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B. Active immunity
Induced after contact w/ foreign antigens
(microorganisms or their products)
consist clinical/subclinical infection
Immunization w/ live or killed infectious agents or their
antigens
Exposure to microbial products (toxins, toxoids)
Transplantation of foreign cells
Advantage: Long-term protection, capacity to respond
Humoral Immunity faster
Always involves the production of antibodies in Disadvantage: Slow onset, need for prolonged or
response to antigen repeated contact w/ the Ag
After Production circulating antibodies remain in TYPES OF ACQUIRED IMMUNITY
blood plasma, lymph, & other body secretions where Active Acquired Immunity
they protect against the specific pathogens that Natural active acquired immunity- Immunity that
stimulate their production is acquired in response to the entry of a live
A person is immune to a particular pathogen because of pathogen into the body (i.e. in response to an
the presence of specific protective antibodies that actual infection) protective Abs
are effective against that pathogen Artificial active acquired immunity -
Immunity that is acquired in response to
Also known as Antibody Mediated Immunity
vaccines
Passive Acquired Immunity
CELL MEDIATED IMMUNITY Natural passive acquired immunity - Immunity that
Involves various cell types, w/ antibodies playing is acquired by a fetus when it receives maternal
only a minor role Abs in utero or by an infant when it receives
cell mediated immune response maternal Abs contained in colostrum
Immune responses significant result is to make Artificial passive acquired immunity - Immunity
person resistant to certain infectious disease that is acquired when a person receives Abs
When resistant one is said to be immune contained in antiserum or gamma globulin
VACCINE o the antigens on the dead cells are usually
Material that can artificially include immunity to an less effective and produce a shorter period
infectious disease, usually after injection or ingestion of immunity
of the material Hep A, flu, Jap B, polio, rabies
A person is deliberately exposed to a harmless version anthrax, typhoid fever (subcutaneous vaccine)
of a pathogen (toxin), w/c will stimulate the persons
immune system to produce protective antibodies & SUBUNIT VACCINE (or acellular vaccine)
memory cells, but will not cause disease in the person uses antigenic (antibody-stimulating) portions of a
The persons immune system is primed to mount a pathogen
strong protective response should the actual pili of N. gonorrheae
pathogen be encountered in the future genes that code for hep B surface protein intro into
yeast cells yeast produced large quantities of that
IDEAL VACCINE protein proteins are injected into people
Contains enough antigenic determinants to stimulate Hep B, whooping cough
the immune system to produce protective antibodies
Contains antigenic determinants from all the strains of CONJUGATE VACCINES
the pathogen that cause the disease (Multivalent or conjugate bacterial capsular antigens (by themselves
Polyvalent) are not antigenic) to molecules that stimulate the
Few or no side effects immune system to produce Abs against the less
Does not cause disease in the vaccinated person antigenic capsular antigens
Hib, meningococcal meningitis, pneumococcal
TYPES OF VACCINE pneumonia
1. Live attenuated vaccines
2. Inactivated vaccines TOXOID VACCINES
3. Subunit vaccines (toxoid) exotoxin that has been inactivated by heat or
4.Conjugate vaccines chemicals
HiB injected safely to stimulate the production of antigens
meningococcal meningitis that are capable of neutralizing the exotoxin of
pneumococcal vaccine pathogens
5. Toxoid vaccines antitoxins antibodies that neutralize toxins
Diphtheria antiserum serum containing antitoxins
tetanus Diptheria, tetanus, botulism
6. DNA vaccines or gene vaccines lab animals
7. Autogenous vaccines Staphylococcus DNA OR GENE VACCINE
experimental, using lab animals
LIVE ATTENUATED VACCINES
particular gene from a pathogen inserted into
avirulent (non-pathogenic) mutant strains of pathogens
plasmids plasmids injected ID or IM inside the
that have been derived from the virulent (pathogenic)
host cells, genes direct the synthesis of a particular
organisms
microbial protein (Ag) copies produced body
growing the org. for many generations under various
conditions or by exposing them to mutagenic produces Abs directed against the protein Abs
chemicals or radiation protect the person from infection w/ the pathogen
should not be administered to immunosuppressed malarial parasite antigen
individual
even weakened pathogens can cause disease in these AUTOGENOUS VACCINE prepared from bacteria isolated
persons from a localized infection, a staph boil pathogens are killed
& then injected into the same person to induce production of
adenovirus, chicken pox (varicella), measles, mumps,
German measles, polio, rotavirus, smallpox, yellow more antibodies.
fever
NONADAPTIVE (INNATE) IMMUNITY
BCG, cholera, typhoid fever (oral vaccine)
Mechanisms of Nonspecific Host Defense:
INNATE, NON-SPECIFIC IMMUNITY
INACTIVATED VACCINES
Infectious agents must overcome innate host defense
made from pathogens that have been killed by heat or
to establish a focus of infection
chemicals
Characterized by physiologic barriers to entry of
can be produced faster and more easily
pathogenic organisms
less effective than live vaccines
Very fast host defense responses
Skin & mucous membranes, phagocytic cells, Oral mucositis Mouth but Viridans strep,
inflammatory mediators, & complement 2 to cancer also entire Capnocytophagiagingivalis
components. Chemo GI tract
Response may vary with age & w/ hormonal or
metabolic activity
INNATE IMMUNOLOGIC MECHANISM
Second Line of defense
INNATE IMMUNOLOGIC MECHANISMS A. Reticuloendothelial cells
1. Physiologic barrier at the portal of entry Phagocytosis - engulfment of
2. Innate immunologic mechanism microorganisms by macrophages
B. Activation of complement by the alternative pathway
First line of defense C. Inflammatory response
Epithelial tissues that cover the whole surface of the release of cytokines from macrophages
body: serves to hold the spread of pathogen until specific
1. Skin adaptive response is initiated
- sweat & sebaceous secretions Fever
- contain lysozyme dissolves bacterial cell walls D. Interferons critical cytokines that play a key role in
- tears, respiratory & cervical secretions defense against viral infection
2. Mucous Membranes E. NK cells large granular lymphocutes, morphology
- Respiratory mucus / cilia / phagocytes related to T Cells, which make up 10 -15 % of leukocytes in
- GIT saliva /acid pH / enzymes / phagocytes the blood
- Normal Flora oppose the establishment of pathogenic
microorganisms A. ALTERNATIVE PATHWAY OF COMPLEMENT ACTIVATION
- After entering tissues, many pathogens are recognized, Important first line of defense
ingested, & killed by phagocytes Activated by microbial surfaces
Proceeds in the absence of antibodies
INTRINSIC EPITHELIAL BARRIERS TO INFECTION Antimicrobial properties: opsonization, lysis of
Mechanical bacteria & amplification of IR
Epithelial cells joined by tight junctions
Longitudinal flow of air or fluid across epithelium
Movement of mucus by cilia
Chemical
Fatty acids (skin)
Enzymes: lysozyme (saliva, sweat, tears), pepsin (gut)
Low pH (stomach)
Antibacterial peptides; defensins (skin, gut), cryptidins
(intestine)
Microbiological
Normal flora compete for nutrients and attachment to
epithelium and can produce antibacterial substances.
Migration, chemotaxis, ingestion & microbial killing REDUCED PHAGOCYTOSIS PREDISPOSES TO INFECTION
PMN (granulocytes), phagocytic monocytes CAUSED BY CERTAIN BACTERIA
(macrophages), fixed macrophages Decreased number of PMNs
Enhanced by opsonins Cancer chemotherapy, total body irradiation
Stimulated to release cytokines that cause the Staph aureus. P aeruginosa
recruitment of more phagocytic cells to the site of Decreased function of PMNs
infection. Chronic granulomatous disease
S. aureus
Decreased function of spleen
Splenectomy, sickle cell anemia
Strep pneumoniae, N. meningitidis, H. influenza
C.INFLAMMATION
3 essential roles:
1. Deliver additional effector molecules &cells to
sites of infection
2. Provide a physical barrier
3. Promte the repair of injured tissue
Is initiated by the response of macrophages to
pathogens
Any injury to tissue elicits In R
Serves to hold the spread of pathogen until adaptive
response is initiated
Pain, redness, heat, swelling
intracellular digestion
B. T Lymphocytes
Lymphocytes that require maturation in the thymus
Utilized to activate B cells & to cope w/ intracellular
pathogens
a. CTL (Cytotoxic T cells) CELL SURFACE RECEPTORS FOR ANTIGEN
destruction of cells in tissue grafts, tumor cells, or 1. B cell receptor for antigen
cells infected by some viruses 2. T cell receptor for antigen
mainly utilized to activate B cell responses and to 3. products of the major histocompatibility complex
cope with intracellular pathogens. (MHC).
b. TH (Helper T cells)
stimulating B cells to produce antibodies 1. B CELL RECEPTOR FOR ANTIGEN
delayed hypersensitivity - membrane-bound receptor
defense against intracellular agents - IgM or IgD
- interacts with other cell surface molecules, known as
T lymphocytes or T cells Ig&Ig
2 major categories: - transduce signals after antigen binding
1. Helper T cells - signals result in biochemical events leading to cell
2. Cytotoxic T cells activation.
Main effects:
1. Opsonization: organisms, Ag-AB complexes (C3b)
2. Chemotaxis: C5a stimulates movement of PMNs
ANTIBODY MEDIATED HUMORAL IMMUNITY 3. Anaphylatoxins: C3a, C4a & C5a degranulation of
mass cells w/ release of mediators inflammation
The Primary Response 4. Cytolysis: insertion of the C5b6789 complex (MAC)
First encounter killing/ lysis of bacteria, tumor cells RBCs
Ab to Ag is detectable in serum within days or weeks
depending on the nature and dose of Ag and the route
of administration
Serum Ab concentration continues to rise for several
weeks & then declines drop to low levels
First Ab formed - IgM followed by IgG, IgA, or both
macrophages present antigen to T lymphocytesvia
their cell surface-situated MHC proteins
antigen-MHC class II complex is recognized by helper
(CD4) T lymphocytes
antigen-MHC class I complex recognized by cytotoxic
(CD8) T lymphocytes
T cells produces cytokines becomes activated,
expands by clonal proliferation
CELL-MEDIATED IMMUNITY
Produce cytokines