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Copyright © 2010 Pearson Education, Inc. CHAPTERS 16 AND 17 Nonspecific and Specific Defenses of the Host

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Nonspecific and Specific Defenses of the Host. Chapters 16 and 17. 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 - PowerPoint PPT Presentation

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Page 1: Chapters 16 and 17

Copyright © 2010 Pearson Education, Inc.

CHAPTERS 16 AND 17Nonspecific and Specific Defenses of the Host

Page 2: Chapters 16 and 17

Copyright © 2010 Pearson Education, Inc.

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

Page 3: Chapters 16 and 17

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An Overview of the Body’s Defenses

Figure 16.1

Nonspecific Specific

Page 4: Chapters 16 and 17

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Nonspecific Defenses of the Host

A. Skin and mucous membranes

Epithelial tissue

Waterproof yet elastic

Mucous membranes produce mucus

Page 5: Chapters 16 and 17

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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

Page 10: Chapters 16 and 17

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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

Page 12: Chapters 16 and 17

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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

Page 13: Chapters 16 and 17

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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

Page 14: Chapters 16 and 17

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Nonspecific Defenses of the Host

E. Phagocytic cells

1. Neutrophils

2. Monocytes/macrophages

Page 16: Chapters 16 and 17

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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

Page 17: Chapters 16 and 17

Copyright © 2010 Pearson Education, Inc.Figure 16.7

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

Page 19: Chapters 16 and 17

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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

Page 20: Chapters 16 and 17

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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

Page 24: Chapters 16 and 17

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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.

Page 38: Chapters 16 and 17

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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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The EndThe End