Chapters 16 and 17
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Transcript of Chapters 16 and 17
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CHAPTERS 16 AND 17Nonspecific and Specific Defenses of the Host
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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
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An Overview of the Body’s Defenses
Figure 16.1
Nonspecific Specific
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Nonspecific Defenses of the Host
A. Skin and mucous membranes
Epithelial tissue
Waterproof yet elastic
Mucous membranes produce mucus
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Skin Epidermis
consists of tightly packed cells with Keratin, a
protective protein
Figure 16.2
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Nonspecific Defenses of the Host
Mucous membranes Mucus: Traps microbes Ciliary escalator: Microbes trapped in mucus are
transported away from the lungs
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Ciliary Escalator
Figure 24.7
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Ciliary Escalator
Figure 16.4
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Nonspecific Defenses of the Host
B. Physical Barriers Lacrimal apparatus: tears wash eye Saliva: Washes microbes off Urine Vaginal secretions Hairs Ciliated cells + mucus
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Lacrimal Apparatus
Figure 16.3
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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
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Interferons (IFNs)
IFN- and IFN-: Cause cells to produce antiviral proteins that inhibit viral replication
Gamma IFN: Causes neutrophils and macrophages
to phagocytize bacteria
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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
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Nonspecific Defenses of the Host
E. Phagocytic cells
1. Neutrophils
2. Monocytes/macrophages
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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
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Phagocytosis
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Inhibit adherence: M protein, capsules
Streptococcus pyogenes, S. pneumoniae
Kill phagocytes: Leukocidins Staphylococcus aureus
Lyse phagocytes: Membrane attack complex
Listeria monocytogenes
Escape phagosome Shigella, Rickettsia
Prevent phagosome-lysosome fusion
HIV, Mycobacterium tuberculosis
Survive in phagolysosome Coxiella burnettii
Microbial Evasion of Phagocytosis
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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
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The Process of Inflammation
Figure 16.8a, b
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Phagocyte Migration and Phagocytosis
Figure 16.8c
[Insert Animation Inflammation: Overview, Steps.]
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Tissue Repair
Figure 16.8d
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Nonspecific Defenses of the Host
G. Fever
Normal body temp. = 37oC (set by hypothalamus)
Increase in temp. = destruction of pathogens; enhancement of immune response
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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
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Specific Defenses
Cellular Immunity
T cells-
CD8 Cytotoxic T cells – killers
CD4 Helper T cells – communicators
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Specific Defenses
Memory cells are produced after challenge to immune system by pathogen or vaccination
2nd response is greater, faster
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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
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Adults reported with AIDS and a history of employment in healthcare, where job is known, by occupation, as of December 2002.
Occupation Number
Nurses 5,378
Health aides 5,638
Technicians 3,182
Physicians 1,792
Therapists 1,082
Dental workers 492
Paramedics 476
Surgeons 122
Other 5,050
Total 23,212
“Surveillance of Healthcare Personnel with HIV/AIDS, as of December 2002”, http://www.cdc.gov/ncidod/dhqp/bp_hiv_hp_with.html
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Healthcare personnel with documented and possible occupationally acquired AIDS/HIV infection, by occupation, as of December 2002.
Occupation Documented Possible
Nurse 24 35
Laboratory worker, clinical 16 17
Physician, nonsurgical 6 12
Laboratory technician, nonclinical 3 -
Housekeeper/maintenance worker 2 13
Technician, surgical 2 2
Embalmer/morgue technician 1 2
Health aide/attendant 1 15
Respiratory therapist 1 2
Technician, dialysis 1 3
Dental worker, including dentist - 6
Emergency medical technician/paramedic - 12
Physician, surgical - 6
Other technician/therapist - 9
Other healthcare occupation - 5
Total 57 139
“Surveillance of Healthcare Personnel with HIV/AIDS, as of December 2002”, http://www.cdc.gov/ncidod/dhqp/bp_hiv_hp_with.html
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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
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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.
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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
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