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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
S. aureus coagulase
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
26
S aureus adhesins
``` Bind host proteins Role in: -tissue adherence -colonisation -deep infections -immune evasion - cloaking ```
27
Staph protein A
An adhesin which binds the Fc portion of IgG
28
Staphylococcal toxins
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
Panton-Valentine Leukocidin (PVL)
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
Scalded skin syndrome
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
Toxic shock syndrome
``` 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
S aureus food poisoning
``` S. aureus superantigens = enterotoxins Ingestion leads to: -rapid brief illness -vomiting +++ -minimal diarrhoea ``` Contamination of food: - manufacture - preparation (if have whitlow etc)
33
S. aureus infections
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
Toxin mediated S. aureus infections
Toxic shock syndrome Scalded skin Food poisoning
35
Coagulase negative Staphylococci
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
S. epidermidis
``` 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
Streptococci
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
Classification of streptococci by haemolysis
Alpha haemolysis is partial and looks green/darker red Beta haemolysis is complete haemolysis - clear Gamma haemolysis - no haemolysis
39
Alpha haemolysis
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
Beta-haemolytic
``` 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
``` 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 ```
Necrotising fascitis
42
Necrotising fasciitis cause
Caused by S. pyogenes infection of deep tissues Production of tissue-destructive enzymes by organisms in stationary phase
43
Necrotising fasciitis symptoms
``` 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
S. pyogenes spectrum of disease
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
S. pyogenes structure and virulence
``` Membrane, wall, capsule Fibronectin-binding proteins Collagen-binding protein C5a peptidase M protein ``` Exotoxins: - superantigens - Streptococcal inhibitor of complement - haemolysins - DNAses - Hyaluronidase - streptokinase
46
Streptococcal M protein
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
M protein
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
Molecular mimicry
Streptococcal M protein in rheumatic fever and post-streptococcal glomerulonephritis Guillan-Barre Syndrome HLA B27-associated spondyloarthropathies
49
E. coli considerations
``` Strain differences Harmless gut commensals Uropathogens Nosocomial infections Enteric pathogens ```
50
Anaerobic pathogens
Gut commensals Wound pathogens C. difficile
51
Non-bacterial pathogens
fungal organisms yeasts, moulds, dimorphic fungi Candida species Aspergillus species
52
Gram negatives
Neisseria Haemophilus E. coli
53
Enterobacteriaciae
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
E. coli
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
E coli virulence mechanisms
``` 4 main virulence mechanisms: adhesins siderophores capsule toxins ```
56
E. coli Adhesins
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
E. coli siderophores
Enterobactin Powerful iron chelators Essential for survival in tissues (very low free Fe3+ environment)
58
E. coli capsule
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
E. coli toxins
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
What does E. coli illustrate?
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
E. coli disease
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
E. coli disease changes
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
Give an example of post infective autoimmune disease in which molecular mimicry is implicated
What infectious agent causes this disease?
64
Name an exotoxin produced by strains of staphylococcus aureus
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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