Objective.Candidaspecies colonize the vagina in at least 20% of women, with rates rising to 30% during pregnancy. This study aimed at determining the prevalence and risk factors of vulvovaginal candidiasis (VVC) in pregnant women at 35-37 weeks of gestation. It also aims at finding possible correlations between VVC and vaginal colonization by other agents, such as Group BStreptococcus(GBS) and bacterial vaginosis.Methodology. Over a one-year period, high vaginal swabs were collected from pregnant women during their regular antenatal checkup in different polyclinics in Beirut and South Lebanon. Swabs were examined microscopically, cultured on Sabouraud Dextrose Agar, andCandidaisolates were identified using ChromaticCandidamedium and Germ Tube Test.Results. VVC was detected in 44.8% of samples, withC. glabrata(44.4%) andC. albicans(43.4%) being the most isolated species. Approximately, half of pregnant women (57.7%) were coinfected withCandidaand bacterial vaginosis, while 26% of them carried simultaneouslyCandidaspp. and GBS. No significant correlation was found between the occurrence of VVC and demographic, clinical, medical, and reproductive health characteristics of pregnant women. In contrast, participants with previous miscarriages and those being hospitalized during the past 12 months were more susceptible to develop vaginalC. kruseiinfection in comparison to otherCandidaspecies (p=0.0316 and p=0.0042, respectively).Conclusion. The prevalence of VVC in pregnant women is an increasing trend in our community. Therefore, routine medical examination and regular screening for candidiasis in the antenatal care program is highly recommended to manage the disease and its complications.

Introduction: The rapid increase in Campylobacter strains resistant to antibiotics represents a major problem for public health. In Lebanon, campylobacteriosis is underdiagnosed since bacteria detection in stool samples is not performed routinely. This study aims to evaluate the prevalence, sources and routes of transmission, risk factors and antimicrobial susceptibility patterns of Campylobacter spp. in Lebanon. Methodology: Stool samples collected from 1000 Lebanese patients with diarrhea, and 150 meat samples taken from supermarkets and slaughterhouses were subjected to Campylobacter detection. Colonies were identified by Gram staining, oxidase and catalase activities. They were then differentiated at the species level by hippurate test and PCR. Susceptibility of Campylobacter spp. to antibiotics was studied by the disc diffusion standard method. Results: Campylobacter spp. were detected in 21.5% of stool samples; the main isolated species being C. jejuni (83.2%) and C. coli (13.9%). The highest Campylobacter infection rates were detected among children (41.8%) and during summer (31.6%). Consumption of contaminated meat and salads, and contact with animals represented the major risk factors for campylobacteriosis, with poultry carcasses and bovine cuts identified as the main bacteria reservoirs. Neither demographic determinants nor season had a major effect on the prevalence of campylobacteriosis. Erythromycin was the most active agent against Campylobacter spp. A multi-resistance rate was observed in 35.9% of isolates. Conclusions: Campylobacteriosis is a major public health concern in Lebanon. Bacteria detection in stool culture should be performed routinely to allow an early diagnosis and a better monitoring of the disease and its burden.

Familial Mediterranean Fever (FMF) is an autosomal recessive autoinflammatory disease caused by mutations in the MEFV (MEditerranean FeVer) gene that affects people originating from the Mediterranean Sea. The high variability in severity and clinical manifestations observed not only between ethnic groups but also between and within families is mainly related to MEFV allelic heterogeneity and to some modifying genes. In addition to the genetic factors underlying FMF, the environment plays a significant role in the development and manifestation of this disease through various epigenetic mechanisms, including DNA methylation, histone modification, and noncoding RNAs. Indeed, epigenetic events have been identified as an important pathophysiological determinant of FMF and co-factors shaping the clinical picture and outcome of the disease. Therefore, it is essential to better understand the contribution of epigenetic factors to autoinflammatory diseases, namely, FMF, to improve disease prognosis and potentially develop effective targeted therapies. In this review, we highlight the latest updates on the role of epigenetics in FMF.

Familial Mediterranean Fever (FMF) is a hereditary autoinflammatory disease characterized by an early onset of recurrent fever and serositis episodes. FMF is caused by mutations in the MEFV gene which encodes the pyrin protein, an IL-1β mediated inflammation regulator. Recent findings have identified a plethora of molecules and pathways involved in the regulation of inflammation and innate immunity, hence increasing our understanding of the etiology and inflammatory nature of FMF. Cytokines, in particular, have been found to play a key role in the pathogenesis and treatment of the disease. Indeed, various studies associated cytokines’ genetic variations and expression with susceptibility to and severity of the disease, which was further supported by the positive response of patients, both children and adults, to targeted cytokine blocking therapies. These studies highlighted the potential use of cytokines as biomarkers and target in resistant/intolerant patients and contributed to improving the early detection of FMF in children, thus enhancing their quality of life and providing alternative treatment for severe cases. The aim of this review is to provide the latest updates on the pivotal role of cytokines in FMF and to discuss the efficacy and safety of anti-cytokine biologics by primarily focusing on pediatric FMF cases.

Familial Mediterranean Fever (FMF) is a recurrent polyserositis characterized by self-limiting episodes or attacks of fever along with serosal inflammation. It mainly impacts people of the Mediterranean and Middle Eastern basin. FMF is a recessive autoinflammatory condition caused by mutation in the MEFV gene located on chromosome 16p13. MEFV mutations lead to the activation of the pyrin inflammasome resulting in an uncontrolled release of IL-1β. Various in vitro, in vivo and ex vivo experimental models have been developed to further comprehend the etiology and pathogenesis of FMF. These models have been proven to be clinically relevant to human FMF and can provide significant information about biological systems with respect to this condition. Additionally, these models have provided pertinent contributions to the development of potent therapeutic strategies against FMF. In this review, we describe the different experimental models utilized in FMF and we focus primarily on the most widely used models that have produced prominent insights into the pathophysiology of the disease.