In Colombia, epidemiological data relating to PMQR is limited. A single case reporting PMQR in Colombia described the qnrB19 gene in E. coli isolates recovered from ALK activation blood cultures of a hospital patient in Monteria

(Cattoir et al., 2008). The gene was linked with ISEcp1-like insertion element responsible for its mobilization and was carried by a novel transposon designated Tn2012 identified on pR4525 (Cattoir et al., 2008). No linkage of qnrB19 with transposon or integron structures was observed in our isolates (data not shown). A high prevalence of qnrB determinants was reported recently in commensal microbial communities cultured from healthy children in Peru and Bolivia (Pallecchi RG7422 ic50 et al., 2009). In a follow-up study, the involvement of ColE-type plasmids and their role in dissemination in these two countries was described (Palecchi et al., 2010). The most prevalent plasmid, designated pECY6-7, was investigated in detail,

and was found to be identical to the plasmid characterized by Hammerl et al. (2010). Both plasmids are indistinguishable from those characterized in the S. Infantis isolate (denoted as S20). These data extend our understanding of the molecular epidemiology of the qnrB19 determinant. In this study, the marker was identified for the first time in Salmonella spp. in Colombia. The fact that the isolates include different serovars, and that they were recovered in different areas of the country from a variety of food samples and over the years (2002–2009), suggests that the reservoir may not be restricted to a specific ecological niche. Further epidemiological studies are required to determine the full extent of the dissemination of PMQR in Colombia and its implications for public health. The authors acknowledge financial support from the Research Stimulus Fund of the Department of Agriculture, Fisheries and Food of Ireland (RSF) (06/TNI-UCD10) and

COST (ATENS) grant COST-STSM-BM0701-05056. Bacterial isolates E. coli Lo qnrA1+, K. pneumoniae B1 qnrB1+ and E. coli S7 qnrS1+ were a kind gift from Professor Patrice Nordmann, E. coli TOP10+pCR2.1WqepA was kindly Carnitine palmitoyltransferase II provided by Dr Marc Galimand and E. coli 78-01 aac(6′)-Ib-cr+ by Professor Johann Pitout. “
“Plastocyanin, encoded by the petE gene, can transfer electrons to photosystem I (PSI) and cytochrome c oxidase during photosynthetic and respiratory metabolism in cyanobacteria. We constructed a petE mutant of Synechocystis sp. strain PCC 6803 and investigated its phenotypic properties under different light conditions. When cultured under continuous light, inactivation of petE accelerated the plastoquinone pool reoxidation, slowed the reoxidation rate of the primary quinone-type acceptor, and decreased the connectivity factor between the individual photosystem II (PSII) photosynthetic units.

As an example, when the extractable solids of the actinomycete CA2, representing each organic solvent were subjected to antimicrobial activity test, the chloroform extract showed the greatest biological activity with the ethyl acetate extract closely behind. The extracts of the other actinomycetes showed a similar profile (not shown). Overall, it appears that the bioactive component(s) have

mostly a lipophilic profile, given their organic solvent preference (Table 2). Culture-dependent studies on sponge-associated actinomycetes (Montalvo et al., 2005; Zhang et al., 2006; Jiang et al., 2007) and marine sediments (Mincer et al., 2002) show that novel Actinobacteria members can be isolated using various isolation media as well as low nutrient media (Jensen et selleck products al., 2005). The presence of novel Actinobacteria members in corals might represent an unexplored resource for pharmaceutical drug discovery. Actinomycetes KU-60019 cell line present in the coral A. digitifera may have a diverse array of antibacterial compounds. This is evident from the different antibiotic activity pattern exhibited by the isolated actinomycetes. Some strains showed antibacterial activity only towards the Gram-positive pathogen S. aureus (CA1, CA8 and CA14). A few strains showed antibacterial activity towards only

Gram-negative pathogens (CA2 and CA4) and a few strains showed antibacterial activity against all the pathogens (CA5, CA7, CA10, CA15 and CA18) (Table 1). Contrary to our study, Shnit-Orland & Kushmaro (2009) report that Actinobacteria Non-specific serine/threonine protein kinase members namely Micrococcus sp. and Arthrobacter sp. isolated from three different

corals did not show any antibacterial activity against any of the tested pathogens. Actinomycetales and Bacillales are responsible for almost 50% of the known bioactive microbial metabolites discovered to date, including many well-known antibiotics (Berdy, 2005). The isolated actinomycetes showed antibacterial activity against both Gram-positive and Gram-negative pathogens. As the results of the extractable solids of the actinomycetes show that the chloroform extract has the greatest biological activity with the n-butanol extract closely behind, it appears that the bioactive component(s) are mostly lipophilic in nature, given their organic solvent preference. Several studies have reported the isolation of novel marine actinomycetes (Jensen et al., 2005) producing bioactive compounds. As it has been shown earlier that mucus from healthy coral harbours bacteria capable of producing antibiotics (Ritchie, 2006), we envisage that coral mucus can be targeted for isolation of actinomycetes with bioactive properties. Within the Actinomycetales, the genus Streptomyces represents the most frequent producers of antibiotic agents (Wiese et al., 2009).

, 1987), pMV158 (Kramer et al., 1995) and pM4

(Yin et al., 2009) were shown to display remarkably decreased plasmid copy number Panobinostat mw and accumulation of single-stranded DNA, while formation of multimers was not reported. We aimed to investigate whether deletion of the ssi of pHW126, in addition to multimerization, also induces accumulation of ssDNA, but failed to detect this molecular species by Southern blot analysis (data not shown). However, it must be emphasized that the amounts of ssDNA formed by several rolling circle may be very low. For instance, pMV158 replicating in Streptococcus pneumoniae forms minute amounts (Kramer et al., 1995) and in the case of pMV158 replicating in Bacillus subtilis (Kramer et al., 1995) or pGT232 (Heng et al., 1999), the abundance is undetectably Dapagliflozin in vivo low. In Rahnella cells containing wild-type pHW126, the ssDNA is likely converted efficiently to dsDNA by the ssi. In constructs lacking the ssi lagging strand synthesis may be primed to some extend at other sites and remaining ssDNA molecules may undergo recombination with ds plasmids

to form di- and multimers as single-stranded DNA is known to be highly recombinogenic (Persky & Lovett, 2008). Rapid multimerization has been reported for different rolling circle plasmids with a failure in termination of replication caused either by specific mutations in the rep gene (Projan et al., 1987; Bidnenko et al., 1993) or by a deletion of a signal in the 5′ part of the replication origin (Yasukawa et al., 1998). Both reasons can be excluded for our pHW126 derivatives because: (1) sequencing confirmed the absence of any mutations within the rep gene, (2) increasing the distance between the replication origin and the accessory region to more than 1 kb had only minor effects [in case of pKYM insertion of even 27 bp induced massive multimerization (Yasukawa et al., 1998)] and (3) the multimerization phenotype could be rescued by including the functional ssi signal of pHW15. Furthermore, insertion

of foreign DNA into rolling circle plasmids may cause formation of high-molecular weight plasmid multimers by an as yet unknown mechanism (Gruss & Ehrlich, 1988, 1989). This high-molecular weight DNA is believed to be composed of head-to-tail linear plasmid multimers (Gruss & Ehrlich, 1988). In contrast, Resminostat the multimers of pHW126 derivatives lacking the accessory region are clearly supercoiled circular DNA molecules. While multimers were rapidly formed from plasmid monomers, the reverse process was less efficient. Monomerization of dimers of rolling circle plasmids may happen if replication is initiated at one origin and terminated at the second origin (Gruss & Ehrlich, 1989). This has also been shown for pHW126 (Rozhon et al., 2010). However, the rate of this process seems to be insufficient to keep constructs lacking the accessory region as monomers.

The RNA probe was transcribed in the presence of [35S]-uridine 5′-[α-thio]triphosphate (specific activity 1000–1500 Ci/mmol;

New England Nuclear, Boston, MA, USA). In situ hybridization was carried find more out as described (Hurd, 2003) by applying the labelled probe to the brain sections at a concentration of 2 × 103 cpm/mm2 of the coverslip area overnight at 55°C in a humidified chamber. Two adjacent sections from each subject were studied. The slides were then apposed to Imaging Plates (FUJIFILM Corporation, Tokyo, Japan) along with 14C-standards (American Radiolabelled Chemicals, St Louis, MO, USA). Films were developed with a phosphoimaging analyzer (FLA-7000), and images were analyzed using the MultiGauge software (FUJIFILM Corporation). We have adopted the nomenclature of Paxinos & Franklin (2001) to describe the organization of the developing mouse brain. In addition, we have relied on the nomenclature introduced by Bons et al. (1998) for the adult mouse lemur to identify brain areas in the developing grey mouse lemur brain. Anti-diabetic Compound Library A comprehensive list of abbreviations of neuroanatomical structures can be found in supporting Table S1. Recent findings demonstrate that scgn is

a CBP identifying neurochemically heterogeneous subsets of neurons in adult rodent, primate (Mulder et al., 2009b) and human forebrain (Attems et al., 2007). However, it remains unknown whether scgn is expressed during neurodevelopment. We assessed scgn mRNA levels in the mouse cerebral cortex (including hippocampus; Fig. 1A) and amygdaloid complex (Fig. 1A1) by qPCR analysis (supporting Fig. S1) during mid- and late-gestation, and in neonates. We established that pallial scgn mRNA expression was robust by E14.5, Tobramycin whilst moderate to low between E16 and P2 in the developing mouse neocortex and hippocampus (Fig. 1A). In contrast, scgn mRNA levels in the amygdaloid complex remained largely stable until birth with a marked decline being apparent after P1 (Fig. 1A1). Within the framework of the Human Protein Atlas program (Uhlen et al., 2005; Mulder et al., 2009a), we have generated antibodies to

> 8000 proteins, including a polyclonal antibody recognizing a phylogenetically conserved scgn epitope (Mulder et al., 2009b). Here, we confirmed that this antibody recognized a single protein target in samples prepared from neonatal mouse forebrain that is identical in size to that seen in adult brain (Fig. 1B; supporting Fig. S2), and corresponds to scgn’s calculated molecular weight of 32 kDa (http://www.ensembl.org). We explored whether scgn is expressed in the developing central nervous system at the protein level by detecting scgn protein upon loading fetal and neonatal forebrain lysates (40 μg/lane) on denaturing SDS-PAGE (Fig. 1C). The developmental dynamics of scgn mRNA expression suggest that this CBP may be transiently expressed by select cell populations in the fetal brain. Alternatively, scgn+ cells may be born by ∼E14.

Under conditions of high aeration and limiting availability of combined nitrogen, A. brasilense cells differentiate into aggregating cells and form dense flocs that are visible to the naked eye (Sadasivan & Neyra, 1985; Burdman et al., 1998). Flocs are formed by cell-to-cell aggregation between nonmotile cells embedded in learn more a dense extracellular matrix (Burdman et al., 2000b). Flocculation correlates with, and likely requires the production of, arabinose-rich exopolysaccharides (Bahat-Samet et al., 2004). Scanning electron and fluorescence microscopy studies of A. brasilense aggregating cells indicate the presence of fibrillar

material connecting cells to each other or to biotic or abiotic substrates (Bashan et al., 1986, 1991). These fibrils seem to be absent in nonaggregating cells or mutant strains that are defective in aggregation, suggesting that they may play a role in promoting this behavior (Burdman et this website al., 1998; Skvortsov &

Ignatov, 1998). The detailed biochemical composition of this fibrillar material remains unknown, although it is possible that it is related to exopolysaccharide production (Bahat-Samet et al., 2004). In support of this idea, the degree of bacterial aggregation appears to correlate with the amount and composition of exopolysaccharide produced by several A. brasilense strains (Burdman et al., 1998). Chemotaxis is perhaps the most-studied signal transduction pathway in bacteria (reviewed in Sourjik, 2004; Wadhams & Armitage, 2004; Parkinson et al., 2005; Hazelbauer VAV2 et al., 2008). Despite the identification of homologous chemotaxis systems in phylogenetically distant bacteria and archaeal species, there is a huge diversity in both the number of chemotaxis operons

encoded within bacterial genomes and their physiological roles (Wadhams & Armitage, 2004). Recent studies have shown that the functions of chemotaxis-like pathways are not limited to the regulation of motility patterns, but also include the regulation of biofilm formation, exopolysaccharide production, and cell-to-cell interactions (Black & Yang, 2003; Hickman et al., 2005; Yang & Li, 2005; Caiazza et al., 2007). In prototypical chemotaxis, the histidine kinase CheA and the response regulator CheY form a two-component signal transduction system, which ultimately modulate the probability of changes in the direction of rotation of flagellar motors in response to specific environmental cues. Changes in the phosphorylation of CheY regulated by the CheA–CheY phosphorylation cascade modulate the affinity of CheY for the flagellar motor switch complex and thus chemotaxis. Surprisingly, in A. brasilense, strains carrying mutations in components of the Che1 chemotaxis-like pathway were found to be affected in their ability to interact by cell-to-cell aggregation and in flocculation.

coli (Vine & Cole,

2011). It is currently unclear whether this ‘activity’ is a previously unreported NO reductase or a combination of a primary chemical reaction (e.g. metal-catalyzed nitrosylation of iron-sulfur centers) followed by a reductive repair pathway. NO reacts directly with metal ions to form nitrosyl complexes. Thus, nitrosylation of iron atoms, especially iron-sulfur clusters, in enzymes such as aconitase and fumarase or in the transcription factors FNR, Fur, SoxR, OxyR, and NsrR inactivates their functions. Under oxidizing conditions, metal nitrosyl complexes can then transfer the NO moiety to –SH groups of proteins, peptides, and cysteine, or to nitrogen atoms of secondary amines. As NarG is a major catalyst for the formation of NO EPZ015666 in the cytoplasm, protection mechanisms become essential when NarL and FNR are both active, which is during anaerobic growth in the presence of a high concentration of nitrate. Consequently, protection against damage by NO must also be activated by NarL, FNR or both. But this poses a dilemma: how can the bacteria survive when NO-induced damage is so severe that FNR can

no longer function? Enteric bacteria appear to have solved this problem by evolving multiple repair pathways, some that function when FNR (and Fur, etc.) are active, and others that deal with the greater threat when damage is so severe that FNR is itself inactivated. Mechanisms to Sirolimus manufacturer minimize damage caused when FNR is active include nitrite reduction by the cytoplasmic nitrite reductase, NirBD, nitrite expulsion by the nitrate and nitrite transporter, NarK (Jia et al., 2009), and possibly repair by the hybrid cluster protein, Hcp, and its reductase. Expression of the genes for all of these proteins is dependent upon FNR activation. However,

contrary to our earlier report (Filenko et al., 2007), hcp expression is not activated by NarL, but instead it is directly regulated by NsrR in response to NO (Chismon et al., 2010). Nitrosative damage to iron-sulfur centers, and possibly other iron proteins as well, is repaired in E. coli by YtfE or Adenylyl cyclase RIC – for repair of iron centers (Justino et al., 2007; Overton et al., 2008). It is not known whether damaged iron-sulfur centers are repaired directly by the removal of the NO moiety, or whether iron is released followed by the reconstruction of the active redox center. If the former is correct, is an acceptor molecule nitrosated in the process and, if so, what is this acceptor and how is that regenerated? Synthesis of three further proteins is strongly up-regulated by nitrate-activated NarL during anaerobic growth in the presence of nitrate but is not dependent on activation by the FNR protein. These are the O6-methyl-guanine methyl transferase, Ogt; and the products of the two-gene operon, yeaR yoaG.

coli (Vine & Cole,

2011). It is currently unclear whether this ‘activity’ is a previously unreported NO reductase or a combination of a primary chemical reaction (e.g. metal-catalyzed nitrosylation of iron-sulfur centers) followed by a reductive repair pathway. NO reacts directly with metal ions to form nitrosyl complexes. Thus, nitrosylation of iron atoms, especially iron-sulfur clusters, in enzymes such as aconitase and fumarase or in the transcription factors FNR, Fur, SoxR, OxyR, and NsrR inactivates their functions. Under oxidizing conditions, metal nitrosyl complexes can then transfer the NO moiety to –SH groups of proteins, peptides, and cysteine, or to nitrogen atoms of secondary amines. As NarG is a major catalyst for the formation of NO Epigenetics activator in the cytoplasm, protection mechanisms become essential when NarL and FNR are both active, which is during anaerobic growth in the presence of a high concentration of nitrate. Consequently, protection against damage by NO must also be activated by NarL, FNR or both. But this poses a dilemma: how can the bacteria survive when NO-induced damage is so severe that FNR can

no longer function? Enteric bacteria appear to have solved this problem by evolving multiple repair pathways, some that function when FNR (and Fur, etc.) are active, and others that deal with the greater threat when damage is so severe that FNR is itself inactivated. Mechanisms to PD-0332991 datasheet minimize damage caused when FNR is active include nitrite reduction by the cytoplasmic nitrite reductase, NirBD, nitrite expulsion by the nitrate and nitrite transporter, NarK (Jia et al., 2009), and possibly repair by the hybrid cluster protein, Hcp, and its reductase. Expression of the genes for all of these proteins is dependent upon FNR activation. However,

contrary to our earlier report (Filenko et al., 2007), hcp expression is not activated by NarL, but instead it is directly regulated by NsrR in response to NO (Chismon et al., 2010). Nitrosative damage to iron-sulfur centers, and possibly other iron proteins as well, is repaired in E. coli by YtfE or Baf-A1 manufacturer RIC – for repair of iron centers (Justino et al., 2007; Overton et al., 2008). It is not known whether damaged iron-sulfur centers are repaired directly by the removal of the NO moiety, or whether iron is released followed by the reconstruction of the active redox center. If the former is correct, is an acceptor molecule nitrosated in the process and, if so, what is this acceptor and how is that regenerated? Synthesis of three further proteins is strongly up-regulated by nitrate-activated NarL during anaerobic growth in the presence of nitrate but is not dependent on activation by the FNR protein. These are the O6-methyl-guanine methyl transferase, Ogt; and the products of the two-gene operon, yeaR yoaG.

For example, we can test H 0: θ1 = θ6 by fitting the unrestricted model given in [1] and fitting

the restricted model where the third row is replaced with (θ5, 0, –(θ5 + θ1), θ1). The likelihood ratio statistic, 2[log L(θ)unrestricted − log L(θ)restricted], has an approximately chi-squared distribution with one degree of freedom if H 0 is true. The observed transition frequencies and the corresponding expected numbers from the models (in parentheses) are listed in Tables A1 and A2 to examine the model fits. As an example, consider the 47 subjects who started in state 1 as HPV negative and with HIV VL > 400 copies/mL (HIV VL model). Of these, 11 subjects remained in state 1, two transitioned to state 2, 28 transitioned to state 3 Etoposide mw and six transitioned to state 4 by week 28. The model estimations for these frequencies are 11.23, 3.57, 27.36 and 4.84, respectively. Overall, the comparisons

of the observed and expected frequencies indicate adequate model fits. “
“Objectives The aim of the study was to investigate the psychological status and the psychosocial experiences of HIV-positive people using Symptom Check List 90 (SCL-90) in eastern China. Methods Two hundred and fourteen HIV-positive people and 200 controls were recruited to the study. Participants were given an anonymous questionnaire which included questions pertaining to demography, SCL-90 and psychosocial experiences. Results The mean subscale scores for SCL-90 in the HIV-positive group were all higher than those of the control group (P<0.001), especially for depression, anxiety, obsessive–compulsive Topoisomerase inhibitor disorder and hostility. Female HIV-positive individuals had significantly

higher depression and anxiety scores (P<0.05) and more scores higher than 2.0 than male HIV-positive individuals. The average number of subscales with mean scores higher than 2.0 was 4.1 for female HIV-positive individuals and 3.7 for male HIV-positive individuals. Histamine H2 receptor The most common psychosocial experiences related to HIV infection were fear (36.9%) and helplessness (31.8%). 90.2% of HIV-positive people would not tell others about their disease because of fear of discrimination against family members (42.2%), exclusion by community members (26.9%) and abandonment (23.3%). Discrimination from acquaintances (38.8%) was a main stressor in the HIV-positive individuals’ daily life. Most members of HIV-positive individuals’ communities expressed negative attitudes: alienation, coldness, aversion and fear. 38.3% of the HIV-positive participants reported that their family members had been discriminated against. Conclusions The results demonstrate that HIV-positive people in eastern China live in a negative psychosocial environment and suffer from psychological distress. It is necessary to provide psychological interventions for people living with AIDS and to educate community members in order to improve the psychosocial environment.

Proportion of patients treated outside of clinical trials for non-genotype 1 who receive therapy with pegylated interferon and ribavirin Proportion of patients treated for non-genotype 1 with a Metavir score of F4 who are offered treatment with pegylated interferon and ribavirin unless contraindicated Proportion of patients with non-genotype 1–4 referred to a tertiary centre Proportion of patients not receiving therapy undergoing repeat non-invasive staging of their liver disease within 1 year The response rate of genotype 4 HCV monoinfection to a PEG-IF/RBV regimen is similar to that seen with genotype

1, with a figure ranging between 43–50% being observed in clinical trials. As with genotypes 2 and 3, neither of the two currently available HCV protease inhibitors has Sirolimus ic50 been studied, but the newer anti-HCV agents are being studied across all genotypes with excellent

initial responses in monoinfected patients [101]. Due to the low rates of success with pegylated click here interferon and ribavirin we suggest that treatment is deferred where possible and treatment with newer agents within clinical trials actively sought. Where the individual has liver disease staging suggestive of Metavir stage 4, a complication of disease, or it is the informed wish of the patient to commence therapy, then treatment is recommended. This should be with pegylated interferon and ribavirin. The duration of therapy should be 48 weeks if an undetectable HCV RNA is achieved at 4 weeks, with a consideration to extend this to 72 weeks if achieved by 12 weeks. If the RNA is still detectable at 12 weeks, consideration should be given to discontinuing treatment. All individuals deferring therapy should undergo hepatic elastography or an alternative non-invasive test at least annually. Individuals infected with genotypes other than 1–4 should be referred to a centre with experience of treating HCV infection with these genotypes for a treatment

plan to be made in consultation with the host centre. We recommend patients without a decrease AZD9291 cost of 2 log10 in HCV RNA at week 4 post diagnosis of acute infection (1D) or with a positive HCV RNA week 12 post diagnosis of acute infection (1C) are offered therapy. We recommend therapy be commenced prior to an estimated duration of infection of 24 weeks (1D). Patients who have not commenced treatment by this time should be managed as for chronic hepatitis C. We recommend all patients be offered combination therapy with pegylated interferon and weight-based ribavirin (1C). We recommend against treatment with PEG-IFN monotherapy (1C). We recommend treatment is discontinued if patients do not achieve an EVR (1C). We recommend patients with re-emergent virus after spontaneous or therapeutic clearance are assessed for relapse or reinfection (1C). We recommend patients with AHC who relapse are managed as for chronic hepatitis C (1D).

“
“Streptococcal histidine triad protein was identified recently as a cell surface-associated protein family. Five members of this family (PhtA, PhtB, PhtD, PhtE and HtpA), derived from Streptococcus pneumoniae and Streptococcus pyogenes, have been shown as antigens that confer protection to the host on infection. In this report, a gene sequence highly homologous to htpA and phtD (designated htpS, the histidine triad protein of Streptococcus suis) was identified from S. suis 2 Chinese strain 05ZYH33. Our data revealed that htpS is extremely conserved in S. suis 2 and widely distributed in 83% (29/35)

of 35 S. suis serotypes. It was also demonstrated by Western blot and flow cytometry that HtpS is a cell surface-associated protein that was expressed during S. suis 2 infection. An antibody against HtpS could increase the deposition of human GSK2118436 ic50 complement 3 on S. suis 2 and also enhance the clearance of S. suis 2 in whole blood. In addition, Regorafenib mice could be immunized against S. suis 2 infection and were well protected after immunization with recombinant HtpS.

Streptococcus suis is an important Gram-positive pathogenic bacterium that can infect piglets and cause many serious diseases such as arthritis, meningitis and septicemia (Lun et al., 2007). It is also an important zoonotic agent for individuals who are in contact with infected swine or healthy carriers (Wertheim et al., 2009). To date, 35 serotypes (types 1/2 and 1–34) of S. suis have been described. Streptococcus suis serotype 2 (S. suis 2) is the most frequently isolated and associated with disease (Higgins & Gottschalk, 1995; Messier et al., 2008). Two outbreaks of severe human S. suis 2 infections in China were characterized by streptococcal toxic shock syndrome in 1998 and 2005, which caused mortality of up to 62.7% and 81.3%, respectively (Tang et al., 2006). This suggested that the prevention and Cell press control of the S. suis 2 infection has become an urgent task in such a grim situation. However, effective control of S. suis 2 infection

was lacking due to the absence of safe and effective vaccines (Haesebrouck et al., 2004). It is well recognized that sequence-conserved, surface-exposed bacterial proteins could be considered as vaccine candidates for subunit vaccine development (Etz et al., 2002; Hamel et al., 2004; Timoney et al., 2007). Based on the sequencing of two virulent S. suis 2 genomes (Chen et al., 2007), a collection of structural and enzymatic proteins that are associated with the bacterial cell wall have been identified from the highly pathogenic isolates (Feng et al., 2007, 2009; Li et al., 2007; Esgleas et al., 2008; Ge et al., 2009; Wang et al., 2009; Zhang et al., 2009). Recently, a study of the divalent-cation-regulated cell surface-associated proteins of S. suis 2 identified several immunogenic proteins in the adcR mutation of S.