The alphaproteobacterium

Caulobacter crescentus divides asymmetrically every cell cycle to form two dissimilar progeny: a nonmotile stalked cell and a motile, polarly flagellated swarmer cell. Assembly of Alectinib purchase the single, polar flagellum in the predivisional cell occurs with the aid of the birth scar markers TipN (Huitema et al., 2006; Lam et al., 2006) and TipF (Huitema et al., 2006). The latter contains an EAL domain homologous to the catalytic domain in bis-(3′-5′)-cyclic dimeric GMP (cyclic-di-GMP) phosphodiesterases (Bobrov et al., 2005; Schmidt et al., 2005; Tamayo et al., 2005; Huitema et al., 2006). Cells that lack TipF are nonmotile and impaired in the PS-341 supplier translation and secretion of the FljK flagellin, a class IV flagellar gene product and major component of the flagellar

filament (Huitema et al., 2006). With the goal of further characterizing the flagellar assembly defect of TipF− cells, we studied flagellar gene expression in ΔtipF cells, comparing it with that of wild-type (WT) cells and other flagellar assembly mutants. Flagellar biogenesis in C. crescentus requires over 50 genes organized into a regulatory hierarchy of four expression classes (Fig. 1) to link the assembly of flagellar gene expression to cell cycle progression (Minnich & Newton, 1987; Ohta et al., 1991; Ramakrishnan et al., 1994). The master cell cycle transcriptional regulator CtrA, encoded at the class I transcriptional level, accumulates

and initiates the transcription of class II flagellar genes in S-phase (Quon et al., 1996). As class II gene products are expressed and assembled into the early (MS-ring basal body) substructure, their transcription ceases as a result of the repressive action of the σ54-dependent transcriptional regulator FlbD http://www.selleck.co.jp/products/sunitinib.html and its interacting partner FliX (Mohr et al., 1998; Anderson & Gober, 2000; Gober & England, 2000) at the time of cell division. Concurrent with the repression of class II genes, FlbD/FliX and σ54-containing RNA polymerase (Eσ54) activate the transcription of class III/IV flagellar genes that form the hook (FlgE), P-, and L-rings and the flagellar filament (Anderson & Gober, 2000). An additional layer of regulation operates on the expression of class IV (flagellin) genes, whose message stability is modulated by the negative regulator FlbT, an RNA-binding protein (Mangan et al., 1999), and FlaF, a protein with unknown biochemical activity (Llewellyn et al., 2005). Collectively, all levels of regulation ensure the accrual of gene products at the time when they are needed for the ordered expression and assembly into the growing flagellum structure.

It remains to be elucidated that the TF1061 glycosyltaransferase is indeed involved in post-translational modification of surface glycoproteins and that glycosylation directly influences the autoaggregation activity. We do not

rule out another possibility that proteolytic processing of S-layer proteins might have increased in the mutant and causally affected the enhanced autoaggregation. To our knowledge, this is the first report on the characterization of a TCS in T. forsythia. We focused on the involvement of TF0022/0023 in the expression of a glycosylation-related gene cluster, post-translational modification of check details S-layer proteins, and autoaggregation of T. forsythia cells. A previous study suggests that the existence of structurally unique HTCSs and their involvement in glycosylation, polysaccharide

synthesis, and carbohydrate metabolism would be a common theme for some species in Bacteroidetes (Sonnenburg et al., 2006). However, further analyses are required to clarify whether the TF0022/0023 HTCS plays such a dedicated role or is also involved in diverse biological functions in this organism. This work was supported in part by a Grant-in-Aid for Scientific Research (KAKENHI 19592139 for K.N.) from the Japan Society for the Promotion of Science. Fig. Selleck Vemurafenib S1. Generation of TF0022-ko mutants. Table S1. Strains, plasmids, and primers used in this study. 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 Liothyronine Sodium to the corresponding author for the article. “
“Very little is known about how the spa gene mutates over time in methicillin-resistant Staphylococcus aureus (MRSA) from the same patient. Copenhagen is an area with low prevalence of MRSA but with high variability in spa types. We collected 1536 MRSA isolates from 319 patients during a 5-year period and found spa type alterations in 30 MRSA isolates (2%) from 13 patients (4%). The alteration most often seen was the deletion of repeats followed by repeat duplication and point mutation. Sequencing of the repeat region of the Staphylococcus aureus protein A gene (spa) has been established as a reliable and discriminative method for typing S. aureus isolates. The spa region consists of a variable number of 24 (or 21 or 27)-bp repeats where variation in nucleotide compositions and order of repeats results in different spa types. In September 2010, >400 unique repeat sequences and >7200 different spa types were recorded (http://spaserver.ridom.de/). The spa types have been shown to give information on short-term epidemiology as well as on long-term phylogeny (Shopsin et al., 1999; Koreen et al., 2004; Kahl et al., 2005; Bartels et al., 2007; Mellmann et al., 2007).

We compared LSO neurons with the native Ih present in both the soma Cobimetinib and dendrites (control) with LSO neurons without Ih (blocked with ZD7288) and with LSO neurons with Ih only present peri-somatically (ZD7288+ computer-simulated Ih using a dynamic clamp). LSO neurons without Ih had a wider time window for firing in response to inputs with short time separations. Simulated somatic Ih (dynamic clamp) could not reverse this effect.

Blocking Ih also increased the summation of EPSPs elicited at both proximal and distal dendritic regions, and dramatically altered the integration of EPSPs and inhibitory post-synaptic http://www.selleckchem.com/products/AZD0530.html potentials. The addition of simulated peri-somatic Ih could not abolish a ZD7288-induced increase of responsiveness to widely separated excitatory inputs. Using a compartmental LSO model, we show that dendritic Ih can reduce EPSP integration by locally decreasing the input resistance. Our results

suggest a significant role for dendritic Ih in LSO neurons, where the activation/deactivation of Ih can alter the LSO response to synaptic inputs. “
“Brain Repair Group, School of Biosciences, Cardiff University, Cardiff, UK Although episodic memory deficits are the most conspicuous cognitive change in patients with Alzheimer’s disease (AD), patients also display alterations in emotional expression, including anxiety and impaired conditioned fear behaviours. The neural circuitry underlying emotional learning is known to involve the amygdala and hippocampus, although the precise impact of amyloid pathology on the interaction between these brain regions remains unclear. Recent evidence suggests that Tg2576 mice, which express a human amyloid precursor protein (APP) mutation associated with early-onset

AD, demonstrate normal acquisition of conditioned freezing to auditory and contextual stimuli paired with footshock. However, examination of the expression of c-Fos revealed altered neural network activity in transgenic mice. In the present oxyclozanide study we examined the effects of the APP mutation on the expression of c-Fos following the retrieval of emotional memories. To this end, stimulus-induced cellular activity was measured by analysing expression of the immediate-early gene c-Fos after the retrieval of auditory or contextual fear memories. To characterize regional interdependencies of c-Fos expression, structural equation modelling was used to compare patterns of neural network activity. Consistent with previous findings, Tg2576 mice displayed reduced freezing elicited by the auditory stimulus but not by the conditioning context.

2a and c), while for the GST fusion proteins, FpdNK + GST and PddNK + GST, it was around 50 kDa, because of the GST part (Fig. 2b and d). Kinetic parameters were determined for purified recombinant PdTK1, PddNK + GST, FpTK1, and FpdNK + GST (Table 1).

The activity was measured at 37 °C, except for FpTK1 and PdTK1, which were tested at 21 °C. All enzyme reactions followed classical Michaelis–Menten kinetics. The FpTK1 specifically phosphorylated dT and dU, having dT as the preferred substrate, because the Km for dT was 2.2 μM, which is ~ 64 times lower Venetoclax than for dU. The apparent maximal velocity (Vm-app) was 5.78 U mg−1 for dT and 4.64 U mg−1 for dU (Table 1, Fig. S2a and b). Similarly, also PdTK1 preferred dT as substrate over dU, with Km for dT being 32 μM, which is ~ 27 times lower than for dU. The Vm-app for dT was 3.43 and 2.11 U mg−1 for dU (Table 1, Fig. S2e and f). The catalytic efficiency (Vm-app/Km) was manyfold higher for FpTK1 than for PdTK1, and the activity with dT was higher for both enzymes. This indicates that FpTK1 has higher specificity toward dT and dU (Table 1). We could not detect any significant phosphorylation of dA, dC, or dG by either FpTK1 or PdTK1. The FpdNK was able to phosphorylate both dA

and dC, but had dA as the preferred substrate, with the Km for dA being 4.5 times lower than for dC. The catalytic efficiency (Vm-app/Km) was manyfold higher for dA than for dC, indicating that dA was the preferred substrate (Table 1, Fig. S2c and d). Also PddNK preferred dA as substrate over dC, the catalytic efficiency being almost 6-fold higher for dA than for dC (Table 1, Fig. S2g and h). In short, both Pifithrin-�� price non-TK1 kinases were much more ADP ribosylation factor specific

for dA than for dC, and none of them was able to phosphorylate dG. Initially, attempts to measure the substrate specificity of pure recombinant PdTK1 and FpTK1 at 37 °C failed; therefore, we decided to determine PdTK1 phosphorylating activity as a function of temperature, by measuring the activity at 500 μM 3H-dT and 2.5 mM ATP, at different temperatures, and with prolonged sampling times. It turned out that the activity of PdTK1 increased with temperature, up to 21 °C, where the highest activity was detected (7.77 ± 1.56 U mg−1); thereafter, the activity decreased with increasing temperature (Fig. 3). Therefore, 21 °C was used for further investigation of PdTK1 and FpTK1. Upon pre-incubating the enzyme at 0 °C for one hour, the obtained activity at 21 °C was considerably lower (0.71 ± 0.04 U mg−1), and after pre-incubation at 37 °C for one hour, the enzyme was irreversibly denatured, because we could not detect any activity at all. One of the approaches to estimate the aquatic bacteria biomass production is the incorporation of 3H-dT into newly synthesized DNA, and it is based on the assumption that all actively growing bacteria can incorporate external dT into DNA (Furhman & Azam, 1982).

Furthermore, a Swedish study found that local analgesia was needed in 60% of sessions, where operative dentistry was performed under N2O/O2 inhalation[6] suggesting a minor analgesic effect of N2O/O2 inhalation. Elucidation of the analgesic effect of N2O/O2 inhalation is important, because efficient pain control during dental treatment of children is essential to reduce the risk for dental anxiety and behaviour management problems[7] with subsequent long-term detrimental consequences for the individuals dental attendance patterns[8, 9] Thus, the purpose of the present experimental study was to determine the analgesic effect of N2O/O2 inhalation in children, with specific aspect

to tooth-pulp pain sensitivity, as well as pressure-induced jaw muscle pain, as both odontogenic and musculoskeletal pain www.selleckchem.com/products/Gefitinib.html problems are commonly encountered in children. The study was conducted during 2010–2011 in the dental clinic in a public school (Sabro-Korsvej School) in the outskirts of the Municipality of Aarhus, Denmark. The children attending this school are from middle-class socioeconomic families. The average DMFS1 of 15-year olds from this school was 0.83 in 2010, compared with 1.89 for the municipality. All families in the school district who

had children 12–15 years of age (a total of 271) were contacted by mail with written information on the study and invited to attend an information meeting at the dental clinic. Furthermore, the primary investigator (ABG) participated selleck compound in meetings in all relevant school-classes as well as evening meetings in the classes with the

parents to inform about the study. At the information meeting, further oral information on the study was given. The child was introduced to the different test procedures, and N2O/O2 was administered as part of the information of the child about the study. In case the parents had not received oral information at one of the evening meetings Resveratrol described above, the parents also attended the information meeting at the clinic. Inclusion criteria were 1: healthy children (ASA Class I and II[10]); 2: able to breathe through the nose. Exclusion criteria were 1: respiratory tract infection; 2: use of analgesics within 48 h before the appointment; 3: pregnancy; 4: traumatic injury to the upper incisors. Power calculations had shown that a total of 28 children were needed in each group to detect a 25% reduction in tooth-pulp pain sensitivity (α = 0.05; β = 0.80). Upon completion of the study, the children were offered a gift certificate of 100 DKr to a sports store in the area. The study was conducted as a placebo-controlled, double-blind, crossover trial, and the children were randomised using a computer-generated list of random numbers to two groups, A and B (Fig. 1). Group A received atmospheric air at the first test session and N2O/O2 at the second test session. Group B received N2O/O2 at the first test session and atmospheric air at the second.

, 1988). In any case, it remains unclear whether the exposure

to IS only inhibited the expression of DPAG-evoked defensive behaviors or attenuated the aversive emotion as well. The dissociation of motor and emotional effects is not unprecedented. Indeed, Maier et al. (1986) showed that uncontrollable stress affects behavioral and hormonal responses differently. If so, the selective inhibition of behavioral responses could explain the paucity of overt flight behaviors in clinical panic. After all, a spontaneous panic attack is conspicuously an uncontrollable stress. In any event, the present study suggests that IS inhibits a DPAG check details in-built motivational system that may be involved in behavioral resilience to stress. This study was part of the Doctorate Thesis of J.W.Q.S. Authors were recipients of postgraduate (C.A.R., C.J.T.M.) and senior

(L.C.S., S.T.) CNPq research fellowships. Research was funded by FAPES (38.413.280/2007), CNPq/FAPES (55203345/11) and UFES/AFIP (23068020409/2010-43) grants. Histology was performed at the Laboratory of Molecular Histology and Immunohistochemistry of the Health Sciences Centre of the Federal University of Espirito Santo. This study was granted the Merit Award at the Torin 1 XXVI Annual Meeting of the Brazilian Federation of Societies of Experimental Biology (FESBE). Authors declare no conflict of interest, financial interest or otherwise, that could have influenced the objectivity of observations herein reported. Abbreviations %OAE percentage of open-arm entries of elevated plus-maze %OAT percentage of open time of elevated plus-maze d.f. degree of freedom DLPAG dorsolateral periaqueductal gray DMPAG dorsomedial periaqueductal gray DPAG dorsal periaqueductal gray EAE enclosed arm entries of elevated plus-maze EPM elevated plus-maze ES escapable shock FS fictive shocks FST forced-swimming test FST-1 forced-swimming training session FST-2 forced-swimming test session I50 median effective intensity IS Elongation factor 2 kinase inescapable shock LPAG lateral periaqueductal gray PAG periaqueductal gray matter PD panic disorder TCP time in central

platform of elevated plus-maze VLPAG ventrolateral periaqueductal gray “
“Electrical synapses formed by neuronal gap junctions composed of connexin36 (Cx36) are a common feature in mammalian brain circuitry, but less is known about their deployment in spinal cord. It has been reported based on connexin mRNA and/or protein detection that developing and/or mature motoneurons express a variety of connexins, including Cx26, Cx32, Cx36 and Cx43 in trigeminal motoneurons, Cx36, Cx37, Cx40, Cx43 and Cx45 in spinal motoneurons, and Cx32 in sexually dimorphic motoneurons. We re-examined the localization of these connexins during postnatal development and in adult rat and mouse using immunofluorescence labeling for each connexin.

, 2007). In addition to the above-mentioned reporter systems, gene expression of C. albicans cells in infected organs can be directly measured by quantitative real-time PCR (qRT-PCR). Sufficient fungal RNA can be extracted from infected organs to allow analysis of expression of

selected subsets of fungal genes (reviewed in Brown et al., 2007). These studies have focused mainly on virulence factors, such as secreted enzymes and adhesins, and have shown that these genes are expressed in specific niches during infection. The addition of an RNA amplification step, following extraction of RNA from fungal cells from infected kidneys, allows fungal gene expression changes during infection to be analysed by transcript profiling. In comparison with C. albicans cells selleck inhibitor grown in vitro, fungal cells from infected mouse kidneys demonstrated altered, mostly downregulated, expression of approximately one-fifth of the genome (Andes et al., 2005). These gene expression changes reflected a switch to a filamentous growth form check details and growth in a glucose-poor environment. Emergence of fungal drug resistance in an antifungal-treated host has also been studied in mouse systemic infection models (Andes et al., 2006). In the mouse, ineffective antifungal dosing regimens

allowed the emergence of resistant isolates, where effective antifungal doses prevented this. In addition, mouse infection models have confirmed that C. albicans Bcl-w strains with specific drug resistance mutations

are more resistant to antifungal therapy, with the greatest resistance seen in strains with multiple genomic mutations (Park et al., 2005; MacCallum et al., 2010). Mouse models have been instrumental in understanding host responses during the initiation and progression of systemic Candida infection, with the advantage of allowing manipulation of the host, either through use of neutralizing antibodies, immunosuppressive treatment or by creating knockout mice. Such host manipulations allow mimicking of susceptible hosts, for example patients depleted in B cells, T cells, macrophages or neutrophils or with specific gene mutations, and allows the effects of these manipulations on host responses or susceptibility to infection to be analysed. Modelling disseminated C. albicans infection by intravenous injection in normal mice demonstrated that fungal growth was controlled in the liver and spleen, while fungal burdens increased in the kidneys (MacCallum & Odds, 2005; Lionakis et al., 2010). In the kidneys, fungal burden increases were accompanied by increasing immune infiltrates (MacCallum et al., 2009a; Castillo et al., 2011). This did not occur in other organs. Analyses of cytokine and chemokine levels in infected organs elucidated obvious organ-specific responses, with high cytokine and chemokine levels in infected kidneys, but reduced responses in the spleen (Spellberg et al., 2003; MacCallum et al., 2009a).

16S rRNA gene was amplified

from the extracted genomic DNA using the universal eubacterial 16S rRNA gene forward primer 5′-AGAGTTTGATCCTGGCTCAG-3′ (Escherichia coli positions 8–27) and the actinomycetes-specific reverse primer 5′-CCGTACTCCCCAGGCGGGG-3′ (ACT878r) (Farris & Olson, 2007). With an objective of finding the number of polymorphic groups among the isolated actinomycetes, all the amplicons representing various isolates were subjected to ARDRA. To examine the ARDRA profile, 10 μL of the PCR product was digested with HinfI, RsaI and MspI at 37 °C for 3 h. Digested DNA samples were analysed in 2% agarose gel. The amplified product (approximately CB-839 ic50 870 bp) was purified and cloned in the pTZ57R/T vector (InsT/Aclone™ PCR Product Cloning Kit #K1214,

MBI Fermentas). Sequencing of the rRNA gene (about 870 bp) for all the coral-associated actinomycetes was carried out in Macrogen (Seoul, Korea). The sequences obtained were matched with previously published sequences available in NCBI using blast (Altschul et al., 1997). Multiple sequence analysis was carried out using clustalx (Thompson et al., 1997) and further NJ plot (Perrière & Gouy, 1996) and PhyloDRAW (Choi et al., 2000) were used for constructing a phylogenetic tree. To click here validate the reproducibility of the branching pattern, a bootstrap analysis was performed. Each actinomycete isolate was grown as a c. 2 cm colony for 10–14 days on Petri plates containing SCA. Bacteria,

on the other hand, were streaked about 1–1.5 cm from the edge of the colony being tested (Zin et al., 2007). Well-characterized Gram-positive and Gram-negative clinical microbial strains Staphylococcus aureus (ATCC 11632), Pseudomonas aeruginosa (ATCC 10145), Aeromonas hydrophila (ATCC 7966), Vibrio parahaemolyticus (ATCC 27519) and Vibrio vulnificus (ATCC 29307) were used as the indicator bacteria for antibacterial activity assay. Growth of the test organisms was evaluated after 24, 48 and 72 h, and recorded as growth, inhibition and no growth as compared with a control plate containing no actinomycetes colonies. Secondary screening was performed by agar well diffusion assay (Harald et al., 2007) with the cell-free supernatant of the actinomycete isolates to confirm the antibacterial activity. The actinomycete Urocanase strains isolated from corals were transferred aseptically into 250-mL Erlenmeyer-baffled flasks with cotton plugs, containing 50 mL of ISP2 medium, which was incubated for 3–5 days at 28 °C with agitation in a rotary shaker at 250 r.p.m. After 3 days of incubation, the culture broth was filtrated through a press to separate mycelium and supernatant. The supernatant was extracted twice with ethyl acetate, chloroform or n-butanol (2 × 100 mL). The solvent extracts were combined and evaporated to dryness under reduced pressure and the extracts obtained were weighed.

Smoking is the most prevalent, modifiable, independent risk factor for CVD in HIV-infected patients [36]. As well as reducing the risk of CVD, these changes also help reduce the risk of progression to diabetes [37]. In high-risk patients, i.e. www.selleckchem.com/ferroptosis.html patients for whom the 10-year risk of CVD is ≥20%, ART modification should be considered, together with specific interventions focused on the principal risk factors for CVD, namely blood pressure, coagulation, and glucose and lipid levels. Similarly, the presence of established CVD or diabetes should also prompt the initiation of lipid-modifying therapy [5]. Impaired glucose tolerance [fasting plasma glucose

<7.0 mmol/L (126 mg/dL)] and impaired fasting glucose [fasting

plasma glucose 6.1–6.9 mmol/L (110–125 mg/dL)] increase the risk of developing diabetes four- to sixfold and increase cardiovascular morbidity and mortality [32]. Patients with glucose abnormalities should be counselled regarding lifestyle changes (Table 2) and those with diabetes [fasting plasma glucose ≥7.0 mmol/L (126 mg/dL) or oral glucose tolerance (2-h value) of ≥11.1 mmol/L (200 mg/dL)] should receive an oral anti-diabetic agent. Metformin is recommended as first-line oral anti-diabetic therapy with the addition of pioglitazone as the preferred SB203580 mw choice for combination therapy if glycated haemoglobin (HbA1c) remains >6.5–7.0% [5]. Blood lipids and blood pressure should be carefully monitored and, where necessary, individuals should be referred

for screening for nephropathy, polyneuropathy and retinopathy. Failure to achieve a target HbA1c of <6.5–7.0% should prompt referral to a diabetes specialist for initiation of insulin therapy [5]. Early screening is not just relevant to metabolic diseases. HIV-infected patients at risk of kidney disease also benefit from early identification and referral [38]. Guidelines from the HIV Medicine Association of the Infectious Diseases Society of America (IDSA) [38] recommend that assessment for existing kidney disease, with a screening urine analysis for proteinuria, a blood test for serum creatinine and a calculated estimate of renal function, should be carried out at the time of HIV click here diagnosis. The recently published EACS guidelines (see ref. 5, p. 36) highlight the potential use of urinary albumin creatinine (UA/C) or urinary albumin protein (UA/P) ratios for screening all patients and assessment of estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease (MDRD) tool developed by the Copenhagen HIV Group (see http://www.cphiv.dk/tools). Both IDSA and EACS guidelines recommend that high-risk HIV-infected patients with proteinuria and/or GFR <60 mL/min are referred to a nephrologist [5,38].

Communication between mother cell and isolated forespore involves a specialised connection system that allows nurturing of the forespore and continued macromolecular synthesis, required to finalise spore maturation. Here,

we review current understanding of this feeding channel formed by a forespore protein, SpoIIQ, and a mother cell protein, SpoIIIAH, in the Lenvatinib research buy model organism Bacillus subtilis and the important human pathogen Clostridium difficile. We also analyse the presence of this channel across endospore-forming bacteria and highlight the main questions still remaining. “
“Streptococcus suis 2 (SS2) is a zoonotic pathogen that can participate in biofilm formation to survive in hostile environments. In this study, virulent SS2 strains HA9801 and ZY05719 displayed increased biofilm formation compared with SS2 avirulent strain T15. In addition, a 58% reduction in adherence to HEp-2 cells was observed

for HA9801 biofilm cells, compared with HA9801 planktonic cells. The 50% lethal dose (LD50) of biofilm cells was 40-fold greater than that of planktonic cells. Quantification of expression levels of known virulence genes by real-time PCR revealed that the transcription levels of the gdh, cps2 and mrp genes in biofilm cells were downregulated, while the sly and gapdh genes were upregulated. HA9801 biofilm and planktonic vaccines MI-503 ic50 provided 60% and 46% protection, respectively, when challenged with 50 times the LD50 of the HA9801 strain. These results suggest a possible connection between virulence and the ability of biofilm formation; cell adhesion, transcription levels and virulence properties are different between biofilm cells and planktonic cells. Furthermore, this work offers a novel insight into bacterium infection mechanisms, which suggests that a virulent strain may be able to decrease its virulence

by forming a biofilm so that it can achieve persistent infection in vivo. Streptococcus suis (SS) is a major pathogen of pigs worldwide and causes septicemia, meningitis, and endocarditis (Gottschalk et al., 1999), which colonizes the respiratory tract, particularly from the tonsils and nasal cavities, as well as the genitals (Gottschalk et al., 2010). Among the 35 different serotypes, SS2 is known to be the most virulent and frequently isolated serotype (Principi & Marchisio, 1999). In addition, SS is believed to be a normal inhabitant of a variety of ruminants (Staats et al., 1997). The pig carrier rate is nearly 100%; however, mortality rates can reach 20% (Cloutier et al., 2003). SS binds to extracellular matrix proteins, including fibronectin and collagen (Esgleas et al., 2005), as well as to endothelial and epithelial cells (Charland et al., 2000; Benga et al., 2004), but the mechanisms by which the bacterium invades, infects, and incubates the host are unclear.