Case 8- virulence factors staph and streph Flashcards
Staphs virulence factors
- Has a capsules- prevents phagocytosis
- Protein A- binds to IgG exerting anti-opsonisation effect
- Fibronectin binding protein- within the cell wall of the bacteria, aids binding to host cell.
- Cytolytic exotoxins- causes haemolysis which destroys red blood cells.
- Panton-valentine leucocidin- causes lyses in Polymorphonuclear lymphocytes (immune cells).
Staphs- superantigens
Staphs also secrete superantigens, which are exotoxins. They cause severe systemic effects away from the site. They can cause damage by over-stimulating the immune system, causing excessive inflammation, tissue damage, loss of blood pressure. The enterotoxins (A, B, C, D, E and G) are half of all s.aureus isolated and cause vomiting and diarrhoea. It is possible to ingest just the toxins and not S.aureus.
Toxic shock syndrome exotoxin
TSST-1
Scaldy skin syndrome toxin
The exfoilatin toxin
MRSA
Methicillin Resistant S.aureus. 1-3% of the population are colonised with MRSA, it is one of the most prevalent causes of nosocomial infections. For treatment you need to ask local microbiology advice, Flucloxacillin does not work. This leads to longer stays and potential for complications. Treatment= Glycopeptides (i.e. Vancomycin), Tetracycline and other 3rd generation penecillins.
How does a pathogen cause diseas?
Disease is caused by the ability to avoid opsonisation, phagocytosis and to adhere to cells, produce toxins and enzymes. It can induce tissue damage and spread from the original site of infection.
What causes systemic infection?
The secretion of toxins that damage surrounding cells
Group A: streptococcus pyogenes toxin- Streptolysin O and S
Causes lysis of eukaryotic cells, so the bacteria can spread
Group A: streptococcus pyogenes toxin- Hyaluronidase
Breaks down connective tissue, facilitates strep.p spread
Group A: streptococcus pyogenes- Pyogenic toxin
Super antigens, responsible for many of the clinical manifestations like toxic shock syndrome and sepsis
Group A: streptococcus pyogenes toxins- Streptokinase
Causes lysis of clots facilitates spread of organism
Group A: streptococcus pyogenes toxins- C5A peptide
Inactivates complement pathway by breaking down C5a, reduces inflammation
Group A: streptococcus pyogenes toxins- Streptodornases
Breaks down DNA in lysed tissue, allows bacteria to spread more quickly as it reduces the viscosity of the surrounding area
S. pneumoniae pathogenicity factors
- Capsule- autophagocytotic.
- Pili- enables attachment of cells of the URT.
- Choline binding proteins- facilitates binding to the carbohydrates in the cells of the URT.
- Autolysins- secreted by the bacteria to facilitate breakdown of the cell to allow release of pneumolysin.
- Pneumolysin- breakdown eukaryotic cells, facilitates spread.
Infection
An inflammatory response to microorganisms or invasion of the normal sterile tissue
Bacteraemia
Presence of bacteria in the blood
Sepsis
Life threatening organ dysfunction caused by a dysregulated host response to infection
Septic shock
Profound circulatory, cellular and metabolic abnormalities, has a greater risk of mortality then sepsis alone. It is sepsis with persisting hypotension (low BP) despite fluid correction and vasopressors. As well as hyperlactatemia, which is a serum lactate (product of anaerobic respiration) greater than 2 mmol/l.
Systemic inflammatory response syndrome (SIRS)
Identifies infection which no longer defines as sepsis, without organ dysfunction
Criteria for SIRS
It requires 2 or more of the following • Temperature- <36 C or >38 C • Pulse rate- >90/min • Respiratory rate- >20/min or PaCO2 <32 mmHg • White cell count- <4 or >12x109/L
What does modified SIRS include
1) New confusion/drowsiness
2) Blood glucose >7.7mmol/L (if not diabetic)
What happens if sepsis is not treated
There is rapid progression to multi-organ failure, septic shock and death
Common bacterial causes of sepsis
Staph A, Pseudomonas spp and E.coli
Sepsis- Respiratory rate changes
Increased vascular permeability causes fluid to accumulate in the lungs, causing a reduction in gas exchange. As the body does not receive enough oxygen the respiratory rate increases to compensate. In addition, the pH of blood falls, this is sensed by chemoreceptors. To compensate the respiratory centre increases rate and depth of breathing , more CO2 is removed from the body, increasing the pH.
