L3 Professional Pathogens Flashcards

(29 cards)

1
Q

Define Infection

A

Organism enters body and increases in number -> damages host in process

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2
Q

Define Colonisation

A

organism lies on body (outside) but no infection caused

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3
Q

Define Pathogen

A

Organism which causes infection (evades immune defences)

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4
Q

Define Commensal

A

Organism which lives on/in gut but does not cause infection

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5
Q

Define Symbosis

A

mutual benefit

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6
Q

Define Parasite

A

unequal

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7
Q

Define Professsional pathogens

A

Almost always cause diseases

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8
Q

Define Opportunistic pathogen

A

Only cause disease in immunocompromised patients

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9
Q

Define Virulence

A

Fundamental properties of the organism

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10
Q

Define Pathogenicity

A

Probability that an organism causes a disease when isolated from a patient

Depends on organism’s virulence, where it is and immune state of patient

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11
Q

Staphylococcus aureus overview

  • where
  • colour on agar
  • gram status and shape
A
Commensal of anterior nares 
20-60% 
Highly adapted - species and nose 
Golden colonies on agar 
Gram +ve cocci in clusters
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12
Q

S. aureus virulence determinants

A

S. epidermidis is less virulent

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13
Q

S. aureus virulence [3/4]

A

Adhesins: bind host proteins (tissue adherence and immune evasion cloaking) - nasal mucosa

Protein A: Binds Fc portion of immunoglobulin - evade immune clearance

Invade - cytotoxins and enzymes

Coagulase: Stimulate clotting and role in immune evasion

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14
Q

Coagulase test

A

Bacteria added to sheep serum

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15
Q

What are the three main staphylococcal toxins?

A

Cytotoxins
(Pore forming toxins, lyse host cells
and Panton-valentine leukocidin (PVL) – lyses polymorphs)

Exfoliative toxins:
Proteases,
Target epidermal structural proteins

Enterotoxins (superantigens)
Stimulate massive T cell activation
immune evasion
Ingestion → vomiting

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16
Q

Describe the staphylococcal capsule

A

Polysaccharide capsule - micro capsule thin compared to other bacteria capsules
Specific Abs to capsular antigens required

Prevents binding of cell wall opsonins to complement receptors and FcRs

17
Q

S. aureus skin infections include

A

Furunculosis
Staph abscess
Impetigo

Bacteraemia - endocarditis, osteomyelitis, septic arthritis + almost anywhere else

18
Q

Gram +ve

A

Thick peptidoglycans layer

Lipoteichoic and teichoic acid

19
Q

Gram -ve

A

Outer membrane: Lipopolysaccharide, proteins and pores
Thin peptidoglycans
Inner membrane

20
Q

Lipopolysaccharide recognition

A

Innate immune system is very sensitive to LPS - early recognition

LPS interacts with Toll-Like Receptors (TLR4) on monocyte, macrophage lineage cells and endothelium

Activates: Inflammatory pathway, coagulation and clotting pathways and changes in endothelial integrity

Gram -ve in blood + endotoxin in blood

21
Q

Lipoteichoic acid / Peptidoglycans recognition

A

Gram +ve dont have endotoxin

Cell wall can stimulate immune responses like LPS

22
Q

Glass test

A

Non-blanching purpuric rash

Meningococcal septicaemia

23
Q

Meningococcal pathogenicity

A

Adhesins - respiratory epithelium and meninges
Lipopolysaccharide
Capsule

Blebbing = shedding of endotoxin

24
Q

Sputum Grain stain

A

Gram +ve diplococci
Pneumococcus

Pneumococcal pneumonia

25
Streptococcus pneumoniae virulence [4]
Specific adhesins for respiratory mucosa Pneumolysin: bind host cell membrane cholesterol, form pores and lyses in ciliated cells and lyse host phagocytic cells Secretory IgA Protease - break down secreted immunoglobulin A (prevent mucosal clearance) Capsule: Polysaccharide coat prevents complement mediated phagocytosis and specific antibodies to capsule required
26
Streptococcus pneumoniae disease overview [5]
Commonest form of pneumonia (~40%) ``` Disseminated disease Bacteraemia Endocarditis (Infection of heart valves) Upper Resp Tract Infections (Sinusitis and Otitis media) Meningitis ```
27
Mechanisms of virulence
Adhesins - Adhesion and Cloaking Toxins: Lysins, Tissue enzymes (elastase, collagenase, coagulase) Exofoliative toxins, enterotoxins Enzymes targeting host immune responses (IgAase) Capsule Endotoxin Lipoteichoic acid / Peptidoglycans
28
Clostridium difficile overview
``` Clostridia include: C. tetani, C. botulinum and C. welchii Gram positive rods Anaerobic Spore forming: Soil and Gut (humans and animals) Wound and GI infections ```
29
C. difficile pathogenicity
Makes toxins – cause fluid secretion into gut Diarrhoea Increased infectivity Production of spores Difficult to control cross infection Relapse on treatment Some virulent strains (027) Lose regulation of toxin genes – hyper-producers Produce additional toxins