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Chapters 16 and 17

Chapters 16 and 17

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Chapters 16 and 17

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  1. Nonspecific and Specific Defenses of the Host Chapters 16 and 17

  2. The Concept of Immunity • Susceptibility: lack of resistance to a disease • Immunity: ability to fight off disease • Innate immunity (nonspecific): built in defenses against any pathogen • Adaptive immunity (specific): resistance to a specific pathogen

  3. An Overview of the Body’s Defenses Nonspecific Specific Figure 16.1

  4. Nonspecific Defenses of the Host A. Skin and mucous membranes Epithelial tissue Waterproof yet elastic Mucous membranes produce mucus

  5. Skin • Epidermis consists of tightly packed cells with • Keratin, a protective protein Figure 16.2

  6. Nonspecific Defenses of the Host • Mucous membranes • Mucus: Traps microbes • Ciliary escalator: Microbes trapped in mucus are transported away from the lungs

  7. Ciliary Escalator Figure 24.7

  8. Ciliary Escalator Figure 16.4

  9. Nonspecific Defenses of the Host B. Physical Barriers • Lacrimal apparatus: tears wash eye • Saliva: Washes microbes off • Urine • Vaginal secretions • Hairs • Ciliated cells + mucus

  10. Lacrimal Apparatus Figure 16.3

  11. Nonspecific Defenses of the Host C. Chemical Defenses • Lysozyme • Gastric juices • Digestive enzymes • pH – stomach (pH 1-3), skin and vagina (pH 3-5) • Sebum/wax • Perspiration • Transferrins – bind iron in blood • Complement – bind to pathogens or increase immune response • Interferons

  12. Interferons (IFNs) • IFN- and IFN-: Cause cells to produce antiviral proteins that inhibit viral replication • Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria

  13. Nonspecific Defenses of the Host D. Normal flora – outcompete pathogens/ produce bacteriocins, etc. Where are they found? Skin Eyes Nose/throat Mouth Large intestine Vagina Lower urethra

  14. Nonspecific Defenses of the Host E. Phagocytic cells 1. Neutrophils 2. Monocytes/macrophages

  15. Phagocytosis • Phago: From Greek, meaning eat • Cyte: From Greek, meaning cell • Ingestion of microbes or particles by a cell, performed by phagocytes Figure 16.6

  16. Phagocytosis Figure 16.7

  17. Microbial Evasion of Phagocytosis

  18. Nonspecific Defenses of the Host F. Inflammation Heat Swelling (edema) Pain Redness Loss of function (sometimes) Purpose: 1. destroy pathogen 2. if not, then wall off pathogen 3. repair tissues

  19. The Process of Inflammation Figure 16.8a, b

  20. Phagocyte Migration and Phagocytosis [Insert Animation Inflammation: Overview, Steps.] Figure 16.8c

  21. Tissue Repair Figure 16.8d

  22. Nonspecific Defenses of the Host G. Fever Normal body temp. = 37oC (set by hypothalamus) Increase in temp. = destruction of pathogens; enhancement of immune response

  23. Specific Defenses Humoral Immunity B cells – produce antibodies (Ab) Ab bind to antigens Antigens (Ag) are any type of molecule which elicits an immune response

  24. Specific Defenses Cellular Immunity T cells- CD8 Cytotoxic T cells – killers CD4 Helper T cells – communicators

  25. Specific Defenses Memory cells are produced after challenge to immune system by pathogen or vaccination 2nd response is greater, faster

  26. HIV/AIDS Review the websites Most common cause of exposure to HIV of healthcare workers – accidental needle stick Health professional with greatest number of cases of HIV acquired on the job – Nurse

  27. “Surveillance of Healthcare Personnel with HIV/AIDS, as of December 2002”,

  28. “Surveillance of Healthcare Personnel with HIV/AIDS, as of December 2002”,

  29. HIV/AIDS Type of pathogen – human immunodeficiency virus Disease – Acquired immune deficiency syndrome Transmission – bodily fluids, in utero; behaviors – unprotected, non-monogamous sex, sharing of needles, pregnancy Prevention – change behaviors, prophylactic treatment of a pregnant woman Treatment


  31. Classes of HIV/AIDS Antiretroviral Drugs Reverse Transcriptase (RT) Inhibitors interfere with the critical step during the HIV life cycle known as reverse transcription. Nucleoside/nucleotide analogs are faulty DNA building blocks. When these faulty pieces are incorporated into the HIV DNA (during the process when HIV RNA is converted to HIV DNA), the DNA chain cannot be completed, thereby blocking HIV from replicating in a cell. Protease Inhibitors interfere with the protease enzyme that HIV uses to produce infectious viral particles. Fusion/Entry Inhibitors interfere with the virus' ability to fuse with the cellular membrane, thereby blocking entry into the host cell. Integrase Inhibitors block integrase, the enzyme HIV uses to integrate genetic material of the virus into its target host cell. Multidrug Combination Products combine drugs from more than one class into a single product. To combat virus strains from becoming resistant to specific antiretroviral drugs, healthcare providers recommend that people infected with HIV take a combination of antiretroviral drugs known as highly active antiretroviral therapy (HAART). Developed by NIAID-supported researchers, the HAART strategy combines drugs from at least two different antiretroviral drug classes.

  32. HIV/AIDS Replication of virus Attachment Penetration Uncoating Reverse transcription Integration of viral DNA into host chromosome Transcription of viral DNA to RNA Translation of RNA to viral proteins Assembly of new viruses Budding through host membrane

  33. The End