Contents

### **Preface XI**


Preface

shock can develop.

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

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‐
