Symbiosis, Disease and Host Defenses An evolutionary arms race.
Transcript of Symbiosis, Disease and Host Defenses An evolutionary arms race.
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Symbiosis, Disease and Host Defenses
An evolutionary arms race
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Symbiosis: Organisms ‘living together’
Three types based on effects:
Commensalism- positive for one organism and neutral for the other
Mutualism-positive for both organisms
Parasitism-positive for one negative for the other
Parasite (Greek parasitos, to dine along side of)
As a matter of convention, parasitology usually covers protist and animals even though bacteria and viruses can be parasites . Microbes are often referred to as pathogens even though they are parasitic.
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Parasitic Organisms• Overarching questions
– How do parasites affect their hosts?– What makes an efficient parasite?– Why are some organisms parasitic and others are
not?– Why is a particular organisms pathogenic sometimes
but not always?
Obligate parasite- can not live without hostOpportunistic parasite/pathogen- can be parasitic under
certain circumstancesVirulence Factor-structural or physiological characteristics
that contribute to the effect that we call disease
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Endosymbiosis
What are the possible costs or benefits to each organism involved?
How does that affect the evolutionary process?
Ancestral symbiotic event between primitive cells
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Selective pressure
Relationship is commensal
Relationship is mutual
Relationship is parasitic
Host fitness Symbiont fitness
No change up
up up
down up
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A biological arms race?
Parasite increases fitness if:• Continues to benefit from the host by resisting defenses
Host increases fitness if:• Excludes parasite• Destroys parasite outside• Destroys/digests parasite inside
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All living things have some defense mechanisms
• Restriction enzymes in bacteria
• Vesicles with chemical defenses in single-celled eukaryotes
• Specialized phagocytic cells in most animals, including arthropods and helminthes
• Pinnacle of host defenses are found in vertebrates (fish, amphibians, reptiles, birds, mammals)
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Non-Specific Host Defenses of Vertebrates
Defense “strategies” include:
External (Exclusion)
chemical-sweat, tears
physical-keratinized structures
Internal
cellular-leukocytes other than lymphocytes
chemical and molecular- complement, interferon
inflammation, fever etc..
Note: regulation is important for all internal defense mechanisms
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Physical barriers: the human integument
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Pathogens subvert physical barriers
Portals of entry include:
Ears
Nose
Mouth
Urogenital tract
Gastrointestinal tract
Wounds
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Leukocytes in non-specific defensesCytoplasm Cell name Function
Granular Neutrophils Phagocytic
Eosinophils Phagocytic, antiworm chemicals released
Basophils Release histamine
Agranular Monocytes Fixed macrophage
Phagocytic, guard tissues
Wandering
macrophages
Phagocytic, Circulate in blood and enter tissues upon infection
Dendritic (Langerhanz) cells
Phagocytic, reside in tissues like epidermis
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Phagocytic cells are non-specific defenses that destroy invaders
Phagocytosis of invader
Lysosome containing digestive chemicals
Phagolysosome formed
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Mechanisms for subverting non-specific defenses
• Structural adaptation-formation of special cell walls, capsules, endospores, cysts
• Physiological adaptations- enzymes that neutralize host chemicals, digest host physical barriers or destroy phagocytes
• Vectors, vehicles, fomites aid in gaining entry into host
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Specific Immunity: defensive cells get ‘smarter’
• “Remembering” invaders allows for faster response upon subsequent encounters of that specific invader
• Specific immunity can be divided into two branches– Humoral immunity- antibodies produced by B cells– Cell-mediated immunity- T cells recognized
invaders and stimulate defense mechanisms• Antigen any molecule that generates an immune
response (antibody generating)• Antibody- a protein that can bind to specific antigens
and help with the immune response in various ways
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Types of Specific Immunity
• Active- antibodies formed by the host– Natural- host forms antibodies naturally upon natural
exposure to antigen– Artificial- host is artificially exposed to antigen i.e.
immunization, vaccination• Passive-antibodies not made by host
– Natural-Maternal antibodies– Artificial-antibodies from other source (horse, cow
etc..), for example antivenin administered after snake bite
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Cells of the Specific Immune System
• B lymphocytes produce antibodies which are special proteins that bind to foreign molecules (antigens) and facilitate an immune response– Plasma cells– Memory B cells
• Natural Killer cells Kill virus- infected cells, bacteria and cancer cells extracellularly
• T lymphocytes differentiate into several types with different immunological functions
– Helper T cells ( TH), CD4 (T4)
– Cytotoxic cells (TC), CD8 (T8)
– Memory T cells
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B lymphocytes produce antibodies (immunoglubulins)
• Antibodies are proteins and therefore are synthesized from the instructions in DNA
• Antibodies can be constructed to fit a variety of immunological functions from cell surface receptors to circulation, or excretion
• The sections of DNA that encode the part the antibody that binds to antigen is highly variable allowing the formation of millions of different antigens so antibodies may be formed to any foreign molecule that is complex enough
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Antibodies
Basic structure of and antibody
Binds to antigen here
Y
Cell with antibody as cell-surface receptor
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Antibodies (immunoglobulins)
IgG-circulating in blood serum, can cross placenta
IgM-first to blood serum, on B cell membrane
IgA-Body secretions, epithelium of GI, Resp, UG tracts
IgD-B cell membrane
IgE-body fluids and skin, affinity for mast cells and basophils, main mediator for type 1 hypersensitivity
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B Cells and Humoral Immunity
Countless B cells are produced expressing a variety of antibodies on the cell surface
Whichever B-cell binds to a specific antigen will be produced in greater numbers to mount an immune response
Some of the newly created B cells will become memory cells and the others will become plasma cells produce and secrete various forms of that specific antibody
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Overview of Cell-mediated Immunity
• Antigen is processed by non-specific immune cells (e.g. macrophages) which present the antigen at the cell surface
• T cells that have a matching receptor bind to the antigen• If the MHC protein is correct, the T cell is activated and it
divides and differentiates
MHC proteins• made from highly variable gene which makes ‘self’
different for almost all individuals• class I MHC on all body cells • class II MHC only on some immune cells
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*
Macrophage presenting antigen in MHC II protein
Y Antibody in the form of T-cell surface receptor
MHC class II
antigen
Helper T cell
Cell-mediated Immunity
Helper T cells are activated. They differentiate into Th1 or Th2 cells which stimulate intracellular destruction of antigen (Th1) or stimulate B cells (Th2)
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*
Infected cell presenting antigen in MHC I protein
Y Antibody in the form of T-cell surface receptor
MHC class I
antigen
Cytotoxic T cell
Cell-mediated Immunity
Cytotoxic T cell are stimulated to attack infected cells
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Phases of Infection
acme
decline
Convalescence period
Pro
drom
al
perio
d
incu
batio
n
invasive
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Immune System Disorders:hypersensitivities
• Hypersensitivities – Type 1 - anaphylactic, immediate, IgE mediated– Type 2- cytotoxic, reaction to cell surface antigens– Type 3- immune complex, persistent antibody-antigen
complexes formed– Type 4 –cell (T cell) mediated, delayed
hypersensitivity
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Immune System Disorders: Autoimmunity
• Caused by lack of self recognition-T-cells and/or antibodies act against self tissues
• Triggers of autoimmunity include:– failure of lymphocyte programming process– new self antigens
• mutation in genes• Haptens (incomplete antigen)
– foreign antigens stimulate cross-reactive antibody production
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Immune System Disorders: Immunodeficiency and Immunosupression
• Causes may be:– Genetic (SCIDS)– Environmental, Chemical (pollution etc..)– Infections (AIDS)– Psychoneuroimmunological (Severe stress)
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Herd Immunity
• Populations of hosts in close proximity may be similarly exposed to diseases (especially crowd diseases)
• The more host there are in the population that are immune to a specific disease, the harder it is for the disease to spread
• Herd immunity can occur naturally as host are exposed over their lifetimes and nature selects for the fittest individuals
• Vaccines can confer artificial herd immunity to limit the spread of disease