26,27 During a pre-travel encounter, the travel practitioner provides the traveler with information about risks and best practices to mitigate risks. Most pre-travel encounters advise regarding local conditions (potential for crime, trauma), safe food and water practices, avoiding endemic communicable diseases (vector avoidance and malaria prevention, safe sexual practices, rabies, tuberculosis), and routine, recommended, and required vaccines. Discussion of these

topics can consume and exceed typically allotted time for the pre-travel encounter; yet, there are little data to ensure understanding and adherence. selleck chemicals Priorities for research to facilitate better understanding of what constitutes effective counseling and how LY294002 supplier to maximize adherence are also shown in Table 2. Research questions to fill knowledge gaps in immunization practice are also imperative. Obtaining accurate immunization history, providing advice regarding immunizations, and administering immunizations for vaccine-preventable travel-related infectious diseases are fundamental to a successful pre-travel encounter. Besides traditionally targeted diseases such as hepatitis A, yellow fever, and typhoid, intriguing data are emerging that demonstrate that respiratory tract infections are extremely common among even short-term travelers,28 and are a common cause for seeking medical attention following travel.29 Mutsch et al. reported that influenza

Janus kinase (JAK) may be the most common vaccine-preventable travel infection for travelers visiting tropical and subtropical regions, with an estimated incidence of 1.0 influenza-associated

events per 100 person-months abroad.13 The recent global emergence of novel influenza A H1N1 illustrates the rapidity with which influenza viruses spread, and serves as a reminder of the imperative to protect travelers and also their home communities from imported respiratory viruses such as influenza. Nearly 50% of travelers encounter diarrhea during travel.2,3 Research priorities around the common problem of travelers’ diarrhea (TD) are included in Table 2. Advising and equipping the traveler to avoid malaria is another paramount role for the pre-travel encounter. Malaria was one of the three most frequent causes of systemic febrile illness among travelers from every GeoSentinel region.29 Centers for Disease and Prevention surveillance shows that about 800 cases of malaria are reported in US civilians each year13 and 453 cases of Plasmodium falciparum were reported by TropNet Europe in 2007.31 Topics that are prioritized for research toward improved malaria chemoprophylaxis and treatment are shown. Research questions concerning special populations and types of travel are included within Table 2. The former includes children, pregnant and/or nursing women, immunocompromised, elderly, and the latter including travelers VFRs, on religious pilgrimages such as the Hajj, and participating in medical tourism.

This needs further investigation. Our findings represent persons with diabetes who sought pre-travel health advice. They may have had a more than average health awareness, particularly having received travel advice Vorinostat and knowing the objectives of the study. As to usage of stand-by antibiotics, its importance was emphasized by an experienced travel health expert, and by means of information leaflets. Nevertheless, 83% of the patients with diarrhea did not use this treatment, even in the case of metabolic dysregulation. Of 152 stand-by

antibiotic courses provided, 141 (92.8%) were not used. Moreover, NIDD only reported hyperglycemias. Indeed, hypoglycemia is uncommon when using only oral anti-diabetics.26 Thus, routine prescription of stand-by antibiotics for uncomplicated diarrhea is probably not more useful than for healthy travelers. For IDD, monitoring blood glucose more frequently, and adjusting insulin dosage and diet accordingly, are probably more helpful check details in minimizing metabolic dysregulation. Stand-by antibiotics may be useful for diabetic travelers to areas where health facilities are lacking in case of more severe illness, for example three or more unformed stools per 24 hours with accompanying symptoms such as fever, or blood in

stools. The merits of this definition could not be assessed in this study. In conclusion, this study showed that medication-dependent Depsipeptide travelers with diabetes to developing countries do not have travel-related symptoms of diarrhea, vomiting, fever, cough, rhinitis, and signs of skin infection more often or longer than travelers without diabetes. The incidence of metabolic dysregulation among travelers with diabetes should be assessed in more detail. Our findings indicate that routine prescription of stand-by antibiotics for travelers with diabetes to areas with good health facilities is probably not more useful than for healthy travelers. The

authors state they have no conflicts of interest to declare. “
“Background. Questionnaires are widely used for data collection in travel medicine studies, but there are no validated instruments that are available to researchers in this field. Our objective was to develop and validate a questionnaire to be used in a prospective study designed to estimate the risk of three viral infections in Australian travelers to Asia. Methods. Qualitative nonexperimental cognitive methods, including cognitive review, task analysis, and cognitive interviews, were selected. A pilot study was performed to assess the instrument in the target population. Results. Recalling dates related to travel or health events was observed and reported to be the most difficult task for travelers. The use of cues embedded into items and provision of memory prompts such as calendars improves the recall of dates during travel.

0 (0.25–4) [23]. The effects Protein Tyrosine Kinase inhibitor of viral load and CD4 cell count when starting salvage therapy were classified as ‘possibly harmful’ and ‘possibly beneficial’ with median hazard ratios of 1.5 (95% CI 0.38–6) and 0.67 (95% CI 0.17–2.7) and with probabilities of being above 1 of 0.72 and 0.28, respectively. Poor adherence and overall GSS were classified as ‘probably harmful’ and ‘probably beneficial’ with median hazard ratios of 2.0 (95% CI 0.5–8) and 0.5 (95% CI 0.13–2) and with probabilities of being above 1 of 0.84 and 0.16, respectively. These priors

correspond to normal distributions for the log hazard ratio with variance 0.5 [23], and the normal cumulative distribution BKM120 purchase function was used to calculate the probability

of a hazard ratio above 1. When considering alternatives to the overall GSS, we compared models using twice the log Bayes factor (2logBF) with the integral of a posterior density calculated by Laplace’s method of approximation [24]. We used SAS version 9.1.3 (SAS Institute Inc., Cary, NC, USA) for our analyses. As of February 2009, 196 patients in the SHCS had started darunavir for the first time but only 130 patients started darunavir as part of a salvage therapy. Of these 130 patients, 115 (88%) had at least one viral load measured 12 weeks or more after starting. Patients starting darunavir as part of a salvage therapy (Table 1) had a median age of 47 years and had been living with HIV for a median of 16 years. Most (81%) received mono or dual antiretroviral therapy prior to starting highly active antiretroviral therapy and since then had experienced virological failure on a median of three PI-based regimens. Prior to starting

darunavir, 77% of patients had been given lopinavir, with 52% recording a viral load above 1000 copies/mL while on a regimen that included this drug. Typically, a considerable period had elapsed between assumed ‘triple class failure’ (i.e. first reporting a viral load above 1000 copies/mL given prior exposure to PI- and Interleukin-2 receptor NNRTI-based therapies for more than 90 days each) and starting darunavir (median 6.6 years), and much of this period (median 3.6 years) was spent at risk of developing resistant mutations, with the patient on therapy while having a viral load above 400 copies/mL. When starting darunavir, only 42% of patients had HIV considered fully susceptible to darunavir. Patients started in reasonable health (median CD4 count 250 cells/μL) given that many patients had an advanced infection [43% Centers for Disease Control and Prevention (CDC) group C] and a relatively high proportion (22%) were coinfected with hepatitis C virus.

This result showed unambiguously that the role of Trk2 in the cell survival of desiccation stress is much more important than that of the Trk1 transporter. One of the reasons for the decreased viability could be the need for the active uptake of potassium during the rehydration process. As mentioned above, desiccation is accompanied by a substantial decrease in cell volume. Such a decrease in cell volume may be not only related to a loss of water but may be accompanied by a loss of ions to preserve

sustainable intracellular osmotic conditions. After obtaining our initial results, we hypothesized that a substantial amount of intracellular selleck compound potassium content may be lost during desiccation, and it is the Trk2 (and not Trk1) transporter that mediates the reuptake of required potassium during the rehydration procedure. To confirm this hypothesis, we followed the survival of cells that were first desiccated in the standard way described in ‘Materials and methods’, and then rehydrated in either water or 50 mM KCl. If the regeneration of internal potassium content during rehydration were crucial, the increased availability Natural Product Library datasheet of potassium in the rehydration solution would enhance the survival of cells. As shown in Table 2, the presence

of KCl during the rehydration of cells had no significant effect. The survival of wild-type BY4741 cells was almost the same under both sets of conditions; the survival of cells lacking potassium exporters (BYT345 and BYT45) Acyl CoA dehydrogenase was slightly decreased in the presence of KCl, probably due to the impaired ability of potassium flux and membrane potential regulation (Zahradka & Sychrova, 2012). The survival of BYT1 cells (trk1Δ) was not changed upon the addition of potassium, and the same was found for cells

lacking either Trk2 alone (BYT2) or in combination with the trk1 mutation (BYT12, trk1Δ trk2Δ). These results showed clearly that the uptake or efflux of potassium by cells during the rehydration process is not crucial for their desiccation survival. Another important role of Trk2 might be supplying potassium to stationary cells. Stationary cells need to have a basal level of continuous potassium influx and efflux to maintain their membrane potential. This role of Trk2 in stationary cells has not been studied in detail so far; the only hint may be the low level of expression of TRK1 in stationary cells (Gasch et al., 2000). To verify the possibility of the effect of the absence of TRK2 on stationary cells, we measured the potassium content in cells from the stationary phase of growth harvested for desiccation. As shown in Table 3, cells lacking the Trk2 transporter contained a significantly lower amount of potassium, which confirmed the presumption that Trk1 was not very active in the stationary cells.

, 2001). Our study shows that each component of the TMS-evoked response is differentially modulated by cTBS. Suppression of the MEPs seems

to be better reflected by inhibition of the P30, consistent with the non-linear correlation between trial-by-trial peak-to-peak N15–P30 and MEPs described by Maki & Ilmoniemi (2010). Our results are also consistent with the study of Ferreri et al. (2011), where trial-by-trial MEPs show a positive correlation with P30 (although on contralateral electrodes where P30 was mainly recorded) and a negative correlation with N44 (equivalent to our N45). However, the other TEPs seem to also play a role. While there is still no clear understanding of the meaning of individual TEPs, our results demonstrate that a combination of the different TEPs,

rather than just one potential, appears to be important for the prediction of MEP amplitude. STI571 mouse To export measures of cTBS-induced plasticity outside the motor cortex, one might need to know in advance the coefficients linking the different TEPs with the estimated excitability. Given the small number of trials collected in each condition, the present study only allows group-level analysis (grand-average). Future studies, with a larger number of trials collected around the time points of interest, will be necessary to extend our observations selleck kinase inhibitor to the individual level. Finally, as cTBS-induced plasticity is known to be altered by age or pathologies (Pascual-Leone et al., 2011), it is reasonable to expect that the relationship between TEPs and MEPs will be population-dependent. Note that some TEPs might not reflect direct brain response to TMS, but rather indirect potentials, such as auditory potentials evoked by the discharge click (Nikouline et al., 1999), or somatosensory potentials evoked by the contraction of the muscle (MEP). Concerning auditory-evoked potentials, the N100 component has, in particular, been associated with this physiological artifact.

However, this same component is also task-dependent and has been associated with inhibitory processes (Bender et al., 2005; Bonnard et al., 2009; Spieser et al., 2010). Although we cannot rule out that in our study cTBS modulated auditory-evoked potentials, we consider it unlikely. On the contrary, it is possible that Acesulfame Potassium modulation of MEP size resulted in modulation of the associated somatosensory-evoked potentials. Future studies with subthreshold stimulation are needed to isolate primary brain responses to TMS from afferent feedback from the target muscle. We found that TMS over M1 induced oscillations before cTBS in the entire frequency range studied. These TMS-induced oscillations were modulated by cTBS. TMS-induced low frequencies (theta and alpha) decreased after cTBS while TMS-induced higher frequencies (high beta) tended to increase after cTBS.

Escherichia coli BW25113 (ΔaraBD) (Datsenko & Wanner, 2000) and BL21 (DE3) were grown in M9 medium supplemented with 0.2% casamino acids and 0.5% glycerol at 37 °C. The primers used in this study are summarized in Table 1. The coding sequences of ygfX alone or ygfYX were PCR-amplified using primers YGFX-F and YGFX-R1, or YGFY-F

and YGFX-R1, respectively. The fragments were cloned into pBAD24 vector (Guzman et al., 1995) and designated as pBAD24-ygfX and pBAD24-ygfYX, respectively. The coding sequence of YgfX in a fusion with His6-tag at the C-terminal (YgfX−His) was also cloned into pBAD24 using YGFX-F and YGFX-R2. A truncated protein of YgfX (YgfX(C); cloned from V49 to Z135) was cloned into Trichostatin A nmr pCold-Km (unpublished results, Inouye laboratory) using YGFXs-F and YGFX-R1. His6-tagged FtsZ and MreB were constructed previously (Tan et al., 2011). FLAG-tagged FtsZ and MreB

were also previously constructed in pET17b, having a tag at the C-terminal end (H. Masuda and M. Inouye, unpublished results). For examining the growth rate, 0.2% arabinose was added to the cultures during the early exponential phase. His6-tagged YgfX(C), FtsZ, and MreB were expressed in E. coli BL21(DE3). Protein expression was induced for 2 h by adding 1 mM IPTG when the OD600 nm reached 0.8. The cells were collected by brief centrifugation at 8000 g and lysed by French pressure press (Thermo Fisher Scientific, MA). FtsZ and MreB were purified as described before (Tan et al., 2011). YgfX(C)−HIS was purified from the insoluble materials after being dissolved CDK inhibitor in 8 M urea (pH 8.0). Proteins were purified

using Ni-NTA agarose according to the manufacturer’s instructions (Qiagen, CA). Inner and outer membrane proteins were isolated following the method described previously (Hobb et al., 2009). Briefly, the total membrane proteins were collected from the lysate by ultracentrifugation at 100 000 g for 1 h. The pellet was washed, then resuspended in 1% (w/v) N-lauroylsarcosine in 10 mM HEPES, pH 7.4, and incubated at 25 °C for 30 min with gentle agitation. The inner and outer membrane fractions were further separated by ultracentrifugation. His6-tag pulldown assays were carried out by incubating the cell lysate containing YgfX−HIS and the cell lysate containing FsZ−FLAG or MreB−FLAG (lysis buffer: 50 mM HEPES-KOH, pH 7.5, 10 mM MgCl2, 200 mM KCl, 0.1 mM EDTA, and 10% Methamphetamine glycerol) overnight at 4 °C. Ni-NTA agarose (0.5 mL) was added to the lysate, and the mixture was incubated at room temperature for 1 h. The beads were washed three times with 20 mL of the same lysis buffer containing 20 mM imidazole. Protein complexes were then separated by 17.5% SDS-PAGE and visualized by Western blot using monoclonal anti-FLAG antibody conjugated with horseradish peroxidase (Sigma-Aldrich, MO). The effect of YgfX on FtsZ and MreB polymerization was determined by a sedimentation method as previously described (Anand et al., 2004) with a few modifications.

Compared with survivors, the deceased patients were older, had a higher BMI and greater menopausal status at diagnosis, were more likely to have reported tubal ligation prior to diagnosis, and had higher parity and ever breastfeeding. A higher proportion of deceased patients was diagnosed at an advanced stage, with ascites and poorly differentiated histopathological grade, and chemotherapy after surgery. There were no significant differences in age at menarche, hysterectomy, hormone replacement therapy, oral contraceptive use, and family history of ovarian cancer between the living and deceased patients. The survival curves in the ovarian

cancer patients according to tubal ligation status were distinctly different visually (see Fig. 1) and, based on the log-rank test for equality of survival distributions, the difference was not a chance occurrence selleck compound (P < 0.001). Only 21 (38.9%) of 54 patients who had tubal ligation survived to the time of interview, in contrast to 95 women (67.4%) still alive among the 141 women without tubal ligation. Table 3 shows the crude and see more adjusted mortality hazard ratios and 95% CI for epithelial ovarian cancer according to selected factors. Compared with patients in FIGO stage I, the adjusted HR were 12.25 (95% CI 2.47–60.78; P < 0.001) and 24.54 (4.50–133.8; P < 0.001) for those who were diagnosed at FIGO stage III and IV. An insignificant

increased HR was observed for ascites 1.27 (95% CI 1.00–1.60; P = 0.05). There was no significant association between cancer survival and age, BMI, World Health Organization (WHO) grade of differentiation, and chemotherapy status. Adjusted HR and 95% CI for reproductive, gynecological and hormone factors are shown in Table 4. HR significantly increased with tubal ligation prior to diagnosis. Compared to patients without tubal ligation, the adjusted HR was 1.62 (95% CI 1.01–2.59; P = 0.04) for patients who had tubal ligation. There was no significant association found with age at menarche, menopausal status, parity, breastfeeding, hormone replacement therapy, oral contraceptive use, and

hysterectomy. The study found that tubal ligation prior to diagnosis had an independently adverse influence on epithelial ovarian cancer survival in Chinese women. The study had a relatively small sample Alectinib purchase size and exposures to some factors were uncommon (e.g. only four cases were exposed to estrogens). There was no relationship found between other reproductive, gynecological, and hormone factors and survival of ovarian cancer, in contrast to substantial effects of these factors on the incidence of the disease reported elsewhere.2–9 In addition to the evidence presented here, previous tubal ligation or hysterectomy, multiparity, oral contraceptive use and breastfeeding have been reported as protective factors against ovarian cancer incidence in several others studies.

4.1 Intrapartum intravenous zidovudine infusion is recommended in the following circumstances.     For women with a viral load of > 1000 HIV RNA copies/mL plasma who present in labour, or with ruptured membranes or who are admitted for planned CS Grading: 1C   For untreated women presenting in labour or with ruptured membranes in whom the current viral load is not known. Grading: 1C   In women on zidovudine monotherapy undergoing a PLCS intravenous zidovudine can be considered.

Continued oral dosing is a reasonable alternative. Grading: 1B 8.1.1 Zidovudine monotherapy is recommended if maternal viral load is < 50 HIV RNA copies/mL at 36 weeks' gestation or thereafter prior to delivery (or mother delivered by PLCS whilst on zidovudine monotherapy). Grading: 1C 8.1.2 Infants < 72 hours old, born to untreated HIV-positive mothers, should immediately initiate

three-drug therapy for 4 weeks. Grading: 1C 8.1.3 Three-drug CT99021 infant therapy is recommended for all circumstances other than Recommendation 8.1.1 where maternal viral load at 36 weeks’ gestation/delivery 3-MA is not < 50 HIV RNA copies/mL. Grading: 2C 8.1.4 Neonatal PEP should be commenced very soon after birth, certainly within 4 hours. Grading: 1C 8.1.5 Neonatal PEP should be given for 4 weeks. Grading: 1C 8.2.1 PCP prophylaxis, with co-trimoxazole, should be initiated from age 4 weeks in:     All HIV-infected infants. Grading: 1C   Infants with an initial positive HIV DNA/RNA test result (and continued until HIV infection has been excluded). Grading: 1C   Infants whose mother's viral load at 36 weeks' gestational age or at delivery is > 1000 HIV RNA copies/mL despite cART or unknown (and continued until HIV infection has been excluded) Grading: 2D 8.3.1 Infants born to HIV-positive mothers Sorafenib research buy should follow the routine national primary immunization schedule. Grading: 1D 8.4.1 All mothers known to be HIV positive, regardless of antiretroviral therapy, and infant PEP, should be advised to exclusively formula

feed from birth. Grading: 1A 8.4.2 Where a mother who is on effective cART with a repeatedly undetectable viral load chooses to breastfeed, this should not constitute grounds for automatic referral to child protection teams. Maternal cART should be carefully monitored and continued until 1 week after all breastfeeding has ceased. Breastfeeding, except during the weaning period, should be exclusive and all breastfeeding, including the weaning period, should have been completed by the end of 6 months. Grading: 1B 8.4.3 Prolonged infant prophylaxis during the breastfeeding period, as opposed to maternal cART, is not recommended. Grading: 1D 8.4.4 Intensive support and monitoring of the mother and infant are recommended during any breastfeeding period, including monthly measurement of maternal HIV plasma viral load, and monthly testing of the infant for HIV by PCR for HIV DNA or RNA (viral load). Grading: 1D 8.5.1 8.5.1.1 8.5.1.

Two other strains originally typed as PT13 were subsequently typed as PT6a. Two strains with original phage types 6 and 8 were subsequently phage typed PT4 and RDNC, respectively. Surprisingly, one strain had converted from a less common phage type PT6 to the most predominant phage type PT4 in Europe and vice

versa, and strains of more prevalent phage types 4, 8 and 13 had converted to less prevalent phage types 1a, RDNC and 6a (Table 1). It should be noted that strains ID 502 and ID 1387 were initially phage typed as PT13 TGF-beta inhibitor and subsequently phage typed as PT6a, thus appearing to become a different clonal lineage. These observations underline the major limitations encountered while using phage typing for epidemiological investigation and severely restrict its value for monitoring the epidemic spread of S. Enteritidis. Our findings confirm previous studies reporting the occurrence of phage conversions. Frost et al.

(1989) reported the conversion of strains of PT4 to strains of PT24 in S. Enteritidis based on the acquisition of IncN plasmids. Inter-relationships were shown between strains of several phage types based on the lost or acquisition of an IncN plasmid (Threlfall et al., 1993). Conversion of PT4 to PT7 and PT1, 4, 6 to PT7 by loss of lipopolysaccharide has been described (Chart et al., 1989). Temperate phages 1, 2, 3, and 6 were used to convert PT4 to PT8, PT6a to PT4, Target Selective Inhibitor Library PT6a to PT7, PT13 to PT13a and PT15 oxyclozanide to PT11 (Rankin & Platt, 1995). Transfer of a plasmid belonging to the IncX into 10 isolates of S. Enteritidis belonging to 10 different phage types (PT1, 2, 3, 4, 8, 9, 9b, 10, 11 and 13) resulted in phage type conversion in 8 of the 10 strains (PT1, 2, 4, 8, 9, 9b, 10 and 11) (Brown et al., 1999). PFGE that is currently the gold standard technique for subtyping S. Enteritidis isolates is laborious, requires precise standardization and displays limited subtyping potential (Hudson et al., 2001; Liebana

et al., 2001). Ribotyping is a laborious procedure that includes multiple steps such as DNA isolation, restriction, electrophoresis, Southern blotting, probe preparation and hybridization (Landeras & Mendoza, 1998). Thong et al. (1995) analysed a total of 61 isolates of S. Enteritidis using PFGE and ribotyping and came to the conclusion that the close genetic similarity observed between epidemiologically unrelated and outbreak-related isolates of S. Enteritidis suggests that both PFGE and ribotyping are of limited value in the epidemiological analysis of these particular isolates. PCR-based methods such as RAPD lack the ability to separate artefactual variation and true polymorphism (Tyler et al., 1997; Landers et al., 1998). The application of RAPD requires the identification of primers capable of recognizing DNA polymorphisms among isolates; however, it is not possible to predict which primers will be useful to differentiate strains of a species or serotype (Landeras & Mendoza, 1998).

The study protocol was approved by the ethics committee of the Hospital Clinic of Barcelona. On June 19, 2009, the medical students traveled from Barcelona to Santo Domingo, Dominican Republic on a scheduled flight with a stopover in Madrid. A bus took them to their hotel located at a beach resort in Punta Cana. Meals were shared depending on daily activities organized and the number of students participating in each activity. The students slept in rooms for two, three,

or four Nutlin-3a manufacturer people with members of their own travel group. Activities were organized according to the interests of the students, and included sightseeing excursions. On June 26, all students traveled on the same bus on a 4-hour trip from Punta Cana to Santo Domingo, where they boarded an Airbus aircraft with 284 economy class and 20 business class seats. The flight back

to Spain lasted 8 hours. Of the 113 students, 86 (76%) were contacted and agreed to participate in the study. The rest could not be contacted or declined to participate. Of the 86 students, 58 (67%) were female. The median age was 24 years, (range 22–56 y). A total of 62 (72%) students developed ILI, and influenza A(H1N1) was confirmed in 39 (45%) (two confirmed cases selleck compound were asymptomatic). Thus, assuming that none of the students who did not participate were ill or infected, the minimum attack rate among all 113 students was 55% for probable influenza and 35% for confirmed influenza. Two of the 37 confirmed cases developed symptoms during the stay in the Dominican Republic. The

first confirmed case first developed symptoms on June 24, followed by a second case on June 25 (2 and 1 d before starting the return trip, respectively). Between June 26 (day of departure Bay 11-7085 from Santo Domingo) and 48 hours after arriving in Barcelona, 29/39 (74%) of the students with confirmed A(H1N1) infection developed symptoms; 6 students (15%) developed symptoms more than 72 hours later, and 2 remained asymptomatic (Figure 1). The predominant symptoms in confirmed cases (Table 1) were cough (87%), malaise (60%), and sore throat (51%). Gastrointestinal symptoms (diarrhea) were reported by 16 (43%) of the confirmed cases. Univariate analyses showed that cough, fever, myalgia, rhinorrhea, and malaise were significantly associated with confirmed infections, and this was supported by the logistic regression analysis (Table 1). Laboratory testing for influenza was more likely to be negative when the time between the onset of illness and the day of diagnostic sampling was longer (Figure 2). The mean time between onset of symptoms and blood sampling was 3.5 days; most (92%) of the positive samples were obtained between 1 and 3 days after onset, whereas most (83%) of the negative samples were obtained 3 or more days after onset. On arriving home from the trip, the students went to their homes, where they lived with family or other students.