Case 8- virulence factors staph and streph

Question 1

Staphs virulence factors

Answer 1

• 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).

Question 2

Staphs- superantigens

Answer 2

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.

Question 3

Toxic shock syndrome exotoxin

Answer 3

TSST-1

Question 4

Scaldy skin syndrome toxin

Answer 4

The exfoilatin toxin

Question 5

MRSA

Answer 5

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.

Question 6

How does a pathogen cause diseas?

Answer 6

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.

Question 7

What causes systemic infection?

Answer 7

The secretion of toxins that damage surrounding cells

Question 8

Group A: streptococcus pyogenes toxin- Streptolysin O and S

Answer 8

Causes lysis of eukaryotic cells, so the bacteria can spread

Question 9

Group A: streptococcus pyogenes toxin- Hyaluronidase

Answer 9

Breaks down connective tissue, facilitates strep.p spread

Question 10

Group A: streptococcus pyogenes- Pyogenic toxin

Answer 10

Super antigens, responsible for many of the clinical manifestations like toxic shock syndrome and sepsis

Question 11

Group A: streptococcus pyogenes toxins- Streptokinase

Answer 11

Causes lysis of clots facilitates spread of organism

Question 12

Group A: streptococcus pyogenes toxins- C5A peptide

Answer 12

Inactivates complement pathway by breaking down C5a, reduces inflammation

Question 13

Group A: streptococcus pyogenes toxins- Streptodornases

Answer 13

Breaks down DNA in lysed tissue, allows bacteria to spread more quickly as it reduces the viscosity of the surrounding area

Question 14

S. pneumoniae pathogenicity factors

Answer 14

• 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.

Question 15

Infection

Answer 15

An inflammatory response to microorganisms or invasion of the normal sterile tissue

Question 16

Bacteraemia

Answer 16

Presence of bacteria in the blood

Question 17

Sepsis

Answer 17

Life threatening organ dysfunction caused by a dysregulated host response to infection

Question 18

Septic shock

Answer 18

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.

Question 19

Systemic inflammatory response syndrome (SIRS)

Answer 19

Identifies infection which no longer defines as sepsis, without organ dysfunction

Question 20

Criteria for SIRS

Answer 20

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

Question 21

What does modified SIRS include

Answer 21

1) New confusion/drowsiness

2) Blood glucose >7.7mmol/L (if not diabetic)

Question 22

What happens if sepsis is not treated

Answer 22

There is rapid progression to multi-organ failure, septic shock and death

Question 23

Common bacterial causes of sepsis

Answer 23

Staph A, Pseudomonas spp and E.coli

Question 24

Sepsis- Respiratory rate changes

Answer 24

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.

Question 25

Sepsis- Blood pressure (BP) and Heart rate (HR)

Answer 25

Bacteraemia causes increased vascular permeability so fluid accumulates in the tissues. There is vasodilation of the vessels reducing systemic vascular resistance, initially septic patients have warm extremities. Both mechanisms reduce blood pressure, the heart rate increases to compensate. There is low blood saturation and tachycardia.

Question 26

Sepsis- kidneys

Answer 26

As less blood is returning to the heart there is a decrease in cardiac output which causes the kidneys to become injured and urine output to decrease.

Question 27

Sepsis- clotting factors

Answer 27

Damage to blood vessel walls due to inflammatory mediators, mean clotting factors are used to repair the damage, making the patient prone to bleeding as they are used up. Less oxygen can get to the tissues causing hypoxia.

Question 28

Sepsis- consciousness and blood glucose

Answer 28

Reduced consciousness is a sign of poor blood supply to the brain. When assessing the patient’s Glasgow Coma Scale (GCS) they may have a reduced score and become more confused. When a patient goes into septic shock they can have raised blood glucose through the actions of cortisol, catecholamines and C-reactive protein (CRP).

Question 29

Sepsis- Temperature

Answer 29

Patients with a higher temperature have a better outcome with sepsis, it may be a protective mechanism. Pyrexia (raised body temp) is generated by pyrogens which affect the Hypothalamus’s ability to regulate temperature.

Question 30

The national early warning score 2 (NEWS2)

Answer 30

Scoring tool used for sepsis. Requires information about RR, oxygen saturation, oxygen requirements, HR, BP, consciousness and temperature

Question 31

Potential infection sources

Answer 31

Urinary tract, joint or skin, brain (meningitis), device related, heart (endocarditis), abdomen and lungs

Question 32

Tests needed to identify sepsis

Answer 32

A CXR, sputum culture, dipstick test, ultrasound or CT scan in the abdomen

Question 33

SOFA score

Answer 33

Used to diagnose sepsis, a change in two point confirms a sepsis diagnosis

Question 34

Risk stratification- sepsis

Answer 34

You can use risk stratification to identify which of the patients symptoms belong in the High risk criteria, Moderate risk criteria and Low risk criteria. This helps to work out the risk of severe illness and death from sepsis.

Question 35

Sepsis 6- 3 in

Answer 35

1. Antibiotics-according to trust policy
2. Oxygen supplementation-if required
3. Intravenous fluids-fluid challenge

Question 36

Sepsis 6- 3 out

Answer 36

1. Bloods-FBC, U&E, CRP, Lactate, Clotting screen, Glucose
2. Blood cultures- take culture prior to antibiotics
3. Fluid monitoring-use a catheter