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Transcript

Internal defense mechanisms to protect body
from pathogens
(A pathogen is a disease causing
microorganism)
immune = “safe” in Latin

Flatworms and roundworms


White blood cells help protect the body from disease.
Here, one type of white blood cell—a macrophage—
engulfs a parasite (magnification: 1950×).

Bacteria
◦ restriction enzymes

Fungi

Plants

◦ thick outer coverings that protect against the host
immune systems and/or host enzymes.
◦ antibiotics that attack bacteria!

Segmented worms
◦ Pathogenesis Related Proteins or PR proteins.

Arthropods
Sponges
◦ protein molecules that cause pathogens to do
apoptosis (self-destruction).
◦ amoebocytes in their blood that engulf pathogens.
◦ special cells called immunocytes that participate in
cellular encapsulation of foreign tissue.
Section 40-1


VECTORS
Physical Contact
◦ Coughing
◦ Sneezing
◦ Touching


Contaminated food and water
Infected animals
In 1890 the German physician and bacteriologist Robert Koch set out
his celebrated criteria for judging whether a given bacteria is the cause
of a given disease
No pathogen
Healthy mouse
Dead mouse
Suspected
pathogen
The pathogen
should always be
found in the body
of a sick
organism and
should not be
found in a
healthy one.
Suspected pathogen
Dead mouse
Pathogen
Injection of organisms
from pure culture
◦ Ex. Mosquitoes
Healthy mouse
When purified
pathogens are
placed in a
new host, they
should cause
the same
disease that
infected the
host.
Suspected
pathogen grown
in pure culture.
Dead mouse
The pathogen
must be
isolated and
grown in the
laboratory in
a pure
culture.
The very same
pathogen should
be reisolated
from the second
host. And it
should be the
same as the
original
pathogen.
1
Section 40-1
Pathogen
Types
Viruses
Bacteria
Protists
Worms
Fungi
Chickenpox
Agent That Causes
Disease
Rhinovirus
Two types (A, B),
plus subtypes
Varicella
Measles
Paramyxovirus
Tuberculosis
Mycobacterium
tuberculosis
Neisseria meningitidis
Vibrio cholerae
Clostridium tetani
Trypanosoma
Disease
Common cold
Influenza
Meningitis
Cholera
Tetanus
African sleeping
sickness
Malaria
Amoebic dysentery
Schistosomiasis
Beef tapeworm
Athlete’s foot
Ringworm
Plasmodium
Entamoeba histolytica
Schistosoma
Taenia saginata
Imperfect fungi
Imperfect fungi
Method of
Transmission
Airborne; direct contact with infected person
Airborne; droplet infection; direct contact with
infected person
Airborne; direct contact with infected person
Droplets in air; direct contact with secretions of
infected person
Droplets in air; contaminated milk and dairy products



non specific
blocks entry of pathogens
Examples:
◦
◦
◦
◦
Direct contact with a carrier
Contaminated drinking water
Contaminated wound; usually puncture wound
Spread by tsetse fly
Spread by Anopheles mosquitoes
Contaminated drinking water
Freshwater streams and rice paddies
Contaminated meat
Contact with infected person
Exchange of hats, combs, or athletic head gear with
infected person
Skin - mechanical and chemical barrier
chemicals in sweat and oil
enzymes in tears can kill bacteria
mucous membranes and hairs trap pathogens
Section 40-2
Also, non specific
Fight infections (chemical and cellular
defense)
1. Killer Cells


◦ Macrophages
Skin
 kill bacteria through phagocytosis
Wound
Phagocytes move into the
area and engulf the bacteria
and cell debris
◦ Neutrophils
 release chemicals, killing bacteria
◦ Natural killer cells
Bacteria enter
the wound
 attack cells infected with microbes by puncturing cell
membrane
 important defense against cancer
Capillary
Video
2.
3.
Proteins - kill invaders
Inflammatory response – sends defensive
cells to area of infection
 1. injured cells release chemical signals
 2. cause expansion of blood vessels, increasing blood
flow
4.
Temperature response
◦ fever – slows or stops bacterial growth
◦ >105 often fatal


Specific defenses
Antibodies are produced to fight pathogens
that have foreign antigens
◦ Antigens
 proteins that ID a cell; act as “flags”
◦ Antibodies
 proteins produced and released by WBC’s to combat
pathogen
2
Section 40-2

Antigenbinding
sites
Antigen

◦ after exposure to a pathogen, body produces
memory cells to destroy pathogen before becoming
ill, if ever exposed again
Antibody
Cell mediated immunity
◦ Marked macrophages and helper T cells signal killer
T cells to divide
◦ The Killer T’s will destroy infected cells

Immunity
Section 40-2
Macrophage
Humoral immunity
◦ Receptor on B cells connects with foreign antigen
◦ B cells divide and produce antibodies that will mark
infected cells for destruction
Helper T cell activates
killer T cells and B cells
T cell binds to
activated
macrophage
Helper
T Cell
Killer
T Cell
T Cell
Antigens are displayed on
surface of macrophage
T cell, activated by macrophage,
becomes a helper T cell
Infected Cell
Killer T cells bind to infected cells,
disrupting their cell membranes and
destroying them

Types of immunity:
◦ Passive immunity
 Develops as a result of passively acquiring antibodies
 ex: mother transfers during pregnancy
◦ Active immunity
 develops after exposure to antigens, which results in
the production of antibodies and memory cells
 ex: Vaccinations
3
Antibody Concentration
Section 40-2
Section 40-3
Interval
between
exposures
First
exposure
Second
exposure
Infection;
Immune
system
eliminates
most of HIV
Symptoms, such as
swollen lymph nodes,
are few
Loss of immune
function more
apparent; appearance
of characteristic
diseases such as
yeast infections
Almost
total loss
of cellular
immunity;
AIDS
Relative HIV
concentration
T cell
concentration
Time
Years
4