Ryuichi Nakano

Bacteremia secondary to Alloscardovia omnicolens urinary tract infection.

A 70-year-old woman was admitted to our hospital with malaise, bilateral leg edema, and oliguria. She had a history of advanced uterine cancer. Bilateral double-J catheters were inserted because growth of intra-abdominal metastases led to bilateral ureteral stricture and hydronephrosis. Two days later, she suddenly developed high fever. Thin gram-positive bacilli of moderate length were detected in the anaerobic blood culture bottles. We performed 16S ribosomal RNA analysis of the isolate and it showed 100% match with Alloscardovia omnicolens DSM 21503(T). She was successfully treated with cefmetazole in addition to percutaneous nephrostomy.

A first case of isolation of Kerstersia gyiorum from urinary tract

An 82-year-old man with percutaneous nephrostomy presented to our Hospital with dysuria for one day. The patients percutaneous nephrostomy tube was exchanged, with about 20xa0mL of creamy purulent urine being collected. Direct smear of the urine specimen showed polymorphonuclear leukocytes and small Gram-negative bacilli, some of which had undergone phagocytosis. This organism was identified as Kerstersia gyiorum using 16S ribosomal RNA gene analysis. He was successfully recovered with exchange of his percutaneous nephrostomy tube and fluoroquinolone internal use treatment. This is the first case report of urinary tract infection due to K.xa0gyiorum.

Suitability of Carbapenem Inactivation Method (CIM) for Detection of IMP Metallo-β-Lactamase-Producing Enterobacteriaceae

Carbapenem-resistant Enterobacteriaceae (CRE) strains have become globally distributed in the past decade, resulting in concern over the control of hospital infections and antimicrobial therapies ([1][1], [2][2]). The majority of CRE isolates are carbapenemase-producing Enterobacteriaceae (CPE)

Comparison of the antiviral effect of solid-state copper and silver compounds.

n Abstractn n Antiviral activities of insoluble solid-state and soluble ionic copper and silver compounds were evaluated against influenza A virus (A/PR8/H1N1) possessing a viral envelope and bacteriophage Qβ lacking an envelope. The viral solutions were exposed on glass samples uniformly loaded with copper and silver compounds. Exposure to solid-state cuprous oxide (Cu2O) efficiently inactivated both influenza A virus and bacteriophage Qβ, whereas solid-state cupric oxide (CuO) and silver sulfide (Ag2S) showed little antiviral activity. Copper ions from copper chloride (CuCl2) had little effect on the activity of bacteriophage Qβ in spite of the fact that copper ions strongly inactivate influenza A in previous studies. Silver ions from silver nitrate (AgNO3) and silver(I) oxide (Ag2O) in solution showed strong inactivation of influenza A and weak inactivation of bacteriophage Qβ. We also investigated the influence of the compounds on the function of two influenza viral proteins, hemagglutinin and neuraminidase. Silver ions from AgNO3 and Ag2O remarkably decreased enzymatic activity of neuraminidase through the breakage of disulfide (SS) bonds, corresponding to the selective inactivation of influenza A virus. By contrast, exposure to Cu2O markedly reduced the activity of hemagglutinin rather than neuraminidase. These findings suggest that solid-state Cu2O disrupts host cell recognition by denaturing protein structures on viral surfaces, leading to the inactivation of viruses regardless of the presence of a viral envelope.n n

The TNF-α of mast cells induces pro-inflammatory responses during infection with Acinetobacter baumannii

Mast cells serve important roles as sentinels against bacterial infection by secreting mediators stored in granules. Much of their effectiveness depends upon recruiting and/or modulating other immune cells. The location of mast cells implies that they recognize pathogens invading tissues or mucosal tissues. Acinetobacter baumannii is a gram-negative bacterium that is considered an emerging nosocomial pathogen and causes a wide range of infections associated with high morbidity and mortality. To date, the interaction of A. baumannii with mast cells remains unclear. In this study, we demonstrated an interaction between human LAD2 mast cells and A. baumannii in vitro. When LAD2 cells were co-cultured with live A. baumannii or Pseudomonas aeruginosa PAO1 in vitro for 4h, TNF-α and IL-8 were produced in the culture supernatant. These inflammatory cytokines were not detected in the supernatant after the cells were treated with live bacteria without serum. Gene expression analysis showed that TNF-α and IL-8 mRNA expression increased in A. baumannii- and P. aeruginosa-infected LAD2 cells. Scanning electron microscopy showed that A. baumannii was tightly attached to the surface of LAD2 cells and suggested that A. baumannii may bind to FcγRII (CD32) on LAD2 cells. TNF-α in the culture supernatant from A. baumannii-infected LAD2 cells, showed that PMN activation and migration increased in Boyden chamber assays. These results suggest that mast cells recognize and initiate immune responses toward A. baumannii by releasing the preformed mediator TNF-α to activate effector neutrophils.

Polymicrobial Anaerobic Bacteremia Caused by Butyricimonas virosa and Brachyspira pilosicoli in a Patient with Peritonitis following Intestinal Perforation

Yoshihiko Ogawa, M.D., Masatoshi Sato, M.D., Takaya Yamashita, Ryuichi Nakano, Ph.D, Satoshi Mochizuki, M.D., Kei Kasahara, M.D., Hisakazu Yano, M.D., and Keiichi Mikasa, M.D. Center for Infectious Diseases and Department of Microbiology and Infectious Diseases, Nara Medical University, Nara, Japan; Department of Infectious Diseases, Department of Clinical Laboratory and Department of Surgery, Nara City Hospital, Nara, Japan

Persimmon-derived tannin has bacteriostatic and anti-inflammatory activity in a murine model of Mycobacterium avium complex (MAC) disease.

Nontuberculous mycobacteria (NTM), including Mycobacterium avium complex (MAC), cause opportunistic chronic pulmonary infections. Notably, MAC susceptibility is regulated by various factors, including the host immune system. Persimmon (Ebenaceae Diospyros kaki Thunb.) tannin is a condensed tannin composed of a polymer of catechin groups. It is well known that condensed tannins have high antioxidant activity and bacteriostatic properties. However, it is hypothesized that condensed tannins might need to be digested and/or fermented into smaller molecules in vivo prior to being absorbed into the body to perform beneficial functions. In this study, we evaluated the effects of soluble persimmon-derived tannins on opportunistic MAC disease. Soluble tannins were hydrolyzed and evaluated by the oxygen radical absorbance capacity (ORAC) method. The ORAC value of soluble tannin hydrolysate was approximately five times greater than that of soluble tannin powder. In addition, soluble tannin hydrolysate exhibited high bacteriostatic activity against MAC in vitro. Furthermore, in an in vivo study, MAC infected mice fed a soluble tannin-containing diet showed significantly higher anti-bacterial activity against MAC and less pulmonary granuloma formation compared with those fed a control diet. Tumor necrosis factor α and inducible nitric oxide synthase levels were significantly lower in lungs of the soluble tannin diet group compared with the control diet group. Moreover, proinflammatory cytokines induced by MAC stimulation of bone marrow-derived macrophages were significantly decreased by addition of soluble tannin hydrolysate. These data suggest that soluble tannin from persimmons might attenuate the pathogenesis of pulmonary NTM infection.

Molecular diagnosis and characterization of a culture-negative mycotic aneurysm due to ST54 Haemophilus influenzae type b with PBP 3 alterations

Mycotic aneurysm is a rare but life-threatening disease that warrants an integrated therapeutic approach involving surgical intervention and prolonged antibiotic use. However, the causative organisms are often unidentified because antibiotics started empirically render blood and tissue cultures negative. Molecular diagnosis has been reported to be useful in such culture-negative cases. We report a case of a culture-negative mycotic aortic aneurysm due to Haemophilus influenzae, diagnosed by direct 16S rRNA polymerase chain reaction (PCR) and sequencing of the resected aneurysm tissue. PCR for serotype revealed type b, and PCR and sequencing of the ftsI gene revealed alterations in penicillin-binding protein 3, suggesting resistance to ampicillin. Multilocus sequence typing demonstrated that the isolate belonged to sequence type 54.

Emergence of VIM-2-producing Citrobacter freundii in Japan

Carbapenemase-producing Enterobacteriaceae show multi-antibiotic resistance; thus, infections with these bacteria are difficult to treat, representing a growing problem worldwide. Carbapenemase is often encoded by a plasmid that spreads via conjugal transfer. In the present journal, a recent report from Zhejiang Province, China payed attention to the increasing emergence of carbapenem resistance in gram-negative bacteria [1]. In 70.4% (59/71) isolates of carbapenem-resistant Enterobacteriaceae, two carbapenemase-encoding genes were detected, namely blaKPC-2 and blaIMP-4/blaIMP-8. Among class B metallo-b-lactamases, blaVIM were detected in Pseudomonas aeruginosa but occurred in none of not 71 isolates of carbapenem-resistant strains of Enterobacteriaceae. Aiming to add information to the present increasing emergence of carbapenemase-producing gram-negatives, we here report our detection of VIM-2-producing Citrobacter freundii in Japan. A carbapenem-non-susceptible C. freundii strain (NR1374) was isolated from a Japanese hospital in 2016. The MICs were determined by agar dilution method according to Clinical and Laboratory Standards Institute (CLSI) guidelines. The isolate was resistant to all broadspectrum cephalosporins except for cefepime (Table 1). The result of the carbapenem inactivation method [2,3] was negative, whereas that of the modified carbapenem inactivation method [4] was positive. This characteristic suggests that strain NR1374 produces carbapenemase. The presence of b-lactamase genes was determined by PCR and DNA sequencing [5,6], which revealed that NR1374 carried the blaVIM-2 gene. This is the first detection of blaVIM-2 from Enterobacteriaceae in Japan. In addition, blaVIM-2 was encoded on a plasmid co-encoding the known resistance genes fosE, aacA31 and sul as gene cassettes on a class I integron structure (Genebank accession no. LC367232). This structure was also detected for a resistant plasmid in P. aeruginosa in Japan [7]; therefore, this plasmid is suspected to have been transferred from P. aeruginosa to C. freundii. To confirm the transferability of blaVIM-2, mating experiments were carried out using the sodium azideresistant Escherichia coli strain J53. Plasmid incompatibility groups were identified by the PCR-based replicon typing method [8]. The plasmid belonged to the IncW group and the transfer frequency was 1.3 10 . Although the plasmid DNA was not transferred in the mating experiment, it could be electroporated into P. aeruginosa PAO1. The transformants showed higher MIC values for all b-lactams except for cefepime, which was conferred by carrying blaVIM-2 encoded on the IncW plasmid (Table 1). The IncW plasmid has high affinity for various bacterial species, and thereby has great potential for broad spread [9]. NR1374 was determined to belong

Role of AmpR in the High Expression of the Plasmid-Encoded AmpC β-Lactamase CFE-1

CFE-1 is a unique plasmid-encoded AmpC β-lactamase with the regulator gene ampR. It imparts high resistance to most cephalosporins with constitutive high-level β-lactamase activity. ABSTRACT CFE-1 is a unique plasmid-encoded AmpC β-lactamase with the regulator gene ampR. It imparts high resistance to most cephalosporins with constitutive high-level β-lactamase activity. Here, the β-lactamase activities and expression levels of ampC with or without ampR were investigated. Results suggested that the resistance of CFE-1 to cephalosporins is caused by a substitution in AmpR, in which the Asp at position 135 is modified to Ala to allow the constitutive high-level expression (derepression) of ampC.