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CHAPTERS 16 AND 17
Nonspecific 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
Nonspecific
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Specific
Figure 16.1
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
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Figure 16.2
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
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Figure 24.7
Ciliary Escalator
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Figure 16.4
Nonspecific Defenses of the Host
B. Physical Barriers
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Lacrimal apparatus: tears wash eye
Saliva: Washes microbes off
Urine
Vaginal secretions
Hairs
Ciliated cells + mucus
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Lacrimal Apparatus
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Figure 16.3
Nonspecific Defenses of the Host
C. Chemical Defenses
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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
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Figure 16.6
Phagocytosis
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Figure 16.7
Microbial Evasion of Phagocytosis
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 HIV, Mycobacterium tuberculosis
fusion
Survive in phagolysosome
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Coxiella burnettii
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
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Figure 16.8a, b
Phagocyte Migration and Phagocytosis
[Insert Animation Inflammation: Overview, Steps.]
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Figure 16.8c
Tissue Repair
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Figure 16.8d
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 cellsCD8 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
57
139
Total
“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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The End
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