Microbiology _ Immunology by gurjitsparhar

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									Inflammation
Wednesday, January 14, 2009
9:00 AM




    Audio recording started: 9:00 AM Wednesday, January 14, 2009


       Hemophyllis influenza (from yesterday)
      o       Even though the organism is in the human host and may have a capsule etc, it can be
         phagocytosed by a macrophages because the B cells produce antibodies which attache to the
         human host
      o       This is not as effective in children because they produce less antibodies

       INFLAMMATION
       Pain
       Edema
       Very effective as a defense mechanism
      o         Protective mechanism against pathogen because the inflammation happens only at the
          site
       Pyogenic: pus forming
       Granulomatous: nodular but without redness and edema

         Steps of inflammatory response (pyogenic)
      o           Compliment: know definition:
      o           C5a, C3a are always in circulation
                          They trigger the mast cells (rich in granulocytes with chemotactic
                  factors/pharmacologically active substances) to degranulate
                                  Usually Cause vasodilation
                                  This causes more immuno competent cells to reach the site
                                           Neutrophils
                                           macrophages
                                  These squeeze out (diapedisis) of the blood vessels and go to the site of
                         infection
                                  If the organism has a capsule or releases toxins, the macrophages and
                         phagocytes will not be able to phagocytose the organism

       Granulomatous Inflammatory response
      o        Can involve the nerve cell because it is near it, therefore when the nodule is moved
          around it can be painful

       M avium causes tuberculosis (esp in HIV patients)
       Listeria: causes meningitis in pregnant women and in the fetus
      o          Caused by ingestion of cheese and other milk products
      o          Not suppose to eat much cheese when pregnant
       Exotoxins: excreted out of the bacterial cell
       Endotoxins: part of the actual bacteria
       No gram +ve organism have endotoxins
       Gram +ve organism s only produce exotoxins
       Gram -ve organisms can produce both endo and exotoxins
       Only gram -ve organisms can produce endotoxins

     Diptheria produces exotoxin (gram +ve)
     Pseudomonas exotin A (gram -ve)
    o         Both above have the same effect

       Cholera toxin (+)
       E coli (-)

       Shiga - shigellosis

       Botulinum toxin
    o           Found in canned food
    o           If see frothing and bubbles found in canned food then there is probably toxin there
    o           Flacid paralysis
    o           E coli channels are being blocked

       Tetanus toxin
    o          Rigid paralysis
    o          Cody becomes a bow shape

       Cholera
    o             Watery stools (15-20 movements per day)

       Membrane damaging exotoxins
    o         Detergent-like action

       C perfringens
    o           Causes gangrene
    o           Destroys tissues
    o           Spreads within hours
    o           anaerobic
    o           Best way to contain the infection is to amputate
    o           Or you can also bombard the infected area with oxygen

     Endotoxin
    o        Casuses Septic schock
    o        Lipopolysaccharides
                    Stimulates B lymphocytes
                    To produce a lot of antibodies and pooling of liquids
    o        Cytokine release
    o        Polyclonal B cells
                    Causes the B cells to reproduce rapidly
                        Different kinds of cells are activated to reproduce A, B C
                                Causes damage to various tissues that each diff type of cell reacts with
                       normally
         Toxin Production
      o          HAVE TO KNOW THE TABLE GIVEN!!!!! Defo on quizzes and on
            sessionals
         Allergy
      o             Hypersensitive reactions

       Immunopathogenesis
      o        Streptococcal infection
      o        Not treated properly and have recurrence
      o        The antibodies produced by this can start attacking the glomerular membrane causing
          glomerular nephritis

         Koch's Postulates

    Questions:
    Which is the most important part of attachment: glycocalyx
    What is Not true about endotoxins? Endotoxins are secreted from cells



Architecture of Immune System
Wednesday, January 14, 2009
11:39 AM




    Audio recording started: 11:40 AM Wednesday, January 14, 2009


       Lymphoid component
      o         specific
       Reticuloendothelial component
      o         Non-specific
      o         React to anything foreign
                        Doesn'ty have to be virus or bacteria\

       1* Lyphoid organs
       Bone Marrow
       All blast cell originate fro the bone marrow (therefore important lyphoid organ)
      o          Hemopoetic blast cells
                          HSC
                                   Develop into B (stay in bone marrow) or T (have to pass through thymus
                         for activation/ to become immunocompetent) lyphocytes
         Thymus
      o            T-cells
         Spleen
      o          2* lymphoid organs
         MHC proteins: major histo compatibility complex
         Complement system
         Chemical mediators: cytokines

    All of the above work together to destroy the organisms

         Agranular vs granular: refer to chart given in slides
         Single blast cell cannot develop with characteristics of both agranular an granular
         The environment determines what they develop into
         At each stage the cells acquire certain markers to develop into

    Polymorphonuclear granulocytes: PNMs

       Neutrophils
      o         If there are more neutrophils being produced then that means the body is producing
          more of them to fight a pyogenic infection
       Eosinophils
      o         best for attacking parasites
      o         Usually increases by 10-20% (this is very important esp in USMLE questions)
      o         If a patient says he/she is eating but is not gaiing weight and is losing weight, do a blood
          test and do a an eosinophil count
       Basophils and Mast Cells:
      o         Important for vasodilation or vasoconstriction
      o         These are protective during inflammation but can be damaging in the case of allergy
      o         Or they can cause septic shock (happens in sever allergies) causing major damage to
          tissues all over the body
      o         Allergy
                        The patient will have a sensitizing dose first
                        Antibodies will be produced by body
                        When the patient is given a second penecillin shot
                        Stimulating dose!
                        The patient will react within minutes

    T Cells

       HIV virus effects the T cells
       Once the t cells are destroyed the other cells cannot work because the T cells are the source
       CD 4, CD8
       All t cells have both odf the above but only one of them is expressed when the cell becomes
    functional and then the cell is designated according to which ever cytokineis expressed
       All other cytokines are produces from CD4 cells (the key)
      o           HIV specifically attacks this in t cells
         T Helper Cells
      o           Type 1 and 2
      Have to know interleukins and TH1 and TH2 slide for sure: will definitely be on the
    exam!!!!

    B cells





Thursday, January 15, 2009
10:26 AM

    SDL
            Present minimum of ten slides



       Globlin fraction of blood: antibodies are found there
       Antibodies definition:
      o         Anti bodies are produced by B cells

         Membrane bound antibodies
      o          These are the receptors on the B cell surface
      o          Not all the antibodies are found on the b cell
      o          These belong to the class Igm and IGG
      o          When a foreign antigen come the antiobodies recofgnize the antigen , these are very
           specific
                         The whole of the antigen does not initiate an immune response, only certain
                 parts
                         B cell gets activated and forms two clones of cells
                                  Plasma cells
                                           They will form soluble antibodies which take part in immune
                              reactions
                                  Memory B cells


                   If same antigen encounters a B cell then the memory b cell takes over and it is much
                     faster,

         Antibodies that take part in the immunological reaction are the secretory antibodies


         B cells
      o             Develop from stem cells in bone marrow
      o             Antigen is encoutneered by the b cell
      o           Move into lymphoid organs, and mature and clonal slection takes place which is the
            division into plasma cells and memory cells
      o           Plasma cells secrete actively antibodies

      o             Hellper T cells\
                           Stimulate the B cells
      o             Cytotoxic T Cells


         Antibody Structure
      o          Page 430

         Variable region versus constant region

         Hinge regions
      o           Proline and cysteine residues
                         Proline: structural conformatino
                         Cysteine: provides sites for disulphide bonds
                         IgE and IgM do not hav any specific hinge regions
                                  CH2 domain acts as hinge region


         Antibody molecule cleaved with pepsin enzyme the FC portion will not be there, LOOK at SLIDE

         Serum concentraion, weight, and half life, know this shit for the five antibodies

         IGA
      o          In secretion it is found as a Dimer
      o          It is joined by a J chain, which is nothing but a polypeptide chain
      o          Attached to the J piece is a secretory component, its role is to add protection to the
            antibody molecule,
      o          Found in the intestinal lumen

       Mucosal surfaces are lined by cells and the igA are there
       You also have poly IG receptors
       Now when the antibody is transferred through the mucosal layer lumen, it has to forma
    complex the Poly IG recepts and the IgA form a complex\
       The Poly IG gets cleaved once it is being transported and once it is outside of the lumen and into
    the cell has the secretory component and adds extra protection to the antibody molecule.

         Newborn has IGG and IGM, how is that?
      o         Infected by some external pathogen or has gotten some infection from the mother
      o         Pathological

         IGM
      o             As long as antigen is there you will find IGM there
      o             Half life is five days
      o             Levels of this indicate that the paitent has been infected with a recent infection
          IGG has four subclasses
          IGA has two subclasses

          IGE
       o           Destroyed by heat, it is heat Labile
       o           Prodeced in persons with allergy


       o          External antigen binds to ige molecule and causes Cross linkage forms and signals
             degranulation and tehn the granules burst and release their contents and that leads to skin
             rashes or whatever allergic reactions


          IGD
       o           Membrane bound receptors on B cells,






PAGE 396 or something...




Tuesday, January 27, 2009
8:07 AM




Audio recording started: 8:07 AM Tuesday, January 27, 2009



     Immunocompetent cells form from what
        Antigen stimulates the body to synthesize biologically active proteins -------chemotaxis
       o        Once the chemotaxis reaches the B & T Lymphocyte it gets activated

        Cells mediated immune response
        Humeral immune response
       o         Antibody mediated immune response

          First line mechanism
       o             Monocytes
       o             Macrophagesdendritic cells
       o             Neutrphils
    o           Eosinpohples
    o           Mast cells
    o           B& T lymphocytes
                       Chemotoxic factors changes the above immunocompetent cells and activates
                them..



       Infection : enlargement and multicplication of organism

       The cells that fail in the first line of defense ; some can become antigen presenting cells
    o           The antigen is taken up by the APC by means of phagocytosis into a small bits of 10-
          25,000 daltons

     MHC : major histocombatiblity complex proteins
    o        MHC class I
                    endogenous
    o        MHC class 2
                    Exogenous antigens

    o           Class 1 and class 2 Determined by exogenous or endogenous antigen
    o           Viruses can be one or two

    o         Linear arrangement of genes, the genetic components of this DNA determines what
          immyunoglobulin will be synthesized
                     If genes are corresponding toward gamma you find IGG
                     If epsolon it si IGE
                     Delta is IGD
                     Alpha is IGA
                     IGM ( the little micro symbol)

    o           The stronger and heavier the chemotaxis reaching the .. You find the IgG antibody
    o           Coming from the mucosal surface you will find IgA
    o           If chemotaxis from allergens, creams, pollen grains you lead to production of IgE

       Promary immune response
    o          Is IgM

       Secondary immune response
    o          Is IgG
    o          Has a very short lag phase if it is same pathogen for the attack,
    o          Will have a profound log phase
    o          It is the same antigen

       Booster doses requried for killed or inactivated vaccines
    o          Live vaccines require lesser booster doses then killed …WHY?

       Clonal selection:





Bacterial Pathogenesis
Tuesday, January 13, 2009
8:07 AM




    Audio recording started: 8:08 AM Tuesday, January 13, 2009


      NEED TO KNOW THE DEFINITIONS!
      Pathogenesis: ability to cause disease
      Normal flora can invade but usually does not causes pathogenesis
      Infection is just entry into the host and multiplication at that site
      Fever is a disease not the actual infection
      Disease refers to the symptoms of a given infection
      Disease is a consequence of an infection
      Ex: ecoli: virulence is low because it is part of the normal flora but can develop virulence is
    exposed to specific structures etc
      Infective dose (ID)
      Lethal Dose (LD)

       Each organism has a ID and LD
       The ID and LD can be different depending on the organism and some organisms have the same
    ID and LD
       Pathogenicity
      o         Virulence
      o         Number of organism
      o         Immune status
                       Example: HIV patient is immunological compromised
                       Therefore a smaller infective dose can cause sickness
                       Ex: cancer patients etc
                       Innate and acquired immune response imbalances can give room for infection

          Carrier state (important. Know the definition)
       o            Subclinical manifestation
       o            Have the pathogen but do not suffer from any infection
          Convalescent carrier: a person carrying the pathogen even after treatment: subclinical

       Paradoxical carrier: a carrier of soemthing else acquires the organism from another person
    (exchange)
      o        Usually happens in a hospital setting
         Zoonotic organism: organism from animals when transferred to humans are pathogenic
      o          Animal infections
      o          Usually the cycle is between the flea and the animal (rat) but when humans intervene it
            can be transferred to them; Ex: Plague

       Non human to human
      o       Know slide
      o       Tetanus manifests in the wound and then creates infection (from soil)
      o       Legionnaire's disease: very severe pneumonia
                      Requiring ventilator etc
      o       Cat-scratch fever: from domestic pets
      o       E coli hemolytic uremic syndrome
                      Bloody diarrhea
                      Patient can die within 4-5 hours
                      From meat sources

         Tuberculosis does not have a carrier state
      o          Can acquire this even from talking to a patient
      o          Therefore have to cover face

         There are some organisms that are always pathogenic (never normal flora)

       Ecoli (normal flora) can become pathogenic when it exchanges DNA with new organisms that
     enter the GIT and have the ability to infect a human host
       Post operative wound infections occur when normal flora of the skin are implanted in the
     perinmeum (ex). The bacteria transplanted there are not normal for that are therefore they are
     pathogenic

1.      Vertical Transmission
      o          Transplacental:
                        As a fetus
                        Within the womb
      o          Within birth canal/ at birth
                        Streptococcal agalactiae
                                Flesh eating disease
                        Gonorrhea
                                Child develops opthalmia after approx 3 days
                                         Can cause color blindness
                                         Or complete blindness
                                         Child has pus emitting from the eye and is unable to open the
                              eyelids
                        Milk can also be infected

         Adherence
      o          Need to have a receptor site
                       Eg: ecoli has to attach in the GIT
                                Receptors only found in GIT
                          Syphyllis
       o          Often the receptor sites are blocked by normal flora therefore the pathogens cannot
             bind the sites
       o          This is why the immunilogical status of the patient is very imprtant
                          People who take unnecessary antibiotics remove all the normal flora and
                   therefore become susceptible to pathogens
                          Immunological suppressed or compromised patients are more at risk
                                  Cancer patients
                                  HIV patients
                                  Common cold

        Gram +ve streptococcus occurs in lines
        E coli with fimbria (different from flagella and pilli)
        Pilli help bacteria attach very strongly to the cells
        E coli pilli: urogenital cells have receptors for them
       o           Therefore infection occurs in them

        Invasion
       o         Some organisms enter the cells instead of just attachin to the cell
                       Produce Toxic enzymes etc
                               Example of various enzymes are given in the slide
                               Collagenase:
                                       Surrounds the organism with chemical and the immunological
                            response cell (B & T cells, macrophages) cannot recognise it therefor it
                            remains and mulitplies
       o         Antiphagocytic
                       Capsulated organisms
                               Macrophages unable to recognise organism because of capsule

          Extracellular Pathogens
       o           Resistant to extra-cellular killing
       o           Killed on phagocytosis
       o           Resist killing
                           By avoiding internalization




Inflammation
Wednesday, January 14, 2009
9:00 AM




    Audio recording started: 9:00 AM Wednesday, January 14, 2009
     Hemophyllis influenza (from yesterday)
    o       Even though the organism is in the human host and may have a capsule etc, it can be
       phagocytosed by a macrophages because the B cells produce antibodies which attache to the
       human host
    o       This is not as effective in children because they produce less antibodies

     INFLAMMATION
     Pain
     Edema
     Very effective as a defense mechanism
    o         Protective mechanism against pathogen because the inflammation happens only at the
        site
     Pyogenic: pus forming
     Granulomatous: nodular but without redness and edema

       Steps of inflammatory response (pyogenic)
    o           Compliment: know definition:
    o           C5a, C3a are always in circulation
                        They trigger the mast cells (rich in granulocytes with chemotactic
                factors/pharmacologically active substances) to degranulate
                                Usually Cause vasodilation
                                This causes more immuno competent cells to reach the site
                                         Neutrophils
                                         macrophages
                                These squeeze out (diapedisis) of the blood vessels and go to the site of
                       infection
                                If the organism has a capsule or releases toxins, the macrophages and
                       phagocytes will not be able to phagocytose the organism

       Granulomatous Inflammatory response
    o          Can involve the nerve cell because it is near it, therefore when the nodule is moved
          around it can be painful

     M avium causes tuberculosis (esp in HIV patients)
     Listeria: causes meningitis in pregnant women and in the fetus
    o          Caused by ingestion of cheese and other milk products
    o          Not suppose to eat much cheese when pregnant
     Exotoxins: excreted out of the bacterial cell
     Endotoxins: part of the actual bacteria
     No gram +ve organism have endotoxins
     Gram +ve organism s only produce exotoxins
     Gram -ve organisms can produce both endo and exotoxins
     Only gram -ve organisms can produce endotoxins

     Diptheria produces exotoxin (gram +ve)
     Pseudomonas exotin A (gram -ve)
    o         Both above have the same effect
       Cholera toxin (+)
       E coli (-)

       Shiga - shigellosis

       Botulinum toxin
    o           Found in canned food
    o           If see frothing and bubbles found in canned food then there is probably toxin there
    o           Flacid paralysis
    o           E coli channels are being blocked

       Tetanus toxin
    o          Rigid paralysis
    o          Cody becomes a bow shape

       Cholera
    o             Watery stools (15-20 movements per day)

       Membrane damaging exotoxins
    o         Detergent-like action

       C perfringens
    o           Causes gangrene
    o           Destroys tissues
    o           Spreads within hours
    o           anaerobic
    o           Best way to contain the infection is to amputate
    o           Or you can also bombard the infected area with oxygen

     Endotoxin
    o         Casuses Septic schock
    o         Lipopolysaccharides
                     Stimulates B lymphocytes
                     To produce a lot of antibodies and pooling of liquids
    o         Cytokine release
    o         Polyclonal B cells
                     Causes the B cells to reproduce rapidly
                     Different kinds of cells are activated to reproduce A, B C
                              Causes damage to various tissues that each diff type of cell reacts with
                    normally
     Toxin Production
    o          HAVE TO KNOW THE TABLE GIVEN!!!!! Defo on quizzes and on
          sessionals
       Allergy
    o             Hypersensitive reactions
         Immunopathogenesis
      o          Streptococcal infection
      o          Not treated properly and have recurrence
      o          The antibodies produced by this can start attacking the glomerular membrane causing
            glomerular nephritis

         Koch's Postulates

    Questions:
    Which is the most important part of attachment: glycocalyx
    What is Not true about endotoxins? Endotoxins are secreted from cells



Architecture of Immune System
Wednesday, January 14, 2009
11:39 AM




    Audio recording started: 11:40 AM Wednesday, January 14, 2009


       Lymphoid component
      o         specific
       Reticuloendothelial component
      o         Non-specific
      o         React to anything foreign
                        Doesn'ty have to be virus or bacteria\

       1* Lyphoid organs
       Bone Marrow
       All blast cell originate fro the bone marrow (therefore important lyphoid organ)
      o          Hemopoetic blast cells
                          HSC
                                   Develop into B (stay in bone marrow) or T (have to pass through thymus
                         for activation/ to become immunocompetent) lyphocytes
       Thymus
      o          T-cells
       Spleen
      o          2* lymphoid organs
       MHC proteins: major histo compatibility complex
       Complement system
       Chemical mediators: cytokines

    All of the above work together to destroy the organisms
         Agranular vs granular: refer to chart given in slides
         Single blast cell cannot develop with characteristics of both agranular an granular
         The environment determines what they develop into
         At each stage the cells acquire certain markers to develop into

    Polymorphonuclear granulocytes: PNMs

       Neutrophils
      o         If there are more neutrophils being produced then that means the body is producing
          more of them to fight a pyogenic infection
       Eosinophils
      o         best for attacking parasites
      o         Usually increases by 10-20% (this is very important esp in USMLE questions)
      o         If a patient says he/she is eating but is not gaiing weight and is losing weight, do a blood
          test and do a an eosinophil count
       Basophils and Mast Cells:
      o         Important for vasodilation or vasoconstriction
      o         These are protective during inflammation but can be damaging in the case of allergy
      o         Or they can cause septic shock (happens in sever allergies) causing major damage to
          tissues all over the body
      o         Allergy
                        The patient will have a sensitizing dose first
                        Antibodies will be produced by body
                        When the patient is given a second penecillin shot
                        Stimulating dose!
                        The patient will react within minutes

    T Cells

       HIV virus effects the T cells
       Once the t cells are destroyed the other cells cannot work because the T cells are the source
       CD 4, CD8
       All t cells have both odf the above but only one of them is expressed when the cell becomes
    functional and then the cell is designated according to which ever cytokineis expressed
       All other cytokines are produces from CD4 cells (the key)
      o           HIV specifically attacks this in t cells
       T Helper Cells
      o           Type 1 and 2
      Have to know interleukins and TH1 and TH2 slide for sure: will definitely be on the
    exam!!!!

    B cells




Bacterial Pathogenesis
Tuesday, January 13, 2009
8:07 AM




    Audio recording started: 8:08 AM Tuesday, January 13, 2009


      NEED TO KNOW THE DEFINITIONS!
      Pathogenesis: ability to cause disease
      Normal flora can invade but usually does not causes pathogenesis
      Infection is just entry into the host and multiplication at that site
      Fever is a disease not the actual infection
      Disease refers to the symptoms of a given infection
      Disease is a consequence of an infection
      Ex: ecoli: virulence is low because it is part of the normal flora but can develop virulence is
    exposed to specific structures etc
      Infective dose (ID)
      Lethal Dose (LD)

       Each organism has a ID and LD
       The ID and LD can be different depending on the organism and some organisms have the same
    ID and LD
       Pathogenicity
      o         Virulence
      o         Number of organism
      o         Immune status
                       Example: HIV patient is immunological compromised
                       Therefore a smaller infective dose can cause sickness
                       Ex: cancer patients etc
                       Innate and acquired immune response imbalances can give room for infection

        Carrier state (important. Know the definition)
       o          Subclinical manifestation
       o          Have the pathogen but do not suffer from any infection
        Convalescent carrier: a person carrying the pathogen even after treatment: subclinical

       Paradoxical carrier: a carrier of soemthing else acquires the organism from another person
    (exchange)
      o        Usually happens in a hospital setting

          Zoonotic organism: organism from animals when transferred to humans are pathogenic
       o          Animal infections
       o          Usually the cycle is between the flea and the animal (rat) but when humans intervene it
             can be transferred to them; Ex: Plague
       Non human to human
      o       Know slide
      o       Tetanus manifests in the wound and then creates infection (from soil)
      o       Legionnaire's disease: very severe pneumonia
                      Requiring ventilator etc
      o       Cat-scratch fever: from domestic pets
      o       E coli hemolytic uremic syndrome
                      Bloody diarrhea
                      Patient can die within 4-5 hours
                      From meat sources

         Tuberculosis does not have a carrier state
      o          Can acquire this even from talking to a patient
      o          Therefore have to cover face

         There are some organisms that are always pathogenic (never normal flora)

       Ecoli (normal flora) can become pathogenic when it exchanges DNA with new organisms that
     enter the GIT and have the ability to infect a human host
       Post operative wound infections occur when normal flora of the skin are implanted in the
     perinmeum (ex). The bacteria transplanted there are not normal for that are therefore they are
     pathogenic

1.      Vertical Transmission
      o          Transplacental:
                        As a fetus
                        Within the womb
      o          Within birth canal/ at birth
                        Streptococcal agalactiae
                                Flesh eating disease
                        Gonorrhea
                                Child develops opthalmia after approx 3 days
                                         Can cause color blindness
                                         Or complete blindness
                                         Child has pus emitting from the eye and is unable to open the
                              eyelids
                        Milk can also be infected

       Adherence
      o        Need to have a receptor site
                       Eg: ecoli has to attach in the GIT
                                Receptors only found in GIT
                       Syphyllis
      o        Often the receptor sites are blocked by normal flora therefore the pathogens cannot
          bind the sites
      o        This is why the immunilogical status of the patient is very imprtant
                       People who take unnecessary antibiotics remove all the normal flora and
                therefore become susceptible to pathogens
                          Immunological suppressed or compromised patients are more at risk
                                Cancer patients
                                HIV patients
                                Common cold

        Gram +ve streptococcus occurs in lines
        E coli with fimbria (different from flagella and pilli)
        Pilli help bacteria attach very strongly to the cells
        E coli pilli: urogenital cells have receptors for them
       o           Therefore infection occurs in them

        Invasion
       o         Some organisms enter the cells instead of just attachin to the cell
                       Produce Toxic enzymes etc
                               Example of various enzymes are given in the slide
                               Collagenase:
                                       Surrounds the organism with chemical and the immunological
                            response cell (B & T cells, macrophages) cannot recognise it therefor it
                            remains and mulitplies
       o         Antiphagocytic
                       Capsulated organisms
                               Macrophages unable to recognise organism because of capsule

          Extracellular Pathogens
       o           Resistant to extra-cellular killing
       o           Killed on phagocytosis
       o           Resist killing
                           By avoiding internalization




Antibodies
Thursday, January 15, 2009
10:26 AM

    SDL
             Present minimum of ten slides



       Globlin fraction of blood: antibodies are found there
       Antibodies definition:
      o         Anti bodies are produced by B cells

          Membrane bound antibodies
      o         These are the receptors on the B cell surface
    o           Not all the antibodies are found on the b cell
    o           These belong to the class Igm and IGG
    o           When a foreign antigen come the antiobodies recofgnize the antigen , these are very
          specific
                        The whole of the antigen does not initiate an immune response, only certain
                parts
                        B cell gets activated and forms two clones of cells
                                 Plasma cells
                                          They will form soluble antibodies which take part in immune
                             reactions
                                 Memory B cells



                 If same antigen encounters a B cell then the memory b cell takes over and it is much
                   faster,

       Antibodies that take part in the immunological reaction are the secretory antibodies


       B cells
    o           Develop from stem cells in bone marrow
    o           Antigen is encoutneered by the b cell
    o           Move into lymphoid organs, and mature and clonal slection takes place which is the
          division into plasma cells and memory cells
    o           Plasma cells secrete actively antibodies

    o             Hellper T cells\
                         Stimulate the B cells
    o             Cytotoxic T Cells


       Antibody Structure
    o          Page 430

       Variable region versus constant region

       Hinge regions
    o           Proline and cysteine residues
                       Proline: structural conformatino
                       Cysteine: provides sites for disulphide bonds
                       IgE and IgM do not hav any specific hinge regions
                                CH2 domain acts as hinge region


       Antibody molecule cleaved with pepsin enzyme the FC portion will not be there, LOOK at SLIDE

       Serum concentraion, weight, and half life, know this shit for the five antibodies
         IGA
      o          In secretion it is found as a Dimer
      o          It is joined by a J chain, which is nothing but a polypeptide chain
      o          Attached to the J piece is a secretory component, its role is to add protection to the
            antibody molecule,
      o          Found in the intestinal lumen

       Mucosal surfaces are lined by cells and the igA are there
       You also have poly IG receptors
       Now when the antibody is transferred through the mucosal layer lumen, it has to forma
    complex the Poly IG recepts and the IgA form a complex\
       The Poly IG gets cleaved once it is being transported and once it is outside of the lumen and into
    the cell has the secretory component and adds extra protection to the antibody molecule.

         Newborn has IGG and IGM, how is that?
      o         Infected by some external pathogen or has gotten some infection from the mother
      o         Pathological

         IGM
      o          As long as antigen is there you will find IGM there
      o          Half life is five days
      o          Levels of this indicate that the paitent has been infected with a recent infection

         IGG has four subclasses
         IGA has two subclasses

         IGE
      o          Destroyed by heat, it is heat Labile
      o          Prodeced in persons with allergy


      o          External antigen binds to ige molecule and causes Cross linkage forms and signals
            degranulation and tehn the granules burst and release their contents and that leads to skin
            rashes or whatever allergic reactions


         IGD
      o          Membrane bound receptors on B cells,






PAGE 396 or something...
Antigen & Antibody Reaction
Tuesday, January 20, 2009
8:03 AM




    Audio recording started: 8:03 AM Tuesday, January 20, 2009


    Amita Shobarao = Umbridge

       Venereal disease research lab (VDRL test for syphillis) - definition not given in slides
       Know examples of different test because we will be given matching exercises on our quizzes
    and sessionals
      o        Eg. Match disease/antigen to a specific test
       Triponemia sopmething something test….the slide before hemagglutination inhibition

    JAVETTS FOR MCQs!!!!!!!!


Architecture of Immune System Continued
Wednesday, January 21, 2009
10:35 AM




    Audio recording started: 11:18 AM Wednesday, January 21, 2009




    Audio recording started: 10:36 AM Wednesday, January 21, 2009



       Lymphocytes
       TH (helper) & TC (cytotoxic)
       Helper cells can be identified using the suface markers (CD4 markers)
      o         There are TH1 and TH2
      o         Difference depends on the type of cytokines they secrete

       Cytotoxic cells have a CD8 marker
       T cells are differenttiated from B cells because T cells occur in a rosette formation vs B cells
    which are free in the serum
       Also use CD2 & CD3 to distinguish T from B because B has CD3, CD19, 20, 21, 22
       If you have both CD4 and CD8 expressed in the same cells you will have very severe
    autoimmune disease with very severe manifestation (mostly leads to death)
       Usually the cells have very well defined characteristics
      o          Marker differences
      o          Functional differences
       T cells cannot be activated without the help of B cells

       B lymphocytes are formed, retained and released in the bone marrow
       Humoral
       Cannot form antibodies without T cells (helper)
      o        Therefore they share the antigen/organism
      o        B cell is activated by T cell and differentiates into a plasma cell
      o        Then the plasma cell creates the antibody
       Generate antibodies against microorganisms that invade the body
       Can generate antibodies against antibiotics and medicines too, and other normal things
      o        Eg: penecillin
      o        Allergies
                        Clothing
                        Food

         B lymphocytes
         Markers that

         TCR = T cell receptor
      o           HIV attacks this

        Natural Killer cells: normally arise from the bone marrow but not from the same erythropoetics
    cells the T and B cells come from
        These are very important because NK cells are highly non-specific
      o           They destroy anything that comes their way
      o           People lacking these usually manifest common etiological diseases even if their B and T
           cells are sufficient
      o           These are also calle large granular killer cells or LG lymphocytes (these terms are often
           inter-changed in reference to these cells
      o           Identified by CD16
                          Functional marker: helps the cell identify the foreign cell/ lymphocyte
           Identified by CD56
                  Structural marker: Differentiates the cell from other cells
        The killer cell degranulates and kills the target cell
        People lacking these show general flu-like symptoms commonly

         Know difference between AIDS and HIV wrt TCR

         Phagocytes
      o          Professional
                        Only does phagocytotic process
                        Only take up bacteria, virus, fungus and destroy using chemicals
                        Types
                                 Lung: alveolar macrophages: against respiratory diseases
                                 Connective tissue: histiocytes
                                 Liver: kupffer cells
                                 Kidney: mesangial cells: prevents hepatobiliary infections
                                 Brain: microglial cells
                        Diapedisis from blood vessels (in resonse to chemicals) and go into tissues to
                  phagocytose organism
                        If organism is not caught, it will spread causing an abcess and further infection
      o           Antigen presenting phagocytes
      o           Mast Cells
                        Degranulate and goes into general circulation causing septic shock
                        Patient can die within 4 to 5 hours

       B cells can be activated remotely without being in actual contact with the organism through
    chemotaxis
       Antigens in general circultion can activate B cells
       T cells are usually not activated by chemotaxis/ antigens in the circulation unless they are larger
    (??? Read up or ask Dr. Raju) (eg. 70,000 Daltons)
       This is why you need antigen presenting cells for T cells. These can be:
      o          B cells
      o          Neotrophils
      o          Somatic cells
       Other cells can act as antigen presenting Cells:
      o          Somatic cells act as APCs and present the HIV virus. In HIV patients after 3-4 yrs, other
          immune cells are exhausted because they have been presented with the HIV virus for

       Terms You should know:
       Adjuvent vs Hapten
       Adjuvent
      o         The particle is smaller than 100,000 but us immunologic, therefore has to be attached to
          a another protein to satisfy the weight restrictions
       Hapten
      o         a given particle is not immunologic but after becoming attached to a carrier protein it
          becomes immunologic and can invoke an immunologic response

         Heterophile antigens:

    Audio recording started: 2:47 PM Thursday, January 22, 2009




Immunity & Inflammation
Thursday, January 22, 2009
2:48 PM




    Audio recording started: 2:48 PM Thursday, January 22, 2009



         Innate = nonspecific immunity
      o           There is not memory or lasting protective immunity

       Its easier to create vaccines for etiological agents with very few variants
      o          Eg. Small pox: only one variant
      o          This is why it was successfully eradicated
       Natural resistance has three different variants
      o          Species resistance
                         HIV injected into humans will cause HIV but will not cause HIV in rabbits
      o          Racial resistance
                         Ppl with sickle cell anemia are resistant to malaria: seen in african population
                         There are some ppl in the world that are resistant to HIV: called Non-responders
      o          Individual resistance
                         Apply cream to face of different females of same race. One may have
                 hyperdensitive reaction & other will not

         Mechanical Barriers
      o         Skin
      o         Mucous membranes
      o         Eyes
      o         Ears
      o         Digestive Tract
      o         Urinary tract
      o         Reproductive system
      o         Circulatory system
      o         CNS

        Gonorrhea: cilia of the epithelial cells in the vagina become rigid and cannot throw out the
    organisms. They get caught there and cause infection
        Droplet nuclei of tuberculosis are smaller than 0.5-1.0 micrometer range (they are 0.3) and the
    cilia in the lungs cannot move them out. They escape tangling in the cilia and pass through into the
    alveolar sac. Multiplication will occur and patient will have very few symptoms until about 3
    months. By this time a lesion is already seen in the lungs. Chemical investigations have to be done to
    test for tuberculosis
       Interferons:
      o         Interferons have an anti-viral effect (not a lot are produced but still called anti-viral)
      o         Very expensive therapy
                        Eg. Hepatitis
      o         Virus is not live when it enters the body
      o         Has to find a cell to be the host so it can become a live virus
      o         Cell Produces soluble proteins that go to other cells and protect them from the virus:
          interferons (? Double check?)

       Complement System
      o       Happens only when all 11 factors come together
      o       Antibody-antigen complexes will bring the complement together
      o       Or a very large foreign particle
                      Eg. Endotoxin part of bacteria
      o       The complement factors together destroy the organism
                      Make a hole in the cell wall fo the bacteria
                      Everything in the bacterial cell spills out, leading to the lysis of the cell
      o       This is also an innate mechanism

         Cellular defenses
      o            See diagram: slide 16 of immunity ppt
      o            Intracellular organisms/pathogens are not killed by phagocytosis
                           In the phagolysosome the organism destroys the phagocyte's enzymes and lives
                   in the macrophage
                           Eg. Salmonella typhi: this one has a coating (typhoid)
                           Tuberculosis
                           Antibody production will not help here because the organisms are intracellular
                   and the antibodies cannot find the antigens

         Inflammation




Summary of Immunity
Tuesday, January 27, 2009
8:05 AM




    Audio recording started: 8:07 AM Tuesday, January 27, 2009


         Chemotaxis reaches B (humoral: AMI) & T (cell: CMI) lymphocytes and they get activated
         First line defense
      o         Monocytes
      o         Macrophages
      o         Dendritic cells
      o         Neutrophils
      o         Eosinophils
      o         Mast cells

        Rearrangement of genes in the cells above when chemical enters them makes them initiate
    their defense mechanism
        In long term viral infections, anitbiotic therapy, chemotherapy patients etc the first line defense
    cells are depleted
      o           Therefore other organisms get a chance to attach and cause infection

       B cell does not have to come intact with the organism: the antigen is enough to activate via
    chemotaxis
       T-cells need to have contact with smaller peptides. They are not activated by the antigen. The
    antigen has to be broken down to a smaller peptide to activate T cells
       Antigen presenting cells
      o          Antigen Taken up by phagocytosis
      o          Broken down within the APC
      o          These are then presented on the outside of the APC cell
      o          MHC (major histo compatibility )proteins are required for the antigen particles to be
          presented on the cell membrane
                        Depending on whether the antigen is endogenous or exogenous
                        MHC class 1
                                 Endogenous antigens
                                 Sometimes viruses can be presented with MHC class proteins
                        MHC class 2
                                 All exogenous antigens attach to these
                                 Viruses can be presented by this class
      o          Physical contact between the presented antigen particle and the T lymphocyte are what
          activates the T cells
                        This is how T cells are activated

       When the chemotaxis reaches B lymphcytes: the cell is activated
      o        Linear rearrangement of genes in the nucleus occurs after contact with antigen
      o        This arrangement determines what immunoglobulin is to be made
      o        Heavier chemotaxis: IgG
      o        Light chemotaxis: IgE
      o        The strength of the chemotaxis determines what linear arrangement occurs to make
         specific immunoglobulins
      o        Allergy: IgE
      o        Once a cell is activated it will produce the same immunoglobulin throughout its life
         because the the DNA other than the linear one is destroyed
      o        Exception: Class switching
                       Occurs when secondary infections etc
                       Can switch from IgG to IgM but the antigen specificity still remains the same
                       The cell still interacts with the same antigen
                         GO OVER THIS!!!! IT WAS UNCLEAR!!!

       Primary Immune Response
      o         Lag phase of antibody production: takes time for immune system to acclimatize to the
          new pathogen
      o         Log phase: After some time the body starts producing antibodies (exponentially)
      o         Stationary phase: The antibody production stabilizes at a certain point and the graph
          becomes parallel to the x axis. The antibodies are interacting with antigens here. Equilibrium.
      o         Decline phase: after some time the antibodies die off (after infection gone)
      o         IgM molecules produced here
       Secondary Immune Phase
      o         If another infection occurs of same kind the patient will have an extremely short lag
          phase because it already has info about organism
      o         In this case IgG is made
      o         Class switching occurs here
      o         Secondary response is always IgG
      o         Second immune response is for a longer period of time (6 months)
      o         Then get boosters to boost IgG production
      o         When testing you test for IgG not IgM
      o         Boosters are given for Killed or inactivated vaccines because they cannot multiply
      o         When live vaccines are given (no virulence) they require less boosters because they
          multiply themselves and create a secondary response on their own without as many boosters
                        This is more dangerous if the vaccines are not stored properly at a low
                temperature
                        Can revert back to vurulwnt strain

       Clonal selection
       The foreign body that enters the body can select its own immunoglobulin depending on amount
    of chemotaxis
       Exceptions: HIV, EBV: can stimulate clonal production of all the different types of B cells
    (polyclonal activation)
      o         Al l the produced antibodies cannot act on the virus only 2 or three clones will act on
          the virus
      o         The rest of the B cells act on the person's visceral organs and cause tissue destruction of
          healthy cells causing Multiorgan system failure
       Myu chain (the symbol)
      o         As long as the immunoglobulins are attached to the cell membrane they are called
          immunoglobulins but as soon as they are released from the membrane into circulation they
          are called antibodies
      o         Antibodies: functional component
      o         Immunoglobulins: structural component
      o         B-lymphocytes produced in bone marrow

         B cell production needs 2 stimuli
      o            Chemotaxis signal
      o            Interleukin-2 has to touch the surface and that activates
                          Differentiation of B cell into plasma and memory cells
                          The plasma cell produces the antibodies
                           The memory cells keep info and create life-long immunity
                           In order to have the antibody production the body has to have activated T cells
                  present
                           Endocrine, paracrine, autocrine effect

       T-cells
       CD4 is the same marker for both TH1 cells and TH2 cells
       TH1
      o         CD2
      o         CD4
       TH2
      o         CD3, 4, 5, 6, 10, 12
       Need to know
      o         interleukins
      o         Class switching
      o         Negative selection
      o         Intracellular killing of viruses my macrophages




Complement System
Wednesday, January 28, 2009
9:05 AM




    Audio recording started: 9:08 AM Wednesday, January 28, 2009


         IgG3 is the most effective in fixing
         C3b + factor B
         C3bB + factor D --> cleaves B into Ba and Bb
         C3bBb is acted upon to get C3bBb3b which is C5 convertase

         Lectin Pathway
      o            Only the first part is different & then when it gets C2C4, it follows the classical pathway
         MASP:
         M: mannose binding lectin
         A:associated (?)
         S:serine
         P: protease


    In the slide regarding regulation of alternative pathway (#2) the cleavage is done by factor I (i) not 1.
MHC Complex
Wednesday, February 04, 2009
9:12 AM




    Audio recording started: 9:12 AM Wednesday, February 04, 2009


       Class 1 genes are present on almost all cells
       Class 2 on antigen presenting cells
       Class 3: not as important in the immune response
    Audio recording started: 9:23 AM Wednesday, February 04, 2009








Type II & Type III Sensitivity
Wednesday, February 04, 2009
2:09 PM




    Audio recording started: 2:09 PM Wednesday, February 04, 2009


       Get Baveja text book
       Diagrams for this ppt are coming from "The Immune System", Garland Science 2005
      o        "Immunobiology," 2005

       Complement is a very important feature in type II hypersensitivity


       Type III hypersensitivity Reactions
       Phalarizine
      o          This drug usually destroys cells
      o          Then the immune system produces antibodies for the nucleus
      o           Systemic Lupus eryththematosus
                        Has a similar response
                        Body itself produces antibodies against its own cell nuclei
                        SLE is an auto immune disorder
                        Type III hypersensitivity due to drugs behaves the same as SLE

         Arthus Reaction
      o           Type III
      o           (type I is similar but I that case weal and flare reaction occurs)
      o           In type III there is extensive edema in comparison to Type I

         Complement system mediated Hypersensitivity will be tested
      o         Need to know the examples because they will be asked in exams


         Type IV (Dleayed hypersensitivity Reactions)
      o           Is not antibody dependent
      o           It is T cell mediated
      o           This reaction occurs 36 to 48 hours after exposure

       Tuberculosis
       If patient has been exposed to Tb in the past
       Intra dermal injection of PPD (tuberculin test)
       Patient forms T cells faster because the body has info already (has already had sensitizing dose)
       Approx 48 hrs later the T cells are activated at the site of injection
       However, in patients who are immuno-compromised the PPD test may give negative result
    without edema or hypersensitivity because there are not enough immuno cells
     o           HIV
     o           Immunosuppression drugs
     o           Measles

       Contact Dermatitis (Type 4)
       Agents act as haptens & combine with skin proteins
       The skin proteins act as the heavy molecule
       Posion Ivy/ oak (Type 4)
      o         Know the interleukins involved
      o         Will be asked on exams
       Mango Sap can cause rash
       Leather reaction
       Granuloma in Leprosy Patient




Micro Lab Feb 04, 2009
Wednesday, February 04, 2009
2:57 PM
Audio recording started: 2:57 PM Wednesday, February 04, 2009


Octerlony technique
Look in Baveja
This will be in our lab practical

CIE: counter immuno electrophoresis
  o     Antigen-antibody line
  o     Antigen -ve (cathode) will move to anode when charged
  o     Antibody +ve charge (anode) will move to cathode when charged
  o     Where they cross in optimal concentrations you will see a line
  o     Precipitation reaction

Rocket Electrophoresis
     Gel already coated with antibodies
     Put antigen at the bottom
     Place the antigen across gel in increase concentration
     Where the antibody and antigen react there is a rocket looking shape
     Tell you how much antigen you need to create a specific antibody reaction
     Can figure out how many antibodies you need to respond adequately

Immuno electrophoresis
Horizontal well
Put patients serum in the well
Run electrophoresis
Will find corresponding proteins in the patient's serum

Identify the spotter and give the importance for the test

Do a rough diagram of all the different tests



Autoimmune Disease & Tolerance
Friday, February 06, 2009
8:47 AM




     Audio recording started: 8:47 AM Friday, February 06, 2009
     This is not covered in the power points. Go over it in book.

     Treatment
1.      Protein inflammatory agents
       a.       SLE
       b.       Rheumatoid arthritis
2.      Plasmapheresis: plasma proteins subjected to electrophoresis and the antibodies are removed.
     The sample is then injected with fresh plasma and put back
       a.       Gullian Barr
       b.       SLE
3.      Anticholinesterases and thymectomy
       a.       Myasthenia gravis
       b.       thymectomy
4.      Metabolic control
5.      Hormone replacement
       a.       Graves
       b.       Hashimoto
6.      Spleenectomy
       a.       Idiopathic thrombocytopenia purpura
7.      Immuno-suppressive agents
       a.       Lympholytic (blocks the initiation and expression of immunity)
            i.          Antiserum
           ii.          Ionizing radiations
       b.       Lymphocytotoxic (blocking the induction by interfering with cell DNA synthesis)
            i.          Antimetabolites
           ii.          Alkalyting agents
                   1.            cyclophosphamide



Autonomic Nervous System & Cholinergics
Monday, February 09, 2009
9:07 AM

       What is pharmacology?
       What is pharmacokinetics?
       What is pharmocodynamics?
       Biotransformation?
       Hoffman Elimination
      o         Drug: Tacryne

       Ach not used for….something….because it gets metabolized very quickly by Ach esterase




Notes for Lab Practical
Wednesday, February 11, 2009
8:41 AM
Antigen-Antibody Serological Tests
ELISA

 o              Classification:
                        Micro-ELISA Antigen-antibody reaction for detection of antibodies in serum or
            plasma.
                        Enzyme immunoassay based on indirect ELISA
 o              Positive result:
                        Test specimens with absorbance value greater than or equal to the cut-off value
            are reactive for anti-HIV by microlisa HIV. (cut off value: 0.240, from handout)
 o              Diagnostic Importance:
                        Used as a screening test for detecting HIV1 and HIV2 in human serum or plasma
            for high risk individulas.

              Also used for:
              Detection of myobacterium antibodies in tuberculosis
              Detection of rotavirus in feces
              Detection of Hep B markers in serum
              Detection of enterotoxin of E. Coli in feces




ASO: Antistreptolysin O Detection Test
 o           Classification:
                     Latex agglutination slide test for detection of antistreptolysin O in serum
 o           Positive result:
                     Clearly visible agglutination
                     ASO content is 200 IU/ml or greater
 o           Diagnostic Importance:
                     Helps in determining streptococcal infection of group A and C.
                     Elevated ASO titres may also be associated with acute glomerulonephritis and
          acute rheumatic fever




RF: Rheumatoid Factor Detection Test

 o           Classification:
                     Rapid Latex agglutination slide test for qualitative and semiquantitative
          determination of RF in serum
 o           Positive result:
                     Agglutination at 2 mins means RF content is 10 IU/ml or greater
                     Has to be read at 2 mins (reading after may be wrong)
 o           Diagnostic Importance:
                     To differentiate between rheumatoid arthritis and other inflammatory and auto
          immune conditions.
                     Higher titres of RF are usually related to the severity of rheumatoid rthritis.
                       In rheumatoid arthritis the presence of RF is nearly 80% where as in Rheumatic
           fever RF is nearly absent




C-Reactive Protein Test

 o             Classification:
                       Latex agglutination slide test for the detection of C-reactive protein in serum
 o             Positive Result:
                       Clearly visible agglutination indicates CRP content is 6mg/L or greater
 o             Diagnostic Importance:
                       CRP can be an early indicator of inflammation and infection because serum
           levels of CRP rise before specific antibody titres
                       It is an acute phase protein because its levels rise during the acute phase of a
           disease
                                 e.g. rheumatic fever or rheumatoid arthritis
                       Its levels fall during the chronic phase
                       Thus CRP can be used monitor the progress of a disorder, its treatment and
           differential diagnosis
RPR: Rapid Plasma Reagin Test

 o           Classification:
                     Antigen-antibody flocculation test causing suspended floccules of precipitate
 o           Positive result:
                     Black Aggregates (carbon) which may be deposited at the periphery of the liquid
          appearing before the 4 minutes of rotation.
 o           Diagnostic Importance:
                     Standard test for diagnosis/screening of Syphillis by precipitating syphyllis
          reagin antibodies in affected individuals
Widal Test

 o                Classification:
                          Tube agglutination test
 o                Positive result:
                          Agglutination titre of 1:240 in enteric fever
                                   H agglutinin titre determines specific organism responsible
                          titre of 1:120 can be significant but the test has to be re-done after a few days
             to see if there is a rise
 o                Diagnostic importance:
                          Diagnosis of typhoid fever
 o                Amnestic Reactions:
                          Persons who have suffered from enteric infection in the past or have received
             TAB vaccine may show appearance of agglutinins when suffering from other unrelated
             illnesses
 o                TAB Vaccination
                          Moderate rise in all 3 H agglutinins simultaneously against all the H antigens id
             suggestive of recent TAB vaccination.
Antigen-Antibody Reactions
Counter Immuno Electrophoresis:

 o           One dimensional double electro-immuno diffusion
 o           Used for detecting:
                    Hepatitis B antigens and antibodies
                    Anitgens of cryptococcus in CSF
 o           More sensitive than standard immunodiffusion technique
 o           See lab book for rest of notes
 o           p 108, Baveja
Rocket Electrophoresis:

 o           Used for quantitation of antigens
 o           See lab book for more notes
 o           P 109, Baveja
Ouchterlony Procedure:

 o           Double Diffusion in two dimensions
 o           Special variety of this procedure is used for detection of C. Diptheriae
 o           P 107, Baveja
Immunoelectrphoresis:

 o              A number of antigens can be identified in human serum using this technique
 o              Particularly useful for detection of normal and abnormal serum proteins like myeloma
     proteins
 o              See lab book for other notes (p108, Baveja)
Monday, February 16, 2009
4:47 PM

MICROBIOLOGY FIRST SESSION NOTES
Introduction and History of Microbiology ppt.
      Koch’s postulates are that an organism should be constantly associated with the
     lesions of disease, it should be possible to isolate the organism in a pure culture, the
     isolated organism should be able to reproduce the same disease in a suitable animal, it
     should be possible to reisolate the organism from the laboratory inoculated animal,
     and antibodies should be demonstrable in the serum of patients.
Infection ppt.
      Saprophytes are free living microorganisms that live on dead or decaying organic
     matter.
      Parasites live on hosts are derive their nutrition from the host without benefiting
     the host.
      Mutualism is when there is a mutually beneficial association between two
     organisms.
      Commensalism is when one benefits and they both live in harmony.
      Parasitism is when there is an intimate relationship where one lives at the expense
     of the other.
    There are many types of infection such as the primary infection, reinfection,
   secondary infection, nosocomial infection, iatrogenic infection, subclinical infection,
   latent infection, and atypical infection.
    Virulence factors, number of initial organisms, and immune status all play a role in
   pathogenicity.
    Bacteria mainly cause disease by two mechanisms, toxin production (endotoxin and
   exotoxin) and invasion/inflammation.
    A person who harbors a pathogenic organism without suffering from it is referred to
   as a carrier.
    Convalescent carriers are those who recovered from the disease but continue to
   harbor the pathogen.
    Paradoxical carrier is one who acquires the pathogen from a patient.
    Modes of spread can be through contact, air borne inhalation, fecal/oral spread,
   transplacental, hospital acquired, zoonotic, and arthropod mediated.
    Unbroken skin is impermeable by most membranes.
    Exotoxins are produced mainly inside gram positive bacteria as part of their growth
   and metabolism.
    Endotoxins are part of the outer portion of the cell wall of a gram negative bacteria
   and are liberated when the bacteria die and the cell wall breaks apart.
    Exotoxins are polypeptids that are highly toxic and have high antigenicity to which
   toxoids are used as vaccines.
    Endotoxins are lipopolysaccharides that show little toxicity such as fever and shock
   and are poorly antigenic hence vaccines are typically not available.
    Toxoids are toxins that have been altered by heat or chemicals and are used in
   vaccines such as diphtheria and tetanus.
    The incubation period the time between the acquisition of the organism and the
   beginning of the symptoms.
    The prodrome period is when non specific symptoms such as fever, malaise, and
   loss of appetite occur.
    The specific illness period is when the characteristic signs and symptoms of a
   disease are present while the recovery period is when the illness diseappears and the
   patient is back to health.
Immunity ppt.
    Immunity is the state or resistance exhibited by the host to toxic molecules,
   microorganisms, and foreign cells.
    Immunity can be innate/natural which is non specific and it can be
   adaptive/acquired which is specific.
    Innate immunity is resistance which an individual possesses by birth due to their
   genetic makeup and all normal healthy individuals are born with innate defenses.
    Species immunity is resistance shown by all members of a particular species, racial
   immunity is immunity that alters with different ravies, and individual immunity is
   that type of immunity which differs from person to person.
    Innate immunity is affected by age, hormones, and nutrition.
    Innate immunity is made up of anatomical factors, cellular factors, and humoral
   factors.
     The skin, mucous secretion, lysozyme in tears, ceruminous glands in the ear,
    mucous lining in the GIT, and low pH of the vagina are all different types of anatomical
    immunity.
     Cellular immunity is brought about by neutrophils, macrophages, natural killer cells,
    and eosinophils.
     Neutrophils play a role in phagocytosis, intracellular killing, inflammation, and
    tissue damage.
     Macrophages play a role in phagocytosis, intracellular killing, extracellular killing of
    infected targets, tissue repair, and antigen presentation for specific immune response.
     Natural killer cells are used for the killing of virus infected and tumor cells.
     Eosinophils are used for the killing of certain parasites.
     Intracellular killing is either oxygen dependent in which there is a respiratory burst
    and the production of hypochlorus acid and oxygen radicals occur, and also through
    oxygen independent methods such as with the help of lysozyme, cathepsin, or
    lactoferrin in which superoxide anion and hydrogen peroxide are formed.
     Inflammation occurs as a result of various mediators, increased blood flow, and the
    aggregation of micro and macrophages by chemotactic mechanisms.
     Humoral barriers such as the complement system, interferon’s, acute phase
    proteins, and defensins all protect against non specific antibacterial substances.
     Complement system results in the lysis of the cell membrane and increased
    phagocytosis while also stimulating inflammation.
     Complement proteins form holes in the bacterial cell walls and allow fluid to enter
    the bacterium which causes it to expand and burst.
     Interferons are a group of soluble proteins in the plasma that are antiviral and there
    are alpha, beta, and gamma types.
     They are produced by WBC’s, fibroblasts, and T-lymphocytes only after a viral
    penetration.
     They act against viruses only and are non specific in their action.
     Aspirin inhibits interferon production and can lead to Reyes syndrome.
     Defensins are highly positive peptides that create pores in bacterial membranes and
    they are mainly present in the GIT and lower respiratory tract.
     Alpha defensins are more predominant in the GIT while beta defensins are more
    concentrated in the lower respiratory tract.
     Acute phase proteins are normal serum proteins that are synthesized in the liver
    and their levels increase dramatically in inflammation, infection, or trauma.
     Common examples of acute phase proteins are C-reactive protein, alpha-1-
    antitrypsin, haptoglobin, and ceruloplasmin.
     Fever is a protective defense mechanism of the body as it inhibits the growth of
    most virusis and bacteria and increases the metabolic reactions in host cells as it
    helps eliminate toxins through urine and sweat and also helpts stimulate the
    production of interferon’s.
     Fever is controlled by the hypothalamus and is activated by pyrogens that are
    released by microbes and injured host cells.
     Acquired immunity can be either active or passive.
      Active immunity is resisitance induced in an individual after effective contact with
     an antigen and requires the active participation of one’s immune system in the
     production of antibodies and cell mediated immunity.
      Active immunity develops slowly over a period of days and weeks but it persists for
     a long time, usually years.
      Active immunity can be natural such as through clinical/subclinical infections or it
     can be artificial such as through vaccinations.
      TAB vaccine for typhoide fever is an inactivated (killed) bacterial vaccine.
      Salk (poliomyelitis) vaccine is an inactivated viral vaccine.
      BCG, anthrax, plague, and brucella vaccines are live attenuated bacterial vaccines.
      MMR, Polio, and smallpox vaccines are live attenuated viral vaccines.
      Passive immunity is resistance that is induced in the recipient by transferring
     preformed (ready made) antibodies against an infective agent or toxin.
      There is no active role for the immune system and it provides an immediate effect
     that only lasts for a couple days or weeks.
      Passive immunity can be natural such as placental transfer of IgG from the mother
     to the fetus or colostral transfer of IgA from the mother to the infant while it can also
     be artificial such as inoculation of the patient with ready made antibodies or special
     immune cells.
      Non specific (innate) immunity is antigen independent, has an immediate maximum
     response, and shows no immunological memory.
      Specific (acquired) immunity is antigen dependent, has a lag time between exposure
     and maximal response, and shows immunological memory.
Structure And Function Of Immune System ppt.
      Immune system is composed of a lymphoid system that is made up of lymphoid
     organs, tissues, and cells and provide a specific immune response along with being
     composed of a reticulo endothelial system which is made up of phagocytic cells and
     provides non specific immunity.
      The primary lymphoid organs are the thymus and bone marrow while the
     secondary are the lymph nodes, spleen, and MALT.
      Neutrophils play a role in the phagocytosis of pyogenic microorganisms.
      Eosinophils play a role in phagocytosis of parasites.
      Basophils play a role in immediate hypersensitivity.
      Lymphocytes play a role in acquired immune response.
      Neutrophils are the most prevalent of the leukocytes and have multilobed nuclei
     which promote inflammation.
      Eosinophils are effective at destroying helminthic parasites and release granules
     that are toxic to the worms.
      Basophils are the least prevalent of the leukocytes and release chemical mediators
     for immediate hypersensitivity such as histamine.
      Lymphoctyes have CD markers (clusters of differentiation) which help in
     identification of different lymphocytes, T cell receptors (TCR) which act as a receptor
     for the antigen bound to MHC complex molecules, and B cell receptors (BCR) which
     are surface immunoglobulin’s that are monomeric IgM.
     T lymphocytes arise in bone marrow but mature and differentiate only in the
    thymus and they all posses the TCR which serves as the CD2 marker and they also
    have the CD3 marker.
     In the cortex of the thymus they first start off as double negative cells (CD4-, CD8-)
    and then proceed into becoming double positive cells (CD4+, CD8+), then depending
    upon whether they make contact with a class II or class I MHC protein they either
    become a CD4+ T helper cell or a CD8+ T killer cell in the medulla of the thymus.
     T helper cells have CD4 on their surface and recognize MHC class II molecules on
    antigen presenting cells.
     There are two subsets in which there are Th1 and Th2 cells.
     Th2 cells interact with B cells and promote the proliferation of B cells to enhance
    antibody synthesis and thus play a role in humoral immunity.
     Th1 cells activate macrophages and cytotoxic T cells and hence they play a role in
    cell mediated immunity.
     T helper cells play a role in both cell mediated immunity as well as in antibody
    mediated immunity (humoral).
     Lymphokines mediate the effects of T helper cells.
     CD8 cells are known as cytotoxic T cells and they contain CD8 on their surface.
     These cells recognize MHC class I molecules on target cells and are responsible for
    the killing of specific target cells whose surface antigens they can recognize.
     Cytotoxic T cells play a role in cell mediated immunity.
     Suppressor cells contain CD8 and suppress the immune response by acting on the T
    helper and B cells.
     T cells are thus involved in cell mediated immunity (Tc cells and Th1 cells), antibody
    mediated immunity (Th2 cells), and delayed hypersensitivity reactions (Th1 cells).
     B lymphocytes mature in the fetal liver and bone marrow and do not require the
    thymus for maturation.
     They have surface immunoglobulines IgM (monomeric) and IgD.
     B cells have markers that distinguish them from other cells and these are CD19,
    CD20, CD21, and CD22.
     The primary development of B cells is antigen independent and it occurs in the bone
    marrow under genetic control where the monomeric IgM is placed on the surface.
     The secondary development is antigen dependent and requires the helping hand of
    T helper cells which usually takes place in the germinal center of peripheral lymph
    organs which leads to the formation of activated B cells and plasma cells which
    produce antibodies to the specific antigens.
     A B cell is triggered when it encounters an antigen, the B cell then engulfs the
    antigen and displays its fragments bound to the MHC which attracts the T helper cell.
    The T helper cell then releases cytokines which help the B cell to multiply and mature
    into antibody producing plasma cells upon which these plasma cells release
    antibodies that bind onto the matching antigens and start a complement cascade or
    facilitate their removal by the liver/spleen.
     Memory B cells are old activated B cells which can remain quiescent for a long time
    and are able to be rapidly activated upon re-exposure to the antigen.
    Memory T cells secrete interleukins that enhance antibody production by memory B
   cells and both memory B and T cells are important in the secondary immune
   response.
    NK cells are part of the innate immunity and mediate direct cytotoxicity as they kill
   virus infected cells and malignant cells.
    NK cells have CD16 and CD56 on their surface and release cytolytic factors such as
   perforins which factor into programmed cell death.
    ADCC (antibody dependent cellular cytotoxicity) cells have surface receptors for IgG
   and are antibody dependent wherease cytotoxic T cells are antibody independent.
    Lymphokine activated killer cells (LAK) are natural killer cells treated with
   interleukin 2 and are cytotoxic to a wide range of tumor cells.
    Foreign antigens cannot be directly presented to CD4 T lymphocytes so they must
   be processed and the fragments are presented on the APC’s with class II MHC
   molecules for their interaction with the TCR.
    The different antigen presenting cells are macrophages, dendritic/langerhan’s cells,
   and B lymphocytes.
    Macrophages arise from the circulating monocytes that have migrated into various
   tissues and have developed into macrophages.
    Lung macrophages are known as alveolar macrophages, connective tissue ones are
   known as histiocytes, liver ones are known as kupffer cells, kidney ones are called
   mesangial, and the ones in the brain are known as microglial cells.
    Macrophages present antigens with MCH class II proteins to CD4 T cells and also
   produce cytokines such as IL-1 which activates helper T cells and TNG which is an
   important inflammatory mediator.
    There are two types of dendritic cells; langerhans cells that are present in the skin
   and follicular dendritic cells which are present in the local lymph nodes.
    Primary/central lymphoid organs are those in which proliferation and
   differentiation of lymphoctyes takes place without antigenic stimulation.
    Precursors of lymphocytes are from the yolk sac/fetal liver/bone marrow and they
   mature in the cortex of the thymus upon which the migrate to the medulla where they
   complete maturation and exit into the blood to reside in the secondary lymph nodes.
    Thymus confers immunological competence on the lyphocyte so that they are
   capable of mounting a cell mediated immune response.
    Absence of thymus results in DiGeorge’s syndrome where there are no T cells and
   are prone to developing recurrent/chronic infections.
    Asplenic individuals suffer from overwhelming bacterial infections from capsulated
   organisms (pneumococcal).
    Secretory IgA is the main immunoglobulin produced by MALT.
Complement ppt.
    Complement is a multicomponent heat labile protein system that is
   characteristically activated by antigen-antibody reactions.
    It consists of 20 or so proteins that augment the effects of other components of the
   immune system and are an important component of our innate host defenses.
    Complement proteins are synthesized mainly in the liver.
    Activation of the complement system can be either by antigen-antibody complexes
   and also by endotoxins.
     There are three pathways which are the classic, lectin, and alternative pathways.
     The lectin and alternative pathways are more important the first time a person gets
    infected and participate in the innate arm of the immune system.
     C3b is the central molecule of the complement cascade and has two important
    functions; it combines with the other complement components to generate C5
    convertase which leads to the formation of the membrane attack complex and it
    opsonizes bacteria because pathogens have receptors for C3b on their surface.
     The three main effects of complement are lysis of the cell, generation of
    inflammatory mediators, and opsonization.
     The antigen-antibody complex activates C1 which cleaves C2 and C4 to form C3
    convertase that cleaves C3 into C3a and C3b where C3a is an anaphylatoxin and C3b
    forms the C5 convertase.
     C5 convertase cleaves C5 to form C5a and C5b where C5a is an anaphyatoxin and
    chemotactic factor. C5b binds with C6, C7, C8, and C9 to form the membrane attack
    complex which causes cytolysis.
     The lectin pathway involves mannan binding lectin (MBL) which binds to the
    surface of microbes bearing mannan.
     Mannan activates proteases that cleave C2 and C4 to activate the classic pathway.
     The alternate pathway is started by endotoxins, cell walls, viral envelops etc. and
    involves the binding between C3 and factor B.
     This complex between factor B and C3 is cleaved by factor D which acts as C3
    convertase to generate C3b.
     The alternative pathway is mediated by factor H which binds to C3b and prevents
    the formation of C5 convertase.
     Decay accelerating factor is a glycoprotein that destabilizes C3 convertase and C5
    convertase in order to prevent the formation of the membrane attack complex.
     CR2 is a complement receptor (CD21) and regulates the antibody production by B
    cells and is also the Epstein-Barr virus receptor.
     C3a, C4a, and C5a are anaphylatoxins because they cause degranulation of mast cells
    which release histamine.
     Complement plays a role in type II (cytotoxic) and type III (immune complex)
    hypersensitivity reactions.
     C3b binding to B cells greatly enhance the rate of antibody production.
     Inherited deficiency of C1 estrase inhibitor results in angioedema.
     Acquired deficiency of decay accelerating factor on the surface of cells results in an
    increase in complement and this clinically results in paroxysmal nocturnal
    hemoglobinuria.
     Immune complexes bind complement and hence complement levels are low in
    immune complex diseases such as SLE.
Hypersensitivity ppt.
     Hypersensitivity is when an immune response is exaggerated or inappropriate
    reaction occur that are harmful to the host.
     Antigens are then called allergens and on the first contact the host cells become
    sensitized and on the subsequent contacts there is an allergic response.
     The types of hypersensitivities are determined by their time, course, and whether T
    cells are the principle elements involved.
     The initial contact with the allergen leads to sensitization and the subsequent
    contacts with the same allergens are known as shocking dose.
     Type I hypersensitivity is immediate/anaphylactic reaction, type II is cytotoxic
    reaction, type III is immune complex reaction, and type IV is delayed/cell mediated
    reaction.
     Type I is an immediate hypersensitivity reaction and occurs when an allergen binds
    to IgE on the surface of mast cells which causes a release of several mediators.
     Type I shows increased vascular permeability, smooth muscle contraction, and
    chemotaxis to the surrounding tissues.
     Anaphylactoid reactions clinically appear similar to anaphylactic ones but they are
    not IgE mediated and the inciting agents are drugs which leads to histamine release
    from mast cells without the involvement of IgE.
     Atopy exhibits a strong familial predisposition and is associated with eleveated IgE
    levels.
     IgE levels in serum are measured by radio allergosorbent test (RAST).
     RIST detects total amounts of IgE while RAST detects amounts of allergen specific
    IgE.
     Type II is cytotoxic hypersensitivity and is due to IgG antibodies against cell surface
    antigens which therefore results in cell damage.
     Type II may be mediated by classic complement cascade or cellular mechanism.
     Hemolytic anemia’s, ABO transfusion reaction, or Rh hemolytic diseases are all
    examples of type II hypersensitivity.
     Drugs can attach to the surface of RBC’s and initiate antibody formation and
    therefore hemolysis occurs.
     Penicillin and quinidine are both known to act in this manner sometimes.
     Myasthenia gravis in which the acetylocholine receptors are internalized by
    antibodies is a type II hypersensitivity.
     Goodpasture syndrome is when an autoantibody against the patients own type IV
    collagen is present in the basement membrane of the kidneys and lungs and is a type
    II hypersensitivity.
     Direct Coombs test is positive in the demonstration of type II hypersensitivity.
     Type III is immune complex hypersensitivity and is characterized by the deposition
    of antigen-antibody complexes in tissues, activation of complement, and infiltration of
    polymophonuclear leucocytes leading to tissue damage.
     The two types are arthus reaction and serum sickness.
     This type of hypersensitivity occurs when antigen-antibody complexes induce an
    inflammatory response in tissues by being deposited in them.
     Immune complexes deposited in tissues also activate the complement system.
     Arthus reaction is when an antigen is given repeatedly in order to create high levels
    of IgG antibody in the body. The antigen is then injected subcutaneously or
    intredermally which will then cause intense edema and hemorrhage to develop.
     Cheese-workers lung, wood workers lung, and wheat millers lung are all clinical
    manifestations of type III hypersensitivities.
     Serum sickness is a systemic inflammatory response to the presence of immune
    complexes deposited in many areas of the body and usually appears after a single
    dose of high concentration foreign serum.
      Immune complexes get deposited on the endothelial lining of blood vessels in
     various parts of the body which causes inflammatory infiltration.
      Complex can also get deposited on the glomerulo basement membrane and the
     damage to the membrane is caused by the enzymes released by the
     polymorphonuclear cells.
      Massive complement activation and fixation by the antigen-antibody complexes
     leads to a fall in the complement concentration.
      Systemic lupus erthematosus is an example of type III hypersensitivity and
     antibodies are formed against DNA and other components of the nucleus of the cell,
     thus activating complement which damages the cells.
      Type IV hypersensitivity is a delayed reaction which is known as cell mediated
     hypersensitivity and the tuberculin test is the most common example.
      Type IV hypersensitivity is a function of T lymphocytes and the response is delayed
     as it starts hours or days after contact with the antigen and lymphokines are leased
     which cause the biological affects on macrophages, leucocytes, and tissue cells.
      The tuberculin type is when a patient previously exposed to M. tuberculosis is
     injected with a small amount of tuberculin (PPD) intradermally and gradually redness
     develops if the patient has been infected earlier.
      Chemicals, poison ivy, topically applied drugs, and cosmetics are all examples of
     contact hypersensitivity as haptens enter the skin and they attach to body proteins to
     become complete antigens. The haptens alter the proteins so much that they are
     recognized as foreign by the body’s immune system.
Antibodies ppt.
      All antibodies are immunoglobulins but all immunoglobulin’s are not antibodies.
      Antigens are phagocytosed by APC that process and present the antigen to T cells,
     and these T cells then interact with B cells, and these B cells that carry surface Ig’s
     proliferate and differentiate into plasma cells that produce specific antibodies.
      Antibodies are Y shaped and have 4 polypeptide chains where 2 are heavy and 2 are
     light.
      The light chains can be kappa or lambda while the heavy chains can be gamma, mu,
     alpha, delta, or epsilon.
      IgG is relatively stable and is the predominant class of Ig as it makes up 70% of all
     immunoglobulins in the serum.
      IgG appears late but also disappears late.
      IgG can cross the placenta and provides passive protection to the fetus and activates
     complement which helps in opsonisation.
      IgA is a dimer and hence it has 4 heavy chains and 4 light chains and is the secretory
     Ig.
      IgM is the largest immunoglobulin as it is a pentamer.
      IgM is produced during the primary immune response and is an indicator of recent
     infection as it is the earliest immunoglobulin to be present and is also the first Ig to be
     synthesized by the fetus.
      The presence of IgM during birth indicates that there was a congenital infection.
      IgE is a monomer and is produced in large amounts during allergies.
      IgE participates in host defenses against certain parasites and bound IgE serves as a
     receptor for allergens and antigens.
     IgD is found associated with the surface of the B lymphocytes as an antigen receptor
    and has no other functions.
     Antibodies that are formed in response to a complex antigen are heterogenous as
    they were produced by several different clones of plasma cells, yet antibodies ariseing
    froma single clone of a B cell against an antigen are homogenous or monoclonal.
Immune Response ppt.
     Immune response is a specific reactivity induced in a host following an antigen
    stimulus.
     The two types of responses are cell mediates and humoral.
     Antibody mediated immunity provides defense against most extracellular bacteria
    and viruses and takes part in the pathogenesis of type I, II, and III hypersensitivities.
     Cell mediated immunity protects against fungi, viruses, intracellular bacteria, and
    parasites.
     It plays an important role in allograft rejection and mediates the pathogenesis of
    delayed hypersensitivity.
     The first line of defense is the skin, the second line of defense are the NK cells, and
    the third line of defense are the antibodies and the leucocytes.
     The stages of phagocytosis are chemotaxis, adherence to the plasma membrane,
    ingestion, and digestion.
     The five major symptoms of inflammation are redness, pain, heat, swelling, and loss
    of function.
     The primary response has a long lag phase and is predominantly IgM modulated.
     The secondary humoral response has a shorter lag phase and has a high level of
    antibodies that persist for a long time which are mainly IgG.
     There are two types of antigens seen in the humoral response and they are T cell
    independent and T cell dependent.
     T cell independent antigens are mainly bacterial capsules and antibody production
    does not require assistance from T cells, but there is a weaker immune response.
     When a B cell encounters an antigen it is stimulated and undergoes clonal
    proliferation into plasma cells which actively secrete antibodies against the antigen it
    binded to.
     In T cell dependent antigens, the antigens are usually proteins on viruses, bacteria,
    or hapten-carrier molecules.
     An APC presents the antigen on MHC class II molecules to a CD4 T cell and the T cell
    receptor binds to this and the APC also secretes IL-1 which activates the T cell.
     The activated T cell interacts with B cells throught the help of IL-4, 5, and 6 to let the
    B cell undergo clonal proliferation and differntiate into plasma cells to secrete
    antibodies.
     An adjuvant is a substance that enhances the immunogenicity of an antigen.
     Antibody binding results in agglutination, activation of complement, opsonization,
    inflammation, neutralization, and antibody dependent cell mediated cytotoxicity.
Cytokines and Immune Regulation ppt.
     Cytokines are biologically active substances that are secreted by monocytes,
    lymphocytes, and other cells.
     The vast majority of cytokines are released by T helper cells.
     Migration inhibiting factor, macrophage activating factor, macrophage chemotactic
    factor, and macrophage stimulating factor are all lymphokines.
     IL-2 is a major activator of T and B cells and converts null cells to lymphokine
    activated killer (LAK) cells.
     IL-3 is the granulocytes macrophage colony stimulating factor.
     IL-4 was formerly known as B cell growth factor and is produced by helper T cells. It
    is required for class switching and enhances the synthesis of IgE.
     IL-5 enhances IgA synthesis.
     IL-6 mainly induces fever be affecting the hypothalamus.
     IL-10 limits gamma interferon release and hence inhibits the development of T
    helper cells.
     IL-12 promotes the development of T helper cells and hence IL-10 and IL-12
    mediate delayed hypersensitivity by regulating the production of T helper cells.
Fever ppt.
     The normal body temperature is 36.8 degrees celcius and is mainly controlled by
    the hypothalamus.
     Fever is defined as a state of elevated core temperature which is often part of the
    defensive response of the host to the invasion of a microorgranism.
     A pyrogen is any substance that causes fever and there are two types; exogenous
    and endogenous.
     Exogenous pyrogens are derived from outside the patient like microbial toxins,
    products, or organisms such as the lipopolysaccharide endotoxin produced by gram
    negative bacteria.
     Endogenous pyrogens are cytokines such as IL-1, IL-6, TNF, IFN-a, and CNTF.
     The hypothalamus releases prostaglandins to increase camp and thus elevate the
    thermo regulatory set point.
     Microbial toxins can induce fever directly without the help of cytokines because the
    hypothalamus has toll like receptors where the microbial toxins bind to them.
     Fevers help us by setting up defenses, speeding up metabolism for tissue repair, and
    increasing the antiviral effects of interferons.
 
Antigen-Antibody Reactions ppt.
      Antigen-antibody reactions are based on a lock and key concept in that there are
     multiple non covalent bonds that are firm but reversible.
      Affinity is the strength of the reaction between a single antigen and a single
     antibody combining site.
      Avidity is the overall strength of binding between an antigen and all the antibodies
     out in the serum.
      The antigen-antibody ratio is explained by the lattice hypothesis which is also
     known as the zone phenomenon.
      When there are equal amounts of antigens and antibodies present, there will be a
     lattice formation.
      Specificity is the ability of an individual antibody combining site to react with only
     one antigenic determinent.
      The more specific a binding site is the less false positives there are.
      Cross reactivity is the ability of an individual antibody to react with more than one
    antigenic determinent and this leads to a decreased sensitivity.
      Temperature, duration of incubation, electrolytes, pH, and the relative
    concentrations of antigens and antibodies all play a role in the reactions.
      Titer is the greatest dilution of serum (hence the lowest concentration of antibody)
    that reacts with the antigen.
      IgM antibodies are more effective than IgG when it comes to agglutination reactions.
      Direct Coomb’s test is used to detect cell bound antibodies whereas indirect
    Coomb’s test is used to detect circulating, non agglutinating antibodies.
      Ouchterlony procedure is when one well is filled with antigen and another well is
    filled with antibodies the they both diffuse to produce a zone of equivalence in the
    middle.
Immunodeficiency Disorders ppt.
      Some clues that are present to hint towards immunodeficiency are recurrent
    infections, chronic infections, unusual infectious agents, poor response to
    antimicrobial therapy, and failure to thrive.
      Primary immunodeficiency is seen in B cell and T cell deficiency while secondary
    immunodeficiency is seen in complement and phagocytic deficiency.
      Causes of primary immunodeficiency are genetic disorders, metabolic disorders,
    vitamin deficiencies, arrest in embryogenesis, and autoimmune deficiencies.
      Secondary/acquired immunodeficiency is seen in viral infections, chronic infections,
    immunosupressive therapy, cancer, chronic renal disease, splenectomy, ageing,
    trauma, and malnutrition.
Transplantation Immunology ppt.
      The different types of grafts are autografts, allografts, isografts, and heterografts.
      Autograft is the transfer of an individuals own tissue to another site in the body.
      Isograft is a graft between identical twins.
      Allograft is a graft between two genetically different members of the same species.
      Heterograft (xenograft) is a graft between members of different species and is
    always rejected.
      The major transplantation antigens are the MHC complex antigens and the major
    blood group antigens.
      The minor transplantation antigens are the non ABO blood group antigens.
      Host vs. graft reaction is when an immuno competent host recognizes the foreign
    antigens on grafted tissue an mounts an immune response which results in rejection
    of the grafted tissue.
      Graft vs. host reaction is when an immuno suppressed hose is grafted with foreign
    immuno competent lymphoid cells and those immuno reactive T cells in the graft
    recognize the foreign antigens on the host tissue and damage the host tissue.
      The acceptance or rejection of a transplant is determined by class I and class II
    MHC/HLA proteins on the donor cells.
      In humans there is the hyper acute rejection, acute rejection, and chronic rejection.
      Hyper acute rejection is due to mismatched blood or the recipient already has
    preformed antibodies to the donor organ and the damage is due to cell mediated lysis.
      Acute reaction is due to sensitization of the CD4 and CD8 cells that become
    activated.
     Chronic rejection takes months to years to occur and the damage is cell and
    antibody mediated.
     Prevention of graft rejection is done by proper ABO typing, tissue typing, and cross
    matching along with immunosuppressive therapy,
     Mucin associated antigen is detected in pancreatic and breast cancer.
     Alphafetoprotein is seen in hepatomas and carcinoembryonic cancer.
     The immune response in malignancies is mainly by complement, ADCC (NK cells),
    and cytokines released by T cells.
     Cyclosporine and corticosteroids can be given for immunosuppressive therapy in
    order to reduce the chances of rejection of the transplanted tissue.
Autoimmunity ppt.
     Tolerance is specific immunologic unresponsiveness which is when an immune
    response to a certain antigen does not occur even though the immune system is
    working normally.
     Antigens that are present during embryonic life are considered self and do not
    stimulate an immunologic response.
     This is due to the way the T cells are matured in the fetal thymus and hence the
    antigens that are not present during the process of maturation are called non self and
    usually elicit an immune response.
     T cell tolerance is the main process by which T lymphocytes acquire the ability to
    distinguish self from non self and there are two types; central and peripheral
    tolerance.
     Central tolerance occurs in the fetal thymus and by clonal deletion the T cells that
    react with self antigens are killed by apoptosis.
     Peripheral tolerance is when some self antigens do not reach the thymus and hence
    some self reactive T cells are not killed and therefore it has to be controlled outside
    the thymus which is called peripheral tolerance.
     The mechanisms of peripheral tolerance can be through the killing of T cells, the
    inactivating of T cells (clonal anergy), suppressing through regulatory T cells, and the
    production of a physical seperation such as the blood brain barrier or the blood testis
    barrier.
     Clonal anergy is a term used to describe self reactive T cells that are not activated
    because proper costimulation does not occur.
     Costimulation is when the B7 protein on the APC interacts with the CD28 on helper
    T cells to fully activate the helper T cell.
     In anergy there is no production of B7 protein on the APC and this results in no
    costimulatory signal.
     B cells become tolerant to the self by 2 mechanisms; clonal deletion and clonal
    anergy where deletion occurs in the bone marrow and anergy occurs in the periphery.
     B cell tolerance is not as well regulated as T cell tolerance and hence this is the
    reason autoimmune diseases are antibody mediated.
     The most important step resulting in autoimmune disease is the activation of self
    reactive helper T cells which induce the antibody mediated immunity.
     HLA-DR4 is strongly associated with rheumatoid arthritis (class II).
     HLA-B27 is strongly associated with ankylosing spondylitis (class I), and reactive
    arthritis.
     The M protein of streptococcus and the myosin of cardiac muscle exhibits molecular
    mimicry and hence antibodies against M protein cross react with cardiac myosin
    which results in rheumatic fever.
     Certain drugs can bind to normal proteins and create neo antigens which are no
    longer recognized as self and hence an immune response is elicited (procainamide
    induced SLE).
     The release of sequestered antigens such as sperm, CNS, uveal tract, lens of the eye,
    and thyroglobulin will elicit an immune response as these tissues were present in
    immunologically privileged sites.
     Localized autoimmune diseases are allergic encephalitis which can follow after
    vaccinations, multiple sclerosis which causes demyelination of white matter of the
    brain (Epstein Barr virus), Hashimoto’s chronic thyroiditis which shows
    autoantibodies to thyroglobulin, hemolytic anemias, myasthenia gravis, grave’s
    disease, insulin resistant diabetes, and insulin dependent diabetes mellitus where
    autoreactive T cells destroy glutamic acid decarboxylase which is an enzyme present
    in the islet cells of the pancrease.
     Graves disease has antibodies to TSH receptors (hyperthyroidism), myasthenia
    gravis has antibodies to acetylcholine receptors, and insulin resistant diabetes has
    antibodies to insulin receptors.
     Guillain-Barre syndrome is the most common cause of acute paralysis in the USA
    and it follows a variety of infectious diseases and is due to antibodies formed against
    myelin proteins which results in this demyelinating polyneuropathy.
     Campylobacter jejuni has the same molecular makeup of GM1 proteins on the
    nerves and hence a cross reaction can occur.
     Pemphigus is when there are autoantibodies against desmoglein which is a protein
    in desmosomes that form the tight junctions between epithelial cells in the skin.
     Celiac disease has a T cell attack on gliadin which is a protein found in wheat and
    hence a gluten free diet must be prescribed.
     IgA nephropathy is the most common types of glomerulonephritis and is
    characterized with immune complexes containing IgA found in the glomeruli.
     Systemic autoimmune diseases are those which involve multiple organs.
     Systemic Lupus Erythematosis (SLE) is a chronic autoimmune disease that results in
    inflammation and tissue damage that harms the joints, skin, and kidneys.
     Auto antibodies are formed against DNA, histones, and nucleoalar proteins of the
    cell nucleus.
     Antibodies against double stranded DNA (dsDNA) is the hallmark of SLE.
     HLA-DR2/DR3 genes is a genetic factor for SLE.
     Diagnosis is made by checking for anti nuclear antibodies (ANA).
     Rheumatoid arthritis is a chronic systemic autoimmune disease affecting the joints
    and multiple organs.
     Rheumatoid arthritis is when autoantibodies (IgM) are formed against IgG.
     These IgM autoantibodies are called rheumatoid factors.
     HLA-DR4 are more prone to rheumatoid arthritis.
     Inflammation of the small joints of the hand and feat are diagnostic of rheumatic
    arthritis.
    Rheumatic fever is when there is a group A streptococcal infection and the M
   protein antibodies also attack the myosin of the cardiac muscle.
    Clinical features are the common polyarthritis, pancarditis, erythema marginatum,
   chorea, and subcutaneous nodules.
    HLA-B27 predisposes one to Reiter’s syndrome that shows a triad of reactive
   arthritis, conjunctivitis, and urethritis.
    Goodpasture’s syndrome is when auto antibodies are formed against the collagen in
   the basement membranes of the kidneys and lungs.
    HLA-DR2 predisposes one to Goodpasteur’s syndrome.
    Wegener’s granulomatosis affects the upper and lower respiratory tracts along with
   the kidneys and its main feature is glomerulonephritis.
    Wegener’s syndrome shows antineutrophilic cytoplasmic antibodies
   (c-ANCA).
Tumor Immunity ppt.
    A tumor is a group of cells which undergo maliganant transformation and when they
   do they express new antigens called tumor antigens.
    There are 2 main types of tumor antigens and they are tumor specifc
   transplantation antigens (TSTA) which are unique to tumor cells and not expressed
   on normal cells, and tumor associated transplantation antigens (TATA) which are
   both expressed by tumor and normal cells.
    Carcinoembyronic antigen is found in the human embryonic gut and is elevated in
   patients with carcinoma of the colon and is a very good prognostic marker.
    Alpha fetoprotein is produced by the fetal liver and is a marker for hepatomas.
    BCG vaccine, corynebacterium parvum, and levamisole are nonspecific active
   immunotherapy which activate macrophages to be tumoricidal.
    Passive immunotherapy is through the administration of antibodies against tumor
   antigens such as antibodies against CD20 that are expressed on non hodgkin’s B cell
   lymphomas and monoclonal antibodies which inhibit protein synthesis.
Immunodeficiency Diseases ppt.
    Immunodeficiency disorders are conditions where the defense mechanisms of the
   host are impaired and leads to increased susceptibility to microbial infections and
   sometimes tumors and autoimmune diseases.
    They can occur due to a defect in any of the 4 major componenets; B cells, T cells,
   complement, and phagocytes.
    X-linked hypogammaglobulinemia is when there is a mutation in the gene encoding
   tyrosine kinase and hence pre B cells fail to differentiate into B cells.
    Severe combined immunodeficiency disease (SCID) is characterized by an absence
   of both B and T cells and the thymus, tonsils, as well as lymph nodes are absent.
    SCID can occur due to a defect in IL-2 (US version) and also due to a defect in
   adenosine deaminase (ADA) or purine necleoside phosphorylase (PNP).
    Wiskott-Aldrich syndrome is associated with normal T cell numbers but reduced
   functions and these patients have a defective WASP protein.
    Hereditary angioedema is due to deficiency of C1 inhibitor.
    C3 deficiency leads to sepsis with staphylococcus aureus while C6, C7, and C8
   deficiency leads to bacteremia with N. meningitides or N. gonorrhoeae.
       Chronic granulomatous disease is formed due to lack of NADPH oxidase activity of
      neutrophils which leads to defective intracellular microbicidal activity.
       Chediak Higashi syndrome is when there is a failure of lysosomes in the neutrophils
      to fuse with the phagosomes which results in defective phagocytic killing of the
      organisms.

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Review for final tips
Monday, February 16, 2009
4:47 PM

MHC class II CD4
MHC class I CD8
This is called MHC restriction. If cross reaction happens between these two, then pt. develops
autoimmunity.

Antibody and Antigen reaction: Principles of agglutinations and examples
Preciptation, neutralizatrion, RIA and complement fixation..ELISA..Know direct, indirect and
Sandwich ELISA.

Immune response
Complement Know C2 to C5
Functions of T and B lymphocytes, Functions of Macrophages, MHC and also Hypersenstivity
rxn Clinical sides Know the basic principles of Type one, two, three and four and also biological
mediators….

One example he gave was…The pt got stung by a bee and what biological mediator u would
see…I think serotonin…Idk if I am rite…

Session # 2
Bacterial Anatomy..Importance of Flagella..hanging drop, pyli thru hemeagglutination…how to
determine or diagnose in lab.

Sterlization clinical approach..spill or clinical thermometer in opd. How do they sterilize it.;
One example he gave was pt got hurt in accidents. Something happened to his eyes. He was
taken to opthamalogist and instruments were sterilized. So what would the opthamalogist would
do? Sterilization by heat for two hrs.

Normal flora
Culture media and Methods
He said questions will telling you the clinical case, they you have to tell how to sterilize and
stuff.
Antimicrobial agents..maybe two questions.

Microbial genetics: conjugation, transduction and Transformation.
Molecular techniques KNOW THE PCR Application and principle of PCR.
And know what heading they fall into all the techniques and stuff there is one slide in lecture.



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Micro Session 1 exam
Monday, February 16, 2009
4:47 PM



Session 1
        1. Which category of hypersensitivity best describes of the newborn
            a. Ectopic immune complex
            b. Cytotoxic (Type II)*

        2. Complement fixation refers to
             a. Ingestion of c3b coated bacteria
             b. The heating (missed)
             c. Binding of complement components by antigen antibody complexes*

        3. If an individual was genetically unable to make J chains, which immunoglobulins would be
           affected? (M and A)
              a. IgG
              b. (missed)
              c. IgG and IgM
              d. IgM and IgA*

        4. Which of the following is NOT true regarding the alternating complement pathway?
            a. It can be triggered by infectious agents in absence of antibody
            b. Does not require c1, c2, or c4
            c. Cannot be initiated unless c3b fragments are already present*
            d. Has same terminal sequence as classic pathways

        5. C3 is cleaved to c3a and c3b by c3 convertase, c3b is involved in all but
             a. Altering vascular permeability*
             b. Promoting phagocytosis
             c. Forming alternate pathway c3 convertase
             d. Forming c5 convertase

        6. During maturation of B lymphocyte the first immunoglobulin heavy chain synthesized is
      a. γ chain (gamma)
      b. μ chain * (mu)
      c. ε chain (epsilon)
      d. α chain (alpha)

7. Which one group of following cells is not phagocytic in nature?
    a. Neutrophil polymorpholeukocyte
    b. B Lymphocytes*

8. Immunoglobulin isotype is determined by
     a. Antigen specificity
     b. L chain variable region
     c. Number of binding sites
     d. H chain constant region*

9. Anaphylaxis can be triggered by cross linkiing of IgE receptors on
    a. Monocytes
    b. Mast cells *
    c. B cells
    d. Neutrophils

10. Radioallergosorbent (RAST) measures
      a. Antigen concentration
      b. IgM antibody
      c. IgE antibody*
      d. IgG antibody
            i.    (RIA – do test by labeling, for id of antigen or antibody, serological very
                  sensitive, expensive so mostly go for ELIZA)

11. The main advantage for passive immunization over active is that
      a. It can be administered orally
      b. Provides antibody rapidly*
      c. Antibody persists for longer period of time
      d. It contains IgM

12. Which type of hypersensitivity cannot be transferred with serum antibody
     a. Type I
     b. Type II
     c. Type III
     d. Type IV *

13. A 3 year old boy has had several bouts with pneumonia. The streptococcal agent was
    isolated and identified. He perhaps had some sort of immunodeficiency. Had normal levels
    of immunoglobulin, but complement system was not working normally. The complement
    system is made of all (missed). Which of the following is the primary opsonization fragment
    in complement system?
      a. Factor b
      b. C5
      c. C3b*
      d. C5a

14. Which of the following is true for class II MHC molecules
     a. Consist of an alpha chain of three domains and beta 2 microglobulin
     b. Are found in all nucleated cells of body
     c. Involved in antigen presentation to CDA cytotoxic lymphocytes
     d. Consist of DP DQ DR molecules*

15. Patient in emergency room was stung by a bee about 15 min ago. A few minutes after being
    stung, became short of breath and saw hives appear in several places on her skin. Which of
    the following is most likely immunological mechanism for this
      a. IgE coated mast cells release histamine and leukotrienes*
      b. Membrane attack complexes of complement damage cells in lung and skin
      c. Cytotoxic helper cells release interleukin2
      d. Immune cells consisting of IgG and hapten release in lung and skin

16. Each of the following concerning hapten is correct EXCEPT
      a. Can combine with antibody
      b. Cannot induce an antibody by itself, rather it may be bound by carrier protein to induce
           something
      c. In both penicillin induce anaphylaxis
      d. Haptens must be processed by cd8 cells to become immunogenic*

17. Direct Coombs test was performed on baby in 7th month (30 weeks), mother has had trouble
    with two early pregnancies and has no RHOgm. The physician is concerned about a possible
    erythroblastosis case. What ingredients would be involved to prove positive direct Coombs
    test?
      a. Rh positive RBs plus mother serum and Coombs reagent
      b. Mothers serum Rh positive
      c. Rh positive from baby and Coombs reagent*
      d. Mothers serum RHOgm and Coombs reagent

18. Complement components are involved in which types of hypersensitivies?
      a. I & III
      b. II & III *
      c. II & IV
      d. III & IV

19. Antibody titer refers to
     a. Highest dilution of antibody still able to give positive result in test system*
     b. Concentration of specific antibody
     c. Availability of specific antibody
     d. Specific amount of specific antibody

20. The site of affinity of antibody for antigen is
      a. Disulfide bond
      b. Fc region
      c. Fab region*
      d.

21. The circulation of a two month old breast fed baby will contain maternal (WARNING:
    teacher was not sure of answer) [answer should be IgA]
      a. IgA
      b. IgM
      c. IgE
      d. IgG*

22. Which of the following is correct about secondary immune response?
     a. Class switching from IgM to IgG will occur and IgG antibody titer will rise*
     b. IgM titer will rise above IgG level for a period of 6 months
     c. IgG titer will continue to fall and IgM titer will rise due to class switching
     d. IgG, IgA titers will continue to rise during secondary immune response
     e.

23. The defense mechanism which is lodged against most extracellular bacterial pathogens that
    infect through respiratory and intestinal tracts is
      a. Immunity involving only macros
      b. Cell mediated
      c. Immunity only involving polymorphonucleocytes
      d. Immune surveillance by immature lymphocytes
      e. Antibody mediated immunity *

24. Which of the following cell types expresses receptors for IgE on surface that mounts a
    response to parasites such as worms
      a. T cells
      b. B cells
      c. Promonocytes
      d. Nk cells
      e. Mast cells*

25. A primary immune response in adult human requires approximately how much time to
    produce detectable (something) levels in blood
      a. 12 hrs
      b. 1 week*
      c. 2 week
      d. 3 week
      e. 4 weeks

26. Biologic fluids (missed a lot) semiquantitatve to detect microbial agents in
      a. Radioimmunoelectroph
      b. Blu nitro
      c. Coombs test
      d. Hemeagglutination inhibition tests
      e. Counter immunoelectrophoresis* (more sensitive)
27. Regarding function of chemokines in host defense , which is most accurate?
      a. Chemokines bind to T cell receptor outside of the antigen binding site and activate many
           T cells
      b. Chemokines induce switching in b cells which increase amount of ige produce
      c. Chemokines penetrate membranes of target cell
      d. Chemokines attract neutrophils to site of bacterial infection thereby playing a role in
           inflammatory response*

28. Which genetic mechanism increases number of different antibody molecules during immune
    response without creating diversity of antigen receptors specificities
      a. Class switching*
      b. Somatic hypermutation
      c. Gene duplication
      d. Multiple J, G gene segments
      e. Imprecise V, D, J joining

29. Immediately after primary immunization which of the following phenomenons would be
    expected to occur?
      a. Production of IgM antibody*
      b. Production of a set of restricted B lymphocytes
      c. Production of low affinity IgG antibody
      d. Degradation of antigen by (missed)

30. Antibody binding site is formed by
     a. Variable regions of L chains
     b. Hyper-variable regions of H & L chains*
     c. Variable regions of H chains
     d. Hyper-variable of H chains
     e. Hyper-variable regions of L chains

31. Which of the following statements about collaboration of T & B lymphocytes is NOT correct
     a. T lymphocytes may stimulate antibody production by B cells
     b. T lymphocytes may depress antibody production by B cells
     c. T lymphocytes that participate in carrier recognition must recognize same antigen
          epitope as B lymphocyte*
     d. Collaboration is not required for all antibody response
     e. Antigen processing by macros may be required to optimize T lymphocytes effects

32. When a precipitation reaction can be converted to an agglutination reaction by coating, it is
    called?
      a. Reverse passive
      b. Coagglutination
      c. Immune adherence
      d. Passive agglutination*

33. Agglutination reaction is more sensitive than precipitation reaction for detection of
      a. Antigens
      b. Antibodies*
      c. Antigen antibody complex
      d. Complement
      e. Heterophil antigen (sp)

34. The role of macrophage during antibody response is to
      a. Make antibody
      b. Lyse virus infected target cells
      c. Activate
      d. Process antigen and present it*

35. Each of the following concerning immunologic tolerance is correct EXCEPT
      a. Tolerance is not antigen specific*
      b. Paralysis of immune cells results in failure to
      c. Tolerance is in t cells than in b cells
      d. Tolerance is induced more in neonates than in adults
      e. Tolerance is induced more by light molecules than heavy

36. Systemic Lupus Erythematosis (SLE) is associated with deficiency of
      a. C1 & C4*
      b. C2 & C3
      c. C5 & C6
      d. C2 & C4

37. Following are autoimmune diseases EXCEPT
      a. DiGeorge syndrome*
      b. Rheumatoid arthritis
      c. Hashimoto’s disease
      d. Myasthenia gravis

38. 1st component of complement that bind to fc of antibody molecule
      a. C1r
      b. C1q*
      c. C1s
      d. C2

39. Due to deficiency of secretory IgA infections occur predominantly in
     a. Respiratory tract
     b. GIT
     c. Other tract options
     d. All of the above *

40. Drug induced immune hemolytic anemia is due to
      a. Type I
      b. Type II *
      c. Type III
      d. Type IV
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Immunology review by Banga Raju
Monday, February 16, 2009
5:20 PM

Microbiology
Immunology Overview

-Immune response by a host to entry of microbes- bacteria, fungus, parasite.
- nearly one billion microbes enter the body just in food. We are protected by immune system.
- to be recognized as an antigen it depends on molecular weight. minimum of 70,000 mol wt. Not all
substances qualify as an ag.
- B (H) and T(CMI) lymphocytes respond at the same time but
       First line- only a fourth of the b cells are mature, others are immature and just travel the body.
       The main advantage is that they don’t come in contact with ag but still get stimulated. Faster! Two
       imp signals
         1. Chemotactic facors need to touch it
         2. Strength of chemotaxis! Greater strength produses IgG (greatest pressure)—IgM—A-D_E
                 a. Most at a threshold which produces IgM; IgM most commonly produced
       Second line
-Ag release pharmacologically active substances, come into physical contact w T lymphocytes. First
signal-Chemotactic reach T cells. DISADV- can not recognize heavy molecules! 70,000 is too big. That’s
why we have mediators- APC!! – Macrophages ,Neutrophils, DendriticCells! Also Microbial cells (brain),
K, S
-inflammation- serum rich in macro and neutrophils
-comes to the point of injury, picks up ag, antigen processing- breaks down the ag into small bits of
peptides so it doesn’t weigh as much and it can be recognized.
- second signal by the t cells activates the other ¾ of the B cells. Paracrine affect
Requires 2 stimulating factors- ag APC and self generated-autocrine-- IL2,4 (7,12,13 also)

Phagocytosis and processing: broken down to small particles, bind to MHC and bind to the surface – can
be presented to cell. (mhc i always DC; CD8) mhc 11- CD4”MHC restriction” never a cross rxn, if so-
then autoimm disease.



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Tuesday, November 25, 2008
12:52 AM


  1. SLE is seen in a def in C2 and c4
     C5 - C8 is seen in Nisseria
     C3 is progenic infection
     C1 is angio edema



2.    Complement lysis cells by insertion of complement protein. Into the cell membrane
3.    Aggulution test rxn is more sensitive than the ppt rxn for detection of antibody
4.    RDS within minutes, and goes into unconsciousness after a bee sting.
      a.     So this is IgE mediated

5.     CNS disorder maintained on drug methyldopa, hemolytic anemia develops, which clears after
     drug withdrawl?
       a.     This is an example of type II sensivity rxn in which CD8 cells are taking out RBC's



           Hypersensitivity (also called hypersensitivity reaction) refers to undesirable (damaging,
           discomfort-producing and sometimes fatal) reactions produced by the normal immune
           system. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. The
           four-group classification was expounded by P. H. G. Gell and Robin Coombs in 1963.[1]
           [edit] Coombs and Gell classification
          Typ Alternative          Often mentioned disorders[2]         Mediators[2]
          e   names [2]

          1     Allergy                                 Atopy                               IgE
                (immediate)                             Anaphylaxis
                                                        Asthma

          2     Cytotoxic,                              Autoimmun                           IgM or
                antibody-                  e hemolytic anemia                   IgG
                dependent                               Thrombocyt                          (Comple
                                           openia                               ment)
                                                        Erythroblast
                                           osis fetalis
                                                        Goodpastur
                                           e's syndrome

          3     Immune                                  Serum                               IgG
                complex                    sickness                                          (Comple
                disease                                 Arthus                 ment)
                                           reaction
                                                        SLE

          4     Delayed-type                            Contact                             T-cells
                hypersensitivi             dermatitis
                ty[3] (DTH),                            Tuberculin
                Cell-mediated              skin test
          immune                                       Chronic
          memory                         transplant rejection
          response,
          antibody-
          independent
     Comparison of hypersensitivity types
     [edit] Type 5
     This is an additional type that is sometimes (often in Britain) used as a distinction from Type
     2.[4]
     Instead of binding to cell surface components, the antibodies recognize and bind to the cell
     surface receptors, which either prevents the intended ligand binding with the receptor or
     mimics the effects of the ligand, thus impairing cell signalling.
     Some clinical examples:
        Graves disease
        Myasthenia gravis
     The use of "Type 5" is rare. These conditions are more frequently classified as Type 2,
     though sometimes they are specifically segregated into its own subcategory of Type 2.


     Pasted from <http://en.wikipedia.org/wiki/Hypersensitivity_response>



f.     C6 def will be seen in nisceria
g.     Chemokines in host, which attract neutrophils to the site of infection plays a role in
   infectious response/
h.     Hapten protein conguate in order to get Anti-Hapten antibodies. It is essential that
          --> hapten attaches to the protein and the protein is recognized by the helper t cell.


9.       3 yrs male pneumonia gave penicillin
           -immunodeficient
           Phagocytic system INTACT
           Normal level of Ig
           Complement not working properly
                 Know the function of C3b
                       Does 2 things


                           Jump to: navigation, search
               The classical and alternative complement pathways.
               C3b is a one of the elements formed by the cleavage of complement
               component 3.
               C3b may bind to microbial cell surfaces within an organism's body. This
               can lead to the production of surface-bound C3 convertase and thus more
               C3b components. Also known as C3bBb, this convertase is similar to
               soluble C3-convertase except that it is membrane bound.
               Alternatively, bound C3b may aid in opsonization of the microbe by
               macrophages.[1] Complement receptor 1 or CR1 on macrophages allows
               the engaging of C3b covered microbes.

               Pasted from <http://en.wikipedia.org/wiki/C3b>



         10, know def of carriers.

11. Which genetic mechanism increases the # of differential antibodies molecules in drug
    when immune respose with out increasing the diversity of the pool Ag receptor
    specification.
          --> Class switching


12. Which category of hypersensivity best describes the hemolytic amenia (type 2) /cd8
    mediated
13. Physicain induced infection -> iatrogenic infection
14. Hemolytic disease in a newborn caused by the Rh factor.
          Incompatibility occurs
                              IgG


      15.       Alternative complement pathway
              1.        Can be triggered by infectious agents
              2.        Does not require C1, C2, C4

                  NOT TRUE
                       It cannot be initiated unless C3b fragments are present.



16. Anaphalytic shock ---====== mast cells
17. Type 4 cannot be transfused with serum????????????
18. Secondary immune response
      1.       Class switching will go from IgM to IgG will occur and IgG titer will rise.
19. Ag Presenting cells that activate helper T cells
            MHC II

20. Which of the groups of the following cells is not phagocytic in nature.
                  B lymphocytes



21. True for MHC II
            DQ< DR< DP
            All have 2 alpha and beta chains



22. Macrophace is an APC
23. Immunologic tolerance is true for all the following except?
      1.       Tolerance is not Ag specific
      2.       More easily induced in T cells and B cells
      3.       More easlily tolerated in neonates rather than adults,.
      4.       Induced by simple molecules.
24. IgG can cross the placenta
25. Loss, of sufrace molecules on Tumor cell target will show some loss of susesptibility by host.
            MHC I

26. Exact # of B cells look at CD 19
    CD -53 = NK cells
    CD-3 = /tcells
27. Role of MHC I in graft Vs. Host reactions\
      1.      (+) Recognized by helper T cells which activate CD 8 to kill donor cells
      2.     /receptor for IL-2
      3.     Induce IgE mediates graft rejection
      4.     Induce Ag that protects Graft



28. An example of articifial active is DPT
29. NK cells are able to kill cells w/ out prior sensitazation
30. //
31. Stem cell in bone marrow is where B and T cells come from
32. Self reactive t cells because of co stimulation is
                Clonal Anergy

                Anergy is a term in immunobiology that describes a lack of reaction by the body's
                defense mechanisms to foreign substances, and consists of a direct induction of
                peripheral lymphocyte tolerance. An individual in a state of anergy often indicates
                that the immune system is unable to mount a normal immune response against a
                specific antigen, usually a self-antigen. Lymphocytes are said to be anergic when they
                fail to respond to their specific antigen. Anergy is one of three processes that induce
                tolerance induction, modifying the immune system to prevent self-destruction (the
                others being clonal deletion and immunoregulation

                Pasted from <http://en.wikipedia.org/wiki/Clonal_anergy>



                clonal anergy
                Functional inactivation of t- or B-lymphocytes rendering them incapable of eliciting
                an immune response to antigen. This occurs through different mechanisms in the
                two kinds of lymphocytes and can contribute to self tolerance

                Pasted from <http://128.240.24.212/cgi-bin/omd?clonal+anergy>




      33.    HLA Genes
                    DR4 = Rhumitoid Arthritis
                    DR2 = Systemic lupus Erythomatus (SLE)
                    DR1 = ulcerative Colitis
                    B27 = Ankylosis spongitis



      34.    Auto immune character by Auto antibodies against AcH
               /mystenia Gravis

                Other options were
Graves diseases which is hyperthyroidism
     Exotholomus

Celiac disease = gluttin free diet cause glutun is seen as an Ag
SLE= against DNA
Wegners =
Wegener's granulomatosis is a form of vasculitis that affects the lungs, kidneys
and other organs. Due to its end-organ damage, it can be a serious disease that
requires long-term immune suppression.[1] It is named after Dr. Friedrich
Wegener, who described the disease in 1936.[2]
Wegener's granulomatosis is part of a larger group of vasculitic syndromes, all
of which feature the presence of an abnormal type of circulating antibody
termed ANCAs (antineutrophil cytoplasmic antibodies) and affect small and
medium-size blood vessels. Apart from Wegener's, this category includes Churg-
Strauss syndrome and microscopic polyangiitis.[

Pasted from <http://en.wikipedia.org/wiki/Wegener%27s_Granulomatosis>




[edit] Signs and symptoms
Initial signs are protean, and diagnosis can be severely delayed due to the
nonspecific nature of the symptoms. Rhinitis is generally the first sign in most
patients.[1]
   Upper airway, eye and ear disease:
          o Nose: pain, stuffiness, nosebleeds, rhinitis, crusting, saddle-nose
               deformity due to a perforated septum
          o Ears: conductive hearing loss due to auditory tube dysfunction,
               sensorineural hearing loss (unclear mechanism)
          o Oral cavity: strawberry gingivitis, underlying bone destruction with
               loosening of teeth, non-specific ulcerations throughout oral mucosa
          o Eyes: pseudotumours, scleritis, conjunctivitis, uveitis, episcleritis
   Trachea: subglottal stenosis
   Lungs: pulmonary nodules (referred to as "coin lesions"), infiltrates (often
        interpreted as pneumonia), cavitary lesions, pulmonary hemorrhage
        causing hemoptysis, and rarely bronchial stenosis.
   Kidney: rapidly progressive segmental necrotising glomerulonephritis
        (75%), leading to chronic renal failure
   Arthritis: Pain or swelling (60%), often initially diagnosed as rheumatoid
        arthritis
   Skin: nodules on the elbow, purpura, various others (see cutaneous
        vasculitis)
   Nervous system: occasionally sensory neuropathy (10%) and rarely
        mononeuritis multiplex
   Heart, gastrointestinal tract, brain, other organs: rarely affected.

[edit] Diagnosis
Wegener's granulomatosis is usually only suspected when a patient has had
unexplained symptoms for a long period of time. Determination of ANCAs can
aid in the diagnosis, but positivity is not conclusive and negative ANCAs are not
sufficient to reject the diagnosis. Cytoplasmic staining ANCAs that react with the
enzyme proteinase 3 (cANCA) in neutrophils (a type of white blood cell) are
associated with Wegener's.[1]
If the patient has renal failure or cutaneous vasculitis, these are the most logical
organs to obtain a biopsy from. Rarely, thoracoscopic lung biopsy is required.
On histopathological examination, a biopsy will show leukocytoclastic vasculitis
with necrotic changes and granulomatous inflammation (clumps of typically
arranged white blood cells) on microscopy. These granulomas are the main
reason for the appellation of "Wegener's granulomatosis," although it is not an
essential feature. Unfortunately, many biopsies can be nonspecific and 50%
provide too little information for the diagnosis of Wegener's.[1]
Differential diagnosis (alternative possible diagnoses) can be extensive. ANCAs
can be positive after the use of certain drugs and other forms of vasculitis can
present with very similar symptoms. The saddle-nose deformity may also be
seen in relapsing polychondritis, cocaine abuse and in congenital syphilis.
[edit] Criteria
In 1990, the American College of Rheumatology accepted classification criteria
for Wegener's. These criteria were not intended for diagnosis, but for inclusion
in randomised controlled trials. Two or more positive criteria have a sensitivity
of 88.2% and a specificity of 92.0% of describing Wegener's.[3]
   Nasal or oral inflammation:
        o painful or painless oral ulcers or
        o purulent or bloody nasal discharge
   Lungs: abnormal chest X-ray with:
        o nodules,
        o infiltrates or
        o cavities
   Kidneys: urinary sediment with:
        o microhematuria or
        o red cell casts
   Biopsy: granulomatous inflammation
        o within the arterial wall or
        o in the perivascular area
According to the Chapel Hill Consensus Conference (CHCC) on the nomenclature
of systemic vasculitis (1992), establishing the diagnosis of Wegener's
granulomatosis demands:[4]
   a granulomatous inflammation involving the respiratory tract, and
   a vasculitis of small to medium-size vessels.
Several investigators have compared the ACR and Chapel Hill criteria.[5]
[edit] Pathophysiology
Inflammation with granuloma formation against a nonspecific inflammatory
background is the classical tissue abnormality in all organs affected by
Wegener's granulomatosis.[1]
It is now widely presumed that the anti-neutrophil cytoplasmic antibodies
(ANCAs) are responsible for the inflammation in Wegener's.[1] The typical
ANCAs in Wegener's are those that react with proteinase 3, an enzyme
prevalent in neutrophil granulocytes.[6] This type of ANCA is also known as
cANCA, with the c indicating cytoplasmic (in contrast to pANCA, which is
perinuclear).
ANCAs activate neutrophils, increase their adherence to endothelium, and lead
to their degranulation. This causes extensive damage to the vessel wall,
particularly of arterioles.[1]
The exact cause for the production of ANCAs is unknown, although some drugs
have been implicated in secondary forms of Wegener's. As with many
autoimmune disorders, the cause is probably genetic predisposition combined
with molecular mimicry caused by a virus or bacterium.
[edit] Treatment
Before steroid treatment became available, mortality within one year was over
90%, with average survival being 5 months. Steroids prolonged average survival
to 8 months. The introduction of cyclophosphamide (CYC) in the 1970s was a
major breakthrough.[7]
Initial treatment is generally with corticosteroids and oral cyclophosphamide
(CYC), 1 mg/kg/day and 2 mg/kg/day, respectively. Occasionally CYC is given in
monthly intravenous (IV) doses. Monitoring of the white blood count is
essential during CYC therapy. Once remission is attained (normally 3 to 6
months), treatment is frequently changed to azathioprine or methotrexate,
which are less toxic drugs. Total duration of therapy should be at least one year,
or longer in high risk patients. Corticosteroids are tapered to a low maintenance
dose, 5-10 mg/day. Plasmapheresis may be beneficial in severe disease or
pulmonary hemorrhage. Experience with other treatment agents is very
limited.[1].
A systematic review of 84 trials examined the evidence for various treatments
in Wegener's granulomatosis. Many trials include data on pooled groups of
patients with Wegener's and microscopic polyangiitis. In this review, cases are
divided between localized disease, non-organ threatening, generalized organ-
threatening disease and severe renal vasculitis and immediately life-threatening
disease.[7]
   In localized disease, treatment with the antibiotic co-trimoxazole is
        recommended, with steroids in case of treatment failure.[8]
   In generalized non-organ threatening disease, remission can be induced
        with methotrexate and steroids, where the steroid dose is reduced after a
        remission has been achieved and methotrexate used as maintenance.
   In case of organ-threatening disease, pulsed intravenous
        cyclophosphamide with steroids is recommended. Once remission has
        been achieved, azathioprine and steroids can be used to maintain
        remission.
   In severe renal vasculitis, the same regimen is used but with the addition
        of plasma exchange.
   In pulmonary hemorrhage, high doses of cyclophosphamide with pulsed
        methylprednisolone may be used, or alternatively CYC, steroids, and
        plasma exchange.
          In severe disease not responsive to previously mentioned treatment, the review
          is positive about mycophenolate mofetil, 15-deoxyspergualin, anti-thymocyte
          globulin, rituximab and infliximab; data was less favourable for intravenous
          immunoglobulin (IVIG) and etanercept.[7]
          In some patients with severe subglottic stenosis, tracheotomy is required to
          maintain an airway.
          Follow-up: general well-being and laboratory organ markers are checked on a
          regular basis to ascertain the patient has remained in remission.
          [edit] Epidemiology
          The incidence is 10 cases per million per year.[7] 90% of the patients are white.
          While it mainly occurs in the middle-aged, it has been reported in much
          younger and older patients.
          [edit] Prognosis
          25 to 40% of patients suffer from flare-ups, but a majority respond well to
          treatment. Anatomical problems (sinusitis, tracheal stenosis) may require
          surgery in a small proportion. Relapses can be long and troublesome.
          Long-term complications are very common (86%): mainly chronic renal failure,
          hearing loss and deafness.[1]

          Pasted from <http://en.wikipedia.org/wiki/Wegener%27s_Granulomatosis>




 Realtionship btw M protein of staph . Pyogens and myosin of cardiac muscle is
          MOLECULAR MIMMICRY


36. Tumor cells use to defend itsself is not true.
      1. Marking of tumor Ag
      2. Escape of Autoreactive clones of t cells
      3. Molecular surface Ag
      4. Producing a blocking activity
      5. Suppression of the T, B cell immunity
37. C reactive protein
          Example is Acute phase proteins

38. Choose for adaptive and not for innate
      1. Physical
      2. Chemical
      3. Clonal expansion of effector cells.

39. NK cells lytic activity increase activity by inceased levels of alpha and beta true except
      Play a role in CD8
      Can resemble Large granular lymphocytes macroscopically to T cells
      Can lyse target cells that have undergone malgnant transformation that plays a
          role in immnue
      NOT =-> derived from same cell lineage as T and B cells.
              40. Ppt rn converted to Agglution rxn with coated soluble Ag on to a latex particle.
                        This is passive Agglution

                        Reverse passive is when the Ab is coated

                        Co agglution is for streptococcus

                        Immune adherence
                            Where Ag-Ab activate complement receptor.




Microbiology Quiz 1
Monday, February 16, 2009
4:47 PM

Microbiology Quiz #1
 1.            Which of the following not one of Koch’s postulate – disease can be treated with broad
     spectrum antimicrobial agents
 2.            Carrier who acquires pathogen from another carrier – paradoxical carrier
 3.            What is the initial step in process of infection - adherence of microorganism to
     susceptible host cells
 4.            Exotoxin part of gram positive organism – produced only upon lysis of the cell
 5.            Mention any two contributions of the person shown below – Louis Pasteur: anthrax,
     vaccines for rabies, father of microbiology
 6.            Substances which is not immunogenic by itself but can react with specific antibody –
     haptens
 7.            Genetic mechanism involved in elaborating large number of diff Igs due to single
     antigenic stimulus is known as – class switching
 8.            individual is unable to synthesize J chains without - IgA, IgM
 9.            matching
 10.           resistance which an indiv possess by birth - innate immunity
 11.           which of following mediators involved in oxygen independent intracellular killing
     mechanism – lactoferrin
 12.           example of natural active immunity dev in person recovering from chicken pox infection
 13.           immunity acquired in person who received pooled human gamma globulins – artificial
     passive immunity
 14.           involved in phagocytosis of parasites – eosinophils
 15.           which is most common surface Igs present on B cells – monomeric IgM
 16.           induced infection resulting from drug therapy – iatrogenic
 17.           null cells are type of – large granular lymphocytes
 18.           CD marker universally present on T cells – CD 3
 19.           Which is NOT an antigen presenting cell – T cells
 20.           Primary lymphoid organ – thymus
Pasted from <file:///F:\A%20K\Microbiology\Session%201\Microbiology%20Quiz%201.doc>




Quiz 2 Microbiology
Friday, February 06, 2009
8:40 AM




       Audio recording started: 8:40 AM Friday, February 06, 2009


       Recording only
       Type up

  1.     Don't have this one. If you have it, please send it out. Thanks.
  2.     Don’t have this one. If you have it, please send it out. Thanks.
  3.     Positive tuberculosis skin test indicates that:
         a.       a humoral immune response has occurred
         b.       A cellular immune response has occurred*
         c.       Both t and b cells systems are functional
         d.       Only the B cell system is functional
  4.     IgE is secreted by:
         a.       Mast cells
         b.       Eosinophils
         c.       Basophils
         d.       Plasma cells*
               i.          (essentially all antibodies secreted by plasma cells)
  5.     Which one of the following does not contain C3B?
         a.       Classic pathway C5 convertase
         b.       Alternative pathway C5 convertase
         c.       Classic pathway with C3 convertase*
         d.       Alternative pathway C3 convertase
  6.     During the maturation of a B lyphocyte the first Ig heavy chain to be synthesized is the
         a.       Mu chain
  7.     Immune response to a hapten protein conjugation order to get antihapten antibodies it is
       essential that
         a.       The hapten be recognized by helper T cells
         b.       The protein be recognized by the helper T cells*
         c.       The protein be recognized by B cells
         d.       The hapten be recognized by….
  8.     A patient with a central nervous system disorder is maintained on the drug methyldopa.
       Hemolitic anemia with…something…. occurs shortly after the drug is withdrawn. This is most
       probably and example of:
        a.      Cytotoxicity (or cytotoxic hypersensitivity)
 9.     The main advantage of passive immunization over active immunization is that:
        a.      Didn't get the answer. If you have it, please send it out. Thanks.
 10.    Each of the following statements concerning class II MHC molecules is correct except:
        a.      They are found on the surface of both B cells and T cells*
        b.      They have a high degree of polymorphism
        c.      They are involved in the presentation of antigens by macrophages
        d.      They present the antigens to CD4 T cells
 11.    Cytokines are:
        a.       not antigen specific*
        b.      Capable of activated something….
        c.      Made by Lymphocytes…..
 12.    Which of the following is not true of class I MHC antigens?
        a.      They are found mainly on macrophages and dendritic cells*
             i.          (this is true for Class II MHC molecules)
 13.    Which of the following is not labelled as a fibrogenic (check this) cytokine?
        a.      Interleukin 2
 14.    The following statements concerning MHC molecules is correct except:
        a.      Corticosteroids increase the expression of class II MHC molecules
 15.    The classic complement pathway is initiated by attraction of:
        a.      Antigen IgG complex



Microbiology Quiz 1
Sunday, February 15, 2009
11:59 AM

Microbio Quiz # 1


1) Immunogenicity most correct:
     Haptens must be attached to heavy molecules
     *proteins and polysaccharides more immunogenic compared to lipid and nucleic acids

2) Primary test for HIV test:
      Uses ELISA, asking for the steps
      HIV antigen, protein serum, ______, enzyme ligand

3) Exotoxins can be turned into toxoids and toxoids are made into vaccines

4) Least likely used in chronic inflammation:
      Neutrophils

5) People who lack antibodies are prone to:
      -recurrent extracellular bacteria
      (remember, viruses are intracellular)
6) Which of the following inflammatory cells is not matched properly?
     -T lymphocytes- antibody mediated cytotoxicity

7) Interferons are:
       Species specific

8) Most antigen sensitive test:
     RIA

9) T cell:
       All of the above

10) IgA secretory part synthesized where?
      Mucosal epithelial cells

11) Helper cells belong to:
      T cells

12) Which of the following cytokines not secreted by T cells?
     L1 (not sure if this is the right answer)

13) Amino end has:
     Variable end

14) Virus infected cells usually killed by:
      Natural killer cells

15) Louis Pasteur:
      Not associated with ___________ (didn’t discover tb)

16) Endotoxins are
      Lipopolysaccharides

17) Myobacterium tetani:
     Doesn’t mach koch’s postulate

18) Radioimmunodiffusion:
      Used to detect serum proteins



Session 1 micro old stuff
Monday, February 16, 2009
4:47 PM


[Enter Post Title Here]
       Clinical infection causes -
  1.              DPT - artifical active
  2.                Parodoxical infections - aquired from another person
  3.                Iatrogenic infections cuased by treatment
  4.                IgE is involved in bee sting of
  5.                SLE -- caused by deficiency of c1 & c4
  6.                Staph aureus and cardiac muscle - molecular mickery
  7.                NK cells whats not true? Same lineage
  8.                Myestenia gravis attacks - ach receptors
  9.                Loss of what class of molecule will lead decreased susceptiablity of tumor host cell - Loss
        of MCH II
  10.              Deficiency of c6 leads to - increased susceptiblity to Nisseria Something
  11.              C Reactive protien is example of - Anaphase protien
  12.              Tumor cells don't use what as a form of immuno escape? Escape from autoreactive
        clonal T-cells
  13.              What IG is responsible for Erythoblastosis Fetlais - IgG
  14.              Child is exposed to chic ken pox from the sister, no symptoms b/c mom had chickenpox
        5 years ago. What immunoglobin is responsible? IgG
  15.              What Gene for rheumatoid arthritis? HLA-DR4
  16.              Which hypersensitivy can't be transferredby antibodies? Type IV
  17.              Patient was given a vaccine - Devloped hemolytic anemia after. Recoverd after removal
        of treatment. What type of reaction? Cytoxic(type II)
  18.              Anti hapten antibodies ? Protien carrier must be recognized (421)
  19.              Agglutination is specific for? antibody
  20.              Precipitation test turned into agglutination by giving latex particles? Passive
        agglutination
  21.              IgE on the surfaceof? mast cells
  22.              Increase antibodies w/o increasing the diversity fo the pool of antigen receptor
        specifities? Class switching (jaewitz)
  23.              What is a characteristic of addaptive immune response and not of innate? Clonal
        expansion of effector cells
  24.              What happens in secondary immune response - Class switching from IgM to IgG
  25.              Cytokines attract neutrophils
  26.              Precipitation is more sensitive than agglutination reaction with regard to – Ag
  27.              (396) What is the role of class II MHC protiens on donor cells in graft rejection? They are
        recognized by helper T cellss which then activate cytoxic t cells to kill the donor cells
  28.              Classical comlement pathway is initiated by inteaction of C1 w/? Antigen - IgG
        complexes
          a.                C3b is involved in all of the following except???? Maybe???
  29.              Infant with no T or B cells has a problem with what? Bone marrow




Pasted from <file:///F:\A%20K\Microbiology\Session%201\Session1Micro.docx>
Microbiology Quiz 2 07-08
Monday, February 16, 2009
4:47 PM

Microbiology Quiz #2
7/8/08
  1.            CD4+ and Th1 cells - IL-2
  2.            What happens in secondary immune response - Class switching from IgM to IgG
  3.            Abs that arise in serum of an indiv immunized with a single complex Ag containing many
      epitopes – heterogeneous in chemical structure
  4.            Macrophages involved in many different activity – role of macrophage during formation
      of Ab – process Ag and present it to T helper CD4 cells
  5.            True of ADCC except – IgG involved, recognition of specific Ag an on MHC class I
  6.            Effector mechanism most likely to act in concert with early IgM production to clear
      infection – complement mediated opsonization
  7.            MAC composed of – C5b, 6, 7, 8, 9
  8.            Not labeled a pyrogenic cytokine – IL-2
  9.            Primary opsonization fragment - C3b
  10.           Bee sting  Ig found in high concentration would be – IgE
  11.           Precipitation is more sensitive than agglutination reaction with regard to – Ag
  12.           Primary test for HIV infection uses – HIV Ag, patient serum, anti-Ig serum and enzyme
      substrate ligand (ELISA)
  13.           Ig isotype is determined by the – H chain constant region
  14.           RAST measures – IgE
  15.           Ab titer refers to – highest dilution of Ab still able to give
  16.           Immunofixation on reaction of Ag - agar
  17.           Healthy child soon after birth would have which Ig – IgG only
  18.           Complement fixation refers to – binding of complement components by Ag-Ab
      complexes
  19.           Cytokines are not – Ag specific
  20.           Which substance is synthesized by hypothalamic endothelium in response to circulation
      pyrogenic cytokine- prostaglandin E2

Pasted from <file:///F:\A%20K\Microbiology\Session%201\Microbiology%20Quiz%202.doc>




Microbiology quiz 3 8-08
Monday, February 16, 2009
4:47 PM

Microbiology Quiz #3

17/8/08

  1.            Which category of hypersensitivty best describes hemolytic disease of the newborn
       caused by Rh compatibility
          a.                Cytotoxic
  1.               During transplantation-The rejection reaction that is caused by the presence of
        preformed Abs in the recipient=white graft rejection-answer hyperacute
  2.               Graft vs. host rxn-when immunocompetatn T cells are present in the graft
  3.               Localized autoimmune disease-idiopathic/immune thrombocytopenic purpura.
  4.               Efficient T cell mediated killing of virally infected cells need MHC class=-needs class 1
        antigen
  5.               Immunofluresecence examination of tissue from goodpastures syndrome-alveolar and
        glomerula basement membrane.
  6.               Which tumor associated antigen is assoicated with hepatocellular carincoma-alpha feto
        protein
  7.               Speicific passive immunotherapyh-anti CD20 monoclonal antibody.
  8.               Hypersensitivity to penicilin and hypersensitivity to poison oak are both initiated by
        haptens.
  9.               Which HLA Ag is implicated in RA=HLA DR4
  10.              HLA B27 (enkelaities spondilitys)
  11.              RF-IgM autoAb against IgG.
  12.              Which autoimmune diase eokeved by a similarity between human GM1 and GM1 ike
        epitope of Campylobacter jejuni lipooligosacchardie-Gullian Barrer syndrome.
  13.              Most automine disease are antibody mediated.
  14.              Enlarged thryoid, exophtalmos, heat intolerance and anxiety. TSH low and high T3 and
        T4 levels.-Graves disease.
  15.              Arthus rxn -intense infilitration of nuetrophils.
  16.              Chronic granulamatous disase due to defect in neutrophil function.
  17.              Digeorge syndrome/thymic aplasia-primary T cell deficiency disease/
  18.              Killed vaccines given to immunocomporeise because more immunogenic then live
        vaccines.
  19.              Live attenuated vaccines available for each of the disease EXCEPT -hepatitis B
        (recombinant vaccine).
  20.              Yellow fever=live vaccine.
  21.              Which type of hyeprsensitivety can not be transffered with serum AB=type 4.


Pasted from <file:///F:\A%20K\Microbiology\Session%201\Microbiology%20Quiz%203.doc>




Microbiology Practice Test
Monday, February 16, 2009
4:47 PM
Micro final review
Monday, February 16, 2009
4:47 PM

Micro final review
 1.            a newly identified pathogenic agent has been isolated from the lung tissue of
     several patients.which of the following charac
       a.              obligate intracellular
 2.            complement fixation is the binding of complement components by ag-ab
     complexes #
 3.            of the following choices, the most important function of antibody in host defences
     against bacteria . ..facilitation of phagocytosis
 4.            which one of the following agents simultaneously contains both DNA and RNA?
       a.              Bacteria
 5.            which of the following statements concerning peptidoglycan is not correct?
       a.              It is thinner in gram positive than in gram –
 6.            A clinical infection leads to
       a.              Active natural immunity
       b.              note that
                   i.           active artificial – vaccines
                  ii.           passive artificial – immunoglobulins
                 iii.           passive natural – from mother to baby in the womb
 7.            in the gram stain, the decolorisation of gram – bacteria by alcohol is most closely
     related to
       a.              lipid rich cell wall
 8.            if an individual was genetically unable to make j chains, which one would he not
     able to make ? G and M
 9.            Creutzfeldt- Jacob disease is caused by prions
 10.           eosinophilic inclusion bodies seen in the cytoplasm of nerve cells …most likely
     caused by rabies virus
       a.              note that herpes simplex type 1, would have basophilic inclusion bodies
 11.           cultures of CSF and blood yielded the same organism on chocolate agar but no
     growth on blood agar
       a.              chocolate agar : hemophilus influenza type b
                   i.           note that neisseria gonorrhea would also show growth on chocolate
                        agar
 12.           normal flora of the vaginal tract and cause meningitis in new borns
       a.              Group B streptococci
                   i.           Note that in new borns 1st causative organism is Group B
                        streptococci, E.coli, klebsiella, viruses and then candida albicans
 13.           viruses cannot replicate by binary fission…know the virus life cycle
 14.           which of the following bacterial components is least likely to contain useful
     antigens…
       a.              ribosomes
15.           Which one of the following cell types expresses receptors for IgE on its cell
    surface that stimulates the cell to mount a response to parasites?
      a.               Mast cells or eosinophils
16.           never considered to be members of normal flora? M. Tuberculosis
17.           what is the initial step in the process of infection?
      a.               Adherence of the microorganism to susceptible host cells
18.           the sequence of steps that each of the virus undergoes during replication are
      a.               absortion, penetration, uncoating, biosynthesis, assembly and release
19.           Enriched medium – culture medium is prepared to meet the nutritional
    requirements of fastidious organisms by addition of substances such as blood serum, and
    egg to a basal medium
20.           the defence mechanism which is lodged against most extracellular bacterial
    pathogens and viruses that infect through the respiratory tract and intestinal tract is
    ….antibody mediated immunity
21.           resident flora not correct?
      a.               Their isolation along with pathogens in clinical samples would give better
          differential diagnosis
22.           Agglutination reaction is more sensitive than precipitation for detection of
    antibody..
      a.               Note soluble …go for antigen
      b.               Heterophile aniten test – for EBV
23.           which of the following agents may cause aseptic meningitis in immunocompro
      a.               c. neoformis
24.           lactose fermenting medium is mac Conkey’s agar
25.           an unculturable gram positive microorganism has been visualized in tissue
    specimens obtained from patients with a previously undescribed disease. Which of the
    following techniques would be most useful in identifying
      a.               PCR amplifications with DNA sequencing
26.           Pathogenesis of rheumatic fever is due to ….cross reacting
27.           all of the following viruses bellown to the picornavirus family
      a.               rhabodovirus
28.           Which antibiotic inhibits an extracellular step in peptidoglycan biosynthesis?
      a.               Penicillin
29.           a simple test used to determine whether a culture contains fimbriated bacilli is
    …hemagglutination test
30.           conjugation is the process by which the acquisition of ressitance occurs by a sex
    pilus….
31.           which of the following is not generally considered when selecting initial
    antimicrobial therapy for an infection
      a.               waiting for culture and susceptibility test results
32.           Ag presenting cells that activate helper t cells must express. MHC II proteins
33.           Carrier who acquires the microorganism from another carrier is known as a
    paradoxical carrier
34.           immediately after primary immunization which of the following phenomena
    would be expected to occur?
      a.               Production of immunoglobulin M antibody
35.           which pathogen is the agent for wool sorter’s diease?
      a.               Bacillus anthracis
36.           Acid fast staining of fresh stools revelaed oocytes…non bloody watery diarrhea
      a.               Cryptosporidium parvam
      b.               Note stronglyoides stercoralis – no oocytes only larval forms
37.           A 7yr old child had a sore throat…sheep blood agar yielded significant colonies
    that were sensitive to bacitracin
      a.               Gram positive cocci in chains, beta hemolysis, catalase –
38.           A 59yr old woman complained of pressure in the upper abdominal area that
    radiated to her chest. She stated that it often improved immediately after meals. She also
    noted occasional heart burn but denied nausea, vomiting or diarrhea
      a.               Urea breath test – for h.pylori
39.           A 61 yr old homeless alcoholic male was found sleeping on the street on a cold
    November night. When awakened he was incoherent and was brough to the emergency
    department. He had a fever of 40C and a production cough, along with the signs of
    malnutrition. He was noted to have foul smelling sputum.
      a.               Go for a gram stain
40.           rusty sputum and pleuritic left sided chest pain. Optochin sensitive
      a.               S. Pneumonia
41.           7 month old male presented with feer and severe vomiting followed by waterly
    diarrhea. Examination …EIA based viral stool antigen test was diagnostic
      a.               Rotavirus
42.           71 yr old…frequent bowel movement …undergone surgery for prostate
    hypertrophy…the patient’s diarrhea resolved after his broad spectrum antibiotics were
    removed
      a.               clostridium difficile
                rd
43.           3 degree burns (think Pseudomonas)…blue green pus…antibiotic resistance to
    most antibiotics
      a.               pseudomonas aeruginosa
44.           it is found in the plasma as a dimmer with a j chain..as it passes through mucosal
    cells i
      a.               IgA
45.           which of the following diseases is most likely to be caused by delayed
    hypersentitivity rxn?
      a.               Contact dermatitis
46.           members of the genus, mycobacterium stain better with the acid fast stain rather
    than gram stain
      a.               they have a large amount of lipid in their cell wall that prevents entry of
           crystal violet
47.           Regarding haptens, which of the following statements is correct
      a.               They cannot induce antibodies unless they are bound to a carrier protein
48.           A 40 yr old woman had blurred vision and slurred speech. She is afebrile. She is
    famous in her neighbourhood for the home – canned vegetables and fruits.
      a.               C. botulinum
                   i.          Note Crytococcus meningitis also has blurred vision
49.           culture in blood agar show beta hemolysis..inhibited by bacitracin
     a.               streptococcus pyogenes
50.           night sweats, chills, and fatigue varying intervals during the past 2 months. Began
    in latin America when eating unpastuerized cheese..small gram – rods.
      a.              Brucella spp
                 i.           Note listeria is most commonly seen in refrigeiated foods
51.           Which genetic mechanism increases the number of different antibody molecules
    during an immune response without increasing the diversity of the pool
      a.              Class switching
52.           Acute aseptic meningitis is diagnosed probably caused by enteroviruses.
    Enteroviruses are characterized by
      a.              Transmission primarily by the feco-oral route
53.           Several different viruses cause hepatitis. One of the following statements applies
    to all four viruses. HA, HC, HD, HE
      a.              Contains single stranded RNA genome
54.           Each of the following statements about M. Tuberculosis is correct except
      a.              Some stains isolated from individuals which previously untreated cases of
           Tuberculosis is resistant to isoniazid
55.           organisms that involve invasion of intestinal mucosa
      a.              Shigella sonnei
                 i.           Know the toxin mediated
56.           All are true about Mycoplasma pneumonia except
      a.              The organism cannot be cultured because of the absence of capsule
57.           Not a characteristic of histoplasmosis
      a.              Person to person transmission
58.           woman with Cystic fibrosis has a slight increase in her frequent cough and
    production of sputum. Gram – bacilli that form mucoid colonies…the bacilli are oxidase
    positive, grow at 42C having grape like odor
      a.              Pseudomonas aeruginosa
59.           Trachoma …is incorrect
      a.              Is readily prevented by a chlamydial vaccine
                 i.           TRIC – trachoma inclusion conjuctivitis
60.           which of the following is not associated with adenoviruses
      a.              carcinoma
61.           a 19yr old female had fever, sore throat and lymphadenopathy accompanied by
    lymphocytosis with atypical cells and an increase in sheep cell agglutinins
      a.              infectious mononucleosis
62.           Several paramyxoviruses can cause pneumonia in infants or children…which one
    has a vaccine
      a.              Measles virus
63.           which toxin inhibits ach release at the neuromuscular junction
      a.              clostridium botulinum toxin
                 i.           tetanus blocks the post syn receptors
64.           60 yr old with history of TB has a cough productive bloody sputum. Chest xray
    reveals round opaque mass within a cavity in his left upper lobe. Culture of the sputum
    grew an organism with septate hyphae
      a.              Aspergillous
  65.          All these intestinal pathogens after attaching to the surface of the epithelial cells
      go into cells and damage them resulting in inflammatory diarrhea except
        a.             Giardia lamblia
  66.          A 3 wk old infant is found to have a particular virus. The family doctor is
      specially concerned because the virus produces disease that is more severe if the infection
      occurs at a very young age. The infact most likely has
        a.             Hepatitis B virus
  67.          the most frequent cause of dysentery is
        a.             shigella sonnei
        b.             not in India though…shigella boyde
  68.          statements about pneumocystis jeroceci is correct except
        a.             can be prevented by administering penicillin orally
  69.          contact lenses and ulceration of the eye
        a.             acanthamoeba
  70.          C3b is involved in all the following except
        a.             Altering vascular permeability
  71.          SLE is associated with deficiency of
        a.             C1 and C 4
  72.          A baby born at 32 weeks…gram + rods
        a.             Listeria monocytogenes
        b.             Neisseria is gram –
  73.

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Micro session 1 tarun
Monday, February 16, 2009
4:47 PM

Micro Session 1 answers

  1.          SLE associated with def of  C1, C4
  2.          Complement lysis cells by  Insertion of compliment protein into cell membrane
  3.          Agglutination reaction inc sensitivity than precip rxn for Antibody
  4.          Resp. distress, unconscious after bee sting  IgE antibody (Type I)
  5.          CNS disorder, hemolytic anemia develops Cytotoxic (Type II)
  6.          Genetic def of C6  Niesseria bacteriemia or Niesseia gonrrheoa
  7.          Function of chemokines  Attract neutrophils to site of infection
  8.          Immune resp to hapten protein conjugate get anti hapten ab Protein be
      recognized by helper T cell (Levinson)
  9.          Comp. opsonization C3b opsonization fragment
  10.         Carrier acquires microorg by another Paradoxical carrier
  11.         Inc # of Antibody molecules without inc diversity of ag  Class switching
  12.         Hypersenstivity , hemolytic disease of newborn  Cytotoxic (Type II)
  13.         Physician induced infection  Iatrogenic infection
  14.              Hemolytic disease in newborn, maternal Antibody into fetal bloodstream  IgG
        antibody
  15.           Not true for Alternate pathway  Cannot be initiated unless C3 fragments are
      already present
  16.           Anaphylaxsis trigger by IgE receptor on  Mast cells
  17.           HS not be transferred with serum Ab. Type IV
  18.           Secondary immune respon  Class switching from IgM to IgG, IgG titer will rise
  19.           APC that act on Th expression MHC II
  20.           Nonphagocytic  B cell
  21.           True of class II MHC  Consist of DP, DQ, DR molecules (presents on APCs)
                   i. APCs Macrophages, B-cells, Dendritic cells (CD4+ Tcells)
       i.               Class I MHC  consists of A, B, C molecules (present on all nucleated
            cells) (CD8+ Tcells)
  22.           Role of macrophage in Ab Response  Process antigen and present it
  23.           Immunologic tolerance is not  Tolerance is not antigen specific (paralysis of
      immune cells results in failure to produce antigen)
  24.           Baby exposed to sister with chicken pox, baby acquired from mom in utero IgG
  25.           (not sure about this question) Loss of molec surface leads to loss of susceptiblitiy
      MHC I
  26.           Bld from flow cytometry, cell marker of B-Cell ?  CD19
  27.           MHC Class II role on donor cells in graft rejection  Recognized by helper T
      cells which activate cytotoxic T cells which kills donor cells (levinson)
  28.           Administration of DPT strain vaccine is ?? immunity  Artificial active
  29.           NK cells are  Able to kill viruses infected without sensitization (levinson)
  30.           Clinical infection leads to  Active natural immunity
  31.           No detectable B/T cells  Stem cell originating in bone marrow (levinson)
  32.           Inactivation of self reactive T cells because lack of costimulation  Clonal
      anergy
  33.           HLA genes strongly assoc wih Rheumatoid Artheritis  HLA-DR4 ???
  34.           Autoimmune with presence of autoab vs. acetylcholine  Myasthenia Gravis
  35.           M protein & myosin of cardiac is seen in rheumatic fever Molecular mimicry
  36.           Not a mechanism by which tumor cells escape immunosurveillance  Escape of
      auto reactive clone of T cells
  37.           C-Reactive Protein is an example of  Acute phase protein
  38.           Adaptive immune response characteristics  Clonal expression
  39.           Not true of NK cells  Derived from same lineage of T and B lymphocytes
  40.           Precipitation reaction converted to agglutination reaction on latex particles 
      Passive agglutination

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Session 1 Lecture Questions
Monday, February 16, 2009
5:16 PM




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Micro questions
Monday, February 16, 2009
5:20 PM

<Q>Complement lyses cells by
<C>enzymatic digestion of the cell membrane
<C>activation of adenylate cyclase
<C+>insertion of complement proteins into the cell membrane
<C>inhibition of elongation factor 2

<Q>A patient with a central nervous system disorder is maintained on the drug methyldopa.
Hemolytic anemia develops, which resolves shortly after the drug is withdrawn. This is MOST
probably an example of
<C>atopic hypersensitivity
<C+>cytotoxic hypersensitivity
<C>immune-complex hypersensitivity
<C>cell-mediated hypersensitivity

<Q>Individuals with a genetic deficiency of C6 have
<C>decreased resistance to viral infections
<C>increased hypersensitivity reactions
<C>increased frequency of cancer
<C+>decreased resistance to Neisseria bacteremia

<Q>Regarding the function of Chemokines in host defenses, which one of the following is the
MOST accurate?
<C>Chemokines bind to the T cell receptor outside of the antigen binding site and activate many
T cells
<C>Chemokines induce gene switching in B cells that increases the amount of IgE Synthesized,
thereby predisposing to allergies
<C>Chemokines penetrate the membranes of target cells during attack by cytotoxic T cells
<C+>Chemokines attract neutrophils to the site of bacterial infection, thereby playing a role in
the inflammatory response

<Q>The defence mechanism which is lodged against most extracellular bacterial pathogens and
viruses that infect through the respiratory tract and intestinal tract is
<C+>Antibody mediated immunity
<C>Immunity involving only macrophages
<C>Cell mediated immunity
<C>Immunity involving only PMNs.
<C>Immune surveillance by immature T cells
<Q> A three-year-old boy has had several bouts with pneumonia. The Streptococcus
pneumoniae organism was isolated and identified. The child was treated with penicillin and his
condition resolved. It was felt that he perhaps had some sort of immune deficiency. It was
determined his phagocytic mechanisms were intact. He had normal levels of immunoglobulins
but it appeared his complement system was not working correctly. The complement system is a
series of several different serum proteins that function to increase inflammation, lyse bacteria,
and opsonize (coat bacteria) for the purpose of phagocytosis by macrophages and other
phagoctyic cells. Which one of the following is the primary opsonization fragment in the
complement system?
<C> Factor B
<C> C5
<C+> C3b
<C> C5a

<Q> Carrier who acquires the microorganisms from another carrier is known as a
<C>Convalescent carrier
<C+>Paradoxical carrier#
<C>Chronic carrier
<C>Contact carrier

<Q> Which genetic mechanism increases the number of different antibody molecules during an
immune response without increasing the diversity of the pool of Ag receptor specificities?
<C+>Class switching#
<C>Somatic hypermutation
<C>Gene duplication like multiple V,D and J gene segments.
<C>Junctional variability due to imprecise V,D,J joining.

<Q> Regarding the function of Chemokines in host defenses, which one of the following is the
MOST accurate?
<C>Chemokines bind to the T cell receptor outside of the antigen binding site and activate many
T cells
<C>Chemokines induce gene switching in B cells that increases the amount of IgE Synthesized,
thereby predisposing to allergies
<C>Chemokines penetrate the membranes of target cells during attack by cytotoxic T cells
<C+>Chemokines attract neutrophils to the site of bacterial infection, thereby playing a role in
the inflammatory response ()




<Q> Which category of hypersensitivity BEST describes hemolytic disease of the newborn
caused by Rh incompatibility?
<C> Atopic or Anaphylactic
<C> Immune complex
<C+> Cytotoxic
<C> Delayed
<Q> Physician induced infection resulting from drug therapy or investigation procedures is
known as
<C>Reinfection
<C>Secondary infection
<C>Latent infection
<C>Subclinical infection
<C+>Iatrogenic infection

<Q> Hemolytic disease of the newborn caused by Rh blood group incompatibility requires
maternal antibody to enter the fetal bloodstream. Therefore, the mediator of this disease is
<C>IgE antibody
<C+>IgG antibody
<C>IgM antibody
<C>IgA antibody

<Q> Which one of the following is NOT true regarding the alternative complement pathway?
<C> It can be triggered by infectious agents in absence of antibody
<C> It does not require C1,C2, or C4.
<C+> It cannot be initiated unless C3b fragments are already present
<C> It has the same terminal sequence of events as the classic pathway.

<Q> Anaphylaxis can be triggered by cross-linking of IgE receptors on:
<C> Monocytes.
<C+> Mast cells
<C> B-cells.
<C> Neutrophils
<Q> Which type of hypersensitivity cannot be transferred with serum antibody?
<C> Type I.
<C> Type II
<C> Type III.
<C+> Type IV.

<Q>Which one of the following is correct about the secondary immune response?
<C+>Class switching from IgM to IgG will occur and the IgG antibody titer will rise.
<C>The IgM titer will rise above the IgG level for a period of 6 months
<C>The IgG titer will continue to fall and 1gA titer will increase due to class switching from
IgG to IgA.
<C>The IgM and IgG titers will continue to both rise during the secondary immune response.
<C>The IgM titer will continue to increase above its level of the primary immune response.

<Q>Reaction to poison ivy or poison oak is
<C>an IgG- mediated response
<C>an IgE- mediated response
<C+>a cell- mediated response
<C>an Arthrus reaction
<Q>A patient with a central nervous system disorder is maintained on the drug methyldopa.
Hemolytic anemia develops, which resolves shortly after the drug is withdrawn. This is MOST
probably an example of
<C>atopic hypersensitivity
<C+>cytotoxic hypersensitivity
<C>immune-complex hypersensitivity
<C>cell-mediated hypersensitivity

<Q> Ag presenting cells that activate helper T cells must express which of the following on their
surfaces
<C>Ig E
<C>Alpha interferon
<C>Class I MHC Proteins
<C+>Class II MHC Proteins #

<Q>The defence mechanism which is lodged against most extracellular bacterial pathogens and
viruses that infect through the respiratory tract and intestinal tract is
<C>Cell mediated immunity
<C+>Antibody mediated immunity#
<C>Immunity involving only macrophages
<C>Immunity involving only PMNs.
<C>Immune surveillance by immature T cells


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Micro quiz 3
Monday, February 16, 2009
5:20 PM




Inserted from: <file://F:\gurjit shit\Unmark2\sem 5\quiz No. 3.ppt>

								
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