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96 Cards in this Set

  • Front
  • Back
Antigen (Ag)
substance that can stimulate the immune system of an animal which reacts specifically with lymphocytes or their products (molecules on a pathogen)
Antibody (Ab)
serum protein produced by immune system in response to antigen presence "immunoglobulin"
primary cells of the adaptive immune system present in the blood stream and lymphoid tissue which react to the presence of specific antigens
Natural Host Defenses (active and passive)
Active - infection
Passive: maternal antibodies
Artificial Host Defenses
(active and passive)
Active - vaccination
Passive: immune serum- animal protein components given to people
Antigens : stimulators of the immune system
Large complex organic molecules, no repeating structure (DNA bad antigen repeating spiral)
Usually Protein or other molecules with protein
Must be foreign substance, found on surface of pathogen
Recognize pathogens by binding to antigens
T-lymph: T cell antigen receptor
B-lymph: Antibody IgD act as antigen receptor
Types of acquired immunity
Humoral immunity (antibody) B-lymph
Cell-mediated response, both very specific to antigen
population of lymphocytes able to recognize millions of pathogens
Functions of B-Lymphocytes
Primary defense against extracellular pathogens
Dont invade cells stay on surface
Specific B-lymphs recognize
Specific antigens produce specific antibody
Antigen recognition
Antibody (IgD)
Recognize Ag by iteslef (T-independent)
Require T-lymphs (T-dependent)
Cell changes metabolism
Plasma cell
B-cell making antibodies
Activated lymphocyte
Divide:identical copies
Produce antibody specific to antigen
Antibody structure
All same basic physical structure, chemical features.
4 polypeptide chains
Ends attach to antigen on microorganism
2 short -light
2 long- heavy
Held by disulfide bonds
Valency # antigen binding sites
Part of heavy and light
Body fluids
Lymph fluids
2 antigen binding sites
4 antigen binding sites
secreting component
surface of epithelial cells (intestinal) turn into plasma cells
10 binding sites
Better at activating complement system
First to appear after antigen stimulation
3 most abundant antibodies
IgA, IgD, IgM
hypersensitivity allergic reactions
surgace of lymphocytes
How do antibodies work
Attach to surface of pathogen due to antibodies specificity for antigen
Pathogen surface becomes coated with antibody
Antibody on pathogen surfaces causes
Activation of complement system- membrane attack complex
Agglutination: coat pathogen, clumping together multiple pathogen
Which antibody is the best agglutinator
igM 10 binding sites
How do antibodies affect viruses and toxins
antibody coats virus, no absorption step, easily phagocytized now
toxins loses physiological effect, neutralized when bound to antigen
Activation of antibody
complement fixation
Cell mediated immunnity
Function of T-lymphocytes
Primary defense against intracellular pathogens
Ab cannot get inside cells, need this
Also effective eukaryotic extracellular pathogens
T- cell effector
cytotoxic T-cells > (Cd-8 ells) > CTL cytotoxic lymphocyte
Specific T lymphocytes
recognize specifi cantigens > lymphocytes become activated (become effector)
Cytotoxic T-L cells
recognize cells with intracellular pathogens
Kills entire cell
Infected host cell as Ag on surface associated with Class I MHC molecule> other proetin on surface of cells > associate with Ag (MHC signal for antibody to recognize)
Immune System Effectors - How cytotoxic cells work
Cytotoxic T- Lmphocytes
Once bound to infected cell or large pathogen, lymphocyte proudces chemicals called lyphotoxins
Lymphotoxins act on infect cell/pathogen
Disrupt cell membrane of infected cell - leaky , lysis
Disrupt metabolism : enters host cell
Initiate apoptosis : turn on preprogrammed death
Infected cell and pathogen killed
Antigen Presenting Cells (APCs)
Certain phagocytic cells (primary macrophages)
engulf entire pathogen > digest pathogen > process
Antigen: presents antigen on its surface > makes available to other cells (associated with class II MHC molecule on surface of APC)
Makes it easier for T-helper cells to recognize the antigen
T- helper cells
Type of T-lymphocte (CD-4 cell)
TH1 helper cytotoxic CD-8 cells
TH2 helps B-lymphocytes
Produces chemicals (lymphokines) which stimulate other lymphocytes
Macrophage presents antigen (what happens APCs)
T helper 2 boost humeral response : antibodies
T-helper 1 helps B lymphocytes
IL -interleukin
IL-1 produced by macrophage when engulfs pathogen
Activate signal for helper cells
Binding of T-lymphocyte to antigen > furthers activation
Interleukins produced
Tells B-Cells to divide and differentiate into plasma cells that make antibodies
Cell Mediated Line
1st and 2nd activation
1st -T helper cells activation by interleukins
Secretes lymphokines
Interleukins activate cytotoxic cells
2nd- infected cells display antigen with MHC1 Molecule
Cytotoxic lymphocyte fully activates
Binds to infected cells makes cells die
Immune Aoidance Mechanisms
Pathogen outsmarts cytotoxic cells
Rapid reproduction :esp. bacteria cells
Prevention of phagocytosis: due to capsule
Bacteria which prevent phagocytosis due to capsule
Keebsiella pneumoniae, Streptococcous pneumoniae
Survival within phagocytes
Mycobacterium tuberculosis (mycolic acids)
Trypanosoma cruzi (chagas Disease)
Chagas Disease
Trypanosoma cruzi (chagas Disease
Intracellular pathogens
Rickettsia and Chlamydia
Changing antigens
Bornelia hermsii (Relapsing fever)
Trypanosoma bruceii (sleeping sickness)
Relapsing fever
Bornelia hermsii
Sleeping sickness
Trypanosoma bruceii
Immune response curve
explains how the immune systems reacts to Ag overtime
Helpful for understanding how active immunization functions
Helps anser:
Why after having a particular infectious disease you are immune from getting same disease later
Introduce new type of immune system cell - memory cell
Primary response : 1st exposure to antigen
Lag period/ latent period : no antibodies produced > interleukins produced
Antibody goes up... goes down
Secondary response: 2nd exposure
No latent/ very little period
Dont disappear as quickly formed quicker
Quickness of formation prevent symptom formation
Memory Cells: IgM
patially activated , dont produce, some turn into plasma cells> make IgG
Active immunization
Ag preparations given to person > guives 1st exposure without pathogen harm, primary response
Requires person to form an immune response
Takes time to develop
Long lasting
used as preventative measure
Passive immunization
Administration of antibody molecules : preformed part of animals immune system
Does not require person to form an immune rsponse
Works immediately but short lasting
Primarily used as treatment
Whole vaccines
Killed/inactivated viruses nonliving > cant be killed> not pathogenic
Pathogen subjeted to chemical or radiation treatment
Antigens inactivate but pathogen destroyed
Advantages - safe cant produce symptoms of disease
Disadvantages - requires larger dose or more frequent application, adverse reaction to other materials in vaccine
Examples pertussis,typhoid cholera
Whole vaccines (examples)
Pertussis, typhoid cholera
Live/attenuated vaccine
PathPathogen made avirulent by modifying growth conditions in the lab
Active but cant cause symptoms of the disease
Antigen intact AND pathogen may be capable of replication
Advantages: produces strong immune response, less adverse reactions because of organism itself
Disadvantages : possible mild symptoms, might revert back to virulent form, transmissible
Examples: Poliio (oral, measles, mumps, rubella
Live/attenuated vaccine examples
Polio (oral), measules, mumps, rubella
Acellular vaccines
subunit vaccines
Contain only antigenic portion of the microbe
Bacterial capsules, cell walls, etc
Some produced through biotechnology
Contain only the single antigenic molecule
Advantages: Fewer adverse reactions, Good/exellent immune response
Disadvantages: newer vaccines, expensive.
Examples: Pneumococcus (bact. infection, HIB (bacterial infection, Hep B
Acellular vaccines examples
Pneumococcus bact. infection, HIB bact. infection, Hep B
Toxoid vaccines
Chemicall denatured pathogen Toxin
Nontoxic and stimulate immune response
Examples tetanus (neurotoxin), diphtheria (bacterial infection)
Complimentary vaccine (...pertussis)
Passive immunization Uses (animal antibody)
Post exposures preventative (treatment after known exposure-hep B, rabies)
Treatment for disease:
Therapy for immunocompromised patients
Treatment of disease due to toxins -Tetanus, Botulism, snake venom
Chemotherapeutic drug
a chemical used in the treatment of a disease
Antimicrobial druge
a chemical used in the treatment of infectios disease
a type of antimicrobial drug which is a natural product of a living organism
First antibiotics isolated from fungi and bacteria
The major drugs used to treat bacterial infections
A few work against protozoa, not antiviral
Antibiotics (cont.)
Many types are synthesized in labs
Penicillin- first antiviotic
First antibiotic
Isolated from the fungi penicillin in 1930s by alexander fleming
purified and used as a drug in 1941
Impact of antibiotics
Civil war > 66% deaths for infectios disease
WWi > 54% deaths from infectios disease
WWII> 28 %
Properties of antimicrobial drugs
Selective toxicity human cells > little effect; microbes> large effect
Must be able to reach infected site
must remain active at infected site
general modes of antimicrobial agents action
Static effects: drugs inhibit growh and replication of microbe, patients immune system kills remaining microbes
Ex. tetracycline

Cidal Drugs: Drug kills the microorganism, often dose dependent
Ex. aminoglybins
Antibacterial drug target sites
Cell wall, DnA, cytoplasm, cell membrane, ribosome: protein synthesis
Cell wall disruption (antimicrobial drugs modes of actions)
Most work by interfering with production of peptidoglycan
Work best on young actively growing cells
Examples : Penicillin, prevents protein crosslinks from forming. Bacitracin, prevents subunits from being transported
Nucleic Acid Disruption (antimicrobial drugs modes of actions)
Inhibit synthesis of nitrogenous bases
Folic acid an essential compound in the synthesis of nitrogenous bases> Drugs interfere with the production of foli cacid
Examples: sulfanamides (sulfa drugs): synthesized chemical, not only one antibiotic
Example: trimethoprim
Sulfa drugs are analogs of PABA > incorporates into folic acid molecule
Sulfanilamide competes for active site of enzyme for folic acid synthesis
Inhibit the unwinding of DNA molecule, block bacterial enzyme used in unwinding DNA gyrases
Examples quinolones
Inhibit RNA polymerase -ex. Rifampin
Protein Synthesis disruption (antimicrobial drugs modes of actions)
Drugs act on the mDNA >ribosome complex
Drugs which bind to 30S subunit
>aminoglycosides: cause misreading of the mRNA
>Tetracycline: block attachment of tRNAs
Drugs that bind to 50s subunit
>Chloraphenicol >prevents peptide bond formation
>Erythromycin (macrolide) prevents movement of ribosome along mRNA
Selective toxicity because different sites of ribosomes of humand and bacteria
Cell membrane disruptions (antimicrobial drugs modes of actions)
Because of similarities between all membranes, drugs tend to be more toxic
are effective against all age cells and relatively inactive cells
> Polymixins: disupts membrane surface by interacting with phospholipids of gram negative bacteria
> Polyenes: form complexes with sterol lipids in fungal cell membranes > abnormal openings
Antiviral Drugs
Selective toxicity hard to obtain (drugs that effect viral replication dirupt living cells)
> viruses are not living but rely on living cells to replicate
No definitive treatment for viral infection ( no antiviral drug by itself can elimainte a patients viral infection) > slow viruses so persons immune system can heal self
Antiviral drugs viral uncoatin
includes durgs to treat influenza
Antiviral drugs slow disrupt neulceic acid synthesis
includes nucleic acid analogs
includes drugs to treat herpes and HIV infections
Inhibit assembly and release of virus
> includes protease inhibitorts to treat HIV
Antimicrobial Drug Resistance
The ability of microorganisms to resist the effect of certain drugs
Microorganisms develop particular mechansim over time
new drug > little or no resistance
As drug used > more and more microbes become resistance
How do microbe acquire drug resistance ? mutation
Rapid reproduction of bacteria can produce beneficial mutations
acquiring the trait from another microbe already resistant to the drug ( intermicrobial gene transfer)
Mechanisms of drug resistance
Synthese of enzymes which degrade the drug
> beta lactamase ( a penicillinase degrades penicillin
produced by staphylococcus
Changing drug receptor sites
> binding site on ribosome altered (macrolides cant attach to ribosome
Increased elimination of drug
> bacteria increase number of efflux pumps or alter pumps
Decrease in cell permeabililty/uptake
> Altering porin proteins in outer membrane of Gram negative
Alterig metabolic pathways
>if pathway blocked by drug, bacteria develops attenuated path
Multiple drug resistance
Microbes resistant to more than one antibiotic
Certain mechanisms of restance work against multiple antibiotics
Example: an efflux pump may be able to remove several types of antibiotic from bacteria
Example: a change in proins may keep several antibitotics from entering cell
Some isolates of certain bacterial species are resistant to all available drugs
Preventing rthe spread of drug resistance
Use antimcrobial drugs only when indicated
Reserve potent antimicrobials for serious infections
Use proper dose and treat for apporpriate length of time
Limit use as growth additive for food animal proudction
-animals grow if given cheap antibiotics but makes vulnerable to exposure to bacteria
Cocci of Medical Importance
Genus Staphylococcus
Genus Streptococcus
Genus Enterococcus
Gram negative
Genus neisseria
Genus Staphylococcus
Graqm positive, major cause of nosocomial infections 15-20% of all infections
Nosocomial infections
Staph contributes to all categores
Staph imporatnt in many categores
-Pneumonia :15-20%
Surgical site infections 35%
Staphylococcus - relevant species
Staphylococcus aureus
methicillin resistant staphylococcus aereus (MRSA)
coagulase negative staphylococcus (CoNS0
S. auerus strain with multiple drug resistnatce
Once established in a clinical setting hard to eradicate
More virulent
Special procedures needed to prevent spread
Coagulase negative staph
Not as pathogenic as S. aereus
Some species normal skin inhabitants
Problems with
- surgican sites, indwelling devices (IV), causes septicemia
Genus Streptococcus
Gram Positive, fastidious, sensitive to many antibiotics
Genus Streptococcus major Pathogens
Streptococcus pyrogenes - strep throat
causes wide variety of diseases
-skin infections, reproductive tract (puerperal fever)> post preg moms
Strep throa
- Rheumatic Fecer ( strep then immune system attackes connective tissues, heart valves) Scarlet fever (toxins made y staph > red skin rash), glomerulonephritis
Streptococcus pneumonia
5-50% of persons normal nasopharynx flora
Pneumococcal ppneumonia
70% of all bacterial pneumonia, most fatalities in elderly or compromised patients
Streptococcus pneumonia
Otitis media (chronic middle ear infection), sinusitis, upper respiratory infections
-common cause : infants, young children
- 30-45% of cases due to strep. pneumoniae
-Penicillin derivatives used for treatment
-17% resistance in S. pneumonia (beta lactamase production)
-Surgical treatment, puncture eardrum and drain
Genus Enterococcus
Gram positive
previously classified in genus streptococus
GI tract commensals, opportunistic pathogens
important and growing cause of nosocomial infections
Genus Neisseria
Gram negative
Diplococci (paired cocci) sometimes beaned shaped
Most species straict pathogens some commensals
Fastidious adn grow best under lots of CO2
Genus neisseria important species
Neisseria gonorrhea (book)
Neisseria Meningitis
-Meningococcal meningitis
-serious infection of lining of the nervous system
-symptoms headache, stiff neck, fever , delirium, convulsions
-disruptions of blood vessels-hemorrhage
-15% mortality with treatment
treatment - penicillin G, other antibiotics
Prevention: vaccine for high reisk groups, epidemics, prophylactic antibioti sc
Bacilli of medical importance
Gram Positive:
-Genus bacillus
Genus Clostridium
-Genus mycobacterium
Gram negative:
-Family enterobacteracea most commensals in intestinal tract
Genus Bacillus
Gram positive
Aerobic spore formers
most sprophytic (organic matter from decaying things), very common in soils and water
Bacillus anthracis antrax
Zoonotic disease: cattle, sheep, goats
Transmission endospores
Wounds/abrasions in skin: eschar lesions (black lesions, raised rims)
Inhalation: very fatal form
Ingestion: rare form, very fatal
Biological warfare bacterium
Genus Clostridium (bacilli)
Gram positive
anaerobic spore formers
many sprophytic soils water
some commensals intenstinal tract
active fermenters
some produce potent toxins
Gas gangrene
C. Septicum and others > cutaneous/subcutaneous infections
Caused by mutlsiple species of Clostridium and once
C. Septicum
- Infection of serious wounds, occasionally surgical sites
- Wounds often deep contaminated with debris (anaerobic conditions)
- Dead tissue , anaerobic conditions spores germinate in tissue
- Gas produced during fermentation builds up in tissues
Bacterium proudce - several toxis and enxymes, gas
- subcutaneous and muscle tisse killed- anaerobic conditions-incread bacterial growth- more tissued destroyed
Treatments : potent comibinaton of antibiotics 02 therapy
-Broad spectrum, --cephalosporins, penicillin
-Hyperbaric o2 therapy
Thorough celaning of wound
prophylactic antibiotics