Preface

Infection is a common clinical condition that may cause local inflammation but, in some cases, can lead to systemic inflammation, with sepsis and organ dysfunction. The inflammatory response is a very complex course that is engendered by the harmful action of various agents, be they infectious, physical, or chemical, towards the host. The inflammatory response, in the biological perspective, should carry out a protective action of the organism, but this response produces several detrimental substances, such as proteolytic enzymes and oxygen metabolites. Usually, the system of host protection performs an effective action and avoids tissue damage. Nevertheless, in some cases, the protective resources are ineffectual or lost and the inflammatory response becomes harmful. Moreover, the tissue damage causes further inflammation with progressive worsening [1].

The clinical scenario of this "malignant inflammation" [2] develops in multiorgan dysfunction, which can progress to multiorgan failure because the final effect of inflammatory tissue damage is diffuse tissue hypoxia, which, if prolonged, causes irreversible cell changes. This is septic shock.

The clinical appearance of the first phase of systemic inflammation, Systemic Inflammatory Response Syndrome (SIRS), is represented by increased temperature, heart rate, respiratory rate, and white blood cell count. Organ dysfunction in Multiple Organ Dysfunction Syndrome (MODS) involves the lungs, kidneys, cardiovascular system, and central nervous system [3].

Septic shock can be evaluated as distributive shock, that is, vasodilatory shock. Distributive shock is based on the increase of intravascular space. In septic shock, especially with gram-negative bacteremia, the lipopolysaccharide endotoxin that comes from the gram-negative bacteria promotes the deliverance of effective vasodilators from damaged cell membranes. In the first phase of septic shock, the most evident clinical appearance is the vascular hyperdynamic state, followed, with the progression of the disease and the expanded intravascular space, by a low cardiac output state. The general clinical condition in distributive shock is insufficient tissue perfusion. In fact, general vasodilation causes a reduction of blood perfusion and tissue damage in the kidneys, brain, and heart. Moreover, in distributive/septic shock there is leakage of fluid from capillaries in the surrounding tissue [4].

The pathophysiology of septic shock is characterized not by altered tissue oxygenation but by cytopathic hypoxia, which is a defect in cellular oxygen availability. Consequently, the tissue level of oxygen can be increased in septic shock [5].

The first section of the book, "Therapeutic Control of Infectious Agents," includes contributions on this wide and complex topic. It provides updates on the bactericidal and bacteriostatic action of antibiotics and on the distribution and molecular detection of methicillin-resistant *Staphylococcus aureus*. It also discusses the therapeutic perspective of potential natural products from tropical fruits, empiric antimicrobial therapy in critically ill septic patients, and bacterial immunotherapy in treating chronic osteomyelitis. This section also includes some interesting studies on the epidemiology and bacterial characteristics of the bacteria *Vibrio cholerae*, including information on its prevalence, antimicrobial resistance, pathogenicity in suburban groundwater supplies of Marrakesh, secretome, and challenges in controlling vibriosis in shrimp farms.

The second section, "Specific Infectious Pathologies," examines diagnostic findings and therapeutic management of some pathological conditions with infective etiology, such as diabetic foot osteomyelitis and infections in neurosurgery.

The third section, "Sepsis Pathophysiology," evaluates some of the most important aspects of the pathophysiology and management of sepsis and septic shock. Topics covered in this section include early diagnosis of sepsis using machine learning; the pathophysiology of septic shock; intestinal barrier dysfunction, bacterial translocation, and inflammation; assessment and management of hypoperfusion in sepsis; sepsis-associated acute kidney injury; and atrial fibrillation during septic shock.

> **Vincenzo Neri** Department of Medical and Surgical Sciences – University of Foggia, Foggia, Italy

> > **Lixing Huang** Jimei University, China

**Jie Li** Chinese Academy of Fishery Sciences, China
