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Members of the genus Staphylococcus and Streptococcus are the causative agnets of many human and animal diseases. Over the past decade the complete sequencing of many staphylococcal and streptococcal genomes has promoted a significant advance in our knowledge of these important pathogens. The pathogenicity of these bacteria is due to the expression of a large variety of virulence factors. Such determinants, which are cell wall-associated and secreted proteins, include adhesins that confer to the pathogen the ability to attach to extracellular matrix/plasma and host cell surfaces, proteins that contribute to host cell invasion and intracellular survival and soluble factors that decrease phagocytosis and modulate the immune response. Furthermore, these Gram-positive cocci in many natural environments (heart valve, lung, oral cavity, throat) and infections on implanted devices live in matrix-encased groups known as biofilms. Biofilms are specialized bacterial communities with high order organization analogous to that of a tissue in multicellular organism that adhere to abiotic or biological substrata and produce an exopolymeric matrix composed of polysaccarides, proteins, DNA or combination thereof. Bacteria within a biofilm persist in adverse conditions, show resistance to killing by antibiotics and to host immune defences and are difficult to eradicate and treat clinically. Therefore, understanding the mechanisms of biofilm development will allow us to effectively combat staphylococcal/streptococcal biofilm-based infections. This Research Topic will focus on the molecular components involved in biofilm formation by staphylococci and streptococci, the role they play in the development, maturation and dispersal of biofilm and on the regulatory aspects of such complex processes. The implication for the pathogenesis of infective diseases and potential therapeutic strategies against biofilm-based infections will be also discussed. The articles will highlight both the recent advances and future challenges inherent in this rapidly evolving area.

Staphylococcus --- Streptococcus --- Biofilm --- Pathogenesis --- colonization

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The present eBook, consisting of a compilation of research and review articles, focuses on the features and mechanisms adopted and explored by pathogenic leptospires to successfully establish infection in the host. Additionally, this eBook provides information to support future work focused on the development of new prevention approaches against this important yet neglected zoonotic disease.

Leptospira --- Leptospirosis --- Pathogenesis --- Virulence --- regulation --- immune response

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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