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  • Author: L.J. Teng x
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Methicillin-resistant Staphylococcus aureus (MRSA) is a major multidrug-resistant bacterial pathogen. The evolution of MRSA is dynamic posing an ongoing threat to humans. The evolution of MRSA includes horizontal gene transfer, which is mediated by mobile genetic elements, plasmids, and bacteriophages, and also mutations. In this review, we clarify the recent trends in MRSA from the perspectives of drug-resistance transfer and uncontrollable infections, particularly those occurring in community settings. We first address the role of MRSA as a disseminator of multidrug resistance. We have studied the cell-to-cell transfer of drug resistance, in which transfer frequencies range from 10-3 to 10-8. The mechanisms of drug-resistance transfers include the self-transmission of large plasmids, the mobilization of small nonconjugative plasmids, the generalized transduction of phages, and the transfer of transposons with circular intermediates. We then discuss uncontrollable infections. Although several anti-MRSA agents have been developed, uncontrollable cases of MRSA infections are still reported. Examples include a case of uncontrollable sepsis arising from a community-associated MRSA (CA-MRSA) with the ST8/SCCmecIVl genotype, and a relapsing severe invasive infection of ST30/SCCmecIVc CA-MRSA in a student athlete. Some of these cases may be attributable to unique adhesins, superantigens, or cytolytic activities. The delayed diagnosis of highly adhesive and toxic infections in community settings may result in CA-MRSA diseases that are difficult to treat. Repeated relapse, persistent bacteremia, and infections of small-colony variants may occur. To treat MRSA infections in community settings, these unique features of MRSA must be considered to ensure that diagnostic delay is avoided.


Helicobacter pylori, one of the most prevalent human pathogens, colonizes the gastric mucosa and is associated with gastric diseases, such as gastritis and peptic ulcers, and is also a bacterial risk factor for gastric cancer. Cytotoxin-associated gene A (CagA) protein, a major virulence factor of H. pylori, is phosphorylated in cells at its Glu-Pro-IIe-Tyr-Ala (EPIYA) motif and is considered to trigger gastric cancer. CagA is classified into two forms, Western CagA with EPIYA-ABC and East Asian CagA with EPIYA-ABD, with the latter associated with a high risk of developing gastric cancer. CagA causes morphological transformation of cells, yielding the “hummingbird” phenotype in AGS cells and possibly membranous pedestals in the gastric epithelium, albeit rarely. H. pylori adherence to the gastric mucosa is not yet fully understood. Here, we describe an intrafamilial infection case of H. pylori, focusing on the gastric epithelium, H. pylori adherence, and a gene mutation in a child with protein-losing gastroenteropathy (characterized by excessive loss of plasma proteins into the gastrointestinal tract). H. pylori, which also infected family members (mother and father), was genetically a single clone with the virulence genes of an East Asian type. The patient’ gastric mucosa exhibited some unique features. Endoscopy revealed the presence of protein plugs on the mucosal surface, which were immunoelectrophoretically similar to serum proteins. Electron microscopy revealed abnormal gastric epithelial cells, totally covered with the secretions or possessing small swollen structures and irregular microvilli. The patient’s H. pylori infection was characterized by frequently occurring thick pedestals, formed along adherent H. pylori. The serum protein level returned to normal and the protein plugs disappeared after the successful eradication of H. pylori, albeit with lag periods for healing. He had a mutation in the OCRL1 gene, associated with Dent disease (asymptomatic proteinuria). Thus, in the patient’s gastric mucosa, we found the abnormal gastric epithelial cells, which may be caused by an OCRL1 mutation or H. pylori, and pedestal-rich H. pylori infection, possibly caused by a higher level of action of CagA in the abnormal epithelial cells. The data suggests a novel H. pylori virulence factor associated with “excessive plasma protein release”.