ZDV was discontinued because of either anaemia or neutropenia in seven patients. In four subjects with renal toxicity, TDF was substituted with ABC, and in one case of lactic acidosis all NRTIs including TDF were discontinued. LPV/r was not discontinued because of toxicity in any patient. Among patients initiating treatment, 55% reported never missing a dose throughout the study period. Likewise, 55% of patients never missed a clinic visit but 29% of patients missed one visit, 11% missed two visits, and 5% missed three visits. Among survivors, the median increase in CD4 count was 142 cells/μL (IQR 66, 263)

at 12 months and 85% of these patients H 89 cell line had HIV-1 RNA<400 copies/mL at 12 months (Fig. 3). Overall, 75% of the 101 patients who started second-line therapy survived and were suppressed (Fig. 3). Of the 13 patients who had HIV-1 RNA>400 copies/mL buy Alectinib at month 12, six were never suppressed and seven had initial suppression but rebounded. On treatment, the HIV-1 RNA suppression rate for patients with wild-type virus was 60% [95% confidence interval (CI) 15–95%]

compared with 94% (95% CI 87–100%) for patients with any TAMs and 95% (95% CI 85–100%) for those with at least three TAMs. HIV-1 RNA suppression rates varied according to the number of active NRTI drugs: at least two active drugs (low), 71% (95% CI 50–93%); one active drug (medium), 92% (95% CI 85–100%); and no active drugs (high), 97% (95% CI 77–100%). Adherence rates (never missed doses) were 48% for those with at least two active

drugs (low), 59% for those with one active drug (medium), and 56% for those with no active drugs (high) (P=0.7), which corresponded to HIV-1 RNA suppression rates of 90% for those with at least two active drugs (low), 96% for those with one active drug (medium), and 89% for those with no active drugs (high) (P=0.6). Among patients who ever missed doses, HIV-1 RNA suppression rates were 55% for those with at least two active drugs (low), 84% for those with one active drug (medium), and 85% for those DNA ligase with no active drugs (high) (P=0.15). Factors associated with HIV-1 RNA>400 copies/mL at 12 months on univariate analysis included having a presenting CD4 count <50 cells/μL and HIV-1 RNA>100 000 copies/mL (Table 3). Paradoxically, having extensive baseline resistance resulted in better virological suppression (Table 3). However, on multivariate analysis, only poor adherence (ever missing a dose) remained statistically significant. Duration on first-line treatment >3 years was not associated with increased risk of failure. In our cohort of ART failure patients identified by clinical and immunological criteria in the public health setting who were confirmed to have virological failure, there is substantial early mortality on second-line ART. Identification of failure by clinical criteria, in particular, was associated with an increased risk of death in the first 6 months as well as new and progressive HIV-associated illnesses.

The ICQ values of the WGA/eGFP-PilACt staining pairs were 0.23 ± 0.06 (mean ± SD) in fruiting bodies, 0.21 ± 0.05 in trail structures and 0.14 ± 0.03 in biofilms, all of which were in the range of 0–0.5 for dependent staining (Li et al., 2004) and significantly different from 0 (random staining, Student’s t-test P < 0.01). Strain SW504 (ΔdifA) is defective in EPS production Tacrolimus in vivo due to a mutation in an EPS regulatory gene (Yang et al., 1998) and was used as an

negative control in our EPS-labeling assay. As SW504 lacks the ability to form starvation biofilms or fruiting bodies, its cell pellets were directly collected from liquid culture and counterstained selleck with Alexa 633-WGA and eGFP-PilACt. Both WGA and eGFP-PilACt failed to stain the cell pellets of SW504 (Fig. 3b). These results demonstrated that eGFP-PilACt specifically labels the EPS structures under native conditions in both fruiting bodies and biofilms. Consistent with the EPS precipitation results (Fig. 2), eGFP alone did not significantly label EPS structures in submerged biofilms and fruiting bodies formed by DK1622 (Fig. 3c) compared with eGFP-PilACt (Fig. 3a). This confirms that the PilACt domain is responsible for the EPS recognition and binding ability of the fusion protein. Thus,

the similarities between patterns of eGFP-PilACt Tolmetin and WGA binding are indicative of direct PilACt binding to the native EPS in biofilms, trails and fruiting bodies. Interestingly, when an elevated amount of WGA (1.5 μM) was added

to the fruiting bodies and biofilms pre-labeled with eGFP-PilACt, the green signals from eGFP-PilACt were reduced and dispersed (Fig. 3c). This result suggested a possible competition between eGFP-PilACt and WGA in binding with EPS. The lectin WGA selectively recognizes N-acetyl-glucosaminyl sugar residues (Wright, 1984); the sugar is one of the carbohydrates identified in the M. xanthus EPS (Behmlander & Dworkin, 1994; Li et al., 2003). Previous findings also showed that GlcNAc blocks TFP retraction and chitin (polymer of GlcNAc) triggers TFP retraction (Li et al., 2003). Therefore, it would appear that PilA of M. xanthus recognizes the GlcNAc moiety in M. xanthus EPS. Type IV pili and EPS are both important cell surface components for many pathogenic and nonpathogenic microbial organisms (Wall & Kaiser, 1999; Sutherland, 2001) and their interactions play pivotal roles in many of biological processes, e.g. motility, development and pathogenesis (Sheth et al., 1994; Li et al., 2003). In M. xanthus, the co-precipitation of sheared pili/pilin and EPS, as well as the triggering of TFP retraction by isolated EPS, indicate specific interactions between these two cell surface components (Li et al., 2003).

Enzyme reactions were confirmed by monitoring the formation of products as well as the disappearance of reactants via HPLC by incubating the activity bands with the appropriate reaction mixtures. GDH expression was determined utilizing the method described in Mailloux et al. (2009a, b). Briefly, the protein samples were solubilized in 62.5 mM Tris-HCl (pH 6.8), 2% SDS, and 2%β-mercaptoethanol at 100 °C for 5 min. Following solubilization, the protein samples were then loaded into a 10% isocratic gel and electrophoresed using a discontinuous buffer system. 5-FU mw Following electrophoresis, the proteins were transferred electrophoretically to

a Hybond™- polyvinylidene difluoride membrane for immunoblotting. Nonspecific binding sites were blocked by treating the membrane with 5% nonfat skim milk dissolved in TTBS [20 mM Tris-HCl, 0.8% NaCl, and 1% Tween-20 (pH 7.6)] for 1 h. Polyclonal antibodies for GDH were obtained from Abcam. The secondary TGF-beta inhibitor antibodies (Li-Cor, Lincoln, NE) consisted of infrared 700 nm tagged goat anti-rabbit. Visualization of the immunoblot was documented using an Odyssey infrared imaging system (Li-Cor). The H2O2-mediated

regulation of KGDH, GDH, and ICDH was studied as follows: 10 mg of protein equivalent of H2O2-treated cells were transferred into the control (without H2O2) medium and a 10 mg protein equivalent of control cells were incubated in a 100/500 μM H2O2-containing medium. Following a 4–8-h incubation period, the cells were isolated and fractionated as described previously to determine enzymatic activities and/or expression. For a proper comparison, control cells (24 h) and H2O2-treated cells (28 h) in a similar growth phase were utilized to inoculate the different media, respectively. Two milligrams of protein equivalent of CFE from control and stressed cells were placed in a reaction SPTBN5 mixture consisting

of 5 mM histidine and 5 mM citrate, in the presence or absence of 5 mM fluorocitrate, an inhibitor of aconitase, in a phosphate buffer (Nasser et al., 2006). After 30 min, the reaction was halted by placing the mixture at 100 °C for 10 min. The reaction mixture was then subjected to HPLC analysis to monitor the production of KG. Data were expressed as means±SDs. Statistical correlations of data were checked for significance using the Student’s t-test (P≤0.05). All experiments were performed at least twice and in triplicate. While both citrate and histidine were utilized readily by the microorganism, it appeared that in the stationary phase of growth, nearly the entire amino acid was consumed (Fig. 1). The biomass yield was relatively similar in these two situations, with the H2O2-stressed bacteria attaining the stationary phase of growth at a slightly later time. Metabolomic analyses of the CFEs revealed that the H2O2-stressed cells contained significantly more KG and succinate (Fig. 2).

Expression levels of popA-lacZYA in the RSc2168 (RK5363) and RSc2167 (RK5366) deletion mutants were 260 and 281 Miller units, respectively, which was not different from the levels in BIBW2992 the wild type (RK5050, Table 2). These results indicate that these two genes do not function

in the regulation of hrp regulon. While the OE1-1 strain is pathogenic to tobacco, the Japanese isolate RS1002 (Mukaihara et al., 2004) is nonpathogenic to tobacco. Instead, it elicits a hypersensitive response (HR). We monitored the expression levels of popA operon in popA-lacZYA fusion strains of RS1002; RK10001 and the three deletion mutants of prhK, prhL, and prhM genes (Table 2). popA expression was reduced to an almost basal level in all three mutants, as was observed in the OE1-1 strain. This demonstrates that the functions of PrhK, PrhL, and PrhM are not strain-specific. Many genome-wide screens for pathogenesis-related genes in R. solanacearum have been performed, both experimentally and in silico. Examples of techniques used are transposon mutagenesis (Boucher et al., 1987; Lin et al., 2008), transposon-based screening of hrpB-dependent genes (Mukaihara et al., 2004), and in silico analysis of

secreted proteins via the twin-arginine translocation system (Gonzalez et al., 2007). These analyses Natural Product Library molecular weight have identified T3SS-related hrp and effector genes, genes for type II secretion system (T2SS), flagellar and motility genes, pilus genes, and genes for biosynthesis of exopolysaccharide. Most of these genes are pathogen-specific. Although none of the screens reached saturation, some genes were identified as virulence determinants in multiple independent screenings. It Bay 11-7085 is interesting that these three pathogenesis-related genes had not been identified, despite this long screening history. Because HrpB controls the hrp regulon (Genin et al., 1992), we examined the influence of prhK, prhL, and prhM on the expression of hrpB. We constructed deletion mutants in RK5046 (hrpB-lacZYA), which resulted in RK5206 (ΔprhK),

RK5210 (ΔprhL), and RK5255 (ΔprhM). In sucrose medium, the expression levels of hrpB were substantially reduced in the prhK, prhL, and prhM deletion mutants (Table 2). These data demonstrate that prhK, prhL, and prhM are necessary for the expression of hrpB. Expression of hrpB is activated by HrpG and PrhG (Brito et al., 1999; Plener et al., 2010). We examined the involvement of prhK, prhL, and prhM in the regulation of hrpB expression by hrpG and by prhG. We constructed deletion mutants of RK5120 (hrpG-lacZYA), which resulted in RK5264 (ΔprhK), RK5260 (ΔprhL), and RK5256 (ΔprhM), and of RK5212 (prhG-lacZYA), which resulted in RK5281 (ΔprhK), RK5262 (ΔprhL), and RK5258 (ΔprhM). Their expression levels were determined in sucrose medium.

Expression levels of popA-lacZYA in the RSc2168 (RK5363) and RSc2167 (RK5366) deletion mutants were 260 and 281 Miller units, respectively, which was not different from the levels in Rapamycin the wild type (RK5050, Table 2). These results indicate that these two genes do not function

in the regulation of hrp regulon. While the OE1-1 strain is pathogenic to tobacco, the Japanese isolate RS1002 (Mukaihara et al., 2004) is nonpathogenic to tobacco. Instead, it elicits a hypersensitive response (HR). We monitored the expression levels of popA operon in popA-lacZYA fusion strains of RS1002; RK10001 and the three deletion mutants of prhK, prhL, and prhM genes (Table 2). popA expression was reduced to an almost basal level in all three mutants, as was observed in the OE1-1 strain. This demonstrates that the functions of PrhK, PrhL, and PrhM are not strain-specific. Many genome-wide screens for pathogenesis-related genes in R. solanacearum have been performed, both experimentally and in silico. Examples of techniques used are transposon mutagenesis (Boucher et al., 1987; Lin et al., 2008), transposon-based screening of hrpB-dependent genes (Mukaihara et al., 2004), and in silico analysis of

secreted proteins via the twin-arginine translocation system (Gonzalez et al., 2007). These analyses Alectinib molecular weight have identified T3SS-related hrp and effector genes, genes for type II secretion system (T2SS), flagellar and motility genes, pilus genes, and genes for biosynthesis of exopolysaccharide. Most of these genes are pathogen-specific. Although none of the screens reached saturation, some genes were identified as virulence determinants in multiple independent screenings. It BCKDHB is interesting that these three pathogenesis-related genes had not been identified, despite this long screening history. Because HrpB controls the hrp regulon (Genin et al., 1992), we examined the influence of prhK, prhL, and prhM on the expression of hrpB. We constructed deletion mutants in RK5046 (hrpB-lacZYA), which resulted in RK5206 (ΔprhK),

RK5210 (ΔprhL), and RK5255 (ΔprhM). In sucrose medium, the expression levels of hrpB were substantially reduced in the prhK, prhL, and prhM deletion mutants (Table 2). These data demonstrate that prhK, prhL, and prhM are necessary for the expression of hrpB. Expression of hrpB is activated by HrpG and PrhG (Brito et al., 1999; Plener et al., 2010). We examined the involvement of prhK, prhL, and prhM in the regulation of hrpB expression by hrpG and by prhG. We constructed deletion mutants of RK5120 (hrpG-lacZYA), which resulted in RK5264 (ΔprhK), RK5260 (ΔprhL), and RK5256 (ΔprhM), and of RK5212 (prhG-lacZYA), which resulted in RK5281 (ΔprhK), RK5262 (ΔprhL), and RK5258 (ΔprhM). Their expression levels were determined in sucrose medium.

Participants also covered a range of pharmacy roles including medicines counter assistants (MCAs) (n = 9), dispensing assistants (n = 6) and pharmacy technicians (n = 6). National multiple (n = 8), small chain (n = 2) and independently owned (n = 2) pharmacies were represented. Participants were recruited by contacting pharmacists in HLPs who nominated support staff for potential participation. Informed consent was obtained prior to conducting interviews. A topic guide was developed and underwent

face validity testing and piloting with one participant. Interviews were audio recorded, transcribed verbatim and analysed using Framework approach. The study was approved Cabozantinib solubility dmso by Robert Gordon University ethics committee. NHS ethics approval was not required. One of the themes identified from the data was integration

of public health activity into traditional pharmacy roles. Participants discussing integration GSK-3 activity of public health activities with other pharmacy duties included examples of advice when conducting product sales and responding to symptoms. An example participants often referred to was sales of nicotine replacement therapy: “…say if it’s somebody [who came in to buy] nicotine replacement therapy, we would say that there are services available, had they thought about giving up. And it’s just basically like a couple of lines like that.” HLP Champion, MCA you don’t realise that you are doing it. Because it’s all part and parcel of the job.” HLP Champion, MCA Whilst participants in this study described integration of public health advice for some pharmacy roles seamlessly, participants were less able to describe integration into dispensing activity despite opportunity in areas such as diabetes and cardiovascular health. Contextualisation of public health activity within community pharmacies for support staff could MTMR9 enable further integration of public health into the role of community pharmacy. Facilitators from achieving this

integration for medicines counter activities should be explored to inform better integration of public health into dispensary based activities. 1. Department of Health 2010 White Paper Healthy Lives Healthy People. Available at: https://www.gov.uk/government/publications/healthy-lives-healthy-people-our-strategy-for-public-health-in-england (Accessed 13/04/14) C. Easthalla,b, N. Taylorc, D. Bhattacharyab aUniversity of Leeds, Leeds, West Yorkshire, UK, bUniversity of East Anglia, Norwich, Norfolk, UK, cUniversity of New South Wales, Sydney, New South Wales, Australia Recent guidelines have called for adherence interventions to be grounded in theory; the Theoretical Domains Framework (TDF) is proposed as a ‘user-friendly’ collation of psychological theories related to the determinants of health behaviours.

1). Streptococcus suis WcgA proteins are similar to the BpOF4_06575 protein predicted to be UDP-galactose phosphate transferase (71% identity) of Bacillus pseudofirmus OF4 (accession number: NC_013791). The initial sugar of the repeat unit is also the donor sugar in the polymerization of the repeat units. The specificity of the Wzy polymerase determines the other component of the CPS linkage (Bentley et al., 2006). The Wzy polymerase is quite different in the 15 serotypes. There are five polymerase HGs associated with WchA, two with WciI, 5 with WcaJ and one with WcgA (Table 1). These associations

are mostly exclusive, with only one polymerase HG (HG39) associated with two HGs of initial transferases. In such cases, the linkages may involve the same acceptor sugar anomerism (α or β isomer) and the same or closely related donor sugar. Wzx flippase can transport the repeat unit across the cytoplasmic membrane after CPS polymerization. Rapamycin chemical structure Except for serotype 16, only one wzx gene is located in the S. suis cps locus. Two wzx genes (cps16N and cps16R) exist in the cps16 locus. cps16O is similar to transposase gene (83% identity) of

Streptococcus mutans at the nucleic acid level. cps16N may be inactivated in the transposition-like events caused by Cps16O transposase. In the serotype 1, 2, 14, 16 and 1/2 cps locus, all the flippases belong to HG7. Each Wzx protein may transport polysaccharides selleck compound with a similar composition and/or structure (Liu et al., 1996). The composition and/or structure were predicted to be similar in the five serotypes. GTs are important enzymes that catalyze the attachment of sugars (donor) to an aglycone (acceptor) in CPS synthesis.

Ignoring initial glycosylphosphotransferase, GTs in all 15 cps loci fall into 38 HGs. Two to seven GTs exist in each cps locus (Table 1). The predicted function of each GT HG is listed in Table S1. A putative GT enhancer (wchJ) is located in serotype 1, 14, 16 and 25. The mechanism and substrate of these enhancers are unknown. Aminotransferase genes are present in the serotype 3, 4, 5, 7, 19 and 23 cps loci. Amino-sugars are important this website components of some bacterial capsules (Hofmann et al., 1985; Beynon et al., 1990; Flahaut et al., 2008). Aminotransferases can transfer amino groups to sugars or form amino linked amidically to the carboxyl group (Beynon et al., 1990). We predicted that the CPS of serotypes 3, 4, 5, 7, 19 and 23 should be amino-sugar. Twelve different putative HGs of acetyltransferase, which play an important role in CPS structure determination (Calix & Nahm, 2010), are present in the 15 cps locus. Five genes (neuA, B, C, D and sialyltransferase) involved in sialic acid synthesis exist in the serotype 1, 2, 14, 16 and 1/2 cps loci. Because the identities of the genes involved in sialic acid synthesis between serotype 16 and 2 are very low (Wang et al.

The JIA patients recruited in this study had relatively low levels of disease activity. It could be postulated Dapagliflozin clinical trial that had patients with more active/severe disease been targeted, that the levels of maternal stress would have exceeded those seen in eczema and enteral feeding. The paper by Lederberg and Golbach[18] referenced in our paper regarding maternal stress in mothers of deaf children suggested mothers of deaf children do not feel a high level of parenting stress.

Stress levels were comparable to normative data. In this study they used another tool (Questionnaire on Resources and Stress [QRS-F]) to measure maternal stress in addition to PSI. By the QRS-F tool mothers of deaf children did express more stress. Most of the patients involved in the study had been enrolled in early intervention programs, which may have helped to reduce stress levels. Patients with JIA in the Australian setting are often not as well supported as those with deafness for which established structures of support are in place. The paper by Powers et al.,[19] which reported on parenting stress in young children check details with diabetes, looked more

specifically at parental stress in response to mealtime behavioral problems. In their paper the level of parental stress measured by PSI Total Stress score was higher in parents of diabetics (218.1) when compared to a control group (195.5) recruited in the study. Thus the Powers et al. paper did not use the established normative data for PSI Total Stress score, which others[14] and us have used as a comparator. In fact if we Idoxuridine were to use the lower 195.5 score rather than 222 it would further strengthen the findings of increased stress in the mothers of children with JIA and further highlights the need for intervention in parents of children with chronic illness, as it appears

to alleviate stress. The literature including Caning et al.[12] regarding outcomes of mothers of children with chronic disease generally agrees that disease severity is not related to psychological outcome. There was not a significant association between current disease activity and maternal stress levels in this study. The overall disease activity was not high with low mean active joint counts, CHAQ scores indicating mild disease activity and low mean physician global assessments. However, half of the patients were taking a disease-modifying anti-rheumatic drug (DMARD) and one-fifth a biologic DMARD, which would suggest that at some point in time the disease activity in at least some of the patients included had been greater. The low levels of disease activity seen in this study were not surprising. Current treatment practices for JIA and all the inflammatory arthritides in general aim for remission and even low levels of disease activity are not accepted. The mothers in this study were recruited at any stage of their child’s disease course.

, 2007), were upregulated in our microarray selleck study, including stx1A, stx1B, and stx2A. Shiga toxins have been shown to play a role in E. coli O157:H7 survival within grazing protozoa, and it has been postulated that the maintenance of shiga toxin genes is important for the protozoal-bacterial interaction and not the mammalian host interaction (Steinberg

& Levin, 2007). The role of the LEE-encoded Type III secretion system (T3SS) in the development of E. coli O157:H7 attaching and effacing lesions and translocation of effectors is well documented (Knutton et al., 1998; Roe et al., 2003; Tobe et al., 2006). Our microarray analysis indicated that genes that comprise part of the LEE-encoded T3SS (espAD, escF) on the transcript expADB-escF-Z5102-Z5104 were upregulated. This result was further confirmed by qRT-PCR analysis estimating the upregulation of espA to be 5.1-fold. A second T3SS described in E. coli O157:H7 (Ideses et al., 2005) that shares homology with

the Salmonella pathogenicity island 1 (eivCAEGF) was also upregulated. Two LEE-encoded and seven non-LEE-encoded T3SS translocated factor transcripts were upregulated. In summary, the analysis of transcript changes in E. coli O157:H7 during its interaction with A. castellanii show that E. coli upregulates genes involved in the response to various stressful environments including iron deprivation and oxidative stress. These results are purely based on transcript levels and www.selleckchem.com/products/17-AAG(Geldanamycin).html need to be confirmed at the protein level. The phenotype changes required for protozoa survival may also include changes in the surface architecture and the translocation of effector molecules by T3SS. Some virulence genes were also upregulated, which suggests that protozoa may serve as the environment that selects for and helps to maintain virulence genes that result in colonization and disease outbreaks in mammalian populations. We would like to thank Dr Greg Phillips for providing A. castellanii.

This study was funded in part by a contract to F.C.M. from the United States Department of Agriculture (Specific Cooperative Agreement 58-3625-2-127). Table S1. Differentially expressed genes of Escherichia coli O157:H7 within selleckchem Acanthamoeba. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“N-deoxyribosyltransferases are essential enzymes in the nucleotide salvage pathway of lactobacilli. They catalyze the exchange between the purine or pyrimidine bases of 2′-deoxyribonucleosides and free pyrimidine or purine bases. In general, N-deoxyribosyltransferases are referred to as cytoplasmic enzymes, although there is no experimental evidence for this subcellular localization.

When the monolayer is not disrupted, the recovered CFU mL−1 should remain essentially constant over the same

time course. The S. Typhimurium 14028s (black diamonds) and S. Typhimurium 14028s ΔsopD2∷FRT (NT060) (white circles) showed a slight decline over the time course of the assay, suggesting that the monolayer integrity was not significantly affected by these strains (Fig. 3). In contrast, CFU mL−1 of S. Typhi STH2370 abruptly decreased until they became undetectable, strongly suggesting that gentamicin leaked due to a monolayer disruption (white squares). When S. Typhi was complemented with sopD2STM gene (in the pNT007 plasmid, see Materials and methods) and used to infect the monolayer, we observed that the corresponding BKM120 order CFU mL−1 showed a sharp difference with the otherwise isogenic wild-type strain resembling the S. AZD1208 molecular weight Typhimurium phenotype (black triangles). The CFU mL−1 numbers from infected cells with S. Typhi carrying the empty plasmid (pCC1) showed no differences with respect to the wild-type strain (data not shown). It has been reported that sopD2 contributes to the synthesis of Sifs, lipid filaments essential for S. Typhimurium intracellular

proliferation (Brumell et al., 2003; Jiang et al., 2004; Birmingham et al., 2005). When we performed a gentamicin protection assay, we observed that S. Typhi sopD2STM showed a significant decrease of CFU recovered from HEp-2-infected monolayers compared with the wild-type strain (Fig. 4). In contrast, S. Typhi sopD2STM showed similar invasion levels compared with S. Typhimurium 14028s ΔsopD2∷FRT (NT060) (P=0.13749). The results suggest that loss of SopD2 function in the serovar Typhi contributes to the bacterial intracellular proliferation in human epithelial cells. In the process of adaptation to humans, bacterial genes no longer compatible with the lifestyle of facultative

pathogens within the host are selectively inactivated. These inactivated genes are called ‘antivirulence genes’ and their loss of function results in the adaptation to a given host (Maurelli, 2007). Salmonella enterica serovar Typhi is a facultative bacterial pathogen that has accumulated a large number of pseudogenes (approximately 5% of the genome), over 75% of which have completely lost their function (McClelland et al., 2004; not Dagan et al., 2006). Compared with free-living organism genomes, facultative pathogens harbor several pseudogenes and a gene population structure that promotes the maintenance of specific mutations. In contrast to free-living bacteria (large genomes, a great diversity of functional genes and low percentage of laterally transferred genes) and obligate parasites (extremely reduced genomes), S. Typhi represents an intermediate step exhibiting some genome erosion directed to inactivation and loss of detrimental or nonessential functions for its environment, i.e. the host (Ochman & Moran, 2001).