THE IMMUNE SYSTEM by 8Es2eL0

VIEWS: 29 PAGES: 126

									     Parts of the Immune System
1. Blood - White Blood Cells in
   particular.
2. Lymph nodes
3. Thymus Gland – Produces T
   Lymphocytes
4. Bone Marrow – Produces B
   Lymphocytes
6.3.1 Define Pathogen
Organism or virus that
causes a disease in
any other organisms.
                Pathogens
 = disease causing micro-organisms

      bacteria
      virus
      fungi,
      protozoa,
        parasite,

        worms

      prion
             Foreign Invaders
 Called Pathogens
   Viruses, bacteria or other
   living thing that causes
   disease/immune
   response.

 Antigens
   Toxins that pathogens
   produce that cause harm
   to an organism.
     The Big three diseases
  Disease           Cause               Pathogen
Tuberculosis   Bacterial infection    Mycobacterium
                                       tuberculosis

   AIDS         Vidal infection           Human
                                     inmunodeficiency
                                        virus (HIV)

  Malaria          Protozoan          Plasmodium sp.
                   infection
Critical considerations
These diseases are classified as the
“neglected tropical diseases” and share
the following criteria.
- They have burdened humanity for centuries
- They are poverty- promoting conditions
- They are associated with social stigma.
- They are most common in low- income
countries.
- Effective, low cost treatment are available.
Protozoan infections
Disease                  Pathogen
African typanosomiasis   Trypanosoma gabiense, T.
                         rhodiense
Kala- azar (viceral
leishamiasis)            Leishmania donovani
         Helmit (worm) infections
Soil transmitted infections:   Pathogen:

Ascaris                        Ascaris lumbricoides
Trichuriasis                   Trichuris trichiura
Hookworm infection             Nectar americanus
Schistosomiasis:              Pathogen

Urinary schistosomiasis       Schistosoma haematobium
Hematobiliary schistomiasis   Schistosoma mansoni
Lymphatic filariasis   Wuchereria ancrofti
Onchocerciases         Onchocerca volvulus
Dracunculiasis         Dracunculus medinensis
Bacterial Infections   Pathogen

Trachoma               Chlamydia trachomitis
Leprosy                Mycobacterium leprae
Buruli ulcer           Mycobacterium ulcerans
1- Suggest factors that might lead these
diseases to be neglected
2- Suggest reasons why these diseases
do not occur in high- income countries.
3- To what extent does using terms such
as “Big three diseases” and “neglect
diseases” limit or affect our thinking?
4- Discuss how “social stigma” might be
a barrier to eradication programmes
and suggest how it might be overcome.
6.3.2 Explain why
  antibiotics are
effective against
 bacteria but not
  against viruses
Antibiotics, such as the
aminoglycosides,
chloramphenicol,
erythromycin, and
clindamycin, block protein
synthesis in bacteria but
not in eukaryotic cells.
Bacteria and animal cells
synthesise proteins in a
similar manner, though the
proteins involved are not
the same.
Those antibiotics that are useful as
antibacterial agents use these
differences to bind to or inhibit the
function of the bacterial proteins. In
this way, they prevent the synthesis
of new proteins and new bacterial
cells without damaging the ‘patient’.
Most bacteria have a cell wall.
Antibiotics may disrupt this cell
wall which will interfere with the
life cycle of the bacteria.
Eukaryotic animal cells do not
have cell walls so are not
affected by the antibiotic. Viruses
do not have a cell wall so are also
not affected by antibiotics.
Viruses invade a cell and get
this host cell to produce the
protein and DNA that the
virus needs to reproduce. As
the virus uses it host’s
processes, antibiotics do not
hurt them. If they did, the
antibiotic would also disrupt
the process of protein
synthesis in the host (which
would be a serious problem).
Many anti-viral
drugs focus on
disrupting the
protein coat
of a virus and will
therefore not
usually cause harm
to the host.
6.3.3 Outline the role of skin
 and mucous membranes in
defence against pathogens.
The skin plays a
major role in this.
When unbroken, it
is almost
impossible for any
microorganism
to penetrate the
skin.
Baby and fungi
 pH of skin
 8
 7
 6
 5
 4                                                            neonates
  3                                                           adults
 2
  1
 0
       Soles    back   abdomen   pamls   forearm   forehad
1- Compare the skin pH of neonates and adults.
2- Suggest how the adult skin pH might be established
3- Suggest why the use of soap (which are basic) might have more irritating
effect on the skin of a neonate.
4- Deduce how basic soaps might undermine the skin’s defensive function.
  First lines of defence
      saliva          tears
      antibacterial   antibacterial
      enzymes         enzymes

                            mucus linings
 skin                       traps dirt and
prevents                    microbes
entry

    stomach acid        “good” gut
    low pH kills        bacteria out
    harmful             compete bad
    microbes
     Second lines of defence
 Involves white blood cells

 Non-specific response
    invading pathogens are targeted by
     macrophages
 Specific response
    lymphocytes produce chemicals
     called antibodies that target
     specific pathogens
Phagocytes
             Phagocytes
 Monocytes and macrophages
   (sangre y tejido)

 Provide a non-specific response to
 infection




 http://www.microbelibrary.org/images/
 tterry/anim/phago053.html
             Phagocytosis
 Stages in phagocytosis
  1. Phagocyte detects chemicals released by a
     foreign intruder (e.g. bacteria)
  2. Phagocyte moves up the concentration
     gradient towards the intruder
  3. The phagocyte adheres to the foreign cell
     and engulfs it in a vacuole by an infolding of
     the cell membrane.
  4. Lysosomes (organelles which are rich in
     digestive enzymes & found in the
     phagocytes cytoplasm) fuse with the
     vacuole & release their contents into it.
             Phagocytosis
  5. The bacterium is digested by the
     enzymes, and the breakdown products
     are absorbed by the phagocyte.

 During infection, hundreds of phagocytes
  are needed.
 Pus is dead bacteria and phagocytes!

 link to phagocytosis
Pus
  An accumulation of : -
     dead phagocytes
     destroyed bacteria
     dead cells
Lymphocyte
               Lymphocytes
Provide a specific immune response to
infectious diseases.
  There are 2 types:
      - T-cells
      - B-cells = They produce antibodies.
                  Antigens

 all cells have surface
 markers called
 antigens.

 body can recognise
 these as self or non-
 self (foreign)
           Specific response
 Lymphocytes detect presence of foreign antigens


 Stimulated to produce
 specific proteins called
 antibodies.
 antibodies combine with their specific antigen
 (like a lock and key)




 this renders the pathogen harmless.
 = primary response
                 Immunity

 = the bodies ability to resist infection


 can be natural or acquired
      Immunological memory
 after an infection is fought off some lymphocytes
 become memory cells.

 if same pathogen returns memory cells stimulate
 the produce the specific antibody very rapidly.

 the infection is fought off before symptoms
 appear = secondary response

 vaccines can stimulate same response
         Immune system
Can you
 Outline the stages in phagocytosis.
 Describe how antibodies work and how
  they are specific.
Blood Cells




              Phagocytes
              Lynphocytes
              Macrophages
Cells of the Immune System
White Blood Cells
 Phagocytes - Neutrophils
                - Macrophages
 Lymphocytes
Phagocytes
 Produced throughout life by the bone marrow.
 Scavengers – remove dead cells and microorganisms.
Macrophages – Phagocytosis
Lymphocytes
 Produce antibodies
 B-cells mature in bone marrow then concentrate in
  lymph nodes and spleen
 T-cells mature in thymus
 B and T cells mature then circulate in the blood and
  lymph
 Circulation ensures they come into contact with
  pathogens and each other
B -Lymphocytes
 There are c.10 million different B-lymphocytes, each of
  which make a different antibody.
 The huge variety is caused by genes coding for abs
  changing slightly during development.
 There are a small group of clones of each type of B-
  lymphocyte
B -Lymphocytes
 At the clone stage antibodies do not leave the B-
  cells.
 The abs are embedded in the plasma membrane of
  the cell and are
  called antibody receptors.
 When the receptors in the membrane recognise
  and antigen on the surface of the pathogen the B-
  cell divides rapidly.
 The antigens are presented to the B-cells by
  macrophages
B -Lymphocytes
B -Lymphocytes
 Some activated B cells  PLASMA CELLS these
  produce lots of antibodies, < 1000/sec
 The antibodies travel to the blood, lymph, lining of gut
  and lungs.
 The number of plasma cells goes down after a few
  weeks
 Antibodies stay in the blood longer but eventually
  their numbers go down too.
B -Lymphocytes
 Some activated B cells  MEMORY CELLS.
 Memory cells divide rapidly as soon as the antigen is
  reintroduced.
 There are many more memory cells than there were
  clone cells.
 When the pathogen/infection infects again it is
  destroyed before any symptoms show.
                    Antibodies
 Also known as immunoglobulins
 Globular glycoproteins
 The heavy and light chains are polypeptides
 The chains are held together by disulphide bridges
 Each ab has 2 identical ag binding sites – variable regions.
 The order of amino acids in the variable region
  determines the shape of the binding site
                 How Abs work
 Some act as labels to identify
  antigens for phagocytes
 Some work as antitoxins i.e. they block toxins for e.g.
  those causing diphtheria and tetanus
 Some attach to bacterial flagella making them less active
  and easier for phagocytes to engulf
 Some cause agglutination (clumping together) of bacteria
  making them less likely to spread
Different Immunoglobulins
Type   Number of    Site of action            Functions
       ag binding
       sites
IgG    2            •Blood                    •Increase
                    •Tissue fluid             macrophage activity
                    •CAN CROSS                •Antitoxins
                    PLACENTA                  •Agglutination

IgM    10           •Blood                    Agglutination
                    •Tissue fluid

IgA    2 or 4       •Secretions (saliva,      •Stop bacteria
                    tears, small intestine,   adhering to host
                    vaginal, prostate,        cells
                    nasal, breast milk)       •Prevents bacteria
                                              forming colonies on
                                              mucous membranes
IgE    2            Tissues                   •Activate mast cells
                                                HISTAMINE
                                              •Worm response
             T-Lymphocytes
 Mature T-cells have T cell receptors which have a very
  similar structure to antibodies and are specific to 1
  antigen.
 They are activated when the receptor comes into
  contact with the Ag with another host cell (e.g. on a
  macrophage membrane or an invaded body cell)
               T-Lymphocytes
 After activation the cell divides to form:
     T-helper cells – secrete CYTOKINES
        help B cells divide
        stimulate macrophages
   Cytotoxic T cells (killer T cells)
        Kill body cells displaying antigen
   Memory T cells
        remain in body
Active and Passive Immunity
Active immunity
 Lymphocytes are activated by antigens on the surface
 of pathogens
 Natural active immunity - acquired due to infection
 Artificial active immunity – vaccination

 Takes time for enough B and T cells to be produced to
 mount an effective response.
Active and Passive Immunity
Passive immunity
B and T cells are not activated and plasma cells have not
  produced antibodies.
The antigen doesn’t have to be encountered for the body
  to make the antibodies.
Antibodies appear immediately in blood but protection
  is only temporary.
Active and Passive Immunity
Artificial passive immunity
 Used when a very rapid immune response is needed
 e.g. after infection with tetanus.
 Human antibodies are injected. In the case of tetanus
 these are antitoxin antibodies.
 Antibodies come from blood donors who have recently
 had the tetanus vaccination.
 Only provides short term protection as abs destroyed
 by phagocytes in spleen and liver.
Active and Passive Immunity
Natural passive immunity
A mother’s antibodies pass across the placenta to the
  foetus and remain for several months.
Colostrum (the first breast milk) contains lots of IgA
  which remain on surface of the baby’s gut wall and
  pass into blood
  This is a specific response to a specific
  pathogen/antigen.
 The response involves the creation of Antibodies.




- Dead cells (tissue)
- Red Blood cells dispersed
- Bacteria or possible infections.
Deactivation of a bacterium by an antibody.
How an antibody operates/works?
    The Pathway of Specific Immune Response
             Step 1
             Pathogens eaten by Macrophage



                                     Step 2
                                     Displays portion of Pathogen
                                     on surface




                                               Step 3

Pathogens



              Helper-T cell recognizes
              Pathogen
Activates Cytotoxic                       Activates B- Cell

T- Cell




                                       Memory B-Cell
                       Memory T-Cell

                                             Antibodies
Kills Infected Cells
              Immune Response Summary
                                                                  Displays copy of antigen
                                                                  on surface of cell
                                             Antigen


                                         Macrophage


                                        Helper T - Cell                Antibody Immunity
  Cellular Immunity

           Active Cytotoxic T-Cell                                     Active B - Cell


Kills Infected Cells        Memory T- Cell             Plasma Cell                  Memory B-Cell


                                                          Antibodies


                                                  Deactivates Antigens
Primary .vs. Secondary Immune Response
 Primary Immune Response
    This is a response to an invader the First time the
     invader infects the body.
        No measurable immune response for first few days.
        Next 10 – 15 days antibody production grows steadily


 Secondary Immune Response
    A more rapid response to an invader the 2nd time it
     invades the body.
        Antibody production increases dramatically and in a much
         shorter time period..
Primary .vs. Secondary Immune Response
11.1.7 Discuss the benefits and
dangers of
vaccination.
Benefits of vaccination
1- Eradication of some diseases (e.g.
smallpox).
2- Fewer people get certain diseases
For example, measles, polio and
diphtheria because when they come
into contact with the pathogen, they
will have a secondary response
rather than a primary response
3- Prevents disability
For example, polio can cause
paralysis and when pregnant women
get rubella, the baby's vision may be
affected. Christina, the youngest
sister of Queen Beatrix of the
Netherlands, has eye problems due
to her mother (Juliana) contracting
rubella during pregnancy.
4- Herd immunity
If many people in a population are
vaccinated, the
disease will not spread and even
the individuals not
vaccinated will be protected
because they probably will
not come into contact with the
disease.
Dangers of vaccination
1- Overloading the immune
system with an antigen will
reduce the ability to handle
other infections (Gulf War
syndrome?).
2- Other pathogens could grow in
the solution with the vaccine.
3- The vaccine could contain other
harmful substances e.g. although no
evidence has been found of harmful
effects of mercury in vaccinations, as a
precaution, it is now used less and less.
4- In tests, vaccines are studied when
administered individually, but usually
the effect of a mixture of
antigens (as in MMR vaccination) is not
considered.
5- Artificial immunity is less
effective; childhood diseases
avoided as a child may cause a
more serious disease as
an adult (e.g. measles).
Side effects of vaccination:
1- In 1998 Dr. Wakefield et al
suggested a possible link between
MMR vaccination and an increased
chance of autism; studies carried
out since have failed to confirm this
link and most of Dr. Wakefield’s
coauthors have retracted the
interpretation of the results.
2- Vaccination against
whooping cough, using a whole
cell vaccine, may increase the
chances of brain
damage; again, further studies
have not shown a link.
3- Malnourished individuals
may not be able to make the
antibodies (which are proteins)
because they do not have
enough amino acids.
                Vaccination
A preparation containing antigenic
material:
 Whole live microorganism
 Dead microorganism
 Attenuated (harmless) microorganism
 Toxoid (harmless form of toxin)
 Preparation of harmless ags
                  Vaccination
 Injection into vein or muscle
 Oral
                 Vaccination
Why aren’t they always effective?
 Natural infections persist within the body for a long
  time so the immune system has time to develop an
  effective response, vaccinations from dead m-os do not
  do this.
 Less effective vaccines need booster injections to
  stimulate secondary responses
                 Vaccination
Why aren’t they always effective?
 Some people don’t respond well/at all to vaccinations
 Defective immune systems
 Malnutrition particularly protein
                 Vaccination
Why aren’t they always effective?
 Antigenic variation caused by mutation
 Antigenic drift – small changes (still recognised by
  memory cells)
 Antigenic shift – large changes (no longer recognised)
                   Vaccination
Why aren’t they always effective?
 No vaccines against protoctists (malaria and sleeping
  sickness)
 Many stages to Plamodium life cycle with many
  antigens so vaccinations would have to be effective
  against all stages (or be effective just against infective
  stage but given in very small time period).
                Vaccination
Why aren’t they always effective?
 Sleeping sickness – Trypanosoma has a thousand
  different ags and changes them every 4-5 days
                  Vaccination
Why aren’t they always effective?
 Antigenic concealment parasites live inside body cells
 Plasmodium – liver and blood cells
 Parasitic worms – cover themselves in host proteins
 HIV – live inside T-helper cells
                    Smallpox
Symptoms
 Red spots containing transparent fluid all over body.
 Spots fill with pus
 Eyelids swell and become glued together
                    Smallpox
Mortality
 12-30% died
 Survivors often left blind and disfigured with scabs.
                   Smallpox
Eradication programme
 Started by WHO in 1956
 Aimed to rid world of smallpox by 1977
 Involved vaccination and surveillance
 Over 80% of populations at risk of the disease were
  vaccinated
 After any reported case everyone in the household and
  30 surrounding households vaccinated – RING
  VACCINATION
                    Smallpox
Eradication programme
 Last case of smallpox reported in Somalia in 1977
 World declared free of smallpox in 1980
  Smallpox
Eradication programme – why was it successful?
 Variola virus stable -> cheap as everyone used same vaccine
 Vaccine made from harmless strain of similar virus (vaccinia)
 Vaccine could be used at high temperatures
 Easy to identify infected people
 Smallpox doesn’t lie dormant in body
  Smallpox
Eradication programme – why don’t all work?
 Political instability
 Poor infrastructure
 Unstable m-os
  Measles
 Caused by an airborne virus
 9th leading cause of death worldwide
 Causes rash and fever
 Can have fatal complications
 Passive immunity from mothers in infants under 8 months
 Now quite a rare disease in developed countries due to
 vaccination
  Measles
 Transmitted easily in overcrowded, insanitary conditions
 Mainly affects malnourished infants with vitamin A
  deficiencies
 Responsible for many cases of childhood blindness and can
  cause severe brain damage
 Herd immunity of 93-95% needed to prevent transmission
  within a population.
Blood from a cut will react with air
and substances from damaged cells
and platelets. Damaged cells will
release the enzyme thrombokinase
(or thromboplastin) which,
together with factor X and factor VII
and Ca2+ ions, will change
prothrombin into thrombin.
Thrombin will hydrolyse soluble
fibrinogen into smaller insoluble
fibrin molecules. These will form
a network which captures
erythrocytes and becomes a
clot.
HIV
H – Human: virus can only infect
 humans
I – Immuno-deficiency: the effect of
 the virus is to create a deficiency, a
 failure to work properly with the
 body’s immune system.
V – Virus: one of its characteristics is
 that it is incapable reproducing by
 itself. It reproduces by taking over
 the machinery of the human cell
How is HIV spread
Bodily Fluids
 Blood
 Semen
 Vaginal secretions
 Breast milk
Sexual Contact
Sexual intercourse
Oral sex
Anal sex
Blood to Blood Contact
Sharing needles or
 syringes
Tattooing - Piercing
Accidental needle stick in
 a medical setting
Incidental Cases
Mother to baby during
 pregnancy and delivery
Mother’s milk to baby
During Dental
 Procedures
The following body fluids are
NOT infectious
Saliva
Tears
Sweat
Feces
Urine
Signs and symptoms HIV
There are no true signs of
 having HIV.
One may experience flu – like
 symptoms of chills, fever, night
 sweats, rashes, etc.
Some will have no signs or
 symptoms.
 How HIV Works
HIV gets into the bloodstream
HIV targets white blood cells (T4 cells)
Virus slowly destroys T4 cells
Forces T4 cells to make copies of HIV
Eventually the cell dies
Moves on to other T4 cells
Can be up to 10 years before person
 shows signs
Phases of HIV infection
Infection with no signs or symptoms
     HIV – does not mean AIDS
Signs and symptoms
AIDS – T4 cells are less than 200 cells
 per microliter of blood or serious
 conditions from long-term, damage
 to immune system
  Opportunistic Infections
 Testing
ELISA – blood test that identifies
 whether a person has antibodies for
 HIV
Western Blot Test – done to confirm the
 results of the Elisa test.
Incubation Window – it can take 6 wks
 to 6 mths for anti. to form after
 exposure to HIV. This test should be
 done at least 6 wks after a person is or
 thinks they are infected.
AIDS
A – Acquired: a condition one must
 acquire or get infected with.
I – Immune: it affects the body’s
 immune system, the part of the body
 which usually works to fight off germs
 such as bacteria and viruses.
D – Deficiency: makes it not work
 properly
S – Syndrome: a group of symptoms
Signs and symptoms of AIDS
There are no common signs or
 symptoms for AIDS
People may experience
 opportunistic infections – when
 the immune system is weakened
 and can attack the body.
 EX.- pneumonia.
AIDS is not spread by:
Casual contact – dry
 mouth kissing, hugging,
 being sneezed on or
 coughed on.
Mosquito bites
How to Protect yourself
Abstinence - 100%
Have Safe Sex - Practice Monogamy
 – (when two people have
 intercourse with only each other for
 their entire lives).
Don’t use dirty needles
Get tested
Some statistical information shows the
extent of the problem.
In 2006, nearly 40 million people were
estimated to be living with HIV/AIDS, of
whom 4.3 million had been newly
infected. More than 60% of the people
infected with HIV/AIDS were living in Sub-
Saharan Africa. Nearly 3 million people
died in 2006 of AIDS-related diseases and
2 million of these lived in Sub-Saharan
Africa.
In North America and Western Europe,
the number of new infections has
remained the same. In many other
countries, the decrease in the number
of new infections has slowed or in other
countries the number of new infections
has increased. It is believed that this is
caused by a reduction in HIV prevention
programmes.
The social implications of AIDS are many
and can be found on any of numerous
websites. Some of these implications
are listed below:
1- People with HIV/AIDS can suffer from
stigma and discrimination.
2- Women are more likely to contract
HIV from sex with an infected partner
than men. This further increases the
inequality between men and women in
some countries.
3- People who die as a result of
HIV/AIDS are often at an
age where they are the most
productive members of
society. In countries were AIDS
causes many deaths, a relatively
large proportion of the work force
may be removed, delaying economic
growth.
4- If both parents die because of
AIDS, the country will need to spend
resources on caring for the orphans.
5- If one adult in a household suffers
from HIV/AIDS, s/he may face
unemployment and not be able to
earn an income. This may push the
entire household into poverty,
further reducing the chances of
obtaining anti-viral drugs.
6- Poverty in itself increases the
chances of contracting HIV/AIDS
due to a lack of information (no
school) and/or being forced to have
sex in exchange for food/money.
Also the incidence of rape may
increase, which is also a factor in
spreading HIV/AIDS.
7- It is expensive to treat people
with HIV/AIDS so obtaining
insurance might be a problem.
8- Use of condoms increases.

								
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