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GRCC > Microbiology Final > Flashcards

Microbiology Final Flashcards

1
Q

What is an antigen?

A

Stimulates an immune response: A substance the body recognizes as forign

Non-self

immunogenic - stimulates an immune response (immunogen)

large, complex molecules

Composed of antigenic determinants - the part of the antigen that actually stimulates and reacts with the immune response

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2
Q

What parts of the bacteria have antigenic determinants?

A

Proteins, lipids, mucleic acids, CHO

Flagellum

Pilli

**Proteins make the best antigenic determinant

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3
Q

What is a hapten?

A

molecule that, by itself, is too small to be immunogenic

**When attached to a larger molecule like a protein then it can be imunogenic

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4
Q

Properties of immune responses

A

Recognition - of self vs. non-self

  • self = host tissue
  • Non-self = forign substances

Specificity - each immune response is directed toward a specific ag but the response to one ag doesn’t affect the response to another. Cross Rx occurs if two ag’s are similar

Diversity - The immune system can respond to many different Ag’s (>1 billion)

Memory - The immune system can recognize ag’s it has previously encountered. It responds quicker the second/subsequent time it encounters that ag

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5
Q

Define tolerance

A

the host doesn’t mount an immune response to self ag’s under normal circumstances

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6
Q

B lymphocytes (B cells)

A

Arise in bone marrow; primarily involved in antibody mediated immunity

Reside in the lympohid organs and in the bloodstream

Receptor: an Ab molecule that recognizes and binds a specific Ag

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7
Q

T lymphocytes (T cells)

A

Arise in thymus gland; Primarily involved in cell-mediated immunity

Reside in lymphoid organs and in the bloodstream

Receptor: T-cell receptor, receptor that recognizes and binds a specific Ag.

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8
Q

Cell-mediated Immune Response

A
  1. Ag is recognized and phagocytosed by macrophages- Ag presenting cells
  2. Macrophages fins corresponding helper T cell; presents Ag (binds)
  3. Helper T cells sound the alarm (CD-4+) - interleukin-1 stimulate T-cells to mature; interleukin-2 stimulates T-cells to rapidly divide
  4. The alarm encourages the production and rapid division of cytotoxic T-cells
  5. Cytotoxic T-cells find and infect cells that present Ag and lyse them
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9
Q

What are cytokines?

A

Cell communication molecules; released by one cell to signal or stimulate another cell.

Released by helper T cells

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10
Q

What are perforins?

A

Released from cytotoxic T cells; forms pores in target cell membrane

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11
Q

What are Antibodies?

A

Proteins that circulate in the bloodstream

sythesize and secreted by plasma cells

Each Ab is specific for 1 particular antigenic determinant

React with Ag that is outside host cell like toxins, bacterial surfaces, viruses

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12
Q

Plasma cells

A

B lymphocytes that circulate in the bloodstream and synthesize & secrete Ab

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13
Q

Antibody mediated (humoral) immune response

A
  1. Macrophages comes across an antigenic determinant
  2. Macrophage must find appropriate B cell with matching surface proteins to the antigenic determinant
  3. Helper T cells help activate and encourage reproduction of B cells by means of cytokines which give rise to plasma cells
  4. Ab find and antigen and mark for destruction
  5. Marked antigens are then easier to phagocytize
  6. Memory B cells created to anticipate the reappearance of certain Ag
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14
Q

IgM Ab

A

Pentamer

First to appear esp. in primary Ab response

In bloodstream on surface of B cells

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15
Q

IgG

A

Monomer

Major circulating Ab

Appears later than IgM esp. in secondary Ab response

Crosses placenta

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16
Q

IgA

A

Monomer/dimer

occurs in serum and in secretions

Secreted into mucosal surfaces, in tears, saliva, colostrum

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17
Q

IgE

A

Monomer

On surface of mast cells and plays a role in allergenic reactions

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18
Q

IgD

A

Monomer

Surface receptor on B lymphocytes

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19
Q

Primary Ab response

A
  • Occurs first time Ag is encountered
  • Ab begins to appear in 5 days
  • First Ab is IgM then wanes
  • Next Ab is IgG appears in greater amount
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20
Q

Secondary Ab response

A
  • Occurs at second/subsequent Ag exposure
  • Results from B memory cells
  • Occurs more quickly than primary response
  • Produces more Ab than primary response
  • Lasts longer than primary response
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21
Q

Neutralizing antibodies

A

Viruses clump them together so they cannot enter cell

Antitoxins - alters the active sites and masks their toxicity, ^ toxins size making it easier to phagocytize

Block adhesions-binds adhesins, prevent from attaching and colonizing host

Opsonize - enhance phagosytosis; handle

Agglutinate - clump insoluble particles together making them easier to phagocytize

Precipitate - Clump soluble molecules together, making them easier to phagocytize

Activate complement - forms MAC, resulting in lysis & killing of pathogen

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22
Q

Natural active immunity

  • Define
  • Whats given to host
  • Immune response
A
  • Immune response develops naturally within a host
  • Example: Getting the chicken pox
  • What’s given to host: You get the virus
  • Immune response is fast; after initial exposure
  • Immune response is either short or long lived
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23
Q

Natural passive immunity

  • Define
  • What’s given to host?
  • Immune response
A
  • Immune response develops naturally and is provided to the host
  • Example: breast milk
  • What’s gien to host: Maternal Ab provided to newborn
  • Immune response is fast
  • Immune response lasts for 3-6 months
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24
Q

Artificial active immunity

  • Define
  • Example
  • Immune response
A
  • Immune response develops after an intentional or purposful action within the host
  • Example: vaccine
  • What’s actually given to host: piece of a bacterium or cead virus
  • Immune response is fast
  • Immune response lasts long
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25
Q

Artificial passive immunity

  • Define
  • Example
  • immune response
A
  • Immune response develops after an intentional or purposful action and is provided to host
  • Snake vaccine
  • immunity taken from someone else (Ab)
  • Immune response is fast
  • Immune response is short lived
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26
Q

Inactivated vaccine

  • Define
  • Advantage
  • Concern
A
  • Whole bacterium or virus is killed and given as an Ag
  • Advantage: No danger or getting the disease from vaccine
  • Concern: Releases endotoxins; short lived immunity
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27
Q

Attenuated Vaccine

  • Define
  • Advantage
  • Concern
A
  • Live organism with reduced pathogenicity is given causing a small subclinical infection
  • Advantage: longer lasting immunity
  • Concern: You can get sick
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28
Q

Subunit vaccine

  • Define
  • Advantage
  • Concern
A
  • Only part of the organism get infected
  • Advantage: Won’t get sick;fewer side effects
  • Concern: Short term immunity
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29
Q

Toxoid

A

Inactivated toxin given as Ag; has lost it’s toxic activity but retained it’s immunogenicity

EX: tetanus

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30
Q

Conjugated vaccine

A

A subunit is linked or conjugated to another molecule to increase its immunogenicity

Hapten is connected with a protein to elict greater immune response

EX: Hib vaccine

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31
Q

Synthetic/recombinant vaccine

A

A subunit or part of an organism if produced using genetic engineering

EX: hep. B vaccine & gardasil

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32
Q

Herd immunity

A

Means that it’s difficult for a disease to spread in the population if a sufficient number of individuals are immunized

90% have to be vaccinated

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33
Q

Adverse reactions to vaccines

A

Soreness at injection site, raised & red; mild fever, malaise

Due to hypersensitivity or allergy to vaccine components

wheel and flare

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34
Q

Hypersensitivity

A

an increased, exaggerated or inappropriate immune response that negatively affects the host

“Too much of a good thing”

A host is sensitized if they are hypersensitive to a particular Ag.

Allergy or allergic response

Ag is often something the host should be tolerant to

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35
Q

Hypersensitivity exposure

A

Sensitizing dose = 1st exposure; usually a large dose

Elicting dose or provocative dose = 2nd or subsequent exposure; can be quite small

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36
Q

Type 1 hypersensitivity

A

immediate-type hypersensitivity

involves IgE on the surface of mast cells and basophils and result in as immediate pharmacologic response

Ag is often an allergen

IgE binds to the surface of cells:

  • Mast cells - CT cells found around respiratory & GI tracts, near blood vessels
  • Basophils - granulocytes that circulate in the bloodstream
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37
Q

Degranulation

A

A rapid release of chemical substances that induce an allergic response from mast and basophil cells

Histamine dilates capillaries; immediate onset

  • increase vascular permeability
  • constricts smooth muscle
  • increase mucus secretions
  • Stimulates nerve endings > itch & pain

This reaction is called anaphylaxis

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38
Q

Localized anaphylaxis - local Ag exposure

A

Rx occurs where allergen enters body

Skin: Wheel & flare - skin Rx characterized by a swollen white center surrounded by redness & itching

Respiratory tract: bronchi constriction, weezing, cough, fluid in lungs, mucous

Digestive tract/food allergy: vomit, diahrea

Treatment: antihistamine stops the release of histamine

Asthma

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39
Q

Systemic anaphylaxis - Ag in bloodstream

A

Systemic Rx –> anaphylactic shock: blood vessels suddenly dilate and become more permeable causing a drop in blood pressure

Can be rapidly fatal (15 min)

EX: Epi pen

Treatment: desensitization-repeated injection of small amounts of denatured Ag. May prevent B cells from maturing into IgE. May induce tolerance to the Ag

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40
Q

Controlling type 1 hypersensitivity

A

Avoid contact with allergen

Antihistamine

Desensitization- repeasted injections of small amounts of denatured Ag; prevent B cells from maturing into IgE secreting plasma cells; May induce tolerance ot the Ag

Block Ab- immunize with the denatured allergen to produce serum IgG; Serum IgG blocks allergen from reaching IgE

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41
Q

Type 2 cytotoxic hypersensitivity

A

Ab usually IgG or IgM
Ag on the surface of cells

Compliment

Adverse effects appear within min-hrs

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42
Q

Hemolytic disease of newborn

A

Rh (rhesus) Ag on erythrocytes

Treatment: shot of RhoGAM - anti Rh Ab

  • administered to mother at birth of first Rh+ child
  • Binds up Rh Ag, preventing it from stimulating mother’s immune system
  • So that Rh Ab is not produced
  • Artificial Passive Immunity
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43
Q

Type 3 immune complex hypersensitivity

A

Ags - usually soluble in lrg amounts entering host

Abs - IgG or IgM

Complement

PMN’s - neutrophils

Adverse effects appear within hrs-days

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44
Q

Serum sickness

A

Type 3

Ab develops to Ags in an antiserum preperation

Next administration: Ag-Ab complexes form and damage kidneys

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45
Q

Type 4 cell-mediated hypersensitivity

A

Ags-usually displayed on cells or have become attached to cell surfaces

Sensitized T cells

  • Generated upon first exposure to Ag
  • React on second exposure to Ag

Often observed as a skin reaction because they are associated with Ag being on the skin

Delayed; starts after >12 hrs; maximal rx 24-72 hrs after Ag exposure. Some takes weeks to develop

46
Q

Contact dermatitis

A

Type 4

CMI response develops to Ag deposited ont he skin

EX: poison ivy

Test with allergen patch

Treatment: antiinflamatory, steroids

47
Q

Tuberculin sensitivity

A

type 4

CMI response develops from infection

tuberculin skin test provides second exposure to Ag

Positive test means you’ve been exposed

48
Q

Granulomatous hypersensitivity

A

type 4

“walled off”

macrophages have phagocytosed pathogens but can’t kill them

Sensitized T cells respond to form a granuloma

49
Q

Autoimmune disorders

A

host mounts immune response against its own Ags, cells, or tissues

host should be tolerant to “self”

“a good thing turned bad”

Auto Ag - the self Ag to which the host is responding

Immune response may involve auto Ab or cellular response

Rx typically results in destruction of host cells or tissues

50
Q

How does autoimmune disprder develop?

A

antigenic mimicry - cross-rx btw a forign and self Ag

Tolerance failed to develop- cells that respond to self ags were not destroyed in development of the immune system

Genetic factors

51
Q

Auto immune disorders

A

Myasthma gravis

  • affects skeletal muscles; unable to contract properly
  • Auto Ab against neurotransmitter receptor at nerve-muscle junction

Rheumatoid arthritis

  • Auto Ag unclear
  • Immune complexes form in the joints

Systemic lupus erythematosus

  • Ab to nuclear compoments of host’s cells
  • Immune complexes form in the skin, organs
52
Q

Immunodeficiency Diseases

A

Immune system responds inadequately to an Ag due to a genetic or acquired defect in the immune system

“too little of a good thing”

Primary immunodeficiency= genetic or developmental defect in immunity

Secondary immunodeficiency= results from damage to the immune cells after they have developed normally

53
Q

Define sterilization

A

the killing or removal of all life forms

54
Q

Define disinfection

A

Reduction in the amount of pathogenic organisms

55
Q

Microbial death curve

A

definite proprtion of organisms die in a given time interval

EX: 20% die one minute; 20% will die the next minute

The more microbes present the more time needed to kill them all so you want to clean before sterilizing.

Nevery really reach 0.

56
Q

Microbial killing with heat

A

function of time and temperature

  • the higher the temp. the shorter the time
  • The lower the temp. the longer the time
  • Depends on the type of organism
  • Depends ont he type of material
  • The presence of organic matter shields oragniams from heat
  • Overkill- use more force that was is needed
57
Q

Microbial killing with Dry heat

A

Standard conditions: 160 C for 2 hrs.

  • penetration is slow
  • Mechanism: oxidizes molecules
  • Materials must be heat stable
  • Doesn’t corrode or dull sharp instruments
  • Sterilze dentures and surgical instruments
58
Q

Microbial killing with moist heat

A

standard conditions for boiling water:

  • Vegatative cells: 100 C for 10 minutes
  • Spores: 100 C for >2 hrs.
  • Water conducts heat more effectively
  • May or may not sterilize
  • Mechanism: denatures proteins & other maccromolecules
59
Q

Microbial killing with autoclave

A

Moist heat and pressure

Standard conditions: 121 C for 15 min. at 15lb/in2

  • pressure increases temp. over 100C
  • pressure helps steam/heat to penetrate
  • Limitations: items wrapped in foil and urea broth
60
Q

Pasteurization removes pathogens

A
  • Targeted at removing oathogens and reducing overall bacterial population
  • Not effective against spores
  • does not sterilize

standard conditions (milk): 62.9 C for 30 min.

61
Q

What is ultrapasteurization?

What is UHT pasteurization?

A

UP: over heating - 82 C for 30 min.

increased shelf life

UHT: 140 C for 3 sec.

62
Q

Filtration traps microorganisms

A
  • liquid or gas is passed through a membrane filter which traps micrpprganisms; .2 pore size
  • May or may not sterilize; viruses pass through still.
  • Use on heat sensitive liquids, culture media, iv solutions, beverages, gases.

Limitations:

  • fliters may clog
  • Breaks, cracks or flaws in filter
  • Some molecules bind to filter

HEPA filter- high efficiency particulate filter

  • air filtration for clean rooms/surgical suites/burn units
  • often used with uv light for sterility
63
Q

UV light control on microbial growth

A

wavelength of 100-400nm

UV light forms thymine dimers in DNA

Requires direct, close contact

useful on air and surfaces

Limitations:

  • doesn’t penetrate
  • less effective at greater distances
  • Damage skin and eyes
64
Q

Ionizing radiation can sterilize materials

A

x-rays & gamma rays

expose materials in lead-lined chamber

Mechanism: excites electrons, creating ions–> inactivate proteins & amino acids

Penetrates well & useful on heat sensitive items

Approved for preservation of food

  • kills foodborne oathogens
  • concerna about safety of workers
  • concerns about saety of consumers
65
Q

Define sanitation

A

reducing the microbial population to a safe level, as determined by some sort of standard

66
Q

Define degerming

A

removing organisms from a surface

67
Q

define -cidal and -static

A
  • cidal: kills organisms
  • static: inhibits the growth of
68
Q

Chemical agent: Halogens

A

Mechanism:

  • oxidize proteins
  • Chlorine & Iodine
  • Bacterial cidal
  • effective against a variety of organisms

Limitations:

  • Work slowly against spores
  • inactivated by organic matter
  • Noticable taste & odor
69
Q

Chlorine

A
  • Release hypochlorous acid in solutions
  • oxidizes proteins
  • water purification - city water & pools
70
Q

Iodine

A

oxidizes proteins

skin antisepsis and surgical prep

EX: betadine

71
Q

Chloroprep Skin antiseptic

A

Gram positive and Negative

Uses:

  • oral rinses
  • skin cleanseres
  • small quanities
72
Q

Phenolics

A

Mechanism:

  • Denatures or coagulates proteins
  • Hydrophobic–> disrupt cell membranes and loosen organisms from surfaces

Useful for disinfecting surfaces

Limitations:

  • More active against Gm +
  • little activity against spores
73
Q

Alcohols

A
  • denature proteins and disrupt membranes
  • ethanol & isopropyl alcohol

Mechanism:

dissolves lipids/disrupts membranes

antisepsis on skin

74
Q

Quaternary Ammonium compounds (quats)

A

have + charged N

amphipathic molecules

Mechanism:

  • dissolve lipids in cell membranes
  • effective against bacteria & enveloped viruses
  • used in cleaning products
75
Q

Ethylene oxide

A

reactive gas

Mechanism: an alkylating agent–> crosslinks proteins and other macromolecules

kills all microorganisms including spores

sterilizes

76
Q

Chemiclave

A

sealed chamber for etO sterilization

EtO for 3 hrs.

Flush with inert gas for 8-12 hr

useful for plastics, medical devices, surgical supplies

77
Q

Chemotherapeutic agent

A

chemical substance that is used in the body for therapy

78
Q

Antimicrobial agent

A

a chemotherapeutic agent used to treat infections caused by microbes

79
Q

Antibacterial agent

A

a drug used to treat infections caused by bacteria

80
Q

Antibiotic

A

an antimicrobial substance produced by a microorganism that inhibits or kills another microorganism

81
Q

Natural products

A

purified from natural sources or from microorganisms

82
Q

Synthetic

A

completely made by chemical synthesis

83
Q

Semi-synthetic

A

initially purified from a natural source, with subsequent synthetic modification

84
Q

Antibacterial class

A
  • general type or group of antibacterial agent
  • Based on mechanism of action or target
  • Usually have similar chemical structure
85
Q

Antibacterial generation

A

groups of agents within a class that represent a major improvement over other members of the class

86
Q

Selective toxicity

A

kills or inhibits the pathogen, but not the host

87
Q

Broad spectrum

A

Active against a wide array of bacteria, including both Gram(+) & Gram(-) organisms

88
Q

Narrow spectrum

A

Active against a limited range of organisms

89
Q

Bactericidial

A

Kills pathogen
Usually requires 99.9% kill to be –cidal

90
Q

Bacteriostatic

A

Inhibits the growth of the pathogen
Relies on host defenses to kill

91
Q

Directed therapy

A

Selection of agent based on results of culture and sensitivity testing
Takes 24-48 hours to get results

92
Q

Granulocytes

A
  • have granules in cytoplasm & lobed nucleus
  • *Neutrophils** [polymorphonuclear leukocytes, PMNs] – professional phagocytes; granules contain lysosomal enzymes
  • *Basophils** – granules contain physiologically active substances (histamine)
  • *Eosinophils** – granules contain toxic substances that defend against parasites
93
Q

Agranulocytes

A

– have no granules in cytoplasm & round nucleus

  • *Monocytes** – can leave the circulation and enter tissues, where they develop or differentiate into macrophages – which are professional phagocytes
  • *Lymphocytes** – include B & T lymphocytes, involved in antibody responses & cellular immune responses
  • *NK cells** (natural killer cells) – involved in extracellular killing of virus-infected cells
94
Q

Lymph

A

fluid that surrounds cells and tissues
extracellular fluid; interstitial fluid

95
Q

Lymph vessels

A

drain lymph from tissues
empties into circulatory system at thoracic duct

96
Q

lymph nodes

A

lymphoid organs positioned along the lymph vessels; they filter out foreign material

97
Q

non-specific resistance

A

3 characteristics:
Exists in all people, all the time
Active at first (and all subsequent) exposures
Protects against all microbes
Also called innate immunity

98
Q

Specific resistance

A

3 characteristics:
Exists only in those previously exposed to a particular parasite
Active at second (and all subsequent) exposures
Protects against only that specific microbe
Also called acquired immunity

99
Q

Physical barriers

A

Cells, structures, or forces that cover or line body surfaces, making it difficult for microbes to penetrate

100
Q

Chemical barriers

A

Chemical molecules produced by the body that inhibit or prevent microbial growth

101
Q

Neutraphils

A

Granulocytes
Reside in blood; recruited to infection site
First-responders in inflammation
Short-lived (~3 day life span)
Tend to die after phagocytosis  pus

102
Q

Macrophages

A

“big eaters”
Mononuclear cells; derived from monocytes
Reside in certain tissues or wandering
Later responders in inflammation
Longer-lived (months/years life span)
Phagocytose and keep on going

103
Q

Chemotaxis

A

Movement in response to a chemical attractant

104
Q

Chemokines

A

the chemical attractants that phagocytes respond to, for example:
Short peptides that bacteria release
Molecules that other phagocytes release

105
Q

Phagocytosis

A
  • *Adherence** – phagocyte binds to specific molecules on microbe’s surface
  • *Ingestion** – phagocyte engulfs microbe and takes it inside within a phagosome
  • *Fusion of phagosome with lysosome** –lysosomes contain many digestive enzymes
  • *Killing & digestion** –can occur within 20 minutes. debris is released outside the phagocyte
106
Q

Inflammation

A

A nonspecific response to tissue injury
Wound, infection, burn, chemical insult
Kills microbes, clears debris, heals tissue
Starts quickly (begins within min, occurs within hr)
Neutrophils are the first responders; Macrophages come later

107
Q

Characteristics of inflammation

A

Redness – increased blood flow to area
Heat – from warmth of blood
Swelling – from accumulation of fluid
Pain – from injury to local nerves
Inflammation & phagocytosis work together to prevent or contain infection

108
Q

Acute inflammation

A

Release of chemical mediators
Capillaries dilate and become leaky
Phagocytes migrate to the site
Phagocytosis
Tissue repair & healing

109
Q

pyrogen

A

substance that causes fever; acts on hypothalamus to “increase” the thermostat

Exogenous pyrogens – come from outside the body;

Endogenous pyrogens – come from inside the body

110
Q

Compliment

A

marks pathogens for destruction

Stimulates inflammation - with chemokines
Promotes phagocytosis - by opsonization
Opsonin = a molecule that promotes phagocytosis when bound to the surface of a microbe; a “handle” for phagocytosis
Destroys pathogens directly - with membrane attack complexes

GRCC (1 decks)

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