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  • Author: Olga V. Peryanova x
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Methicillin-resistant Staphylococcus aureus (MRSA) is a major multidrug-resistant nosocomial pathogen. This class of MRSA, first reported in the early 1960s and now termed healthcare-associated MRSA (HA-MRSA), was followed by a newer class of MRSA, community-associated MRSA (CA-MRSA). The unique feature of the initial CAMRSA included Panton-Valentine leukocidin (PVL), an abscess-associated toxin and also S. aureus spread factor. CA-MRSA usually causes skin and soft-tissue infections, but occasionally causes invasive infections, including (necrotizing) pneumonia, sometimes preceded by respiratory virus infections. The most successful CA-MRSA USA300 (ST8/SCCmecIVa) caused an epidemic in the United States. In Russia, we first detected PVL-positive CAMRSA (ST30/SCCmecIVc) in Vladivostok in 2006, but with no more PVL-positive MRSA isolation. However, we recently isolated four lineages of PVL-positive MRSA in Krasnoyarsk. Regarding chemotherapy against invasive MRSA infections, vancomycin still remains a gold standard, in addition to some other anti-MRSA agents such as teicoplanin, linezolid, and daptomycin. For resistance, vancomycin-resistant MRSA (VRSA) with MICs of ≥16 μg/mL appeared in patients, but cases are still limited. However, clinically, infections from strains with MICs of ≥1.5 μg/mL, even albeit with susceptible MICs (≤2 μg/mL), respond poorly to vancomycin. Some of those bacteria have been bacteriologically characterized as vancomycin-intermediate S. aureus (VISA) and heterogeneous VISA (hVISA), generally with HA-MRSA genetic backgrounds. The features of the above PVL-positive Krasnoyarsk MRSA include reduced susceptibility to vancomycin, which meets the criteria of hVISA. In this review, we discuss a possible new trend of PVL-positive hVISA, which may spread and threaten human health in community settings.


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”.