Results

from the 24- and 36-month study visits are presented here. Twelve-month study visit results have been published previously in the 52-week follow-up study Maraviroc report [14]. Nineteen patients were available for the 24-month analysis, and 17 patients remained at the 36-month analysis having been followed up for a period of at least 12 months since their last treatment. Mean weight at 24 months was 77.7 ± 11.6 kg (P=0.16 vs. baseline) and at 36 months was 79.1 ± 12.1 kg (P<0.05 vs. baseline). At baseline, all 20 patients received an injection of hyaluronic acid in each cheek in the nasogenian area. The mean volumes of gel injected into each cheek at baseline were 1.77 mL (range 1–2.2 mL). Fifteen patients received a touch-up treatment at week 4 (mean volume 1.9 mL in each cheek; range 0.6–3.0 mL). At the 12-month follow-up visit, 13 patients were treated (mean volume 1.9 mL in each cheek; range 0.8–3.0 mL) and 1 patient was given a touch-up treatment of 1 mL selleckchem of gel in each cheek. The final study treatment was given at the 24-month visit, where 13 patients were treated (mean volume 1.9 mL in each cheek; range 1.0–3.0 mL) and 6 patients had a touch-up treatment (mean volume 1.6 mL in each cheek; range 1.0–2.7 mL). Approximately 6 weeks after each

treatment, patients attended a post-treatment consultation. Mean (± standard deviation) total cutaneous thickness increased from 6 ± 1 mm at baseline to 12 ± 2 mm at 24 months (P<0.001) and 12 ± 1 mm at 36 months (P<0.001 vs. baseline). At 24 months, the response rate, defined as total cutaneous thickness >10 mm, was 85% (17/20, 1 patient missing) and at 36 months was 70% (14/20, 3 patients missing). Five patients received treatment only at the baseline visit. Of these five patients, three had higher total cutaneous thickness scores at 36 months measured by

ultrasound, one patient had a higher total cutaneous thickness score at 24 months before he was lost to follow up, and no follow up ultrasound was performed on the last patient. Two patients received treatment only at the baseline and 12-month visits. At 36 months, 2 years later, both patients had higher total cutaneous thickness scores. One of these patients Tryptophan synthase was a treatment responder with a total cutaneous thickness >10 mm. When evaluating the effect of treatment using the Global Aesthetic Improvement Scale at 24 months, 14 out of 19 patients classified their facial appearance as very much improved or moderately improved (Table 1). At the 36-month study visit, which was at least 12 months after the last treatment session, 15 out of 17 patients classified their facial appearance as very much improved or moderately improved. Patient visual analogue assessments and self-esteem scores increased significantly from baseline and persisted through to 36 months (Table 2). No serious adverse events were reported at the 6-week post-treatment consultations.

After vortexing, the samples were boiled in a water bath for 10 min and subsequently refrigerated at 4 °C for 10 min. Finally, the samples were centrifuged at 16 000 g for 2 min and 100 μL of the

supernatant was used as template DNA. All samples were immediately used for multiplex click here and real-time PCR assays after preparation. The PCR assay was optimized using an MJ PTC 100 thermocycler (Bio-Rad, Hercules, CA). The primer sets for the PCR assay are listed in Table 2. All primers were synthesized by Integrated DNA Technologies (IDT, Coralville, IA). The reactions resulted in a 90-bp fragment for C. jejuni, a 150-bp fragment for E. coli O157:H7 (Sharma et al., 1999), and a 262-bp fragment for S. Typhimurium. (Cheng et al., 2008). The Campylobacter spp. primers were designed

by targeting a conserved region of the hsp60 gene. Reactions specific for each pathogen were first carried out independently and each reaction consisted of a 25-μL total volume mixture with 12.5 μL of SYBR Green Premix Ex Taq™ (Takara, Fisher Scientific, Pittsburg, PA), 800 nM of each primer, 1.6 μL of bovine serum albumin (BSA, 20 mg mL−1), 1 μL of DNA template, and water to volume. After CDK inhibitor each PCR reaction was optimized independently, an m-PCR reaction was optimized to detect all three pathogens simultaneously and three independent experiments were performed to verify the reproducibility. The m-PCR reaction consisted of 25 μL of total volume mixture with 12.5 μL of SYBR Green Premix Ex Taq™ (Takara, Fisher Scientific), 400 nM of Campylobacter spp.-specific primers, 400 nM of E. coli O157:H7-specific primers, 960 nM of Salmonella spp.-specific primers, 1.6 μL of BSA (20 mg mL−1), 3 μL of three DNA templates, and water to volume. The PCR reaction was optimized to conditions of 94 °C for 2 min. and then 35 cycles

of 94 °C for 30 s, 55 °C for 30 s, and 72 °C for 30 s, with a final extension cycle at 72 °C for 5 min. The PCR products were separated in a 2% agarose gel at 100 V for 20 min. Gels were stained with ethidium bromide (10 mg mL−1) and viewed using a UV transilluminator. The SYBR green real-time PCR assay was optimized using an Eppendorf Masterplex thermocycler ep (Eppendorf, Westbury, NY). Gradient Technology in the Eppendorf unit was used to optimize annealing and extension temperatures and times. Real-time PCR assays were conducted Loperamide as three independent experiments and triplicate samples per experiment. The same primer sets utilized for conventional PCR, listed in Table 1, were also used for the SYBR green real-time PCR reaction. A 25-μL total volume reaction mixture consisted of 12.5 μL of SYBR Green Premix Ex Taq™ (Takara, Fisher Scientific), 800 nM of each primer, 1.6 μL of BSA (20 mg mL−1), 1 μL of DNA template, and water to volume. The PCR reaction was optimized to the conditions of 95 °C for 2 min., followed by 40 cycles of 95 °C for 15 s, 55 °C for 15 s, and 68 °C for 20 s, with fluorescence being measured during the extension phase.

faecalis is grown under respiration-permissive conditions, that is, in the presence of heme. Glycerol can be metabolized by E. faecalis via two different pathways (Jacobs & Vandemark, 1960; Bizzini et al., 2010). One of them,

which is predominant in strain OG1RF, comprises BMN 673 price the enzyme glycerol-3-phosphate oxidase (GlpO) that oxidizes glycerol-3-phosphate to dihydroxyacetone phosphate and reduces molecular oxygen to hydrogen peroxide. It was shown previously that an E. faecalis Npr-defective mutant grows poorly on media containing glycerol as carbon source due to accumulation of hydrogen peroxide in the cell (La Carbona et al., 2007). The npr transposon-insertion mutant EMB15 used in this study showed the same phenotype when grown on TSB agar plates supplemented with 0.3% glycerol. Supplementation of the medium with 8 μM hemin allowed normal growth of strain EMB15 also in the presence of glycerol. To investigate the role of catalase in resistance Doxorubicin chemical structure to endogenous hydrogen peroxide stress, we grew E. faecalis strains OG1RF and EMB15 in TSB with and without hemin added until mid-exponential growth phase. Then, glycerol was added and the incubation was continued. Shortly after glycerol

addition, the Npr-defective mutant, but not the wild type, stopped growing in medium without hemin. In contrast, only little difference in growth between these strains was seen in heme-supplemented medium (Fig. 4). These results show that heme supplementation can complement Npr deficiency. Catalase-mutant EMB2 grown in medium with and without heme behaved like the wild-type strain OG1RF in this type of experiment (data not shown) which emphasize the role of Npr in resistance to endogenous hydrogen peroxide stress. In this study, we show that catalase in E. faecalis plays a partially protective role against toxic effects of externally added hydrogen peroxide. Ixazomib Suppression of the glycerol-sensitive phenotype of an Npr-deficient mutant by heme supplementation of the growth medium indicates that catalase also protects against endogenous hydrogen peroxide stress. Although heme is found in many environments (Lechardeur et al., 2011), its availability is often limited, for

example, in animal tissues by binding to specialized heme-binding proteins. Most pathogenic bacteria have evolved mechanisms to acquire heme from host proteins (Anzaldi & Skaar, 2010). No heme uptake system has yet been identified in E. faecalis, and the mechanism of how this bacterium obtains heme for catalase biogenesis from the environment is not known. Interestingly, no homolog of katA, encoding the catalase protein, can be found in the available genomes of other Enterococcus species, nor in the phylogenetically closely related Lactococci and Streptococci. Thus, E. faecalis apparently harbors catalase as an extra layer of protection against oxidative stress under conditions where heme is available. This work was supported by grant 621-2010-5672 from the Swedish Research Council.

1), streptococcal culture Selleckchem ABT-263 supernatants were harvested

by centrifugation exactly at the mid log phase (A600 = 0.6–0.7) (Svensson et al., 2002). In addition, to ensure the absence of the zymogene (40 kDa) and active form (28 kDa) of the SpeB protease, the proteins of mid log phase culture supernatants were precipitated using 100% trichloroacetic acid and were evaluated by standard 12% SDS-PAGE and Coomassie blue staining (Svensson et al., 2002). The culture supernatants were subsequently filtered through 0.22-μm filter (Whatman, Germany) and stored at −70 °C until use. For each colorimetric assay, 50 μL of the culture supernatant was incubated at 37 °C with 100 μL 50 mM Tris–HCl, pH 7.4 in microplate containing 50 μg mL−1 of human Plg (Sigma) for 15 min. The S-2251 substrate (50 μL of 2.5 mM) was added, and absorbance was measured at 405 nm every 5 min for 60 min. Each assay was performed in duplicate, both in the presence and absence of Plg/S-2251. Assays containing the intact (unused) THB media and culture supernatants of the reference strains were also employed as negative and positive controls, respectively. Serial dilutions of Streptase® (CSL, Behring, Germany), a commercial SK, were used to prepare the standard curve for

SK Talazoparib molecular weight activity. Optical densities were plotted against time, and activity rates were determined from linear portion of the curve. The level of SK activity in each bacterial culture supernatant was converted to IU mL−1 using the standard curve. The PCR product of a representative of each digestion pattern (Fig. 1) was selected for nucleotide sequencing. DNA sequencing data were used for alignment studies and restriction site mapping via application many of the Molecular Evolutionary Genetic Analysis (mega 4) analytical package (Tamura et al., 2007). Difference in SK activities among GAS and GCS/GGS groups was determined using the one-way

anova test. The Kruskal–Wallis analysis of variance was employed to calculate the level of significance of SK activity among variants. All statistical analyses were carried out using spss version 16.0 (SPSS, Inc., Chicago, IL). A value of P < 0.05 was considered significant. PCR-based amplification of the sk-V1 region produced the expected 339-bp fragments (Fig. 1). Digestion of the PCR products (sk-V1) by MluI, PvuII, DraI and DdeI restriction enzymes also provided exactly the earlier described restriction patterns of the DNA fragments (Tewodros et al., 1996) (Fig. 1, Supporting Information, Table S1). The reference strains GCS/GGS and NZ131 were classified as sk5 and sk1, respectively, as expected. In total, 21 sk allelic variants were detected among strains investigated in our study (Fig. 2). Besides the several previously reported sk allelic variants of GAS and GCS/GGS isolates (Tewodros et al.

547 pupils (aged 11–15 years), from two different schools, participated in

the study. Half the participants were given full-face photographs of a boy and girl without an enamel defect, and the other half were given the same two photographs with the subjects’ RXDX-106 incisors digitally modified to show enamel opacities. Participants completed the attribute questionnaire to rate the photographic subjects according to six positive and five negative descriptors using a four-point Likert scale. The total attribute score (TAS) could range from 11 (most negative) to 44 (most positive). TAS was significantly lower for photographic subjects with enamel defects compared to the same subject with normal enamel appearance (P < 0.001, one sample t-test). Gender had a significant impact on TAS, with boys making more negative judgements than girls. Age and socio-economic status did not have an effect. Young people may make negative psychosocial

judgements on the basis of enamel appearance. “
“The objective of this study was to assess the brushing abrasion effects of toothpastes containing chitosan and propolis on sound and demineralized primary tooth enamel. Pairs of enamel specimens were prepared from human extracted primary teeth, embedded in epoxy resin and polished. An artificial subsurface lesion was created in one specimen from each pair. All samples were divided into four groups (Chitodent, Aagaard propolis, Elmex, and Control) and brushed with slurry of toothpastes and artificial saliva in a brushing machine. The brushing abrasion depths were evaluated using computer-guided optical profilometry. Trametinib chemical structure Methane monooxygenase No significant differences existed in terms of brushing depths between artificial carious enamel and brushed sound enamel specimens (P > 0.05). The abrasion values of the sound enamel samples brushed with Aagaard propolis and control samples

were significantly lower than the Elmex group (P < 0.05). The lowest brushing abrasion values of demineralized enamel specimens were observed in the Chitodent group (P > 0.05). The tested toothpastes exhibited similar effects in terms of brushing abrasion on both sound and artificially demineralized enamel. Based on mean values without statistical significance, the lowest brushing abrasion values in the demineralized brushed enamel samples were detected in the Chitodent group. “
“International Journal of Paediatric Dentistry 2013; 23: 116–124 Objective  This epidemiological study aimed to compare the caries experience in 10-year-olds with and without molar incisor hypomineralisation (MIH). Methods  About 693 children from an ongoing birth cohort study (GINIplus10) were examined for caries lesions to determine the DMF index. Furthermore, enamel hypomineralisation (EH) was scored on all permanent teeth/surfaces, according to the criteria of the European Academy of Paediatric Dentistry.

The allele frequency of HLA-B*5801 has been reported to be as high as 6–8% among Southeast Asian populations, and <1% among Western European populations, respectively.[7, 8] In their study, Hung et al.[9] used a case-control association study in the Han Chinese in Taiwan, to identify genetic markers for allopurinol-induced severe cutaneous adverse reactions (allopurinol-SCAR). Allopurinol-SCAR

included the drug hypersensitivity syndrome, SJS and TEN. They used two groups of controls, the first being 135 patients who had been on allopurinol for at least 6 months without adverse events, and a second control group of 93 subjects from the general population. They found that all 51 patients (100%) with allopurinol-SCAR carried the HLA-B*5801 gene. The presence of chronic renal insufficiency also increased the risk of developing CHIR-99021 mouse allopurinol-SCAR RO4929097 (odds ratio 4.7; confidence interval [CI] 2.3–9.3). Tassaneeyakul[10] and Kaniwa[11] found a strong association

between HLA-B*5801 and allopurinol-related SJS and TEN in Thai (100%) and Japanese (4/5) patients, respectively. Kang[12] studied 25 Korean patients with allopurinol-SCAR and found a HLA-B*5801 frequency of 92% in these patients versus 10.5% in controls. Furthermore, Jung[13] discovered that the incidence of allopurinol-SCAR in Korean patients with chronic renal insufficiency was considerably higher if they also carried the HLA-B*5801 gene.

In fact, the association between HLA-B*5801 allele and allopurinol-SCAR has been found to be consistent across different populations, both Asian and non-Asian.[14] A major limitation of individual studies arises from the low incidence of allopurinol-SCAR, which results in observational studies with small sample sizes and insufficient power. Somkrua and colleagues performed a systematic review and meta-analysis in order to accumulate and quantitatively analyze the genetic association between HLA-B*5801 and allopurinol-induced SJS/TEN as well as to elucidate any between-study heterogeneity.[15] They 4-Aminobutyrate aminotransferase analyzed four studies which included 55 SJS/TEN cases and 678 matched controls (allopurinol-tolerant control) and five studies with 69 SJS/TEN cases and 3378 population controls (general population). They concluded that allopurinol users with HLA-B*5801 have a 80–97 times increased risk of developing SJS/TEN compared to those who do not have this gene. Furthermore, sensitivity analyses suggested that the summary odds ratios remained significant regardless of populations, thus highlighting the potential of genotyping in different populations. The pathogenesis of AHS is likely to represent the interplay between different factors, mainly immunological and genetic, and with the drug and accumulation of its metabolite (oxypurinol).

, 2008a, b). Further analysis must be carried out to determine how these

characteristics are involved in protein functionality. In the interaction between Rhizobium strain NGR234 and Tephrosia vogelii, both positive and negative T3SS effectors have been described, resulting in the generation of the ‘equilibrium hypothesis’, which suggests that the combination of these effects determines whether T3SS acts positively, negatively, or has no effect on nodule formation (Skorpil et al., 2005; Kambara et al., 2009). A dual effect selleck of T3SS effectors also was described for plant-bacterial pathogens (Oh et al., 1990; Boureau et al., 2011). Okazaki et al. (2010) attributed a negative effect for Mlr6361 on Lo. halophilus nodulation. Our results also indicate a negative effect for Mlr6361 in competitiveness on Lo. japonicus MG-20 and could not discard the same on Lo. tenuis. However, the negative role of Mlr6361 does not appear to be the only factor responsible for the negative effects of T3SS functionality on both plants. Besides the putative M. loti T3SS effectors

studied here, several other candidate effectors remain to be analyzed. Some arose from our bioinformatic search of promoter regions containing sequences significantly homologous to the tts box (Sánchez et al., 2009). Other candidate effectors arose from the analysis of Yang et al. (2010), and by homology to known phytopathogen T3SS effectors, other two putative PLX3397 T3SS proteins in M. loti MAFF303099 were identified (Grant et al., 2006). The results obtained from kinetic nodulation Palmatine and competitiveness analysis on Lo. tenuis cv. Esmeralda also indicate a better performance for the rhcN mutant than for the mutant affected in the expression of the three putative T3SS effectors. This is in concordance

with the idea that a mutation that affects T3SS functionality prevents both positive and negative T3SS effects. However, the rhcN mutant induced a lower number of nodules than the wt strain in spite of the higher competitiveness of the former. This indicates that high competitiveness not necessarily reflects high nodulation capacity and suggests that the participation of the positive and negative effects resulting from T3SS functionality may affect different phenotypes in a different manner. In conclusion, the results presented here demonstrate the capacity of Mlr6331 and Mlr6316 N-terminal regions to direct secretion through M. loti T3SS. The results also show that Mlr6358, Mlr6361, Mlr6331, and Mlr6316, either individually or in combination, play a role in the symbiotic competitiveness on Lo. tenuis and/or Lo. japonicus. Data also show that the function of T3SS in the symbiotic process with lotus results from a balance between positive and negative effects. Further analysis is needed to identify other M. loti T3SS effectors or components involved in T3SS functionality in symbiosis.

Better evidence to support when such screening is appropriate and worthwhile would be valuable. We have described priority research questions for which answers will help to

expand the evidence base in travel medicine. Proposing these potential topics for future research has been difficult in itself, but conducting high-quality research with findings that can be translated PARP inhibitor into improved travel medicine services will be even more challenging. This discussion of research priorities serves to highlight the commitment that ISTM has in promoting quality travel-related research. L. H. C. has received CDC funding for research through the Boston Area Travel Medicine Network (BATMN), honoraria for serving on the editorial board of Travel Medicine Advisor, and honoraria for chairing ISTM courses on travel medicine. C. S. has received royalties from Elsevier, University of Washington Press, and Merck, speaking fees for The Everett Clinic, Everett,

WA, USA, and National Wilderness Medicine Conferences as well as consultant fee from the Boeing Company. The other authors state that they have no conflicts of interest to declare. Members of the Research Committee of the International Society of Travel Medicine include: Anne McCarthy, buy GDC-0068 MD, Chair (University of Ottawa, Ottawa, ON, Canada), Irmgard Bauer, PhD, Co-chair (James Cook University, Townsville Queensland), Elizabeth A. Talbot, MD (Dartmouth Medical School, Lebanon, NH), Lin H. Chen, MD (Mount Auburn Hospital, Cambridge, MA, and Harvard Medical School, Boston, MA), Christopher Sanford,

MD, MPH, DTM&H (University of Washington, Seattle, WA), Patricia Schlagenhauf, PhD (University of Zurich, Zurich, Switzerland), and Annelies Wilder-Smith, MD, PhD, MIH, DTM&H (National University Hospital Singapore). Adenosine “
“Background. International travel plays a significant role in the emergence and redistribution of major human diseases. The importance of travel medicine clinics for preventing morbidity and mortality has been increasingly appreciated, although few studies have thus far examined the management and staff training strategies that result in successful travel-clinic operations. Here, we describe an example of travel-clinic operation and management coordinated through the University of Utah School of Medicine, Division of Infectious Diseases. This program, which involves eight separate clinics distributed statewide, functions both to provide patient consult and care services, as well as medical provider training and continuing medical education (CME). Methods. Initial training, the use of standardized forms and protocols, routine chart reviews and monthly continuing education meetings are the distinguishing attributes of this program. An Infectious Disease team consisting of one medical doctor (MD) and a physician assistant (PA) act as consultants to travel nurses who comprise the majority of clinic staff. Results.

sanguinis have been detected in clinical specimens of atheromatous plaque (Chiu, 1999; Nakano et al., 2006; Koren et al., 2011). Moreover, foam cell formation was accelerated by heat-inactivated S. sanguinis

as well as viable bacteria (Fig. 1). Activation of macrophages by bacterial components such as LPS has been reported to be sufficient to induce foam cell formation (Funk et al., 1993; Kakayoglu & Byrne, 1998). Based on recent understanding of atherosclerosis as an inflammatory disease (Erridge, 2008), our results suggest that both live and dead S. sanguinis may be potential atherogenic Etoposide stimuli, as each were shown to be promoters of inflammatory foam cell formation. Although the periodontal pathogen P. gingivalis is known to induce

foam cell formation (Giacona et al., 2004; Qi et al., 2003), our literature search indicated that the involvement of oral streptococci in foam cell formation has not been reported. Thus, the molecular mechanism by which S. sanguinis induces foam cell formation requires Selumetinib in vivo further investigation. Our subsequent experiment revealed that infection with viable S. sanguinis at higher doses (MOI > 100) induced cell death of differentiated THP-1 macrophages (Fig. 2). Induction of cell death of macrophages may contribute to atherosclerosis, because several investigations have suggested that dead macrophages are involved in the development of atherosclerosis plaque (Tabas, 2010). Therefore, S. sanguinis is potentially able to stimulate Methocarbamol the progression of atherosclerosis by inducing cell death of macrophages, as well as by stimulating foam cell formation. Recent investigations have reported that several pathogenic streptococci and staphylococci induce cell

death of macrophages (Fettucciari et al., 2000; Craven et al., 2009; Harder et al., 2009). Those studies suggested that bacterial pore-inducing toxins such as streptolysin O, β-hemolysin and α-hemolysin trigger the cell death of infected macrophages. As S. sanguinis has no pore-forming toxins, our finding that S. sanguinis-induced cell death of macrophages was unexpected. Therefore, we examined the possible involvement of the cell death pathway in phagocytic cells. The initial recognition of microorganisms is mediated by pattern recognition receptors such as toll-like receptors, which recognize bacterial components (Ishii et al., 2008). Another class of pattern recognition receptors, intracellular nucleotide-binding oligomerization receptors (NLRs), have been identified (Ishii et al., 2008). A group of NLRs participates in the formation of protein complexes called inflammasomes, which mediate the induction of caspase-1 activation in response to microbial stimulation (Yu & Finlay, 2008; Schroder & Tschopp, 2010). In the present study, we found that S. sanguinis infection induced the secretion of IL-1β and ATP (Fig. 4), which are known to be implicated in activation of inflammasomes (Petrilli et al., 2007).

Almost all adults have protective anti-HAV antibodies as a result of subclinical exposure during early childhood. However, because of rising socioeconomic and educational status, improved access to clean water and sanitation as well CT99021 cost as vaccination, seroprevalence rates have

decreased in developing countries during the last three decades.1–13 Acquisition of infection has shifted from childhood to adulthood. Seroconversion has occurred at a later age. The proportion of “naturally immunized” decreased in the young. Our results are compatible with these epidemiologic data as well as with European seroprevalence studies.14–18 In Amsterdam, the Netherlands, in 2004 three fourths of 89 immigrants of Surinamese and Caribbean origin and almost 100% of 317 Turks and 281 Moroccans over 15 years of age were immunized against hepatitis A.14 In a multiethnic neighborhood in Rotterdam, the Netherlands15, in 2004 seroprevalence of hepatitis A in non-Dutch ethnic groups was 50

and 55% in 64 Surinamese and 40 Caribbean immigrants, respectively, and over 90% in 61, 50, and 14 subjects of Turkish, Moroccan, and Cape Verdean origin, respectively. In the age group between 18 and 29 years, 54% of the emigrant population had no antibodies to HAV. In Padua, Italy, in 2005, of 221 medical students, antibodies against hepatitis A were found in 94.7% of students of African origin, 60.9% of Asian and Central or Southern American GW-572016 order origin, and in 52.7% of East Europeans.16 In Verona, Italy, in 2004 to 2005, of a group of 182 illegal sub-Saharan African immigrants 99.5% had hepatitis A antibodies.17 In a vaccination center at Bordeaux, France in 2007, hepatitis

A seroprevalence of 466 travelers Thiamine-diphosphate kinase was 83%. The study population included not only immigrants but also people who were born and lived in France, if they had a history of jaundice, or one hepatitis A vaccine or had been born before 1955.18 Hepatitis A incidence is 2.15/100,000 in France19 and 3.9/100,000 in the European Community20 in 2006. In France 41% of infections were acquired while traveling in a country at risk.19 The growing traveling population including immigrants with their diminishing naturally acquired immunity against hepatitis A and frequent visits to countries of risk call for new vaccination tactics, for both individual and public health reasons. It will be useful to extend screening for immunity and in case of lack of time, to increase vaccination in this population. We thank Pascale Ozier, Anne Puisais, Claire Fosse, Automne Picot, Hantaniaina Rafanoson, and Marie Paule Saint Lu. The authors state they have no conflicts of interest to declare. “
“We treated a case of severe murine typhus in a Japanese traveler after returning from Thailand. Although the disease is typically self-limited or mild, the patient showed shock and multiple organ failure including acute respiratory distress syndrome.