The analysis of the published information and the sequences deposited in the public databases

allowed a first classification of these plasmids into a selleck screening library restricted number of groups according to the proteins involved in the initiation of replication, plasmid partition and conjugation. The sequence comparisons demonstrated that the plasmids from sphingomonads encode for four main groups of replication initiation (Rep) proteins. These Rep proteins belong to the protein superfamilies RepA_C (Pfam 04796), Rep_3 (Pfam 01051), RPA (Pfam 10134) and HTH-36 (Pfam 13730). The ‘degradative megaplasmids’ pNL2, pCAR3, pSWIT02, pCHQ1, pISP0, and pISP1, which code for genes involved in the degradation of aromatic hydrocarbons, carbazole, dibenzo-p-dioxin and γ-hexachlorocyclohexane, carry Rep proteins which either belong to the RepA_C- (plasmids

pNL2, pCAR3, pSWIT02), Rep-3- (plasmids pCHQ1, pISP0) or RPA-superfamily (pISP1). The classification of these ‘degradative megaplasmids’ into three groups is also supported by sequence comparisons CT99021 solubility dmso of the proteins involved in plasmid partition (ParAB) and the organization of the three genes on the respective plasmids. All analysed ‘degradative megaplasmids’ carry genes, which might allow a conjugative transfer of the plasmids. Sequence comparisons of these genes suggest the presence of at least two types of transfer functions, which either are closer related to the tra- or vir-genes previously described for plasmids from other sources. The sphingomonads represent a group of Alphaproteobacteria, Megestrol Acetate which encompass in our days the genera Novosphingobium, Sphingobium, Sphingomonas, Sphingopyxis, Sphingosinicella, Sphingomicrobium, Sphingorhabdus and Parasphingopyxis. These genera share a number of phenotypic traits, such as the presence of sphingolipids in their outer membranes, the formation of usually yellow-pigmented colonies and a specific pattern of polyamines (Kämpfer et al., 2012; Uchida et al., 2012; Jogler et al., 2013). Sphingomonads have been

intensively studied during the last years because of their pronounced ability to degrade recalcitrant natural and xenobiotic compounds, such as various polycyclic aromatic hydrocarbons (PAHs), nonylphenols, sulphonated naphthalenes, chlorinated dibenzofurans and dibenzodioxins, carbazole, polyethylene glycols and different herbicides and pesticides (Stolz, 2009). It was shown in the last years that many sphingomonads possess (often several) plasmids and especially that rather large plasmids are common in this bacterial group. These large plasmids are commonly designated as ‘megaplasmids’ if their sizes exceed about 100 kbp (Basta et al., 2004, 2005; Aylward et al., 2013). These ‘megaplasmids’ often carry genes coding for degradative pathways, which are often found either on different replicons (as e.g.

We compared foreign-born (FB) travelers with US-born travelers because previous studies have shown that immigrant adults and their children are less likely to be current on routine immunizations than their US-born counterparts.7,8 The case definition used for travel-associated influenza-like illness (ILI) was fever with cough or sore throat during the trip or within 1 week after return. Because of small numbers, we used exact logistic regression

to analyze ILI in the post-travel survey. The survey protocol and questionnaires were reviewed and exempted as research by the institutional review board at the Centers for Disease Control and Prevention. We approached 3,935 travelers to Asia, of whom 2,046 (52%) Selleck Ku-0059436 were ineligible (visitors to the United States returning home, short-term US residents for less than 6 months, or people with language barriers). Of 1,889 eligible travelers, 1,301 (69%) completed the pre-travel questionnaire. Of these, 600 provided their contact information and agreed to complete the post-travel survey after returning from Asia, and 337 (56%) completed the post-travel survey either by mail, telephone, or online. Participants in the pre-

and post-travel surveys differed ALK activation significantly by age, race, occupation, and country of birth (Table 1). Of the 1,301 participants who answered the pre-travel survey, 494 (42%) planned to visit more than one Asian country during their trip. The top three destination countries were China (including Hong Kong), Japan, and India (Table 2). The main reasons for travel were vacation (40%), visiting friends Sulfite dehydrogenase and relatives (37%), and

business (26%) (Table 2). US-born travelers were more likely to travel for work or vacation while FB travelers were more likely to visit their friends and relatives (VFR). FB travelers were also more likely to travel for longer duration than US-born travelers (Table 2). US-born travelers were more likely than FB travelers to plan the following activities: attend large gatherings/events, visit food markets, eat from street food vendors, and travel into rural areas (Table 2). Both FB and US-born travelers were aware of most influenza symptoms and prevention measures (Table 2), but US-born travelers were more aware that the following symptoms could indicate influenza: nausea (OR = 2.67, CI = 2.08–3.43), vomiting (OR = 2.88, CI = 2.22–3.73), diarrhea (OR = 2.58, CI = 1.92–3.48), and muscle ache (OR = 3.04, CI = 2.29–4.03). Overall, 692 (56%) participants did not receive influenza vaccine during the previous season and 3% did not know whether they had received the vaccine.

Total scores and subscale scores of the three clinical groups were compared through ANOVA. Results.  There was no significant difference in mean total scale score and subscale scores between functional and headgear groups (P > 0.05). Significant differences were found in

both mean total and subscale scores between the malocclusion and nonmalocclusion groups (P < 0.001) except oral symptoms subscale (P > 0.05). Conclusions.  The results of this Selleck Compound C study reveal that functional and headgear appliances do not differ in terms of impact on daily life during the treatment. Moreover, both groups have poorer OHQoL compared to malocclusion group. “
“Traumatic dental injury (TDI) has been considered a significant problem in youth, not only because PLX4032 chemical structure of its consequences to the craniofacial structures but also for its potential impact on the quality of life of affected individuals. The aim of this study was to investigate the impact of TDI with treatment needs on the oral health–related quality of life (OHRQoL) of South Brazilian schoolchildren. A cross-sectional study was performed in Porto Alegre, Brazil, using a multistage probability sampling strategy. Of 1837 eligible 12-year-old schoolchildren attending public and private schools,

1528 were examined. OHRQoL was assessed by the Brazilian version of the Child Perceptions Questionnaire for 11-to 14-year-old children (CPQ11–14) – 16-item short form. Clinical examination was conducted to assess the presence of TDI in permanent incisors (Children’s Dental Health Survey criteria), malocclusion, and dental caries. Parents/legal guardians answered questions on socioeconomic status. Statistical analyses were performed using Poisson regression models. The overall CPQ11–14 score was not associated with TDI. In the functional limitations domain, individuals presenting TDIs with treatment needs experienced significantly higher mean

CPQ11–14 than individuals with no TDI or without treatment needs (RR = 1.21; 95% CI = 1.05–1.39), after adjusting for malocclusion, OSBPL9 dental caries, gender, and socioeconomic status. No other domains were associated with TDI. This study revealed that TDI with treatment needs negatively affects the OHRQoL in this population of 12-year-old schoolchildren and that this impact is related to oral functions. “
“Toothbrushes harbor a high number of cariogenic microorganisms. To investigate the viability of mutans streptococci (MS) on toothbrushes bristles and the production of extracellular polysaccharide (ECP) related to drying time. Twenty children were submitted to brushing without dentifrice. Toothbrushes were kept at room temperature from 0 to 48 h and then submitted to microbiological processing. The number of MS colonies/biofilms was expressed according to scores: 0 = no colonies were detected; 1 = 1 to 50; 2 = 51 to 100; 3 = over 100.

Morphological changes of cochlear

tissue, expression of nestin mRNA and protein and cell proliferation were investigated in these models. Our observations show that ototoxic injury has modest effects on nestin expression and cell proliferation. On the other hand, the addition of growth factors to the injured cochlear explants induced the appearance of nestin-positive cells in the supporting cell area of the organ of Corti. The vast majority of nestin-expressing cells, however, were not proliferating. Growth factors also had a robust stimulatory effect on axonal sprouting and the proliferative response, which was more pronounced in injured cochleae. On the whole, our findings indicate that nestin expression after kanamycin ototoxicity is related to tissue reactivity rather than activation of resident progenitors attempting to Carfilzomib chemical structure replace the lost receptors. In addition, administration of growth factors significantly enhances tissue remodelling, suggesting that cochlear repair may be promoted by the exogenous application of regeneration-promoting buy ITF2357 substances. “
“Tonic inhibition mediated by extrasynaptic GABAA receptors (GABAARs)

is an important regulator of neuronal excitability. Phosphorylation by protein kinase C (PKC) provides a key mode of regulation for synaptic GABAARs underlying phasic inhibition; however, less attention has been focused on the plasticity of tonic inhibition and whether this can also be modulated by receptor phosphorylation. To address this issue, we used whole-cell patch

clamp recording in acute murine brain slices at both room and physiological temperatures to examine the effects of PKC-mediated phosphorylation on tonic inhibition. Recordings from dentate gyrus granule cells in the hippocampus http://www.selleck.co.jp/products/CHIR-99021.html and dorsal lateral geniculate relay neurons in the thalamus demonstrated that PKC activation caused downregulation of tonic GABAAR-mediated inhibition. Conversely, inhibition of PKC resulted in an increase in tonic GABAAR activity. These findings were corroborated by experiments on human embryonic kidney 293 cells expressing recombinant α4β2δ GABAARs, which represent a key extrasynaptic GABAAR isoform in the hippocampus and thalamus. Using bath application of low GABA concentrations to mimic activation by ambient neurotransmitter, we demonstrated a similar inhibition of receptor function following PKC activation at physiological temperature. Live cell imaging revealed that this was correlated with a loss of cell surface GABAARs. The inhibitory effects of PKC activation on α4β2δ GABAAR activity appeared to be mediated by direct phosphorylation at a previously identified site on the β2 subunit, serine 410.

3, with OD440 nm of 0.1 corresponding to 24 mg dry biomass (L)−1 was used. Protein was quantified according to Bradford (1976) using bovine serum albumen standards. Methylococcus capsulatus (Bath) was grown in 500 mL

volumes of NMS medium in 2-L Erlenmeyer flasks under air supplemented with 19% (v/v) methane and 1% (v/v) carbon dioxide. Flasks were sealed with red rubber ‘Suba Seal’ vaccine stoppers and were incubated at 45 °C in see more an orbital incubator (Gallenkamp, Loughborough, UK) at 120 r.p.m. Cells were harvested at late exponential phase by centrifugation at 13 000 g for 30 min at 4 °C with one wash in NMS and resuspension in 50 mM PIPES-HCl at pH 7.2. QuickFit Erlenmeyer flasks of capacity 250-mL were modified by the Glass Workshop at the University of Warwick to attach QuickFit test tubes of 8-mL volume with a short length of glass tubing (Fig. 1), in the style of BioMeter flasks. Hereafter, the Erlenmeyer (A) is termed ‘flask’ and the test tube (B),

‘trap’. Both openings were sealed using ‘Suba Seal’ vaccine stoppers (C) with three coats of polytetrafluoroethylene dry lubricant spray (RS www.selleckchem.com/products/Roscovitine.html Components) to minimize methane adsorption. Vaccine stoppers were pierced with 19G, blunt-ended, hollow surgical steel needles (Beckton, Dickinson & Co., Rutherford, NJ or Studley Surgical Needle Co., Studley, UK), sufficiently long to reach the bottom of the flask and the trap (D), with integral Luer-Slip™ female tapers. Luer-Lok™ Interleukin-2 receptor polycarbonate taps (E; Cole-Parmer Instrument Company Ltd, Hanwell, UK) were attached to the needles. Cell suspensions in

NMS (50 mL containing 12 mg dry biomass) were placed in flasks with 5 mL 21.6 M KOH solution in the trap, ensuring that it could not enter the flask. Killed controls were prepared by incubating flasks containing cells suspended in 5.2 M formaldehyde in NMS on ice for 10 min. Experimental flasks were also preincubated in this way to avoid any variance. Cell-free controls were performed with or without the addition of formaldehyde, and no significant difference in carbon partitioning between trap and flask was observed (data not shown). Radiorespirometry experiments were conducted at 45 °C in a gyrotory water bath shaker (New Brunswick, Edison, NJ) with moderate agitation. Nine millilitres of methane and 1 mL of carbon dioxide were injected, and flasks were allowed to preincubate for 10 min. 2.3μCi [14C]-methane (43 nmol) was injected along with, in some flasks, 0.5 mL of 1 M HgCl2 solution to give a final concentration of 10 mM. At 5 min intervals, 2 mL volumes of cell suspension were removed with 0.5 mL volumes from the trap for scintillation counting. Cells were harvested onto nitrocellulose filters of 0.2-μm pore size (Whatman LTD, Maidstone, UK) supported on 0.45-μm glass fibre filters (Whatman LTD) using a vacuum and were washed with 25 mL 0.1 M HCl to remove [14C]-carbonates followed by 25 mL of NMS.

3, with OD440 nm of 0.1 corresponding to 24 mg dry biomass (L)−1 was used. Protein was quantified according to Bradford (1976) using bovine serum albumen standards. Methylococcus capsulatus (Bath) was grown in 500 mL

volumes of NMS medium in 2-L Erlenmeyer flasks under air supplemented with 19% (v/v) methane and 1% (v/v) carbon dioxide. Flasks were sealed with red rubber ‘Suba Seal’ vaccine stoppers and were incubated at 45 °C in SB431542 cost an orbital incubator (Gallenkamp, Loughborough, UK) at 120 r.p.m. Cells were harvested at late exponential phase by centrifugation at 13 000 g for 30 min at 4 °C with one wash in NMS and resuspension in 50 mM PIPES-HCl at pH 7.2. QuickFit Erlenmeyer flasks of capacity 250-mL were modified by the Glass Workshop at the University of Warwick to attach QuickFit test tubes of 8-mL volume with a short length of glass tubing (Fig. 1), in the style of BioMeter flasks. Hereafter, the Erlenmeyer (A) is termed ‘flask’ and the test tube (B),

‘trap’. Both openings were sealed using ‘Suba Seal’ vaccine stoppers (C) with three coats of polytetrafluoroethylene dry lubricant spray (RS see more Components) to minimize methane adsorption. Vaccine stoppers were pierced with 19G, blunt-ended, hollow surgical steel needles (Beckton, Dickinson & Co., Rutherford, NJ or Studley Surgical Needle Co., Studley, UK), sufficiently long to reach the bottom of the flask and the trap (D), with integral Luer-Slip™ female tapers. Luer-Lok™ Nintedanib (BIBF 1120) polycarbonate taps (E; Cole-Parmer Instrument Company Ltd, Hanwell, UK) were attached to the needles. Cell suspensions in

NMS (50 mL containing 12 mg dry biomass) were placed in flasks with 5 mL 21.6 M KOH solution in the trap, ensuring that it could not enter the flask. Killed controls were prepared by incubating flasks containing cells suspended in 5.2 M formaldehyde in NMS on ice for 10 min. Experimental flasks were also preincubated in this way to avoid any variance. Cell-free controls were performed with or without the addition of formaldehyde, and no significant difference in carbon partitioning between trap and flask was observed (data not shown). Radiorespirometry experiments were conducted at 45 °C in a gyrotory water bath shaker (New Brunswick, Edison, NJ) with moderate agitation. Nine millilitres of methane and 1 mL of carbon dioxide were injected, and flasks were allowed to preincubate for 10 min. 2.3μCi [14C]-methane (43 nmol) was injected along with, in some flasks, 0.5 mL of 1 M HgCl2 solution to give a final concentration of 10 mM. At 5 min intervals, 2 mL volumes of cell suspension were removed with 0.5 mL volumes from the trap for scintillation counting. Cells were harvested onto nitrocellulose filters of 0.2-μm pore size (Whatman LTD, Maidstone, UK) supported on 0.45-μm glass fibre filters (Whatman LTD) using a vacuum and were washed with 25 mL 0.1 M HCl to remove [14C]-carbonates followed by 25 mL of NMS.

3a). It was important to verify that the C-terminal HemA truncations encode functional enzymes and exhibit normal regulation. Plasmid-encoded, truncated, and tagged S. enterica hemA complemented an E. coli hemA mutant. Regulation in response to heme was tested by Western blot (Fig. 3b). To eliminate the possibility that a partial defect in the enzyme activity of the truncated proteins could affect the results of the test, an E. coli host that is wild type for hemA was used, and the plasmid-encoded proteins were specifically detected by an additional C-terminal FLAG tag. Truncated HemA exhibited

normal regulation in response to heme limitation. His-tagged C-terminally truncated HemA was selleck chemical purified by Ni-NTA affinity chromatography. The purified protein was red in color, suggesting the presence of bound heme. The absorption spectrum of purified HemA protein (Fig. 1a) contains features characteristic of heme, including a prominent peak at 424 nm (the http://www.selleckchem.com/products/gsk126.html Soret band). Upon reduction with Na-dithionite, the peak at 424 nm became sharper and shifted toward a longer wavelength (426 nm), and two other peaks appeared: one at 530 nm and another at 560 nm. The spectrum of reduced heme (hemin), which was used as a control, was very similar to that of the purified protein (data not shown). Three separate protein preparations

averaged 0.055 mol heme mol−1 protein monomer as determined by the pyridine hemochromogen assay. HemA1−412 [C170A]-His6 was purified according to the Interleukin-3 receptor same protocol as that used for HemA1−412-His6. The C170A mutant protein was colorless, suggesting that it is unable to bind heme. The absence of heme was also demonstrated by its absorption spectrum, which lacks the peaks characteristic of heme-containing proteins (Fig. 1b). The HemA spectrum is that of a b-type heme; this class of molecules is attached noncovalently. Treatment with the strong denaturant, 6 M guanidine-HCl, removed a maximum of 7% of heme from HemA, and in two trials, failed

to remove any (Supporting Information). The ability to retain noncovalently bound heme in the presence of strong denaturants has been documented for other proteins (Hargrove & Olson, 1996; Wójtowicz et al., 2009). Although these results demonstrate a strong association between heme and HemA, covalent binding cannot be inferred from this assay. Thiol reagents, which have been used to distinguish covalent heme-protein bonds, are incompatible with Ni-NTA. The nature of the association between heme and HemA was further examined using a different method. Heme-associated peroxidase activity, which can be measured by standard ECL reagents (a Western blot without the antibody; Dorward, 1993), detects heme-binding proteins (such as cytochrome c). Purified proteins were separated by SDS-PAGE and then assessed for heme-associated peroxidase activity.

Greater CD4 increases from 12 weeks with nevirapine could have caused more serious immune reconstitution inflammatory syndrome (IRIS) [20]. However, week 4 and 12 viral load

changes were similar in the two groups, and the clinical events diagnosed were not predominantly IRIS-type events. Furthermore, there was no clear association between developing clinical events and rapidity of viral load changes, nor did the difference between nevirapine and abacavir vary with pre-ART CD4 cell count, both strong predictors of IRIS [21,22], nor was there evidence that the differences between groups were restricted to the first 6 months on ART when IRIS events would be likely to predominate. Emergence of HIV resistance mutations is described separately [5] but, given that higher viral load suppression was substantially and significantly greater in the nevirapine group, it is unclear how any Fulvestrant nmr differences in resistance accumulation GDC-0199 ic50 or the relative fitness cost of NNRTI and NRTI mutations could have increased overall disease progression relative to the abacavir group. If suboptimal virological potency of abacavir was driving results, either

more ART modifications or more clinical events (or both) would be expected in the abacavir group – neither was observed. While patients initiating ART with advanced HIV disease and low CD4 cell counts may be at higher risk of opportunistic infections, it is unclear why their risk would be greater on nevirapine- than abacavir-containing regimens. Furthermore, we found no evidence to suggest that absolute levels of CD4 and HIV RNA had different prognostic values for clinical outcomes in the nevirapine and abacavir groups, Molecular motor and after adjustment for time-updated CD4 cell count, haemoglobin and weight, differences between randomized groups were similar to those obtained in unadjusted analyses. Without stored cells, we are unable to explore whether the quality rather than the quantity of CD4 immune restoration differed between the abacavir and nevirapine groups. The only published data appear to be

those of a small study in children simplifying from boosted protease inhibitor to triple NRTI therapy, which demonstrated increased functionality [23]; whether this would be similar in ART-naïve adults in NORA is unclear. Nevertheless, our findings highlight the importance of close follow-up and high-quality clinical management (including primary and secondary prophylaxis/treatment for opportunistic infections) for patients initiating ART with advanced disease. The timescale for changes in prognostic markers to influence clinical outcome could differ; i.e. inferior 48-week immunological/virological response in the abacavir group might lead to poorer clinical outcome only later on. We noted a trend towards superior weight gain with nevirapine at 48 weeks but not before; and a nonsignificant (P=0.

Silver diamine fluoride (SDF) has been shown to be a successful treatment for arresting IWR-1 in vitro caries. However, the mechanism of SDF is to be elucidated. Aim.  To characterize the effects of SDF on dentine carious induced by Streptococcus mutans and Actinomyces naeslundii. Design.  Thirty-two artificially demineralized human dentine blocks were inoculated: 16 with S. mutans and 16 with A. naeslundii. Either SDF or water was applied to eight blocks in each group. Biofilm morphology, microbial kinetics and viability were evaluated by scanning electron microscopy, colony

forming units, and confocal microscopy. The crosssection of the dentine carious lesions were assessed by microhardness testing, scanning electron microscopy with energy-dispersive x-ray spectroscopy and Fourier transform infrared spectroscopy. Results.  Biofilm counts were reduced in SDF group than control (P < 0.01). Surfaces of carious lesions were harder after SDF application than after water application (P < 0.05), in S. mutans group, Ca and P weight percentage after SDF application than after water application (P < 0.05). Lesions showed a significantly reduced level of matrix to phosphate

after SDF treatment (P < 0.05). Conclusion.  Present study showed that SDF posses an anti-microbial activity against cariogenic biofilm of S. mutans or A. naeslundii formed on dentine surfaces. SDF slowed down demineralization of dentine. This dual activity could be the reason MAPK inhibitor behind clinical success of SDF. “
“Resins used in dental composites, derived from bisphenol-A (BPA), have been shown to alter immune cells. The objective of this

study was to explore children’s immune function changes in relation to resin composite treatment. We conducted secondary data analysis of the New England Children’s Amalgam Trial immune function substudy (N = 59). Immune function was measured pre-treatment and up to five times post-treatment through 5-year follow-up. Multivariable generalized linear regression models were used to estimate the association between three classes of resin composites (bisphenol-A-diglycidyl-dimethacrylate [BisGMA]-based flowables used for preventive sealants; urethane dimethacrylate [UDMA]-based compomer restorations; bisGMA-based restorations) and changes in immune function markers ifenprodil measured annually. Total white blood cell counts and responsiveness of T cells or neutrophils were not appreciably altered by composite treatment levels. Changes in B cell responsiveness were greater throughout follow-up among children with more bisGMA-based composite restorations, which opposed findings for amalgam treatment levels. Monocyte responsiveness changes were decreased at 6 months with greater treatment, but not over longer follow-up. Results of this analysis showed no overt immune function alterations associated with resin composites.

This ferredoxin domain substitutes the portion of colicin M required for receptor binding and translocation, presumably fulfilling this role by parasitizing an existing ferredoxin-based

iron acquisition pathway. The ability of susceptible strains of Pectobacterium to utilize plant ferredoxin as an iron source was also demonstrated, providing additional evidence for the existence of such a system. If this hypothesis is correct, it represents the first example of iron piracy directly from a host protein by a phytopathogen and serves as a testament of the flexibility of evolution in creating new bacteriocin specificities. Iron is essential for most life due to its role as a cofactor in the transport and storage of oxygen and in numerous redox reactions buy INK 128 (Lindley, 1996). While abundant, iron is effectively insoluble under aerobic conditions making it the limiting nutrient for microbial life in many environments (Krieg et al., 2009). To overcome this obstacle and to obtain iron in a form available for growth, bacteria produce and secrete a diversity of molecules with strong affinity for ferric iron (Fe3+) or iron-containing compounds. These molecules range in size from small organic acids (citrate) to larger siderophores (catecholate) and proteins (haemophores; Ratledge & Dover, 2000). In Gram-negative bacteria, the outer

membrane serves as a permeability barrier protecting the cell from antibiotics, detergents and cell-wall-degrading enzymes Montelukast Sodium (Delcour, 2009). However, the outer membrane bilayer also serves as a barrier STA-9090 to the uptake of iron-scavenging compounds and as such it contains a conserved family of β-barrel receptors (TonB-dependent receptors), which selectively transport iron and other nutrient-containing compounds using energy derived from the proton motive force, through interaction with the TonB–ExbB–ExbD

complex (Pawelek et al., 2006). Some bacteria also produce receptors for the import of noncognate siderophores (xenosiderophores), providing an advantage to the microorganisms in a mixed community where the vast majority of soluble iron exists in a siderophore complex (Jurkevitch et al., 1992; Greenwald et al., 2009). The availability of iron can also be a deciding factor in the success or failure of bacterial infection, and consequently, mammalian hosts restrict the availability of iron through the production of iron-binding proteins, transferrin, lactoferrin, haemoglobin and ferritin. Siderophores produced by some pathogens bind iron with ultra-high affinity and so are able to scavenge iron directly from host-binding proteins (Weinberg, 2009). Other bacteria acquire iron directly from these host proteins, either through binding to a cell surface receptor or through the production and secretion of binding proteins (Cornelissen & Sparling, 1994).