Detection of <i>Helicobacter ganmani</i>‐Like 16S rDNA in Pediatric Liver Tissue

Tolia, Vasundhara; Nilsson, Hans Olof; Boyer, K.; Wuerth, Anne; Al‐Soud, Waleed Abu; Rabah, Raja; Wadström, Torkel

doi:10.1111/j.1083-4389.2004.00266.x

Cited by 35 publications

(22 citation statements)

References 37 publications

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“…Strains from human bile, liver and gallbladder samples have also been identified as H. bilis by 16S rRNA gene sequence comparisons (Fox et al 1998a;Tolia et al 2004). Polyphasic analysis of the phenotypic and genotypic characteristics of what was previously referred to as Flexispira taxa 2, 3 and 8, isolated from humans, sheep and pigs, have shown them also to be members of the species H. bilis (Dewhirst et al 2000a;Hanninen et al 2005).…”

Section: Helicobacter Bilismentioning

confidence: 99%

The Family Helicobacteraceae

et al. 2014

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Section: Helicobacter Bilismentioning

confidence: 99%

The Family Helicobacteraceae

et al. 2014

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“…Especially susceptible are humans with immunodeficiencies such as AIDS (2) and X-agammaglobulinemia (3)(4)(5). These organisms may be associated with diarrhea, bacteremia, and/or visceral disease, including cholecystitis, hepatitis, and possibly hepatic cancer (6), and have been detected in livers of patients with ulcerative colitis and concomitant liver disease, as well as in children with other liver diseases (7,8).…”

Section: Case Reportmentioning

confidence: 99%

Helicobacter canis Bacteremia in a Patient with Fever of Unknown Origin

et al. 2013

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A 57-year-old woman with common variable immune deficiency and liver failure of unknown etiology presented with recurrent fevers over a 5-month period. She was found to have Helicobacter canis bacteremia. Immunocompromised hosts with exposure to cats or dogs may be at risk for infection with this organism, which may be challenging to diagnose. CASE REPORTA 57-year-old woman from Montana was referred to our institution for Infectious Diseases consultation for recurrent fever and chills for 3 months. She had common variable immunodeficiency (for which she received intermittent intravenous immune globulin infusions), and presumed pulmonary sarcoidosis (treated intermittently with prednisone), and had undergone prior splenectomy. She had a 2-year history of elevated alkaline phosphatase. She had developed intermittent fever 3 months prior to consultation and had been previously hospitalized locally for fever and clinical sepsis with negative blood cultures. Laparoscopic liver biopsy had shown mildly active steatohepatitis with periportal fibrosis, and had been procedurally complicated by intra-abdominal hemorrhage. She had been hospitalized for fever on several subsequent occasions and had received multiple courses of empirical antibacterial therapy despite negative blood cultures and no clear definition of an infectious process.Upon presentation for initial Infectious Diseases consultation, fevers were described as low grade and intermittent and were accompanied by chills and sweats. She had taken prednisone (20 mg daily) for the previous 3 months for abdominal pain ascribed to possible gastrointestinal sarcoidosis. She reported a 1-year history of diarrhea and a 2-year 160-pound weight loss. A colonoscopic biopsy 5 months prior had shown findings consistent with common variable immunodeficiency. Stool studies showed no evidence of enteric infection. She had two dogs and three cats. The patient's blood cultures, serologic testing for HIV, blood PCR for cytomegalovirus, and chest X-ray were negative. Serum IgG was 408 mg/dl (767 to 1,590 mg/dl), and IgA was 2 mg/dl (61 to 356 mg/dl). Total bilirubin was 0.4 mg/dl (0.1 to 1 mg/dl), alkaline phosphatase 566 units/liter (46 to 118 units/liter), and alanine transaminase 155 units/liter (7 to 45 units/liter). Computed tomography of the chest, abdomen, and pelvis was notable only for a fluid collection around the liver. Aspiration of this collection was attempted, but no fluid was obtained, and the finding was ascribed to a resolving hematoma. A positron emission tomography scan was unremarkable. She was empirically treated with ciprofloxacin and metronidazole for 5 days. Fever resolved and she was discharged home.She was admitted to a local hospital 2 months later for recurring fevers and worsening cholestasis. Total bilirubin was 21.6 mg/dl (0.1 to 1 mg/dl), alkaline phosphatase 359 units/liter (46 to 118 units/liter), and alanine transaminase 384 units/liter (7 to 45 units/liter). She was subsequently transferred to our hospital, at which time she was afebrile in the a...

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“…in hepatobiliary diseases in animals and humans [1][2][3][4]. Helicobacter DNA, or cross-reacting DNA, has been detected in hepatic tissues from both adults and children with and without liver disease [5][6][7][8][9][10][11][12]. Liver diseases in which Helicobacter sp.…”

Section: Introductionmentioning

confidence: 99%

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

et al. 2008

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Although Helicobacter pylori have been identified in the liver, the role of Helicobacter sp. in human liver diseases remains unclear. This study explored whether H. pylori were internalized and could persist in hepatocytes. The majority of an inoculum of H. pylori (1 × 10 7 colony forming units) adhered to hepatocytes. Using the gentamicin invasion assay we found that approximately 2% were internalized and persisted following passage for more than 2 months. Electron microscopy confirmed the presence of intracellular Helicobacter. The number of adherent or internalized H. pylori was significantly greater with hepatocytes than with gastric epithelial cells (P <0.05) and was also dependent on cag pathogenicity island (PAI), VacA, OipA, or BabA status. Transmission electron microscopy was used to confirm adherence and invasion of H. pylori into hepatocytes. Internalization of H. pylori was inhibited by antibodies to β1-integrin receptors, genistein, and cytochalasin D (P < 0.05) consistent with β1-integrin acting as a surface receptor with additional requirements for tyrosine kinase phosphorylation and actin polymerization. In summary, H. pylori both adhered to and invaded into hepatocytes in vitro, depending on the virulent factors, and persisted within hepatocytes during subcultures. β1-integrin is likely a receptor involved in internalization of H. pylori into hepatocytes.

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Detection of Helicobacter ganmani‐Like 16S rDNA in Pediatric Liver Tissue

Cited by 35 publications

References 37 publications

The Family Helicobacteraceae

The Family Helicobacteraceae

Helicobacter canis Bacteremia in a Patient with Fever of Unknown Origin

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

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