IC17 C.difficile Flashcards
bacteria type
Gram-positive, spore forming anaerobic bacillus
causes of infection
- antibiotic-associated diarrhoea & colitis
- Nosocomial diarrhoea → increases duration of hospitalisation & healthcare cost
transmission route
where can the bacteria be found
faecal-oral route
where it is found
* rooms of patients with CDI
* On hands of healthcare workers
* On medical instruments
pathogenesis
toxin; role of Ab
- Colonisation of intestinal tract with C.difficile via faecal-oral route
Facilitated by AB use → disrupts barrier function of normal colonic flora (imbalance of normal flora) ⇒ C.difficile can multiply & produce toxins - Toxigenic C.difficile releases toxin A & toxin B
Toxin B ⇒ more clinically important; causes more severe disease - Toxins leads to inflammation & diarrhoea
Antibodies can be protective against toxins
* Asymptomatic carriers → higher serum levels of Ab compared to those who develop severe disease
risk factors
GA2T2 RICH2
- Advanced age > 65 years ⇒ impaired immunity
- Multiple or severe comorbidities
- Immunosuppression
- History of CDI ⇒ more vulnerable & susceptible
- GI surgery ⇒ disruption of GI lining & microbiota
- Tube feeding (enteral-feeding)
- Prior hospitalisation (last 1 year); Duration of hospitalisation
- Residence in nursing home or long‐term care facilities
- Use of antibiotics
- Use of gastric acid suppressive therapy ⇒ affects normal microbiota of GI
risk factors: AB
causative, protective, general guide
Greatest risks: clindamycin, 3rd/4th gen cephalosporins, Fluoroquinolones
* Highest risks while receiving AB, but still elevated even up to 12 weeks after stopping
Protective AB: doxycycline, tigecycline, metronidazole
* Active against C.difficile growth & inhibits toxin production
* Minimal effects on gut flora
Generally, increased risks with: (dose-dependent risk)
* Increased cumulative exposure of AB
* use for >2 weeks
* larger number of AB used
infection control & prevention
I HEA2P
Isolation
* Patients should have a private room with dedicated toilet → to decrease transmission to other patients
* If have limited number of private single rooms
Prioritise patients with stool incontinence for private rooms
Hand hygiene
* Wear gloves & gown
* Wash hands with soap and water > alcohol hand rub
To remove spores
Environmental cleaning With sporicidal agents
AMS
* Minimise frequency & duration of high-risk AB therapy
* Minimise number of AB agents prescribed
Acid suppression
* Unnecessary PPIs should be discontinued in general
Probiotics (Not routinely recommended)
range of clinical presentation
- asymptomatic
- mild symptoms
- moderate symptoms
- severe symptoms
- fulminant symptoms
clinical presentation: mild
Diarrhoea, abdominal cramps
clinical presentation: moderate
WBC
Fever, diarrhoea, nausea & malaise
Abdominal cramps & distension
Leukocytosis → elevated WBC count
Hypovolemia → decreased fluid volume due to dehydration
clinical presentation: severe
WBC & SCr
Fever, diarrhoea, diffuse abdominal cramps & distension
WBC ≥ 15 x 109 /L
Scr ≥ 133 μmol/L (1.5 mg/dL) → due to dehydration
clinical presentation: fulminant
hypotension/ shock
Ileus (inability of gut to move; no more peristalsis) & megacolon (inflammation of colon)
* Risks of perforation → bacteria can be released to other parts of the body
diagnostics
- Presence of diarrhoea (3 unformed stools in 24 hours) OR radiographic evidence of ileus/ toxic megacolon → symptoms
- Positive stool test result for C.difficile/ toxins OR colonoscopic/ histopathologic evidence of pseudomembranous colitis
stool test
requirements; stance on retesting
- Only perform tests for symptomatic patients → stool test cannot distinguish between colonisation & infection
Asymptomatic ⇒ likely just colonisation - To confirm patient did not receive laxative within prior 48 hours before sending test
Do not repeat testing <7 days Or when documenting care
* >60% with favourable clinical responses will still test positive
management of CDI
principles of treatment
who to treat, actions required (2)
Only patients with symptoms consistent with CDI ⇒ prescribe therapy
- To discontinue any AB not specifically treating CDI
- If additional AB therapy required
Select narrowest agent possible
Larger spectrum = more disrupted gut flora
Avoid agents with strong association with CDI
management of CDI (initial)
duration of treatment
10 days
Extend to 14 days if symptoms not completely resolved
management of CDI (initial)
definition of infection types
Non-severe
WBC <15 x 109 /L
AND
Scr <133 μmol/L (1.5 mg/dL)
Severe
WBC ≥ 15 x 109 /L
OR
Scr ≥ 133 μmol/L (1.5 mg/dL)
Fulminant
Hypotension OR ileus OR megacolon
management of CDI (initial)
treament for infection types
Non-severe
* First line
PO fidaxomicin 200 mg BD
PO vancomycin 125 mg QDS
* Alternative
PO metronidazole 400 mg TDS
Severe
PO fidaxomicin 200 mg BD
PO vancomycin 125 mg QDS
Fulminant
IV metronidazole 500 mg q8h
* + PO vancomycin 500 mg QDS
* ± PR Vancomycin 500mg QDS
(per rectal)
management of CDI (recurrence)
definition
Resolution of CDI symptoms → subsequent reappearance of symptoms after discontinuing treatment
management of CDI (recurrence)
risk factors
- Administration of other AB during/ after initial CDI treatment
- Defective humoral immune response against C.difficile toxins
Cannot produce Ab against C.difficile - Advanced age & underlying disease
- Continued usage of PPIs
management of CDI (recurrence)
treatment
fiaxomicin/ vancomycin initial
- PO fidaxomicin 200 mg BD x 10 days
- PO fidaxomicin 200 mg BD x 5 days, then 5 mg EOD x 20 days
- PO vancomycin tapered/ pulsed:
125 mg QDS x 10-14 days, then
125 mg BD x 7 days, then
125 mg OD x 7 days, then
125 mg every 2-3 days x 2-8 weeks
management of CDI (recurrence)
treatment
metronidazole initial
PO vancomycin 125 mg QDS x 10 days
monitoring responses
if >14 days no response; managing poor response
Symptoms should resolve in 10 days
* If not can extend treatment for another 4 days (total 14 days)
Do not continue C.difficile treatment >10-14 days
* No evidence of reduced recurrence
* Also to allow for patient to continue other current ABs
Additional diagnostics/ escalation of pharmacologic treatment ⇒ if poor response
