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302/308 > Bacterial pathogenesis and infectious disease > Flashcards

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
Q

Toxic shock syndrome

A
  • Historically most notorious as “Tampon shock”

- Caused by bacterial toxins

26
Q

Symptoms of toxic shock syndrome

A
  • Rash
  • Renal failure
  • Septic shock
  • Multiorgan failure
  • Skin desquamation on recovery
27
Q

S. aureus food poisoning

A
  • S. aureus superantigens = enterotoxins
  • Ingestion –> rapid brief illness
  • Vomiting
  • Minimal diarrhoea

Contamination of food

  • Manufacture
  • Preparation
28
Q

S. aureus infections

A
  • Normal commensal
  • Pathogen in skin/soft tissue infections
  • Vascular line related infections
  • Bacteraemia - commonest cause
  • Surgical site infections
  • Toxin mediated
29
Q

S.aureus bacteraemia

A
  • Endocarditis
  • Osteomyelitis
  • Septic arthritis
  • Almost anywhere else
30
Q

S.aureus toxin mediated

A
  • Toxic shock
  • Scalded skin
  • Food poisoning
31
Q

Coagulase negative staphylococci

A
  • 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
Q

S. epidermis

A
  • 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
Q

What are streptococci

A
  • A huge family of gram positive bacteria which colonise the GI tract and skin
34
Q

Ways of classifying streptococci

A

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
Q

Classification of streptococci by haemolysis

A
  • alpha haemolysis = partial
  • beta haemolysis = complete
  • gamma haemolysis = none
36
Q

What are organisms which cause alpha haemolysis sometimes called

A
  • Viridians-type streptococci
  • Common commensals of the mouth
  • S. milleri, S. mitis, S. Sanguis
  • Also S. pneumoniae
37
Q

Which lancefield groups of streptococci are beta haemolytic

A
  • 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
Q

What is necrotising fasciitis caused by

A
  • Caused by S.pyogenes infection of deep tissues

- Production of tissue-destructive enzymes by organisms in stationary phase

39
Q

Effects of necrotising fasciitis

A
  • 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
Q

S.pyogenes - superficial infections

A
  • Pharyngitis

- Cellulitis

41
Q

S.pyogenes - deep infections

A
  • Severe soft tissue infection
  • Myositis
  • Necrotising fasciitis
42
Q

S.pyogenes - autoimmune sequelae(v.rare in UK)

A
  • Rheumatic fever - a major cause of heart disease

- Glomerulonephritis

43
Q

S.pyogenes structue and virulence

A
  • Fibronectin-binding proteins
  • Collagen-binding protein
  • C5a peptidase
  • M protein
  • Capsule
  • Wall
  • Membrane
44
Q

Exotoxins released by s.pyogenes

A
  • Superantigens
  • Streptococcal inhibitor of complement
  • Haemolysins
  • DNAses
  • Hyaluronidase
  • Streptockinase
45
Q

Streptococcal M protein

A

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
Q

Molecular mimicry and autoimmune sequelae

A

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
Q

What is molecular mimicry also implicated in aetiology of

A
  • Guillain-barre syndrome

- HLA B27-associated spondyloarthropathies

48
Q

Enterobacteriaciae(E.coli etc)

A
  • 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
Q

E. coli

A
  • Hugely diverse species
  • Hundreds of serotypes
  • Cell wall ‘O’ flagella ‘H’ and capsular ‘K’ antigens
50
Q

Three major human disease caused E.coli

A
  • UTI
  • Enteric
  • Meningitis(neonatal, elderly, immunocompromised)
51
Q

E.coli virulence mechanisms

A
  1. Adhesins (fimbrae = pili)
  2. Siderophores
  3. Capsule
  4. Toxins
52
Q

E.coli - Adhesins

A

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
Q

E.coli - siderophores

A
  • Enterobactin
  • Powerful iron chelators
  • Essential for survival in tissues(very low free fe3+ environment)
54
Q

E.coli - capsule

A
  • 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
Q

E.coli - toxins

A
  • Endotoxin
  • Exotoxins positive streptolysins)
  • Enterotoxins
  • Verotoxins
56
Q

Exotoxins

A
  • cytolysins(like gram positive streptolysins)
57
Q

Enterotoxins - e.coli

A
  • Very different from staphyloccocal enterotoxins - cause fluid leak in the GI tract
58
Q

Verotoxins

A
  • Disrupt ribosomal protein synthesis
  • Verotoxin producing strains cause haemorrhagic diarrhoea
  • Enterohaemorrhagic e.coli (ehec)
  • Associated with haemolytic uraemic syndrome (HUS)
59
Q

What does e.coli illustrate

A
  • 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
Q

E.coli disease

A
  • 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
Q

Two big changes in E.coli disease going on

A
  1. Invasive infection(bacteraemia) is becoming much more common
  2. Strains are increasingly resistant to first-line antibiotics

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