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Vibrios are Gram-negative bacilli that occur naturally in marine, estuarine, and freshwater systems. Some species include human and animal pathogens capable of causing gastroenteritis, wound infections, cholera, and fatal septicemia. Over the past decades, cutting edge research on Vibrio genomics has promoted a tremendous advance in our knowledge of these pathogens. Significant developments include the discovery of emerging epidemic clones, tracking the spread of new strain variants, and an intensified appreciation of the role of mobile genetic elements in antibiotic resistance spread as well as pathogenesis. Furthermore, improved understanding of the interaction of Vibrios with a variety of living organisms in the aquatic environment has documented the significant role of environmental reservoirs in their seasonal cycle favoring persistence of the pathogen during inter-epidemic periods and enhancing disease transmission. This Research Topic is dedicated to our current understanding in these areas and will bring together leading experts in the field to provide a deep overview of Vibrios ecology and evolution, and will suggest the pathway of future research in this field.

Vibrio --- Ecology --- Genome --- evolution --- Pathogenesis

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Sudden Infant Death Syndrome (SIDS) is the leading cause of death among infants in the first year of age. The more known definition of SIDS is the sudden unexpected death of an infant less than 1 year of age, with onset of the fatal episode apparently occurring during sleep, that remains unexplained after a thorough investigation, including performance of a complete autopsy and review of the circumstances of death and the clinical history. Despite the success of the “Back to Sleep” campaigns to reduce the risks introduced worldwide, the frequency of SIDS (striking one infant every 750-1,000 live births) has not significantly declined in the last years. Sudden Intrauterine Unexplained Death Syndrome (SIUDS), referring to fetuses that die unexpectedly, particularly in the last weeks of gestation, without any cause even after a complete autopsy, including examination of the placental disk, umbilical cord and fetal membranes, has a six-eightfold greater incidence than that of SIDS. Even if the pathogenetic mechanism of these deaths has not yet been determined, the neuropathology seems to be a consistent substrate in both SIUDS and SIDS. Subtle common developmental abnormalities of brainstem nuclei checking the vital functions have been highlighted, frequently related to environmental risk factors, such as cigarette smoke, air and water pollution, pesticides, food contamination, etc. Exogenous toxic factors can in fact interact in complex ways with the genetic constitution of the infant leading to polymorphisms and/or mutations of specific genes (as polymorphisms of the serotonin transporter gene 5-HTT, the regulator of the synaptic serotonin concentration, and of the PHOX2B, the key gene in the Congenital Central Hypoventilation Syndrome). These interactions can directly injure the development of the autonomic nervous system, frequently resulting in hypoplasia of the vital brainstem centers, and consequently in sudden death. It is very important to continue studying these syndromes and in particular identify all possible congenital alterations and their correlation with the exposure to environmental risk factors, in order to reduce their incidence and mitigate the surrounding social concern. The goal of this research topic is to propose new approaches to explain the pathogenesis of both SIUDS and SIDS and consequently new prevention strategies to decrease the incidence of these unexpected and very devastating events for families. Expert authors in the Topic field are encouraged to submit original research articles aimed to widen the current knowledge on the pathological substrates of these deaths, also considering the correlations with possible risk factors. Submissions of hypotheses, opinions and commentaries are also welcome. This Research Topic would lead to development of targeted risk-lowering strategies to reduce the incidence of both SIUDS and SIDS. Furthermore, the adoption of appropriate preventive measures could also lead to improve the quality of life in adults, promoting active and healthy aging.

SIDS --- sudden fetal death --- pathogenesis --- hypotheses --- guidelines

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Mycoplasma pneumoniae (Mp) is a major human pathogen that causes both upper and lower respiratory infections, and is one of the leading causes of community acquired pneumonia (CAP), accounting for 11–15% of CAP throughout the world. Additionally it is known to induce an inflammatory process which depends on several mechanisms such as virulence of Mp (lipoproteins, community acquired respiratory distress syndrome (CARDS) toxin, oxidative products) and host defenses (cellular immunity and humoral immunity). Although it is a common pathogen, the pathogenesis for Mp infections is not yet fully understood. From the clinical point of view, since the pioneer studies in the 1960s and 1970s on the clinical presentation of Mp associated disease, the diagnostics approaches have changed dramatically leading to a better understanding of the clinical presentation and new issues have emerged - such as antibiotics resistance. The purpose of this Frontiers ebook is to thoroughly review and discuss the clinical presentation in view of the improved diagnostics, microbiological and immunological analysis of Mp infections, with focus on the history of Mp, clinical features of disease, bacterial structure of Mp and mechanism of gliding, clinical and laboratory diagnostics, the role of lipoproteins and Toll-like receptor, CARDS toxin, subtyping of Mp isolates and genome analysis, macrolide resistance and treatment.

Mycoplasma pneumoniae --- pathogenesis --- epidemiology --- treatment --- clinical presentation antimicrobial resistance --- outcome

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Unfolded protein response (UPR) is a cellular adaptive response for restoring endoplasmic reticulum (ER) homeostasis in response to ER stress. Perturbation of the UPR and failure to restore ER homeostasis inevitably leads to diseases. It has now become evident that perturbation of the UPR is the cause of many important human diseases such as neurodegenerative diseases, cystic fibrosis, diabetes and cancer. It has recently emerged that virus infections can trigger the UPR but the relationship between virus infections and host UPR is intriguing. On one hand, UPR is harmful to the virus and virus has developed means to subvert the UPR. On the other hand, virus exploits the host UPR to assist in its own infection, gene expression, establishment of persistence, reactivation from latency and to evade the immune response. When this delicate balance of virus-host UPR interaction is broken down, it may cause diseases. This is particularly challenging for viruses that establish a chronic infection to maintain this balance. Each virus interacts with the host UPR in a different way to suit their life style and how the virus interacts with the host UPR can define the characteristic of a particular virus infection. Understanding how a particular virus interacts with the host UPR may pave the way to the design of a new class of anti-viral that targets this particular pathway to skew the response towards anti-virus. This knowledge can also be translated into the clinics to help re-design oncolytic virotherapy and gene therapy. In this research topic we aimed to compile a collection of focused review articles, original research articles, commentary, opinion, hypothesis and methods to highlight the current advances in this burgeoning area of research, in an attempt to provide an in-depth understanding of how viruses interact with the host UPR, which may be beneficial to the future combat of viral and human diseases.

Unfolded Protein Response --- Endoplasmic Reticulum Stress --- ERAD --- Autophagy --- innate immunity --- Gene Therapy --- Pathogenesis --- virus-host interaction

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Streptococcus pneumoniae has been for decades the number one bacterial killer of children in the world. Although vaccination with pneumococcal vaccines [PCV7, PCV10, and PCV13 (children) or PPSV23 (adults)] has helped decrease the burden of pneumococcal disease (PD), mortality remains high. Therefore, pathogenesis studies are still key toward our understanding of PD and its control. The introduction of pneumococcal vaccines has also created a niche for vaccine-escape clones. Moreover, the rise of multi-drug resistant clones around the world has also posed a serious threat in recent years. The proposed special issue of Frontiers in Cellular and Infection Microbiology highlights many of the recent advances that have been made in pneumococcal pathogenesis, colonization and antibiotic resistance by groups in Latino America, Europe, and the USA.

Streptococcus pneumoniae --- pathogenesis --- gene regulation --- biofilm --- co-infection --- drug resistance --- microbial --- macrophages