19.3 Principles of Infectious Disease (Table 19.1)


1. A primary pathogen causes disease in otherwise healthy individuals; an opportunist causes disease only when the body's innate or adaptive defenses are compromised.

2. Virulence refers to the degree of pathogenicity of an organism.

Characteristics of Infectious Disease

1. Communicable or contagious diseases spread from one host to another; ease of spread partly reflects the infectious dose.

2. Stages of infectious disease include the incubation period, illness, and convalescence; during the illness a person experiences signs and symptoms of the disease (Figure 19.2).

3. Infections may be described as acute, chronic, or latent, depending on the timing and duration of symptoms.

4. Infections may be localized or systemic.

19.4 Establishing the Cause of Infectious Disease

Koch's Postulates

1. Koch's Postulates may be used to establish the cause of infectious disease.

482 Chapter 19 Host-Microbe Interactions

Molecular Postulates

1. Molecular Postulates may be used to identify virulence factors that contribute to disease.

Mechanisms of Pathogenesis

19.5 Establishment of Infection


1. Bacteria use adhesins to bind to host cells (Figure 19.3)


1. Rapid turnover of pili, antigenic variation, and IgA proteases enable bacteria to avoid the effects of IgA.

2. Siderophores enable microbes to scavenge iron.

Delivery of Effector Molecules to Host Cells

1. Type III secretion systems of Gram-negative bacteria allow them to deliver compounds directly to host cells. (Figure 19.4)

19.6 Invasion—Breaching the Anatomical Barriers

Penetration of Skin

1. Bacteria take advantage of trauma that destroys the integrity of the skin or rely on arthropods to inject them.

Penetration of Mucous Membranes

1. Some pathogens induce mucosal epithelial cells to engulf bacterial cells; others exploit antigen-sampling processes. (Figures 19.5, 19.6)

19.7 Avoiding the Host Defenses

Hiding Within a Host Cell

1. Some bacteria can evade the innate defenses, as well as some aspects of the adaptive defenses, by remaining inside host cells.

Avoiding Killing by Complement Proteins

1. Some serum-resistant bacteria are able to postpone the formation of the membrane attack complex by interfering with activation of the complement system via the alternative pathway. (Figure 19.8)

Avoiding Destruction by Phagocytes (Figure 19.9)

1. Mechanisms to prevent encounters with phagocytes include C5a peptidase, which degrades the chemoattractant, and membrane-damaging toxins, which destroy phagocytic cells.

2. Mechanisms to avoid recognition and attachment by phagocytes include capsules, M protein, and Fc receptors. (Figures 19.10,19.11)

3. Mechanisms to survive within the phagocyte include escape from the phagosome, preventing phagosome-lysosome fusion, and surviving within the phagosome.

Avoiding Antibodies

1. Mechanisms to avoid antibodies include IgA protease, antigenic variation, and mimicking "self."

19.8 Damage to the Host

Exotoxins (Table 19.2)

1. Exotoxins are proteins that have very specific damaging effects; they may act locally or cause dramatic systemic effects. Many can be grouped into categories such as neurotoxins, enterotoxins, or cytotoxins.

2. The toxic activity of A-B toxins is mediated by the A subunit; binding to specific cells is mediated by the B subunit. (Figure 19.12)

3. Superantigens override the specificity of the T-cell response, causing systemic effects due to the massive release of cytokines. (Figure 19.13)

4. Membrane-damaging toxins disrupt cell membranes either by forming pores or by removing the polar head group on phospholipids in the membrane.

5. Various other proteins can have detrimental effects; hydrolytic enzymes can break down tissue components.

Endotoxin and Other Bacterial Cell Wall Components

1. The symptoms associated with endotoxin are due to a vigorous host response. Lipid A of lipopolysaccharide is responsible for its toxic properties. (Figure 19.14)

2. Peptidoglycan and certain other components induce various cells to produce pro-inflammatory cytokines.

Damaging Effects of the Immune Response

1. The release of enzymes and toxic products from phagocytic cells can damage tissues.

2. Antigen-antibody complexes can cause kidney and joint damage; cross-reactive antibodies can promote an autoimmune response.

19.9 Mechanisms of Viral Pathogenesis

Binding to Host Cells and Invasion

1. Many viruses bind to and infect cells along mucous membranes; others enter at sites that are damaged or penetrated.

2. Viruses attach to specific receptors on the target cell.

Avoiding Immune Responses

1. Some viruses can avoid the effects of interferon; some can regulate apoptosis of the host cell. (Figure 19.15)

2. To subvert the role of antibodies, some viruses transfer directly from cell to cell; the surface antigens of some viruses change quickly, outpacing the production of antibodies.

Viruses and Damage to the Host

1. Mechanisms of damage include direct damage by the virus, virally induced apoptosis, and the immune response to the infection.

19.10 Mechanisms of Eukaryotic Pathogenesis


1. Saprophytes are generally opportunists; dermatophytes cause superficial infections of skin, hair, and nails. The most serious fungal infections are caused by dimorphic fungi.

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