Question

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Describe in brief which lucosites are involved in preventation of bacterial diseases and explain the process.

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Answer 1

Bacterial infections are a common, recurrent complication of cirrhosis associated with poor outcome [1]. Decompensated cirrhosis has more frequent episodes of infections than compensated cirrhosis. Once infection develops, renal failure, shock, and encephalopathy may follow, which adversely affect survival. Recent prospective studies have shown that 32–34% of cirrhotic patients develop a bacterial infection either at the time of admission or later during their hospitalization [2]. Among cirrhotic patients being admitted for gastrointestinal hemorrhage, the rate of infection is even higher at an estimated 45% and has been shown to be associated with failure to control bleeding and with early variceal rebleeding [3–7]. These numbers contrast sharply with the 5–7% overall infection rates for the general population and emphasize the concept of cirrhosis as an acquired immunodeficient state. The development of infection in cirrhosis is associated with a significantly higher mortality that has been shown to be independent of the severity of liver disease [2, 8–10]. In fact, the in-hospital mortality of cirrhotic patients with infection is approximately 15%, more than twice that of patients without infection. More importantly, infection is directly responsible for 30–50% of deaths in cirrhosis [11].

The mechanisms of increased susceptibility to infections in cirrhosis are unclear. Numerous mechanisms implicated in altered and diminished immunity include increased shunting of blood away from the liver, qualitative dysfunction of the reticuloendothelial system, decreased opsonisation capacity of the ascitic fluid, and increased intestinal permeability of bacteria and associated endotoxins [12]. It has been suggested that there is a role for deficiencies in C3 and C4, downregulation of monocyte human leukocyte antigen-DR expression (and subsequent impaired antigen presentation ability), and impairment of macrophage Fcγ-receptor-mediated clearance of antibody-coated bacteria. Patients with alcoholic cirrhosis have depressed neutrophil phagocytic and intracellular killing of microorganisms [13, 14].

The most common infections in cirrhotics are spontaneous bacterial peritonitis (SBP) (25%), followed by urinary tract infection (20%), pneumonia (15%), bacteremia following a therapeutic procedure, cellulitis, and spontaneous bacteremia [1]. Infections are culture positive in 50%–70% of cases. The causative organisms of community-acquired infection are Gram-negative bacilli (GNB), especially Escherichia coli, in about 60%, Gram-positive cocci (GPC) in about 30%–35%, and mixed in the last 5%–10%. Nosocomial infections behave differently with 60% GPC and 30%–35% positive for GNB, as a result of the use of therapeutic procedures and previous antibiotic therapies [15]. Beside Escherichia coli, the most frequently isolated bacteria areStaphylococcus aureus, Enterococcus faecalis, andStreptococcus pneumoniae. In cirrhotics less virulent organisms cause infections suggesting that, in advanced cirrhosis, bacteria do not need to develop strategies to circumvent host defenses and invade the host [16]. While GNB notablyEscherichia coli are the causative agents in spontaneous bacterial peritonitis (SBP) and urinary tract infections, Gram-positive bacteria (GPB) predominate in pneumonia (Streptococcus pneumoniae) and procedure-associated bacteremia (Staphylococcus aureus). Fungal infections especially Candida species are involved in up to 15% of severe sepsis in cirrhosis [17].

Most of the available information on bacterial infections in cirrhosis refers to SBP, an entity that is essentially unique to the cirrhotic patient and shares its pathogenesis and management with spontaneous bacteremia and spontaneous bacterial empyema. Gram-positive infections in cirrhosis such as pneumonia or secondary bacteremia are managed according to conventional criteria.

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Answer 2

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The front line of host defense
Microorganisms that cause pathology in humans and animals enter the body at different sites and produce disease by a variety of mechanisms. Many different infectious agents can cause pathology, and those that do are referred to as pathogenic microorganisms or pathogens. Invasions by microorganisms are initially countered, in all vertebrates, by innate defense mechanisms that preexist in all individuals and act within minutes of infection. Only when the innate host defenses are bypassed, evaded, or overwhelmed is an induced or adaptive immune response required. In the first part of this chapter we will describe briefly the infectious strategies of microorganisms before examining the innate host defenses that, in most cases, prevent infection from becoming established. Thus we will look at the defense functions of the epithelial surfaces of the body, the role of antimicrobial peptides and proteins, and the defense of body tissues by macrophages and neutrophils, which bind and ingest invading microorganisms in a process known as phagocytosis.