Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sophie - Principles of Pathology - Year 2 > 33.5 Specific Pathogenic Bacteria > Flashcards

33.5 Specific Pathogenic Bacteria Flashcards

1
Q

What are all of the different important bacterial pathogens listed in the spec?

A

Gram positive:

  • Streptococcus pneumoniae
  • Streptococcus pyogenes
  • Staphylococcus aureus (including MRSA)
  • Clostridium difficile
  • Clostridium tetani

Gram negative (O-antigen possessing):

  • Escherichia coli
  • Shigella
  • Salmonella

Gram negative (Non-O-antigen possessing):

  • Neisseria gonorrhoeae
  • Neisseria meningitides

Mycobacteria:

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

For Streptococcus pneumoniae, state:

  • Gram type
  • Diseases it causes
A
  • Gram positive
  • Causes: Primary lobular pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

For Streptococcus pyogenes, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram positive
  • Causes:
    • Pharyngitis (sore throat)
    • Cellulitis (skin infection)
    • Rheumatic fever
    • Glomerulonephritis (glomerulus injury)
  • Features:
    • CO2 may regulate the expression of virulence determinants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

For Staphylococcus aureus, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram positive
  • Causes:
    • Abcesses (a form of skin infection)
    • Surgical wound and burn infections
    • Food poisoning
  • Features:
    • Examples of adhesins, aggressins (e.g. toxins) and antibiotic resistance genes carried by mobile genetic elements (in Staphs & Streps).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What Streptococcus species makes up most of Streptococcus group A?

A

Streptococcus pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is MRSA resistant to?

A

Penicillins, such as methicillin.

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

For Clostridium difficile and Clostridium tetani, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram positive
  • Causes:
    • Clostridium difficile -> Watery diarrhea
    • Clostridium tetani -> Tetanus
  • Features:
    • Anaerobic
    • Spore forming
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

For Escherichia coli, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram negative (O-antigen-possessing)
  • Causes:
    • Travellers’ diarrhoea
    • Dysentery (intestinal inflammation and cramps)
    • Food poisoning
    • Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

For Shigella species, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram negative (O-antigen-possessing)
  • Causes:
    • Travellers’ diarrhoea
    • Dysentery (intestinal inflammation and cramps)
    • Food poisoning
    • Fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

For Salmonella species, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram negative (O-antigen-possessing)
  • Causes:
    • Travellers’ diarrhoea
    • Dysentery (intestinal inflammation and cramps)
    • Food poisoning
    • Typhoid fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

For Neisseria gonorrhoeae, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram negative (Non-O-antigen-possessing)
  • Causes:
    • Gonorrhoea
  • Features:
    • There are differences between men and women in terms of asymptomatic carriage
    • Main steps of infection and transmission cycle, key interactions, importance of sialylation and capsule for evasion (ADD FLASHCARDS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

For Neisseria meningitides, state:

  • Gram type
  • Diseases it causes
  • Features mentioned in the spec
A
  • Gram negative (Non-O-antigen-possessing)
  • Causes:
    • Meningitis
  • Features:
    • Main steps of infection and transmission cycle, key interactions, importance of sialylation and capsule for evasion (ADD FLASHCARDS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Compare how frequently Neisseria gonorrhoeae infections are asymptomatic in men and women.

A

Women are much more likely to carry asymptomatic infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the difference between EHEC and EPEC E.coli?

A

Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) are closely-related bacterial pathogens. EHEC infection causes bloody diarrhea and haemolytic uremic syndrome in developed nations, while EPEC is responsible for paediatric diarrhea in developing countries. Major differences between EHEC and EPEC include:
*EPEC rearranges host cell actin and EHEC does not
*EHEC secretes a Shiga-like toxin and EPEC does not
*EHEC possesses a type III secretion system and EPEC does not
*EPEC passes through the placenta to infect the foetus and EHEC does not
EHEC strains are considered to have evolved from EPEC strains through acquisition of bacteriophages encoding Shiga-like toxins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common pyogenic G+ organisms

A

Staphs and streps

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

Staphylococcus - commensalism?

A

Normally commensal

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

Staphylococcus activation

A

Death signals:
- Poor perfusion, tissue necrosis, anaerobic conditions
- Signal host is dead = can no longer survive as commensal
- Activation of destructive enzymes and toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Staphylococcus shape

A

Cocci

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

Staphylococcus Gram stain

A

G+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Staphylococcus motility

A

Non-motile

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

Staphylococcus ability to form spores

A

No

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

Streptococcus shape

A

Cocci

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

Staphylococcus catalase test

A

Positive (oxygen gas bubbles)

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

Staphylococcus aureus - distinguished from other staphs because (3)

A
  • Coagulase test positivity (coagulase present, coagulates blood plasma)
  • Ferments mannitol
  • Haemolysis of RBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Staphylococcus aureus causes what diseases?

A

Abscesses, surgical wound and burn infections, food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Staphylococcus aureus - Gram status and shape

A

G+ cocci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Staphylococcus aureus - catalase positive; facilitates what?

A

Breakdown of toxic oxygen products

Salt tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Staphylococcus aureus - commensalism and where (3)?

A

Common component of normal flora
- Well-oxygenated sites like the skin
- Survives for long periods in the environment; reinfection/recolonisation
- Vagina of ~5% of women (predisposition to TSS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Staphylococcus aureus - predisposition

A
  • Heavily contaminated environment
  • Compromised immune system
  • Diabetes
  • IV drug use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Staphylococcus aureus - adhesion

A

Teichoic acids and polymers of ribitol phosphate bind to mucosal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Staphylococcus aureus - immune evasion (7)

A
  • Protein A in cell wall binds to Fc portion of IgG at complement binding site, preventing complement activation, C3b production and reducing opsonisation and phagocytosis
  • Catalase positive; breaks down PMN’s ROS
  • Antiphagocytic capsule
  • Coagulase enzyme clots plasma around infection site, forming fibrin barrier impermeable to phagocytes
  • Produce toxins, e.g. phospholipase that damage cell membranes
  • Produce leukocidins, which kill leucocytes
  • Produce IgA protease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Staphylococcus aureus - cause damage by (2)

A

Exozyme production, e.g. proteases inducing local tissue damage

Aggresin production:
- Alpha toxin causes necrosis of skin, forming holes in cell membrane
- Beta toxin degrades sphingomyelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

mRSA - resistant because

A

Methicillin-resistant staphylococcus aureus:

  • 90%: Spreading of plasmids encoding beta-lactamase
  • 20%: Changes in PBP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

mRSA - alternative drug and its MOA

A

Vancomycin - inhibits cell wall synthesis by binding to peptides rather than transpeptidase enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Staphylococcus morphology

A

Clusters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Streptococcus activation

A

Death signals:
- Poor perfusion, tissue necrosis, anaerobic conditions
- Signal host is dead = can no longer survive as commensal
- Activation of destructive enzymes and toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Streptococcus - commensalism?

A

Normally commensal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Streptococcus Gram stain

A

G+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Streptococcus motility

A

Non-motile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Streptococcus ability to form spores

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Streptococcus catalase test

A

Negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Streptococcus morphology

A

Chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Streptococcus pneumoniae causes what disease

A

Primary lobar pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Primary lobar pneumonia

A

Form of pneumonia characterised by inflammatory exudate within alveolar space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Streptococcus pneumoniae - Gram status and shape

A

G+ diplococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Streptococcus pneumoniae distinguished from other Streps because

A

It is alpha-haemolytic, not beta-haemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Streptococcus pneumoniae adhesion

A

Lipoteichoic acids bind to fibronectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Streptococcus pneumoniae immune evasion (2)

A
  • Anti-phagocytic polysaccharide capsule
  • Secretion of IgA protease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

IgA protease

A

Enzyme that cleaves IgA. Secreted by S. pneumoniae, H. influenzae type B, and Neisseria (SHiN) in order to colonise respiratory mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Streptococcus pneumoniae cause damage by

A
  • Lipoteichoic acid trigger immune response
  • Phagocytosis can’t clear bacteria
  • Inflammatory response = damage & pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Streptococcus pneumoniae susceptible to what drug

A

Penicillins

52
Q

Streptococcus pyogenes (Group A) GRT what diseases

A
  • Pharyngitis
  • Cellulitis
  • Rheumatic fever
  • Glomerulonephritis
53
Q

Streptococcus pyogenes (Group A) - Gram status and shape

A

Spherical G+ cocci arranged in chains

54
Q

Streptococcus pyogenes (Group A) - type of pathogen

A

Facultative aerobe

55
Q

Streptococcus pyogenes (Group A) - distinguished from other Streps because

A

Beta haemolytic (complete lysis) and Lancefield typing (group A glycoprotein)

56
Q

Streptococcus pyogenes (Group A) - commensalism?

A

Normal flora of skin and oropharynx

(small numbers, less common than staph. aureus)

57
Q

Streptococcus pyogenes (Group A) - adhesion (2)

A

Protein F and lipoteichoic acids allow binding to fibronectin

M proteins allow binding to cell surface sugars

58
Q

Streptococcus pyogenes (Group A) - adherence to pharyngeal epithelium (pharyngitis)

A

Pili covered in lipoteichoic acid and M proteins

59
Q

Streptococcus pyogenes (Group A) - immune evasion (3)

A
  • M proteins bind the Fc region of IgA/IgG and prevent complement activation/opsonisation
  • Anti-phagocytic hyaluronic capsule
  • Molecular mimicry; hyaluronic acid is normal in body
60
Q

Streptococcus pyogenes (Group A) - cause damage by (2)

A

Production of:
- Exoenzymes
- Toxins and haemolysins

61
Q

Streptococcus pyogenes (Group A) - main exotoxin and its function

A

Exotoxin B - protease that rapidly destroys tissue and is produced in large amounts

62
Q

Streptococcus pyogenes (Group A) - quorum sensing

A

Detects CO2 levels to up regulate virulence factors in the body when they are greater (death signal)

63
Q

Streptococcus pyogenes (Group A) - treatment

A
  • Susceptible to penicillins unless rheumatic fever or acute glomerulonephritis arise
  • Can use macrolides, but resistant stains have emerged
64
Q

Clostridia Gram stain

A

Positive

65
Q

Clostridia shape

A

Bacillus/rod

66
Q

Clostridia catalase test

A

Negative

67
Q

Clostridia haemolysis test

A

Negative

68
Q

Clostridia oxidase test

A

Negative

69
Q

Clostridia oxidative-fermentative

A

Anaerobic

70
Q

Clostridia fermentation

A

Mannitol, glucose, fructose, mannose

71
Q

Clostridia ability to form spores

A

Yes

72
Q

Clostridia motility

A

Non-motile

73
Q

Clostridia - commensalism?

A

Normal part of flora found in intestinal
tract (anaerobic)

74
Q

Clostridia strains on spec

A
  • Clostridium difficile
  • Clostridium tetani
75
Q

Clostridium difficile infection causes what

A

Diarrhoea and colic

76
Q

Clostridium tetani causes what

A

Tetanus - sustained muscular contraction due to rapid series of nerve impulses, e.g. lockjaw

77
Q

Clostridium tetani - reservoir

A

Soil

78
Q

Three most common enteric O-antigen-possessing G- bacteria

A

E. coli
Shigella
Salmonella

79
Q

Common virulence factors of E. coli, Shigella and Salmonella (3

A
  • LPS (endotoxin)
  • O-antigen in LPS (outermost portion); protective against bile salt
  • Anti-phagocytic polysaccharide capsule
80
Q

E. coli - Gram stain and shape

A

G- bacillus

81
Q

E. coli - distinguished from shigella and salmonella because

A

Ferments lactose

82
Q

E. coli - commensalism?

A

Some strains commensal, others pathogenic

83
Q

E. coli - enterotoxinogenic strain invasion

A

Invade epithelium

84
Q

E. coli - enteropathogenic strain invasion

A

Do not invade epithelium

85
Q

E. coli - adhesion

A

P pili

86
Q

E. coli - motility

A

Motile due to flagellar protein

87
Q

E. coli - enterotoxigenic strains cause damage by

A
  • Produce heat-labile toxin and/or heat-stable toxin (enterotoxins)
  • Inhibit channels leading to salt and water retention in lumen = watery diarrhoea
88
Q

E. coli - enteropathic strains cause damage by

A
  • Disruption of microvilli in small intestine
  • Alter absorption and inflame epithelium
  • Bloody diarrhoea (dysentery)
89
Q

Salmonella - Gram stain and shape

A

G- bacilli

90
Q

Salmonella - distinguished from Shigella and E. coli because

A

Does not ferment lactose (different to E.coli) but does produce H2S (different to Shigella)

91
Q

Salmonella - motility

A

Motile due to flagellum

92
Q

Salmonella - pathogenesis

A
  • Penetrates epithelium in terminal SI, taken up by M cells and then spreads
  • Migrates to lamina propria and initiates inflammatory response
  • Prostaglandins activate adenylate cyclase, increase cAMP and disrupt NaCl absorption
  • Causes diarrhoea, sometimes dysentery
  • Severe strains invade, causing chronic inflammation and fever due to LPS presence
93
Q

Salmonella - reservoirs

A

Many animal reservoirs; associated with food poisoning

94
Q

Salmonella - SPI-1 function

A

Produces T3SS

95
Q

Salmonella - SPI-2 function

A

Prevent lysosomal fusion and improve replication

96
Q

Shigella - Gram stain and shape

A

G- bacillus

97
Q

Shigella - distinguished from salmonella and E. coli because

A

Do not ferment lactose (unlike E. coli) and does not produce H2S (unlike Shigella and E. coli), also non-motile

98
Q

Shigella - motility

A

Non-motile

99
Q

Shigella - pathogenesis

A
  • Shigella enters epithelial cells of the large intestine through endocytosis mediated by plasma-encoded membrane proteins
  • Escapes from phagosome and begins to move cell-to-cell using actin filaments
  • Movement causes mucous dysentery
100
Q

Mycobacterium tuberculosis shape (M. TB)

A

Bacillus

101
Q

M. TB - cell wall structure

A

Very thick lipid wall containing mycolic acids that confer negative charge to OM

102
Q

M. TB - immune evasion

A
  • Few surface targets
  • Resistant to phagolysosomal killing
  • Macrophage subversion
103
Q

M. TB - culture time

A

Slow growing, 4-6 weeks to culture

104
Q

M. TB - Features of primary infection

A

Ghon focus and granuloma formation

105
Q

M. TB - Ghon focus Vs Granuloma

A

Tissue inside granuloma dies due to caseous necrosis; necrotic area known as Ghon focus

106
Q

M. TB - granuloma formation

A
  • Mtb phagocytose by alveolar macrophages
  • TLR2 recognises lipids, triggers MyD-88 dependent signalling
  • Secretion of TNF-alpha recruits phagocytes, development of granuloma
  • VEGF recruits small vessels, allowing more lymphocytes, macrophages and DCs to the infection
107
Q

M. TB - granuloma structure

A

Immune cells (foamy macrophages, giant cells and CD4 T cells) surround bacteria, which becomes enclosed in a fibrous cuff

108
Q

M. TB - latency

A

Granuloma becomes hypoxic due to fibrous cuff, bacteria enter dormant phase

109
Q

M. TB - reactivation

A

Cavitation due to increasing bacterial load

110
Q

M. TB - treatment

A

Antibiotic cocktail over long period of time due to latent infection

111
Q

Examples of non-O-antigen-possessing G- bacteria

A

Neisseria gonorrhoea and neisseria meningitidis

112
Q

Professional non-O-antigen-possessing G- bacterial pathogen

A

Neisseria gonorrhoea

113
Q

Non-professional non-O-antigen-possessing G- bacterial pathogen

A

Neisseria meningitidis

114
Q

Neisseria meningitidis - Gram stain and shape

A

G- diplococci

115
Q

Neisseria meningitidis - commensalism

A

Normally colonises nasopharynx as harmless commensal

116
Q

Neisseria meningitidis - spread from nasopharynx

A

Colonisations spread to blood/CSF but not evolved, disease-causing phenotype because bacteria can’t be transmitted once in CSF; disease causing strains are not infectious

117
Q

Neisseria meningitidis - pathogenesis (3)

A
  • Pilus with adhesive properties and molecular mimicry of host structures
  • Opacity (Opa) proteins bind to epithelial cells and macrophages, allowing invasion
  • LPS
118
Q

Neisseria meningitidis - immune evasion (2)

A
  • IgA protease production
  • Anti-phagocytic polysaccharide capsule (virulent strains = sialic acid also found in human membranes)
119
Q

Neisseria meningitidis - treatment

A

Penicillin

120
Q

Neisseria gonorrhoea - Gram stain and shape

A

G- diplococcus

121
Q

Neisseria gonorrhoea - commensalism

A

No - normally colonises genital tract, almost always leading to infection go gonorrhoea

122
Q

Neisseria gonorrhoea - difference in pathogenesis to neisseria meningitidis

A

N. meningitidis causes immune response when in blood, N. gonorrhoea rapidly induces pus formation at infected surface

123
Q

Neisseria gonorrhoea - men Vs women symptoms

A

Men have more noticeable symptoms: urethritis, dysuria and purulent discharges

Women can be asymptomatic carriers with undetected local tissue damage (aids transmission because no precautions taken)

124
Q

Neisseria gonorrhoea - adhesion

A

Pili and Opa proteins, important to prevent washing away of bacteria by urine/discharge

125
Q

Neisseria gonorrhoea - immune evasion

A
  • Anti-phagocytic pili (no capsule)
  • IgA protease; without this would be unable to attach to the mucosa
  • Porin protein in cell walls inactivated C3b complement fragment
126
Q

Neisseria gonorrhoea - pathogenesis

A

Local damage due to inflammatory response

127
Q

Neisseria gonorrhoea - treatment

A

Penicillin, but more strains becoming resistant due to plasmids for penicillinase transport

Sophie - Principles of Pathology - Year 2 (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions