Preface

Sepsis is as a complex body response to infectious agents (bacteria, virus, fungi, multicellu‐ lar parasites, etc.). The human species, as all mammals, has three defense mechanisms against pathogens: anatomical barriers, nonspecific immunity, and specific immunity. The anatomical barriers are the skin; the mucous surface, such as conjunctiva and the oral cavity with the protection of lysozyme; the mucous layer of the respiratory tract, secreted by muci‐ parous cells, and removed by eyelashes; and the acidic environment in the stomach, vagina, and on the skin. The first step of the organism reaction is tissue response to the damage caused by foreign viable agents that have passed the anatomical barriers, the body's first defense, or by pathological action of endogenous agents, present as commensals in various organs. This response is called inflammation and its purpose is to bring in the damaged site cells and serum molecules. The inflammation develops through the following phases: incre‐ ment of hematic perfusion in the site, increase of capillary permeability, and cellular migra‐ tion from blood vessels to tissues. The inflammation is a local reaction and the results are positive, mostly because its action is confined in a site. The next phase of inflammation, after increase of perfusion, is the nonspecific cellular response. The macrophages and neutrophils are the main cells that perform the action of phagocytosis of pathogens. Viral infections cause, by various cellular types, the secretion of an antiviral substance called interferon that prevents viral multiplication in the cells. Many pathogens induce the multifactorial tissue response of acute inflammation; in fact, if surface protection mechanisms and nonspecific cellular mechanisms fail to prevent invasion of pathogenic microorganisms, specific defined immune responses go into action. Many pathogens can activate specific immune responses. The activation of the immune system leads the recognition of particular characteristics of specific pathogens that are specific surface macromolecules, called antigens. Therefore the antigens produce responses, antibodies, intended to destroy them and the pathogen. This last phase of the organism's response takes place in the systemic dimension. The systemic involvement of specific immune responses can evolve in the onset of systemic inflammatory response and sepsis, which is conditioned in its severity by the response of the organism, amplified by the cascade of inflammation mediators. In this way, severe sepsis and septic shock can develop.

The introductory chapter "Surgical Infections" summarizes the pathogenesis, defense mech‐ anisms, and clinical problems of autonomous infectious pathologies of single organs treated with surgical procedures, wound infections, and surgical site infections. The chapter "Im‐ munodepression in Sepsis" focuses on the down-regulation of the innate and adaptive im‐ mune capabilities caused by anti-inflammatory substances. It emphasizes the control of the immune system and the perspectives of therapeutic strategies. The chapter "Microbiota-Ori‐ ented Diagnostics and Therapy in Sepsis: Utopia or Necessity" regards the disruption of mi‐ crobiota as an indicator of the role they play in sepsis. The changes of the gut microbiota and the characteristics of interactions in the septic microbiome can allow advances in diagnosis and therapy of sepsis. The chapter "Cytokine Gene Polymorphism and Sepsis" discusses the importance of cytokines for host immune response. The study suggests that variations in the promoter and structural regions of cytokine genes are involved in the inflammatory re‐ sponses and in inter-individual differences in sepsis severity. The chapter "Hemostatic As‐ pects of Sepsis" analyzes the changes of the hemostatic system under septic conditions, such as coagulopathy with disseminated intravascular coagulation and increase of developing or‐ gan dysfunction, morbidity, and mortality. The final chapter, "The Invariant Peptide Clus‐ ters of Serum Amyloid A Are Humoral Checkpoints for Vital Innate Functions as Probed by Monoclonal Antibodies, Including in Sepsis: Induction by Febrile Temperatures and Path of Discoveries," subdivides the argument in sections and subsections and clarifies the complex topic of the role of serum amyloid A in the acute phase of sepsis.

> **Prof. Vincenzo Neri** University of Foggia, Italy

**Chapter 1**

**Provisional chapter**

**Introductory Chapter: Surgical Infections**

Surgical infections are infectious diseases that can be treated with surgical procedures or occur in the surgical site. Synthetically, these are a localized, closed infectious disease. In the first group, the autonomous infectious pathologies of single organs or closed sites, as abscesses, appendicitis, cholecystitis, colonic diverticulitis, etc., are included. However, in the other group, there are the surgical site infections, surgical wound infections, etc. It is important to remind that the post-surgical infections can develop as local disease or as general disease with startup of systemic inflammatory response syndrome (SIRS) and then sepsis, severe sepsis, and septic shock. The surgical site and wound infections can come from the external environment or from an endogenous contamination. The infections from external environment, hospital ward, operating room, and surgical equipment, are controlled and resolved by sterilization procedures. Very crucial is the role of perioperative nurses, which should control and save the sterile techniques, detect the occurred breaks, and communicate actively to all team members. Less easily the contaminations from endogenous infective agents, pathologic aerobes and anaerobes, that are present, as commensals, in the digestive, biliary and urinary tract, airways, etc., can be controlled. In the perspective of infective risk, surgical procedures have been subdivided into four types. This classification enables proper risk stratification of occurrence of infective complications [1]. Obviously, this risk is not only connected with the environmental or endogenous sources of contamination involved during surgical procedures, but is conditioned by the general conditions of patients, characteristics of occurred intraoperative contamination, etc. [2]. The surgical procedures are classified as following: class I clean intervention—during these procedures, there is no opening of the lumen of intestinal, urinary, respiratory, genital tract; also there is no treatment for inflamed tissues or septic outbreaks. Among these interventions, there are abdominal parietal hernias, thyroid and breast surgery, exploratory abdominal surgery, etc. Class II clean-contaminated intervention—in this class, interventions during which the opening of digestive, urinary, and respiratory tract is scheduled, with checked normal situation and without uncommon contamination are collected. We

DOI: 10.5772/intechopen.92259

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and eproduction in any medium, provided the original work is properly cited.

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

distribution, and reproduction in any medium, provided the original work is properly cited.

**Introductory Chapter: Surgical Infections**

Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.92259

Vincenzo Neri

Vincenzo Neri

**1. Introduction**

### **Introductory Chapter: Surgical Infections Introductory Chapter: Surgical Infections**

DOI: 10.5772/intechopen.92259

### Vincenzo Neri Vincenzo Neri

crobiota as an indicator of the role they play in sepsis. The changes of the gut microbiota and the characteristics of interactions in the septic microbiome can allow advances in diagnosis and therapy of sepsis. The chapter "Cytokine Gene Polymorphism and Sepsis" discusses the importance of cytokines for host immune response. The study suggests that variations in the promoter and structural regions of cytokine genes are involved in the inflammatory re‐ sponses and in inter-individual differences in sepsis severity. The chapter "Hemostatic As‐ pects of Sepsis" analyzes the changes of the hemostatic system under septic conditions, such as coagulopathy with disseminated intravascular coagulation and increase of developing or‐ gan dysfunction, morbidity, and mortality. The final chapter, "The Invariant Peptide Clus‐ ters of Serum Amyloid A Are Humoral Checkpoints for Vital Innate Functions as Probed by Monoclonal Antibodies, Including in Sepsis: Induction by Febrile Temperatures and Path of Discoveries," subdivides the argument in sections and subsections and clarifies the complex

**Prof. Vincenzo Neri**

University of Foggia, Italy

topic of the role of serum amyloid A in the acute phase of sepsis.

VIII Preface

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.92259
