In order to maximize the utilization of this surgical modality, it should be applied not only on clinical cases but also for resident surgical training. Technological advancement and, above all, industry competition could reduce the cost

of the robotic instrumentation, making the robotic technology more affordable and cost-effective. The authors declare that there are no conflicts of interest. “
“More than 1,050 individuals served as special referees for The Journal of Obstetrics and Gynaecology Research (JOGR). The Editorial Board, Asia and Oceania Federation of Obstetrics and Gynaecology (AOFOG) and Japan Society of Obstetrics and Gynecology (JSOG) take this opportunity to acknowledge these reviewers who have contributed many hours and much effort in the evaluation of manuscripts submitted to JOGR during the Adriamycin mouse past year. We also continue to seek advice from reviewers and readers alike with regards to their overall evaluation of JOGR. Abdalla, Hossam eldin Abdelazim, Ibrahim Abdel-Hady, El-Said Abdool, Zeelha Abdullah, Mohamed Abe, Yasuhito Abeysena, Chrishantha Abildgaard, U. Abou-Elela, Ashraf

Abu-Asab, N. Adachi, Kumiko Adamo, Ciro Adams, Samantha Aggarwal, Nidhi Agur, Wael Ahmed, Hamdia Aizawa, Shihoko Akihira, Jun-ichi Akinaga, Chieko Akira, Shigeo Al, Ragip Alkhaja, F. Allen, Robert Allison, Kim Alonso, Justo Alqahatani, Noura Altinbas, Sibel Alva, Teresa Amer, S. A. Ando, Hisao Andreeva, Petya Anim-Somuah, Millicent Aoki, Showa Aoki, Yoichi Api, O. Araki, Ryuichiro Araki, Yoshihiko Araujo Júnior, Edward Arimoto, Takahide Aris, Aziz Arrabal-Polo, Miguel http://www.selleckchem.com/products/ensartinib-x-396.html Angel Asai, Satoshi Atacag, Tijen Aubuchon, Mira Augustin, Goran Awonuga, A. O. Aydin, Suleyman Azzaroli, F. Baba, Tsukasa Bacon, James Badawy, Ahmed Badiglian-Filho, Levon Bagos, Pantelis Bajory, Zoltan Bakkum-Gamez, Jamie Baksu, Basak Balbi, Giancarlo Baldwin, Maureen Banas, Tomasz Banerjee,

Saikat Banno, Kouji Barad, D. H. Barbesino, G. Barbosa, Caio Barrientos, Gabriela Bartha, José Barut, Aykut Bateman, B. Bauer, Melissa Bauer, Sam Beierwaltes, W. H. Bekiesińska-Figatowska, Monika Bellomo, Gianni Benagiano, Giuseppe Benaglia, Laura Benian, Ali Benson, M. Benson, M. D. Bhat, Ramesh Bhide, P. Bilgin, Tufan Billah, Syed Binhamdan, Mukhri Blitek, A. Bolukbasi, Y. Bonino, Luca Bose, cAMP Chinmoy Bos-Mikich, A. Bowen, Angela Bowman, Zachary Brännström, Mats Brown, Mary Brun, Jean Luc Buckett, William Bugano, D. D. Bullarbo, Maria Bunyavejchevin, Suvit Bushnell, Cheryl Byme, B. Cakir Gungor, Ayse Nur Cardaropoli, Simona Cardonick, E. Carey, Vincent J. Carmina, Enrico Carmona, F. Caroppo, Ettore Casart, Y. Casper, R. F. Castelo-Branco, C. Cebekhulu, Sylvia Cervigni, Mauro Chae, Hee-Dong Chamley, Larry Chan, Karen Chan, Symphorosa S. C. Chan, Te-Fu Chan, Wee-Shian Chan, Yee Chandra, Prasanta Chandraharan, Edwin Chang, P. T. Chanrachakul, Boonsri Chatterjee, Jayanta Chattopadhyay, S. Cheang, K. I.

It is possible that most of these patients get infected by contact with a taenia carrier.

The time AMPK activator elapsed between disease acquisition and symptoms occurrence suggests that, at least in some patients, clinical manifestations are related to reactivation of an infection that has previously been controlled by the host immune system. Neurocysticercosis is the most common helminthic infection of the nervous system, and a major cause of acquired epilepsy worldwide.1 The disease occurs when humans become intermediate hosts of the tapeworm Taenia solium by ingesting its eggs from contaminated food or, most often, directly from a taenia carrier (fecal-oral route). Within the central nervous system, parasites may lodge in the brain parenchyma, subarachnoid space, ventricular system, or spinal cord, causing a myriad of pathological changes that are responsible for the clinical pleomorphism of neurocysticercosis. Neurocysticercosis is endemic in most selleck chemicals llc of the developing world. There, millions of people are infected by cysticerci, and many of them will eventually experience the clinical consequences of this infection.2 Neurocysticercosis was rare in developed countries up to the past few decades. Together with the growing number of immigrants from endemic areas, there has been

an increase in the number of patients with cysticercosis in some of these countries.3,4 Also, increased tourism and international business affairs have rendered people from nonendemic areas more susceptible to acquire this parasitic disease. Neurocysticercosis in travelers has not been well characterized, and available information on these individuals is scarce and incomplete.5 The main purpose of this study is to present a review of the literature on neurocysticercosis in citizens from nonendemic countries who developed the disease after a travel to disease-endemic regions, to estimate the magnitude of the disease, and to describe the pattern of disease expression in this population. A literature search of neurocysticercosis occurring

all in citizens from nonendemic countries who had history of travel to disease-endemic countries over the past 30 years (1981–2011) was performed using the electronic database of MEDLINE (National Library of Medicine, Bethesda, MD, USA). Key words “cysticercosis” and “neurocysticercosis” were combined with “travel,”“traveler,” and with the name of each of the countries traditionally considered as nonendemic, including Western European countries, African and Middle-East countries of the Arab World, Israel, some American countries (Argentina, Belize, Canada, Surinam, United States, and Uruguay), Islands of the Caribbean Basin (except Haiti and Dominican Republic), and some countries of Asia and Oceania (Australia, Japan, Malaysia, and New Zealand).

It is possible that most of these patients get infected by contact with a taenia carrier.

The time Ponatinib research buy elapsed between disease acquisition and symptoms occurrence suggests that, at least in some patients, clinical manifestations are related to reactivation of an infection that has previously been controlled by the host immune system. Neurocysticercosis is the most common helminthic infection of the nervous system, and a major cause of acquired epilepsy worldwide.1 The disease occurs when humans become intermediate hosts of the tapeworm Taenia solium by ingesting its eggs from contaminated food or, most often, directly from a taenia carrier (fecal-oral route). Within the central nervous system, parasites may lodge in the brain parenchyma, subarachnoid space, ventricular system, or spinal cord, causing a myriad of pathological changes that are responsible for the clinical pleomorphism of neurocysticercosis. Neurocysticercosis is endemic in most Selleckchem Enzalutamide of the developing world. There, millions of people are infected by cysticerci, and many of them will eventually experience the clinical consequences of this infection.2 Neurocysticercosis was rare in developed countries up to the past few decades. Together with the growing number of immigrants from endemic areas, there has been

an increase in the number of patients with cysticercosis in some of these countries.3,4 Also, increased tourism and international business affairs have rendered people from nonendemic areas more susceptible to acquire this parasitic disease. Neurocysticercosis in travelers has not been well characterized, and available information on these individuals is scarce and incomplete.5 The main purpose of this study is to present a review of the literature on neurocysticercosis in citizens from nonendemic countries who developed the disease after a travel to disease-endemic regions, to estimate the magnitude of the disease, and to describe the pattern of disease expression in this population. A literature search of neurocysticercosis occurring

Org 27569 in citizens from nonendemic countries who had history of travel to disease-endemic countries over the past 30 years (1981–2011) was performed using the electronic database of MEDLINE (National Library of Medicine, Bethesda, MD, USA). Key words “cysticercosis” and “neurocysticercosis” were combined with “travel,”“traveler,” and with the name of each of the countries traditionally considered as nonendemic, including Western European countries, African and Middle-East countries of the Arab World, Israel, some American countries (Argentina, Belize, Canada, Surinam, United States, and Uruguay), Islands of the Caribbean Basin (except Haiti and Dominican Republic), and some countries of Asia and Oceania (Australia, Japan, Malaysia, and New Zealand).

In contrast, neurons in this RVLM region, including catecholamine-synthesizing neurons, did express c-Fos following induced hypotension, which reflexly activates RVLM sympathetic premotor neurons. The highest proportion of NTS-projecting neurons that were double-labelled

with c-Fos after air puff stress was in the ventrolateral PAG (29.3 ± 5.5%), with smaller but still significant proportions INK 128 of double-labelled NTS-projecting neurons in the PVN and PeF (6.5 ± 1.8 and 6.4 ± 1.7%, respectively). The results suggest that the increased sympathetic activity during psychological stress is not driven primarily by RVLM sympathetic premotor neurons, and that neurons in the PVN, PeF and ventrolateral PAG may contribute to the resetting of the baroreceptor-sympathetic reflex Selleckchem AZD1208 that is associated with psychological stress. “
“Some central nervous system neurons express receptors of gastrointestinal hormones, but their pharmacological actions are not well known. Previous anatomical and unit recording studies suggest that a group of cerebellar Purkinje cells express motilin receptors, and motilin depresses the spike discharges of vestibular nuclear neurons that receive direct cerebellar inhibition in rats or rabbits. Here, by the slice-patch recording method, we examined the pharmacological

actions of motilin on the mouse medial vestibular nuclear neurons (MVNs), which play an important role in the control of ocular reflexes. A small number of MVNs, as well as cerebellar floccular Purkinje cells, were labeled with an anti-motilin receptor antibody. Ribose-5-phosphate isomerase Bath application of motilin (0.1 μm) decreased the discharge frequency of spontaneous action potentials in a group of MVNs in a dose-dependent

manner (Kd, 0.03 μm). The motilin action on spontaneous action potentials was blocked by apamin (100 nm), a blocker of small-conductance Ca2+-activated K+ channels. Furthermore, motilin enhanced the amplitudes of inhibitory postsynaptic currents (IPSCs) and miniature IPSCs, but did not affect the frequencies of miniature IPSCs. Intracellular application of pertussis toxin (PTx) (0.5 μg/μL) or guanosine triphosphate-γ-S (1 mm) depressed the motilin actions on both action potentials and IPSCs. Only 30% of MVNs examined on slices obtained from wild-type mice, but none of the GABAergic MVNs that were studied on slices obtained from vesicular γ-aminobutyric acid transporter-Venus transgenic mice, showed such a motilin response on action potentials and IPSCs. These findings suggest that motilin could modulate small-conductance Ca2+-activated K+ channels and postsynaptic γ-aminobutyric acid receptors through heterotrimeric guanosine triphosphate-binding protein-coupled receptor in a group of glutamatergic MVNs.

A mechanistic and causal understanding must consider individual neurons and their synaptic interactions within complex highly-distributed neuronal networks. The difficulty

of such analyses may be significantly aided by investigating relatively simple sensory systems in genetically tractable animals, such as the mouse. Mice are nocturnal animals living in tunnels, and they rely heavily upon tactile information from their whiskers in order to sense their immediate environment. The tactile whisker sensorimotor system of the mouse is therefore one attractive model system for beginning a detailed synaptic and circuit-level analysis of the neural mechanisms underlying perception (Kleinfeld click here et al., 2006; Petersen, 2007; Diamond et al., 2008; O’Connor et al., 2009). In the laboratory environment, motivated by reward, mice can learn to use their whiskers to locate objects (Celikel & Sakmann, 2007; O’Connor et al., 2010) and discriminate textures (Mazarakis et al., 2005). Here, in this review, we will focus on the functional mapping and the underlying anatomy of the signalling pathways involved in processing whisker sensory information

in the mouse (White & DeAmicis, 1977; Porter & White, 1983; Hoogland et al., 1987; Welker et al., 1988; Brown & Dyck, 2005). Deflections of the mystacial whiskers are rapidly signalled to the primary somatosensory neocortex (S1) via two synapses, one in the brain GSK3 inhibitor stem and the other in the thalamus (Fig. 1A). Mechanosensitive sensory

neurons of the trigeminal ganglion fire reliable direction-selective action potentials with different velocity thresholds in response to deflection of single whiskers (Szwed et al., 2003; Jones et al., 2004; Arabzadeh et al., 2005; Leiser & Moxon, 2007). This sensory information is signalled to neurons in the principal and spinal trigeminal nuclei via excitatory glutamatergic synapses in the brain stem. The brain stem neurons, in turn, signal across tuclazepam excitatory glutamatergic synapses to somatosensory thalamocortical neurons of the ventroposterior medial (VPM) and posterior medial (POM) thalamus (among other targets). Projections from these two thalamic nuclei to primary somatosensory barrel cortex of the mouse have begun to be characterized anatomically and functionally. The primary somatosensory barrel cortex can be divided along its depth into anatomically defined layers, from superficial layer 1 to deep layer 6. Thalamocortical neurons located in so-called ‘barreloids’ of the VPM densely innervate layer 4 (with a more sparse innervation of upper layer 6), with each whisker being individually represented by a segregated termination field of somatotopically arranged thalamocortical axons defining the cortical barrel map (Fig. 1B and C; Woolsey & Van der Loos, 1970).

These findings, which show an increase over time in the use of triple drug PEP for infants Y-27632 cost born to HIV-infected women, highlight the impact that changes in national guidelines have had on clinical practice. Combined with effective antiretroviral therapy in pregnancy and careful management of delivery, neonatal prophylaxis contributes to the success

of MTCT prevention programmes across the UK and Ireland. National surveillance of obstetric and paediatric HIV infection is undertaken through the National Study of HIV in Pregnancy and Childhood (NSHPC) in collaboration with the Health Protection Agency Centre for Infections, and Health Protection Scotland. We gratefully acknowledge the contribution of the midwives, obstetricians, genito-urinary physicians, paediatricians, clinical nurse specialists and all other colleagues who report to the NSHPC through the British Paediatric Surveillance Selleckchem Roxadustat Unit of the Royal College of Paediatrics and Child Health, and the obstetric reporting scheme run under the auspices of the Royal College of Obstetricians and Gynaecologists. We thank Janet Masters who co-ordinates the study and manages the data, and provided comments on drafts

of this paper, and Icina Shakes for administrative support. We also thank Mario Cortina-Borja, Catherine Peckham and Hermione Lyall for their helpful comments on this manuscript. Author contributions: HH-S and CLT carried out the statistical analyses and jointly drafted the paper. All authors contributed to the interpretation of the results, commented on all drafts of the paper, and approved the final version.

PAT is the guarantor. Sources of financial support: The National Study of HIV in Pregnancy and Childhood receives core funding from the Health Protection Agency (grant number GHP/003/013/003). CLT was funded by the UK Medical Research DOK2 Council (MRC) between 2006 and 2009 (grant number G0501895). This work was undertaken at the Centre for Paediatric Epidemiology and Biostatistics which benefits from funding support from the MRC in its capacity as the MRC Centre of Epidemiology for Child Health. The University College London (UCL) Institute of Child Health receives a proportion of funding from the Department of Health’s National Institute for Health Research Biomedical Research Centres funding scheme. Any views expressed in this paper are those of the authors, and not necessarily those of the funders. Ethics approval: Ethics approval for the NSHPC was renewed following review by the London Multi-Centre Research Ethics Committee in 2004 (ref. MREC/04/2/009). Disclosure of interests: We declare that we have no conflicts of interest. “
“Treated HIV-1-infected patients with lipodystrophy often develop insulin resistance and proatherogenic dyslipidaemia.

Each series selleck inhibitor contained at least 40 sections. Sections were viewed and analyzed with a light Axio Imager A1 (Carl Zeiss) microscope; images were captured using an AxioCam (Carl Zeiss) digital camera with the software axiovision ac. Trace software igl trace 1.26b (Fiala, 2002) was used

to adjust serial sections by their contours. The 3D images were exported to WRML format, with final rendering using 3D Studio Max9 (Autodesk). Electron microscopy of the cell surfaces of yeasts grown in oil-containing media revealed profound structural alterations in the cell walls as compared with yeasts grown without hydrocarbons. Depending on the species, the yeasts could be divided into two groups. Group one included several species of Candida, Torulopsis and Shwanniomyces. When grown on either hexadecane, n-alkane mixtures (C12–C20) or crude oil, these yeasts formed ‘canals’ in their cell walls. The canals were numerous, with up to 100 canals per cell, and were especially vivid on the carbon–platinum replicas of the cell surface (Fig. 1a and b). The formation of the canals was substrate-dependent. When cells that had been grown on oil were transferred

to a medium with glucose as a sole carbon source, the canal-forming yeasts reverted to a morphotype without canals (Fig. 1c). Along with canal formation, the yeasts S. occidentalis, T. candida and C. maltosa also secreted copious amounts of fibrilar substances when cultivated in media with hexadecane, a mixture of n-alkanes or crude oil. Ultrathin sections and freeze fraction micrographs vividly click here demonstrated that this exosubstance was anatomically bound with the canal features (Fig. 2a–c). Cytochemical staining Etofibrate of these cells with diaminobenzidine further revealed the presence of oxidative enzymes

that were concentrated in the canals (Fig. 3a and b). The oxidative enzymes could also be observed in canals of partially purified cell wall fractions from these yeasts, suggesting that these enzymes are ionically or covalently bound with these modified sites of the cell wall (Fig. 3c). Immunocytochemical staining (Fig. 3d) further showed that cytochrome P-450 was concentrated in distinct locations within the cell walls. All of these facts confirmed the supposition that primary oxidation of hydrocarbons by yeasts occurs mainly in the canals where degradative enzymes are entrapped in a polymer matrix. In contrast to the canal-forming yeast, a second group of yeasts including C. lipolytica and C. paralipolytica did not form canals when grown in hydrocarbon- or crude oil-containing media, but instead secreted large amounts of fibrilar substances. The carbon–platinum replicas of these yeasts were quite smooth (Fig. 3e) and the yeasts appeared to secrete the fibrilar substances over their entire cell surface. The products of the cytochemical staining reaction targeting oxidative enzymes were located both on the cell surfaces and on the exocellular films (Fig. 3f).

The restricted word limit may also encourage pharmacy practice researchers to publish the qualitative and quantitative components separately, thereby jeopardizing the usefulness of mixed-methods research. Therefore, we urge all the pharmacy practice/education journal editors to consider increasing the word limit for mixed-methods research to allow the inclusion of sufficient detail to ensure Olaparib cost high-quality reporting of studies. In cases where increasing the word limit in print format is not practical, publishing

online supplemental material can also help to overcome the word-limit problem. Like any other research design the conduct of mixed-methods research has its challenges and limitations. These should be carefully considered before embarking on mixed-methods research. The biggest challenge perhaps is to possess the required knowledge and skills for both qualitative and quantitative data collection, analysis and interpretation. This can be overcome by developing teams of researchers with the required range of expertise, collaborating with researchers in other disciplines where necessary.[8] Mixed-methods study designs, especially sequential study

designs, may take significantly more time and resources Volasertib datasheet to undertake the distinct phases of a study.[13] For concurrent study designs it may be difficult for a single researcher to collect both qualitative and quantitative data together and several data collectors may be required.[14, 15] Since mixed-methods research is a relatively new methodology, convincing and enlightening others about its usefulness may be challenging[8] and providing a sound rationale for this approach is important. In light of these limitations we

suggest the following four questions to assist researchers to clearly think through before choosing a mixed-methods design. Firstly, after stating the research question the researcher must ask: Is mixed-methods methodology best suited to answer the research question? Secondly, which mixed-methods research design is the most appropriate to answer the research question? Thirdly, do I or other members of the research Dapagliflozin team have the necessary knowledge and skills to conduct both qualitative and quantitative studies and meaningfully combine them to comprehensively answer the research question(s)? Finally, do we have adequate time and resources to carry out a mixed-methods study? Well-designed and -executed research is essential for the development of pharmacy practice. Pharmacy practice research can benefit from mixed-methods as it allows combining the strengths of both qualitative and quantitative methodologies to gain greater understanding of the research problem.[6] The ‘numbers’ can demonstrate the effectiveness of the service/intervention and the ‘words’ can describe how/why the intervention works. It also gives the researcher the freedom to choose and mix different methods.

Then, the opposite fusion protein, GST–SpiA protein (6 mg), was applied to the column. When needed, dithiothreitol, which was added to the refolding buffer, was substituted with 1 mM diamide. Eluted protein samples were analyzed by SDS-PAGE. Purified maltose-binding BKM120 protein (5 mg)

was applied to a Ni-NTA column with bound His6–WhcA protein and treated as described above to assess nonspecific binding. HL1387 cells were grown to log phase in nonselective media, followed by diamide addition to a final concentration of 0.25–0.5 mM. After an additional 2-h incubation, transcripts were isolated and the amount of his3 mRNA was analyzed by RT-qPCR. If necessary, diamide was substituted with menadione, which was added to a final concentration of 0.5 mM. A BacterioMatch II Two-Hybrid System was used to search

for proteins that interact with WhcA. After transformation of the reporter strain with CT99021 pSL482 (pBT-whcA) and C. glutamicum target library, five clones that exhibited efficient growth on selective media were recovered, and the plasmids were isolated and sequenced. One of the plasmids contained a 243-bp fragment of the ispG gene encoding the C-terminal region (starting from the amino acid at position 151) of the 4-hydroxy-3-methylbut-2-en-1-yl diphosphate synthase. Four others contained out-of-frame genes that expressed peptide sequences. Subsequently, we searched genes whose protein products had a high homology with the peptides. ORFs NCgl1708- (hypothetical protein), NCgl0108- (NADPH-dependent dehydrogenase), NCgl0899- (dioxygenase), and NCgl1141 (nitrate reductase)-encoded proteins showed a homology with the respective peptide

sequences (Table 1). To verify the interaction of the encoded proteins with WhcA, we cloned the full-length ORFs of the above five clones into the pTRG vector, introduced them into reporter cells carrying the bait vector pBT-whcA, and monitored growth on selective media. Aside from the cells carrying pTRG-NCgl1141, all others grew efficiently on the media. These protein–protein interactions were then quantified by measuring the transcript level of the reporter gene his3 by RT-qPCR. Cells carrying pTRG-NCgl0899 showed the highest transcript level, which corresponded to 37% compared with the positive Ribonucleotide reductase control cells (Fig. 1). The transcript level for cells carrying pTRG-NCgl0108 was 25% relative to the positive control cells. In contrast, the transcript levels for cells carrying the NCgl1708- and NCgl1938-encoded proteins were close to the background level (Fig. 1). As the NCgl0899-encoded protein (now designated as SpiA) showed the strongest interaction with WhcA, we further analyzed and characterized this interaction. A direct physical interaction between WhcA and SpiA was tested by a protein-binding ‘pull-down’in vitro experiment using His6–WhcA fusion that was bound on beads and incubated with the GST–SpiA fusion protein.

The RT-PCR techniques developed appear to be sensitive, specific, and fast and could be helpful to detect those mycoses. However, it is also essential that physicians consider histoplasmosis and PCM in individuals coming from endemic areas and that they perform differential diagnosis. We are grateful to the Spanish National Health Hospitals listed below which have contributed by sending samples and data on their patients: Hospital Carlos III (Madrid), Hospital Clinico San Carlos (Madrid), Hospital Comarcal de Orihuela-Vega Baja (Orihuela, Alicante), Hospital Donostia (San Sebastian), Hospital General de Asturias (Oviedo), Hospital General de Lanzarote (Lanzarote), Hospital General Universitario Gregorio

Marañón (Madrid), Hospital General La Mancha Centro (Alcazar INCB024360 de San Juan, Ciudad Real), Hospital General Universitario Morales Meseguer, Hospital de Hellín (Hellín, Albacete), Hospital Marina Baixa (Villajoyosa, Alicante), Hospital do Meixoeiro (Vigo, Pontevedra), Hospital Mutua de Terrassa (Terrassa, Barcelona), Hospital Universitario Carlos Haya (Málaga), Hospital Universitario Clinic de Barcelona (Barcelona), Hospital Universitario Doce de Octubre (Madrid), Hospital Universitari La Fe de Valencia (Valencia), Hospital Universitario Miguel Servet (Zaragoza), Trametinib clinical trial Hospital Universitario de Mostoles (Mostoles, Madrid), Hospital Universitario Principe de Asturias (Alcala de Henares, Madrid), Hospital Universitario Ramon y Cajal (Madrid), Hospital Universitario

Son Dureta (Mallorca), Hospital Universitario

Amoxicillin Virgen de la Arrixaca (Murcia), Hospital Universitario Virgen de la Macarena (Sevilla), Hospital Vall d’Hebron (Barcelona), Hospital Virgen del Camino (Pamplona), and Hospital Virgen de la Salud (Toledo). L. B.-M. has a research contract from REIPI (Red Española de Investigación en Patología Infecciosa, Project MPY 1022/07_1) The authors state that they have no conflicts of interest to declare. “
“Background. Mediterranean spotted fever (MSF) is a tick-borne infection caused by Rickettsia conorii conorii mainly endemic in the Mediterranean Basin. Although usually considered as a benign disease, severe forms of MSF have been sporadically reported. Methods. We report on three patients who developed severe MSF complications after a stay in Morocco. Literature was reviewed to assess the frequency and pattern of MSF complications in the largest reported case series in endemic countries. Results. Each of our three patients diagnosed with MSF presented with a different complicated course: one with meningoencephalitis, one with lung embolism and one with septic shock and multi organ failure. In published series, rate of complications (defined as severe organ involvement) ranged from 1% to 20%. However, study designs and settings were highly variable and did not allow for relevant comparisons. Meningoencephalitis and shock with multi organ failure were the most frequently observed complications. Mortality of severe course was up to 20% in some series.