L3 Professional Pathogens

Question 1

Define Infection

Answer 1

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

Question 2

Define Colonisation

Answer 2

organism lies on body (outside) but no infection caused

Question 3

Define Pathogen

Answer 3

Organism which causes infection (evades immune defences)

Question 4

Define Commensal

Answer 4

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

Question 5

Define Symbosis

Answer 5

mutual benefit

Question 6

Define Parasite

Answer 6

unequal

Question 7

Define Professsional pathogens

Answer 7

Almost always cause diseases

Question 8

Define Opportunistic pathogen

Answer 8

Only cause disease in immunocompromised patients

Question 9

Define Virulence

Answer 9

Fundamental properties of the organism

Question 10

Define Pathogenicity

Answer 10

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

Question 11

Staphylococcus aureus overview

• where
• colour on agar
• gram status and shape

Answer 11

Commensal of anterior nares 
20-60% 
Highly adapted - species and nose 
Golden colonies on agar 
Gram +ve cocci in clusters

Question 12

S. aureus virulence determinants

Answer 12

S. epidermidis is less virulent

Question 13

S. aureus virulence [3/4]

Answer 13

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

Question 14

Coagulase test

Answer 14

Bacteria added to sheep serum

Question 15

What are the three main staphylococcal toxins?

Answer 15

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

Question 16

Describe the staphylococcal capsule

Answer 16

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

Question 17

S. aureus skin infections include

Answer 17

Furunculosis
Staph abscess
Impetigo

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

Question 18

Gram +ve

Answer 18

Thick peptidoglycans layer

Lipoteichoic and teichoic acid

Question 19

Gram -ve

Answer 19

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

Question 20

Lipopolysaccharide recognition

Answer 20

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

Question 21

Lipoteichoic acid / Peptidoglycans recognition

Answer 21

Gram +ve dont have endotoxin

Cell wall can stimulate immune responses like LPS

Question 22

Glass test

Answer 22

Non-blanching purpuric rash

Meningococcal septicaemia

Question 23

Meningococcal pathogenicity

Answer 23

Adhesins - respiratory epithelium and meninges
Lipopolysaccharide
Capsule

Blebbing = shedding of endotoxin

Question 24

Sputum Grain stain

Answer 24

Gram +ve diplococci
Pneumococcus

Pneumococcal pneumonia

Question 25

Streptococcus pneumoniae virulence [4]

Answer 25

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

Question 26

Streptococcus pneumoniae disease overview [5]

Answer 26

Commonest form of pneumonia (~40%)

Disseminated disease
Bacteraemia
Endocarditis (Infection of heart valves)
Upper Resp Tract Infections (Sinusitis and Otitis media)
Meningitis

Question 27

Mechanisms of virulence

Answer 27

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

Question 28

Clostridium difficile overview

Answer 28

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

Question 29

C. difficile pathogenicity

Answer 29

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