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PubMed2004

Recurrent Staphylococcus aureus chalazia in hyperimmunoglobulinemia E (Job's) syndrome.

PURPOSE: To report a case of recurrent Staphylococcus aureus chalazia in a patient with hyperimmunoglobulinemia E syndrome (Job's Syndrome). DESIGN: Case report. METHODS: Three separate surgical incisions and curettages of multiple, recurrent chalazia of the right upper eyelid were performed over a course of 3 months. Cultures and pathologic specimens were obtained. Postoperative treatment consisted of oral erythromycin and amoxicillin/clavulonate, topical tobramycin/dexamethasone ointment, and warm compresses. RESULTS: Pathology of the tarsus confirmed the diagnosis of multiple chalazia. Cultures of the chalazia contents were positive for Staphylococcus aureus. No further recurrence was observed following the third surgical procedure over a 3-month follow-up period. CONCLUSION: Characteristic Staphylococcus aureus skin infections in immunodeficient patients with hyperimmunoglobulinemia E syndrome can involve the eyelids and may be recurrent despite appropriate medical and surgical therapy.

Adolescent↗
PubMed2003

Evaluation of intraspecies interference due to agr polymorphism in Staphylococcus aureus during infection and colonization.

In Staphylococcus aureus infection, intraspecies cross-inhibition mediated by the regulatory system agr may lead to the exclusion of heterologous strains at the site of infection or colonization. We analyzed consecutive and cocolonizing strains (classified as different clones by pulsed-field gel electrophoresis) from patients with cystic fibrosis (CF) and healthy individuals. Strain replacement was accompanied by a change in the agr group in 80% of the patients with CF and in 63% of the healthy individuals. Cocolonizing strains from patients with CF were shown to belong to interfering agr groups in 6 of 10 cases. In contrast, in healthy individuals, cocolonization of the nares with strains of interfering agr groups was rarely observed. agr polymorphism has no impact on the colonization dynamics of S. aureus in patients with CF but may influence nasal colonization in health individuals.

Bacterial Proteins↗
PubMed1999

Resistance to gentamicin and related aminoglycosides in Staphylococcus aureus isolated in Brazil.

Isolates of Staphylococcus aureus obtained from a Brazilian university hospital were characterized in relation to resistance to gentamicin and related aminoglycosides. Thirty-six isolates were susceptible to methicillin (MSSA) and 14 were resistant (MRSA). All isolates were sensitive to nucleic acid-binding compounds. All MRSA isolates and one MSSA isolate were demonstrated to be resistant to gentamicin and were coincidentally resistant to amikacin, kanamycin, neomycin and tobramycin. Among the gentamicin sensitive MSSA isolates, five isolates were found to be resistant only to kanamycin/neomycin. The resistance to gentamicin (and related aminoglycosides: kanamycin and tobramycin) must be due to AAC(6')-APH(2") activity. As these isolates also showed resistance to neomycin, they must carry an additional genetic element, probably the one responsible for APH(3')III activity, which accounts for the high level of resistance to kanamycin and to amikacin. The resistance to kanamycin/neomycin in the gentamicin sensitive isolates could not be attributed to the AAD(4')(4") activity because of the tobramycin sensitivity, and so could be ascribed to the APH(3')III activity. Curing and transfer experiments, as well as electrophoresis procedures, indicate that gentamicin resistance in Staph. aureus strains here studied has, characteristically, chromosomal localization.

Anti-Bacterial Agents↗
PubMed2005

Evidence of an intracellular reservoir in the nasal mucosa of patients with recurrent Staphylococcus aureus rhinosinusitis.

Severe infections due to Staphylococcus aureus require prolonged therapy for cure, and relapse may occur even years after the first episode. Persistence of S. aureus may be explained, in part, by nasal carriage of S. aureus, which occurs in a large percentage of healthy humans and represents a major source of systemic infection. However, the persistence of internalized S. aureus within mucosal cells has not been evaluated in humans. Here, we provide the first in vivo evidence of intracellular reservoirs of S. aureus in humans, which were assessed in endonasal mucosa specimens from patients suffering from recurrent S. aureus rhinosinusitis due to unique, patient-specific bacterial clonotypes. Heavily infected foci of intracellular bacteria located in nasal epithelium, glandular, and myofibroblastic cells were revealed by inverted confocal laser scan fluorescence and electron microscopic examination of posttherapy intranasal biopsy specimens from symptom-free patients undergoing surgery on the sinuses. Intracellular residence may provide a sanctuary for pathogenic bacteria by protecting them from host defense mechanisms and antibiotic treatment during acute, recurrent S. aureus rhinosinusitis.

Biopsy↗
PubMed1994

Gentamicin-resistant menadione and hemin auxotrophic Staphylococcus aureus persist within cultured endothelial cells.

Staphylococcus aureus menadione and hemin auxotrophs, generated by in vitro gentamicin selection, demonstrated reduced hemolytic activity and enhanced intracellular survival within cultured bovine aortic endothelial cells relative to their hemolytic parent. Supplementation of the auxotrophs with exogenous menadione or hemin resulted in rapid growth, increased hemolytic activity, and reduced intracellular persistence to the level found for the hemolytic clinical parent. Aminoglycoside selection of staphylococcal menadione and hemin auxotrophs and subsequent persistence of these variants in the intracellular milieu may adapt S. aureus for evasion of host defenses and resistance to antimicrobial therapy.

Animals↗
PubMed2005

Antibiotic resistance in Staphylococcus aureus and its relevance in therapy.

Staphylococcus aureus is a major cause of infections. Only approximately 20% of the strains remain sensitive to penicillin. Beta-lactamase stable penicillins such as flucloxacillin form the mainstay of treatment of staphylococcal infection. Meticillin-resistant S. aureus (MRSA) are resistant to all beta-lactam antibiotics. Glycopeptide antibiotics are effective against most MRSA strains but, in the last few years, isolates of MRSA that have reduced susceptibility to glycopeptides (glycopeptide-intermediate S. aureus) have been isolated. Some strains exhibit frank resistance to glycopeptides (vancomycin-resistant S. aureus). Infections due to these strains are difficult to treat. This review summarises the therapeutic options for MRSA, glycopeptide-intermediate S. aureus and vancomycin-resistant S. aureus. Novel therapeutic strategies such as immunotherapy and vaccines are also discussed.

Acetamides↗
PubMed1978

Characterization of small plasmids from Staphylococcus aureus.

Small molecular weight plasmids from Staphylococcus aureus were characterized with respect to size, restriction enzyme cleavage pattern and transforming capacity. The plasmids pS194 and pC194 which encode streptomycin and chloramphenicol resistance respectively contained 3.0 and 2.0 megadaltons of DNA as determined by zonal rate centrifugation and electron-microscopy. Both plasmids transformed S. aureus wigh high efficiency. Plasmid pC194 contained only one cleavage site for endonuclease HindIII and pS194 contained single cleavage sites for HindIII and EcoRI. A natural recombinant between these two plasmids, pSC194, shared the high transforming capacity of the parental plasmids and contained one EcoRI site and two HindIII sites. pSC194 DNA also transformed B. subtilis with high efficiency. The recombinant plasmid pSC194 may be used as an EcoRI vector for construction and propagation of hybrid DNA in S. aureus as shown in the following paper (Löfdahl et al., 1978).

Bacillus subtilis↗
PubMed2003

Polarization of cytokine responses in B- and T-lymphocytes during Staphylococcus aureus infection.

The destructive course of Staphylococcus aureus arthritis is due to certain leukocytes and their products, mainly cytokines. The cellular source of cytokines mediating this inflammatory process has not been previously assessed on a protein level. Using a mouse model of hematogenously induced S. aureus infection the intracellular production of IFN-gamma, IL-4 and IL-10 in splenic B and T cells have been determined. This has enabled us to define distinct Th1 vs Th2 and Be1 vs Be2 populations of lymphocytes participating in S. aureus infection. Spleen cells were obtained before, and at different time intervals during the first week of infection and re-stimulated in vitro with staphylococcal peptidoglycan, formalin killed staphylococci and TSST-1. The different antigens used for re-stimulation gave rise to different cytokine profiles in analysed T cells (identified as CD4+) and B cells (identified as CD19+). TSST-1 acted as the most potent re-stimulator and we found that 40% of the CD4+ cells responded with IFN-gamma production, and unexpectedly almost 20% of the CD19+ cells. As to IL-4 and IL-10 production, the percentage of B cells expressing these cytokines was higher than the percentage T cells and the peak of their appearance appeared later than that of IFN-gamma. This finding indicates that Be1 cells are an important source of IFN-gamma early during the infection and that the production of the Th2 cytokines in B cells downregulates its production of IFN-gamma. In conclusion this study shows that both B and T cells contribute to the cytokine production during S. aureus infection in a complex pattern.

Animals↗
PubMed2005

Mechanism and consequences of invasion of endothelial cells by Staphylococcus aureus.

It has become clear that Staphylococcus aureus is a facultative intracellular microorganism. Adherence and invasion are a prerequisite for endovascular infections caused by S. aureus, such as infective endocarditis. These phenomena may also be involved in the pathogenesis of invasive and metastatic infection upon hematogenous dissemination, such as osteomyelitis and abscess formation. The underlying molecular mechanism has been elucidated in detail, including its likely relevance in vivo. However, the mode of action of recently identified modulators of invasion, such as pls/Pls have not yet been clarified. The potential outcome for host cells and S. aureus following invasion are diverse. Surprisingly, induction of apoptosis in human endothelial cells is more complex than previously thought, since it appears to involve multiple virulence factors. In the light of increasing resistance to antimicrobial therapy, understanding the multifacetted pathogenesis of S. aureus infection in detail is needed for a better prevention and therapy.

Adhesins, Bacterial↗
PubMed1992

Topical antibiotic therapy for the treatment of experimental Staphylococcus aureus keratitis.

A rabbit model of Staphylococcus aureus keratitis was developed to study the chemotherapeutic efficacy of ciprofloxacin, vancomycin, and cefazolin. Intrastromal injection of 100 colony forming units of log phase S. aureus ATCC strain 25923 resulted in rapid growth in the cornea, peaking at 10(7) cfu/cornea by 12 hr post-infection. Slit-lamp examination revealed that infected eyes reached 30% of maximum inflammation by 10 hr and 60% by 22 hr post-infection. Antibiotic therapy (one drop every 15 min for 5 hr) was initiated at 4 hr post-infection (experiment 1) or 10 hr post-infection (experiment 2). Another group was initiated at 10 hr post-infection and treated for 10 hr (experiment 3). In experiment 1, treatment from 4-9 hr post-infection with 0.3% ciprofloxacin drops decreased the cfu per cornea 6.1 logs, compared to placebo-treated controls (P = 0.0001), and rendered 50% of inoculated eyes sterile. Vancomycin (5.0%) and cefazolin (5.0%) each lowered the cfu per cornea 4.6 logs (P = 0.0187) but did not sterilize any eyes. In experiment 2, therapy from 10-15 hr post-infection with 0.3% ciprofloxacin reduced the cfu per cornea 0.9 logs (P = 0.0001). Vancomycin (5.0%) and cefazolin (5.0%) decreased the cfu per cornea 0.2 logs (P = 0.3973) and 0.3 logs (P = 0.1307), respectively. In experiment 3, therapy from 10-20 hr post-infection with 0.3% ciprofloxacin reduced the cfu per cornea 3.9 logs (P < 0.0001). In this keratitis model, ciprofloxacin was more effective than vancomycin or cefazolin in killing S. aureus.

Animals↗
PubMed2004

Identification of bacteriophage types and their carriage in Staphylococcus aureus.

Conserved genomic sequences distinctive of Staphylococcus aureus phage types 3A, 11, 77, 187 and Twort, representative of phage serogroups A, B, F, L and D, were identified and characterized. PCR primers designed for the above sequences were used for development of a multiplex PCR assay which enabled us not only to classify all phages of the International Typing Set plus 16 additional phages, but also to detect prophages in S. aureus genomes. One to four different prophages were unambiguously detected in experimentally lysogenized S. aureus strains, and substantial variation in prophage content was found in 176 S. aureus clinical strains of different provenance. In addition, by using a comparative genomics approach, all the prophages in the S. aureus genomes sequenced to date could be revealed and classified.

DNA Primers↗
PubMed2006

The importance of the development of antibiotic resistance in Staphylococcus aureus.

Hospital- and community-acquired Staphylococcus aureus infections pose a substantial burden in terms of morbidity, mortality and health care costs. The introduction of new antibiotics to counter this pathogen has frequently been closely followed by the emergence of resistant strains. Most significantly, S. aureus isolates resistant to beta-lactams have become common, and many of these are also resistant to beta-lactamase-resistant penicillins. The rapid spread of methicillin-resistant S. aureus (MRSA) clones across the world often results in hospital outbreaks, but implementation of appropriate control measures usually reduces prevalence to sporadic levels. However, the recent emergence of MRSA infections in the community, affecting patients with no established risk factors for MRSA acquisition, is likely to impact significantly on future strategies for control of nosocomial MRSA. In contrast to other antibiotic classes, S. aureus resistance to glycopeptides did not emerge until nearly 40 years after their clinical introduction, and as a result this drug class has remained the mainstay of treatment for MRSA infections. However, a number of vancomycin-intermediate S. aureus isolates have emerged worldwide and four fully resistant S. aureus isolates have been reported in the USA. This raises the concern that the current first-line treatment for MRSA infection may become ineffective in an increasing proportion of cases in the near future. New classes of antibiotic are urgently needed to treat infections with this growing population of multidrug-resistant S. aureus, and the recently introduced oxazolidinone linezolid and the cyclic lipopeptide daptomycin are welcome additions to the ever-narrowing range of therapies effective against this pathogen.

Aminoglycosides↗
PubMed1995

[Carrier status of Staphylococcus aureus among students of different courses].

Staphylococcus aureus is a frequent pathogen of nosocomial infections. The main part in the spread of these microorganisms take symptomless carriers. The aim the research was defining the carrierstate of S. aureus among students of Medical Academy and University. The investigation showed a greater carrierstate in the group of Medical students (33%) than in the group of University students. Strains isolated from the Medical students were more differentiated in biochemical tests and they were more drug-resistant mainly to Augmentin (51.5% resistant strains) and doxycycline (24% resistant strains). A great percentage of ampicillin-resistant strains (94%) was found among the strains isolated from both groups. Results of the research showed greater carrierstate among people who had direct contact with patients and infectious materials and proved a wide range of drug-resistance among hospital strains. Carriers of S. aureus among medical personnel could influence the spreading of nosocomial infections mainly on ICU and Newborn Wards.

Drug Resistance, Microbial↗
PubMed2003

Specificity of the action of lysoamidase on Staphylococcus aureus 209P cell walls.

Specificity of Staphylococcus aureus 209P cell wall hydrolysis by the L1 and L2-bacteriolytic enzymes from lysoamidase lytic complex was studied. L1-peptidase was shown to display both glycyl-glycine endopeptidase and N-acetylmuramyl-L-alanine amidase enzymatic activities on the S. aureus peptidoglycan molecule, whereas L2-peptidase acts as N-acetylmuramyl-L-alanine amidase.

Amino Acid Sequence↗
PubMed1996

Clusterin, a putative complement regulator, binds to the cell surface of Staphylococcus aureus clinical isolates.

The ability of Staphylococcus aureus Cowan I strain and a number of S. aureus clinical isolates to bind to the human blood glycoprotein clusterin was investigated. Binding of clusterin to these strains was tested by both enzyme-linked immunosorbent assay and flow cytometry. All of the S. aureus strains examined appeared to bind clusterin to some extent, while nonpathogenic control strains Bacillus subtilis BR151 and Escherichia coli JM109 did not. Three S. aureus isolates were selected for more detailed study; binding of labeled clusterin was saturable, inhibited in the presence of excess unlabeled clusterin, and prevented by pretreatment of bacteria with proteases. From the saturation binding studies, estimates of the affinity constants for the binding of clusterin to the bacteria ranged from 31 to 57 nM. Addition of clusterin to S. aureus cultures was also found to result in aggregation of the bacterial cells; aggregation was not detected when clusterin was added to B. subtilis BR151 or E. coli JM109 cultures. These results suggest that at least some S. aureus strains possess specific proteinaceous receptors for clusterin. Such receptors may be an important new bacterial virulence determinant for S. aureus, as clusterin has been proposed to have a role in the regulation of complement activity.

Clusterin↗
PubMed1992

Carotenoid pigment levels in Staphylococcus aureus and sensitivity to oleic acid.

Staphylococcus aureus mutants lacking pigment, or expressing only low levels of pigment, were more sensitive to oleic acid than were the parent strain and mutants making more pigment than the parent. One class of mutants (colour index 5), although possessing significant levels of pigment, were nevertheless quite sensitive to oleic acid. This suggested that only certain carotenoids in the biosynthetic pathway were capable of imparting resistance to fatty acids. The phenotypic expression of pigment also affected the sensitivity of a strain to oleic acid. The parent S. aureus strain 18Z, when grown to express its maximal pigment potential, was more resistant to oleic acid than when it was grown to express minimal levels of pigment.

Carotenoids↗
PubMed1999

Development and characterization of a Staphylococcus aureus nasal colonization model in mice.

Staphylococcus aureus nasal carriage is a risk factor for infection in humans, particularly in the hospital environment. Attenuation of carriage has proven effective in reducing the prevalence of infection in some high-risk groups. To study staphylococcal factors that influence nasal colonization, a mouse model of S. aureus nasal colonization was developed. Mice were inoculated intranasally with S. aureus Reynolds, and nasal carriage was evaluated by quantitating cultures of the nasal tissues from mice sacrificed at various time points after inoculation. The majority of mice inoculated with 10(8) CFU of S. aureus maintained nasal carriage for at least 20 days. Nasal colonization rates were similar for inbred (BALB/c and C57BL/6) and outbred (ICR) mice. Colonization was not affected by mouse passage of strain Reynolds. Lower inoculum doses (<10(7) CFU) resulted in reduced colonization after 7 days. However, mice given streptomycin in their drinking water developed long-term carriage of S. aureus, and they were colonized with inocula as low as 10(5) CFU. Nasal colonization was also established with two other S. aureus strains (one strain each of human and murine origins). S. aureus recovered from the nares of experimentally colonized mice expressed high levels of capsule, and the ability of a capsule-defective mutant to persist in the nares was reduced in comparison to that of the parent strain. This nasal colonization model should prove useful for studies of factors that mediate S. aureus colonization and for assessment of targets for antimicrobial intervention or vaccine development.

Animals↗
PubMed2004

Bacterial evasion of innate host defenses--the Staphylococcus aureus lesson.

Bacterial pathogens such as Staphylococcus aureus use highly efficient mechanisms to evade recognition and elimination by the innate immune system. S. aureus produces sophisticated anti-inflammatory molecules and it employs several mechanisms protecting the bacteria against host cationic antimicrobial molecules such as defensin-like peptides and bacteriolytic enzymes such as lysozyme. Cell wall teichoic acids and lipoteichoic acids, complex Gram-positive surface polymers, and modified membrane lipids such as lysylphosphatidylglycerol are crucial in defensin resistance and other important aspects of staphylococcal virulence such as nasal colonization and biofilm formation on biomaterials. Certain S. aureus genes conferring escape from innate host defenses are conserved in many human pathogens suggesting that the underlying mechanisms are of general significance in bacterial virulence.

Biofilms↗