T4L3 - Professional Pathogen Flashcards
Infection
Organism enters body and multiples -> damage host in process (invasion, replication and damage)
Colonisation
Organism lies on body (outside) - NO infection
Pathogen
Organism which causes infection (evade immune defences)
Commensal
Organism lives on us/in gut - NO infection
Symbiosis
Mutual benefit
Parasite
Unequal
Professional Pathogen vs Opportunistic pathogen
Professional pathogens: almost always cause disease
Opportunistic pathogens: only cause disease in immunocompromised patients
Pathogenicity depends on
Probability of organism causing disease once isolated
Virulence - fundamental property
Immune state of patient
Location
Pathogen vs commensal
Immune status of patient
Site/sample in question
Disease causing properties of bacteria
Sterile??
Blood, urine (normally sterile)
Stool, throat (not normally sterile)
Staphylococcus aureus overview [3]
Commensal of anterior nares
20-60%
Highly adapted: species & nose
Staphylococcus aureus virulence
Adhesins - bind host proteins
Tissue adherence and immune evasion
Protein A - Binds Fc portion of immunoglobulins
Staphylococcus aureus binding proteins
Elastin
Collagen
Fibronectin
Clumping factor
Coagulase
Protein A
Enterotoxin B
Coagulase [3]
Stimulate clotting
Role in immune evasion
Bacteria added to sheep serum
Staphyloccocal toxins
Cytotoxins
Exfoliative toxins
Enterotoxins
Cytotoxins
Pore forming toxins, lyse host cells
Panton-valentine leukocidin (PVL) – lyses polymorphs
Exfoliative toxins
Proteases
Target epidermal structural proteins
Enterotoxins (superantigens)
Stimulate massive T cell activation ?immune evasion
Ingestion → vomiting
Staphylococcal capsule
Antibodies can’t bind to antigens - peptidoglycans etc
Binding of cell wall opsonins to complement receptors and FcRs is prevented by capsule
S. aureus skin infections
Furunculosis
Staph abscess
Impetigo
S.aureus infection
• 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
Food poisoning
S. aureus enterotoxins
Ingestion →
Rapid brief illness, Vomiting +++ & Minimal diarrhoea
Contamination of food
- Manufacture
- Preparation
Gram positive and Gram negative virulence
Gram positive
Thick peptidoglycans layer
Lipoteichoic and teichoic acid
Gram negative Outer membrane Lipopolysaccharide Proteins and pores Thin peptidoglycans Inner membrane
Lipopolysaccharide recognition
Innate immune system VERY SENSITIVE to LPS
LPS interact with TLRs (TLR4) on monocyte/macrophage/endothelium)
Lipopolysaccharide results in activation of
Results in activation of
Inflammatory pathways
Coagulation and clotting pathways
Changes in endothelial integrity
Lipoteichoic acid / Peptidoglycans recognition
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
Meningococcal pathogenicity
Adhesins: Respiratory epithelium& Meninges
Lipopolysaccharide
Capsule