Respiratory syncytial virus (RSV) is the leading cause of hospitalizations in infants worldwide. https://www.selleckchem.com/products/atn-161.html Palivizumab, a humanized monoclonal antibody against the RSV F protein, is the only licensed agent for prevention of severe RSV infection in high-risk infants. Palivizumab is administered intramuscularly, every month during the RSV season, usually 5 doses are required. In recent years, the resolution of the structure of the RSV F protein, with identification of potent neutralizing epitopes, and new technologies for production of monoclonal antibodies (mAbs) have facilitated the development of new alternative strategies for the prevention of RSV infections. One promising approach is a new generation of mAbs directed to new neutralizing epitopes and with prolonged half life. These enhanced mAbs are expected to provide adequate protection during the complete RSV season with a single intramuscular (IM) dose. The long-term goal of this approach is to provide passive immunization for the prevention of RSV lower respiratory tract infection to all infants (preterm and full term) in the first months of life before their initial exposure to RSV.Lyme disease is a multisystem disease caused by Borrelia burgdorferi infection and accounts for well-defined manifestations, appearing either at an early or late stage. Appropriate antibiotic therapy generally leads to a favorable outcome. Still, unspecific persisting symptoms such as fatigue, myalgia, arthralgia or cognitive dysfunction are reported by several patients months to years after adequate treatment. Their underlying pathophysiologic mechanism is unclear. However, there is no evidence for microbiological persistence in these cases and attempts to resolve the symptoms by repeated or prolonged antibiotic treatment have not been convincingly successful, but they may rather be harmful. To narrow down the controversially handled entity of posttreatment Lyme disease syndrome (PTLDS) and to avoid overdiagnosis and overtreatment, case definitions have been proposed, acknowledging PTLDS as a complex of nonspecific, subjective symptoms, which are neither caused by ongoing infection nor by any other identifiable disease. PTLDS is mainly a diagnosis of exclusion and requires careful evaluation of differential diagnosis followed by counseling about optimal management in light of missing specific therapeutic options.Ureaplasma species are increasingly recognized as relevant pathogens in prenatal, perinatal and postnatal morbidity. They are commonly found as commensals on the mucous membranes of the lower urogenital tract of pregnant women, but when ascending, they can cause bacterial vaginosis, chorioamnionitis, premature birth and postnatal morbidities such as bronchopulmonary dysplasia, and early-onset neonatal sepsis and meningitis. The detection of Ureaplasma species is challenging and is not covered by routine diagnostics, and current empiric antibiotic treatment in neonates suspected of infection is not directed against Ureaplasma species. The aim of this review is to discuss the pathophysiology of Ureaplasma infections, the clinical consequences and the current difficulties in diagnosis and treatment by providing an overview of the current literature.Up to 10% of hospitalized patients have an antibiotic allergy label in their medical file, most frequently concerning penicillins. However, the vast majority of reported allergies to antibiotics does not represent a "true" allergy but are due to drug intolerance, idiosyncratic reactions or symptoms of the concurrent infectious disease. Since antibiotic allergy labels result in deviation from first-choice antimicrobial therapy, tackling the issue of incorrect antibiotic allergy labelling, already at young age, is a core element of antibiotic stewardship. In this article, we describe the structured approach to the patient with a presumed antibiotic allergy with emphasis on key elements of allergy-specific history taking and the limited risk of cross-allergic reactions between beta-lactam subclasses.Since the early 1900s, Bartonella species were known only to cause human disease resulting from very restricted geographic (bartonellosis) or environmental influences ("trench fever"). In the 1990s, and in parallel, cat scratch disease and bacillary angiomatosis were definitively linked to Bartonella species. Subsequently, widespread use of modern diagnostic methods revealed the broad ecologic niche of this organism and greatly expanded our knowledge of the epidemiology and clinical presentations associated with this genus. A large number of reservoirs and vectors involved with Bartonella propagation and transmission to humans have been identified; cats and various arthropods remain the most well-studied to date. Though not completely understood, it appears that specific immune-modulated interactions between the infecting species and host-related factors play a major role in the observed breadth of human clinical syndromes associated with Bartonellae, the large differences in immunopathologic features of tissue samples among different syndromes and potentially the varied responses to antimicrobial therapy. Further, the clinical management for cat scratch disease in particular is quite variable among clinicians, reflecting a poor evidence base. No preventive measures have been developed beyond suggestions to avoid at-risk behavior with known vectors.Widespread availability of antiretroviral therapy among pregnant women living with HIV has greatly reduced the rate of mother-to-child transmission (MTCT) of HIV across the globe. However, while Joint United Nations Programme on HIV/AIDS has set targets to reduce the annual number of new pediatric HIV infections to fewer than 40,000 in 2018 and fewer than 20,000 in 2020, progress towards these targets has plateaued at an unacceptably high global estimate of greater than 160,000 children newly infected with HIV in 2018. Moreover, it has become clear that expansion of maternal antiretroviral therapy alone will not be sufficient to close the remaining gap and eliminate MTCT of HIV. Additional strategies such as maternal or infant passive and/or active immunization that synergize with maternal antiretroviral therapy will be required to end the pediatric HIV epidemic. In this review, we outline the landscape of existing maternal interventions and emerging maternal immune-based approaches to prevent MTCT of HIV.