects on systemic immune and intestinal epithelial cell function has led to new credence for the use of probiotics and nutraceuticals in clinical medicine. Level I evidence now exists for the therapeutic use of probiotics in infectious diarrhea in children, recurrent Clostridium difficile-induced infections and post-operative pouchitis. Additional evidence is being acquired for the use of probiotics in other gastrointestinal infections, irritable bowel syndrome and inflammatory bowel disease. Not all individual probiotic strains have the same efficacy, and future clinical trials may focus on multistrain preparations agents with known efficacy. The use of nutraceuticals and probiotics as therapeutic agents for gastrointestinal disorders is rapidly moving into clinical usage. Scientific studies are providing mechanisms of action to explain the therapeutic effects, and randomized controlled trials are providing the necessary evidence for their incorporation into the therapeutic armamentarium.

7.

1.                   Woo PC, Lau SK, Teng JL, Yuen KY. Current status and future directions for Laribacter hongkongensis, a novel bacterium associated with gastroenteritis and traveller's diarrhoea. Curr Opin Infect Dis. 2005 Oct;18(5):413-9. Review.

Department of Microbiology and Research Centre of Infection and Immunology, Faculty of Medicine, The University of Hong Kong, Hong Kong, ROC.

PURPOSE OF REVIEW: Despite extensive investigations, a microbiological cause cannot be found in about half of the patients with infectious disease. Throughout the years, scientists have spent tremendous efforts in looking for microorganisms associated with these "unexplained infectious disease syndromes". Recently, a novel bacterium, Laribacter hongkongensis, was discovered and shown to be associated with gastroenteritis and traveller's diarrhoea. This review summarizes the current status, and shares with the readers the authors' experience in the microbiology, classification, epidemiology, clinical disease, laboratory diagnosis, antibiotic resistance and treatment of L. hongkongensis. It also discusses the importance and perspective of describing novel pathogenic bacterial species. RECENT FINDINGS: L. hongkongensis was shown to be associated with gastroenteritis and traveller's diarrhoea. Consumption of fish was associated with recovery of L. hongkongensis. Freshwater fish was a reservoir of L. hongkongensis. Genotypic typing revealed the possibility of virulent clones of L. hongkongensis. The class C beta-lactamase of L. hongkongensis has been cloned and characterized. SUMMARY: In 2001, L. hongkongensis, a novel genus and species, was first discovered in Hong Kong from the blood and empyema pus of a patient with alcoholic cirrhosis. Subsequently, it was isolated from patients in other parts of the world. Recently, this bacterium was found to be associated with community-acquired gastroenteritis and traveller's diarrhoea using cefoperazone MacConkey agar as the selective medium. Further studies, including setting up of animal and tissue culture models and characterization of virulence factors, should be performed. For pathogenic microbes, even one strain of a novel species should be described, so that global concerted efforts can be drawn to look for more cases associated with such a pathogen.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:  

13799.   Aly SM, El-Zawawy LA, Said DE, Fathy FM, Mohamed ON. The utility of lactoferrin in differentiating parasitic from bacterial infections. J Egypt Soc Parasitol. 2005 Dec;35(3 Suppl):1149-62.

13800.   Aro P, Ronkainen J, Talley NJ, Storskrubb T, Bolling-Sternevald E, Agreus L. Body mass index and chronic unexplained gastrointestinal symptoms: an adult endoscopic population based study. Gut. 2005 Oct;54(10):1377-83.  

13801.  Arroyo LG, Rousseau J, Willey BM, Low DE, Staempfli H, McGeer A, Weese JS.  Use of a selective enrichment broth to recover Clostridium difficile from stool swabs stored under different conditions. J Clin Microbiol. 2005 Oct;43(10):5341-3.

13802.  Asha NJ, Fawley WN, Freeman J, Wilcox MH. Increased rate of DNA recovery from United Kingdom epidemic Clostridium difficile PCR ribotype 1 strains stored cryogenically. J Clin Microbiol. 2005 Nov;43(11):5794-5.

13803.  Assa'ad A. Detection of causative foods by skin prick and atopy patch tests in patients with eosinophilic esophagitis: things are not what they seem. Ann Allergy Asthma Immunol. 2005 Oct;95(4):309-11.  

13804.   Burt BM, Javid PJ, Ferzoco SJ. Stump appendicitis in a patient with prior appendectomy. Dig Dis Sci. 2005 Nov;50(11):2163-4.  

13805.   Cardona AF, Ramos PL, Casasbuenas A. From case reports to systematic reviews in neutropenic enterocolitis. Eur J Haematol. 2005 Nov;75(5):445-6.  

13806.  Graham DY. Is real-time testing for helicobacter pylori and corpus atrophy clinically useful in 2005? Endoscopy. 2005 Oct;37(10):1006-7.  

13807.   Harris MC, D'Angio CT, Gallagher PR, Kaufman D, Evans J, Kilpatrick L. Cytokine elaboration in critically ill infants with bacterial sepsis, necrotizing entercolitis, or sepsis syndrome: correlation with clinical parameters of inflammation and mortality. J Pediatr. 2005 Oct;147(4):462-8.

13808.   Kawashima D, Oshitani N, Jinno Y, Watanabe K, Nakamura S, Higuchi K, Arakawa T. Augmented expression of secondary lymphoid tissue chemokine and EBI1 ligand chemokine in Crohn's disease. J Clin Pathol. 2005 Oct;58(10):1057-63.

13809.   Kornbluth A, Colombel JF, Leighton JA, Loftus E; ICCE. ICCE consensus for inflammatory bowel disease. Endoscopy. 2005 Oct;37(10):1051-4.  

13810.   Maunula L, Von Bonsdorff CH. Norovirus genotypes causing gastroenteritis outbreaks in Finland 1998-2002. J Clin Virol. 2005 Nov;34(3):186-94.

13811.   Mera R, Fontham ET, Bravo LE, Bravo JC, Piazuelo MB, Camargo MC, Correa P.  Long term follow up of patients treated for Helicobacter pylori infection. Gut. 2005 Nov;54(11):1536-40.  

13812.   Pardi DS, Limsui D. Utility of symptom-based criteria for evaluating patients with chronic diarrhea. Gastrointest Endosc. 2005 Oct;62(4):649.  

13813.   Phan TG, Nguyen TA, Shimizu H, Yagyu F, Okitsu S, Muller WE, Ushijima H.  Identification of enteroviral infection among infants and children admitted to hospital with acute gastroentritis in Ho Chi Minh City, Vietnam. J Med Virol. 2005 Oct;77(2):257-64.

13814.   Rugge M, Genta RM. Staging gastritis: an international proposal. Gastroenterology. 2005 Nov;129(5):1807-8.  

13815.   Scherubl H, Zeitz M. Tuberculous colitis. Gut. 2005 Dec;54(12):1820.  

13816.   Van den Berg RJ, Bruijnesteijn van Coppenraet LS, Gerritsen HJ, Endtz HP, van der Vorm ER, Kuijper EJ. Prospective multicenter evaluation of a new immunoassay and real-time PCR for rapid diagnosis of Clostridium difficile-associated diarrhea in hospitalized patients. J Clin Microbiol. 2005 Oct;43(10):5338-40.

13817.   Zagari RM, Pozzato P, Martuzzi C, Fuccio L, Martinelli G, Roda E, Bazzoli F. 13C-urea breath test to assess Helicobacter pylori bacterial load. Helicobacter. 2005 Dec;10(6):615-9.

 

Pathogenesis:

 13818.  Al-Haddad S, Riddell RH. The role of eosinophils in inflammatory bowel disease. Gut. 2005 Dec;54(12):1674-5.  

13819.   Abreu MT. Nod2 in normal and abnormal intestinal immune function. Gastroenterology. 2005 Oct;129(4):1302-4.  

13820.   Bamias G, Nyce MR, De La Rue SA, Cominelli F; American College of Physicians; American Physiological Society. New concepts in the pathophysiology of inflammatory bowel disease. Ann Intern Med. 2005 Dec 20;143(12):895-904. Review.  

13821.   Basu D, Lopez I, Kulkarni A, Sellin JH. Impact of race and ethnicity on inflammatory bowel disease. Am J Gastroenterol. 2005 Oct;100(10):2254-61.

13822.  Cao W, Fiocchi C, Pricolo VE. Production of IL-1beta, hydrogen peroxide, and nitric oxide by colonic mucosa decreases sigmoid smooth muscle contractility in ulcerative colitis. Am J Physiol Cell Physiol. 2005 Dec;289(6):C1408-16.  

13823.  Chompook P, Samosornsuk S, von Seidlein L, Jitsanguansuk S, Sirima N, Sudjai S, Mangjit P, Kim DR, Wheeler JG, Todd J, Lee H, Ali M, Clemens J, Tapchaisri P, Chaicumpa W. Estimating the burden of shigellosis in Thailand: 36-month population-based surveillance study. Bull World Health Organ. 2005 Oct;83(10):739-46.  

13824.   Collins SM. Dysregulation of peripheral cytokine production in irritable bowel syndrome. Am J Gastroenterol. 2005 Nov;100(11):2517-8.  

13825.   Elphick DA, Mahida YR. Paneth cells: their role in innate immunity and inflammatory disease. Gut. 2005 Dec;54(12):1802-9. Review.

13826.   Furuta GT, Nieuwenhuis EE, Karhausen J, Gleich G, Blumberg RS, Lee JJ, Ackerman SJ. Eosinophils alter colonic epithelial barrier function: role for major basic protein. Am J Physiol Gastrointest Liver Physiol. 2005 Nov;289(5):G890-7.

13827.   Gupta A, Derbes C, Sellin J. Clinical indications of the use of antineutrophil cytoplasmic antibodies and anti-Saccharomyces cerevisiae antibodies in the evaluation of inflammatory bowel disease at an Academic Medical Center. Inflamm Bowel Dis. 2005 Oct;11(10):898-902.

13828.   Hamano M, Kuzuya M, Fujii R, Ogura H, Yamada M. Epidemiology of acute gastroenteritis outbreaks caused by Noroviruses in Okayama, Japan. J Med Virol. 2005 Oct;77(2):282-9.

13829.   Hapfelmeier S, Hardt WD. A mouse model for S. typhimurium-induced enterocolitis. Trends Microbiol. 2005 Oct;13(10):497-503. Review.

13830.   Kutluana U, Simsek I, Akarsu M, Kupelioglu A, Karasu S, Altekin E. Is there a possible relation between atrophic gastritis and premature atherosclerosis? Helicobacter. 2005 Dec;10(6):623-9.

13831.   Latasa C, Roux A, Toledo-Arana A, Ghigo JM, Gamazo C, Penades JR, Lasa I.  BapA, a large secreted protein required for biofilm formation and host colonization of Salmonella enterica serovar Enteritidis. Mol Microbiol. 2005 Dec;58(5):1322-39.

13832.   Lemee L, Bourgeois I, Ruffin E, Collignon A, Lemeland JF, Pons JL. Multilocus sequence analysis and comparative evolution of virulence-associated genes and housekeeping genes of Clostridium difficile. Microbiology. 2005 Oct;151(Pt 10):3171-80.

13833.   Lo WY, Li JY, Chan YK, Lai LS, Yeung YW, Lo ST, Tsui WM, Ng CS. Instability of clonality in gastric lymphoid infiltrates: a study with emphasis on serial biopsies. Am J Surg Pathol. 2005 Dec;29(12):1582-92.

13834.   Makino SI, Kawamoto K, Takeshi K, Okada Y, Yamasaki M, Yamamoto S, Igimi S.  An outbreak of food-borne listeriosis due to cheese in Japan, during 2001. Int J Food Microbiol. 2005 Oct 15;104(2):189-96.

13835.   Martin MC, Oliver J, Urcelay E, Orozco G, Gomez-Garcia M, Lopez-Nevot MA, Pinero A, Brieva JA, de la Concha EG, Nieto A, Martin J. The functional genetic variation in the PTPN22 gene has a negligible effect on the susceptibility to develop inflammatory bowel disease. Tissue Antigens. 2005 Oct;66(4):314-7.

13836.   Palmer S, Brown D, Morgan D. Early qualitative risk assessment of the emerging zoonotic potential of animal diseases. BMJ. 2005 Nov 26;331(7527):1256-60. Review.  

13837.   Parsot C. Shigella spp. and enteroinvasive Escherichia coli pathogenicity factors. FEMS Microbiol Lett. 2005 Nov 1;252(1):11-8.   Review.

13838.   Reidy N, O'Halloran F, Fanning S, Cryan B, O'Shea H. Emergence of G3 and G9 rotavirus and increased incidence of mixed infections in the southern region of Ireland 2001-2004. J Med Virol. 2005 Dec;77(4):571-8.

13839.   Rockx B, Baric RS, de Grijs I, Duizer E, Koopmans MP. Characterization of the homo- and heterotypic immune responses after natural norovirus infection. J Med Virol. 2005  Nov; 77 (3) : 439-46.

13840.   Schreiber S. Of mice and men: what to learn about human inflammatory bowel disease from genetic analysis of murine inflammation. Gastroenterology. 2005 Nov;129(5):1782-4.  

13841.   Taguchi A, Ohmiya N, Shirai K, Mabuchi N, Itoh A, Hirooka Y, Niwa Y, Goto H.  Interleukin-8 promoter polymorphism increases the risk of atrophic gastritis and gastric cancer in Japan. Cancer Epidemiol Biomarkers Prev. 2005 Nov;14(11 Pt 1):2487-93.

13842.   Vermeire S, Rutgeerts P. Current status of genetics research in inflammatory bowel disease. Genes Immun. 2005 Dec;6(8):637-45. Review.

Vaccines:

13843.   Orr N, Katz DE, Atsmon J, Radu P, Yavzori M, Halperin T, Sela T, Kayouf R, Klein Z, Ambar R, Cohen D, Wolf MK, Venkatesan MM, Hale TL. Community-based safety, immunogenicity, and transmissibility study of the Shigella sonnei WRSS1 vaccine in Israeli volunteers. Infect Immun. 2005 Dec;73(12):8027-32.

Therapy:

13844.     Hanauer SB, Sandborn WJ, Kornbluth A, Katz S, Safdi M, Woogen S, Regalli G, Yeh C, Smith-Hall N, Ajayi F. Delayed-release oral mesalamine at 4.8 g/day (800 mg tablet) for the treatment of moderately active ulcerative colitis: the ASCEND II trial. Am J Gastroenterol. 2005 Nov;100(11):2478-85.

13845.   Hanauer SB. Infliximab or cyclosporine for severe ulcerative colitis. Gastroenterology. 2005 Oct;129(4):1358-9;  

13846.   Ingram JR, Thomas GA, Rhodes J, Green JT, Hawkes ND, Swift JL, Srivastava ED, Evans BK, Williams GT, Newcombe RG, Courtney E, Pillai S. A randomized trial of nicotine enemas for active ulcerative colitis. Clin Gastroenterol Hepatol. 2005 Nov;3(11):1107-14.

13847.   Roberta P, Antonino B, Paolo P. Inflammatory bowel disease and drug intake. Inflamm Bowel Dis. 2005 Oct;11(10):951.  

13848.   Rutgeerts P, Sandborn WJ, Feagan BG, Reinisch W, Olson A, Johanns J, Travers S, Rachmilewitz D, Hanauer SB, Lichtenstein GR, de Villiers WJ, Present D, Sands BE, Colombel JF.  Infliximab for induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2005 Dec 8;353(23):2462-76.

13849.   Sandborn WJ, Colombel JF, Enns R, Feagan BG, Hanauer SB, Lawrance IC, Panaccione R, Sanders M, Schreiber S, Targan S, van Deventer S, Goldblum R, Despain D, Hogge GS, Rutgeerts P; International Efficacy of Natalizumab as Active Crohn's Therapy (ENACT-1) Trial Group; Evaluation of Natalizumab as Continuous Therapy (ENACT-2) Trial Group. Natalizumab induction and maintenance therapy for Crohn's disease. N Engl J Med. 2005 Nov 3;353(18):1912-25.

 

Back

 

July 2006

Some selected abstracts:

1.

Neville KA, Verge CF, Rosenberg AR, O'Meara MW, Walker JL. Isotonic is better than hypotonic saline for intravenous rehydration of children with gastroenteritis: a prospective randomised study. Arch Dis Child. 2006 Mar;91(3):226-32.

Department of Endocrinology, Sydney Children's Hospital, Sydney, Australia. kristen.neville@sesiahs.health.nsw.gov.au

AIMS: To determine whether the risk of hyponatraemia in children with gastroenteritis receiving intravenous (IV) fluids is decreased by the use of 0.9% saline. METHODS: A prospective randomised study was carried out in a tertiary paediatric hospital. A total of 102 children with gastroenteritis were randomised to receive either 0.9% saline + 2.5% dextrose (NS) or 0.45% saline + 2.5% dextrose (N/2) at a rate determined by their treating physician according to hospital guidelines and clinical judgement. Plasma electrolytes, osmolality, and plasma glucose were measured before (T(0)) and 4 hours after (T(4)
starting IV fluids, and subsequently if clinically indicated. Electrolytes and osmolality were measured in urine samples. Results were analysed according to whether children were hyponatraemic (plasma sodium <135 mmol/l) or normonatraemic at T(0). RESULTS: At T(0), mean (SD) plasma sodium was 135 (3.3) mmol/l (range 124-142), with 37/102 (36%) hyponatraemic. At T(4), mean plasma sodium in children receiving N/2 remained unchanged in those initially hyponatraemic (n = 16), but fell 2.3 (2.2) mmol/l in the normonatraemic group. In contrast, among children receiving NS, mean plasma sodium was 2.4 (2.0) mmol/l higher in those hyponatraemic at baseline (n = 21) and unchanged in the initially normonatraemic children. In 16 children who were still receiving IV fluids at 24 hours, 3/ 8 receiving N/2 were hyponatraemic compared with 0/8 receiving NS. No child became hypernatraemic. CONCLUSIONS: In gastroenteritis treated with intravenous fluids, normal saline is preferable to hypotonic saline because it protects against hyponatraemia without causing hypernatraemia.
 

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:  
 

14329. Banning M. Bacteria and the gastrointestinal tract: beneficial and harmful effects. Br J Nurs. 2006 Feb 9-22;15(3):144-9. Review.

14330. Curry A, Appleton H, Dowsett B. Application of transmission electron microscopy to the clinical study of viral and bacterial infections: present and future. Micron. 2006; 37(2):91-106.

14331. Moanna A, Bajaj R, del Rio C. Emphysematous cholecystitis due to Salmonella derby.Lancet Infect Dis. 2006 Feb;6(2):118-20.

14332. Okumura A, Watanabe K, Negoro T, Hayakawa F, Kato T, Maruyama K, Kubota T, Suzuki M, Kurahashi H, Azuma Y. Long-term follow-up of patients with benign partial epilepsy in infancy. Epilepsia. 2006 Jan;47(1):181-5.
 

Pathogenesis:

14333. Ojo DA, Mafiana CF, Oluloro YJ. Study of pathogenic bacteria commonly associated with gastroenteritis in school children in Abeokuta Southlocal Government area of Ogun state, Nigeria. Biosci, Biotechnol ResAsia.2004; 2(2): 89-92.
 

Vaccines:
 

14334. Haupt RM, Isikci O, Kimble WL, Sotos GL, Fu J. Physicians' knowledge and attitudes  about rotavirus gastroenteritis and rotavirus vaccine. Pediatr Ann. 2006 Jan;35(1):54-61.

Therapy:

14335. McCollough M, Sharieff GQ. Abdominal pain in children. Pediatr Clin North Am. 2006 Feb;53(1):107-37, vi. Review.

 Back

 

October 2006

 

Some selected abstract:

1

Freedman SB, Adler M, Seshadri R, Powell EC. Oral ondansetron for gastroenteritis in a pediatric emergency department. N Engl J Med. 2006 Apr 20;354(16):1698-705. 

Division of Pediatric Emergency Medicine, Hospital for Sick Children, University of Toronto, Toronto, ON, Canada. stephen.freedman@sickkids.ca

 

BACKGROUND: Vomiting limits the success of oral rehydration in children with gastroenteritis. We conducted a double-blind trial to determine whether a single oral dose of ondansetron, an antiemetic, would improve outcomes in children with gastroenteritis. METHODS: We enrolled 215 children 6 months through 10 years of age who were treated in a pediatric emergency department for gastroenteritis and dehydration. After being randomly assigned to treatment with orally disintegrating ondansetron tablets or placebo, the children received oral-rehydration therapy according to a standardized protocol. The primary outcome was the proportion who vomited while receiving oral rehydration. The secondary outcomes were the number of episodes of vomiting and the proportions who were treated with intravenous rehydration or hospitalized. RESULTS: As compared with children who received placebo, children who received ondansetron were less likely to vomit (14 percent vs. 35 percent; relative risk, 0.40; 95 percent confidence interval, 0.26 to 0.61), vomited less often (mean number of episodes per child, 0.18 vs. 0.65; P<0.001), had greater oral intake (239 ml vs. 196 ml, P=0.001), and were less likely to be treated by intravenous rehydration (14 percent vs. 31 percent; relative risk, 0.46; 95 percent confidence interval, 0.26 to 0.79). Although the mean length of stay in the emergency department was reduced by 12 percent in the ondansetron group, as compared with the placebo group (P=0.02), the rates of hospitalization (4 percent and 5 percent, respectively; P=1.00) and of return visits to the emergency department (19 percent and 22 percent, P=0.73) did not differ significantly between groups. CONCLUSIONS: In children with gastroenteritis and dehydration, a single dose of oral ondansetron reduces vomiting and facilitates oral rehydration and may thus be well suited for use in the emergency department. Copyright 2006 Massachusetts Medical Society.

 

Vaccines:

14713.  Molinaro GA, Lee DA, Parashar UD.  Rotavirus vaccines. N Engl J Med. 2006 Apr 20;354(16):1747-51; author reply 1747-51.

Back