Week 1: Basics of Bacteriology Flashcards

1
Q

The ratio of cellular domains in the human body

A

10x more prokaryotic cells than eukaryotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bacterial functions in the human body

A
  • physiological
  • nutritional
  • protective functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some things that can affect the normal flora of the human body

A
  • antibiotics
  • tissue damage
  • medical procedures
  • changes in diet
  • introduction of new pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Potential clinical implications of human microbiome

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Types of relationships between microbes and humans

A
  • Mutualism
  • Commensalism
  • Parasitic
  • Pathogenic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe a mutualism

A

Both the host and the microbe benefit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe a commensalism

A

One partner of the relationship benefits (usually the microbe) and the other partner (usually the host) is neither benefited nor harmed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Decribe a parasitic relationship

A

The microbe benefits at the expense of the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe a pathogenic relationship

A

The microbe causes damage to the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the relationships between microbes and humans and what they mean

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are opportunistic pathogens?

A
  • Only cause disease in those with a compromised immune defense
  • Often organisms that are typically normal flora or can normally be controlled by a competent immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of opportunistic pathogens

A

T-cell immune compromise:

  • Pneumocystis jerovecii pneumonia
  • Cytomegalovirus

Patients receiving broad-spectrum antibiotics

  • Clostridium difficile colitis

Patients with intravenous catheters

  • Staphylococcus epidermidis bacteremia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Compromised T-cell opportunistic pathogens

A
  • Pneumocystis jerovecii pneumonia
  • Cytomegalovirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Broad-spectrum antibiotics opportunistic pathogens

A
  • Patients receiving broad-spectrum antibiotics
  • Clostridium difficile colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Intravenous catheters opportunistic pathogens

A

Staphylococcus epidermidis bacteremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are frank pathogens?

A

Always associated with disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Examples of frank pathogens

A
  • Neisseria gonorrhoeae
  • Shigella
  • Human Immunodeficiency Virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are facultative pathogens?

A

Fall between the two extremes (opportunistic and frank) and the majority of organisms that cause disease fall into this group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Examples of Facultative pathogens

A
  • Staphylococcus aureus
  • Escherichia coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Size of prokaryotes

A

0.2-2.0 um

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

size of eukaryotes

A

typically 10-100 um

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nucleus of prokaryotes

A

no nuclear-bound nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Nucleus of Eukaryotes

A

True nucleus with nuclear membrane and nucleoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Prokaryote membrane-wrapped organelles

A

Absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Eukaryote membrane-wrapped organelles
Present (Golgi, lysosome, ER, mitochondria, chorplast)
26
Cell wall of prokaryotes
Usually present and complex
27
Cell wall of Eukaryotes
When present is chemically simple
28
Ribosomes of prokaryotes
70S Ribosome
29
Eukaryotes Ribosomes
80S
30
DNA of prokaryotes
* Single circular chromosome * smaller
31
Eukaryotes DNA
Multiple linear chromosomes
32
Cell division of prokaryotes
Binary Fission
33
Cell division of eukaryotes
Mitosis
34
Sexual reproduction of prokaryotes
* No meiosis * transfer of DNA fragments only
35
Sexual reproduction of eukaryotes
Meiosis
36
Gram stain reaction
37
Clinically relevant exceptions of the gram stain
* Mycobacterium * Nocardia * Mycoplasma * Ureaplasma * Chlamydia
38
E coli gram stain
Negative
39
Klebsiella gram stain
Negative
40
Bacteriodes gram stain
Negative
41
Staphylococcus gram stain
Positive
42
Streptococcus gram stain
Positive
43
Listeria gram stain
Positive
44
Gram stain process
Fixation crystal violet decolorization counter stain safranin
45
Describe the structural differences between gram-negative and gram-positive bacteria
Gram-positive bacteria * have a thick peptidoglycan layer * 3D crosslinking * degraded by lysozyme * Teichoic Acid * links peptidoglycan too lipids in the cell membrane Gram-negative bacteria * thin peptidoglycan layer * 3D cross-linking * degraded by lysozyme * Outer membrane * maintains bacterial structure * permeability barrier * Lipopolysaccharide (LPS) * endotoxin
46
Describe the features of Gram-positive bacteria
47
Describe the features of Gram-negative bacteria
48
List of organisms with poor or no gram-staining 5 listed
* Mycobacteria * Nocardia * Mycoplasma/Ureaplasma * Chlamydia/Rickettsia * Treponema
49
Cause of Mycobacteria gram-stain appearance
Contain many mycolic acids and lipids in the cell wall that do not allow the gram stain to penetrate completely
50
Cause of Nocardia gram-stain appearance
contain mycolic acid and lipids but fewer than mycobacteria
51
Cause of Mycoplasma/Ureaplasma gram-stain appearance
No cell wall layer (contain a tri-layered cell membrane)
52
Cause of Chlamydia/Rickettsia gram-stain appearance
Obligate intracellular organisms, gram reaction does not perform well for intracellular organisms, technically they are gram-negative
53
Cause of Treponema gram-stain appearance
organisms are very small (\<1 um), dark-field microscopy is used to visualize, technically, they are gram-negative
54
Describe the different forms of bacteria propagation
55
Describe Bacterial division
56
Describe Bacterial sporulation
57
Describe the bacterial association with disease
58
Mechanisms of bacterial pathogenesis
* Adhesion * Invasion * Evasion * Disruption * Destruction * Induction
59
Describe adhesion as a mechanism of bacterial pathogenesis
(host cell surface binding)
60
Describe Invasion as a mechanism of bacterial pathogenesis
invasion to host cell or physical barrier
61
Describe Evasion as a mechanism of bacterial pathogenesis
of immune surveillance
62
Describe Disruption as a mechanism of bacterial pathogenesis
disruption of host cell function
63
Describe destruction as a mechanism of bacterial pathogenesis
destruction of host cell
64
Describe Induction as a mechanism of bacterial pathogenesis
induction of host immune response leading to * inflammation * anaphylaxis * autoimmune
65
Routes of bacterial infection
Respiratory tract Gastrointestinal tract Genitourinary tract Unnatural routes opened up by breaks in mucous membranes or skin different levels of hos degree mechanisms are enlisted depending on the number of organisms entering and their virulence
66
Examples of diarrheal pathogens
67
General characteristics
Streptococcus pyogenes
68
Clinical syndromes of streptococcus pyogenes
* Tonsillopharyngitis * Scarlet fever * Toxic shock syndrome * Skin & soft tissue infections
69
Virulence factors of Streptococcus pyogenes (GAS) 8 listed
* M protein * Hyaluronic acid capsule * Pyogenic exotoxins * Streptokinase * Proteinkinase * C5a petidase * Streptolysin S and Streptolysin O * DNase
70
Describe M protein
* Key virulence factor * anti-phagocytic * may act as an adhesin * may play a role in invasiveness
71
Describe hyaluronic acid capsule
anti-phagocytic
72
Describe pyrogenic exotoxins
* associated with invasive disease and streptococcal toxic shock syndrome * can act as a superantigen
73
Describe streptokinase
Can dissolve fibrin clots
74
Describe proteinase
can damage a variety of cell types
75
Describe C5a peptidase
Can inactivate complement component C5a adversely affecting chemotaxis
76
Describe Streptolysin S and Streptolysin O
Hemolysins that can damage a variety of cell types
77
Describe DNase
Degrades DNA
78
Describe the general characteristics of Staphylococcus aureus
79
Clinical syndromes of Staphylococcus aureus
* Skin & soft tissue infections * Bone & Joint infections * Bacteremia * Hospital-acquired pneumonia
80
Staphylococcus aureus Virulence factors 10 listed
* Nuclease * Cytotoxins * Lipases * Enterotoxins * Adhesins * Leukocidins * immunoglobulin binding proteins * Autolysins * Superantigens * Proteases
81
Describe S. aureus nuclease
Cleaves DNA and RNA
82
Describe S. aureus cytotoxins
toxic for many cell types
83
Describe S. aureus lipases
hydrolyzes lipids
84
Describe S. aureus Enterotoxins
Superantigens (TSST-1)
85
Describe S. aureus Adhesins
* Bind cell surface receptors on host tissues, host cells and soluble factors in the blood * Bind to complement factors to inhibit complement activation cascade
86
Describe S. aureus Leukocidins
Secreted virulence factors, including toxins and peptides Selectively target and kill key classes of host immune cell
87
Describe S. aureus Immunoglobulin binding proteins
* Bind IgGs via Fc * Immobilize IgGs and inhibit engagement of host immune factors
88
Describe S. aureus Autolysins
Highly immunogenic cell wall transglycosylases that facilitate invasion of non-professional phgocytes
89
Describe S. aureus Superantigens
* Potent immunostimulatory exotoxins * Activate T cells and trigger cytokine release
90
Describe S. aureus Proteases
* Surface-bound and secreted forms of target host immune factors and tissues * GluV8 cleaves IgGs via hinge and inactivates effector functions
91
E. Coli general characteristics
92
Clinical syndromes of E. coli
93
Clinical presentations of E. coli
94
Clinical presentation of S. aureus
95
Clinical presentation of S. pyogenes
96
E. Coli virulence factors
* Endotoxin * Fimbriae * K-1 capsule * Toxigenic E. coli * ETEC * EHEC * EPEC * EIEC