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MICROM 442 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Robert Hooke and Antoni Van Leeuwenhoek (1600s)

A

developed single-lensed microscopes

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2
Q

Edward Jenner (1700s)

A

smallpox vaccine

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3
Q

Florence Nightingale (1800s)

A

hygiene is a great way to avoid infection

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4
Q

Pasteur and Koch (1800s)

A

microbes as causative agents of disease

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5
Q

Hans Christian Gram (1800s)

A

Gram’s stain

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6
Q

Paul Erlich (1900s)

A

606 salvarsan/arsphenamine for syphilis

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7
Q

Alexander Fleming (1900s)

A

penicillin

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8
Q

Gerhard Domagk (1900s)

A

sulfonamides

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9
Q

Avery, MacLeod, McCarty (1900s)

A

DNA as a transforming principle

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10
Q

Rich Roberts (1900s)

A

restriction enzymes

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11
Q

Herb Boyer, Stanley Cohen (1900s)

A

constructing recombinant DNA

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12
Q

Kary Mullis (1900s)

A

PCR

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13
Q

Taxonomy

A

classification into groups

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14
Q

Phylogeny

A

study of evolution and ancestry

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15
Q

Metabiome

A

cataloguing constituent members of microbial populations

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16
Q

Path of pathogen

A

colonize, multiply, transmit

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17
Q

Transient

A

colonize skin

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18
Q

Carrier state

A

has organism, but is unaffected

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19
Q

Microbiota on skin

A

Staphylococcus epidermidis, other staph, propionibacterium, diphtheroids

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20
Q

Conjunctiva

A

S. epidermidis and corynebacteria

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21
Q

Mouth

A

Streptococcus mutans, Neisseria, and Moraxella

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22
Q

Stomach and small intestine

A

sparsely inhabited

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23
Q

Colon

A

Bacteroides, Fusobacterium, Clostridium perfingens, E. Coli, enterobacteriaceae, enterococci, and yeasts

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24
Q

Nares

A

Staphylococcus aureus

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25
Q

Nasopharynx

A

Similar to mouth, Steptococcus pneumoniae, neisseria meningitidis, Haemophilus influenzae

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26
Q

Larynx and below, middle ear, and sinuses

A

Protected by mucociliary escalator

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27
Q

Urinary tract

A

mainly sterile

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28
Q

Vagina

A

Things from skin, colon, and perineum

Child bearing years: Lactobacillus, anaerobic GNRs, GPC, Gardenerella, Mycoplasma, Ureaplasma

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29
Q

Beneficial effects of bacteria

A

priming immune system, excludes other bacteria, and helps with nutrition

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30
Q

Identification of etiological agents (why they happen)

A

1) determine nature of disease
2) predict course and potential outcomes
3) tailor therapy
4) exclude non-infectious causes of symptoms

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31
Q

Conventional intervention

A

1) gross phenotype
2) biochemical characteristics
3) Antigenic structures
4) Toxin production
5) Nucleic acid sequences
6) Flow of information (DNA, RNA, enzymatic functions, structures)

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32
Q

Conventional Molecular Detection

A

1) probes for culture confirmation
2) PCR
3) Next Generation Sequencing

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33
Q

Primary pathogen

A

infects competent host

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34
Q

Opportunistic pathogen

A

infects compromised host

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35
Q

Virulence

A

quantitative measure of likelihood of causing disease

36
Q

Infectivity

A

quantitative measure of a pathogen’s ability to infect another host

37
Q

Colonization

A

1) adherence
2) motility
3) survival or fitness in an environment outside host

38
Q

Multiply

A

1) nutrition

2) avoiding host immune surveillance

39
Q

Host Defense Mechanisms

A

1) non-specific
2) Innate immunity/acute inflammation
3) Adaptive (Acquired/Specific) Immunity

40
Q

Non-specific

A

First line of defense, always there and don’t require sensor/response mechanism

41
Q

Innate Immunity

A

Early warning system, senses presence of invader, “alert” response

42
Q

Adaptive Immunity

A

“Immune response”, targeted to invader, provides immunologic memory

43
Q

GI Tract Normal secretions (non-specific)

A

Lysozyme (saliva)
Low pH
Bile salts
Mucus

44
Q

GI Tract Normal microbiota (non-specific)

A

Compete for nutrients
Compete for host receptors
Produce bacteriocins
Stimulate production of antimicrobial peptides

45
Q

Gut-associated lymphoid tissue (non-specific)

A
  • Poised to deal with microbes that penetrate intestinal lining
  • Secretory antibodies (slgA) are transported into gut lumen
  • Specialized regions called Peyer’s patches sample the intestinal flora
  • Phagocytic cells capture bacteria and bring them to the draining lymph node
46
Q

Complement activation

A
  • Induces inflammation
  • Recruits leukocytes
  • Opsonizes bacteria
  • Kills bacteria by lysis
47
Q

The Membrane Attack Complex (MAC) lyses:

A
  • gram bacteria
  • enveloped viruses
  • host cells that display foreign proteins on their surface
48
Q

Cells of the Innate Immune System

A 
First to see pathogens
-Epithelial cells
-Endothelial cells
Phagocytic Cells
-Neutrophils
-Dendritic cells
-Macrophages
49
Q

Triggers of Inflammation

A

Physical trauma, tissue damage

Bacterial products
-lipopolysaccharide (LPS), lipoproteins, peptidoglycans (PGN), lipoteichoic acid, DNA, others

50
Q

Pattern Recognition Receptors

A

Central to innate immunity.
Toll-like receptors (TLRs): extracellular pathogens
Nod-like receptors (NLRs): intracellular pathogens

51
Q

TLR 4

A

LPS

GRAM NEGATIVE

52
Q

TLR 2

A

lipoproteins, peptidoglycans (PGN), lipoteichoic acid, glycolipids

GRAM POSITIVE

53
Q

TLR 5

A

bacterial flagellin

54
Q

TLR 9

A

bacterial DNA

55
Q

TLR 3

56
Q

TLR 7,8

A

Independently activated by an antiviral compound

57
Q

TLR 1

A

Binding partner with TLR 2; inhibits signaling by some bacterial products

58
Q

Cationic Antimicrobial Peptides

A

Produced by epithelial, endothelial, and phagocytic cells to kill gram +/- bacteria, fungi, and some viruses.

Bind to the negatively charged microbial membranes and form pores that kill the cell

59
Q

Pro-inflammatory cytokines

A

Dilation of capillaries
Extravasation of fluid
Diapedesis of leukocytes

Low conc.= activate cells in the local area
High conc.=induce fever and production of acute phase proteins

60
Q

IL-8

A

recruits cells to site of infection

61
Q

IL-6, TNF alpha, IL-1

A

activate cells (epithelial, endothelial, and phagocytes)

62
Q

Phagocytic Defenses

A
  • Opsonins (antibody) increase phagocytosis
  • Microbes are taken up into phagosome
  • Phagosomes fuse with lysosomes to form phagolysosomes
  • Microbes are killed/degraded within the phagolysosome
63
Q

Polymorphonucelear Leukocytes (PMNs)

A 
Develop from bone marrow cells
Short half-life
Degrade phagocytosed bacteria and produce IL-8, IL-1, TNF
First phagocytic cells mobilized
Chemotaxis toward C5a
64
Q

Macrophages and Dendritic Cells

A

Derived from blood monocytes

Act as antigen presenting cells (APC)

65
Q

B cells

A

produces antibodies with a unique antigenic specificity

66
Q

Antibodies

A
  • Block attachment to host
  • Neutralize toxins
  • Promote opsonization
  • Activate complement
67
Q

IgM

A

primary antibody response

68
Q

IgG

A

cross the placenta

69
Q

IgE

A

triggers release of histamines

70
Q

IgA

71
Q

CD8

A 
MHC class I
Directly lyse infected cells
72
Q

CD4

A

MHC class II
T helper cells
Produce cytokines

73
Q

Cell wall antibiotics

A

B-lactams (penicillin and cephalosporins)

Glycopeptides (vancomycin)

74
Q

Cell membrane antibiotics

A

polymyxins

75
Q

DNA antibiotics

A

Fluroquinolones
Sulfonamides and trimethoprim
Metronidazole

76
Q

Transcription antibiotics

77
Q

Protein synthesis antibiotics

A

Aminoglycosides (gentamycin)
Macrolides
Tetracyclines
Lincosamides (clindamycin)

78
Q

General mechanisms of resistance

A

Efflux
Restricted access to target
Inactivating enzymes
Target modification

79
Q

Multi-resistant drug strains

A

Encode multiple genes
Encode a gene that can target multiple antibiotics
Selective pressure

80
Q

B-lactams

A

Penicillins
Cephalosporins
Monobactams
Carbapenems

81
Q

Vancomycin

A

Kills gram positive bacteria

Used to treat MRSA

82
Q

Strains of Enterococcus

A

E. faecalis (susceptible)

E. faecium (more resistant)

83
Q

Cephalosporin subclasses

A 
1st Cefazolin (skin infection, surgical prophylaxis)
2nd (non important)
3rd Ceftriaxone (meningitis, endocarditis, etc)
4th Cefepime (life-threatening infection)
5th Ceftaroline (MRSA)
84
Q

Rifampin

A

Targets transcription

Rapid selection for resistance

85
Q

Aminogylcosides

A

Used against gram negative

MICROM 442 (1 decks)

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