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Background Viral gastroenteritides are among the causes of higher morbidity and mortality in the childhood period, especially in infants. Although viral-induced diarrheal diseases are important problems in Erzurum, there have been no studies on the molecular prevalence of viral gastroenteritis agents in this region's children. The aim of the prospective study is to determine the molecular prevalence of the most commonly seen viral etiologic agents and their coinfection rates in children under 5 years of age with gastroenteritis in Erzurum, Turkey. Methods Stool samples from 375 children between 0 and 5 years of age who suffered from acute diarrhea were investigated for the presence of Rotavirus, Norovirus, Astrovirus and Adenovirus by reverse transcriptase polymerase chain reaction, followed by conventional PCR techniques. The presence of Rotavirus, Norovirus, Astrovirus and Adenovirus in the specimens was detected by amplification of the VP6, RdRp, ORF-1b and Hexon regions, respectively. Stool samples were also investigated non-viral enteropathogens by conventional techniques. Results At least one viral pathogen was detected in 59.2% of the stool samples. Rotavirus was the most frequently observed agent (32.3%), followed by Norovirus (20.3%), Adenovirus (9.6%) and Astrovirus (5.6%). All specimens were negative for bacterial pathogens. Twenty seven (7.2%) specimens were positive for intestinal helminths and protozoan. A total of 39 coinfection (10.4%) including 38 dual and 1 triple were detected. The most frequent coinfections were observed between Norovirus plus Rotavirus and Norovirus plus Adenovirus. Conclusions Single infections or coinfections of the enteropathogenic viruses occur at a significant rate in Erzurum's children. This study draws attention to the necessity of taking account of multiple viral infections in studies on combined vaccines and the treatment of gastroenteritis.

Objective: to determine the proportion of adenovirus gastroenteritides in the structure of acute enteric infections of uncertain etiology among the children of Baku. Subjects and methods. A total of 155 children aged less than 14 years with acute enteric infections of uncertain etiology who had been admitted to the Clinic of Infectious Diseases, V. Akhundov National Research Institute of Medical Prevention, in 2014–2015, were examined. The etiological diagnosis of adenovirus gastroenteritis was made by immunochromatographic assay. To rule out the bacterial etiology of acute enteric infection, all the children underwent fecal bacteriological examination. The examinees included babies under 6 months (17,4%), infants aged 7 months to 1 year (6,4%), those 1–2 years of age (29,6%), and children aged 2–14 years (46,4%). Adenoviruses in conjunction with rotavirus were detected in 7 (4,5%) patients. Adenovirus monoinfection was seen in 23 (15%) children. The contribution of adenoviruses in the etiological structure of acute enteric infections in children was 19,3%. There was no significant difference in the frequency of adenoviruses depending on gender. Adenovirus monoinfection wasregistered in the children all year round. Adenovirus monoinfection occurred as moderate diarrhea whereas mixed adenovirus-rotavirus infection was characterized by the severe course of diarrheal syndrome and catarrhal manifestations.

Viruses are sometimes transmitted through foods. Hepatitis A (HA) and some viral gastroenteritides are the diseases now known to be spread most frequently in this way, but any virus from the human intestines probably could be. Bacterial indicators of fecal contamination show limited correlation with the incidence of viruses in foods, so tests to detect the viruses themselves are needed. The epidemiologic record has led to selection of shellfish (bivalve molluscs) and vegetables and fruits as foods for which test methods should be described, and ground beef and raw milk are also considered here because of the great interest they have attracted among research workers. Viruses in foods are presently detected on the basis of the infections they cause in cultured primate cells, but these cell culture methods do not permit detection of the HA virus nor the most important of the foodborne gastroenteritis viruses. Current methods of virus detection entail liquefaction of the food sample, clarification of the sample suspension, possibly concentration of the clarified food extract, and inoculation of cell cultures; a certain amount of specialized equipment is required for some of these procedures. The inclusion of the proper controls is critical to interpretation of results that are obtained.

Markedly increased blood eosinophilia (ie,or =1.5 x 10(9)/L), whether discovered fortuitously or found with signs and symptoms of associated organ involvement, commands diagnostic evaluation and often therapeutic interventions. This degree of hypereosinophilia is often but not uniformly associated with eosinophilic infiltration of tissues that can potentially lead to irreversible, life-threatening organ damage. Initial approaches focus on ascertaining that eosinophilia is not secondary to other underlying disease processes, including helminthic parasite infections, varied types of adverse reactions to medications, and other eosinophil-associated syndromes, such as eosinophilic gastroenteritides, eosinophilic pneumonias, and Churg-Strauss syndrome vasculitis. If evaluations exclude eosinophilia attributable to secondary causes or other eosinophil-related syndromes or organ-specific diseases, attention must be directed to considerations of varied other forms of the hypereosinophilic syndromes, which include myeloproliferative variants, lymphocytic variants, and many of still unknown causes. Cognizant of the capacities of eosinophils to mediate tissue damage, the varied causes for hypereosinophilia are considered, and a contemporary stepwise practical approach to the diagnosis and treatment of patients with hypereosinophilia is presented.

Aim. While collagenous colitis represents the most common form of the collagenous gastroenteritides, the collagenous entities affecting the proximal part of the gastrointestinal tract are much less recognized and possibly overlooked. The aim was to summarize the latest information through a systematic review of collagenous gastritis, collagenous sprue, and a combination thereof. Methods. The search yielded 117 studies which were suitable for inclusion in the systematic review. Excluding repeated cases, 89 case reports and 28 case series were reported, whereas no prospective studies with or without control groups were identified. Further, no randomized, controlled trials were identified. The total number of patients with proximal collagenous gastroenteritides reported was 330. Results. An overview of clinical presentations, prognosis, pathophysiology and histopathology, as well as management of these disorders is presented. The prognosis of both collagenous gastritis and sprue seems not to be as dismal as considered previously. Data point to involvement of immune or autoimmune mechanisms potentially driven by luminal antigens initiating the fibroinflammatory condition. Conclusions. To reach the diagnosis it is recommended that biopsies are obtained during gastroduodenoscopies. Therapies with anti-secretory strategies, glucocorticoids, and in some cases iron supplementation are suggested, although rational treatment options from randomized, controlled trials do not exist for these rare or even overlooked disorders.

This year's literature on the pathology of the small intestine will again be subdivided into sections on the enterocyte and its general environment, inflammatory changes exclusive of inflammatory bowel disease, infections, and tumors. Special attention is given to the eosinophilic gastroenteritides with a proposal of a new conceptual framework for classification.

Based on the premise that dietary nitrate is detrimental to human health, increasingly stringent regulations are being instituted to lower nitrate levels in food and water. Not only does this pose a financial challenge to water boards and a threat to vegetable production in Northern Europe, but also may be eliminating an important non-immune mechanism for host defence. Until recently nitrate was perceived as a purely harmful dietary component which causes infantile methaemoglobinaemia, carcinogenesis and possibly even teratogenesis. Epidemiological studies have failed to substantiate this. It has been shown that dietary nitrate undergoes enterosalivary circulation. It is recirculated in the blood, concentrated by the salivary glands, secreted in the saliva and reduced to nitrite by facultative Gram-positive anaerobes (Staphylococcus sciuriandS. intermedius) on the tongue. Salivary nitrite is swallowed into the acidic stomach where it is reduced to large quantities of NO and other oxides of N and, conceivably, also contributes to the formation of systemic S-nitrosothiols. NO and solutions of acidified nitrite, mimicking gastric conditions, have been shown to have antimicrobial activity against a wide range of organisms. In particular, acidified nitrite is bactericidal for a variety of gastrointestinal pathogens such asYersiniaandSalmonella.NO is known to have vasodilator properties and to modulate platelet function, as are S-nitrosothiols. Thus, nitrate in the diet, which determines reactive nitrogen oxide species production in the stomach (McKnightet al.1997), is emerging as an effective host defence against gastrointestinal pathogens, as a modulator of platelet activity and possibly even of gastrointestinal motility and microcirculation. Therefore dietary nitrate may have an important therapeutic role to play, not least in the immunocompromised and in refugees who are at particular risk of contracting gastroenteritides.

Introduction: Isolated collagenous gastroduodenitis (CGD) with no colonic involvement is an extremely rare entity with only 2 cases reported in the literature. We report a case of isolated CGD presenting as nausea, vomiting, abdominal pain and profound weight loss. Case: A 63-year-old African American woman presented with two-year history of nausea, vomiting, upper abdominal pain and sixty pounds weight loss. There was no history of diarrhea, gastrointestinal (GI) bleeding or skin changes. Prior evaluation, including esophagogastroduodenoscopy, colonoscopy with biopsies and a video-capsule endoscopy only revealed gastric mucosal edema. Celiac serologies were negative and a gluten free diet failed to improve her symptoms. She was hospitalized for severe malnutrition and total parenteral nutrition (TPN) was started. Laboratory evaluation revealed Hemoglobin of 12.4g/dl, albumin 2.6g/dl, positive antinuclear antigen (1:640), and positive anti SCL-70 antibody. Push enteroscopy showed inflammatory changes in the stomach and the small bowel (SB) wall mucosa appeared edematous and nodular. Biopsies revealed inflammatory changes and thickened collagen table consistent with CGD. She was started on oral prednisone, mycophenolate mofetil (MMF), and high dose proton pump inhibitors. Prednisone was eventually tapered off and the TPN was discontinued. At 4 months, repeat push enteroscopy showed normal looking SB mucosa. Biopsies revealed no collagen table. She has regained her baseline weight and is currently maintained only on MMF. Discussion: Collagenous gastroenteritides are characterized by marked subepithelial collagen deposition with mucosal inflammatory infiltrate. Isolated collagenous gastritis presents with anemia, weight loss, dyspepsia and epigastric pain. Endoscopy shows thickened and nodular mucosa, erosions, and ulcerations. Diagnosis is made by histology, with increased subepithelial collagen band thickness to at least 10 μm and inflammatory cell response with predominant mononuclear infiltrate in the lamina propria. GI involvement in scleroderma can also present similarly, however, endoscopic findings are more consistent with gastric antral vascular ectasia (GAVE) and histology is characterized by mucosal capillary dilatation with fibromuscular hyperplasia. The histological features in our case typify CGD and were not consistent with GI scleroderma. A variety of therapies for CGD have been tried including corticosteroids, Bismuth subsalicylate, Mesalazine, and hypoallergenic diets. Steroids can lead to clinical improvement, however, endoscopic or histological improvement has not been documented. The uniqueness in our case is significant clinical, endoscopic and histologic response to steroid and MMF therapy. With increased awareness and reporting of such cases, diagnostic and management strategies may be better elucidated.

Introduction: Isolated collagenous gastroduodenitis (CGD) with no colonic involvement is an extremely rare entity with only 2 cases reported in the literature. We report a case of isolated CGD presenting as nausea, vomiting, abdominal pain and profound weight loss. Case: A 63-year-old African American woman presented with two-year history of nausea, vomiting, upper abdominal pain and sixty pounds weight loss. There was no history of diarrhea, gastrointestinal (GI) bleeding or skin changes. Prior evaluation, including esophagogastroduodenoscopy, colonoscopy with biopsies and a video-capsule endoscopy only revealed gastric mucosal edema. Celiac serologies were negative and a gluten free diet failed to improve her symptoms. She was hospitalized for severe malnutrition and total parenteral nutrition (TPN) was started. Laboratory evaluation revealed Hemoglobin of 12.4g/dl, albumin 2.6g/dl, positive antinuclear antigen (1:640), and positive anti SCL-70 antibody. Push enteroscopy showed inflammatory changes in the stomach and the small bowel (SB) wall mucosa appeared edematous and nodular. Biopsies revealed inflammatory changes and thickened collagen table consistent with CGD. She was started on oral prednisone, mycophenolate mofetil (MMF), and high dose proton pump inhibitors. Prednisone was eventually tapered off and the TPN was discontinued. At 4 months, repeat push enteroscopy showed normal looking SB mucosa. Biopsies revealed no collagen table. She has regained her baseline weight and is currently maintained only on MMF. Discussion: Collagenous gastroenteritides are characterized by marked subepithelial collagen deposition with mucosal inflammatory infiltrate. Isolated collagenous gastritis presents with anemia, weight loss, dyspepsia and epigastric pain. Endoscopy shows thickened and nodular mucosa, erosions, and ulcerations. Diagnosis is made by histology, with increased subepithelial collagen band thickness to at least 10 μm and inflammatory cell response with predominant mononuclear infiltrate in the lamina propria. GI involvement in scleroderma can also present similarly, however, endoscopic findings are more consistent with gastric antral vascular ectasia (GAVE) and histology is characterized by mucosal capillary dilatation with fibromuscular hyperplasia. The histological features in our case typify CGD and were not consistent with GI scleroderma. A variety of therapies for CGD have been tried including corticosteroids, Bismuth subsalicylate, Mesalazine, and hypoallergenic diets. Steroids can lead to clinical improvement, however, endoscopic or histological improvement has not been documented. The uniqueness in our case is significant clinical, endoscopic and histologic response to steroid and MMF therapy. With increased awareness and reporting of such cases, diagnostic and management strategies may be better elucidated.

To the Editor: Burckhardt et al. (1) recently reported on Clostridium difficile–associated disease (CDAD) in Saxony, Germany. In contrast to the observation by Wilcox and Fawley in the United Kingdom (2), the report from Germany argued against a reporting bias for gastroenteritides as a cause of the observed increase in the incidence of CDAD diagnoses from 2002 through 2006. To explore this issue further, I examined the potential influence of such reporting bias on the observed increase in the incidence of hospitalizations of patients with CDAD in the United States from 2000 through 2005. In the 2000–2005 data from the National Inpatient Sample data from the Agency for Healthcare Research and Quality (3,4), I identified hospitalizations for gastrointestinal infections caused by C. difficile, Salmonella, rotavirus, and other unspecified infectious agents, using the corresponding diagnosis codes from the International Classification of Diseases, 9th Revision, Clinical Modification. I obtained censal and intercensal data on the numbers of the U.S. population from 2000 through 2005 from the U.S. Census Bureau (5). Based on these records, I calculated hospitalization incidence for each of the infectious causes. Annual incidence of CDAD increased from 49.2 to 101.6 per 100,000 population within the period examined. Within the same time frame, the incidence of CDAD as the principal diagnosis also more than doubled, increasing from 11.6 to 25.8 hospitalizations per 100,000. Although the incidence of hospitalizations for Salmonella infections per 100,000 population remained stable, rotavirus infection showed a slight increase (from 10.8 to 14.5) as did other infectious gastroenteritides (from 38.9 to 49.9/100,000) (Figure). Thus, although a slight increase in the incidence was exhibited, a reporting bias for gastroenteric infections with organisms other than C. difficile does not appear to account fully for the observed doubling of the overall incidence of hospitalizations with CDAD in the United States from 2000 through 2005. Figure Annual incidence per 100,000 population of all hospitalizations for Clostridium difficile–associated disease (CDAD) compared with hospitalizations for a primary diagnosis of CDAD and with gastroenteritides caused by Salmonella, rotavirus, and ...

• A critical analysis of the literature shows that only a few viral agents have been proved by accepted criteria to cause acute gastroenteritis. Rotavirus, of the RNA family reoviridae, is the cause of most childhood gastroenteritis. The parvovirus-like agents (Norwalk, Hawaii, MC, and W) are proved agents of epidemic gastroenteritis. There is good evidence that the Marcy, FS, and Niigata agents were the causes of gastroenteritis outbreaks. Thirty percent of all acute gastroenteritis episodes in large investigations are still etiologically unaccounted for. Much work remains to be done to define the pathogenesis and immunology of viral gastroenteritides. ( Am J Dis Child 132:302-307, 1978)