Thus, the question of whether hypoxia modulates eye movement beha

Thus, the question of whether hypoxia modulates eye movement behavior remains open. Here we examined the effects of short-term hypobaric hypoxia on the velocity of saccadic eye movements and intersaccadic drift of Spanish Air Force pilots

PI3K cancer and flight engineers, compared with a control group that did not experience hypoxia. Saccadic velocity decreased with time-on-duty in both groups, in correlation with subjective fatigue. Intersaccadic drift velocity increased in the hypoxia group only, suggesting that acute hypoxia diminishes eye stability, independently of fatigue. Our results suggest that intersaccadic drift velocity could serve as a biomarker of acute hypoxia. These findings may also contribute to our understanding of the relationship between hypoxia episodes and central nervous system impairments. “
“The mirror-neuron system

(MNS) connects sensory information that describes an action with a motor plan for performing that action. selleck chemical Recently, studies using the repetition-suppression paradigm have shown that strong activation occurs in the left premotor and superior temporal areas in response to action-related, but not non-action-related, stimuli. However, few studies have investigated the mirror system by using event-related potentials (ERPs) and employing more than one sensory modality in the same sample. In the present study, we compared ERPs that occurred in response to visual and auditory action/non-action-related stimuli to search for evidence of overlapping activations for the two modalities. The results confirmed previous studies that investigated auditory MNS and extended these studies

by showing that similar activity existed for the visual modality. Furthermore, we confirmed that the responses to action- and non-action-related stimuli were distinct by demonstrating that, in the case of action-related stimuli, activity was restricted mainly to the left hemisphere, whereas for non-action-related stimuli, activity tended to be more bilateral. The time course of ERP brain check sources showed a clear sequence of events that subtended the processing of action-related stimuli. This activity seemed to occur in the left temporal lobe and, in agreement with findings from previous studies of the mirror-neuron network, the information involved appeared to be conveyed subsequently to the premotor area. The left temporo-parietal activity observed following a delay might reflect processing associated with stimulus-related motor preparation. “
“MC 228-77, California Institute of Technology, Pasadena, CA, USA There is accumulating evidence implicating a set of key brain regions in encoding rewarding and punishing outcomes, including the orbitofrontal cortex, medial prefrontal cortex, ventral striatum, anterior insula, and anterior cingulate.

At many synapses, and at physiological temperature, the entire se

At many synapses, and at physiological temperature, the entire sequence of events takes place in < 1 ms. In particular, one subtype of GABAergic cells, the fast-spiking, parvalbumin (PV)-expressing interneuron, releases the neurotransmitter very rapidly and with high temporal precision (Kraushaar & Jonas, 2000). Other types of synapses release neurotransmitters more asynchronously, FG-4592 purchase especially during and after trains of

stimuli (Barrett & Stevens, 1972; Goda & Stevens, 1994; Atluri & Regehr, 1998). In particular, asynchronous release is very prominent at the output synapses of hippocampal interneurons containing the neuropeptide cholecystokinin (CCK) (Hefft & Jonas, 2005; Daw et al., 2009; Karson et al., 2009). Thus, whereas synchrony of transmitter

release is a hallmark property of transmission at PV-interneurons, asynchrony of release characterizes CCK-interneurons. In addition to these differences in the time course of neurotransmitter release, CCK-interneurons differ from PV-interneurons in several ways. Whereas PV-interneurons exclusively use P/Q-type Ca2+ channels for transmitter release, CCK-interneurons rely on N-type Ca2+ channels (Hefft & Jonas, 2005). Furthermore, whereas PV-interneurons have presynaptic terminals endowed with M2 muscarinic acetylcholine and μ opioid receptors, the terminals of CCK-interneurons express cannabinoid (CB1) receptors (Freund

& Katona, 2007). Importantly, CB1 receptors situated on the presynaptic terminals find more of CCK-interneurons mediate depolarization-induced suppression of inhibition (DSI), a form of short-term synaptic plasticity induced by depolarization of postsynaptic cells (Pitler & Alger, 1994; Wilson et al., 2001). This depolarization induces endocannabinoid synthesis and release from the postsynaptic cell, leading to activation of CB1 receptors, which transiently blocks transmitter release from the presynaptic terminals. Asynchronous GABA release was originally reported at output synapses of CCK-interneurons on principal cells (Hefft & Jonas, 2005). Whether asynchronous release also G protein-coupled receptor kinase occurs at connections between CCK-interneurons and other interneurons has remained unclear. Three recent publications shed light on this question, using paired recordings between synaptically connected neurons. Daw et al. (2009) examined synapses between CCK-interneurons in the hippocampal CA3 and CA1 region. Karson et al. (2009) demonstrated asynchronous release at synapses between CCK-interneurons and PV-interneurons in CA1. Finally, in this issue of EJN, Ali & Todorova (2010) studied synapses between CCK-interneurons in the stratum lacunosum moleculare-radiatum (LM-R) of the CA1 subfield, a region highly enriched in CCK-immunoreactive cells.

The field dose of each fungicide differed according to manufactur

The field dose of each fungicide differed according to manufacturer instructions and was 125 g ha−1 (1250 mg L−1) and 250 g ha−1 (1500 mg L−1) of propiconazole and tebuconazole, respectively. Fungicide spraying was repeated after 14 days to IDH inhibitor strengthen the effect of azoles on Fusarium isolates. In the positive control group, wheat plants were inoculated with fungal biomass without fungicide spraying. In the negative control group, wheat plants were not inoculated with fungal biomass without fungicide treatment. In addition, 25 wheat heads from each

plot we collected 24 h after the first fungicide treatment for azole quantitation. Azoles were assessed using gas chromatography (GC; Łozowicka et al., 2009, 2011) at the Plant Protection Institute, National Research Institute in Białystok. GC analysis was performed with an Agilent (Waldbronn, Germany) model 7890 A gas chromatograph equipped with electron capture (ECD) and nitrogen-phosphorus (NPD) find more with a non-polar column HP-5 ((5%-Phenyl)-methylpolysiloxane; 30 m × 0.32 mm and film thickness 0.50 μm) and Chemstation chromatography manager data acquisition and processing system (Hewlette-Packard, version A.10.2). For confirmation of residues, a mid-polarity column HP-35 ((35%-Phenyl)-methylpolysiloxane; 30 m × 0.32 mm and film thickness 0.50 μm) was used. The operating conditions were as follows: for detectors – injector temperature, 210 °C; carrier

gas, helium at a flow-rate of 3.0 mL min−1; detector temperature, 300 °C (ECD and NPD); make up gas, nitrogen at a flow-rate of 57 mL min−1 (ECD) and 8 mL min−1 (NPD), hydrogen 3.0 mL min−1, air 60 mL min−1; for oven-initial temperature, 120 °C increase to 190 °C at 16 °C min−1, then to 230 °C at 8 °C min−1

and finally to 285 °C at 18 °C min−1 and hold 10 min (ECD and NPD). The volume of final sample extract injected at 210 °C in splitless mode (purge off time 2 min) was 2 mL. Total time of analysis: 20.43 min. The amounts of trichothecene genotypes (3ADON, 15ADON, and NIV) were quantitated in pooled samples by three qPCR assays specific to 3ADON, 15ADON, and NIV producers within F. culmorum/F. graminearum (Kulik, 2011). Each pooled sample (100 g) contained kernels pooled from c. 500 wheat heads per sample. Amoxicillin Kernels were ground to a fine powder for 5 min in A11 basic analytical mill (IKA, Germany). Preparation of cell lysates from 0.1 g of grounded kernels was made in triplicate from each sample as previously described (Kulik, 2011). Each qPCR reaction was prepared in at least three repetitions. The levels of DON, 3ADON, 15ADON, NIV, and 4ANIV in an in vitro experiment were determined in 10 pooled samples by GC-MS analysis as previously described by Perkowski et al. (2003) (Tables 2 and 3). Each pooled sample contained lyophilized fungal biomass pooled from seven replicates (7 Petri plates per variant). Each pooled sample was analyzed once.

[6, 7] The French armed forces epidemiological surveillance syste

[6, 7] The French armed forces epidemiological surveillance system also made it possible to identify epidemic transmission in the French West Indies since June 2010, and therefore to increase mosquito control measures. This outbreak enabled a comparison between incidence rates from the local civilian surveillance system Selleck BAY 73-4506 and the French military system (respectively 10% and 6%, p < 10−9).[13] However, similar upward trends were observed. Civilian and military epidemic peaks occurred at the same time, in August 2010. Either military mosquito control measures protected soldiers from dengue infection, or the military surveillance system was less efficient or

sensitive. In these French territories, many soldiers consulted civilian instead of military physicians. That is not the case in foreign territories. However, similar upward trends were observed, with the epidemic peak occurring at the same time. A new, very sensitive Selleckchem Omipalisib early warning system is now being deployed in the French armed forces and will enable detection of very low increases of dengue-like fevers.[14] Therefore, French soldiers could serve as sentinels within the local population, with military epidemiological surveillance making it possible to detect increased virus circulation, in particular in countries without epidemiological tools. Military epidemiological surveillance systems

can detect dengue circulation where soldiers are stationed. Therefore, these systems could be used to evaluate dengue risk in countries without a local epidemiological surveillance system. The authors state that they have no conflicts of interest. Venetoclax cell line
“We report two cases of symptomatic neurocysticercosis in two migrants whose negative serology delayed appropriate treatment for 9 and 6 months, respectively. Seroconversion occurred after treatment, which was associated with paradoxical reaction in one patient. Long-term outcome was good in both patients. In Western countries, neurocysticercosis

(NCC) is mostly seen in migrants, native to endemic areas, and occasionally in travelers returning from such countries.[1, 2] The diagnosis relies on the association of compatible clinical symptoms, typical images on cranial computed tomography (CT) scan or magnetic resonance imaging (MRI), and positive serodiagnosis.[3-5] However, serologic tests display a high rate of false negatives[6, 7] Hence, a negative serology can cause futile and invasive procedures to confirm the diagnosis and delay the treatment by months as illustrated in the two following cases. A 35-year-old man native to South Africa, who moved to France in 2003, was admitted to a French university hospital in October 2009 complaining of headaches and photophobia. Physical examination was normal. Cerebrospinal fluid (CSF) showed no abnormalities.

Although

still hypothetical, it looks as if themes arise

Although

still hypothetical, it looks as if themes arise that may be common pathways leading to or contributing to motor neuron degeneration (see Fig. 5). Intracellular (axonal) transport (motors and cytoskeleton) is one of them (De Vos et al., 2008). KIFAP3 (kinesin), Elp3 (tubulin), UNC13A BIBF1120 (vesicle release) and dynactin (dynein) are examples. Interestingly, mutations in other transport-related proteins have been identified in related motor neuropathies such as Charcot–Marie–Tooth disease (e.g. NEFL; Mersiyanova et al., 2000) and hereditary spastic paraparesis (e.g. KIF5A; Reid et al., 2002). Another emerging theme has to do with RNA processing (TDP-43, FUS/TLS, Elp3), a theme also encountered in spinomuscular atrophy,

senataxin-related motor neuron disease and others (Lemmens et al., 2010). It can be predicted that more RNA-interacting proteins that play an etiologic or mediating role in ALS will be identified. Neurovascular molecules seem to establish another mechanism in ALS (VEGF, angiogenin) and related diseases (e.g. progranulin in FTLD; Lambrechts et al., 2006). The involvement ZVADFMK of ER stress is yet another one (SOD1, VAPB and others; Kanekura et al., 2009). In addition, there is the mechanism of excitotoxicity that comes up in many models generated so far and that could explain the selective vulnerability of motor neurons (Van Den Bosch et al., 2006). Finally, there is the contribution of glial cells to motor neuron death (Ilieva et al., 2009). It remains Rucaparib in vivo to be seen how these themes will fit together. Most importantly, however, it is uncertain whether they are also at play in human motor neuron degeneration. This is difficult to investigate, as the human material we have is usually from patients in the terminal stages of disease, often poor in quality and, for many researchers, difficult to get hold of. For ∼15 years, ALS research has been limited to mutant SOD1-induced

motor neuron degeneration, as it was the only known cause of this disease. The discovery of other disease-causing mutations and the generation of animal models for them will allow a much broader approach and enable investigators to study compounds with a potential therapeutic effect in several different models. Hopefully these new opportunities will soon yield novel treatment strategies and make a difference for the many patients with ALS, their families and caregivers. A.B. is supported by the Laevers Foundation for ALS research and Fundacao para a Ciencia e a Tecnologia of the Portuguese Government (Postdoctoral grant BPD/SFRH/2009/66777). P.V.D., L.V.D.B. and W.R. are supported by grants from the Fund for Scientific Research Flanders (F.W.O.

, 2009) Interestingly, CaTrk1 and CaTok1 have been proposed to b

, 2009). Interestingly, CaTrk1 and CaTok1 have been proposed to be the effectors in killing C. albicans with the cationic protein Histatin 5, with Trk1 providing the essential pathway for the ATP loss observed during treatment with this toxic protein (Baev et al., 2004). Many nonconventional yeasts (Hansenula polymorpha, Debaryomyces, C. albicans) as Ion Channel Ligand Library in vitro well as mycelial fungi (Neurospora crassa; Haro et

al., 1999) contain, besides Trk, a second type of K+ transporter coded by HAK genes (High Affinity K+ transporter) (Table 1; Rodriguez-Navarro, 2000; Arino et al., 2010). Yeast HAK transporters are homologous to the Kup system of Escherichia coli. The role of Hak1 in potassium transport has been studied in two Debaryomyces species, D. occidentalis (Banuelos et al., 1995, 2000) and D. hansenii (Prista et al., 2007), containing both the TRK1 and HAK1 genes. Heterologous expression of DoHAK1 in S. cerevisiae mutants with defective K+ uptake improved both their growth at low K+- and potassium-transport capacity. It has been proposed that HAK transporters work as K+–H+ symporters with a high concentrative capacity and that they are expressed under K+ starvation. Under certain conditions, Na+ can substitute for H+ in D. hansenii and in this case, K+–Na+ symport would be the operating Ku-0059436 chemical structure mechanism of transport. The expression of DhHAK1

requires not only low external K+ but also low Na+, because in the absence of K+, the presence of Na+ prevents the expression of the gene. Further, the addition of millimolar concentrations of Astemizole either K+ or Na+ to D. hansenii cells provokes a fast decrease in HAK1 gene expression (Martínez et al., 2011). The existence of a third type of K+ uptake system, ACU ATPases (Alkali Cation Uptake), has been reported recently. This system is not widely distributed in nonconventional yeasts, but is present in some of them, such as Ustilago maydis or Pichia sorbitophila (Benito et al., 2004). The ACU ATPases form

a novel subfamily of P-type ATPases involved in high-affinity K+ or Na+ uptake. In U. maydis, two ACU genes have been identified and studied (Umacu1 and Umacu2). Deletion of the acu1 and acu2 genes and subsequent transport studies showed that they encode transporters mediating a high-affinity K+ and Na+ uptake. This finding was also confirmed by the heterologous expression of UmAcu2 ATPase in S. cerevisiae mutants. Besides P. sorbitophila, other yeasts have genes or pseudogenes whose translated sequences show high similarity to the Acu proteins of U. maydis (Benito et al., 2004), for example Pichia stipitis (Jeffries et al., 2007). Whereas a database search indicates that the genomes of most Candida, Zygosaccharomyces, Yarrowia or Pichia yeast species contain a gene orthologous to the S. cerevisiae TOK1 (coding for the only known yeast outward K+ rectifier), the best-known nonconventional yeasts S. pombe and D. hansenii seem to lack a similar system.

In order to examine which activity patterns were related to succe

In order to examine which activity patterns were related to successful classification, we also assessed decoding performance when the feature space was restricted to only those voxels activated during a general linear model (GLM). For this purpose, we retrained the classifier post hoc on a restricted feature space of only those clusters activated in a GLM on the localizer task. Using this approach, we examined whether multivariate or average activity patterns within each cluster drove classifier performance. Finally, to assess if representation selleck compound of object-based attention is distributed across multiple brain regions, we applied multivariate decoders

to individual clusters activated in the GLM. If the object representation is distributed across various brain regions, then these individual clusters should yield poorer decoding performance compared with

whole-brain or GLM-restricted decoders. Because brain state predictions are available for every scan in real-time fMRI, these online detected brain states can be used as neurofeedback to train subjects to modulate their ongoing brain activity. Such brain-state dependent stimulation provides a new avenue for investigating the neuronal substrate of cognition (Hartmann et al., 2011; Jensen et al., 2011). To ascertain how this brain-state dependent stimulation impacted subjects’ task performance, we conducted each attention trial twice, once with fMRI neurofeedback and once without it. However, find more due to the lack of statistically significant differences between feedback and non-feedback conditions, we will focus primarily on the non-feedback condition and refer the reader to the Supporting Information for a detailed analysis of the feedback condition. Results for both the

feedback and non-feedback conditions showed that object-based attention can be successfully decoded within a real-time fMRI paradigm. Seven subjects (six males, one female) with an average age of 23.4 years (SD = 4.6) participated in Docetaxel chemical structure the study. All participants had normal vision, and received either monetary compensation or study credits for their participation. The study was approved by the local ethics committee (Commissie Mensgebonden Onderzoek Regio Arnhem-Nijmegen) and conformed with The Code of Ethics of the World Medical Association (Declaration of Helsinki), printed in the British Medical Journal (18 July 1964). Subjects gave written informed consent before the experiment. To keep them motivated during the experiment, participants were promised a monetary reward if their task performance (i.e. average decoding accuracy) in the experiment exceeded 95%. The stimulus set consisted of color pictures of famous faces and famous places collected from the World Wide Web. Previous studies have shown larger activations for familiar faces and places compared with unfamiliar faces and places, respectively (Shah et al., 2001; Pierce et al., 2004; Rosenbaum et al., 2004).

Changes in levels of acetaldehyde, methanol and ammonia were also

Changes in levels of acetaldehyde, methanol and ammonia were also observed. These compounds are not Trichostatin A manufacturer unique to mycobacteria and will be of limited

value as individual markers for detecting M. tuberculosis complex bacteria. Their value may increase if used in combination as components of a mycobacterial VOC profile or ‘fingerprint’. Technical difficulties also arise from the variety and size of the compounds to be investigated, which range from organic compounds to simple gases. Whereas the zNose may be used for real time detection of VOC production from bacterial cultures (Casalinuovo et al., 2006; Dawson et al., 2011), concurrent measurement of gases such as ammonia will require sophisticated analytical instrumentation not readily available to microbiology laboratories. SIFT-MS and GC-MS are large expensive instruments well suited to these types of analysis. However, although sensitive and with the ability to resolve several hundreds of compounds, they are not readily suited to field deployment. The z-nose in comparison is small, rapid and much less expensive. However, it is less able to differentiate compounds and sensitivity is lower. It has been suggested that VOC may be used to detect tuberculosis disease. Detecting mycobacterial VOC in the headspace of clinical materials or in breath

will be challenging as VOC markers produced by mycobacteria in vitro check details may not be detected in

vivo. In addition, the relatively low concentration of such markers produced in vivo may make their detection in the presence of host VOCs difficult (Syhre et al., 2009). A more robust approach is likely to be achieved by obtaining the whole spectra of samples for TB diagnosis and subjecting these to multivariate Methamphetamine analysis and extensive validation to derive diagnostic algorithms. The dependency of PEA production on growth of the bacteria suggests that it could be used to assist LJ-based tests for susceptibility to anti-tuberculosis drugs. However, when directly testing headspace for PEA with the zNose, large numbers of bacteria were needed, and for rapid drug resistance testing, a VOC preconcentration step or a more sensitive detection method would be required. A number of other volatile compounds have recently been reported as potential markers for M. tuberculosis complex bacteria including 1-methylnaphthalene, 3-heptanone; methylcyclododecane; 2,2,4,4,6-pentamethyl heptane (isododecane); benzene, 1-methyl-4-(1-methylethyl)-; cyclohexane, 1,4-dimethyl-; 3,5-dimethylamphetamine; butanal, 3-methyl- (isopentanal); 2-hexene; trans-anti-1-methyldecahydronaphthalene (Phillips et al., 2007); and methyl phenylacetate, methyl p-anisate, methyl nicotinate and o-phenylanisole which are metabolites of nicotinic acid (Syhre & Chambers, 2008).

32 The most common symptoms were fever (100%), rash (57%), lympha

32 The most common symptoms were fever (100%), rash (57%), lymphadenopathy (37%), and severe headache (29%). R typhi infections are reported in Greece and mostly in the island of Crete.12,33 The predominant clinical manifestations were fever (100%), headache (88%), chills (86.7%), and rash Torin 1 research buy (79.5%).12 In Italy, murine typhus was the most widespread rickettsioses,

especially in Sicily during World War II.34Rickettsia typhi still exist, at least in Sicily; in particular, asymptomatic cases of murine typhus were reported in Sicily in the late 1980s.34 In the south of Spain a prospective study over 17 years (1979–1995) identified 104 cases of murine typhus.17Rickettsia typhi infection was the cause in 6.7% of 926 cases of fever lasting Trichostatin A supplier for 7 to 28 days. Sero-epidemiological

studies reveal that murine typhus probably exists in other Mediterranean countries. In Morocco indirect immunofluorescence test on human sera obtained from 300 donors and 126 patients from clinical laboratories identified R typhi antibodies in 1.7 and 4%, respectively.35 In France R typhi antibodies were identified in homeless patients from Marseille.36 An R typhi-positive serology was identified in 68.1% of the residents in the northern Dalmatian islands of Croatia in an epidemiological study.37Rickettsia typhi has also identified and cultivated from Monopsyllus sciurorum sciurorum fleas collected in southern Slovenia.38 There is evidence that murine typhus also exists in North Spain as the R typhi seroprevalence was in 7.6% of the people living in urban, 8.5% in semirural, and 21.4% in

rural areas.39 In Malta, contrary to current belief, R typhi did not account for any of the cases seen.40 Finally, there have not been any studies to determine if murine typhus is endemic in Libya, Lebanon, Syria, Turkey, Albania, Serbia, and Montenegro. In the countries of North Europe autochthones cases of murine typhus have not been described. However, sporadic cases are identified in travelers who visited endemic areas like the countries of Non-specific serine/threonine protein kinase the south Mediterranean area. As a result, R typhi infection was found in a Norwegian tourist with fever, chills, and severe headache who had visited the island of Crete.41 The patient did not present a rash and recovered without sequelae. The diagnosis of murine typhus was based on the detection of IgM antibodies against R typhi in serum samples during reconvalescence.41 Murine typhus was also identified in a traveler from the UK after her return from Spain.42 The patient presented fever (39.5°C), chills, severe headache, photophobia, a sore throat, neck stiffness, purpuric rash, and she was passing very little urine. Unfortunately, murine typhus was not considered from the beginning of the symptoms and she was treated with IV cefotaxime.

32 The most common symptoms were fever (100%), rash (57%), lympha

32 The most common symptoms were fever (100%), rash (57%), lymphadenopathy (37%), and severe headache (29%). R typhi infections are reported in Greece and mostly in the island of Crete.12,33 The predominant clinical manifestations were fever (100%), headache (88%), chills (86.7%), and rash TSA HDAC mw (79.5%).12 In Italy, murine typhus was the most widespread rickettsioses,

especially in Sicily during World War II.34Rickettsia typhi still exist, at least in Sicily; in particular, asymptomatic cases of murine typhus were reported in Sicily in the late 1980s.34 In the south of Spain a prospective study over 17 years (1979–1995) identified 104 cases of murine typhus.17Rickettsia typhi infection was the cause in 6.7% of 926 cases of fever lasting GSK J4 cost for 7 to 28 days. Sero-epidemiological

studies reveal that murine typhus probably exists in other Mediterranean countries. In Morocco indirect immunofluorescence test on human sera obtained from 300 donors and 126 patients from clinical laboratories identified R typhi antibodies in 1.7 and 4%, respectively.35 In France R typhi antibodies were identified in homeless patients from Marseille.36 An R typhi-positive serology was identified in 68.1% of the residents in the northern Dalmatian islands of Croatia in an epidemiological study.37Rickettsia typhi has also identified and cultivated from Monopsyllus sciurorum sciurorum fleas collected in southern Slovenia.38 There is evidence that murine typhus also exists in North Spain as the R typhi seroprevalence was in 7.6% of the people living in urban, 8.5% in semirural, and 21.4% in

rural areas.39 In Malta, contrary to current belief, R typhi did not account for any of the cases seen.40 Finally, there have not been any studies to determine if murine typhus is endemic in Libya, Lebanon, Syria, Turkey, Albania, Serbia, and Montenegro. In the countries of North Europe autochthones cases of murine typhus have not been described. However, sporadic cases are identified in travelers who visited endemic areas like the countries of Teicoplanin the south Mediterranean area. As a result, R typhi infection was found in a Norwegian tourist with fever, chills, and severe headache who had visited the island of Crete.41 The patient did not present a rash and recovered without sequelae. The diagnosis of murine typhus was based on the detection of IgM antibodies against R typhi in serum samples during reconvalescence.41 Murine typhus was also identified in a traveler from the UK after her return from Spain.42 The patient presented fever (39.5°C), chills, severe headache, photophobia, a sore throat, neck stiffness, purpuric rash, and she was passing very little urine. Unfortunately, murine typhus was not considered from the beginning of the symptoms and she was treated with IV cefotaxime.