In most instances, to establish infection, microorganisms must penetrate or circumvent the host’s physical barriers (i.e., skin or mucosal surfaces); overcoming these defensive barriers depends on both host and microbial factors. When these barriers are broken, numerous other host defensive strategies are activated.

Disruption of Surface Barriers

Any situation that disrupts the physical barrier of the skin and mucosa, alters the environmental conditions (e.g., loss of stomach acidity or dryness of skin), changes the functioning of surface cells, or alters the normal flora population can facilitate the penetration of microorganisms past the barriers and into deeper host tissues. Disruptive factors may vary from accidental or intentional (medical) trauma that results in surface destruction to the use of antibiotics that remove normal, protective, colonizing microorganisms (Box 1). It is important to note that a number of these factors are related to medical interventions and procedures.

Box1. Factors Contributing to Disruption of the Skin and  Mucosal Surface

Responses to Microbial Invasion of Deeper Tissues

Once surface barriers have been bypassed, the host responds to microbial presence in the underlying tissue in various ways. Some of these responses are nonspecific, because they occur regardless of the type of invading organism; other responses are more specific and involve the host’s immune system. Both nonspecific and specific host responses are critical if the host is to survive. Without them, microorganisms would multiply and invade vital tissues and organs, resulting in severe damage to the host.

Nonspecific Responses. Some nonspecific responses are biochemical; others are cellular. Biochemical factors remove essential nutrients, such as iron, from tissues so that it is unavailable for use by invading microorganisms. Cellular responses are central to tissue and organ defenses, and the cells involved are known as phagocytes.

Phagocytes. Phagocytes are cells that ingest and destroy bacteria and other foreign particles. The two major types of phagocytes are polymorphonuclear leukocytes, also known as PMNs or neutrophils, and macro phages. Phagocytes ingest bacteria by a process known as endocytosis and engulf them in a membrane-lined structure called a phagosome (Figure 1). The phagosome is then fused with a second structure, the lysosome. When the lysosome, which contains toxic chemicals and destructive enzymes, combines with the phagosome, the bacteria trapped within the structure, referred to as a phagolysosome, are neutralized and destroyed. This destructive process must be carried out inside membrane-lined structures; otherwise the noxious substances contained within the phagolysosome would destroy the phagocyte itself. This is evident during the course of rampant infections when thousands of phagocytes exhibit “sloppy” ingestion of the microorganisms and toxic substances spill from the cells, damaging the surrounding host tissue. This process is referred to as phagocytosis.

Fig1. Overview of phagocyte activity and possible outcomes of phagocyte-bacterial interactions. 

Although both PMNs and macrophages are phagocytes, these cell types differ. PMNs develop in the bone marrow and spend their short lives (usually a day or less) circulating in blood and tissues. Widely dispersed in the body, PMNs usually are the first cells on the scene of bacterial invasion. Macrophages also develop in the bone marrow but first go through a cellular phase in which they are called monocytes. Macrophages circulating in the bloodstream are called monocytes. When deposited in tissue or at a site of infection, monocytes transform into mature macrophages. In the absence of infection, macrophages usually reside in specific organs, such as the spleen, lymph nodes, liver, or lungs, where they live for days to several weeks, awaiting encounters with invading bacteria. In addition to the ingestion and destruction of bacteria, macrophages play an important role in mediating immune system defenses.

In addition to the inhibition of microbial proliferation by phagocytes and by biochemical substances such as lysozyme, microorganisms are “washed” from tissues during the flow of lymph fluid. The fluid carries infectious agents through the lymphatic system, where they are deposited in tissues and organs (e.g., lymph nodes and spleen) heavily populated with phagocytes. This process functions as an efficient filtration system.

Inflammation. Because microbes may survive initial encounters with phagocytes (see Figure 1), the inflammatory response plays an extremely important role as a primary mechanism against microbial survival and proliferation in tissues and organs. Inflammation has both cellular and biochemical components that interact in various complex ways (Table 1).

Table1. Components of Inflammation

The complement system is composed of a coordinated group of proteins activated by the immune system or as a result of the presence of invading microorganisms. On activation of this system, a cascade of biochemical events occurs that attracts (chemotaxis) and enhances the activities of more phagocytes. Because PMNs and macro phages are widely dispersed throughout the body, signals are needed to attract and concentrate these cells at the point of invasion, and serum complement proteins provide many of these signals. Cytokines are chemical substances, or proteins secreted by a cell, that have effects on the activities of other cells. Cytokines draw more phagocytes toward the infection and activate the maturation of monocytes to macrophages.

Additional protective functions of the complement system are enhanced by the coagulation system, which works to increase blood flow to the area of infection and also can effectively wall off the infection through the production of blood clots and barriers composed of cellular debris.

The manifestations of inflammation are evident and familiar to most of us and include the following:

 • Swelling—caused by increased flow of fluid and cells to the affected body site

 • Redness—results from vasodilation of blood vessels and increased blood flow at the infection site

• Heat—results from increased cellular metabolism and energy production in the affected area

• Pain—due to tissue damage and pressure on nerve endings from increased flow of fluid and cells

On a microscopic level, the presence of phagocytes at the infection site is an important observation in diagnostic microbiology. Microorganisms associated with these host cells are frequently identified as the cause of a particular infection. An overview of inflammation is depicted in Figure 2.

Fig2. Overview of the components, signs, and functions of  inflammation. 

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مواضيع ذات صلة

Microorganism Colonization of Host Surfaces

The Encounter Between Host and Microorganism

Systemic Approach to Anemia

Comparison of Etiologies of Anemia in Adults and Children

Mechanisms of Anemia

Peptic Ulcer Disease

Nosology of Hemoglobinopathies

Infections of the Urinary Tract: Types of Infection and Their Clinical Manifestations

Toxic Goitre

Infections of the Urinary Tract : Pathogenesis

Infections of the Urinary Tract : Etiologic Agents

Infections of the Sinuses