Lack of Vancomycin Tolerance in
            <i>Streptococcus pneumoniae</i>
            Strains Isolated in Barcelona, Spain, from 1999 to 2001

Ortega, Mar; Marco, Francesc; Soriano, Álex; García, Elisa; Martínez, José Antonio

doi:10.1128/aac.47.6.1976-1978.2003

Cited by 7 publications

(9 citation statements)

References 9 publications

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“…No strain showing vancomycin tolerance was detected in our work. In a recent regional survey (5), we did not detect any vancomycin-tolerant strains among invasive isolates from French children, and a similar observation was established by two different authors in Spain (2,24). Despite the relatively limited number of strains studied, the distribution of serogroups among PNSSP seemed similar to those in other countries (15) whereas the predominance of serotypes 1 and 3 among penicillin-susceptible strains was of concern.…”

supporting

confidence: 53%

Invasive Streptococcus pneumoniae in France: Antimicrobial Resistance, Serotype, and Molecular Epidemiology Findings from a Monthly National Study in 2000 to 2002

Decousser

Pina

Viguier

et al. 2004

Antimicrob Agents Chemother

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supporting

confidence: 53%

Invasive Streptococcus pneumoniae in France: Antimicrobial Resistance, Serotype, and Molecular Epidemiology Findings from a Monthly National Study in 2000 to 2002

Decousser

Pina

Viguier

et al. 2004

Antimicrob Agents Chemother

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“…The VTSP strain S3 (serotype 23F) (Sung et al ., 2006) was kindly provided by M‐N Kim (Department of Laboratory Medicine, University of Ulsan and Asan Medical Center, Seoul, Republic of Korea). The VTSP Tupelo strain (serotype 14), a clinical pneumococcal isolate considered a model of Van tolerance (McCullers et al ., 2000), was kindly provided by F. Marco (Department of Microbiology, Hospital Clinic, Barcelona, Spain) (Ortega et al ., 2003). Unless stated otherwise, pneumococcal strains were grown in C medium either supplemented (C + Y) or not supplemented with 0.08% yeast extract, or on reconstituted tryptose blood agar base plates (Difco Laboratories) supplemented with 5% defibrinated sheep's blood.…”

Section: Methodsmentioning

confidence: 99%

“…Given reports of frequent meningitis treatment failures as a result of multidrug‐resistant bacteria (Tan, 2003), vancomycin (Van) is often added to standard therapy regimens for meningitis and so far, no Van‐resistant pneumococci have been identified. However, there have been reports of the emergence of Van‐tolerant S. pneumoniae (VTSP) in some countries (McCullers et al ., 2000; Henriques Normark et al ., 2001; Boost et al ., 2003; Hidalgo et al ., 2003; Gillis et al ., 2005; Sung et al ., 2006) but not in others (Antón et al ., 2001; Ortega et al ., 2003; Decousser et al ., 2004a,b).…”

Section: Introductionmentioning

confidence: 99%

Vancomycin tolerance in clinical and laboratory Streptococcus pneumoniae isolates depends on reduced enzyme activity of the major LytA autolysin or cooperation between CiaH histidine kinase and capsular polysaccharide

Moscoso¹,

Domenech²,

Garcı́a³

2010

Molecular Microbiology

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SummaryVancomycin is frequently added to standard therapy for pneumococcal meningitis. Although vancomycinresistant Streptococcus pneumoniae strains have not been isolated, reports on the emergence of vancomycin-tolerant pneumococci are a cause of concern. To date, the molecular basis of vancomycin tolerance in S. pneumoniae is essentially unknown. We examined two vancomycin-tolerant clinical isolates, i.e. a purported autolysin negative (LytA -), serotype 23F isolate (strain S3) and the serotype 14 strain 'Tupelo', which is considered a paradigm of vancomycin tolerance. S3 was characterized here as carrying a frameshift mutation in the lytA gene encoding the main pneumococcal autolysin. The vancomycin tolerance of strain S3 was abolished by transformation to the autolysin-proficient phenotype. The original Tupelo strain was discovered to be a mixture: a strain showing a vancomycin-tolerant phenotype (Tupelo_VT) and a vancomycinnontolerant strain (Tupelo_VNT). The two strains differed only in terms of a single mutation in the ciaH gene present in the VT strain. Most interestingly, although the vancomycin tolerance of Tupelo_VT could be overcome by increasing the LytA dosage upon transformation by a multicopy plasmid or by externally adding the autolysin, we show that vancomycin tolerance in S. pneumoniae requires the simultaneous presence of a mutated CiaH histidine kinase and capsular polysaccharide.

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“…4,53,62,131 Epidemiology and Prevalence of Macrolide Resistance Globally, macrolide resistance among S. pneumoniae escalated dramatically in the 1990s. 3,4,53,174,251 By the mid-1990s, macrolide resistance rates exceeded 20% in several countries, including Spain, 252 Greece, 253 Slovakia, 130 Bulgaria, 254 Rumania, 254 Uruguay, 255 and several Asian countries. 81,82,241 Rates of macrolide resistance were highly variable among countries (< 3% to > 70%).…”

Section: Macrolide Resistancementioning

confidence: 99%

Streptococcus pneumoniae: Does Antimicrobial Resistance Matter?

Lynch

Zhanel²

2009

Semin Respir Crit Care Med

113

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Over the past 3 decades, antimicrobial resistance among Streptococcus pneumoniae, the most common cause of community-acquired pneumonia (CAP), has escalated dramatically worldwide. In the late 1970s, strains of pneumococci displaying resistance to penicillin were described in South Africa and Spain. By the early 1990s, penicillin-resistant clones of S. pneumoniae spread rapidly across Europe and globally. Additionally, resistance to macrolides and other antibiotic classes escalated in tandem with penicillin resistance. Six international clones (serotypes 6A, 6B, 9V, 14, 19F, 23F) were responsible for most of these resistant isolates. Currently, 15 to 30% of S. pneumoniae worldwide are multidrug-resistant (MDR) (i.e., resistant to > or = 3 classes of antibiotics). Despite the dramatic escalation in the rate of antimicrobial resistance among pneumococci worldwide, the clinical impact of antimicrobial resistance is difficult to define. Treatment failures due to antibiotic-resistant pneumococci have been reported with meningitis, otitis media, and lower respiratory tract infections, but the relation between drug resistance and treatment failures has not been convincingly established. Clinical failures often reflect factors independent of antimicrobial susceptibility of the infecting organisms. Host factors (e.g., extremes of age; underlying immunosuppressive or debilitating disease; comorbidities), or factors that affect intrinsic virulence of the organisms (e.g., capsular subtype) strongly influence prognosis. Mortality rates are higher in the presence of: multilobar involvement, renal insufficiency, need for intensive care unit (ICU) care, hypoxemia, severe derangement in physiological parameters, and comorbidities. Given these confounding factors, dissecting out the impact of antimicrobial resistance on clinical outcomes is difficult, if not impossible. Prospective, randomized trials designed to assess the clinical significance of antimicrobial resistance among pneumococci are lacking, and for logistical reasons, will never be done. Does in vitro resistance translate into clinical failures? Should changing resistance patterns modify our choice of therapy for CAP or for suspected pneumococcal pneumonia? In this review, we discuss several facets, including mechanisms of antimicrobial resistance among specific antibiotic classes, epidemiology and spread of antimicrobial resistance determinants regionally and worldwide, risk factors for acquisition and dissemination of resistance, the impact of key international clones displaying multidrug resistance, the clinical impact of antimicrobial resistance, and strategies to limit or curtail antimicrobial resistance among this key respiratory tract pathogen.

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Lack of Vancomycin Tolerance in Streptococcus pneumoniae Strains Isolated in Barcelona, Spain, from 1999 to 2001

Cited by 7 publications

References 9 publications

Invasive Streptococcus pneumoniae in France: Antimicrobial Resistance, Serotype, and Molecular Epidemiology Findings from a Monthly National Study in 2000 to 2002

Invasive Streptococcus pneumoniae in France: Antimicrobial Resistance, Serotype, and Molecular Epidemiology Findings from a Monthly National Study in 2000 to 2002

Vancomycin tolerance in clinical and laboratory Streptococcus pneumoniae isolates depends on reduced enzyme activity of the major LytA autolysin or cooperation between CiaH histidine kinase and capsular polysaccharide

Streptococcus pneumoniae: Does Antimicrobial Resistance Matter?

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