Immunology Midterm Flashcards

(110 cards)

1
Q

What is the difference between innate immunity and acquired immunity?

A

Innate: defense mechanism from birth. Often non specific (ie skin)

Acquired: defense mechanisms acquired by exposure to specific pathogens

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2
Q

What are the three lines of defense? What are examples?

A
  1. First - surface protection - anatomical (cilia), physiological (skin), genetic (32bp deletions), non specific chemical barriers (stomach acid)
  2. Cellular and more specific chemical barriers - enzymes, phagocytosis, inflammation, fever
  3. Specific Immune responses - B&T lymptocytes
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3
Q

What is the mucociliary escalator/ blanket?

A

System of defense found in the trachea. Involves epithelial tissues (physical), mucous secreted to trap particles (chemical) and cilia to sweep mucous out of the trap (anatomical)

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4
Q

What are some examples of first line behavioural barriers?

A
  1. Hygiene - handwashing, avoiding sweage
  2. Contagion avoidance
  3. Healthy lifestyle choices
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5
Q

What are some examples of first line physical barriers?

A
  1. Skin - can be breached. If so, increases risk of entry
  2. Mucous/ Wax - lines POE to prevent entrance of pathogens
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6
Q

What are some examples of first line chemical barriers?

A
  1. Acid - stomach acid, lactic acid in sweat
  2. Salt - in tears or sweat
  3. Proteins - lysozymes and defensins in tears, digestive ensymes
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7
Q

What are some examples of a first line genetic barrier?

A

HIV-1 (R5) partially requires CCR5 cells to infect.

Some caucasians have a 32pb deletion which can lead to partial resistance to infection

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8
Q

How does H. Pylori overcome first line defenses?

A

Physical - overcomes physical by using flagella to burrow into the mucosal layer of the stomach

Chemical - once inside the mucosal layer, releases a basic substance to neutralize the stomach area

Genetic - h. pylori has adapted to survive in the human stomach

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9
Q

What cells are not part of the innate system?

A

B & T lymphocytes

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10
Q

Where are WBCs found in the body?

A
  1. Blood stream
  2. Lymphatic vessels
  3. Reticuloendothelial system - meshlike network of connective tissue that holds the tissue together
  4. extracellular fluid
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11
Q

What is the difference between plasma and serum? What is the buffy coat?

A

Plasma - blood without protein or cells (Cloudy)

Serum - plasma minus the clotting factors (clear)

Buffy coat - WBC layer (white)

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12
Q

What are platelets, mast cells, basophils, eosinophils, neutrophils and monocytes?

A

Platelet: clotting cells

Mast / Basophils: inflammation / allergy

Eosinphil: Fungal/ parasitic infection

Neutrophil/ Monocyte/ Macrophage: Phagocytosis

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13
Q

WHat are characteristics of neutrophils?

A

Most abundant WBC - 55-95%

Filled with digestive granules

Eats invading microbes

Has multiple nuclei - visible when stained

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14
Q

How do WBCs recognize foreign cells?

A

WBCs “feel” the surface of every cell they encounter using pattern recognition receptors

PRPs recognize abnormal proteins on foreign cells aka Pathogen associated molecular patterns

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15
Q

What are the special pattern recognition receptors on phagocytes?

A

Toll-like receptors

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16
Q

What is the process of phagocytosis?

A

  1. Pattern recognitions receptors recognize pathogen associated molecular patterns 2. Phagocytic cell engulfs the pathogen 3. A bubble forms around the pathogen = phagosome 4. Lysosome store digestive enzymes and chemicals. Stored in granules. Fuses with phagosomes 5. Fused phagosome + lysosome = phagolysosomes 6. Digestion and nutrient absorption into the celll 7. Water is excreted from the cell via exocytosis
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17
Q

How are oxygen dependant intracellular killing mehcanisms different than oxygen independent mechanisms? What are examples of each?

A

Oxygen dendent - require O2 to form reactice toxic species. Reaction occurs inside granules. ie OH radicals, hydrogen peroxide, hypochlorite. Can cause DNA instability. Oxygen independent mechanism - ie Electrically charged proteins - damage membrane of bacteria, fungi or yeasts Lysozomes - damage cell wall Lactoferrins - compete for iron binding proteases - digest and degrade proteins

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18
Q

what are characteristics of thrombocytes?

A

anucleated, fragment of megakaryote Aggregate to seal up fissures in blood vessels and skin to form clots

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19
Q

What is the difference between chemokine and chemotaxis?

A

Chemokine is an attractive chemical signal to attack other WBCs chemotaxis - movement of WBC along the chemokine gradient

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20
Q

What are the characteristics of macrophages?

A

Can digest more than neutrophils Attracted by chemokine released by neutrophil movement by chemotaxis Somewhat specific Have granules promotes cytokines and inflammation Mature form of monocytes

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21
Q

what are characteristics of eosinophils?

A

Granulocytes targets fungus and parasites that are too large to consume Secretes peroxides, lysozymes and other toxins into the invader release cytokine

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22
Q

what are characteristics of mast cell and basophils?

A

release cytokines stored in granules weakly phagocytic Basophils = circulate. Mast cells - in tissues.

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23
Q

What are cytokines? examples?

A

Large class of chemical messnegers which coordinates vasoactive or chemoactive effects of inflammation

ie Histamine (released immediately after exposure to allergen) prostaglandins (synthesis starts when allergin detected) Cuases inflammation

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24
Q

What are classic signs of inflammation?

A

redness - increased circulation and vasodilation,

warmth - heat from increase blood flow

swelling - fluid in circulation assumulates in tissue

pain - nerve endings stimulated

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25
What are vasoactive cytokines?
1. histamines - formed by basophils. Pre-stored in granules Act rapidly 2. Prostaglandin- formed from basophils. Made as needed. Slow acting 3. Serotonin - involved in intestinal movements. Secreted by platelets to induce clotting 4. bradykinin - increase the sensation of pain
26
What are the events of inflammation?
1. **Margination** - WBCs to edge of capillary in areas which have **intercellular adhesion molecules** (ICAMs) expressed 2. **Diapedes** - endothelial cells shrink. Makes opening for WBCs to exit 3. **Chemotaxis** - WBCs are pulled to the site of infection following the cytokine gradient
27
What are examples of chemotactic factors?
**Elements of pathogens or toxin**s: endotoxin, PAMPS **Signals of infection**: platelet activating factor, secreted chemotactic factor
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What is TNF?
Tumor necrotic factor: Made by mscrophages, B & T cells. Increases chemotaxis (attracts more WBCs to area), phagocytosis (increases tastiness of pathogen) and pyrogen (too much may cause fever)
29
What is interferon?
Made by leukocytes and fibroblasts. Anti-viral or anti-tumors
30
What are the different types of interleukins (1, 6, 8, 12)
1. Macrophages/ epithelial cells - causes vasodilation, B&T cell activation, pyrogen 6. macrophage, B&T cell, fibroblast - B&T cell activation, pyrogen 8. Macrophage / epithelial cells - non pyrogenic, chemotactic 12. macrophage - non pyrogenic, activates NK cells and T helper cells
31
What is a niche?
a compartment with unique properties (ability to survive in a temp, pH or with certian nutrients
32
What are the differences between commensalism, mutualism and parasitism?
Commensalism - organisms that benefits from another without harming the host (normal microbiota, indiginous microflora) Mutalism - two organisms cooperate to both benefit (cows and bacteria to digest grass) Parasitism - one organ benefits at the expense of another
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What is the process of colonization in a new born?
Baby is sterile until birth until baby comes into contact with microbes during delivery Colonization (90%) within 8-12 hrs
34
What bacteria are related to bottle feeding vs breast milk?
Bottle feeding: coliforms, lactobacilli, enteric streptococci, stapylococcus Breast feeding: bifidobacterium
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What is the process of colonization?
1. Contact - microbes adhere to the body surface 2. Colonization of microbiota 3. Invasion - erode lines of defense and enters sterile tissue 4. Infection - pathogenic material multiplies in tissues. May causept to become asymptomatic carrier, may allow the defenses to fight off the infection or destruction of tissue occurs
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What is microbial antagonism?
When "good" microbes defend humans against harmful pathogens
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What are the differences between pimary pathogens and oppotunistic ones?
Primary - likely cause disease when infecting human with normal immune system Opportunistic - cause disease in immunocompromised pts but not usually healthy ones
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What is pathogenicity?
The capacity of a microbe to cause disease
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What stage does pathogenicity generally occur?
During invasion (vibrio cholerae) or infection
40
## Footnote What is the complimentary system? Where is it produced?
## Footnote A complex of proteins which results in a porous membrane of a pathogen. Second line of defense. Inactive proteins are produced in the liver
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## Footnote What is an acute phase protein?
## Footnote A protein that increases significantly during the early stage of inflammation. Part of a positive feedback loop
42
## Footnote What are the three pathways of the complementary system?
## Footnote 1. Classic pathway - antibodies and proteins combine to activate C3. Rapid and specific 2. Sugar on the surface of pathogen - mannosee binding lectin binds to mannose on pathogen cells. Mannose not found in humans. Nonspecific for bacteria and viruses 3. Alternative - C3 binds to pathogens directly (viruses, bacteria, fungi, viruses) All these pathways activates C3
43
## Footnote what happens when c3 is activated?
## Footnote C3 is broken down into C3a (inflammation) and C3b (phagocytosis) C3b activates C5 C5 is broken down into C5a (inflammation) and C5b (oponisation) C5b is the start point for the formation of a MAC complex
44
## Footnote what is a membrane attack complex and how is it formed?
## Footnote Proteins which create a pore in a pathogen's membrane C5b causes C6, C7 and C8 to bind to the pathogen membrane. induces C( to form a pore through membrane. One pore may not destroy cell, but several will
45
## Footnote what is opsonization and opsonin?
## Footnote Opsonization: enhanced phagocytosis - cell is made more delicious Opsonin- any protein which opsonizes cell (C3b, C5b)
46
## Footnote what properties of complement factors make the complement fixation test possible?
## Footnote Complement factors are destroyed 56 degrees C and antibodies are not
47
## Footnote How can the complement fixation test be used to determine flu strains?
## Footnote 1. Serum from the patient is isolated. It is heated to destroy the compliment proteins; however, the natural antibodies are still intact. A pre-measured amount of compliment factors are added to the blood. 2. Pre-processed sheeb RBCs (sRBCs) have sRBC antibodies on them are added into the pt serum 3. Antigen of question is added to the serum. 4. If the test is positive. The serum will remain red, because the compliment factors have formed complexes with the antibody and antigens. If the test is negative it will be pink because the factors cannot fuse with pts antibodies, and instead form complexes with the sRBC antibodies causing the RBCs to lyse
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## Footnote What is virulence?
## Footnote the degree of harm caused by a pathogen
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## Footnote What are virulence factors?
## Footnote intrinsic characteristics of a pathogen which can cause harm
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## Footnote What is the infectious dose?
## Footnote Minimum number of microbes required to cause illness
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## Footnote What is lethal dose?
## Footnote the minimal number of microbes to cause death
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53
## Footnote what is ecoli O157? ID and VR?
## Footnote infects lower intestine. Pathogenic strains aka food poisoning. Produces tocins to break down gut lining ID: 10 or more cells VF: toxins, rapid growth, ability to enter gut
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## Footnote what is vibrio cholera? ID and VF?
## Footnote Found in the small intestine and aquatic environments. Produces toxin whichdraws salt and H2O which causes severe diarrhea ID: 10^6 - 10^11 VF: toxins
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## Footnote ID 50/50
## Footnote Minimum amount of microbe required to infect 50% of the population
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## Footnote what is LD 50?
## Footnote amount required to kill 50% of a given population
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## Footnote What are different virulence factors?
Adhesion Immune Evasion - anti-phagocytic factors, physiological, immunocompromised Invasiveness - extracellular enzymes, toxins, invasion factors toxins - endotoxins & exotoxins Nutrient Competition genetic
58
## Footnote What are the differences between bacterial and viral adhesion?
## Footnote Bacteria: capsules - slimy, sticky outer layer (molasses) & fimbrae - sticky hair like structures that stick to almost all surfaces Virus: glycoproteins adsorb to cells because of specific interactions with cellular proteins (aka - receptors) ie HIV specifically adapted to fit Cd4 receptors inside of neutrophils. Hemagglutinin - protein spikes of influenza bind to surface of respiritory tract
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## Footnote What are evasie anti-phagocytic virulence factors?
## Footnote 1. Capsules - slimy layer prevents phagocytosis by covering PAMPs and making it difficult to eat 2. toxins - offensive defensive technique 3. Leukocidins - toxins that directly kill WBC (type of toxins) 4. Intracellular microbes - hide inside host cells by secreting molecules to make it easier to enter ie TB, Malaria
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## Footnote How do microbes surpass host physiological barriers?
## Footnote ie hpylori. Uses flagella to burrow into mucosa and releases urease that produces ammonia making the environment basic Urea + H2O + urease = CO2 + Ammonia
61
What are the differences between the development of B & T cells?
B: mature in the bone marrow T: mature in the thymus
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What are antigen presenting cells?
Cells which display the antigens of phagocytized pathogens on the surface using the MHC II protein complex Neutrophils, macrophages, T & B cells
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What are antigens?
A specific molecule (protein) which can be used by the immune system to identify a specific pathogen Evokes the production of Ab Substances which bind to lymphocyte receptors
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What happens when B cells encounter antigens? When T helper cells? Cytotoxic cells?
B-cells - makes antibodies T helper cells - activate B cells or cytotoxic T cells using cytokines Cytotoxic T cells - phagocytize cells
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What are the different between memory and effector cells? What are examples in B & T cells?
Memory - immunological memory of diseases Memory B cells & Effector B cells (Plasma B cells) Memory T cells & Effector T cells (helped & cytotoxic)
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What are the jobs of antibodies?
1. Agglutination: Antibodies stick together causing the target to clump 2. Neutralization: Bind to the suface of a pathogen and toxin and prevent it's function 3. Opsonization: make pathogens more likely to be digested 4. Complement activation
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What is the difference between MHC I and MHC II?
MHC I recognizes changes in genes inside of cells (degraded proteins). Works for all nucleated cells. Detects tumors, intracelllular viruses (HIV) and intracellular microbes (Malaria) and stimulated Tc cells MHC II - antigen presenting cells (neutrophils, macrophages & B cells). Recognizes peptides from phagocytized pathogens and exotoxins. Detect microbes, EC viruses and EC exotoxins. Stimulates Th which may cause Tc or B cell response. Stronger response = more sensitive
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What are epitopes?
The segment of an antigen which is specifically recognized by lymphocyte receptors (receptor has oposite shape of epitopes) 3D receptor sequence of 4-6 amino acids
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What are immunogens?
Agents which can provoke and immune response and react with the products of such responses All immunogens are antigens but not all antigens are immunogens
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When are antigens not immunogens? How can they become immunogens? Whar are examples?
1. When they're too small (haptens). Can be bound to larger molecules to cause immuno response. (sugars, drug metabolites, amino acids) 2. When they are too similar to normal cellular proteins (Streptococcus pyogenes - has cell surface proteins which mimic human proteins) 3. When they have static (unchanging) structures ie lipids or globular proteins 4. When they have a highly repeating structure (starch, glycogen)
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What don't structures similar to cellular proteins cause an immunologic response? How does S pyogenes take advantage of this?
If T/B cells reacted to structures similar to the body, it could cause an auto-immune reaction S pyogenes has surface proteins similar to human proteins
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What is cross reactivity?
When the immune system recognizes that a pathogen has proteins similar antigens to human cells, it makes antibodies These antibodies may attack normal cells while trying to attack the pathogen
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What are the intrinsic and extrinsic factors which determine an antigen's immunogenicity?
Intrinsic 1. Chemical composition 2. Size 3. Complexity 4. Genetic Disparity 5. APC processing Extrinsic 1. Adjuvants
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What is more immunogenic? Proteins or lipids? Why
Proteins are more immunogenic than carbs. Lipids are not immunogenic All cells have a lipid bi-layer. If lipids were immunogenic, it would cause a mass reaction
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What is more likely to cause an immunogenic response? Larger or smaller molecules
Larger (100,000 MW)
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What cell structures are more liekly to cause an immunogenic response?
Linear hydrocarbons are less immunogenic than aromatic ring structures
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What are hospitals scent free zones?
If patients are hypersensitive, they are more liekly to be hypersensitive to scents because of the aromatic compounds. Avoiding use of any scents can prevent this.
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What is serum sickness?
Old practice making antibodies involved exposing the horse to botulism toxin. The horse generated antibodies from toxin. Serum from the horse was administered to humans as anti-toxin However, the immune system recognized the serum as foreign antigen, and attacked in the serum. Those injected experiences skin eruptions, fever, joint pain,
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What is the difference between autograft, isograft, allograft and xenograft? Which is the best to use?
Autograft: from self Isograft - from twin Allograft- from an unrelated person Xenograft- from animal Closer to self is best because the body is less likely to recognize it as foreign
80
What are different methods to have autologous transplants?
1. Umbellical cord blood banking - cord has hematopoetic stem cells 2. Autologous Bone Marrow Transplant - bone marrow harbest during remission and stored, during relapse can receive their own bone marrow 3. Autologous blood transfusion - remove blood a month before surgery, its on hand
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What are autoantigens and alloantigens?
autoantigens - modification of normal proteins causing stimulation of an autoimmune response which causes normal proteins to be recognized as an antigen alloantigens- antigens derived from other people (MHC I)
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What are heterophilic antigens?
Two different pathogens with similar antigens which can be mistaken for each other ie syphilis and lupus Cardiolipins are found on the syphilis bacteria. Syphilis is tested with anti-cardiolipin Lupus, cardiolipins are auto-antigens therefore if tested with anti-cadiolipins, the antibodiy enters the cell
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What are adjuvants?
External factors which can make a substance more immunogenic ie - alum (aluminum hydroxide), oil & water emulsion
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What are immunoglobulins?
Specialized receptors on the surface of B & T cells
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What is VJD recombination?
Formation of unique immunoglobuins by the random selection of variable, diverse and joining genes. The combinations are all different New clones
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What is the difference between active naturally acquired immunity and artificially? Passive naturally acquired and artificial?
Active - the body is exposed to an immunogen that stimulates the immune system. Stimulates memory * Natural - body exposed to pathogen * Artificial - exposure after vaccine Passive - individual receives protective immune products but doesn't retain the memory after products cease * Natural - breast feeding or placenta * Artificial- premade antibodies in serum
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What are the different sources which antigens are produced
1. Inactivated/ Killed pathogen 2. Attenuated pathogen 3. Purified molecules 4. Recombinant protein
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How are killed/ inactivated pathogens produced? Which vaccines are produced this way? What are pros and cons?
Pathogen is killed by heat, radiation or chemical treatment ie polio, influenza Pros: almost always dead and safe Cons: Does not multiply, higher dose required. May require booster shots, might not be completely dead
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How are attenuated pathogen produced? Which vaccines are produced this way? What are pros and cons?
Pathogens grown in lab conditions so they aren't as virulent in humans ie - TB, oral polio vaccine Pros - multiplies somewhat, confers long lasting protection Cons - Risk for reversion
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How are purified molecules produced? Which vaccines are produced this way? What are pros and cons?
Fragments or purified components of pathogens are used rather than living organisms ie anthrax, hepatitis B Pros - no living pathogen Cons - antigen may change shape during purification
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How are recombinant proteins produced? Which vaccines are produced this way? What are pros and cons?
DNA encoding the protein of a pathogen is expressed in yeast ie - Hepatitis B Pros - cheap, safe Cons - clonal, pathogen can evolve resistance easily (only one protein is represented)
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What is heard immunity?
Large scale immunization campaign which targers the at risk population. Used to prevent epidemics by estabilshing a high level (over 95% of the people in the population) of immunization
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What are exoenzymes? what are diseases which cause the following? Mucinase Keratinase collagenase hyalurondiase coagulase
Enzymes secreted by certain pathofens to help disrupt tissues and enter into them further Mucinase - disrupts protective mucous membranes - dysentry Keratinase - ringworm Collagenase - digests connective tissue - clostridium Hyal - digests acid which cemesnts tissue - flesh eating Coagulase - prevents clotting - staphlococci
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What are different invasive virulence factors?
1. exoenzymes - invades between tight junctions of cell (black plague) 2. Toxins to kill surface endothelium cells - ecoli 3. secretion systems - salmonella
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## Footnote What are the differences between endotoxins and exotoxins?
Endotoxins are non specific lipopolysaccrides from cell wall. Have systemic inflammation effects but require higher doses for cause. Released from cell wall after lysis ie - meningitis, salmonellosis Exotoins are small proteins which are specific to a cell, and only a small amount can cause reactions. Effects are dependent on which cell is targeted. Secreted from live cells ie - tetanus, anthrax, cholera
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What are the effects of endotoxins on humans?
Fever, inflammation, shock, hypotension
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What are the two exceptions of exotoxins which cannot be detroyed by heat?
S. Aureus and B. Cereus emetic
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What are the two domains of an exotoxin?
Proteins have two domains 1. Binding domain - binds to a receptor 2. Active domain - action of the toxin
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What are examples of enterotoxins? which bacteria are they produced from?
Ecoli - verotoxin aka s. disenteriae shiga toxin - degrades lining of blood vessels Vibrio Cholera - choleragen toxin - stimulates water secretion into the gut
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What are examples of neurotoxins? What are their effects?
1. Botulism toxin - flaccid paralysis (numbness, no muscle strength) ## Footnote 2. Tetanospasmin - spastic paralysis (constant contractions)
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What are examples of hemolytic toxins?
Hemolysins - destroy RBCs ie - streptococcus pyogens (Group A streptococcus) Leukocydins - destroy WBCs Streptococcus aureus - targets neutrophils - necrotizing pneumonia. Can kill patient in 72 hrs
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What is the difference between blood and chocolate agars?
Blood: agar mixed with nutrient growth mediums and living RBCs. Helps characterize alpha, beta, and gamma bacteria (tests for the presence of hemolysins) Chocolate: for more fussy bacteria which require the nutrients of RBC (iron) to propogate, but cannot get it by itself dt lack of hemolysins
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What would an alpha, beta and gamma hemolyti bacteria look like on a blood agar?
Alpha: Partial RBC hemolysis, but incomplete digestion. Agar turns green. ie S. viridians Beta: Complete RBC hemolysis. Halo around colonies. ie S. haemolytics Gamma: not hemolytic
104
How is competition with the host for nutrients a virulence factor
By robbing the host of nutrients that it requires to grow, the pathogen can cause harm to the host
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What is the difference between siderophores and hemoproteins? What are examples of hemoproteins?
Siderophores: bacteria which scavenge free iron from the host. Can dissolve off of hemoproteins Hemoproteins: How a host retains Fe. ie Transferrin, Ferritin, Lactoferrin?
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Nomenclature difference between hemoproteins and siderophores?
Hemoproteins - ends with "rins Siderophores end in "bactins. ie Mycobaterium = Myctobactin
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How can genetic defenses be a virulene factor?
Pathogens change their 3D epitope so it doesn't feel the same to the antigen, which means the T cells may not recognize it and antibodies may no longer be efective against it
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What is variable surface glycoproteins?
A method of pathogens changing their antigen shape by covering the surface with sugars ie - Trypanosome - african sleeping sckness
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What is the difference between antigenic drift and antigenic shift? WHich is more dangerous?
1. Drift- mistakes in RNA reproduction can help the pathogen evolve- ie Flu virus every year 2. Shift: virus gains foreign genetic material from another species -**genetic reassortment**. Human body cannot recognize the new DNA (HA has changed). Very dangerous. Avian flu (Avian HA is mized with human influenza)
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