Staphylococcus aureus nasal carriage as a marker for subsequent staphylococcal infections in intensive care unit patients.

Infectious Disease Service, Hospital de Bellvitge, University of Barcelona, Spain.
European Journal of Clinical Microbiology (Impact Factor: 2.54). 05/1997; 16(5):351-7. DOI: 10.1007/BF01726362
Source: PubMed

ABSTRACT From January to December 1994, 752 consecutive patients admitted to intensive care units (ICU) for more than two days were studied prospectively for Staphylococcus aureus colonization and infection. Nasal swabs were obtained at admission and weekly during the ICU stay. At ICU admission 166 patients (22.1%) were Staphylococcus aureus nasal carriers, while 586 were free of nasal colonization. Of the 166 nasal carriers, 163 harbored methicillin-sensitive Staphylococcus aureus (MSSA) and three methicillin-resistant Staphylococcus aureus (MRSA). During the ICU stay 24 of the 586 noncolonized patients became nasal carriers (11 MSSA and 13 MRSA), and one nasal carrier initially colonized by MSSA was reconlonized by MRSA. Staphylococcal infections were documented in 51 (6.8%) of the total 752 patients. After 14 days of ICU stay, the probability of developing staphylococcal infections was significantly higher for those patients who were nasal carriers at ICU admission than for those found to be initially negative (relative risk 59.6, 95% CI 20.37-184.32; p < 0.0001). In patients with ICU-acquired nasal colonization, most infections were documented prior to or at the time of the detection of the nasal colonization; thus, in this group of patients nasal carriage showed a lower predictive value for subsequent Staphylococcus aureus infections that that described classically. Paired isolates of nasal colonizing and clinical strains were studied by pulsed-field gel electrophoresis (PFGE) and mecA polymorphism analysis in 30 patients; identity was demonstrated in all but two patients. The results suggest that, outside the setting of an outbreak of MRSA, the detection of Staphylococcus aureus nasal carriers on admission may be particularly useful in identifying those patients who are at high risk for developing staphylococcal infections during their ICU stay.

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    ABSTRACT: In apparent contrast to its invasive potential Staphylococcus aureus colonizes the anterior nares of 20-80% of the human population. The relationship between host and microbe appears particularly individualized and colonization status seems somehow predetermined. After decolonization, persistent carriers often become re-colonized with their prior S. aureus strain, whereas non-carriers resist experimental colonization. Efforts to identify factors facilitating colonization have thus far largely focused on the microorganism rather than on the human host. The host responds to S. aureus nasal colonization via local expression of anti-microbial peptides, lipids, and cytokines. Interplay with the co-existing microbiota also influences colonization and immune regulation. Transient or persistent S. aureus colonization induces specific systemic immune responses. Humoral responses are the most studied of these and little is known of cellular responses induced by colonization. Intriguingly, colonized patients who develop bacteremia may have a lower S. aureus-attributable mortality than their non-colonized counterparts. This could imply a staphylococcal-specific immune "priming" or immunomodulation occurring as a consequence of colonization and impacting on the outcome of infection. This has yet to be fully explored. An effective vaccine remains elusive. Anti-S. aureus vaccine strategies may need to drive both humoral and cellular immune responses to confer efficient protection. Understanding the influence of colonization on adaptive response is essential to intelligent vaccine design, and may determine the efficacy of vaccine-mediated immunity. Clinical trials should consider colonization status and the resulting impact of this on individual patient responses. We urgently need an increased appreciation of colonization and its modulation of host immunity.
    Frontiers in Immunology 01/2014; 4:507. DOI:10.3389/fimmu.2013.00507
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    ABSTRACT: Background: Staphylococcus aureus is a major cause of serious hospital and community acquired infections, particularly in colonized individuals. Objectives: The study was carried out in a tertiary care center in Tehran, Iran to identify the frequency of hospital acquired methicillin resistant Staphylococcus aureus (HA-MRSA ) colonization and its antibiotic susceptibility pattern and molecular characteristics. Patients and Methods: This point-prevalence study was performed on 631 children who were admitted for at least 48 hours in different wards of Mofid children’s hospital in Tehran, Iran. Samples from anterior nares of these children were taken with sterile swab and cultured. If Staphylococcus aureus (S. aureus) was isolated, methicillin resistance and antibiotic susceptibility pattern were diagnosed according to Center for Disease Control and Prevention (CDC) guidelines of 2011 and Clinical and Laboratory Standards Institute (CLSI), and molecular analysis were determined by minimum inhibitory concentration (MIC) and polymerase chain reaction (PCR) methods. Results: Rate of colonization with S. aureus and methicillin resistant Staphylococcus aureus (MRSA) were 3.2% and 1.1% (1.1% of total and 35% of S. aureus isolates), respectively. All MRSA isolates were susceptible to rifampin and clindamycin. Resistance to vancomycin was reported in six Staphylococcus strains. Resistance to linezolid was detected in 19/20 Staphylococcus. Molecular analysis of isolates showed that all vancomycin resistant S. aureus isolates contained Van A or Van B gene, and 15/19 linezolid resistant strain was positive for chloramphenicol-florfenicol resistant gene ( cfr gene). Conclusions: The rate of MRSA colonization varies in any area, and the knowledge of acquisition risk factors and antibiotic susceptibility pattern are essential in prevention and treatment of MRSA infections. Based on our study, we suggest that clindamycin and rifampin are good choices in empiric treatment of patients suspected to have HA- MRSA infections until results of culture and antibiotic susceptibility pattern are prepared. In respect to the prevalence of linezolid resistance in this study, we suggest avoiding the use of linezolid as empiric therapy in HA-Staphylococcus infection.
    10/2012; 1(1):4-8. DOI:10.5812/pedinfect.5190
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    ABSTRACT: Nasal decolonisation has a proven effect on the prevention of severe Staphylococcus aureus infections and in the control of methicillin resistant S. aureus (MRSA). However, rising rates of resistance to antibiotics highlights the need for new substances for nasal decolonisation. LTX-109 is a broad spectrum, fast-acting bactericidal antimicrobial drug for topical treatment, which causes membrane disruption and cell lysis. This mechanism of action is not associated with cross-resistance and has a low propensity for development of resistance. In the present study persistent nasal MRSA and methicillin sensitive S. aureus carriers were treated for three days with vehicle, 1%, 2% or 5% LTX-109, respectively. A significant effect on nasal decolonisation was observed already after 2 days of LTX-109 treatment in subjects treated with 2% or 5% LTX-109 compared to vehicle (P≤0.0012, Dunnett's test). No safety issues were noted during the 9-week follow-up period. Minimal reversible epithelial lesions were observed in the nasal cavity. The systemic exposure was very low with a Cmax 1-2 h post dosing (3.72-11.7 ng/mL). One week after treatment initiation LTX-109 was not detectable in any subject. Summary: Intranasal treatment of S. aureus with LTX-109 is safe and reduces the bacterial load already after a single day of treatment. Hence, LTX-109 has the potential as a new and effective antimicrobial agent with low propensity of resistance development that can prevent infections by MSSA/MRSA during hospitalization. NCT01158235.
    Antimicrobial Agents and Chemotherapy 10/2014; 59(1). DOI:10.1128/AAC.03513-14 · 4.45 Impact Factor