Microbiology - Virulence Flashcards
what is a virulence factor?
a characteristic of a pathogen that contributes to its effectiveness in causing a pathology
give examples of types of virulence factors and what they do
adhesin - allows organism to bind to host tissue
invasion - enables organism to invade host tissue
impeding - enables organism to avoid host defence
aggressin - direct damage to host
modulin - indirect damage to host
what type of organism is most likely to cause an infection in the skin?
part of natural skin flora
i.e - gram +ve (eg - staph or strep)
where are infections likely to occur in the skin and how can microbes invade?
moist areas (axilla, groin etc) can enter through hair follicle, sweat pore or sebaceous glands
how are staphylococci distinguished? what does this mean?
coagulase test
coagulase +ve = aureus
coagulase is a bacterial enzyme that gives staph aureus the ability to coagulate blood, hence acting as a virulence factor
how can staph aureus infection arise?
skin colonised with staph aureus in some parts like nostrils and perineum
can be hospital or community acquired
MRSA usually hospital acquired and common in immunocompromised/unwell patients
how can strep epidermidis infection arise?
colonizes 100% of skin surface and mucous membranes so can arise from break in skin
or hospital acquired via catheters etc
describe the pathogenicity of staph aureus
very versatile and can adapt to many different environments so can infect many sites and cause a wide range of symptoms
give examples of symptoms caused by different staph aureus infections
superifical skin leasions like boils or abscesses
toxinoses like toxic shock or scalded skin syndrome
systemic life threatening effects
what gives staph aureus its versatility?
different strains carry different virulence factors (all staph aureus have coagulase)
Give 3 examples of toxinoses caused by staph aureus
Toxic shock (TSST-1)
staph food poisoning
Scalded skin syndrome
give an example of a superantigen and what it doesq
TSST-1 (toxic shock syndrome)
toxin from staph aureus causes huge activation of T cells (1 in 5 compared to normal 1 in 10,000) resulting in a cytokine storm and overstimulation of immune response
what are the diagnostic criteria for toxic shock syndrome?
fever >39 diffuse macular rash (red and bumpy) desquamation (skin peeling) hypotension <90 >3 organ systems involved (including skin/mucous membranes)
what are adhesins and what are the 2 types?
components of bacteria that increase coagulation of blood
also present on epithelial and endothelial surfaces
2 types = fibrinogen binding an =d collagen binding
name 5 aspects of staph aureus that help it to evade the immune system
protein A (binds IgG in wrong position) superantigens (TSST-1) coagulase (plasma clotting) capsule (protects from phagocytosis) production of PVL and alpha toxin
what 2 types of capsule can exist on staph aureus?
mucoid and microcapsule
what is PVL?
Panton-Valentine Leukocidin
toxin produced by staph aureus that attacks leukocytes
present in most community acquired skin infections
what is PVL associated with?
CA-MRSA which causes severe skin infections like sepsis/necrotising fasciitis/pneumonia and recurrent furunculosis
what is necrotizing pneumonia and why cant it be treated with antibiotics?
rapidly progressing flu like syndrome of necrotizing haemorrhagic pneumonia (necrosis of lung parenchyma)
knocks out immune system so antibiotics not enough
what are the symptoms of necrotizing pneumonia?
preceeding flu like symptoms > acute respiratory distress > deterioration in pulmonary function > hypoxaemia > multi organ failure
how does understanding of virulence factors have a clinical benefit?
if you know the virulence factor you know the risk and allows you to think of a strategy for treatment/isolate patients etc and develop treatments
describe strep pyogenes
gram +ve cocci in chains
Beta haemolysis
catalase negative
type of group A strep
what diseases is strep pyogenes associated with?
impetigo
cellulitis
necrotising fasciitis
Toxic Shock Like Syndrome (TSLS)
what is the lancefield system?
system of classifying catalase negative strep into groups (strep A, strep B etc) using cell wall carbohydrates
groups then further divided due to M protein antigens in cell wall
what is impetigo?
contagious infection of strep pyogenes (usually in face) immediately below the surface
what diseases can be caused by invasive group A strep (iGAS)?
cellulitis
necrotizing fascitis
what is necrotizing fasciitis?
invasive strains of strep A penetrate mucous membrane and develop in the lesion, rapidly destroying connective tissue
how can strep A cause tissue/cell distruction?
hemolysins eg - streptolysin S (SLS)
= pore forming cytolysin which is toxic to organelles, platelets and PMN
how can the importance of SLS be shown?
if you knock out the gene for SLS in the bacteria, the infection is far less aggressive and doesn’t cause the damage
what causes toxic shock like syndrome?
exotoxins of strep pyogenes
complication of invasive infection (e.g pharyngitis)
what causes the variation in virulence between bacteria?
strain evolution through passing of genes encoding for virulence factors via transformation, transduction or conjugation
how is the incidence of GAS and iGAS infections changing?
increasing
where is strep pyogenes typically found?
pharynx
how do both staph aureus and strep pyogenes cause toxic shock?
production of similar exotoxins, common virulence factors and disease mechanisms
