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Bacterial pathogenesis and infectious disease Flashcards

1
Q

Process of gram staining

A
  • Fixation
  • Crystal violet
  • Iodine treatment
  • Decolonisation
  • Counter stain (safranin)
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2
Q

Types of bacteria shapes

A
  • Cocci
  • Rods(bacilli)
  • Spirals
  • Vibrio
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3
Q

Gram positive bacteria membrane structure

A
  • Thick peptidoglycans layer

- Lipoteichoic and teichoic acid

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4
Q

Gram negative bacteria membrane structure

A
  • Outer membrane(lipopolysaccharide, proteins and pores)
  • Thin peptidoglycans
  • Inner membrane
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5
Q

S.aureus - type of growth

A
  • Aerobic

- Use O2 as final electron acceptor (very efficient)

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6
Q

Clostridium spp - type of growth

A
  • Anaerobic
  • Fermentation - yields final electron acceptor is organic molecule
  • Ok when substrates are plentiful
  • Oxygen usually toxic to anaerobic bacteria
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7
Q

What are facultative anaerobes

A
  • Can switch between aerobic and anaerobic metabolism

- E.coli

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8
Q

Terms used to classify streptococci

A
  • alpha haemolytic ‘viridians’ streptococci - these cause partial haemolysis of blood agar and a greenish colour
  • Beta haemolytic streptococci - these cause complete haemolysis making the blood agar translucent
  • gamma(non)-haemolytic streptococci
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9
Q

Streptococci typing

A

Relatedness of strains within a species e.g:

  • E. coli 0157:H7
  • (sero-) group A N.meningitidis
  • M3T3 S. pyogenes

Primarily serological types
- antibodies to expressed antigens

Now frequently correlating genotypes eg: S. pyogenes emmtype = M type

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10
Q

Commensal

A
  • Something which is probably not causing disease when identified from a clinical sample
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11
Q

Pathogen

A
  • Something which is probably causing disease when identified from a clinical sample
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12
Q

What determines whether an organism is a pathogen or a commensal

A
  1. The immune status of the patient
  2. The site/sample in question
  3. The disease causing properties of the bacteria(virulence)
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13
Q

Virulence of S. aureus

A

Coagulase
Adhesins: Bind host proteins
Protein A

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14
Q

Coagulase

A
  • Stimulates clotting
  • Role in immune evasion
  • Not expressed by less virulent ‘coagulase negative’ staphs
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15
Q

Adhesins

A

Bind host proteins

  • Tissue adherence
  • Colonisation
  • Deep infections
  • Immune evasion ‘cloaking’
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16
Q

Protein A

A
  • An adhesin

- Binds the Fc portion of IgG

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17
Q

What can S.aureus sepsis present with on a chest x-ray

A
  • Lung abscesses

- Also splenic abscesses (not on an x-ray tho lol)

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18
Q

Staphylococcal toxins

A
  • Cytotoxins
  • Exfoliative toxins
  • Enterotoxins(superantigens)
  • Complement inhibitors

Many of these are encoded on mobile genetic elements (only present on a proportion of strains)

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19
Q

Cytotoxins

A
  • Pore forming toxins, lyse host cells

- Panton-valentine leukocidin (PVL) - lyses polymorphs

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20
Q

Exfoliative toxins

A
  • Proteases

- Target epidermal structural proteins

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21
Q

Enterotoxins (superantigens)

A
  • Stimulate massive T cell activation, immune evasion
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22
Q

Panton valentine leukocidin (PVL)

A
  • Neutrophil pore-forming lysin
  • Present in around 2% of S.aureus strains
  • Family and community outbreaks
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23
Q

What is PVL disease associated with

A
  • Associated with community onset MRSA cases in USA - not yet in Europe
  • Severe, purulent, necrotizing skin infections
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24
Q

Scalded skin syndrome

A
  • Ritter’s disease
  • Exfoliative toxins (ET)A, B etc
    (Serine proteases - specific for desmoglein I)
  • Outbreaks in nurseries (ET+ve strains, no immunity)
  • Local infection - eg. umbilicus
  • Distant bullae
  • Sheet-like desquamation
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25
Toxic shock syndrome
- Historically most notorious as "Tampon shock" | - Caused by bacterial toxins
26
Symptoms of toxic shock syndrome
- Rash - Renal failure - Septic shock - Multiorgan failure - Skin desquamation on recovery
27
S. aureus food poisoning
- S. aureus superantigens = enterotoxins - Ingestion --> rapid brief illness - Vomiting - Minimal diarrhoea Contamination of food - Manufacture - Preparation
28
S. aureus infections
- Normal commensal - Pathogen in skin/soft tissue infections - Vascular line related infections - Bacteraemia - commonest cause - Surgical site infections - Toxin mediated
29
S.aureus bacteraemia
- Endocarditis - Osteomyelitis - Septic arthritis - Almost anywhere else
30
S.aureus toxin mediated
- Toxic shock - Scalded skin - Food poisoning
31
Coagulase negative staphylococci
- Gram positive cocci in clusters (like S. aureus) - Don't make coagulase (less virulent, differentiated in the lab) - Includes several species (S.epidermis most commonly)
32
S. epidermis
- Lives on the skin - Frequently contaminates blood culture - Also a pathogen - Central venous line infection Endocarditis(prosthetic valve), orthopaedic surgical infections, foreign material in a 'sterile' place(grafts, implants etc)
33
What are streptococci
- A huge family of gram positive bacteria which colonise the GI tract and skin
34
Ways of classifying streptococci
1) Appearance on blood agar(haemolysis) e.g 'beta haemolytic strep 2) Lancefield groups(A, B, C etc) - Surface carbohydrate antigens - e. 'group A strep' 3) True species names(S. pyogenes, S. pneumoniae etc) e.g S.pyogenes = group A strep and is a beta haemolytic strep
35
Classification of streptococci by haemolysis
- alpha haemolysis = partial - beta haemolysis = complete - gamma haemolysis = none
36
What are organisms which cause alpha haemolysis sometimes called
- Viridians-type streptococci - Common commensals of the mouth - S. milleri, S. mitis, S. Sanguis - Also S. pneumoniae
37
Which lancefield groups of streptococci are beta haemolytic
- A, B, C, G - V similar organisms - Site and species adapted(S. pyogenes - pharynx of man, S. equi, S.canis etc, same disease in other species) - All can cause pharyngitis and cellulitis
38
What is necrotising fasciitis caused by
- Caused by S.pyogenes infection of deep tissues | - Production of tissue-destructive enzymes by organisms in stationary phase
39
Effects of necrotising fasciitis
- Pain out of proportion to physical signs - Bruising and blistering - Generalised toxaemia - Renal impairment - Very high inflammatory response (CRP) - Raised creatine kinase - Diagnosis by surgical exploration
40
S.pyogenes - superficial infections
- Pharyngitis | - Cellulitis
41
S.pyogenes - deep infections
- Severe soft tissue infection - Myositis - Necrotising fasciitis
42
S.pyogenes - autoimmune sequelae(v.rare in UK)
- Rheumatic fever - a major cause of heart disease | - Glomerulonephritis
43
S.pyogenes structue and virulence
- Fibronectin-binding proteins - Collagen-binding protein - C5a peptidase - M protein - Capsule - Wall - Membrane
44
Exotoxins released by s.pyogenes
- Superantigens - Streptococcal inhibitor of complement - Haemolysins - DNAses - Hyaluronidase - Streptockinase
45
Streptococcal M protein
A major antigenic determinant of S.pyogenes (immunity is type specific) A major virulence factor - Binds serum factor H - regulator of complement activation - Prevents opsonisation Involved in pathogenicity - Has an alpha-helical 'coiled-coil' protein - Molecular mimickry
46
Molecular mimicry and autoimmune sequelae
M protein - alpha helical coiled coil structure - Homology with cardiac myosin/trophomyosin, glomerular basement membrane - Recurrent childhood infection associated with cross-reactive anti-self responses - Rheumatic fever - Post-streptococcal glomerulonephritis
47
What is molecular mimicry also implicated in aetiology of
- Guillain-barre syndrome | - HLA B27-associated spondyloarthropathies
48
Enterobacteriaciae(E.coli etc)
- Commensals of the gut (hence entero) - Note NOT enterococcus (a gram positive coccus) - GNRs including klebisella, enterobacter, citrobacter - Opportunistic infections where organisms gain access to sterile sites(wound infections, biliary infections, hospital acquired pneumonia) - Specific syndromes of infections associated with specific virulence mechanisms
49
E. coli
- Hugely diverse species - Hundreds of serotypes - Cell wall 'O' flagella 'H' and capsular 'K' antigens
50
Three major human disease caused E.coli
- UTI - Enteric - Meningitis(neonatal, elderly, immunocompromised)
51
E.coli virulence mechanisms
1. Adhesins (fimbrae = pili) 2. Siderophores 3. Capsule 4. Toxins
52
E.coli - Adhesins
P fimbria - P = RBC P antigen - Also binds uroepithelial antigen - Also known as pyelonephritis associated adhesin Non-fimbral GI adhesins - Diarrhoeal diseases EPC, EIEC
53
E.coli - siderophores
- Enterobactin - Powerful iron chelators - Essential for survival in tissues(very low free fe3+ environment)
54
E.coli - capsule
- Protects from complement mediated responses - Important early in life (lack of antibody) - Some associated with particular manifestations e.g. K1 capsular serotype and neonatal meningitis (mechanism? adhesin interactions with blood brain barrier)
55
E.coli - toxins
- Endotoxin - Exotoxins positive streptolysins) - Enterotoxins - Verotoxins
56
Exotoxins
- cytolysins(like gram positive streptolysins)
57
Enterotoxins - e.coli
- Very different from staphyloccocal enterotoxins - cause fluid leak in the GI tract
58
Verotoxins
- Disrupt ribosomal protein synthesis - Verotoxin producing strains cause haemorrhagic diarrhoea - Enterohaemorrhagic e.coli (ehec) - Associated with haemolytic uraemic syndrome (HUS)
59
What does e.coli illustrate
- Gram negative bacteria can make exotoxins too - Within a species, very different pathogens can exist - Usual virulence mechanisms (adhesion, toxins) - Also, specific 'fimbral' adhesins, iron chelation
60
E.coli disease
- Commonest cause of urosepsis - Major contributor to GI-related and biliary sepsis - Major cause of nonsocomial infections(wounds, devices, pneumonia) - Commonest pathogen grown in blood
61
Two big changes in E.coli disease going on
1. Invasive infection(bacteraemia) is becoming much more common 2. Strains are increasingly resistant to first-line antibiotics

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