Raoultella planticola associated with Meckel's diverticulum perforation and peritonitis in a child: Case report and systematic review of the paediatric literature.

Raoultella planticola (R. planticola) is a Gram-negative, aerobic, rod bacteria found in water and soil that has been on rare occasions associated with clinical infections. However, in recent years, there has been both an increase in the frequency and severity of R. planticola infections. We present the first case of Meckel's diverticulum perforation and peritonitis in a child associated with R. planticola infection and a systematic review of the paediatric literature. At present, in the paediatric population, R. planticola presents good susceptibility to a variety of antibiotics with the exception of ampicillin.

[Detection rate of Helicobacter pylori and its clinical significance in children with Meckel's diverticulum].

OBJECTIVE: To determine the detection rate of Helicobacter pylori (Hp) in children with Meckel's diverticulum (MD) and its clinical significance among children with MD. METHODS: Eighty-one children with MD were divided into two groups according to the presence (n=45) or absence (n=36) of digestive hemorrhage. The detection rates of Hp in MD tissues and stomach tissues were determined by immunohistochemistry. The detection rates of Hp were compared between the two groups and between the MD tissues with different clinical features in the hemorrhage group. RESULTS: The detection rate of Hp in MD tissues for the hemorrhage group was 76% (34/45), which was significantly higher than that for the non-hemorrhage group (47%, 17/36) (P<0.05). The detection rate of Hp in stomach tissues for the hemorrhage group (87%, 39/45) was insignificantly higher than that for the non-hemorrhage group (67%, 24/36) (P>0.05). Among patients in the bleeding group, the detection rate of Hp in MD tissues showed no relationship with age, sex, preoperative hemorrhage frequency, amount of hemorrhage, length of MD, basal diameter of MD, and pathological type (P>0.05), but was related to location of MD, presence or absence of ulcer, and depth of ulcer (P<0.05). For the hemorrhage group, a significant positive correlation was found between the detection rates of Hp in MD tissues and stomach tissues (P<0.05), as shown by the Spearman correlation analysis. CONCLUSIONS: The detection rate of Hp in MD tissues is increased in children with MD complicated by digestive hemorrhage. Hp infection may play some role in the hemorrhage process among children with MD.

Helicobacter species and gut bacterial DNA in Meckel's diverticulum and the appendix.

AIM: To analyse the possible association of various Helicobacter species and certain common gut bacteria in patients with Meckel's diverticulum and appendicitis. METHODS: A nested-polymerase chain reaction (PCR), specific to 16S rRNA of the Helicobacter genus, was performed on paraffin embedded samples, 50 with acute appendicitis, 50 normal appendixes, and 33 Meckel's diverticulum with gastric heterotopia and/or ulcer. Helicobacter genus positive samples were sequenced for species identification. All samples were also analysed for certain gut bacteria by PCR. RESULTS: Helicobacter pullorum DNA was found in one out of 33 cases and Enterobacteria in two cases of Meckel's diverticulum. Helicobacter pylori (H. pylori) was found in three, Enterobacter in 18, and Bacteroides in 19 out of 100 appendix samples by PCR. Enterococcus was not found in any MD or appendix samples. All H. pylori positive cases were from normal appendixes. CONCLUSION: Helicobacter is not an etiological agent in the pathogenesis of symptomatic Meckel's diverticulum or in acute appendicitis.

Evaluation for Helicobacter pylori in Meckel's diverticulum by using real-time PCR.

BACKGROUND: Although Helicobacter pylori (H. pylori) has been identified in heterotopic gastric mucosa of Meckel's diverticulum, controversial results are reported in the pertinent literature. AIMS: The aim of this study was to evaluate for the presence of H. pylori histologically using hematoxylin-eosin and Toluidine Blue in Meckel's diverticulum and by real-time TaqMan polymerase chain reaction (PCR) in those with heterotopic gastric mucosa. METHODS: The study included 21 consecutive patients who had undergone resection of Meckel's diverticulum at our hospital between 1995 and 2007. The paraffin-embedded tissues were retrieved and reviewed for the presence of histological abnormalities and H. pylori-like organisms and for the presence or absence of heterotopic mucosa. H. pylori was sought in those cases that contained heterotopic gastric mucosa using real-time TaqMan PCR to amplify a fragment of the 23S ribosomal RNA (rRNA) gene of H. pylori. RESULTS: Upon histological examination, heterotopic gastric mucosa was found to be present in 12 cases. H. pylori was not identified in any of the sections examined. A genomic PCR product was also not obtained in real-time PCR study. CONCLUSIONS: We have confirmed that colonization of H. pylori, if it occurs at all, is exceedingly rare in heterotopic gastric mucosa of Meckel's diverticulum.

Role of Helicobacter pylori infection in complications from Meckel's diverticulum.

Our purpose was to evaluate the role of Helicobacter pylori in complications arising from Meckel's diverticulum in the Jewish and Arab populations of Jerusalem. Diverticular tissues were studied by hematoxylin-eosin, Giemsa, and two immunohistochemical stainings. Three groups of patients were identified: (1) 20 patients in whom Meckel's diverticulum was an incidental finding during laparotomy for other causes; (2) 7 patients with heterotopic gastric mucosa who underwent laparotomy because of bleeding from Meckel's diverticulum--3 were infected with Helicobacter pylori; and (3) 15 patients who underwent operations because of complicated Meckel's diverticulum except for bleeding--7 patients had heterotopic gastric mucosa; only 1 patient had Helicobacter pylori. Demographic, clinical, and pathological findings within the gastric mucosa were not different in patients with and without colonization with Helicobacter pylori. In conclusions, Helicobacter pylori colonizes heterotopic gastric mucosa with Meckel's diverticulum, but probably has a minor role in the complications of Meckel's diverticulum.

Does colonization of Helicobacter pylori in the heterotopic gastric mucosa play a role in bleeding of Meckel's diverticulum?

BACKGROUND/PURPOSE: Helicobacter pylori is a microorganism known to colonize in gastric type of mucosa and is associated with gastritis and peptic ulceration. The aim of the study was to determine whether colonization of H pylori in heterotopic gastric mucosa plays a role in bleeding of Meckel's diverticulum. METHODS: Histopathologic slides of patients who had undergone resection of Meckel's diverticulum in recent 5 years were reexamined for the presence of H pylori in heterotopic gastric mucosa. Polimerase chain reaction (PCR) test was used to trace the genetic material of urease gene and 16s rDNA amplifications for H pylori. RESULTS: Thirteen of the 30 histopathologic slides of Meckel's diverticula had heterotopic gastric mucosa. Ten of the 13 patients presented with acute bleeding of the diverticula, whereas 3 of them were asymptomatic. None of the 13 gastric mucosa bearing diverticula were colonized with H pylori. PCR was unable to show any trace of genetic material for H pylori. CONCLUSION: Although the role of H pylori is well established in the gastric mucosal ulceration, its presence is not essentially required to induce "heterotopic gastritis" that may result in bleeding of the Meckel's diverticulum. .

Helicobacter pylori and Meckel's diverticula.

BACKGROUND: Helicobacter pylori is known to infect only gastric mucosa and is strongly associated with gastroduodenal ulceration. The authors studied whether H. pylori colonizes the gastric mucosa of Meckel's diverticula, and determined its relationship to "gastritis" and bleeding. METHODS: A 10-year retrospective review identified 45 children with Meckel's diverticulum. Hematoxylin-eosin and Diff-Quik stains were used to assess the presence and severity of gastritis, and to highlight organisms in the resected diverticula. Cases with organisms were then studied with antibodies specific for H. pylori using immunoperoxidase methods. RESULTS: Twenty-eight children, 7 months to 12.6 years of age, had lower gastrointestinal hemorrhage caused by Meckel's diverticulum and had positive radionuclide scans. All had acid-secreting mucosa in their diverticula, and ulceration. "Chronic gastritis" and eosinophilia were constant findings; "acute gastritis" was present in four patients. Twenty specimens exhibited lymphoid follicles in the gastric mucosa. Seventeen patients with Meckel's diverticula (age range, 1 month-14.7 years) who presented with acute abdominal pain associated with intussusception were used for comparison. Acid-secreting gastric mucosa was seen in four patients. H. pylori was identified in only one of the 45 patients; this patient had ulceration and moderate "acute gastritis." CONCLUSIONS: H. pylori does not colonize a substantial number of children who have ulcerated and bleeding Meckel's diverticulum in the presence of acid-secreting mucosa. Although H. pylori is a notable cause of ulceration, the authors confirm that ulceration is possible in its absence, and alternative mechanisms of ulceration are important. The presence of lymphoid follicles in Meckel's diverticula, unlike gastric biopsies, is not associated with H. pylori.

Clinicopathological features of Meckel's diverticula in 32 patients, with emphasis on the presence of Helicobacter pylori.

Meckel's diverticula (MD) with areas of gastric heterotopia (metaplasia) are more likely to become symptomatic than those that contain mucosa of purely an intestinal type. Helicobacter pylori has been associated with the pathogenesis of various diseases. The aim of the study was to evaluate whether H. pylori could be identified within metaplastic gastric mucosa in MD. A retrospective evaluation of the histopathological features and the clinical presentation of patients with MD was undertaken. The study group included 32 cases (20 paediatric and 12 adults). The commonest modes of presentation were acute pain (25%), obstruction (19%), bleeding (12.5%) and hernias (9%). On histological examination, heterotopic gastric mucosa was noted to be present in 12 cases. Of these, 3 specimens were noted to have H. pylori organisms present using a specific immunostaining technique. Two patients had concurrent gastric biopsies; one stained positively for H. pylori but the second (1 mm biopsy) was rapid urease-test positive only. In conclusion, the study provides strong evidence that H. pylori may colonise heterotopic gastric mucosa in a minority of MD. H. pylori is apparently not involved in the pathogenesis of most cases of complicated MD. Nonetheless, all 3 patients who had evidence of H. pylori were symptomatic.

[Helicobacter pylori and Meckel's diverticulum]. / Helicobacter pylori et diverticule de meckel.

One quarter of Meckel's diverticula are covered by ectopic gastric mucosa and many may present histological inflammatory changes. Helicobacter pylori grows preferentially on an acid ground but has been found in different parts of the gastrointestinal tract. A prior hypothesis of a pathogenic role for this bacterium in some of Meckel's diverticula with ectopic mucosa is not confirmed by this study covering 21 cases.

Helicobacter pylori in Meckel's diverticulum with heterotopic gastric mucosa in a population with relatively high H. pylori prevalence rate.

BACKGROUND: Helicobacter pylori (H. pylori) colonize only foveolar gastric-type mucosa and are associated with active chronic gastritis and peptic ulcer. The aim of this study was to investigate whether H. pylori can also be found in Meckel's diverticulum which contains heterotopic gastric mucosa. METHODS: Biopsy specimens of Meckel's diverticulum resected in Queen Mary Hospital, University of Hong Kong, during the 10 year period 1986-1995 were retrieved and reviewed. Those containing gastric heterotopia were examined for the presence of H. pylori, using Warthin-Starry silver stain. RESULTS: In the 59 cases of Meckel's diverticula studied, 16 were found to contain heterotopic gastric mucosa. Helicobacter pylori were not identified in any of these cases. In one of the 16 patients a concomitant gastric biopsy was performed. Although the gastric mucosa of this patient was heavily colonized by H. pylori, again no H. pylori was found in the heterotopic gastric mucosa in the Meckel's diverticulum. CONCLUSIONS: The absence of H. pylori in all the Meckel's diverticula examined, even when the stomach was heavily colonized by the organisms, suggests that colonization of Meckel's diverticulum by H. pylori is a rare event. This, together with the overall rarity of H. pylori in all reported series of Meckel's diverticulum, argues against its causative role in complications of Meckel's diverticulum.

[Actinomycosis with abdominal manifestation]. / Abdominális manifesztációjú actinomycosis.

During the last 4 years the authors observed 3 actinomycotic cases with abdominal localization. The disease was found in all the three cases to be localized to those parts of the intestinal tract where stasis of fecal contents may occur, i. e. to the appendix, to Meckel's diverticle and to the left colonic flexure. The relatively rare incidence and preoperative diagnostic difficulties make publication of these cases worthwhile. Based on own experience and literary data they describe natural history, clinical picture, histology and treatment of the disease, respectively.

Helicobacter pylori and Meckel's diverticulum.

Helicobacter pylori is invariably associated with peptic ulceration of the upper gastrointestinal tract. This has led to speculation about its pathogenic role in peptic ulceration. The literature and this present study show that H. pylori is not often associated with peptic ulceration in Meckel's diverticulum and hence it is unlikely that it has any significant role in peptic ulceration at this site.

Does Helicobacter pylori colonize the gastric mucosa of Meckel's diverticulum?

Helicobacter pylori (formerly, Campylobacter pylori) is a highly adapted organism that seems to infect only gastric-type mucosa. In this study, we attempted to determine whether gastric epithelium at a site distant from the stomach, the heterotopic gastric mucosa of Meckel's diverticulum, was susceptible to colonization by H. pylori. Retrospectively, we examined biopsy specimens from 23 patients who had undergone resection of Meckel's diverticulum that contained heterotopic gastric mucosa. As a methodologic control, we also reviewed antral biopsy specimens from 18 patients with chronic duodenal ulcer who had undergone antrectomy. Heterotopic gastric mucosa in Meckel's diverticulum was of antral type in 13 patients and fundic type in 10 patients. Six patients had an ulcer in the diverticulum. No evidence of chronic or active chronic gastritis was detected in the heterotopic gastric mucosa. H. pylori was not found in any Meckel's diverticula but was present in the antrum of 89% of patients with duodenal ulcer. These results suggest that H. pylori may not colonize the heterotopic gastric mucosa of Meckel's diverticulum and has no role in the development of ulceration at this site.

Campylobacter pylori infection in Meckel's diverticula containing gastric mucosa.

A retrospective survey was undertaken of 228 resected Meckel's diverticula to determine if there was any evidence of Campylobacter pylori infection in diverticula containing gastric mucosa. Among the 65 diverticula with gastric mucosa one was heavily infected with organisms having the morphological appearances of C pylori. The specimen had been removed from a six year old Samoan boy who had been admitted with small bowel obstruction. Infection and associated mucosal inflammatory infiltrate were limited to areas of gastric mucosa only. The detection of the organism at this site remote from the gastroduodenal environment suggests the organism may be transmitted by the orofaecal route.

Campylobacter-like organisms and heterotopic gastric mucosa in Meckel's diverticula.

To assess the possibility that Campylobacter pylori might colonise heterotopic gastric mucosa a detailed histological review of 69 cases of Meckel's diverticula resected over 17 years was undertaken. Twenty three were resected incidentally while 46 were excised as the suspected cause of symptoms. Gastric mucosa was found in 13 diverticula (19%), 10 from the symptomatic group and three from the incidental cases, of which eight showed active gastritis affecting the heterotopic mucosa. Specific staining showed spiral bacteria with the typical morphology of C pylori adherent to gastric mucosa in four of the diverticula showing active gastritis. Campylobacter-like organisms were not seen on normal heterotopic gastric mucosa or on adjacent intestinal epithelium. The findings show that Campylobacter-like organisms, identical in appearance, staining, and distribution with C pylori, colonise and possibly inflame heterotopic gastric mucosa in Meckel's diverticulum.