SCCmec typing of PVL-positive community-acquired Staphylococcus aureus (CA-MRSA) at a Japanese hospital.

The epidemiology of Panton-Valentine leukocidin (PVL)-positive MRSA in community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) was examined. Three hundred and forty-two CA-MRSA strains that were susceptible to imipenem and cefazolin were isolated from 1107 samples (intravenous catheter, blood, sputum, urine, skin, wound, and pharynx) from outpatients at Showa University Hospital in Japan between September 2009 and March 2017. The PVL gene was detected in 46 of 342 CA-MRSA strains, accounting for 13.5%. The type of SCCmec was determined by detection of each SCCmec-specific region, class complex, and ccr. SCCmec type IV comprised 33 strains, type V comprised 5 strains, type VII comprised 4 strains, and the unclassified type comprised 4 strains. Among the type IV strains, subtype IVa was dominant, comprising 23 of 33 strains, and the remaining 10 strains were of varying subtypes. The SCCmec type III-specific region, CZ049, was amplified in 2 type V strains, 4 type VII strains, and 4 unclassified strains. In 4 unclassified strains, CZ049 and ccr5 were detected, but neither the SCCmec-specific region nor class complex was detected. The PVL-positive rate was lower than that in Western countries. The SCCmec types of PVL-positive CA-MRSA strains were found to vary, indicating a diverse spreading route.

Detection of metallo-ß-lactamase genes in clinically isolated Klebsiella pneumoniae and Klebsiella oxytoca.

We detected and characterized metallo-ß-lactamase genes (blaIMP-1 and blaIMP-11) in third generation cephalosporin-resistant Klebsiella pneumoniae and Klebsiella oxytoca isolated at Showa University Hospital between January 1, 2011 and December 31, 2012. The cephalosporin-resistant K pneumoniae strains were frequently isolated from the urine, while one strain of K. pneumoniae, which was resistant to carbapenem, was isolated from the stool. We analyzed the phenotypes and genotypes of the metallo-ß-lactamase genes from the 16 strains of cephalosporin-resistant-K pneumoniae and 6 strains of -K. oxytoca isolated from the same ward. The minimum inhibitory concentrations of imipenem were below 4 µg/ml in 21 out of the 22 isolated strains. The double disc synergy test using ceftazidime and sodium mercaptoacetic acid revealed enlargements in the inhibitory zones of 14 of the 16 strains of K. pneumoniae and all 6 strains of K. oxytoca. Metallo-ß-lactamase genes were detected in all of the tested strains, with blaIMP-1 in 3 K. pneumoniae and 1 K. oxytoca, blaIMP-11 in 13 K pneumoniae and 4 K. oxytoca, and both blaIMP-1 and blaIMP-11 in one K. oxytoca. Our results indicate that third generation cephalosporin-resistant and imipenem-susceptible K. pneumoniae and K. oxytoca possess the metallo-ß-lactamase gene. The active surveillance of metallo-ß-lactamase genes should be performed in clinical laboratories. (Original).

[Analysis of the relevance of the mutations of the precore and basic core promoter in HBV genome with the DNA amount of HBV viremia].

In the course of hepatitis B, serum concentrations of the virus usually fall following sero-conversion, characterized by the loss of HBe antigen and appearance of detectable anti-HBe. However, hepatitis B viremia may persist even after sero-conversion. We assessed the association of continuous viremia with the precore (PC) (G1896A) mutation, basic core promoter (BCP) (A1762T, G1764A) mutations, the viral genotype and the quantity of viral DNA. Neither PC nor BCP mutations were detected in the viral DNA isolated from cases in which HBV became negative during the course of infection. The virus quantity increased after sero-conversion in all of the cases of persistent viremia with HBV genotype C harboring BCP mutations, indicating that the BCP mutation in genotype C is a determinant of continuous viremia. This feature was not evident in infections with HBV genotype B. Although the PC mutation was detected in the viral DNA from both genotypes B and C in continuous viremia, the mutation was not relevant to the quantity of virus. Our data suggest that HBV genotype C has a predisposition to acquire BCP mutations and these mutations activate virus replication after sero-conversion. This mechanism may be a cause of the poor prognosis of hepatitis with HBV genotype C. In conclusion, analyses of HBV genotype and BCP mutations are imperative to determine the prognosis of hepatitis B.