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Microbiologyh > Chapter Thirteen And Fifteen > Flashcards

Chapter Thirteen And Fifteen Flashcards

1
Q

Viruses

A

-parasites
-contain RNA and DNA
-have a protein coat
-spikes

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2
Q

Virion

A

A matured particles
-containing all ingredients
-virus

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3
Q

What makes a virion different (4)

A

-genome
-capsid
-envelope
-spikes on envelope

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4
Q

Own genome of a virion

A

The DNA or RNA (never both)
-determines lifecycle

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5
Q

Capsid of a virion

A

Contains genome, is a protein molecule

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6
Q

Capsid of virion function

A

-identifies virus by capsomere
-transportation
-attachment of host cell

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7
Q

Capsomere

A

What makes up capsid

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8
Q

Envelope of a virus is made up of

A

-Protein
-carbohydrates
-phospholipid on more complex ones

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9
Q

Spikes on envelope of virus

A

Found on COVID/influenza
-increases virulence

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10
Q

Two types of spikes

A

HA and NA

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11
Q

HA/ Hemoagglutination spikes

A

Attach to host cell
-strain match by spike “H1N1” or “H9N1”

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12
Q

The number beside H in H1N1 stands for

A

Each spike that has mutated once

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13
Q

NA spike or Neuramin

A

After infection, populates host cell membrane
-strain detection

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14
Q

HIV stands for

A

Human immunodeficiency virus

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15
Q

Four things the HIV virus contains

A

-RNA genome
-capsid
-envelope
-spikes

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16
Q

Spikes are made up of

A

GP (carbohydrate + protein) 41+120

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17
Q

Three facts about HIV

A

-is a retro virus
-only replicates in humans
-only kills/invalids helper T cells

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18
Q

What does it mean by retro virus

A

Going backwards then forwards

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19
Q

Transcription

A

Copying 2 dna strands into rna

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20
Q

Life cycle of HIV: initially contains

A

2 rna strands
-ssrna (single strand)

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21
Q

Life cycle of HIV: begins penetrating cell with ___ and ____

A

Spike and enzyme reverse transcriptase

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22
Q

Reverse transcriptase cannot be made in

A

Humans

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23
Q

Life cycle of HIV: spike/enzyme attaches to

A

Helper T cell
-CD4 cells

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24
Q

Life cycle of HIV: enters cell via and does what

A

Endocytosis (receptor mediated)

Mergers with CD4 cell

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25
Q

Life cycle of HIV: how does the cell enter via endocytosis

A

Using spike gp 41+120

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26
Q

Life cycle of HIV: begins to ___ and releases

A

Uncoat, RNA + reverse transcriptase

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27
Q

Life cycle of HIV: multiplies within cytoplasm to

A

Synthesize own model

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28
Q

Life cycle of HIV: reverse transcription occurs via

A

Reverse transcriptase

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29
Q

What is reverse transcription

A

RNA to DNA

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30
Q

Steps of the reverse transcriptase

A
  1. Copy rna into a single dna
  2. RNA degrades, left with 1dna
  3. Recoup dna to create a double strand
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31
Q

Provirus stage of HIV

A

Has established and integrated itself into dna
-can synthesize new virgins
-can become latent virus
-converts cell into cancerous cell

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32
Q

Latent means the virus is

A

Waiting four host helalth to diminish then act

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33
Q

HIV 1

A

USA and Europe

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34
Q

HIV 2

A

West Africa

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35
Q

CDC

A

Center for disease control

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36
Q

How many stages of HIV

A

Three

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37
Q

HIV stage 1

A

TH = 500 cells/mm2
-50 percent or less

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38
Q

Normal TH count is

A

1000 to 1500 cells/mm2

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39
Q

Stage 2 HIV

A

Amount of CD4 is declining
-TH = 499 to 200 cells/mm2
-immunodeficiency symptom

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40
Q

Immunodeficiency symptom

A

Swollen lymph nodes
-suspeptible to (shingles, fungal/UTI, diarrhea, fever)

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41
Q

Stage 3 HIV

A

TH = 200 cell/mm2
-cancer stage
-other infections

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42
Q

Cancer in stage 3

A

Kaposis sarcomma
-cancer of skin and blood vessels

43
Q

Other infections in stage 3

A

TB, pneumonia, eye infections

44
Q

Simian immunodeficiency

A

HIV 2 came from
-monkeys to us

45
Q

HIV treatment

A

Several different drugs help to destroy enzyme RT
-cocktail mixture

46
Q

Two examples of HIV treatment drugs

A

Zidovudine (AZT) and laminuridine (3TC)

47
Q

Why is there no vaccine development for HIV

A

Process of copying the dna has many mutations
-its different for each person

48
Q

What type of vaccine is being studied for HIV

A

MRNA vaccine
-to reduce speed of HIV

49
Q

How does HIV spread

A

-blood
-sexual transition (semen)
-breast milk

50
Q

Lyric viral infection

A

Good infection
-kills cell but gets rid of virus as it dies
Example- cold, rhino virus

51
Q

Persistent viral infection

A

Slow, mythological, deadly over long period fo time
Example- brain degeneration in measles

52
Q

Latent viral infections

A

Hides in cells then emerges

Example- herpies 1: causes cold sores, shingles, mono

53
Q

Cancer viral infections

A

Normal cells turns into cancer cell

Example- burkitts lymphoma (b lymphocytes around jaw region)

54
Q

Three main avenues for pathogens to enter

A

-mucous membrane of major organ systems
-skin
-parenteral

55
Q

Mucous membrane of major organ systems

A

-respiratory tract
-GI tract
-GU tract
-eye/conjectiva

56
Q

Skin

A

Innate but still vulnerable
-fungal infections

57
Q

Parenteral

A

Broken skin that gives direct entery into blood
-bite, catheter, needle

Example- malaria

58
Q

Adherence

A

Ability to attach to cells and invade tissues
-forms link with host

59
Q

Host contains

A

Receptors (sugar, present on cell membrane)

60
Q

Pathogen contains

A

Adhesions (enable sugar to match up)

61
Q

Adhesions are made up of

A

Glycoproteins or lipoproteins

62
Q

Adhesions can be found in what four forms

A

-on capsule
-fimbrae
-flagella
-cell wall

63
Q

An example of capsule adhesions

A

S. Mutants

64
Q

S.mutants and adhesions: attach…

A

Attach by capsule, and use enzyme glucosyltransferaze to metabolize sugar

65
Q

S.mutants turns sugar into

A

Glucose and fructose, then glucose into glucose and fructose into acid

66
Q

Glucose into glucan

A

Is the gummy sugar found on teeth that forms plaque

67
Q

Plaque and acid

A

Acid soaks into gummy sugar and begins breaking down teeth

68
Q

Examples of fimbrae

A

E.coli and n.gonorrhea

69
Q

N.gonorrhea and fimbrae

A

Contains protein called opa, that is found on fimbrae

70
Q

S. Pyogenes and attachment

A

Contains an M protein, that is found outside cell wall that is resistant to heat/acid and phagocytosis

71
Q

Invasion technique

A

Penetrating host defences
-exoenzymes (there are four)

72
Q

Four exoenzymes that process invasion

A

-coagulase
-kinase
-hyaluronidase
-collagenase

73
Q

Coagulase

A

Turns fibrinogen to fibrin, creating a CLOT

Example- s.aureus

74
Q

Kinase

A

Breaks fimbrae clot and leaves body vulnerable to more invasion
-more bacteria released to travel through body

Example- s.pyogenes

75
Q

Hyaluronidase

A

Fragment/breaks down tissue

Example- colistridum perfringes (necrotic tissue)
s.Pyogenes (flesh eating disease)

76
Q

Collagenase

A

Breaks Down tissue

Example- c.diff (colitis)

77
Q

Toxaemia

A

Toxin in hosts blood

78
Q

Toxoid

A

Inactivated toxin found in vaccines

79
Q

Types of toxins

A

Exotoxin and endotoxin

80
Q

Exotoxin definition/example

A

Secretes in human body to cause disease

Example- tetanus (opstitholonos or C shape back spasm)

81
Q

Exotoxin notes

A

-can be gram + or -
-byproduct of metabolism
-protein
-circulates in body fluids
-s/s are specific/easily recognizable
-no fever in response

82
Q

Exotoxin —> antitoxin

A

Antitoxin is produced by body
-then neutralized
-then toxoid is used to make vaccine

DTaP

83
Q

Three classes of exotoxins

A

-classic A+B
-membrane disrupting
-super antigens

84
Q

Classic A+B

A

A protein—> ACTIVE (cells react and kill)

B protein—> BINDS (to whole cell then drag A in)

85
Q

Membrane disrupting exotoxins

A

-making protein channels (disrupt plasma mem)
-phospholipid bilayer is disrupted (cellular contents flow out)

86
Q

Super antigens exotoxins

A

Activate an intense immune response (cytokines)

Symptoms: violent behaviour, nausea, diarrhea, shock

Example- TSS, S.aureus (food poisioning)

87
Q

Endotoxin

A

Always present, just needs to release
-lipids
-released more during lyse of bacteria cells

88
Q

Disseminated intramuscular coagulation

A

Consequence of endotoxins, activation of blood clotting proteins
-blood clot formation
-gram negative !!!

-decreased blood supply/tissue death

89
Q

Endotoxic shock

A

Related to secretion of cytokine by macrophages
-secrete TNF, damages capillaries, lowers bp —> shock

90
Q

Endotoxins are apart of the

A

Gram negative cell wall

91
Q

Endotoxins are produced by

A

Gram negative

92
Q

Two large effects of gram negative cells

A

-fever/pyrogenic

-shock response

93
Q

Fever

A

-is a good and natural process
-eventually need to break the process or could potentially end up in coma/brain reaction

94
Q

Process of fever

A

Macrophage/monocyte engulf GN bacteria, lipid A is released and triggers monocyte to release INTERLEUKIN-1

95
Q

What does interleukin-1 do?

A

Initiates fever by interacting with hypothalamus

96
Q

Chills stage of fever

A

Abundance of IL-1 in blood
-shivering

97
Q

crisis stage

A

IL-1 decreasing, sweating

98
Q

Septic shock occurs due to

A

Change in blood pressure
-lipid A releases Cachein and travels to vital organs changing the permeability of the blood vessels there and causes shock

99
Q

Which of the two is good for the body? Fever or shock

A

Fever
-shock is never good

100
Q

Cachein

A

Tumour necrosis factor, TNF

101
Q

Shock symptoms

A

Nausea, vomiting, kidney failure, turning pale, breathing heavy

102
Q

Lipid A comes from

A

Lipopolysacharides

103
Q

Lipid A causes

A

Fever, nausea, vomiting, diarrhea, dysentery and eventually septic shock

104
Q

Can you neutralize endotoxins by antibiotics

A

No

Microbiologyh (18 decks)

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