Midterm 1 Flashcards
1
Q
Robert Hooke and Antoni Van Leeuwenhoek (1600s)
A
developed single-lensed microscopes
2
Q
Edward Jenner (1700s)
A
smallpox vaccine
3
Q
Florence Nightingale (1800s)
A
hygiene is a great way to avoid infection
4
Q
Pasteur and Koch (1800s)
A
microbes as causative agents of disease
5
Q
Hans Christian Gram (1800s)
A
Gram’s stain
6
Q
Paul Erlich (1900s)
A
606 salvarsan/arsphenamine for syphilis
7
Q
Alexander Fleming (1900s)
A
penicillin
8
Q
Gerhard Domagk (1900s)
A
sulfonamides
9
Q
Avery, MacLeod, McCarty (1900s)
A
DNA as a transforming principle
10
Q
Rich Roberts (1900s)
A
restriction enzymes
11
Q
Herb Boyer, Stanley Cohen (1900s)
A
constructing recombinant DNA
12
Q
Kary Mullis (1900s)
A
PCR
13
Q
Taxonomy
A
classification into groups
14
Q
Phylogeny
A
study of evolution and ancestry
15
Q
Metabiome
A
cataloguing constituent members of microbial populations
16
Q
Path of pathogen
A
colonize, multiply, transmit
17
Q
Transient
A
colonize skin
18
Q
Carrier state
A
has organism, but is unaffected
19
Q
Microbiota on skin
A
Staphylococcus epidermidis, other staph, propionibacterium, diphtheroids
20
Q
Conjunctiva
A
S. epidermidis and corynebacteria
21
Q
Mouth
A
Streptococcus mutans, Neisseria, and Moraxella
22
Q
Stomach and small intestine
A
sparsely inhabited
23
Q
Colon
A
Bacteroides, Fusobacterium, Clostridium perfingens, E. Coli, enterobacteriaceae, enterococci, and yeasts
24
Q
Nares
A
Staphylococcus aureus
25
Nasopharynx
Similar to mouth, Steptococcus pneumoniae, neisseria meningitidis, Haemophilus influenzae
26
Larynx and below, middle ear, and sinuses
Protected by mucociliary escalator
27
Urinary tract
mainly sterile
28
Vagina
Things from skin, colon, and perineum
| Child bearing years: Lactobacillus, anaerobic GNRs, GPC, Gardenerella, Mycoplasma, Ureaplasma
29
Beneficial effects of bacteria
priming immune system, excludes other bacteria, and helps with nutrition
30
Identification of etiological agents (why they happen)
1) determine nature of disease
2) predict course and potential outcomes
3) tailor therapy
4) exclude non-infectious causes of symptoms
31
Conventional intervention
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)
32
Conventional Molecular Detection
1) probes for culture confirmation
2) PCR
3) Next Generation Sequencing
33
Primary pathogen
infects competent host
34
Opportunistic pathogen
infects compromised host
35
Virulence
quantitative measure of likelihood of causing disease
36
Infectivity
quantitative measure of a pathogen's ability to infect another host
37
Colonization
1) adherence
2) motility
3) survival or fitness in an environment outside host
38
Multiply
1) nutrition
| 2) avoiding host immune surveillance
39
Host Defense Mechanisms
1) non-specific
2) Innate immunity/acute inflammation
3) Adaptive (Acquired/Specific) Immunity
40
Non-specific
First line of defense, always there and don't require sensor/response mechanism
41
Innate Immunity
Early warning system, senses presence of invader, "alert" response
42
Adaptive Immunity
"Immune response", targeted to invader, provides immunologic memory
43
GI Tract Normal secretions (non-specific)
Lysozyme (saliva)
Low pH
Bile salts
Mucus
44
GI Tract Normal microbiota (non-specific)
Compete for nutrients
Compete for host receptors
Produce bacteriocins
Stimulate production of antimicrobial peptides
45
Gut-associated lymphoid tissue (non-specific)
- 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
Complement activation
- Induces inflammation
- Recruits leukocytes
- Opsonizes bacteria
- Kills bacteria by lysis
47
The Membrane Attack Complex (MAC) lyses:
- gram bacteria
- enveloped viruses
- host cells that display foreign proteins on their surface
48
Cells of the Innate Immune System
```
First to see pathogens
-Epithelial cells
-Endothelial cells
Phagocytic Cells
-Neutrophils
-Dendritic cells
-Macrophages
```
49
Triggers of Inflammation
Physical trauma, tissue damage
Bacterial products
-lipopolysaccharide (LPS), lipoproteins, peptidoglycans (PGN), lipoteichoic acid, DNA, others
50
Pattern Recognition Receptors
Central to innate immunity.
Toll-like receptors (TLRs): extracellular pathogens
Nod-like receptors (NLRs): intracellular pathogens
51
TLR 4
LPS
GRAM NEGATIVE
52
TLR 2
lipoproteins, peptidoglycans (PGN), lipoteichoic acid, glycolipids
GRAM POSITIVE
53
TLR 5
bacterial flagellin
54
TLR 9
bacterial DNA
55
TLR 3
Viral RNA
56
TLR 7,8
Independently activated by an antiviral compound
57
TLR 1
Binding partner with TLR 2; inhibits signaling by some bacterial products
58
Cationic Antimicrobial Peptides
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
Pro-inflammatory cytokines
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
IL-8
recruits cells to site of infection
61
IL-6, TNF alpha, IL-1
activate cells (epithelial, endothelial, and phagocytes)
62
Phagocytic Defenses
- 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
Polymorphonucelear Leukocytes (PMNs)
```
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
Macrophages and Dendritic Cells
Derived from blood monocytes
| Act as antigen presenting cells (APC)
65
B cells
produces antibodies with a unique antigenic specificity
66
Antibodies
- Block attachment to host
- Neutralize toxins
- Promote opsonization
- Activate complement
67
IgM
primary antibody response
68
IgG
cross the placenta
69
IgE
triggers release of histamines
70
IgA
secretion
71
CD8
```
MHC class I
Directly lyse infected cells
```
72
CD4
MHC class II
T helper cells
Produce cytokines
73
Cell wall antibiotics
B-lactams (penicillin and cephalosporins)
| Glycopeptides (vancomycin)
74
Cell membrane antibiotics
polymyxins
75
DNA antibiotics
Fluroquinolones
Sulfonamides and trimethoprim
Metronidazole
76
Transcription antibiotics
Rifampin
77
Protein synthesis antibiotics
Aminoglycosides (gentamycin)
Macrolides
Tetracyclines
Lincosamides (clindamycin)
78
General mechanisms of resistance
Efflux
Restricted access to target
Inactivating enzymes
Target modification
79
Multi-resistant drug strains
Encode multiple genes
Encode a gene that can target multiple antibiotics
Selective pressure
80
B-lactams
Penicillins
Cephalosporins
Monobactams
Carbapenems
81
Vancomycin
Kills gram positive bacteria
| Used to treat MRSA
82
Strains of Enterococcus
E. faecalis (susceptible)
| E. faecium (more resistant)
83
Cephalosporin subclasses
```
1st Cefazolin (skin infection, surgical prophylaxis)
2nd (non important)
3rd Ceftriaxone (meningitis, endocarditis, etc)
4th Cefepime (life-threatening infection)
5th Ceftaroline (MRSA)
```
84
Rifampin
Targets transcription
| Rapid selection for resistance
85
Aminogylcosides
Used against gram negative
