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Infectious Disease > Week 1: Basics of Bacteriology > Flashcards

Week 1: Basics of Bacteriology Flashcards

1
Q

The ratio of cellular domains in the human body

A

10x more prokaryotic cells than eukaryotic

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2
Q

Bacterial functions in the human body

A
  • physiological
  • nutritional
  • protective functions
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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
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4
Q

Potential clinical implications of human microbiome

A
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5
Q

Types of relationships between microbes and humans

A
  • Mutualism
  • Commensalism
  • Parasitic
  • Pathogenic
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6
Q

Describe a mutualism

A

Both the host and the microbe benefit

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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

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8
Q

Decribe a parasitic relationship

A

The microbe benefits at the expense of the host

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9
Q

Describe a pathogenic relationship

A

The microbe causes damage to the host

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10
Q

Describe the relationships between microbes and humans and what they mean

A
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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
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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
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13
Q

Compromised T-cell opportunistic pathogens

A
  • Pneumocystis jerovecii pneumonia
  • Cytomegalovirus
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14
Q

Broad-spectrum antibiotics opportunistic pathogens

A
  • Patients receiving broad-spectrum antibiotics
  • Clostridium difficile colitis
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15
Q

Intravenous catheters opportunistic pathogens

A

Staphylococcus epidermidis bacteremia

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16
Q

What are frank pathogens?

A

Always associated with disease

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17
Q

Examples of frank pathogens

A
  • Neisseria gonorrhoeae
  • Shigella
  • Human Immunodeficiency Virus
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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

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19
Q

Examples of Facultative pathogens

A
  • Staphylococcus aureus
  • Escherichia coli
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20
Q

Size of prokaryotes

A

0.2-2.0 um

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21
Q

size of eukaryotes

A

typically 10-100 um

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22
Q

Nucleus of prokaryotes

A

no nuclear-bound nucleus

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23
Q

Nucleus of Eukaryotes

A

True nucleus with nuclear membrane and nucleoli

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24
Q

Prokaryote membrane-wrapped organelles

A

Absent

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25
Q

Eukaryote membrane-wrapped organelles

A

Present (Golgi, lysosome, ER, mitochondria, chorplast)

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26
Q

Cell wall of prokaryotes

A

Usually present and complex

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27
Q

Cell wall of Eukaryotes

A

When present is chemically simple

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28
Q

Ribosomes of prokaryotes

A

70S Ribosome

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29
Q

Eukaryotes Ribosomes

A

80S

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30
Q

DNA of prokaryotes

A
  • Single circular chromosome
  • smaller
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31
Q

Eukaryotes DNA

A

Multiple linear chromosomes

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32
Q

Cell division of prokaryotes

A

Binary Fission

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33
Q

Cell division of eukaryotes

A

Mitosis

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34
Q

Sexual reproduction of prokaryotes

A
  • No meiosis
  • transfer of DNA fragments only
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35
Q

Sexual reproduction of eukaryotes

A

Meiosis

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36
Q

Gram stain reaction

A
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37
Q

Clinically relevant exceptions of the gram stain

A
  • Mycobacterium
  • Nocardia
  • Mycoplasma
  • Ureaplasma
  • Chlamydia
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38
Q

E coli gram stain

A

Negative

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39
Q

Klebsiella gram stain

A

Negative

40
Q

Bacteriodes gram stain

A

Negative

41
Q

Staphylococcus gram stain

A

Positive

42
Q

Streptococcus gram stain

A

Positive

43
Q

Listeria gram stain

A

Positive

44
Q

Gram stain process

A

Fixation

crystal violet

decolorization

counter stain safranin

45
Q

Describe the structural differences between gram-negative and gram-positive bacteria

A

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
Q

Describe the features of Gram-positive bacteria

A
47
Q

Describe the features of Gram-negative bacteria

A
48
Q

List of organisms with poor or no gram-staining

5 listed

A
  • Mycobacteria
  • Nocardia
  • Mycoplasma/Ureaplasma
  • Chlamydia/Rickettsia
  • Treponema
49
Q

Cause of Mycobacteria gram-stain appearance

A

Contain many mycolic acids and lipids in the cell wall that do not allow the gram stain to penetrate completely

50
Q

Cause of Nocardia gram-stain appearance

A

contain mycolic acid and lipids but fewer than mycobacteria

51
Q

Cause of Mycoplasma/Ureaplasma gram-stain appearance

A

No cell wall layer (contain a tri-layered cell membrane)

52
Q

Cause of Chlamydia/Rickettsia gram-stain appearance

A

Obligate intracellular organisms, gram reaction does not perform well for intracellular organisms, technically they are gram-negative

53
Q

Cause of Treponema gram-stain appearance

A

organisms are very small (<1 um), dark-field microscopy is used to visualize, technically, they are gram-negative

54
Q

Describe the different forms of bacteria propagation

A
55
Q

Describe Bacterial division

A
56
Q

Describe Bacterial sporulation

A
57
Q

Describe the bacterial association with disease

A
58
Q

Mechanisms of bacterial pathogenesis

A
  • Adhesion
  • Invasion
  • Evasion
  • Disruption
  • Destruction
  • Induction
59
Q

Describe adhesion as a mechanism of bacterial pathogenesis

A

(host cell surface binding)

60
Q

Describe Invasion as a mechanism of bacterial pathogenesis

A

invasion to host cell or physical barrier

61
Q

Describe Evasion as a mechanism of bacterial pathogenesis

A

of immune surveillance

62
Q

Describe Disruption as a mechanism of bacterial pathogenesis

A

disruption of host cell function

63
Q

Describe destruction as a mechanism of bacterial pathogenesis

A

destruction of host cell

64
Q

Describe Induction as a mechanism of bacterial pathogenesis

A

induction of host immune response leading to

  • inflammation
  • anaphylaxis
  • autoimmune
65
Q

Routes of bacterial infection

A

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
Q

Examples of diarrheal pathogens

A
67
Q

General characteristics

A

Streptococcus pyogenes

68
Q

Clinical syndromes of streptococcus pyogenes

A
  • Tonsillopharyngitis
  • Scarlet fever
  • Toxic shock syndrome
  • Skin & soft tissue infections
69
Q

Virulence factors of Streptococcus pyogenes (GAS)

8 listed

A
  • M protein
  • Hyaluronic acid capsule
  • Pyogenic exotoxins
  • Streptokinase
  • Proteinkinase
  • C5a petidase
  • Streptolysin S and Streptolysin O
  • DNase
70
Q

Describe M protein

A
  • Key virulence factor
  • anti-phagocytic
  • may act as an adhesin
  • may play a role in invasiveness
71
Q

Describe hyaluronic acid capsule

A

anti-phagocytic

72
Q

Describe pyrogenic exotoxins

A
  • associated with invasive disease and streptococcal toxic shock syndrome
  • can act as a superantigen
73
Q

Describe streptokinase

A

Can dissolve fibrin clots

74
Q

Describe proteinase

A

can damage a variety of cell types

75
Q

Describe C5a peptidase

A

Can inactivate complement component C5a adversely affecting chemotaxis

76
Q

Describe Streptolysin S and Streptolysin O

A

Hemolysins that can damage a variety of cell types

77
Q

Describe DNase

A

Degrades DNA

78
Q

Describe the general characteristics of Staphylococcus aureus

A
79
Q

Clinical syndromes of Staphylococcus aureus

A
  • Skin & soft tissue infections
  • Bone & Joint infections
  • Bacteremia
  • Hospital-acquired pneumonia
80
Q

Staphylococcus aureus Virulence factors

10 listed

A
  • Nuclease
  • Cytotoxins
  • Lipases
  • Enterotoxins
  • Adhesins
  • Leukocidins
  • immunoglobulin binding proteins
  • Autolysins
  • Superantigens
  • Proteases
81
Q

Describe S. aureus nuclease

A

Cleaves DNA and RNA

82
Q

Describe S. aureus cytotoxins

A

toxic for many cell types

83
Q

Describe S. aureus lipases

A

hydrolyzes lipids

84
Q

Describe S. aureus Enterotoxins

A

Superantigens (TSST-1)

85
Q

Describe S. aureus Adhesins

A
  • 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
Q

Describe S. aureus Leukocidins

A

Secreted virulence factors, including toxins and peptides

Selectively target and kill key classes of host immune cell

87
Q

Describe S. aureus Immunoglobulin binding proteins

A
  • Bind IgGs via Fc
  • Immobilize IgGs and inhibit engagement of host immune factors
88
Q

Describe S. aureus Autolysins

A

Highly immunogenic cell wall transglycosylases that facilitate invasion of non-professional phgocytes

89
Q

Describe S. aureus Superantigens

A
  • Potent immunostimulatory exotoxins
  • Activate T cells and trigger cytokine release
90
Q

Describe S. aureus Proteases

A
  • Surface-bound and secreted forms of target host immune factors and tissues
  • GluV8 cleaves IgGs via hinge and inactivates effector functions
91
Q

E. Coli general characteristics

A
92
Q

Clinical syndromes of E. coli

A
93
Q

Clinical presentations of E. coli

A
94
Q

Clinical presentation of S. aureus

A
95
Q

Clinical presentation of S. pyogenes

A
96
Q

E. Coli virulence factors

A
  • Endotoxin
  • Fimbriae
  • K-1 capsule
  • Toxigenic E. coli
    • ETEC
    • EHEC
    • EPEC
    • EIEC

Infectious Disease (82 decks)

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