T4L3 - Professional Pathogen Flashcards

1
Q

Infection

A

Organism enters body and multiples -> damage host in process (invasion, replication and damage)

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2
Q

Colonisation

A

Organism lies on body (outside) - NO infection

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3
Q

Pathogen

A

Organism which causes infection (evade immune defences)

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4
Q

Commensal

A

Organism lives on us/in gut - NO infection

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5
Q

Symbiosis

A

Mutual benefit

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6
Q

Parasite

A

Unequal

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7
Q

Professional Pathogen vs Opportunistic pathogen

A

Professional pathogens: almost always cause disease

Opportunistic pathogens: only cause disease in immunocompromised patients

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8
Q

Pathogenicity depends on

A

Probability of organism causing disease once isolated
Virulence - fundamental property
Immune state of patient
Location

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9
Q

Pathogen vs commensal

A

Immune status of patient
Site/sample in question
Disease causing properties of bacteria

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10
Q

Sterile??

A

Blood, urine (normally sterile)

Stool, throat (not normally sterile)

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11
Q

Staphylococcus aureus overview [3]

A

Commensal of anterior nares
20-60%
Highly adapted: species & nose

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12
Q

Staphylococcus aureus virulence

A

Adhesins - bind host proteins
Tissue adherence and immune evasion

Protein A - Binds Fc portion of immunoglobulins

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13
Q

Staphylococcus aureus binding proteins

A

Elastin
Collagen
Fibronectin

Clumping factor
Coagulase
Protein A
Enterotoxin B

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14
Q

Coagulase [3]

A

Stimulate clotting
Role in immune evasion
Bacteria added to sheep serum

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15
Q

Staphyloccocal toxins

A

Cytotoxins
Exfoliative toxins
Enterotoxins

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16
Q

Cytotoxins

A

Pore forming toxins, lyse host cells

Panton-valentine leukocidin (PVL) – lyses polymorphs

17
Q

Exfoliative toxins

A

Proteases

Target epidermal structural proteins

18
Q

Enterotoxins (superantigens)

A

Stimulate massive T cell activation ?immune evasion

Ingestion → vomiting

19
Q

Staphylococcal capsule

A

Antibodies can’t bind to antigens - peptidoglycans etc

Binding of cell wall opsonins to complement receptors and FcRs is prevented by capsule

20
Q

S. aureus skin infections

A

Furunculosis
Staph abscess
Impetigo

21
Q

S.aureus infection

A
• Normal commensal
	• Pathogen in skin / soft tissue infections
	• Surgical site infections
	• Vascular line related infections
	• Bacteraemia – commonest cause
		• Endocarditis
		• Osteomyelitis
		• Septic arthritis
Almost anywhere else
22
Q

Food poisoning

A

S. aureus enterotoxins
Ingestion →
Rapid brief illness, Vomiting +++ & Minimal diarrhoea

Contamination of food

  • Manufacture
  • Preparation
23
Q

Gram positive and Gram negative virulence

A

Gram positive
Thick peptidoglycans layer
Lipoteichoic and teichoic acid

Gram negative
Outer membrane
Lipopolysaccharide
Proteins and pores
Thin peptidoglycans
Inner membrane
24
Q

Lipopolysaccharide recognition

A

Innate immune system VERY SENSITIVE to LPS

LPS interact with TLRs (TLR4) on monocyte/macrophage/endothelium)

25
Q

Lipopolysaccharide results in activation of

A

Results in activation of
Inflammatory pathways
Coagulation and clotting pathways
Changes in endothelial integrity

26
Q

Lipoteichoic acid / Peptidoglycans recognition

A

Gram positive bacteria don’t have endotoxin

Cell wall components: Lipoteichoic acid
and Peptidoglycans

Can stimulate immune responses just like LPS
Different Toll-like receptors

27
Q

Meningococcal pathogenicity

A

Adhesins: Respiratory epithelium& Meninges

Lipopolysaccharide
Capsule