aureus and so it may be here that these proteins have their most important functions. Our data also have potential implications for the use of the Isd proteins

as vaccinogens against S. aureus as they do not have an apparent crucial role in pathogenesis, although they may still elicit opsonic antibodies. This work was funded by the Medical Research Council (Ref: 78981). “
“Streptococcus tigurinus is a new member of the Streptococcus viridians group and is closely related SP600125 molecular weight to Streptococcus mitis, Streptococcus pneumoniae, Streptococcus pseudopneumoniae, Streptococcus oralis, and Streptococcus infantis. The type strain AZ_3aT of S. tigurinus was originally isolated from a patient with infective endocarditis. Accurate identification of S. tigurinus is facilitated only by newer molecular methods like 16S rRNA gene analysis. During the course of study on bacteraemia and infective endocarditis with reference to periodontitis and viridians group of streptococci, a strain of S. tigurinus isolated from subgingival

plaque of a patient with periodontitis identified by 16S rRNA gene analysis, which was originally identified as Streptococcus pluranimalium by Vitek 2. Confirmation by BMN 673 concentration 16S rRNA gene analysis showed 99.39% similarity (1476/1485 bp) with S. tigurinus AZ_3aT(AORU01000002). To the best of our knowledge, this is the first report of isolation of S. tigurinus from the oral cavity of a periodontitis patient. “
“Light conditions during mycelial growth are known to influence fungi in many ways. The effect of visible-light exposure during mycelial growth was investigated on conidial tolerance to UVB irradiation and wet heat of Metarhizium robertsii, an insect-pathogenic fungus. Two nutrient media and two light regimens were compared. Conidia were produced on (A) potato dextrose agar plus yeast extract medium (PDAY) (A1) under dark conditions or (A2) under continuous visible light (provided by two fluorescent lamps with intensity 5.4 W m−2). For comparison, the fungus was also produced on (B) minimal medium (MM) under

continuous-dark incubation, which is known to produce conidia with increased tolerance to heat and UVB radiation. The UVB tolerances the of conidia produced on PDAY under continuous visible light were twofold higher than conidia produced on PDAY medium under dark conditions, and this elevated UVB tolerance was similar to that of conidia produced on MM in the dark. The heat tolerance of conidia produced under continuous light was, however, similar to that of conidia produced on MM or PDAY in the dark. Conidial yield on PDAY medium was equivalent when the fungus was grown either under continuous-dark or under continuous-light conditions. Light sensing is conserved throughout the three domains of Bacteria, Archaea, and Eukarya (Purschwitz et al., 2006; Swartz et al., 2007).

Detection was carried out using either 6A3 monoclonal antibody, which was raised against purified Apa (Lara et al., 2004), or concanavalin A (ConA)

conjugated with peroxidase (Sigma), both at a 1 : 1000 dilution. For detection of the hemagglutinin epitope in tagged Pmt proteins, membrane fractions were subject to electrophoresis in 10% SDS-polyacrylamide gels, transferred to PVDF membranes, and incubated with 3F10 high-affinity anti-hemagglutinin-Peroxidase antibodies find more (Roche) at a 1 : 1000 dilution. Detection was carried out with the BM Chemiluminescence Western blotting kit (Roche). Purification of membrane fractions from Streptomyces mycelium was carried out as described by Kim et al. (2005), and c-Met inhibitor fractionation of M. smegmatis membranes used for standardization of Ppm activity was carried out as described by Cascioferro et al. (2007). Assay of Ppm activity in membrane fractions was carried out as described by Gurcha et al. (2002), using GDP-[U-14C]mannose,

262 mCi/mmol (PerkinElmer). Pmt activity was determined in a coupled assay using the Apa-derived peptide A3 (Invitrogen) as described by Cooper et al. (2002). Detailed description is provided in Data S1. The bacterial two-hybrid system of Karimova et al. (1998) was used, based on plasmids pKT25 and pUT18 with modified polylinker regions (Karimova et al., 2001). β-galactosidase activity was determined according to Miller (1972). The sco1423 gene (ppm) encodes Ppm of S. coelicolor (PpmSco; Cowlishaw & Smith, 2002; Wehmeier et al., 2009). We constructed strain IB31 carrying a deletion of this gene in the J1928 background, which is wild type except for a pgl mutation that allows bacteriophage φC31 to form plaques (Table 1). As expected, φC31 was able to form plaques in J1928 (Fig. 1a,

plate 1), but not in the Δppm mutant IB31 Verteporfin solubility dmso (Fig. 1a, plate 2; Table S2), confirming that PpmSco is required for infection by φC31. To determine whether PpmSco is required for glycosylation of the Apa protein of M. tuberculosis by S. coelicolor, we cloned the apa gene (Rv1860) under the control of the PtipA promoter in the integrative vector pRT802 and introduced the resulting plasmid (pBL1, Table 1) into the wild-type (J1928) and Δppm (IB31) strains. The Apa protein obtained from supernatants of J1928 carrying the cloned apa gene (in pBL1) could be seen as a clear band in Western blots, both when detection was based on a monoclonal antibody (Fig. 1b, lane 1) and when it was based on reaction to the ConA lectin (Fig. 1c, lane 1), meaning that S. coelicolor is able to express, secrete, and glycosylate the Apa protein, as has been previously shown for S. lividans; in contrast to S. lividans, the Apa protein secreted by S. coelicolor was subject to some degradation, as revealed by the presence of a faint faster migrating band not observed in S. lividans (Lara et al., 2004).

, 2010). Random DNA fragments

were generated with RsaI, ligated into SmaI digested cloning vector pBluescript SK and transformed in Escherichia coli XL1-blue (Stratagene) with electroporation according to the manufacturer’s instructions (Bio-Rad micropulser). The positive clones were sequenced by capillary sequencer; these DNA fragments served as the initial templates for the genome walking. Overlapping sequencing reactions (141 reactions using Life Tech’s Genetic Analyzer 3500) were used to cover the whole phage DNA, the mean usable read length was 861 bases, so that each nucleotide of the 40 058 bp phage DNA was covered on the average 3.03 times (each nucleotide was covered selleck chemicals llc Ixazomib in vitro at least by two capillary sequencing reads). NGS data (2 827 891 reads with a mean read length of 45.15 bases, altogether 127 685 564 bases) were used to correct the possible sequencing errors of the sequence backbone revealed by capillary sequencing method. The average coverage of each nucleotide by SOLiD reads was 3187. CLC Genomics Workbench software (CLC Bio, Aarhus, Denmark) was used to generate contigs and

to assemble NGS and capillary sequencing data. GenBank accession number: JN991020. ORFs were assigned using the ORF finder programs RAST (Aziz et al., 2008; http://rast.nmpdr.org/ ), Glimmer (http://www.ncbi.nlm.nih.gov/genomes/MICROBES/glimmer_3.cgi), NCBI ORF finder (http://www.ncbi.nlm.nih.gov/projects/gorf/), and GeneMark (Lukashin & Borodovsky, 1998, http://exon.biology.gatech.edu/). Reverse transcriptase Translated sequences identified by ORF finders were further analyzed by homology searching using NCBI blastp (Altschul et al., 1997). Molecular masses, isoelectric points, and codon statistics

were calculated using CLC Genomics Workbench. For the comparative genomic studies, we screened for sequence homologies with NCBI blastx (Altschul et al., 1997) against the Entrez Query ‘Viruses (ORGN)’ databases to looking for potential relationships as recommended by Lavigne et al., 2003. To confirm the resulted relations, we used CoreGenes 3.1 program to create pairwise comparisons, using default stringency setting (‘75’) at http://binf.gmu.edu:8080/coreGenes3.1/. Sixteen broad host range bacteriophages against P. tolaasii LMG 2342T and P. putida DSM 9278 were obtained after the repeated isolation cycles. The results of the spot lysis assay against different pseudomonads are summarized in Table 2. The most effective phages were Bf3 and Bf7, which infected 16 strains of the treated pseudomonads, but Bf10 and Bf16 had also remarkable abilities (infecting 15 and 13 strains, respectively). The nucleic acid of the phages proved to be DNA as they were susceptible to deoxyribonuclease but not to ribonuclease digestions. The genome sizes were approximately 38 kb based on restriction enzyme digestion experiments.

Typhi to produce a systemic infection in humans. sopD2 gene corresponds to an SPI-2-regulated effector protein (Brumell et al., 2003). In S. Typhi this gene carries a nucleotide deletion that produced a nonsense mutation and probably Protein Tyrosine Kinase inhibitor the loss of an essential protein translocation motif [WEK(I/M)xxFF; data not shown] (Brumell et al., 2003; Brown et al., 2006). Our results confirm that sopD2 in S. Typhi is a pseudogene supporting previous studies of Salmonella spp. comparative genomics (Parkhill et al., 2001; McClelland et al., 2004). The SPI-1 encodes T3SS effectors that mediate the invasion by Salmonella of nonphagocytic cells via cellular host cytoskeleton manipulation (Bueno et al., 2010). SPI-2

is induced after bacterial internalization and is essential for bacterial survival and proliferation within SCV. In addition, intracellular Salmonella interferes with the actin cytoskeleton in an SPI-1 T3SS-independent manner and in SPI-1-dependent effectors contributing to the SCV establishment (Abrahams & Hensel, 2006; Bakowski et al., 2008). This has been described as a regulatory and functional SPI cross-talk (Knodler et al., 2002; Steele-Mortimer et al., 2002). It is therefore not surprising that although sopD2 in S. Typhimurium corresponds to a SPI-2-regulated

effector, PI3K Inhibitor Library it is also expressed under SPI-1 conditions and participates in epithelial cell invasion (Brumell et al., 2003). The previous observation is supported by S. Typhimurium ΔsopD2∷FRT null mutant strain (NT060), which Flucloronide showed a decreased invasion level in HEp-2 human epithelial cell line. In S. Typhimurium, SCV synthesis depends on SopD2 and the sopD2 gene mutation decreases intracellular proliferation and bacterial virulence in mice (Jiang et al., 2004; Birmingham et al., 2005). However, the presence of a fully functional sopD2 gene interferes with

S. Typhi proliferation within human epithelial cells and the bacterial capacity to alter cellular permeability. Because S. Typhimurium SopD2 participates in the endosome (SCV) synthesis and concomitantly in the generation of Sif structures (Brumell et al., 2003; Jiang et al., 2004; Birmingham et al., 2005), we suggest that SopD2STM in S. Typhi interferes directly in the intracellular traffic of this pathogen in epithelial cells. Our previous studies showed that this permeability alteration is directly related to cytotoxicity (Trombert et al., 2010). In this work, we observed that the functional transfer of sopD2 from S. Typhimurium to S. Typhi decreased cellular permeability and more likely decreased cytotoxicity. It has been observed that S. Typhi increases cytotoxicity within the host by inactivating or acquiring new genes (Oscarsson et al., 2002; Fuentes et al., 2008; Faucher et al., 2009; Trombert et al., 2010). Thus, the inactivation of some genes (i.e. sopD2) and the acquisition of others could contribute to cytotoxicity toward the epithelial barrier and might ensure the development of systemic infection in the human host.

The results showed that the pathogen was a new Scytalidium species, here named Scytalidium auriculariicola. Scytalidium auriculariicola was characterized by its rapid growth rate, the catenate conidia of variable size, and the pale brown to brown chlamydoconidia. Phylogenetic analyses based on internal transcribed spacer regions and RPB2 sequences on the pathogen isolated and related species supported that S. auriculariicola was a true Scytalidium species. It was congeneric with and close to Scytalidium lignicola, the type species of Scytalidium.

However, it differed from the latter species in the size of conidia, 33 different nucleotide bases in ITS sequences and 30 different nucleotide bases in RPB2 sequences. “
“In Saccharomyces EPZ015666 chemical structure cerevisiae,Nce102 encodes a 173 amino acid transmembrane protein, which acts as a key player in eisosome assembly and plasma membrane organization. Here, we check details describe the characterization of Nce102 homologue in the human pathogen, Aspergillus fumigatus. Our results demonstrated that AfuNce102 is continuously expressed during fungal growth. In addition, microscopic examination of an AfuNce102-GFP-expressing

transformant confirmed the localization of the fusion protein to the endoplasmic reticulum with higher density fluorescence at the tip of the mycelium. During conidiogenesis, the protein was localized to the conidiophores and the conidia. Abnormal conidiation of AfuNce102 deletion mutant suggests a potential role for AfuNce102 in sporulation process. A nonclassical export pathway has been proposed in yeast as an alternative route for the secretion

of proteins lacking signal sequence (Cleves et al., 1996; Nombela et al., 2006). Based on a screen for gene products involved in this nonclassical export pathway, three genes, Nce101, Nce102, and Nce103, have been identified as being involved Methane monooxygenase in protein secretion (Cleves et al., 1996). In Saccharomyces cerevisiae, Nce102 encodes a 173 amino acid peptide containing four transmembrane domains. Early functional studies on Nce102 demonstrated that the deletion of this gene can severely disrupt the nonclassical secretion of heterologous mammalian galectin-1. This observation has led to a hypothesis that Nce102-related nonclassical export pathway may be involved in the transport of virulence factors to the cell surface of pathogenic microorganisms (Nombela et al., 2006). The yeast deletion mutant of Nce102 was also found to be more sensitive to diethylmaleate toxicity, suggesting a possible role for Nce102 in protection of the cell against oxidative stress (Desmyter et al., 2007). Recently, a genome-wide screen in yeast has identified the Nce102 as a key player in plasma membrane organization (Frohlich et al., 2009). In yeast, the plasma membrane is highly organized and laterally divided into two overlapping compartments, membrane compartment of Can1 (MCC) and membrane compartment of Pma1 (MCP).

In particular, a study conducted in our cohort in the early era of HAART [13] showed that intolerance/toxicity was the main reason for discontinuing first-line HAART in the first year. Treatment strategies have evolved dramatically over recent years, and data are lacking regarding the possible impact of the use of currently recommended regimens in first-line therapy on

the incidence of, and reasons for, drug discontinuation. Therefore, the aim of our analysis was to investigate whether the incidence of first-line treatment discontinuations and their causes have changed according to the year of starting HAART. The study population was drawn from that of the Italian COhort Naïve Antiretrovirals (ICoNA) Foundation LDK378 supplier Study, a multicentre buy PD-0332991 prospective observational study of HIV-1-positive persons which began in 1997 with the aim of following the enrolled patients for a minimum of 10 years. Recently it has been agreed to re-open enrolment and to extend the follow-up of existing patients to a minimum of 10 additional years. Patients eligible for inclusion in the cohort

are those who, for whatever reason, are naïve to antiretrovirals at the time of enrolment regardless of the stage of the disease. Demographic, clinical and laboratory data and information on therapy are collected for all participants and recorded online [http://www.icona.org]. All data are updated at the occurrence of any clinical event and, otherwise, at least every 6 months. When a patient discontinues a drug in 3-mercaptopyruvate sulfurtransferase the antiretroviral regimen, regardless of whether or not he/she switches to another regimen, clinicians are asked to report the reason

for discontinuation. A coded computer form is provided in which reasons for discontinuation are categorized as follows: clinical contraindication, immunological failure, virological failure, clinical failure, gastrointestinal intolerance, hypersensitivity, lipodystrophy, nervous central system symptoms, other side effects/symptoms, toxicity based on laboratory data (haematological, renal, hepatic, glucose/lipid metabolism or other), presumed cardiovascular toxicity, poor compliance, patient’s decision, simplification in the case of undetectable HIV plasma viraemia, change of drug formulation, changes in international guidelines, therapy discontinuation after clinician’s decision, therapy discontinuation after patient’s decision, and ‘other reasons’. The clinician is asked to choose only one of these reasons for each drug stopped. Patients included in this analysis were those who started HAART (>2 drugs) when ART-naïve before 1 January 2007, and who underwent at least one follow-up clinical visit after starting therapy.

0004). Comparison of mean healing time in the pimecrolimus versus placebo group, demonstrated a significant acceleration

both in intention-to-treat analysis (10.7 vs. 20.7 days, F = 17.466, P < 0.0001) and treatment-completed analysis (8.3 vs. 20.7 days, F = 29.289, P < 0.0001). Conclusion:  Pimecrolimus is safe and efficient in the treatment of BD genital ulcers, by accelerating the healing process. "
“Systemic lupus erythematosus (SLE) is an autoimmune disease in which organs undergo damage. Hypoparathyroidism IDO inhibitor is a rare disease, which presents in two forms: hereditary and acquired. Cases of hypoparathyroidism and SLE rarely co-exist. Only six cases have been reported; five of them first presented with lupus and then hypoparathyroidism or simultaneously. We present here developing lupus disease in a woman who had idiopathic hypoparathyroidism. Vorinostat research buy According to increasing data about the autoimmune origin of idiopathic hypoparathyroidism, these case reports suggest that there may be an autoimmune process linking these diseases. “
“Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with unknown etiology. Genetic and environmental factors play important roles in the pathogenesis of SLE. The primary objective of this study was to investigate the possible association of eNOS gene intron 4b/a, Glu298Asp and T-786C polymorphisms with SLE in southeast Iran populations. This was a case-control study comparing eNOS polymorphisms in 106 SLE patients

and 196 age- and sex-matched healthy controls. The 4b/a, Glu298Asp and T-786C polymorphisms were analyzed using polymerase chain reaction and restriction fragment length polymorphism.

Our findings indicated that the 4b/a polymorphism was associated with SLE, and the risk of SLE was 3.5- and 1.75-fold higher in patients with aa and ba genotypes than in patients with bb genotype. No association was observed between Glu298Asp and T-786C polymorphisms and SLE. There were no differences in eNOS gene polymorphisms between the Balouch and Fars population. Statistically significant differences were observed in genotypes and allele frequencies of 4b/a polymorphism between patients with SLE and healthy controls in southeast Iran. “
“Behcet’s disease Thymidine kinase (BD) is a rare disease mostly seen along the Silk Road. The prevalence has been reported as 0.12 (USA) to 370 (in a single village, northern Turkey) for 100 000 inhabitants.[1] During the past four decades, due to immigrations, the prevalence in Europe and North America has gradually increased.[2] It is now 4.2 in Germany, 7.2 in France and 8.6 in the US. Behcet’s disease is classified among the vasculitides and the pathophysiology is thought to be autoimmune, although some propose it as an autoinflammatory disease. Human leukocyte antigen (HLA)-B51 is recognized as a genetic factor. Hyperfunction of neutrophils, reactive oxygen species production, T-cell abnormalities, heat shock proteins (microbial and viral) are all involved in the ethiopathogenesis.

In this study, we found that under oxidative stress, antioxidant gene expression is also partially impaired in the Δskn7 mutant but to a milder extent than in the Δchap1 mutant, whereas in the double mutant – Δchap1-Δskn7 – none of the tested selleck inhibitor genes was induced, with the exception of one catalase gene, CAT2. Both single mutants are capable of infecting the plant, showing similar virulence to the WT. The double mutant, however, showed clearly decreased virulence, pointing

to additive contributions of ChAP1 and Skn7. Possible mechanisms are discussed, including additive regulation of gene expression by oxidative stress. Histidine kinase-based phosphorelays are widespread in prokaryotes and are also found in lower eukaryotes and in plants (Wuichet et al., 2010). Some of these two-component signaling systems have important roles in stress responses. Histidine kinases respond to specific signals and are activated by autophosphorylation of a conserved histidine residue; after a cascade of phosphotransfers from His-to-Asp, the phosphoryl group is transferred to a conserved aspartate residue in the receiver domain of a response regulator. The details were worked out first for the osmotic stress response in Saccharomyces cerevisiae (Fassler & West, 2011). In budding

yeast, three phosphotransfers follow activation of the membrane-localized histidine kinase Sln1: First, the conserved sensor domain histidine is phosphorylated in response to the stress signal; the phosphate is transferred to an aspartate residue, then to the phosphorelay protein Ypd1, and finally from FG-4592 manufacturer Ypd1 to either of two downstream response regulators, Ssk1 or Skn7. The response regulators’ phosphorylation levels control their activity. Osmotic stress decreases Sln1 phosphorylation, decreasing the phosphorylation of the phosphorelay Ypd1 and consequently of Ssk1. Dephosphorylation of Ssk1 allows activation of Hog1. The other branch of the pathway downstream of Sln1 is mediated by Skn7,

a highly conserved, stress-responsive transcription factor whose ZD1839 manufacturer activity depends on osmotic, cell wall and oxidative stresses. The mechanism by which Skn7 responds to these stresses is different. In response to cell wall stress, Skn7 is phosphorylated, again via Ypd1, on the conserved aspartate residue, D427, while hyperosmotic stress has the opposite effect, dephosphorylating Skn7 (Fassler & West, 2011). The Skn7 response to oxidative stress is independent of the Sln1 pathway, however. In budding yeast, Skn7 cooperates with the redox-sensitive transcription factor Yap1. Phosphorylation on the D427 residue of Skn7 is not absolutely necessary for Yap1 recruitment; rather, phosphorylation on threonine 437 is required for stabilization of the Skn7-Yap1 complex (He et al., 2009; Fassler & West, 2011).

, 2000), adenylate kinase 2 of L. donovani (Villa et al., 2003), cysteine protease type A and B (CPA and CPB) genes of L. infantum (Rafati et al., 2003). In practice, it is usually worthwhile to test several different vector/host combinations to obtain the best possible yield of protein in its desired form. Hence,

a number of commercially available strains of E. coli host cells and expression vectors were tested in an attempt to produce LdSSN in the soluble form. Screening of experimental conditions were carried out to obtain high yields of recombinant protein, including growth temperature, medium type and hours of growth after IPTG induction. For maximum overexpression of SSN protein in the soluble fraction, various parameters were standardized viz. E. coli host strains, IPTG concentrations, incubation temperatures before and after induction SP600125 purchase and incubation period after induction. Because the pET-28a-SSN recombinant vector has T7 promoter, various hosts compatible with T7 promoter viz. BL21 (DE3), Rosetta and codon plus cells were attempted for the expression of soluble SSN protein. The maximum solubility of SSN protein was found in BL21 (DE3)

cells as compared with Rosetta and codon plus cells; therefore, further expression of recombinant SSN protein was carried out in BL21 (DE3) cells. IPTG concentrations varying from 0.1 to 1 mM were attempted BMN 673 mw so as to observe the amount of expressed SSN protein. However, no difference in the amount of expressed protein was observed with the above used concentrations. 0.1 mM IPTG concentration the was used for protein induction and overexpression

studies. Addition of >0.1 mM IPTG to the cultures did not lead to further increase in the amount of overexpressed recombinant LdSSN. The level of expression of recombinant LdSSN was tested under various temperatures ranging from 20 to 37 °C. At temperatures 37, 30 and 28 °C, the recombinant SSN protein was expressed at a significant level, but all the expressed protein appeared as inclusion bodies. Reducing the temperature to 20 °C resulted in the expression of the recombinant protein in a soluble form; however, below 20 °C, the solubility of the protein was increased but the total amount of expressed SSN protein was also decreased, and therefore, in further studies, BL21 (DE3) cells were induced at 20 °C with 0.1 mM IPTG. The induction time was varied from 6 to 12 h. The amount of recombinant soluble SSN protein was increased from 6 to 12 h; therefore, in further studies, the induction time was extended to 12 h to obtain the maximum amount of soluble protein. The best suitable parameters selected resulted in nearly 30% of the recombinant protein in the soluble fraction, whereas most of the protein was found in inclusion bodies.

The mean age was 43.2 years, the mean nadir CD4 count Selleckchem Olaparib was 200 cells/μL, and the mean duration of HIV infection from the time of diagnosis was 9 years. Only 21.5% of our patients were classified as MSM by self-report. The proportion of underlying medical comorbidities was similar in both groups, with the exception of hepatitis B virus coinfection which was twice as prevalent among our cases as among our controls (Table 1). Univariate logistic regression identified several variables

associated with MRSA colonization or infection (Table 2); however, after multivariate analysis only a nadir CD4 count <200 cells/μL and prior antibiotic exposure were independent risks for MRSA colonization or infection. Use of ART within the previous year conferred a protective effect, significantly decreasing the risk of MRSA colonization or infection among selleckchem our patient population (Table 2). Eighty-four per cent of control patients were on ART within the previous year, compared with only 50% of case patients. The protective effect of ART was seen regardless of whether patients were receiving protease inhibitors (PIs) or nonnucleoside reverse transcriptase inhibitors (NNRTIs). Sixty-four (89%) of 72 patients with MRSA colonization or infection

had isolates available for PFGE strain typing. Forty-nine (77%) of these isolates were USA-300 CA-MRSA strains. Of our 60 patients with MRSA infection, 48 (80%) were infected with a USA-300 CA-MRSA strain. Univariate analysis identified SSTI as the only variable associated with having MRSA colonization or infection with USA-300 CA-MRSA. Of note, the presence of a dermatological disorder was negatively associated with having MRSA colonization or infection with the USA-300 strain. Following multivariate IMP dehydrogenase analysis, each of these variables retained independent statistical significance

[odds ratio (OR) 5.9; 95% confidence interval (CI) 1.4–24.3; P=0.01; OR 0.19; 95% CI 0.05–0.75; P=0.02, respectively]. Antibiotic susceptibilities were reported for 55 (85%) of the infecting MRSA isolates. Eight of these isolates were multidrug resistant, which we defined as resistance to two or more antibiotic classes other than beta-lactams. Only one isolate was resistant to trimethoprim-sulfamethoxazole and this was a non-USA-300 MRSA strain. There were no significant differences between the antibiotic susceptibilities of USA-300 CA-MRSA strains and non-USA-300 MRSA strains. Of the eight multidrug-resistant strains, five were USA-300 and all of these were associated with SSTI. A measurable proportion of our HIV-infected patients were MRSA colonized or infected, usually with USA-300. Reported rates of MRSA colonization among HIV-infected patients have varied from 1.6% to 34.8% in previous studies [11–13].