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Microbiology > Exam 3 (Viruses, Antimicrobial Drugs, Innate Immunity, Adaptive Immunity) > Flashcards

Exam 3 (Viruses, Antimicrobial Drugs, Innate Immunity, Adaptive Immunity) Flashcards

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1
Q

Penicillin G & V

A
  • Natural penicillins
  • Beta-lactum drug
  • Inhibition of cell wall synthesis
  • Narrow spectrum and bacteriocidal
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2
Q

Amoxicillin

A
  • Semisynthetic penicillin
  • Beta-lactum drug
  • Inhibition of cell wall synthesis
  • Broad spectrum and bacteriocidal
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3
Q

Vancomycin

A
  • Inhibition of cell wall synthesis
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4
Q

Beta-lactum drugs

A

Bind to penicillin binding proteins which are enzymes used by bacteria to synthesize their cell walls. This action stops these enzymes from making their cell walls.

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5
Q

Streptomycin

A
  • Taken topically, not by mouth
  • Last chance drug
  • Binds to 70s ribosomes (perm)
  • Bacteriocidal and broad spectrum
  • Inhibition of protein synthesis
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6
Q

Tetracylcine

A
  • Taken topically, not by mouth
  • Last chance drug
  • Binds to 70s ribosomes (temp)
  • Bacteriostatic and broad spectrum
  • Inhibition of protein synthesis
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7
Q

Polymyxin B

A
  • Taken topically, not by mouth
  • Last chance drug
  • Bacteriocidal and broad spectrum
  • Interferes with fatty acid synthesis used to help synthesize the plasma membrane
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8
Q

Rifampin

A
  • Bacteriocidal and narrow spectrum
  • Inhibits the synthesis of mRNA by interfering with RNA polymerase
  • Inhibition of nucleic acid synthesis
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9
Q

Ciprofloxacin

A
  • Bacteriocidal and broad spectrum
  • Inhibits of bacterial DNA by interfering DNA gyrase
  • Inhibition of nucleic acid synthesis
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10
Q

Sulfa Drugs

A
  • Combined with trimethoprim (have to be taken together to be more effective)
  • Trimethoprim slows down PABA
  • Bacteriostatic and broad spectrum
  • Inhibition of metabolism
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11
Q

4 Ways to Antibiotic Resistance:

A

1) Inactivation of the drug by enzymes (plasmids and horizontal gene transfer)
2) Alter the drugs target site (mutations in the targeted proteins)
3) Stop the uptake of the drug (ex. a modified cell wall protein // bacteria have altered the number and/or character of their porins to limit drug entry)
4) Ejection of drug (efflux pumps or multidrug resistant pumps)

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12
Q

Narrow Spectrum of Activity:

A

Where one specific type of microbe is targeted and killed by an antimicrobial drug

  • Important because if you are trying to kill a eukaryotic cell (human cells), you need to be specific in what cell structure is targeted so we don’t attack our own cells
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13
Q

Broad Spectrum of Activity:

A

Most microbes are targeted and killed by an antimicrobial drug

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14
Q

Bacteriostatic

A

Impedes growth of the microbe but does not kill it

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15
Q

Bacteriocidal

A

Able to kill the microbe

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16
Q

Criteria for “Magic Bullet”

A
  1. Selectively toxicity - drug can kill the microbe and not us
  2. Route of Administration - make sure the drug goes to the correct areas
  3. Cost of research/making the drug affordable
  4. Limit the side effects
  5. Half-life/Shelf-life - keep the drug effective
  6. Dosage - per each persons size thats effective
  7. Limit the development of antimicrobial resistance
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17
Q

Kirby-Bauer Test

A

Also known as disk-diffusion test – tests how effective an antibiotic is against bacteria.

After the incubation period, the susceptibility or resistance against the antibiotic is observed based on the zone of inhibition

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18
Q

Minimum Inhibitory Concentration (MIC)

A

the junction of the ZOI where the concentration of the antimicrobic has become too low to effectively stop growth.

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19
Q

Minimum Bactericidal Concentration (MBC)

A

The lowest concentration of an antimicrobial agent that kills 99.9% of the original bacterial inoculum.

Essentially, determines how much of the specific antibacterial drug is needed to kill a certain bacteria

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20
Q

Broth Dilution Tests

A

Often used to determine the MIC.

Involves diluting the antimicrobial agent in a liquid medium, inoculating it with the bacteria, and then assessing the growth of the bacteria to find the lowest concentration that inhibits visible growth.

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21
Q

Lysogenic bacteriophages are responsible for the transduction of bacterial cells

A
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22
Q

Generalized Replication in Bacteriophages (Lysogenic cycle of Lambda Phage)

A

Attachment - Tail fibers help with viral adhesion to bacterial surface proteins

Penetration - injection of genetic material through the cell wall and plasma membrane. The empty capsids remain outside

Uncoating - does not happen with bacteriophages
- Extracellular

Replication - binary fission
- Biosynthesis 3A: host cells transcription and translation machinery is turned off.
- Prophage replicates with the host -> switches to lytic cycle (virus becomes induced and exists the host genome)

Assembly - viral factors pack the genome parts into the capsid

Release - Lysozyme will be encoded which will result in lysis, release, and subsequent infection

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23
Q

Lytic Cycle for Phages

A

99.9% of viruses

Attachment via tail fibers

Penetration Uncoating: Extracellular; lysozyme makes the hole for the virus

Virus nucleic acid is released from phage outside the membrane into the intracellular fluid

DNA is getting destroyed to make copies of itself

The host cells transcription and translation machinery is turned off

Replication: Biosynthesis

Maturation: new phages get assembled into virions (complete infectious virus)

Released by new the phages using lysosome

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24
Q

Generalized Replication in Animal Virus (lytic cycle for human viruses)

A

Attachment - capsid proteins or spikes will bind to hose cell membranes

Penetration:
1) Naked - endocytosis; viral binding to host cell surface receptors will trigger their intake
2) Enveloped - endocytosis or membrane fusion; host cell plasma membrane and viral envelope will blend together and release the viral capsid into the cytoplasm

Uncoating - capsid is entirely or partially broken down -> release of viral genome
- Intracellular

Replication - takes over the host cell for transcription and translation of viral genes. DNAases; building blocks of new phage particles & enzymes that will copy the viral genome
(turns off biosynthesis)

Assembly - some capsids are packaged before they are finished.
- Capsids will be assembled around the genome.
- Enveloped viruses often require viral proteins to be embedded in the host plasma membrane before virion release (for budding)

Release:
1) Enveloped - budding -> taking portions of the host cell’s plasma membrane
2) Naked - lysis -> cell death

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25
Lysogeny
An alternative pathway for bacteriophages. - After the Penetrative Step of the Lytic Cycle, the phage DNA integrates itself into the host DNA, forming a prophage; they are able to confer new pathogenic properties to bacterial cells. - As the host cell undergoes scheduled replication, it replicates BOTH host and phage genomes, increasing the number of infected cells - If the prophage receives an external stressor, it may excise itself an re-enter the lytic cycle in an attempt to find a new host cell
26
Latency
This type of infection is distinguished by flare-ups with intermittent periods of dormancy - During flare-ups, virions are shed and the infected person experiences symptoms; triggers infection with another pathogen, fever, sunburn, hormone level changes, immune repression
27
Latent humans viruses cause:
- Persistent infections: genital herpes (comes and goes) - Chronic infections: hepatitis C & HIV (always active) - Latent infections: HIV (asymptomatic)
28
Chronic infections
Characterized by continuous release virions over time and a slow progression of disease
29
Oncogenic (oncoviruses)
viruses that can cause cancer
30
Cancer causing mechanisms:
1) Viral genes can cause uncontrolled cell division 2) Chronic inflammation from the virus is hypothesized to trigger host cell DNA damage and mutations
31
Antivirals
Attachment: - Maraviroc: covers the receptor for the HIV virus and Enfuvirtide which blocks viral penetration of HIV Intracellular Uncoating: - Amantadine Inhibition of Nucleic Acid synthesis: - Acyclovir (Zovirax, Valtrex): mimics guanosine nucleotides - AZT (Retrovir, Zidovudine): inhibits reverse transcriptase enzymes Inhibition of assembly/maturation: - Protease inhibitors (lopinavir, amprenavir, atazanavir)
32
Prions
Cause dementia in humans and animals Sheep: Scrapie Cows: Made cow disease Humans: (plaques in brain), Kuru, Creutzfeldt-Jakob disease
33
Function of capsid
The protein shell that packages and protects the genome and also accounts for the bulk of the virion's mass They are able to self assemble or can use the host cell machinery to make capsids
34
Shapes of Viruses
1. Helical Capsid 2. Icosahedral Capsid 3. Complex Structure
35
Plaque Forming Units
- The quantity of bacteriophages in an initial volume of sample - Plaques are clear zones on the plates that is evidence of the phages lysing out of the host cells
36
Nonspecific Host Defenses
Innate Immunity - Responses that defend against any invader or abnormal material - triggered by general molecular patterns associated with pathogens or other drugs - Contains the first and second lines of defenses
37
First line of defenses:
- Skin (hair, dry, sloughing off dead skin, slightly acidic, normal flora, salty, oils, sweat) - Mucous membranes
38
Second line of defenses:
- Phagocytes - Fever - NK cells - Antimicrobial proteins - Inflammation (Occurs in Lymphoid tissues)
39
Lactoferrin/transferrin function:
molecules that bind to free-floating iron to keep the iron away from invading microbes - iron works as a cofactor for bacterial growth
40
Margination:
CAMs on capillary cells cause leukocytes to stick to capillary walls - roll along the sides of the blood vessels
41
Diapedesis
Leukocytes can squeeze through the blood vessel to move into a tissue
42
Chemotaxis
Leukocytes follow chemical trails to damaged tissue - how the leukocytes know where to go
43
Opsonins
chemical placed on non-self cell by immune system, link to phagocytosis
44
Bacterial cell markers:
- PAMPS: pathogen-associated molecular patterns - TLR: toll-like receptors - PRR: pathogen recognition receptors
45
Phagocytes:
1) Survey the tissue and discover microbes 2) ingest and eliminate 3) extract immunogenic information (anitgens)
46
Phagocytosis
The process of cell eating - Performed by phagocytes which are WBCs
47
Cytokines
Chemical that causes cells to move to the site of infection
48
C3b tags pathogens for Phagocytosis
CR1 (compliment receptor 1) - bind to C3b deposited on microbial surfaces for phagocytosis
49
Phases of Phagocytosis
1) Chemotaxis and adherence of microbe to phagocytosis (WBC attracted to chemical substance microbe is producing) 2) Ingestion of microbe by phagocyte 3) Formation of phagosome 4) Fusion of phagosome with a lysosome to form a phagolysosome 5) Digestion of ingested microbe by enzymes 6) Formation of residual body containing a indigestible material 7) Discharge of waste materials
50
Complement
- A cascade system that consists of about 30 proteins that lead to 3 outcomes: 1. Increased opsonization/increased phagocytosis 2. Inflammation 3. Cytolysis: hole in membrane of pathogen
51
Inflammation
- Temporary and localized - designed to bring phagocytes and plasma proteins to injured area
52
Inflammation in four stages:
1. Reddening which is caused by histamine - vasodilation -> increased blood flow (redness, heat) - increased capillary permeability -> plasma proteins flow out -> edema (swelling, pain) 2. Swelling caused by pyogens 3. Pain which caused by histamine 4. Heat/fever which is caused by pyrogens
53
Inflammation Response Stages:
Stage 1: vasodilation and increased permeability of blood vessels to bring WBC's to the damaged area Stage 2: phagocytic migration and diapedesis - margination: phagocytes stick to blood vessels - diapedesis: phagocytes squeeze between endothelial cells - phagocytes invade the bacteria Stage 3: repair of tissues
54
Cytolysis:
Formation of the Membrane Attack Complex
55
Interferon
1. Released by virus-infected cells, triggers production of virus-blocking enzymes in nearby cells 2. Enhances role of phagocytes and other immune cells on virus-infected and cancer cells
56
Neutrophils
highly mobile phagocytes
57
Eosinophils
secrete chemicals that kill parasitic worms, involved in allergic reactions
58
Basophils
release histamine and heparin involved in allergic reactions
59
Lymphocytes
Can reproduce outside bone marrow B lymphocytes: secrete antibodies - mature in bone marrow T Lymphocytes: destroy virus infected and cancer cells - mature in thymus
60
Complement System
Plasma protein precursors activated by exposure to pathogen or antibodies 1. Lysis non-self cells (when activated) - Membrane attack complex (MAC) inserts itself into bacterial membrane and pokes holes 2. Serve as chemotaxins and opsonins 3. Promote vasodilation and histamine release 4. Activate kinins (enhancements)
61
Specific Host Immune (Adaptive Immunity)
This system can determine "self" cells from "nonself" cells - Act on particular invaders - Third line of defense
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B Cells
Originate: bone marrow Maturation: bone marrow Antibody production: Yes Involved in Humoral immunity (HI) Functional forms: one (antibodies) Creates memory cells
63
T cells
Origination: bone marrow Maturation: thymus No antibody production Involved in cell mediated immunity (CMI) Functional forms: 4 - T helper cells - T cytotoxic cells Creates memory cells
64
Humoral Immunity (HI)
- Affords us protection in our body fluids - Helps us fight off extracellular infections - Involves B cells, and the production of antibodies through B cells (B cells have to be induced in order to make antibodies) - The induction and production of antibodies by B cells mediated by antigens
65
Cell-mediated immunity (t cells)
- macrophages "present antigen" to T cells 1. Macrophages phagocytizes antigen and places it on its surface 2. Appropriate type of T cell binds and is activated to reproduce and differentiate - Requires both non-self and self antigen to bind and destroy a cell
66
Antigens
- Chemical substances that are recognized by host immune system as foreign substances - Inducer of the B cells - Composed of three molecules: 1. proteins 2. Carbohydrates 3. Nucleic acids/Fats: do not induce host immune response
67
Epitopes
A specific region that the cell recognizes as foreign in an antigen
68
Antibodies
- microbe binds to the antibody - proteins made in response to antigen Functions: 1. mark a microbe for destruction (opsonization) 2. Neutralization of a microbe 3. Agglutination cause microbes to clump together (prevents from binding to the host) 4. Activation of classical complement 5. Involved in antibody dependent cellular cytotoxicity (ADCC)
69
IgG Antibody:
- Most prevalent antibody found in blood - Involved in chronic infections - Counterpart: macrophages - High levels of macrophages means high levels macrophages - Cross the placenta
70
IgM Antibody
- first antibody synthesized in response to most infections - counterpart: neutrophil - involved in acute infections
71
IgA Antibody
- Most prevalent antibody in the body - Found in breastmilk
72
IgD Antibody
- unknown function but works as a B cell receptor
73
IgE Antibody
- Involved in parasitic infections allergic reactions - Counterpart: basophils and eosinophils
74
Primary Response:
- 7-10 days - Very effective - Plasma cells involved (b cells) - Memory cells are NOT involved
75
Secondary Response:
- Min.-Hours - Effectiveness is enhanced - No plasma cells involved - Memory cells are involved
76
T helper cells functions:
- delayed hypersensitivity reactions
77
Tc cells functions:
- destroys cells by releasing perforin
78
Self-cell recognition
Important for our cells to distinguish "self" vs. "non-self". This is called tolerance. When our cells lose this ability, we can develop an autoimmune disease
79
How to distinguish self cells:
- A set of molecules called the Major Histocompatibility Complex (MHC); part of the human leukocyte antigen system MHC 1: - found in all host cells except for RBCs - recognized by Tc cells - intracellular antigen uses proteasome MHC 2: - found only on antigen presenting cells (APCs) - recognized by T helper cells - extracellular antigen in endocytic vesicle
80
MHC 1 Outcomes:
Scenario A: - cytokines are released to help recruit Tc cells - Antibody not made Scenario B: - cytokines are released to help recruit t-helper cells - t-helper cells call for more macrophages (fusion), Tc cells, and B-cells
81
MHC 2 Outcomes
- Cytokines are released to help recruit t-helper cells - t-helper cells release different cytokines and recruit b-cells
82
Two pathways that are used in conjunction with HI and CMI
1. T-cell dependent antigen pathway: uses T cells - recognizes if the antigen is foreign 2. T-cell independent antigen pathway: doesn't use T cells, B cells only
83
T-cell Independent antigen pathway
- used when we don't recognize if the antigen has been formed
84
What happens if a microbe is too big for phagotcytosis?
Antibody Dependent Cellular Cytotoxicity - macrophage takes a piece of the microbe and presents it on the surface - cytokines are released and recruit t-helper cells
85
T-helper cells (2 forms)
1. Td cells - delayed hypersensitivity 2. Treg - turns on CMI, Tsupp - turns off CMI
86
Antigen Presenting Cells (APC)
- displays an antigen bound by a major MHC protein on its surface
87
Which of the following is not cytolytic, cytotoxic, or phagocyte?
Interferon - a cell thats been attacked releases interferons. - No cytolytic and phagocytic toxins
88
Whats the commonality of all viruses and antibodies?
- both are specific
89
Minimum time to make antibodies (primary response)
7-10 days
90
Classical Complement
- requires antigen-antibody complexes for activation (specific immune response) - opsonize antibodies
91
Alternative Complement
- can be activated by spontaneous complement component C3 hydrolysis, foreign material, pathogens, or damaged cells - opsonize C3b
92
Pseudopod functions:
1. locomotion 2. capture of prey or engulfing of food
93
What does oil and bacteriophages have in common?
both contain lysozymes
94
Two types of transduction:
1. specialized: specific genes are transferred between bacteria by a phage - corynebacterium 2. generalized: random genes are transferred between bacteria by a phage
95
Leukocyte Migration steps:
1. tethering 2. rolling 3. activation 4. firm adhesion
96
Phagocytosis:
1. chemotaxis 2. attachment 3. formation of phagosome 4. formation of phagolysosome/digestion 5. release
97
Can a macrophage directly make an antibody?
No. Macrophages present antigens to B cells, which then activate and differentiate into antibody-producing plasma cells
98
Can a t-helper cells make an antibody
No, needs a B cell (indirectly can help)

Microbiology (7 decks)

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