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BSMS302 > 4. Bacterial pathogenesis and infectious disease > Flashcards

4. Bacterial pathogenesis and infectious disease Flashcards

1
Q

How are bacteria described?

A 
Staining
Growth:
conditions (e.g. atmosphere)
morphology - both microscopic and macroscopic (colonies on agar)
typing
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2
Q

Gram stain steps

A 
Fixation
Crystal violet
Iodine treatment
Decolourisation
Counter stain (safranin)
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3
Q

Gram stain results

A

Gram positive - purple

Gram negative - pink

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4
Q

Colony shapes

A

Cocci
Bacilli
Spirals
Vibrio

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5
Q

Gram positive bacterial envelope structure

A

Thick peptidoglycan layer

Lipoteichoic acid and teichoic acid

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6
Q

Gram negative bacterial envelope structure

A

Outer membrane w lipopolysaccharide, proteins and pores
Thin peptidoglycans
Inner membrane

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7
Q

Aerobes

A

Use O2 as final electron acceptor so very efficient

e.g. Staph aureus

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8
Q

Anaerobes (obligate)

A

Ferment, so final electron acceptor is organic molecule
grow ok when substrates are plentiful
oxygen usually toxic
e.g. Clostridium spp.

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9
Q

Facultative anaerobes

A

Can switch between aerobic and anaerobic metabolism

e.g. E. coli

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10
Q

Streptococci classification

A

Haemolytic streptococci:
alpha haemolytic viridans strep - partially haemolyse blood agar to give a greenish colour
Beta haemolytic strep - cause complete haemolysis making the blood agar translucent

Non-haemolytic strep/gamma haemolytic strep

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11
Q

Typing

A

Relatedness of strains within a species e.g.
E.coli O157:H7
group A N. meningitidis
M3T3 S. pyogenes

Primarily serological types - use antibodies to detect expressed antigens
Now frequently given correlating genotypes e.g. S. pyogenes emmtype = M type

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12
Q

Commensals vs pathogens

A

Commensals are something which is probably not causing disease when identified from a clinical sample

Pathogens are something which is probably causing disease when identified from a clinical sample

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13
Q

Whats a common commensal organism?

A

Lactobacillus casei

Propionibacterium acnes

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14
Q

What is a common commensal which has the ability to cause disease

A

Staph epidermididis

Candida albicans

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15
Q

What is an absolute pathogen

A

Malaria, HIV, Strep pneumoniae, Neisseria meningitidis

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16
Q

When are commensals pathogens?

A

If a patient is ill or immunocompromised, their commensals can become pathogenic e.g. patient w burns, neutropenic patients

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17
Q

What determines if a microorganism is a pathogen or a commensal?

A

the immune status of the patient
the site/sample in question
the disease causing properties of the bacteria (virulence)

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18
Q

Gram positive cocci

A

Staphylococci:
S. aureus
Coagulase negative staphylococci

Streptococci:
Group A streptococcus (S pyogenes)
Group B
Group C and G
Group D - enterococcus
S. pneumoniae
Viridans type streptocci
Peptococcus/peptrostreptococcus
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19
Q

Gram positive rods (bacilli)

A 
Bacillus e.g. B. cerus and B. anthracis
Corynebacterium
Propionibacterium
Listeria monocytogenes
Clostridium e.g. C difficile
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20
Q

Gram negative cocci

A

Neisseria e.g. N meningitidis
N. gonorrhoe
Moraxella (Branbamella) catarrhalis

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21
Q

Gram negative rods

A 
Haemophilus influenzae
Enterobacteriaciae:
- Salmonella & shigellaa
- E. coli
-Klebsiella and Enterobacter
- Proteus
Pseudomonas e.g. P aeruginosa
Bacteroides e.g. B fragilis
Campylobacter and Helicobacter
Vibrio cholerae
Bordatella pertussis
Legionella
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22
Q

Staphylococcus aureus

A 
Commensal of nose 60%
Gram positive cocci in clusters
Furunculosis
Abscesses
Impetigo
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23
Q

Virulence factors for S. aureus - surface proteins

A

Surface proteins - effective in exponential phase:
Coagulase
protein A
elastin-binding protein
collagen-binding protein
fibronectin-binding protein
Agr system - quorum-sensing accessory gene regulator

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24
Q

Virulence factors S. aureus - secreted proteins

A

effective in stationary phase
Superantigens (TSST-1, SEA, SEB etc)
Exfoliative toxins
Cytolysins e.g. alpha-toxin, PVL

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25
Q

S. aureus coagulase

A

stimulates clotting
role in immune evasion
not expressed by less virulent coagulase-negative staphs
can be shown w coagulase test - precipitate in positive and clear in negative

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26
Q

S aureus adhesins

A 
Bind host proteins
Role in:
-tissue adherence
-colonisation
-deep infections
-immune evasion - cloaking
27
Q

Staph protein A

A

An adhesin which binds the Fc portion of IgG

28
Q

Staphylococcal toxins

A

Cytotoxins - form pores which lyse host cells - e.g. PVL (panton-valentine leukocidin) which lyses polymorphs

Exfoliative toxins - proteases which target epidermal structural proteins

Enterotoxins - Stimulate massive T cell activation - maybe role in immune evasion

Complement inhibitors

All of these toxins encoded on mobile genetic elements

29
Q

Panton-Valentine Leukocidin (PVL)

A

neutrophil pore-forming lysin
present in ~2% of S. aureus strains
Family and community outbreaks

PVL disease - associated with community onset MRSA cases in USA, not yet in Europe - sports teams/gym/army outbreaks which result in severe purulent necrotising skin infections

30
Q

Scalded skin syndrome

A

Ritter’s disease
Exfolitive toxins (ET)A, B etc - serine proteases, specific for desmoglein I
Outbreaks in nurseries - ET+ve strains, no immunity
Local infection e.g. umbillicus
Distant bullae
Sheet-like desquamation

31
Q

Toxic shock syndrome

A 
Tampon shock, more commonly now non-menstrual related TSS e.g. wound packs
Superantigen exotoxins
rash
renal failure
septic shock
multiorgan failure
skin desquamation (peeling) on recovery
32
Q

S aureus food poisoning

A 
S. aureus superantigens = enterotoxins
Ingestion leads to:
-rapid brief illness
-vomiting +++
-minimal diarrhoea

Contamination of food:

  • manufacture
  • preparation (if have whitlow etc)
33
Q

S. aureus infections

A

normal commensal
pathogen in skin/soft tissue infections
Vascular line related infections
Bacteraemia - commonest cause
endocarditis, osteomyelitis, septic arthritis and almost anywhere else
Surgical site infections
Toxin mediated e.g. toxic shock. scalded skin, food poisoning

34
Q

Toxin mediated S. aureus infections

A

Toxic shock syndrome
Scalded skin
Food poisoning

35
Q

Coagulase negative Staphylococci

A

Gram positive cocci in clusters like S. aureus
Don’t make coagulase, so less virulent
differentiated in the lab by coagulas test
includes several species e.g. S. epidermidis most commonly

36
Q

S. epidermidis

A 
Lives on the skin
frequently contaminates blood culture
Also a pathogen
Causes central venous line infection
endocarditis (prosthetic valve),
orthopaedic surgical infections,
foreign materials in a sterile place e.g. grafts, implants, etc
37
Q

Streptococci

A

huge family of Gram positives which colonise GI tract and skin
Classified by 3 ways:
-Haemolysis on blood agar
-Lancefield groups (surface carbohydrate antiens e.g. A,B,C)
-True species names (S. pyogenes, S. pneumoniae etc) e.g. S. pyogenes is group A and beta-haemolytic

38
Q

Classification of streptococci by haemolysis

A

Alpha haemolysis is partial and looks green/darker red
Beta haemolysis is complete haemolysis - clear
Gamma haemolysis - no haemolysis

39
Q

Alpha haemolysis

A

Results in green colour
Sometimes alpha-haemolytic organisms are called viridans-type Streptococci
Common commensals of the mouth
S. milleri, S. mitis, S. sanguis, S. pneumoniae

40
Q

Beta-haemolytic

A 
Lancefield groups A,B,C,G
V similar organisms
Site and species adapted
S. pyogenes - pharynx of man
S. equi, S. canis etc
Same diseases in other species
All can cause pharyngitis and cellulitis
41
Q 
flu-like illness
6 hours worsening pain and swelling leg
Hot red leg
Temp 38 deg C
Tachycardia
develops into generalised rash
hypotension
Cardiovascular collapse
A

Necrotising fascitis

42
Q

Necrotising fasciitis cause

A

Caused by S. pyogenes infection of deep tissues

Production of tissue-destructive enzymes by organisms in stationary phase

43
Q

Necrotising fasciitis symptoms

A 
Pain out of proportion to physical signs
bruising and blistering
generalised toxaemia
renal impairment
v high inflammatory response (CRP)
Raised creatinine kinase

Diagnosis by surgical exploration

44
Q

S. pyogenes spectrum of disease

A

Superficial infections e.g. pharyngitis, cellulitis

Deep infections e.g. severe soft tissue infection, myositis, necrotising fasciitis

Autoimmune sequelae (v rare in UK) - rheumatic fever - major cause of heart disease; glomerulonephritis

45
Q

S. pyogenes structure and virulence

A 
Membrane, wall, capsule
Fibronectin-binding proteins
Collagen-binding protein
C5a peptidase
M protein

Exotoxins:

  • superantigens
  • Streptococcal inhibitor of complement
  • haemolysins
  • DNAses
  • Hyaluronidase
  • streptokinase
46
Q

Streptococcal M protein

A

Major antigenic determinant of S. pyogenes
-immunity is type specific

Major virulence factor:

  • binds serum factor H which regulates complement activation
  • prevents opsonisation

Involved in pathogenicity

  • has an alpha-helical coiled-coil protein
  • molecular mimicry
47
Q

M protein

A

M protein has an alpha helical coiled-coil structure

Involved in molecular mimicry which leads to autoimmune sequelae

Has homology w cardiac myosin/trophomyosin AND glomerular basement membrane

Recurrent childhood infection is associated w/ cross-reative anti-self responses, rheumatic fever, and post-streptococcal glomerulonephritis

48
Q

Molecular mimicry

A

Streptococcal M protein in rheumatic fever and post-streptococcal glomerulonephritis

Guillan-Barre Syndrome
HLA B27-associated spondyloarthropathies

49
Q

E. coli considerations

A 
Strain differences
Harmless gut commensals
Uropathogens
Nosocomial infections
Enteric pathogens
50
Q

Anaerobic pathogens

A

Gut commensals
Wound pathogens
C. difficile

51
Q

Non-bacterial pathogens

A

fungal organisms
yeasts, moulds, dimorphic fungi
Candida species
Aspergillus species

52
Q

Gram negatives

A

Neisseria
Haemophilus
E. coli

53
Q

Enterobacteriaciae

A

Commensals of the gut
NOT enterococcus which are Gram positive coccus

Gram negative rods including Klebsiella, Enterobacter, Citrobacter

Cause opportunistic infections where organisms gain access to sterile sites - wound infections, biliary infectiona, hospital pneumonia

Specific syndromes of infections are determined by specific virulence mechanisms

54
Q

E. coli

A

hugely diverse species w hundreds of serotypes

Antigens:
Cell wall O
Flagella H
Capsular K

Three major human diseases:
UTI
Enteric
Meningitis (neonatal, elderly, immunocompromised)

55
Q

E coli virulence mechanisms

A 
4 main virulence mechanisms:
adhesins
siderophores
capsule
toxins
56
Q

E. coli Adhesins

A

Fimbrae - pilli e.g.

  • P fimbria: P is the RBC P antigen, but also binds uroepithelial antigen, also known as pyelonephritis associated adhesin
  • Non-fimbrial GI adhesins - diarrhoeal diseases - EPEIC, EIEC
57
Q

E. coli siderophores

A

Enterobactin
Powerful iron chelators
Essential for survival in tissues (very low free Fe3+ environment)

58
Q

E. coli capsule

A

Protects from complement mediated responses
important early in life (lack of antibody)
some associated with particular disease manifestations .e.g K1 capsular serotype and neonatal meningitis - due to interactions with blood brain barrier

59
Q

E. coli toxins

A

Endotoxin
Exotoxins e.g. cytolysins which are like Gram positive streptolysins
Enterotoxins v different from staphylococcal enterotoxins because they cause fluid leak in the GI tract

Verotoxins - disrupt ribosomal protein synthesis, and strains which have verotoxin cause haemorrhagic diarrhoea
Enterohaemorrhagic E. coli (EhEC) e.g. O157:H7
associated w haemolytic uraemic syndrome (HUS)

60
Q

What does E. coli illustrate?

A

Gram negative bacteria can make exotoxins too
Very diff pathogens can exist within a species
Can have usual virulence mechanisms of adhesion and toxins and also evolved unique ones such as specific fimbral adhesins and iron chelation

61
Q

E. coli disease

A

commonest cause of urosepsis
Major contributor to GI-related and billiary sepsus
Major cause of nosocomial infections - wounds, devices, pneumoniae
Commonest pathogen grown in blood

62
Q

E. coli disease changes

A

Invasive infection - bacteraemia - becoming much more common
More E. coli BSI/year than MRSA or C diff cases
Strains increasingly resistnat to first-line Abx

63
Q

Give an example of post infective autoimmune disease in which molecular mimicry is implicated

A

What infectious agent causes this disease?

64
Q

Name an exotoxin produced by strains of staphylococcus aureus

A

What syndrome of infection is this toxin associated with?

Describe the mechanism through which this toxin causes disease

BSMS302 (10 decks)

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