Methicillin-resistant Staphylococcus aureus (MRSA) is one of the most common nosocomial pathogens. In April 1997, there were five MRSA-infected patients among 16 patients in the Neonatal Intensive Care Unit (NICU), Seoul National University Hospital, which is a tertiary-care hospital with 1,500 beds. The infections had spread from twin patients with MRSA who had transferred from Hospital C. MRSA was isolated from the axilla of 15 (94%) of the 16 patients, including the two patients with obvious infections. Three (19%) of 16 doctors and nine (30%) of 30 nurses had MRSA colonization of the anterior nares. Six different PFGE patterns (A through F) were identified in the 53 isolates of MRSA tested. Twelve of 13 isolates from infected sites of five patients showed pattern F. Three MRSA strains obtained from hospital C showed closely or possibly related pattern F. MRSA of type F was isolated from three of 16 patients' axilla, and one of 3 doctors' and three of 30 nurses' nasal swabs. The antibiogram code for 12 of 13 MRSA isolates from five infected patients was 66,754. PFGE patterns of these isolates were either F, F1, F2 or Fa. Only one of three strains isolated from clinical specimens of patients in Hospital C showed the antibiogram code 66754, although they were all PFGE types F1 and Fa. In conclusion, the presumptive sources of the outbreak of MRSA infection in NICU were the twin patients transferred from hospital C. Antibiogram correlated reasonably well to the PFGE type. An effective notification system is needed when a MRSA-infected patient is transferred to another hospital to control the spread of the infection.
Bacterial Typing Techniques* ; Electrophoresis, Gel, Pulsed-Field* ; Human ; Methicillin Resistance/physiology* ; Microbial Sensitivity Tests* ; Staphylococcus aureus/physiology* ; Staphylococcus aureus/classification*

Methicillin-resistant Staphylococcus aureus (MRSA) produces specific penicillin-binding protein, PBP2', which shows remarkably low affinities to most beta-lactam antibiotics except those such as penicillin G and ampicillin. The region surrounding mecA has been called additional DNA or mec and is thought to be of extraspecies origin. From the study of mec, we found that mec is a novel mobile genetic element and designated as staphylococcal cassette chromosome mec (SCCmec). There are three types of SCCmec. In the past decades, MRSA has become resistant to many antibiotics, such as carbapenems, new quinolones, and minocycline etc. It seems to be a characteristic of MRSA to acquire multi-resistance by accumulating multiple resistance genes around the mecA gene inside SCCmec.
Drug Resistance, Microbial/physiology* ; Drug Resistance, Multiple/physiology* ; Methicillin Resistance/physiology* ; Staphylococcus aureus/physiology*

Antibiotic resistance has evolved over the past 50 years from a merely microbiological curiosity to a serious medical problem in hospitals all over the world. Resistance has been reported in almost all species of gram-positive and -negative bacteria to various classes of antibiotics including recently developed ones. Bacteria acquire resistance by reducing permeability and intracellular accumulation, by alteration of targets of antibiotic action, and by enzymatic modification of antibiotics. Inappropriate use of an antibiotic selects resistant strains much more frequently. Once resistant bacteria has emerged, the resistance can be transferred to other bacteria by various mechanisms, resulting in multiresistant strains. MRSA is one of the typical multiresistant nosocomial pathogens. A study of the PFGE pattern of endonuclease-digested chromosomal DNA showed that MRSA of a few clones were disseminated among newborns in the NICU of a Japanese hospital. In this regard, it is important to choose appropriate antibiotics and then after some time, to change to other classes to reduce the selection of resistant strains. Since the development of epoch-making new antibiotics is not expected in the near future, it has become very important to use existing antibiotics prudently based on mechanisms of antibiotic action and bacterial resistance. Control of nosocomial infection is also very important to reduce further spread of resistant bacteria.
Cross Infection/physiopathology ; Drug Resistance, Microbial/physiology* ; Enzymes/physiology ; Methicillin Resistance/physiology ; Staphylococcus aureus/physiology

Similar to multicellular animals, single-cell organisms, such as bacteria show the phenomenon of programmed cell death (PCD). The PCD not only can play an important role in various physiological procedures, but also can eliminate bacteria with irreversible injuries. The PCD of single cell in a colony is for the benefits of other bacteria in the same colony to achieve the development and reproduction of the whole colony. Disturbing or destroying such PCD may provide a new way for antibiotic drug research and development.
Autophagy ; physiology ; Bacteria ; cytology ; Staphylococcus aureus ; cytology ; physiology ; Streptococcus pneumoniae ; cytology ; physiology

BACKGROUNDDiversity of orthopedic infections with various local environments affects the pattern and prevalence of pathogens. It is not well-characterized whether different pathogens have different propensity to cause different types of orthopedic infections. We aimed to investigate the frequency of different pathogens derived from orthopedic infections, and determine the relationship between the prevalence of clinical isolates and the type of orthopedic implants, especially focusing on staphylococci.

METHODSFrom January 2006 to December 2011, orthopedic infections were identified retrospectively from clinical microbiology laboratory and orthopedic medical records. The sources of orthopedic infections were divided into two main groups: those associated with implants and those not associated with implants. Implants-associated infections were further subdivided into five subgroups: arthroplasty, internal fixation, external fixation, internal and external fixation, and others. We analyzed microbiological spectrum in different groups and subgroups. Antibiotic susceptibility of staphylococci was analyzed.

RESULTSOnly coagulase-negative staphylococci (CoNS) was significantly more likely to be associated with implants-associated infections (P = 0.029). The overall pathogens prevalence of arthroplasty was significantly different from other subgroups (P < 0.05). 65% isolates from external fixation was Gram-negative bacteria. Some percentage (55%) of S. aureus and (83%) CoNS were resistant to methicillin. No resistance to glycopeptide was seen in all of staphylococci.

CONCLUSIONSStaphylococcus aureus was the most frequent isolates in orthopedic infections but was not associated with the presence or absence of implants. Only CoNS was implants-associated, especially for arthroplasty infection. Cefazolin alone is not enough for orthopedic surgery prophylaxis in settings with a high prevalence of methicillin-resistant staphylococci.

Humans ; Orthopedic Procedures ; adverse effects ; Prostheses and Implants ; microbiology ; Retrospective Studies ; Staphylococcus aureus ; pathogenicity ; physiology

Treatment of bovine mastitis caused by Staphylococcus (S.) aureus is becoming very difficult due to the emergence of multidrug-resistant strains. Hence, the search for novel therapeutic alternatives has become of great importance. Consequently, bacteriophages and their endolysins have been identified as potential therapeutic alternatives to antibiotic therapy against S. aureus. In the present study, the gene encoding lysin (LysSA4) in S. aureus phage SA4 was cloned and the nucleotide sequence was determined. Sequence analysis of the recombinant clone revealed a single 802-bp open reading frame encoding a partial protein with a calculated mass of 30 kDa. Results of this analysis also indicated that the LysSA4 sequence shared a high homology with endolysin of the GH15 phage and other reported phages. The LysSA4 gene of the SA4 phage was subsequently expressed in Escherichia coli. Recombinant LysSA4 induced the lysis of host bacteria in a spot inoculation test, indicating that the protein was expressed and functionally active. Furthermore, recombinant lysin was found to have lytic activity, albeit a low level, against mastitogenic Staphylococcus isolates of bovine origin. Data from the current study can be used to develop therapeutic tools for treating diseases caused by drug-resistant S. aureus strains.
Animals ; Base Sequence ; Cloning, Molecular ; Gene Expression Regulation, Viral/physiology ; Mucoproteins/genetics/*metabolism ; Phylogeny ; Polymerase Chain Reaction/methods ; Recombinant Proteins ; Staphylococcus Phages/genetics/*metabolism/physiology ; Staphylococcus aureus/*virology

OBJECTIVETo evaluate the efficacy of teacher tablets in the treatment of pharyngitis.

METHODOne hundred and thirty six patients with acute pharyngitis or chronic pharyngitis in attack were randamly divided into two groups: treated group (n=68), the patients were given teacher tablets for 7 days, control group (n=68), the patients were given Qinlian capsule for 7 days. Before and after the experimental medicine-taking test, general condition, clinical symptoms and features of examinations on laryngo-pharynx, throat swab bacterial culture were measured.

RESULTAfter 7 day medicine-taking experiment, teacher tablets can improve clinical symptoms (at an efficacy rate of more than 60%) and features (at an efficacy rate of more than 80%) of laryngopharynx, in treated group, the inhibition ratios of alpha streptococcus, neisseria and staphylococcus aureus are more than 50%. There are no significant difference between treated group and control groups in those detected index.

CONCLUSIONTeacher tablets is effective for pharyagitis.

Adolescent ; Adult ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Hypopharynx ; pathology ; Male ; Middle Aged ; Neisseria ; physiology ; Pharyngitis ; drug therapy ; microbiology ; pathology ; Staphylococcus aureus ; physiology ; Streptococcus ; physiology ; Young Adult

OBJECTIVETo explore the mechanisms involved in Staphylococcus aureus (S. aureus) invading human monocytic U937 cells.

METHODSS. aureus were added to U937 cells at multiplicity of infections (MOI) of 20:1 for 0, 15, 30, 60, and 90 minutes, respectively. Cell apoptosis was analyzed with Hoechst 33258 staining and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry analysis. Akt and nuclear factor-kappaB (NF-kappaB) activities were detected by Western blotting.

RESULTSInfection of U937 cells with S. aureus induced rapid cell death in a time-dependent manner, and the cells displayed characteristic features of apoptosis. S. aureus-induced apoptosis was associated with a prominent downregulation of activated (phosphorylated) Akt and NF-kappaB. The inhibition of phosphorylated Akt by LY294002 led to the inhibition of NF-kappaB in a dose-dependent manner. Inhibition of Akt with LY294002 caused further increase in apoptosis of U937 cells.

CONCLUSIONSS. aureus can stimulate the apoptosis of U937 cells. S. aureus induces apoptosis of U937 cells by inhibiting Akt-regulated NF-kappaB.

Apoptosis ; Chromones ; pharmacology ; Humans ; Morpholines ; pharmacology ; NF-kappa B ; physiology ; Phosphatidylinositol 3-Kinases ; physiology ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; antagonists & inhibitors ; physiology ; Staphylococcus aureus ; pathogenicity ; U937 Cells

To assess the ability of the previously selected human vaginal isolates of Lactobacillus crispatus (L. crispatus) T79-3, T90-1 and Lactobacillus jensenii (L. jensenii) T118-3, T231-1 to inhibit the growth of Staphylococcus aureus and block their adhesion to HeLa cells. The inhibitory bioactive substances produced by these Lactobacillus were also identified. Inhibitory substances interaction tests were carried out by using a streak-diffusion method on agar plates. Three types of interaction were performed to determine the inhibitory effect of Lactobacillus on adhesion of Staphylococcus aureus to HeLa cells: Exclusion Group (Lactobacillus and HeLa followed by pathogens), Competition Group (Lactobacillus, HeLa and pathogens together) and Displacement Group (pathogens and HeLa followed by the addition of Lactobacillus). The number of HeLa cells adhered to Staphylococcus aureus was quantified by bacteria colony counts on LB plate. The results showed that lactic acids produced by the Lactobacillus are the main substances that can inhibit Staphylococcus aureus growth and there is variation among the three types of interaction regarding the inhibitory activity against Staphylococcus aureus. The effects of Lactobacillus on blocking the adhesion to HeLa cells were concentration dependent. All four Lactobacillus isolates displayed the ability to inhibit Staphylococcus aureus growth and block Staphylococcus aureus adherence to HeLa cells. Exclusion Group was the most effective, and T79-3 showed greater capacity to block Staphylococcus aureus adherence compared with the other three isolates. The present study suggests the potential ability of L. crispatus T79-3 as probiotic for the treatment and prevention of urogenital infections in women.
Bacterial Adhesion ; physiology ; Cell Wall ; chemistry ; Female ; HeLa Cells ; Humans ; Lactobacillus ; classification ; physiology ; Probiotics ; Staphylococcus aureus ; growth & development ; pathogenicity ; Vagina ; microbiology

Staphylococcus aureus (S. aureus) is an important human pathogen which can cause a chronic condition with a high relapse rate despite the aggressive antimicrobial treatment. Recent studies showed that intracellular pattern recognition receptors (including NOD) in response to bacteria or bacterial products play a proinflammatory role by activating nuclear transcription factor-κB (NF-κB). But how NOD2 mediates the proinflammatory response to S. aureus in mast cells (MCs) is unclear. So, in this study, we attempted to examine the role of NOD2 in inflammatory responses of MCs to S. aureus. P815 cells (a mouse mast cell line) were cultured. Real-time PCR was used to detect the NOD2 mRNA expression in P815 cells during S. aureus infection. The siRNA against NOD2 gene was synthesized and transfected into S. aureus-infected P815 cells. By using the methods of ELISA and flow cytometry, the effects of NOD2 gene silencing on cell phagocytosis, cytokine secretion, NF-κB activation and cell apoptosis of the S. aureus-infected P815 cells were examined. It was found that S. aureus infection could increase the expression of NOD2 mRNA in P815 cells. NOD2 gene interference in P815 cells reduced the number of S. aureus engulfed by P815 cells, the level of cytokines and the activation of NF-κB. In addition, S. aureus could induce the apoptosis of P815 cells, but NOD2 gene silencing did not affect the cell apoptosis rate. Our data suggested that NOD2 plays a key role in pathogen recognition, signal transduction, and NF-κB activation in the inflammatory responses of MCs infected by S. aureus.
Animals ; Cell Line ; Cytokines ; immunology ; Inflammation Mediators ; immunology ; Mast Cells ; immunology ; microbiology ; Mice ; NF-kappa B ; immunology ; Nod2 Signaling Adaptor Protein ; immunology ; Staphylococcus aureus ; physiology