Both groups also matched for age and country of birth, but selleck compound not for gender: travelers with diabetes were more often male. Yet, prospective studies on travel-related infectious diseases found no association of symptoms of infectious diseases and gender.20,21 Theoretically, if one

of the sexes document their symptoms better than the other, differences between travelers with diabetes and their travel companions may have been underestimated or overestimated. Groups did not match for cardiovascular disease and dyslipidemia. However, we are not aware of any association of travel-related infection and cardiovascular disease or dyslipidemia. The prevalence of diabetes among visitors of our clinic was 3.1%, comparable with the general population.12 Also, age and male–female ratio of our subjects with diabetes were comparable with the general diabetic population. Participants’ travel destinations were equally distributed across the four regions. Their median travel duration of 20 days corresponded well with the median travel duration GSI-IX ic50 of the average traveler.22,23 Thus, the study sample can be considered representative, and results can reasonably be applied to the average traveler with diabetes to a developing country.

This study also had some limitations. Sample size may not have been large enough to detect small differences. Secondly, some of the symptomatic illnesses could have been due to a non-infectious cause. Although the study design with a travel companion serving as a matched control minimized differences in exposure to environmental and infectious agents between the two groups, this may have overestimated AZD9291 in vivo the (absolute) rate of infection in all groups. Thirdly, although the diary provided information on symptom duration, it did not distinguish mild symptomatology from severe. For example, travelers with diabetes could

have had more bowel movements or more water loss. Finally, travelers with diabetes and controls differed in counseling and prescription; some travelers with diabetes did use the stand-by antibiotics. Therefore, the data may be skewed toward seeing less differences in outcome measures between both groups. Regular testing of blood glucose levels during travel was not part of the study protocol. Yet, three IDD (4.3%) and two NIDD (2.4%) reported dysregulation of blood glucose levels during travel. Two IDD reported hypoglycemia coinciding with non-febrile diarrhea, for which one took stand-by antibiotics. Both NIDD only reported hyperglycemia; in one traveler this coincided with non-febrile diarrhea, for which no stand-by antibiotics were taken. There is only one previous publication on travel-related dysregulation, which suggested that travel to the tropics is a risk factor for metabolic dysregulation.4 Yet, data were collected retrospectively, by telephone interviewing, and the study sample comprised only 19 subjects, all IDD.

The flasks were then inoculated with this suspension to an initial OD600 nm of 0.05 in 25 mL of fresh DM with or without thiamine and incubated at 37 °C with shaking. The OD600 nm was then measured at appropriate intervals throughout isocitrate dehydrogenase inhibitor review the growth. Cultures grown in 25 mL BHI in 250 mL flasks with shaking at 37 °C were assayed for acid tolerance by diluting 1 : 10 into BHI medium adjusted to pH 3.0. At suitable intervals, samples were removed, serially diluted, and 10 μL aliquots of each dilution were plated on BHI agar plates. Colonies were counted after 24 h at 37 °C and survival was calculated as a percentage of the

cell count at time zero. For acid-adapted cultures, cells were first diluted 1 : 10 into BHI medium adjusted to pH 5.0, incubated for 1 h, and then further diluted 1 : 10 into BHI medium adjusted Ku-0059436 manufacturer to pH 3.0. For experiments on thiamine-depleted cells, cultures were grown in DM either with or without thiamine supplementation (3 μM), and then after 12 h of growth, cells were diluted 1 : 20 into DM adjusted to pH 3.0 (which contained thiamine). Survival was determined by serial dilution and plating on BHI agar plates

as described above. Relative transcript levels of thiT in exponentially growing cells (OD600 nm = 0.6) at pH 5.5 or pH 5.0 compared to pH 7.0 were measured by real-time RT-PCR as previously described (Utratna et al., 2011). Acetoin was determined by the modified Voges–Proskauer reaction of Westerfeld (1945), with slight modification. Stationary phase cultures of L. monocytogenes wild-type and mutant grown in both DM supplemented with thiamine and DM without thiamine were recovered and centrifuged at 14 500 g for 5 min. The supernatants were used to measure the acetoin production. To 1.0 mL of culture supernatant in DM, diluted appropriately to give a reading within the range of the calibration curve for acetoin, 0.2 mL of 0.5% (w/v) l-arginine monohydrochloride and 0.2 mL

of 5% (w/v) α-naphthol in 2.5 N NaOH were added, in that order. The pink color that developed after Cyclin-dependent kinase 3 1-h incubation was measured by recording the absorbance at 530 nm using a UV-VIS spectrophotometer (Spectronic® 20 Genesys™). The concentration of acetoin was estimated from a linear calibration curve based on measurements of standard acetoin solutions (0.01–40 μg mL−1). To identify genetic determinants of acid tolerance in L. monocytogenes, a library of 4800 transposon (Tn917-lacZ) mutants was screened for mutants displaying an acid-sensitive phenotype at pH 3.0. One acid-sensitive mutant, initially designated ads12, was found to induce a poor adaptive ATR at pH 5.0 compared to the wild-type, indicated by a dramatically reduced ability to survive at pH 3.0 (Fig. 1a).

For example, deletion and homologous overproduction experiments have shown that red light absorption by the RsbP protein can activate a stress response in Bacillus subtilis (Avila-Perez et al., 2010). Blue light, either sensed by a photoreceptor or initiating photosynthetic electron transport, has the opposite effect on the transcription of photosynthesis-related genes in Rhodobacter sphaeroides (Happ et al., 2005). Furthermore, a blue light–activated histidine kinase (HK), frequently used for environmental sensing by bacterial two-component transduction systems (TCSTS), has been shown to regulate Brucella abortus virulence (Swartz et al.,

2007). Blue light photoreceptors are of the utmost importance for some organisms, allowing the development of DNA-repair IDH inhibitor clinical trial systems in light illumination (Weber, 2005), the formation of protective (shielding) substances or for allowing learn more motile organisms to escape from regions with a high UV/blue light intensity (Armitage & Hellingwerf, 2003). Per-ARNT-Sim (PAS) domains are important signalling modules that monitor changes in light, oxygen, voltage (LOV), small ligands and the overall

energy level of a cell (Taylor & Zhulin, 1999). Prokaryotic genome analysis with bioinformatics methods has revealed the presence of PAS-domain-containing proteins (thereafter PAS proteins) in approximately 15% of all sequenced genomes, and 81.36% of the more than 22 000 identified PAS domains were found in bacteria (Letunic et al., 2006). Increasing experimental evidence suggests

that many PAS domains act as photoreceptors. Although sequence identity is low in the PAS superfamily (Taylor & Zhulin, 1999), the three-dimensional structures of PAS domains are highly conserved (Zhong et al., 2003), suggesting that common mechanisms may be used for signalling. The revealed general secondary structure of a PAS domain is ββααααβββ, and cofactors frequently interact with α helixes (Möglich et al., 2009; Jaiswal et al., 2010). Light promotes the detachment of the Jα helix from the central beta-sheet Amoxicillin (Harper et al., 2003) and its subsequent unfolding of the second PAS domain in oat phototropin (Hoersch et al., 2010). Therefore, the secondary structure topology (SST) of the PAS domain is valuable to reveal the activation sites of PAS domains and further to analyse functions of PAS proteins. The integration of SST analysis and determining the sequence of PAS domains will be an effective and promising methodology. Xanthomonas campestris pv. campestris (Xcc) is the causative agent of crucifer black rot disease, which causes severe losses in agricultural yield worldwide (Swings et al., 1993). This organism generally invades and multiplies in cruciferous plant vascular tissues, resulting in the characteristic ‘black rot’ symptoms of blackened veins and V-shaped necrotic lesions at the foliar margin (Alvarez, 2000).

At the investigated early time point of cold adaptation, the transcriptome is reprogrammed in almost all functional categories, but the protein profile has still not adapted to the change of living conditions in the cold. S.F. received a predoctoral

stipend from the DFG-supported IRTG 653 ‘Pseudomonas: Pathogenicity and Biotechnology’. Financial support was provided by BMBF within the framework of the SysMO consortium, part PSYSMO ‘Towards a quantum increase in the performance of P. putida as the cell factory of choice for white biotechnology,’ project 3: Key determinants of abiotic stress response of P. putida KT2440′. Table S1. Genes that were PD-0332991 chemical structure detected to be differentially expressed upon cold shock according to Illumina cDNA sequencing. Table S2. Calculated SD of biological replicates at 10 °C. Table S3. Calculated SD of biological Androgen Receptor Antagonist molecular weight replicates at 30 °C. 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. “
“Saccharomyces boulardii is a probiotic strain that confers many benefits to human enterocolopathies and is used against a number of enteric pathogens. Candida albicans is an opportunistic pathogen that causes intestinal infections in immunocompromised patients, and after translocation into the bloodstream, is responsible for serious systemic candidiasis. In this study, we investigated the influence of S. boulardii cells and its culture extract 3-mercaptopyruvate sulfurtransferase on C. albicans adhesion to Caco-2 and Intestin 407 cell lines. We also tested the proinflammatory IL-1β, IL-6 and IL-8 cytokine expression by C. albicans-infected Caco-2 cells, using real-time RT-PCR. We found that both S. boulardii and its extract significantly inhibited C. albicans adhesion to epithelial cell lines. The IL-8 gene expression by C. albicans-infected

Caco-2 cells was suppressed by the addition of S. boulardii extract. Our results indicate that S. boulardii affects C. albicans adhesion and reduces cytokine-mediated inflammatory host response. The natural microbiota and the surface of the intestinal mucosa interact with each other and act as a barrier to prevent colonization of the intestine surface by pathogenic microorganisms. Pathogen infections induce the secretion of many cytokines by epithelial cells, including tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-4, IL-6 and IL-8 (Kagnoff & Eckmann, 1997; Xing et al., 1998; Apte & Voronov, 2002). Candida albicans is the most common opportunistic fungal pathogen isolated from the human body. It possesses many virulence factors such as adhesion, biofilm formation and morphological transformation. The first and necessary step in infection is adherence.

Statistically significant differences in motility diameters were identified by one-way anova in R (Chambers et al., 1993). Viable cell counts were performed on the same cultures used for each paired bioassay and western blot experiment.

Serial dilutions were plated and colony-forming units (CFU) were calculated to determine the number of viable cells for each culture. Each mutant strain was compared with the wild type in three biological replicates. Statistically significant differences in viable cell numbers were identified by one-way anova in R (Chambers et al., 1993). The R. capsulatus SB1003 (Strnad et al., 2010) regulatory gene orthologs discussed in this work are rcc01663 (ctrA), rcc01662 (sciP), rcc03000 (chpT), and rcc01749 (cckA); all four genes are predicted to be transcribed as independent mRNAs based on genomic context (Strnad et al., 2010) and transcriptome data (Mercer et al., 2010). We compared the R. capsulatus phosphatase inhibitor library CtrA, CckA, ChpT, and SciP sequences to the C. crescentus orthologs, and the regions of similarities and the conserved protein domains identified (Marchler-Bauer et al., 2010) are shown in Fig. 1. We made strains with disruptions in the chpT and sciP genes to test whether

these proteins were involved in the regulation of motility and RcGTA production, as found for CtrA and CckA (Lang & Beatty, 2000, 2002). Additionally, we constructed a new cckA mutant because the original R. capsulatus mutant strains (Lang & Beatty, 2000, 2002) retained ~70% of the cckA coding sequence undisrupted before the insertional mutation site (between the HA and REC domains; Fig. 1), possibly allowing for the expression of Selleck Bafetinib a partially functional protein. We also created a ctrA/sciP double mutant. Flagellar motility of the cckA, chpT, sciP, and ctrA/sciP mutants was assayed using soft agar stabs and compared with wild-type strain SB1003 and the ctrA mutant (Fig. 2). Motility in both the chpT and cckA mutants was reduced, but not as severely as for the ctrA and ctrA/sciP strains, while sciP disruption had no observable effect. Complementation in trans of chpT

and cckA restored motility. Wild-type ctrA does restore motility in the ctrA mutant, but neither ctrAD51E nor ctrAD51A were able to restore motility in the Fossariinae ctrA, cckA, or chpT mutants. The ctrAD51E gene was able to partially restore motility in the ctrA/sciP double mutant (Fig. 2e). Tests for significant differences in swimming distances were performed, and all anova results are available in Supporting Information, Table S1. RcGTA gene transfer activity was assayed for the ctrA, cckA, chpT, sciP, and ctrA/sciP mutants (Fig. 3a). This was paired with analyses of RcGTA capsid protein levels in both cell and culture supernatant samples by western blotting (Fig. 3b–f). As expected, the ctrA and ctrA/sciP mutants had no detectable RcGTA activity (Fig. 3a) or capsid protein expression (Fig.

, 2008, 2010). Although the assumption that ionotropic glutamate receptors are expressed by cholinergic JAK inhibitor terminals would provide a straightforward mechanism underlying these glutamatergic–cholinergic transient interactions, to our knowledge the presence of ionotropic glutamate receptors on cholinergic terminals has not been investigated. Thus, a more complex, multi-synaptic mechanism underlying the relationship between prefrontal cholinergic and glutamatergic signaling cannot be excluded. We will return

to the discussion of potential synaptic mechanisms further below following the discussion of the cognitive functions of cholinergic transients. Cholinergic inputs to the cortex are necessary for attentional performance and specifically for the detection and use of instructive cues to guide decisions about ongoing behavior (Muir et al., 1992; McGaughy et al.,

1996; Turchi & Sarter, 1997; Dalley et al., 2004; Botly & De Rosa, 2009). The use of cues to guide behavior buy Antiinfection Compound Library henceforth is termed ‘detection’, as defined in Posner et al. (1980). Importantly, this definition integrates the perceptual with the cognitive processes involved in the decision to report a signal – ‘By detection, we will mean the entry of information concerning the presence of a signal into a system that allows the subject to report the existence of the signal by an arbitrary response indicated by the experimenter’ (Posner et al., 1980, p. 162). Cholinergic activity in the cortex serves both neuromodulatory and deterministic functions, albeit via separate mechanisms. Our current model assumes that that the cholinergic neurons that modulate cortical circuitry form a separate population from those that generate the transient release events that are integrated into cortical information processing and exert deterministic functions (Hasselmo & Sarter, 2011; see also Hasselmo & Bower, 1992). This assumption awaits further testing, but separate cholinergic cell populations may be revealed based on, for example, their topographic organisation in the basal forebrain, differential

Lck histological markers, and/or their differential cortical vs. subcortical afferent organisation (Unal et al., 2012; Zaborszky, 2002; Zaborszky et al., 2005, 2013; Fig. 1). In the present context, the neuromodulatory component of cholinergic activity is hypothesised to influence the probability and amplitude of cortical glutamatergic–cholinergic transients, primarily via stimulation of nAChRs (as described above). The level of this neuromodulatory influence has been shown to co-vary with demands on attentional control, not level of performance. That is, performance-associated increases are highest when performance is low as a result of distractors, extended time on task, or pharmacological challenges (Kozak et al., 2006; Sarter et al., 2006; St Peters et al., 2011).

Sclerosing cholangitis presents with right upper quadrant pain, vomiting and raised alkaline phosphatase levels. 4.4.3.3 Diagnosis. The diagnosis of cryptosporidiosis is made by a stool flotation method with subsequent Ziehl–Neelsen, auramine phenol or acid-fast trichrome staining to differentiate oocysts from yeasts [71]. Oocysts may be detected more easily by direct

immunofluorescence or enzyme-linked immunosorbent assay [72], which have a similar sensitivity to PCR techniques [73]. In individuals with profuse diarrhoea, cryptosporidiosis may be detected in a single stool sample, but multiple samples may be required in those with less severe infection Vorinostat as oocyst excretion may be intermittent. Small bowel and rectal histology may be useful although the latter has a low sensitivity for diagnosis. In individuals with abdominal pain, endoscopic retrograde cholangio-pancreatography (ERCP) may reveal ampullary stenosis and sclerosing cholangitis with associated thickening of the gall bladder wall. 4.4.3.4 Treatment. There is no check details specific treatment targeting cryptosporidium directly. Early HAART is imperative and is associated with complete resolution of infection following restoration of immune function [74,75]. In individuals with profuse diarrhoea, therapeutic drug monitoring may be required to confirm adequate absorption of antiretroviral

agents. Paromomycin is active in animal models [76], although a recent meta-analysis has shown no evidence for clinical effectiveness [77]. A study combining paromomycin with azithromycin reported substantial reduction in stool frequency and volume, together with diminished oocyst shedding [78].

Paromomycin was given orally as 500 mg four times daily or 1 g twice daily for up to 12 weeks. The dose of azithryomycin was 500 mg daily. However the small numbers in this study and the limited experience of this combination preclude its choice as a front line therapy. Nitazoxanide has been approved for use in immunocompetent individuals but has not been shown to be superior to placebo in the severely immunocompromised [79]. If used, nitazoxanide is given at a dose of 500 mg twice daily for 3 days, but may be required for up to 12 weeks. Trials have also investigated a larger dose of 1 g bd po [80]. When an anti-cryptosporidial agent is chosen nitazoxanide CYTH4 is the preferred agent but its efficacy is limited in more immunocompromised patients. Supportive therapy with iv fluid replacement/antimotility agents is essential. First-line treatment for cryptosporidiosis is with effective antiretroviral therapy (category recommendation III). 4.4.3.5 Impact of HAART. The use of optimized HAART should be continued to prevent relapse 4.4.3.6 Prevention. Standard drinking water chlorination techniques are not sufficient to eradicate the parasite. Specific filtration employing an ‘absolute’ 1-micron filter is required [81].

Resolved proteins were transferred to polyvinylidene difluoride membranes (Thermo Scientific), and detected with mouse anti-FLAG Ab M2 (1 : 5000) and alkaline phosphatase-conjugated goat anti-mouse IgG (1 : 10 000) as described previously (Uzzau et al., 2001). Salmonella Typhi strains were grown overnight in LB broth at 37 °C with shaking. Aliquots of these cultures were subcultured in LB broth and supplemented with chloramphenicol Vincristine when required. To induce STY1365 expression, isopropyl-β-d-thio-galactoside (IPTG, Sigma) was added

at a final concentration of 1 mM. Cultures were incubated with shaking at 37 °C and growth was measured at OD600 nm. Salmonella Typhi strains were grown overnight in LB broth at 37 °C with shaking. Subcultures of strains were grown in LB broth and supplemented with chloramphenicol and IPTG when required. At an OD600 nm of 0.2, bacteria were harvested by centrifugation, and extraction of outer-membrane proteins was performed as described above. Proteins

were quantified using the Pierce® BCA Protein Assay Kit (Thermo Scientific). Twenty micrograms of proteins were resolved by SDS-PAGE (12.5%) as described by Lobos & Mora (1991). The intensity of bands was analyzed using imagemeter software (Adobe) Exposure of bacteria to crystal violet (1.5 μg mL−1) was performed by the method described previously (Onufryk et al., 2005). The efficiencies of plating were calculated by dividing the number of CFUs of a given strain on supplemented LB plates by

the number of CFUs of the same strain on LB plates. below Assays for each strain were performed Alectinib in duplicate and repeated three times with three independent isolates. All results are expressed as the means±SD of an individual experiment performed in triplicate. P-values were calculated according to Student’s t-test, and a value of P<0.05 was considered to be statistically significant. According to S. Typhi CT18 genome, STY1365 corresponds to a sequence interrupted by a premature stop codon (TGA). This observation was correlated to the data obtained by the STY1365 sequencing in S. Typhi STH2370 (Rodas et al., 2010). To find sequences with identity to STY1365 and flanking regions a blast algorithm was used. We found two sequences both with identity to a prophage-like element of S. Typhimurium DT104 (Saitoh et al., 2005; Fig. 1a). One sequence corresponds to artA and the other sequence to artB. Although no putative ORFs were annotated downstream of artB, our analysis showed that this region has 89% of identity to STY1365, suggesting that this is probably a prophage-like element (Fig. 1a). No dual-start motif was found in the predicted amino acid sequence of STY1365, but our blast searches revealed that the closest homologues of STY1365 amino acid sequence (57 residues) are all putative holins of different E. coli strains and the phage ΦP27. STY1365 showed 76% identity (e=6e−12) to EcolTa2 holin of E. coli TA271, 78% identity (e=4e–11) to ECDG_01257 holin of E.

1b) with MicrobesOnline Operon Predictions (http://www.microbesonline.org/operons/). Five operons, mlr6787-mlr6788, mlr6792-mlr6793, mlr6796-mlr6798-mlr6799, mlr6801-mlr6802-mlr6803-mlr6804, and mlr6806-mlr6807, are polycistronic. Other operons are monocistronic.

Two operons, beginning with mlr6796 and mlr6801, encode proteins that are related to ABC transporters. The functions of three monocistronic genes, mlr6789, mlr6790 and mll6800, are unknown. Besides the mlr6787 operon, five transcriptional units are related to the vitamin B6 degradation pathway I. Additional potential operator sites associated with these genes were searched for. Although several palindrome sequences were found upstream of genes, none of them was similar to the Selleckchem Dasatinib previously identified palindrome sequence (GATTGTCAGACAATC) and we could not find any predicted PyrR binding sites. As a next step, gel retardation assays against the potential regulatory regions should be performed. selleck chemical The effect of the PyrR concentration on the gel-shift of the 135-bp fragment was examined (Fig. 4). The gel-shift was concentration-dependent. With a high concentration

of PyrR (Fig. 4, lanes 8–10), the fragment moved upward as an additional band, suggesting that tetrameric assembly of the PyrR protein had occurred. There are examples of such assembly following DNA binding by Gnt superfamily proteins (Hoskisson & Rigali, 2009). Although the dissociation constant of PyrR was estimated to be 167.9 ± 57.5 μM, based on the density of the main band in lanes 4–7, the value was high and may be an artifact of the blotting technique. Thus, accurate determination of the dissociation constant by another method is required. Pyridoxine induced activities of degrading enzymes (Table 2), indicating that it could work

as an effector molecule. Therefore, pyridoxine and related compounds, Methane monooxygenase pyridoxamine and pyridoxal, were added to the gel retardation assays. When pyridoxal and pyridoxamine were added, the relative amount of the free form of the nucleotide probe increased (Fig. 5), demonstrating that these compounds had an inhibitory effect on binding of PyrR to the DNA. On the other hand, pyridoxine did not appear to prevent DNA binding. Further study will reveal the mode of interaction between PyrR and its effector molecules. “
“Penicillium digitatum, causing citrus green mold, is one of the most devastating pathogenic fungi for postharvest fruits. The disease control is becoming less efficient because of the dispersal of fungicide-resistant strains. However, genome-scale analyses of its resistance mechanism are scarce. In this work, we sequenced the whole genome of the R1 genotype strain Pd01-ZJU and investigated the genes and DNA elements highly associated with drug resistance. Variation in DNA elements related to drug resistance between P.

After all, travelers play a central role in the global spread of STIs, especially travelers to tropical and subtropical regions with the highest worldwide prevalence of STIs including HIV.[38, 39] Accidents were the only risk perceived higher after travel but significantly lower by travelers than by experts (Figure 3). Injuries, particularly road traffic accidents, are the second most common cause of death abroad

after cardiovascular disease[40-43] and the leading cause of death of those aged 15 to 29 years worldwide.[44] Over 90% of road traffic fatalities occur in low- and middle-income countries,[44] including Talazoparib order many tourist destinations in the tropics and subtropics. Higher mortality rates due to vehicle accidents have been found among travelers than among the local population.[45] Travelers are often not familiar with poor road conditions and different, partly insufficient or insufficiently enforced[44] road traffic laws, and they might engage in high-risk behavior during vacation. Despite their potential

for disability[44] and other complications, little is known about the incidence, type, and severity of nonfatal 3MA accidents among travelers. Injuries were reported by 6 to 16% of travelers in three different studies,[14, 46, 47] most of them due to road traffic accidents. The most vulnerable groups on the road are pedestrians, (motor) Dapagliflozin cyclists, and users of unsafe or overcrowded public transport.[44] Some studies suggest that (young) men are most likely to be involved in (fatal) vehicle crashes[43, 48] and engage in more

risk-taking activities than women.[14, 49] However, there were no gender- or age-related differences in the perception of accidents in this study (Figure 4). The post-travel increase in perception is most likely due to observed danger abroad. In other studies, accidents were also rated as a more important health problem during or after a stay abroad than before.[10, 50] In order to raise awareness of this potentially life-threatening risk before departure, information about accidents abroad including practical preventive measures needs to be an integral part of pre-travel health advice. PRISM has only been validated for the assessment of the subjective burden of a present illness, not for the perception of health risks in the near future and past. Nevertheless, a fast, nonverbal visual tool[16] may take into account the emotional quality of (risk) perception which is subjective among both travelers and experts. Statistical correlation of the perception of risks with their incidence was not an option as up-to-date, comparable data were not available or collected. However, the experts’ risk assessment, used as a reference point, proved to be consistent with current literature. Generalization of the results is limited owing to the single location of the study.