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Link: Comparison
OBJECTIVES: To determine which method of determining the MIC of teicoplanin produces a result closely related to outcome in the critically ill patient. METHODS: Four methods of teicoplanin susceptibility testing--disc diffusion, Etest, VITEK (Legacy and VITEK 2) and agar incorporation--were compared for 47 methicillin-resistant Staphylococcus aureus (MRSA) isolates from invasive intensive care unit (ICU) infections and 83 isolates from ICU patients colonized with the organism. Clinical outcome was recorded prospectively for all the patients. Another 13 reference laboratory strains of MRSA with reduced susceptibility to teicoplanin were tested. RESULTS: Both VITEK systems failed to demonstrate resistance in the three isolates identified as resistant by Etest or agar incorporation, and disc testing detected only one resistant isolate. A higher MIC, as found by Etest or agar incorporation, was associated with lower survival (n = 130, 95% CI -0.082 to -0.006, P = 0.023, Etest; n = 130, 95% CI -0.156 to -0.020, P = 0.011, agar). The findings for the 13 reference strains were similar, with a >/=4-fold reduction in MIC between agar incorporation or Etest and VITEK2 for six isolates. CONCLUSIONS: Neither disc diffusion nor the VITEK systems are reliable for detection of teicoplanin resistance in MRSA. Etest and agar incorporation remain the methods of choice.
Link: Paediatric nosocomial infections: resistance pattern of clinical isolates..
Hospital acquired infections are transmitted to patients by hospital personnel and other patients, or they may arise from patient's own endogenous flora. Children are one of the most susceptible subjects associated in the hospital-acquired infections and have a higher prevalence rate for infections. This problem is at its extremes in developing countries like Pakistan where in most of cases the severity depends on the hygienic conditions of the Hospitals and lack or lapse of infection control measures. To have a surveillance type of data in this regard, one hundred and twenty four isolates of Pseudomonas aeruginosa/Pseudomonas species, Staphylococcus aureus (MRSA/MSSA) and Klebsiella species, that are commonest among the nosocomial infection causing organisms, were collected from pediatric hospital settings in Karachi. A study of incidence and resistance pattern by Kirby Baur disc diffusion method, with selected antimicrobials, was carried out. These isolates were resistant against most antimicrobials tested. Drugs like mmipenem, meropenem, amikacin, vancomycin (especially in MRSA or BRSA), Fucidic acid (for burns and other infections) and some of the 3rd generation cephalosporins were found quite effective.
Link: HighWire Press -- Medline Abstract.
The aim of this study was to determine resistance to co-trimoxazole among 476 strains of methicillin-resistant Staphylococus aureus (MRSA) and 2137 strains of methicillin resistant coagulase-negative staphylococci (MRCNS) isolation during three years (2001-2003). Their susceptibility testing were performed by the disc-diffusion techniques according to recomendation of NCCLS (National Committe for Clinical Laboratory Standards). Co-trimoxazole resistance was demonstrated more frequently among MRCNS (52,8%, 51,4%, 63,9% in 2001, 2002, 2003), than among MRSA (23,4%, 19,5%, 16,8% adequately).
Link: Antimicrobial Agents and Chemotherapy.
Forty-five Panton-Valentine leukocidin (PVL)-positive, methicillin-resistant Staphylococcus aureus strains were isolated in Algeria between 2003 and 2004; 18 isolates were isolated in the community and 27 in a hospital. Five PVL-positive hospital isolates were resistant to multiple antibiotics, including ofloxacin and gentamicin for three isolates.
Link: HighWire Press -- Medline Abstract.
To assess whether the occurrence of rifampicin (RFP) resistance in methicillin-resistant Staphylococcus aureus (MRSA) is related to treatment of tuberculosis, we determined the RFP susceptibility of MRSA isolates obtained from tuberculosis patients and screened for mutation(s) in the rpoB gene of these isolates. The MICs of RFP for 84 MRSA isolates obtained from two hospitals in Japan were determined. DNA was sequenced in the region 1318-1602 nucleotides (nt) of the rpoB gene, which includes RFP resistance-determining clusters I (1384-1464 nt, 462-488 amino acids). The majority of MRSA isolates from tuberculosis wards, i.e., 48 of 51 (94%) [33 of 34 in a Tokyo hospital (97%) and 15 of 17 in a Chubu hospital (88%)], were resistant to RFP. Meanwhile, no isolates of 33 from the other wards were resistant to RFP. All RFP-resistant MRSA isolates had a mutation(s), including novel mutation(s) such as Val453AEPhe, Asp471AEAsn, and Ile527AELeu, in rpoB. An emergence of RFP-resistant MRSAs in tuberculosis wards in Japan was strongly suggested.
Link: HighWire Press -- Medline Abstract.
Methicillin resistant Staphylococcus aureus (MRSA) is an important nosocomial pathogen. We report the prevalence and antibiotic susceptibility pattern of MRSA in major southern districts of Tamilnadu. METHODS: A total of 7172 clinical specimens and 1725 carrier screening samples were collected from different centers and subjected to MRSA screening using conventional microbiological methods. Subsequently the antibiotic sensitivity test was performed for the confirmed MRSA isolates. RESULTS: Out of 906 strains of S. aureus isolated from clinical and carrier samples, 250 (31.1%) and 39 (37.9%) were found to be methicillin resistant respectively. Almost all clinical MRSA strains (99.6%) were resistant to penicillin, 93.6% to ampicillin, and 63.2% towards gentamicin, co-trimoxazole, cephalexin, erythromycin, and cephotaxime. All MRSA strains (100%) of carrier screening samples had resistance to penicillin and about 71.8% and 35.9% were resistant to ampicillin and co-trimoxazole respectively. Multidrug resistance was observed among 63.6% of clinical and 23% of carrier MRSA isolates. However, all strains of clinical and carrier subjects were sensitive to vancomycin. CONCLUSION: The determination of prevalence and antibiotic sensitivity pattern of MRSA will help the treating clinicians for first line treatment in referral hospitals.
Link: Experts warn of six drug-resistant killer germs.
Life-threatening diseases are becoming more drug-resistant while the development of new drugs is stagnating, medical school scientists warned Wednesday.The Infectious Diseases Society of America published a list of six microbes for which it said doctors have "an inadequate medicine cabinet." "What is worse is that our ammunition is running out and there are no reinforcements in sight." Neglect by major pharmaceutical companies that are more interested in profitable treatments for chronic diseases than in new antibiotics was cited as one factor in the failure to find effective new drugs.
In an article titled "Bad Bugs Need Drugs" in Wednesday's issue of the society's journal, Clinical Infectious Diseases, the team of experts listed the six priority infections: — Methicillin-resistant staphylococcus aureus (MRSA), a disease that has plagued hospitals for several decades and is now showing up in a new, more virulent form in people who acquired it outside of hospitals. — Escherichia coli and Klebsiella, bacteria that cause often fatal urinary and intestinal tract infections and are evolving resistance to more and more antibiotics. — Acinetobacter baumannii, a growing cause of both hospital-acquired pneumonia with mortality rates that range from 20 to 50 percent and increasing numbers of highly resistant wound infections among U.S. soldiers returning from Iraq and Afghanistan. — Aspergillus, a fungus that causes mortality as high as 60 percent, even with the best antifungal drugs. — Vancomycin-resistant enterococcus faecium (VRE), a major cause of bloodstream infections, meningitis and abdominal infections. — Pseudomonas aeruginosa, cause of severe pneumonia and urinary tract infection, particular among cancer patients and other persons with compromised immune systems.
Link: Journal of Antimicrobial Chemotherapy
This article reports on the proceedings of a meeting held in London in July 2005 organized by the Specialist Advisory Committee on Antimicrobial Resistance in conjunction with the UK National Prescribing Centre and UK Department of Health. The focus of the meeting was the developing role of the antibiotic pharmacist. The main presentations tackled four aspects of hospital antimicrobial prescribing: the development, maintenance and presentation of guidelines; the role of prescriber education; the importance of team working in multidisciplinary prescribing networks; and preliminary findings on hospital antibiotic consumption in England. The speakers highlighted the progress that has been made and gave examples of good practice, in addition they drew attention to deficiencies and hence the challenges that lie ahead. These include the need for accurate hospital antibiotic usage data in the UK and more integration of clinical outcome data in studies on the control of antimicrobial consumption through the implementation of prescribing guidelines.
Link: The Journal of Bacteriology
Custom-designed gene chips (Affymetrix) were used to determine genetic relatedness and gene expression profiles in Staphylococcus aureus isolates with increasing MICs of vancomycin that were recovered over a period of several weeks from the blood and heart valve of a patient undergoing extensive vancomycin therapy. The isolates were found to be isogenic as determined by the GeneChip based genotyping approach and thus represented a unique opportunity to study changes in gene expression that may contribute to the vancomycin resistance phenotype. No differences in gene expression were detected between the parent strain, JH1, and JH15, isolated from the nares of a patient contact. Few expression changes were observed between blood and heart valve isolates with identical vancomycin MICs. A large number of genes had altered expression in the late stage JH9 isolate (MIC = 8 �g/ml) compared to JH1 (MIC = 1 �g/ml). Most genes with altered expression were involved in housekeeping functions or cell wall biosynthesis and regulation. The sortase-encoding genes, srtA and srtB, as well as several surface protein-encoding genes were downregulated in JH9. Two hypothetical protein-encoding genes, SAS016 and SA2343, were dramatically overexpressed in JH9. Interestingly, 27 of the genes with altered expression in JH9 grown in drug-free medium were found to be also overexpressed when the parental strain JH1 was briefly exposed to inhibitory concentrations of vancomycin, and more than half (17 of 27) of the genes with altered expression belonged to determinants that were proposed to form part of a general cell wall stress stimulon
Link: HighWire Press -- Medline Abstract.
Objective: To investigate antibiotic resistance and genetic relatedness of methicillin-resistant Staphylococcus aureus (MRSA) isolated in a general hospital in Kuwait over a period from 1996 to 1998 and 2001. Material and Methods: The isolates were characterized by antibacterial susceptibility testing, coagulase serotyping, coagulase gene polymorphism (coag-RFLP) and pulsed-field gel electrophoresis (PFGE). Results: The MRSA isolates were highly resistant to gentamicin, kanamycin, ciprofloxacin, tetracycline, fusidic acid and mupirocin. The prevalence of gentamicin, kanamycin, streptomycin, tetracycline and erythromycin resistance remained high (80-96%) throughout the study period, but the prevalence of resistance to ciprofloxacin, fusidic acid and mupirocin steadily increased. The already high mupirocin resistance level increased from 12.5 in 1996, to 85.7% in 2001, and the fusidic acid resistance varied between 70.8 and 85.7%. In contrast, chloramphenicol and trimethoprim resistance declined from 25 and 29% in 1996 to 4.7 and 14.2% in 2001, respectively. The majority (91.5%) of the isolates were coagulase serotype 4. AluI restriction endonuclease analysis of amplified coagulase gene generated four coag-RFLP patterns: 92% of them were coag-RFLP type 1, while types 2, 3 and 4 were 3.5, 4.6 and 1.1% respectively. PFGE differentiated them into seven pulsotypes (PFGE types 1-7). The PFGE type 1 pulsotype constituted 90.2% of the isolates. Isolates with the type A coag-RFLP also had the type1 PFGE pulsotypes. Conclusion: The concordant results of PFGE and coag-RFLP demonstrated the presence of a persistent MRSA clone in the hospital during the study period. Copyright (c) 2006 S. Karger AG, Basel.
Link: Hospital "super super bug" stronger than MRSA.
According to reports eleven patients at a British hospital have acquired a superbug said to be stronger than MRSA. The bug known as gentamicin resistant MRSA, does not react to standard drugs used to treat the bacteria and apparently causes blood poisoning and chest infections. Walsgrave hospital in Coventry says it is not aware of any deaths associated with the strain which was first identified during routine screening in June. A hospital microbiologist has said the strain is particularly recognisable because of its very resistant sensitivity pattern. The super strain has apparently occurred in two intensive care units, and in a high dependency unit. Five incidents have occurred in just 10 days between August and September, while eight were likely to have been acquired in the hospital. As well as gentamicin, a frontline antibiotic in the treatment of MRSA, the strain is also resistant to mupirocin, fucidin, rifampicin.
Link: icBirmingham
Patients at a Warwickshire hospital have acquired a new superbug, thought to be stronger than MRSA, it was revealed yesterday. Gentamicin-resistant MRSA does not react to standard drugs used to treat other strains of the bacteria and it is thought to cause blood poisoning and chest infections. According to a leaked document, 11 patients at Walsgrave Hospital have acquired the superbug - the first of which was identified in an intensive care patient during routine screening in June.
Link: In vivo transfer
We examined the molecular basis of the emergence of mupirocin resistance in a methicillin-resistant Staphylococcus aureus (MRSA) strain colonizing a nursing home resident undergoing mupirocin prophylaxis. Patient and methods: A persistent carrier of mupirocin-susceptible MRSA participated in a trial of mupirocin for nasal decolonization among nursing home residents. During prophylaxis a high-level mupirocin-resistant MRSA emerged in the nasal isolates from this patient. S. aureus and coagulase-negative staphylococci were isolated prior to, during and after 14 days of mupirocin treatment. The staphylococcal isolates and their plasmids were examined by molecular genetic methods. RESULTS: All mupirocin-susceptible and -resistant MRSA isolates possessed the same genotype. The patient was also colonized by a single mupirocin-resistant Staphylococcus epidermidis strain. The mupirocin-resistant MRSA and S. epidermidis strains harboured identical plasmids that carried the mupA determinant and genes for conjugative DNA transfer in staphylococci. These plasmids could be transferred in vitro from both clinical isolates to S. aureus RN2677. CONCLUSIONS: The MRSA strain contained a conjugative plasmid expressing mupA that was identical with that found in the S. epidermidis strain which colonized the patient. These findings suggest that transfer of mupA from S. epidermidis to MRSA probably occurred during mupirocin prophylaxis.
Link: Physorg.
Antibiotic resistant bacteria, which are proliferating in hospitals and causing major headaches for physicians, cheat death by finding ways to fortify their cell walls against the deadly drugs. The question is: how? New research from the laboratory of Alexander Tomasz shows that one gene, called mecA, enables some bacteria to withstand penicillin and other drugs in its class. Part of a larger group called beta-lactam antibiotics, these drugs work by inhibiting proteins the bacteria need to construct their cell wall. If a Staphylococcus aureus bacterium has the mecA gene, however, it can still build a cell wall even in the presence of the antibiotics. But mecA is an acquired gene in S. aureus, and Tomasz and colleagues show that these bacteria probably picked mecA up from another bacteria called S. sciuri. S. sciuri, which is only very remotely related to S. aureus, lives on the skin of domestic and wild animals, including mice, rats and squirrels. While all S. sciuri carry a gene closely related to mecA, they are virtually all fully sensitive to beta-lactam antibiotics. On rare occasions, a mutation occurs in mecA that renders them resistant. Tomasz’s group introduced this mutated gene into S. aureaus and showed that they then also became resistant to beta-lactam antibiotics. “This suggests that the mecA gene originated in S. scuiri and then found its way into S. aureus,” says Tomasz, head of the Laboratory of Microbial Cell Biology and the Dr. Plutarch Papamarkou Professor. “Even though the two bacteria use different molecules to make their cell walls, we found that the mecA protein can use what is available to build the cell wall.
Link: The Journal of Bacteriology.
Staphylococcus haemolyticus is an opportunistic bacterial pathogen that colonizes human skin and is remarkable for its highly antibiotic-resistant phenotype. We determined the complete genome sequence of S.haemolyticus to better understand its pathogenicity and evolutionary relatedness to the other staphylococcal species. A large proportion of the open reading frames in the genomes of S.haemolyticus, Staphylococcus aureus, and Staphylococcus epidermidis were conserved in their sequence and order on the chromosome. We identified a region of the bacterial chromosome just downstream of the origin of replication that showed little homology among the species but was conserved among strains within a species. This novel region, designated the "oriC environ," likely contributes to the evolution and differentiation of the staphylococcal species, since it was enriched for species-specific nonessential genes that contribute to the biological features of each staphylococcal species. A comparative analysis of the genomes of S.haemolyticus, S.aureus, and S.epidermidis elucidated differences in their biological and genetic characteristics and pathogenic potentials. We identified as many as 82 insertion sequences in the S.haemolyticus chromosome that probably mediated frequent genomic rearrangements, resulting in phenotypic diversification of the strain. Such rearrangements could have brought genomic plasticity to this species and contributed to its acquisition of antibiotic resistance.
Link: HighWire Press -- Medline Abstract.
From 1990 to 1995 at Hospital Universitrio Clementino Fraga Filho, patients colonized or infected with methicillin-resistant Staphylococcus aureus (MRSA) were treated with mupirocin to eliminate MRSA carriage. In 1995, 65% of MRSA patients at this hospital had mupirocin-resistant isolates. Starting in 1996, mupirocin use was restricted to patients colonized, but not infected, with MRSA. . RESULTS: The incidence density of MRSA patients increased slightly over time, whereas the purchase of mupirocin decreased dramatically. Mupirocin-resistant MRSA infections decreased from 65% in 1994-1995 to 15% in 1999-2000. The MRSA Brazilian clone, detected in 1992, was still highly prevalent. The same ileS-2 encoding plasmid found in 1994-1995 persisted in three identical MRSA isolates from 1999-2000 belonging to the Brazilian clone. CONCLUSIONS: After mupirocin use decreased, the ileS-2 encoding plasmid persisted in only a few Brazilian clone isolates. Our data on mupirocin-resistant MRSA incidence and mupirocin use strongly suggested that restricted use was related to decreased rates of mupirocin resistance at our hospital.
Link: Journal of Antimicrobial Chemotherapy.
Progress on rational intervention to prevent increasing antibiotic resistance has been slow. We suggest that this is because the science of resistance epidemiology has received little attention, and that a systematic, co-operative investigation of this area might yield a relevant knowledge base, analogous to the basis for effective public health intervention in infectious disease given by infection epidemiology. The steps required to progress this approach in the UK are discussed, along with a summary of what is known and speculation on what might emerge.
Link: Antimicrobial Agents and Chemotherapy.
Very technical but it basically means that some strains of MRSA can pump the drugs out that are sent to kill them
Efflux is an important mechanism of multidrug resistance (MDR) in bacteria. The multidrug and toxin extrusion (MATE) family is the most recently described group of MDR efflux proteins, none of which have previously been identified in Staphylococcus aureus. Two independently derived S. aureus mutants having efflux-related MDR phenotypes were studied using microarray technology and a marked overexpression of an open reading frame (ORF; mepA) encoding a protein homologous with MATE family proteins was observed in both.
The rate of FQs-resistant MRSA was 80 approximately 90%, being markedly higher than that of FQs-resistant MSSA. The FQs-resistance rate of MRCNS was also higher than that of MSCNS, however, it was lower than that of MRSA.
Link: Attack of the Superbug.
A report this week indicated that hospital-acquired infection rates have worsened in the United States during the last several years, including antibiotic-resistant bacterial infections. Along with a warning from the Centers for Disease Control and Prevention (CDC) that more than 70 percent of the bacteria that cause infections are resistant to at least one antibiotic used to treat them, a USC pharmacist advises being more selective in using these drugs.
Link: As science gets wiser, so do the bugs.
Researchers at the Baylor College of Medicine and Texas Children's Hospital conducted a three-year study of S. aureus infections in children. They found that among S. aureus isolates acquired in the community, the proportion of isolates that were MRSA had reached 76 percent in 2003. Over the preceding three years, the number of MRSA infections acquired in the community had more than doubled. The MRSA isolates caused skin and soft tissue infections in most cases, and more than 60 percent of these children were admitted to the hospital. The rapid rise in pediatric community-acquired MRSA infections in Texas should raise red flags for health care workers everywhere. "There have been deaths related to this organism, although the vast number are skin and soft tissue infections," said Sheldon Kaplan, MD, lead author of the Texas study. He added that because of this "very dramatic increase" in MRSA infections, physicians should learn what percentage of staphylococcal isolates are drug-resistant in their own communities so they can monitor for increases and adjust treatment accordingly. And if regular drug-resistant bacteria weren't bad enough, some bacteria have become multidrug resistant (MDR). Researchers at the Beth Israel Deaconess Medical Center and Harvard Medical School studied the prevalence of bacteria resistant to three or more drugs over a six-year period. From 1998 to 2003, there was a significant increase in the incidence of patients carrying MDR bacteria when they were admitted to the hospital. Of the four species of MDR bacteria that the researchers examined, three of them--including Escherichia coli, a familiar bug that can cause urinary tract infections--were involved in the upswing.
Link: HighWire Press -- Medline Abstract.
In this sample, MSSA isolates were almost three times more likely to have inducible MLS resistance compared to MRSA isolates. Inducible resistance may compromise the efficacy of clindamycin. The frequency of inducible resistance in this series of "clindamycin sensitive" S. aureus isolates is 26%. It is likely that the true percentage of clindamycin resistance is being underestimated since testing for inducible resistance is not routinely performed.
Twenty-three rifampicin-resistant methicillin-resistant Staphylococcus aureus (MRSA) isolated in three wards at a university hospital in Turkey between June, 2000, and February, 2001, were studied for their genetic relatedness using a combination of antibiogram, coagulase serotyping, coagulase gene polymorphism (coa-RFLP), and pulsed-field gel electrophoresis (PFGE). They all expressed high-level rifampicin resistance (MIC, >256 mg/L) and were resistant to gentamicin, kanamycin, amikacin, ciprofloxacin, tetracycline, and cadmium acetate and were susceptible to fusidic acid, vancomycin, trimethoprim, and mupirocin. They belonged to the same coagulase serotype (serotype IV) and had identical coa-RFLP patterns. In contrast, PFGE generated nine banding patterns designated type A, types A1-A5, B, C, and D. The most common PFGE pattern (type A) and its subtypes (types A1-A5) were seen in 20 (87%) of the 23 isolates in the three wards. The results demonstrated the acquisition of rifampicin resistance by different MRSA clones and the spread of one clone among patients in the three wards.
Link: Antimicrobial Agents and Chemotherapy.
The erm gene product confers clindamycin resistance on Staphylococcus aureus. We report a clindamycin clinical failure where resistance developed on therapy in a D-test-positive strain. D tests of 91 clindamycin-susceptible, erythromycin-resistant S. aureus isolates showed that 68% of methicillin-susceptible and 12.3% of methicillin-resistant S. aureus strains were D-test positive.
A short introduction from Dave Roberts
This 12 minute introduction will help you grasp the key facts and the key issues surrounding drug resistant staph aureus (mersa, mursa)
