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Infection. Chapter 9. Microorganism/Human Relationship. Mutual relationship Normal flora Relationship can be breached by injury Leave their normal sites and cause infection elsewhere Opportunistic microorganisms. Stages of Infection. Colonization Invasion Multiplication Spread.
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Infection Chapter 9
Microorganism/Human Relationship • Mutual relationship • Normal flora • Relationship can be breached by injury • Leave their normal sites and cause infection elsewhere • Opportunistic microorganisms
Stages of Infection • Colonization • Invasion • Multiplication • Spread
Factors for Infection • Mechanism of action • Infectivity • Pathogenicity • Virulence • Immunogenicity • Toxigenicity • Portal of entry
Classes of Infectious Microorganisms • Virus • Chlamydia • Rickettsia • Mycoplasma • Bacteria • Fungi • Protozoa • Helminths
Pathogen Defense Mechanisms • Surface coats • Inhibit phagocytosis, surface receptors to bind host cells, and toxins • Antigenic variation • Mutation • Antigenic drift • Recombination • Antigenic shifts • Gene switching
Bacterial Virulence and Infectivity • Bacteria must have iron to multiply • Siderophores (iron receptors) • Presence of polysaccharide capsules • Suppression of complement activation • Bacterial proliferation rates can surpass protective response
Bacterial Virulence and Infectivity • Toxin production • Exotoxins • Enzymes released during growth causing specific responses • Immunogenic • Antitoxin production • Endotoxins • Lipopolysaccharides contained in the cell walls of gram-negative organisms • Pyrogenic effects
Bacterial Virulence and Infectivity • Bacteremia or septicemia • Presence of bacteria in the blood due to a failure of the body’s defense mechanisms • Usually caused by gram-negative bacteria • Toxins released in the blood cause the release of vasoactive peptides and cytokines that produce widespread vasodilation
Viral Infection and Injury • Obligate intracellular parasites • Dependent on host cells • No metabolism or incapable of independent reproduction • Permissive host cell • Virion binds to receptors on the plasma membrane • Usually a self-limiting infection • Spreads cell to cell
Viral Replication • DNA or RNA • Single or double stranded • Protein receptor–binding site • Virus uncoats • Most RNA viruses directly produce mRNA • DNA “provirus” enters nucleus is are transcribed into mRNA
Viral Replication • Translation of mRNA results in the production of viral proteins • New virions are released through budding • Viral DNA that is integrated in host cell DNA is transmitted to daughter cells by mitosis
Cellular Effects of Viruses • Inhibition of host cell DNA, RNA, or protein synthesis • Disruption of lysosomal membranes • Promotion of apoptosis • Fusion of infected, adjacent host cells • Alteration of antigenic properties • Transformation of host cells into cancerous cells • Promotion of secondary bacterial infections
Fungal Infection and Injury • Large microorganisms with thick cell walls • Eukaryotes • Exist as single-celled yeasts, multicelled molds, or both • Pathogenicity • Adapt to host environment • Wide temperature variations, digest keratin, low oxygen • Suppress the immune defenses
Fungal Infection and Injury • Diseases caused by fungi are called mycoses • Superficial, deep, or opportunistic • Fungi that invade the skin, hair, or nails are known as dermatophytes • The diseases they produce are called tineas (ringworm) • Tinea capitis, tinea pedis, and tinea cruris • Deep fungal infections are life threatening and are commonly opportunistic
Clinical Manifestations of Infectious Disease • Variable depending on the pathogen • Directly caused by the pathogen or indirectly caused by its products • Fever • Resetting the hypothalamus • Exogenous pyrogens • Endogenous pyrogens
Countermeasures • Vaccines • Induction of long-lasting protective immune responses that will not result in disease in a healthy recipient • Attenuated organism • Killed organisms • Recombinant viral protein • Bacterial antigens • Toxins
Countermeasures • Antimicrobials • Inhibit synthesis of cell wall • Damage cytoplasmic membrane • Alter metabolism of nucleic acid • Inhibit protein synthesis • Modify energy metabolism
Pathogenic Adaptations • Suppression of immune response • Antigenic changes • Development of resistance