L40: Healthcare associated infections

Question 1

Device-associated infection

Answer 1

• Through procedure of placing device and device itself
• Bladder catheters used a lot + high rate of infection (10-30%): usually mild, not likely to be life-threatening
• Central venous catheters used a lot + relatively high rate of infection (3-8%): bloodstream infection serious and can be deadly

Question 2

Biofilm

Answer 2

• Impt in device-associated infection
• Microbial community of cells that attach to substrate or interface with each other, embedded in matrix of extracellular polymeric substance
• Commonly on plastic, titanium, metal and can occur in infection without prosthetic material
• Hard to treat
• Consider host, device and bacteria

Question 3

Device -associated causative bacteria

Answer 3

Most common = Staph. epidermidis, Staph. aureus, E. coli

• Gram positives: 50-60% of nosocomial bacteraemic events (mainly S. epidermidis and S. aureus)
• Gram negatives: 30% of all episodes of bacteraemia (mostly E. coli, Klebsiella pneumonia, pseudomonas aeruginosa, enterobacter aerogenes
• Fungi: mostly candida

Question 4

Device-associated bacterial factors

Answer 4

(Allowing them to cause infection around prosthetic materials)

• Non -specific (hydrophobicity, electrostatic forces)
• Adhesive proteins (MSCRAMMs)
• Polysaccharide intracellular adhesion

Question 5

Device factors that favour bacterial adhesion

Answer 5

• Device material: PVC > teflon, PE, > PU, steel > titanium, latex > silicon
• Source of material: synthetic > biomaterial
• Surface of device: textured > smooth, irregular > regular
• Shape of device: polymeric tubing > wire mesh

Question 6

Problems with biofilm associated bacteria

Answer 6

• Antibiotics hard to reach bacteria deeper in biofilm
• Change of phenotype = different gene expression
• Change of cell surface properties = increased antibiotic tolerance
• Slower growth rate = more resistant to antibiotics
• Persister cells: specialised survivors resistant to antibiotics
• Difficult to determine antibiotic resistance (cannot do standard dilution tests)

Question 7

Prevention of device-associated infection

Answer 7

• Reconsider requirement for device
• Handwashing before and after touching device
• Place device under aseptic conditions (avoid femoral site)
• Monitor devices carefully for signs of infection
• Remove unnecessary devices
• Reduced venous catheter infection by 66%

Question 8

Management of cellulitis around cannula

Answer 8

• Remove cannula and drain pus
• Pus and blood samples to microbiology lab
• Can remove catheter tip and send to lab
• Cannula removed and replaced
• IV antibiotics for 14 days (7 days too short)
• E.g. staph aureus give flucloxacillin (90% resistant to penicillin)

Question 9

On broad spectrum antibiotics and development of increased freq of bowel movements, changing over a few days to explosive, watery, bloodless diarrhoea

Answer 9

= clostridium difficile

• C. difficile part of normal gut flora
• Carriage is 5% in community and 20% in hosp
• Spread from person to person via hospital wards: diarrhoea contaminated environment or long lived bacterial endospores
• Toxin A and B cause damage

Question 10

Most at risk of C. difficile

Answer 10

1. Hosp patients receiving antibiotics
   - Beta lactams and clindamycin especially
   - Fluoroquinolones (epidemic strain)
2. Longer than 1 wk in hosp (time to be colonised)
3. Other treatments disrupting colonic flora (removes competition, allowing C. difficile to grow)

Question 11

C. difficile colonisation factors and route

Answer 11

• Antibiotics reduce number of major genera of non-endospore forming anaerobes in colon
• C. difficile grows to high numbers and produces toxins
• C. difficile may be sensitive to antibiotics but survive as endospores and outcompete other species when treatment stoppped

Question 12

Endospores

Answer 12

• Only produced by species of bacillus and clostridium
• Dormant, survival structure not reproductive
• Endospore formation for survival in hosp environment
• Killed by: heat-autoclaving, chemicals (needs to be sporicidal)
• Not killed by: heat-pasteurisation, antibiotics (resistant as cells dormant), oxygen (C. difficile obligate anaerobes)

Question 13

Process of C. difficile

Answer 13

1. Attaches to surface of colonic mucosal cell
2. Endocytosis
3. Acidification and release
4. G-protein glucosylation (proteins e.g. Rho normally maintain cytoskeleton)
5. Actin depolymerisation

Question 14

Infection with C. difficile

Answer 14

• Toxin A causes epi cells to become round + apoptosis –> toxin B can access submucosa and colon bacteria/LPS can enter blood
• Loss of barrier integrity = pseudomembrane (ulceration) –> loss of water (diarrhoea)
• Severely inflamed colon and sepsis = toxic megacolon (can perforate and may be fatal, may need surgical removal)

Question 15

Diagnostic tests for C. difficile

Answer 15

• Test stool from suspected C. difficile infection
• Antibody based assay for toxins
• PCR for toxin genes
• Presence of bacteria may not be diagnostic, colonisation common
• Very likely to have raised white cell count

Question 16

Treatment of C. difficile

Answer 16

• Discontinue antibiotic (sometimes enough if mild)
• Treat with IV metranidazole or oral vancomycin
• Support fluid loss and pain
• Restoration of normal microflora (faeces donor - injected into colon or oral tablets OR pharmaceutically grown)

Question 17

C. difficile how is ward affected?

Answer 17

• Potential for outbreak
• Attention to hygiene and cleanliness
• Limited use of predisposing antibiotics
• 20% relapse rate