Important Infections - 2

?
  • Created by: LBCW0502
  • Created on: 29-11-19 10:24
Describe features of C. difficile (1)
Gram positive rod, spore-forming (produces toxins), anaerobic, bacillus. Caused of severe colitis in adults. Pseudomembraneous colitis (severe, gut contents out of GIT) or Antibiotic-associated colitis. Toxin producing strains cause diarrhoea
1 of 38
Describe features of C. difficile (2)
Toxin A (enterotoxin), toxin B (cytotoxin - cause of diarrhoea). Hypervirulent strains exist such as ribotype 027, may express a binary toxin. Can be colonised quickly with C. difficile in healthcare
2 of 38
Describe features of C. difficile (3)
Gene codes for production of toxins – not always switched on. Can be colonised to toxigenic C. difficile (able to produce toxins). PCR (check gene), enzyme assay (check toxin), identify organism (+/-)
3 of 38
Describe features of the pathogenesis (1)
C. difficile lives harmlessly in the gut in some people. If newly acquired/allowed to proliferate can cause symptoms. Can be fatal. Infection occurs by ingestion of spores via faecal-oral route. Spores can persist for months/years in environment
4 of 38
Describe features of the pathogenesis (2)
Spores can pass through GIT and come into contact with bile acids and other substances, stimulates germination of vegetative growth forms, produce toxins depending on surrounding microflora
5 of 38
Describe features of the pathogenesis (3)
Cross-infection of C. difficile (poor hand hygiene, exposure to environment). Spores – allows organism to survive long enough to be transmitted (dormant form, contamination in environment)
6 of 38
Describe features of the pathogenesis (4)
Toxins – produces severity of disease, increase chances of transmission. Hand to mouth transmission, can remain dormant/spore form in the gut, can colonise patient’s gut, can produce toxins/cause diarrhoea
7 of 38
Describe features of the pathogenesis (5)
Presence driven by bile acids, presence of immunoglobulins. If gut microflora disrupted (overuse of antibiotics), allows C. difficile to overgrow/proliferate, less bacterial diversity, disruption can persist for weeks after antibiotics
8 of 38
Describe features of the pathogenesis (6)
Absence of antibody response to toxins can lead to infection. Stay in hospital/long term care facility - increases colonisation rates
9 of 38
Describe features of the pathogenesis (7)
Patient colonised with C. difficile, given antibiotics (impact on other organisms in the gut). C. difficile resistant to antibiotics and some other organisms sensitive to antibiotics. Gut microbiome - kills of organisms in gut
10 of 38
Describe features of the pathogenesis (8)
Reduce competition for C. difficile (e.g. more nutrients, reduced population of other organisms), C. difficile proliferates/overgrowth. Less bacterial diversity in patient (limited organisms in stool). Disruption lasts for 6 months-1 year
11 of 38
Describe features of the pathogenesis (9)
Can prime gut overgrowth. Issues with immunoglobulin, risking of developing C. difficile. Colonisation rate increased with long stay (hospital/care home) - diagram of pathophysiology
12 of 38
Outline the factors contributing to the develop of C. difficile colonisation and diarrhoea following acquisition of toxigenic strain (1)
Disruption of flora, acquire C. difficile, protective factors (antibodies, become a carrier, low chance of C. difficile diarrhoea, could spread organism to others), risk factors, low serum antibodies, GIT disease, immunosuppression
13 of 38
Outline the factors contributing to the develop of C. difficile colonisation and diarrhoea following acquisition of toxigenic strain (2)
Develop C. difficile diarrhoea, younger people – single episode of C. difficile/low chance of recurrence, older people with exposure to antibiotics prior – increased risk of recurrent C. difficile
14 of 38
What are the risk factors for CDI? (1)
Prolonged use of broad-spectrum antibiotics (can kill other gut flora and allow C. difficile to multiply/overgrow). Acid suppressive agents (PPIs, H2 antagonists). Patient age (>65 yrs more vulnerable). Co-morbidities
15 of 38
What are the risk factors for CDI? (2)
Recent hospital stay (within last 3 months). Living in a residential or care home. Immunosuppression. Chronic inflammatory GI diseases
16 of 38
Why do acid suppressive agents increase the risk of CDI?
Acid suppressive agents – low pH breaks down organism before it can reach the gut, H2/PPI (protective factor not present)
17 of 38
What are the symptoms of CDI? (1)
Distinguish between mild and severe disease (severe - fatal, dehydration occurs quickly if fluid not replaced, impact on co-morbidities e.g. renal impairment, diabetes, HF, can develop constipation - poor prognosis)
18 of 38
What are the symptoms of CDI? (2)
Range from simple mucosal irritation and watery, soft diarrhoea to severe colitis. Diarrhoea can be frequent/profound (>10 stools/day). Patients rapidly dehydrated, develop constipation. Sign of ileus developing (not a good marker)
19 of 38
What are the symptoms of CDI? (3)
High WBC, high temperature, concomitant sepsis (markers of poor outcome), low BP, high HR, high RR (poor markers). Morality rate increases with severity
20 of 38
Describe features of recurrence (1)
Relapses occur in 20% of cases following initial treatment. Usually within 2-6 weeks after treatment. Risk factors - age >75, number of unformed stools in past 24h (>10), serum creatinine (>107 micromol/L), prior episodes
21 of 38
Describe features of recurrence (2)
Use of fidaxomicin or vancomycin. Inflammation, colitis, CDI, worse diarrhoea - more likely to have an occurrence
22 of 38
Describe features of infection control for CDI (1)
C. difficile spores can't to inactivated by alcohol based products. Patients infected with C. difficile need to be isolated - single rooms/cohort isolation, individual toilet facilities, wash hands with soap/water, mechanical removal of spores
23 of 38
Describe features of infection control for CDI (2)
Antimicrobial stewardship - crucial in reducing CDI (data, targets). Use narrow spectrum agents alone/combination, avoid clindamycin/2nd and 3rd generation cephalosporins, minimise use of quinolones/carbapenems, prolonged courses of aminopenicillins
24 of 38
Describe the treatment for CDI (1)
Supportive care is essential. Hydration/electrolytes/nutrition. Avoid anti-peristaltic agents (e.g. loperamide, opioids, want infection flushed out) in acute infection. Stop causative antibiotics where possible/switch. Treat with specific antibiotics
25 of 38
Describe the treatment for CDI (2)
Mild disease may not need treating. Moderate-severe should always be treated. Metronidazole, vancomycin, fidaxomicin, all equivalent for initial cure of CDI. Fidaxomicin leads to less recurrence than vancomycin (economically viable). Algorithm
26 of 38
What could be used to prevent CDI?
Probiotics
27 of 38
Describe new treatment methods for CDI (1)
Faecal microbiota transplantation - highly effective in cases of recurrent CDI, given after extensive pre-screening of donor. By either nasogastric or naso-jejunal tube or via colonoscopy. Also oral encapsulated forms under investigation
28 of 38
Describe new treatment methods for CDI (2)
Vaccinations being investigated. Other drugs being investigated also - similar structure to fidaxomicin
29 of 38
What is sepsis? (1)
A life-threatening reaction to an infection. It happens when your immune system overreacts to an infection and starts to damage your body's own tissues and organs. Septicaemia or blood poisoning
30 of 38
What is sepsis? (2)
Infection and organ dysfunction (inappropriate response of body to infection). E.g. renal impairment associated with pneumonia
31 of 38
What are the signs and symptoms of sepsis? (1)
Slurred speech/confusion, extreme shivering/muscle pain, passing no urine in a day, severe breathlessness, feel like you're going to die, skin mottled/discoloured
32 of 38
What are the signs and symptoms of sepsis? (2)
Children - breathing fast, convulsion, bluish/pale/mottled, rash, lethargic, abnormally cold, not feeding, vomiting, no wee/wet nappy for 12 hours
33 of 38
What are the sepsis red flags?
Responds only to voice/pain, unresponsive, acute confusional rate, systolic <90 (or >40 drop from normal), HR >130, RR >25, needs O2 to keep >92%, non-blanching rash, mottled/ashen/cyanotic, not passed urine in 18h, lactate >2, recent chemotherapy
34 of 38
What is the time frame to administer antibiotics for sepsis?
Management patients with sepsis within an hour – administer antibiotics
35 of 38
What is the Sepsis Six? (1)
Ensure a senior clinician attends, oxygen if required, obtain IV access/take bloods (blood cultures, blood sample, blood gas analyser, measure lactate in the blood/measure of metabolic function
36 of 38
What is the Sepsis Six? (2)
Higher lactate/low metabolism, lactate 2+ is an issue, measure urine output), give IV antibiotics (within 1 hour of diagnosis), give IV fluids (to increase BP, improve perfusion), monitor (fluid balance input/output) - UK Sepsis Trust (website)
37 of 38
What other factors are considered about antibiotics?
Antimicrobials used to treat MRSA - need to know how drugs used, available formulations and routes of administration. Antimicrobials used to treat Pseudomonas - need to know drugs used, available formulations and routes of administration
38 of 38

Other cards in this set

Card 2

Front

Describe features of C. difficile (2)

Back

Toxin A (enterotoxin), toxin B (cytotoxin - cause of diarrhoea). Hypervirulent strains exist such as ribotype 027, may express a binary toxin. Can be colonised quickly with C. difficile in healthcare

Card 3

Front

Describe features of C. difficile (3)

Back

Preview of the front of card 3

Card 4

Front

Describe features of the pathogenesis (1)

Back

Preview of the front of card 4

Card 5

Front

Describe features of the pathogenesis (2)

Back

Preview of the front of card 5
View more cards

Comments

No comments have yet been made

Similar Pharmacy resources:

See all Pharmacy resources »See all Important Infections - 2 resources »