Helicobacter pylori is naturally competent for transformation, but the DNA uptake system of this bacterium is only partially characterized, and nothing is known about the regulation of competence in H. pylori. To identify other components involved in transformation or competence regulation in this species, we screened a mutant library for competence-deficient mutants. This resulted in the identification of a novel, Helicobacterspecific competence gene (comH) whose function is essential for transformation of H. pylori with chromosomal DNA fragments as well as with plasmids. Complementation of comH mutants in trans completely restored competence. Unlike other transformation genes of H. pylori, comH does not belong to a known family of orthologous genes. Moreover, no significant homologs of comH were identified in currently available databases of bacterial genome sequences. The comH gene codes for a protein with an N-terminal leader sequence and is present in both highly competent and less-efficient transforming H. pylori strains. A comH homolog was found in Helicobacter acinonychis but not in Helicobacter felis and Helicobacter mustelae.

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Lymphocytic cholangitis (LC) in cats is a biliary disease of unknown etiology. Helicobacter spp. were recently implicated in human primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC). Because of the similarities between PSC/PBC with LC, we hypothesized that Helicobacter spp. are involved in feline LC. A PCR with Helicobacter genus-specific 16S rRNA primers was performed on DNA isolated from feline bile samples. Four of the 15 (26%) LC samples were positive, whereas only 8/51 (16%) of non-LC samples were PCR positive (p=0.44). Sequence analysis of the amplicons revealed a 100% identity with the Helicobacter pylori specific DNA fragments. Our data suggest an etiological role of H. pylori in feline LC and that cats are a potential zoonotic reservoir.

The causes of hepatitis in dogs are mostly unknown. Known causes of canine hepatitis are infectious (CAV-1), toxic (e.g. aflatoxin), and metabolic (copper accumulation). In order to understand the unknown causes, research in this field is necessary. Despite the marked progress in the knowledge on viral causes for human hepatitis, the involvement of infectious agents in the pathogenesis of hepatitis in the dog is still largely unknown. It is, like in human hepatitis, very likely that more than one causative infectious agent may cause hepatitis in the dog. This review presents the various forms of hepatitis in the dog, the known infectious and non-infectious causes of canine hepatitis, the infectious causes of hepatitis in man and other animals, and finally our recent infection and molecular studies to investigate possible infectious causes of canine hepatitis.

Helicobacter species DNA has been detected in liver tissue of patients affected by primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). To investigate a potential causative relation between Helicobacter species and PBC/PSC, we compared the presence of Helicobacter species-specific DNA in liver tissue of patients with PBC/PSC (n=18/n=13) with those of a control group of patients with various liver diseases with known cause (n=29). A PCR with Helicobacter genus-specific 16S rRNA primers was performed on DNA isolated from paraffin embedded liver tissue. Control patients had hepatitis-B (n=9), alcoholic cirrhosis (n=14), or non-cirrhotic metabolic liver disease (n=6). There was no significant difference between the incidence of Helicobacter spp.-specific DNA in PBC/PSC (9/31; 29%) and the control group (10/29; 34%). Sequence analysis confirmed Helicobacter spp. DNA. Because Helicobacter spp. DNA can be found in approximately one-third of all samples tested, it is unlikely that PSC and PBC are caused by Helicobacter infection.