L3 Professional Pathogens Flashcards
(29 cards)
Define Infection
Organism enters body and increases in number -> damages host in process
Define Colonisation
organism lies on body (outside) but no infection caused
Define Pathogen
Organism which causes infection (evades immune defences)
Define Commensal
Organism which lives on/in gut but does not cause infection
Define Symbosis
mutual benefit
Define Parasite
unequal
Define Professsional pathogens
Almost always cause diseases
Define Opportunistic pathogen
Only cause disease in immunocompromised patients
Define Virulence
Fundamental properties of the organism
Define Pathogenicity
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
Staphylococcus aureus overview
- where
- colour on agar
- gram status and shape
Commensal of anterior nares 20-60% Highly adapted - species and nose Golden colonies on agar Gram +ve cocci in clusters
S. aureus virulence determinants
S. epidermidis is less virulent
S. aureus virulence [3/4]
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
Coagulase test
Bacteria added to sheep serum
What are the three main staphylococcal toxins?
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
Describe the staphylococcal capsule
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
S. aureus skin infections include
Furunculosis
Staph abscess
Impetigo
Bacteraemia - endocarditis, osteomyelitis, septic arthritis + almost anywhere else
Gram +ve
Thick peptidoglycans layer
Lipoteichoic and teichoic acid
Gram -ve
Outer membrane: Lipopolysaccharide, proteins and pores
Thin peptidoglycans
Inner membrane
Lipopolysaccharide recognition
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
Lipoteichoic acid / Peptidoglycans recognition
Gram +ve dont have endotoxin
Cell wall can stimulate immune responses like LPS
Glass test
Non-blanching purpuric rash
Meningococcal septicaemia
Meningococcal pathogenicity
Adhesins - respiratory epithelium and meninges
Lipopolysaccharide
Capsule
Blebbing = shedding of endotoxin
Sputum Grain stain
Gram +ve diplococci
Pneumococcus
Pneumococcal pneumonia