Clostridioides di

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Clostridioides di
colitis and diarrhoea.
Transmission\: occurs via the faecal-oral route, commonly in healthcare settings; spores can survive on surfaces for
prolonged periods.
Risk factors\: recent antibiotic use (especially broad-spectrum penicillins, cephalosporins,
advanced age, immunosuppression, prolonged hospitalisation, PPI use.
Clinical features\: watery diarrhoea (≥3 loose stools in 24 hours), fever, lower abdominal pain, nausea, and anorexia.
Investigations\: stool PCR (
megacolon are suspected.
Management\: oral vancomycin (125mg QDS for 10 days), IV
intervention if toxic megacolon or perforation.
Recurrent CDI\: 25% relapse rate;
Complications\: pseudomembranous colitis, fulminant colitis, toxic megacolon, intestinal perforation, dehydration, and
sepsis.
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Introduction

C l o s t r i d i o i d e s d i
associated colitis and profuse diarrhoea. It is one of the most common nosocomial infections and is associated with
signi
1-3
There are approximately 500,000 cases of CDI and 29,000 deaths annually in the US. Over 16,000 cases were reported in
2022-2023 by NHS trusts in England.
3

Aetiology

C . d i
asymptomatically colonises approximately 5% of the population.
2-3
Colonisation rates may be as high as 18% in healthcare facilities and 51% in long-term care facilities.
4
C . d i
normal intestinal
5
Hence, CDI most commonly presents in conditions where the normal intestinal
antibiotic therapy.
2-3, 5
TransmissionC . d i
with infectious diarrhoea. C . d i
spread. Person-to-person transfer occurs as a consequence of inadequate infection control measures and poor
handwashing technique.
2-3
The typical incubation period of CDI is 2-3 days.
2-3
Hand washing
Alcohol-based hand sanitisers are inehand
washing before and after contact with all suspected or con
Pathophysiology
C . d i
toxins. The most notable virulence factor of C . d i
2-3
In addition to enzymatic degradation of the colonic mucosa, toxins A and B produce an in
mucosal integrity and inducing the characteristic colitis and diarrhoea observed with CDI. Toxin levels have been shown to
correlate closely with disease severity.
2, 5
In severe cases, CDI can be complicated by the formation of pseudomembranes, large intraluminal aggregates of cellular
debris, neutrophils, mucin and
3, 5-6

Risk factors

The most signi
antibiotic treatment, however, symptoms may manifest up to 8 weeks following treatment cessation.
Antibiotics associated with C . d i
However, CDI is most strongly associated with the '4 Cs'
2, 7
\:
Broad spectrum penicillins (e.g. co-amoxiclav)
Cephalosporins
Fluoroquinolones (e.g. cipro
Clindamycin
All antibiotics can cause dysbiosis and predispose to CDI.
Other notable risk factors include\:
2-3
Advanced age
Prolonged hospitalisation or long-term residential care
Occupational exposure (i.e. healthcare professionals)
Immunosuppression
Previous CDI
Comorbidities
Gastric acid suppression (e.g. proton pump inhibitors (PPI) and H2 receptor antagonists)

Clinical features

History
CDI should be suspected in all patients who present with diarrhoea following recent antibiotic use.Watery diarrhoea (≥3 loose stools in a 24-hour period) is the hallmark symptom of CDI. It is common for mucous or occult
blood to be present in the diarrhoea, however, melaena or haematochezia are rare. The presence of these features may
suggest an alternative diagnosis.
8
Other typical symptoms of CDI include\:
3, 8
Fever
Lower abdominal pain
Nausea
Vomiting
Anorexia
Clinical examination
Patients with suspected CDI should have a full general and abdominal examination.
Examination
3, 8
Abdominal tenderness
Abdominal distension
Signs of dehydration (e.g. dry mucous membranes, decreased skin turgor)
If severe abdominal tenderness, distension or features of peritonitis are present, complications such as toxic megacolon or
intestinal perforation should be suspected. These may be accompanied by signs of shock (e.g. tachycardia, hypotension).

Di

Important di
3, 8
Bacterial or viral gastroenteritis
Other causes of antibiotic-associated diarrhoea (e.g. side e
a u r e u s or K l e b s i e l l a o x y t o c a )
Ischaemic colitis
In

Investigations

Bedside investigations
Relevant bedside investigations include\:
Basic observations\: regular monitoring to assess for fever, tachycardia, hypotension, altered consciousness level etc.
ECG\: electrolyte derangement is common in CDI and may trigger arrhythmias
Additionally, all patients should have a stool chart to monitor the frequency and character of loose stool. Fluid balance
should also be closely monitored and recorded.
Laboratory investigations
Blood tests
Initial blood tests should include\:
Full blood count\: elevated white cells are common
Urea and electrolytes\: electrolyte derangement is common in diarrhoeal illness, particularly hypokalaemia
Liver function tests
C-reactive protein
Venous blood gas\: if acute abdomen is present, to measure lactate
Blood cultures\: if febrile or systemically unwell
In
MicrobiologyEnteric investigations are the mainstay of diagnosing CDI.
Numerous options are available, including\:
3, 8
Stool polymerase chain reaction (PCR) test\: highly sensitive and moderately speci
Enzyme immunoassay (EIA) for glutamate dehydrogenase (GDH) antigens\: high sensitivity and speci
distinguish between toxigenic and non-toxigenic strains
EIA for toxins A and B\: moderate sensitivity and high speci
Cell culture cytotoxicity assay\: high sensitivity and speci
Enteric investigations should ideally be obtained before initiation of treatment, but treatment should not be delayed to
facilitate this.
Imaging
Imaging studies are not required for uncomplicated illness.
If marked abdominal pain or distension is present, an abdominal X-ray (AXR) may be requested. This may show dilated
bowel loops in complications such as toxic megacolon.
3
If severe abdominal pain, features of peritonitis or absent bowel sounds are present, CT abdomen is the preferred
investigation. CT
submucosal oedema. Severe colonic dilatation (>7cm) is suggestive of toxic megacolon. Features of pseudomembranous
colitis are highly suggestive of CDI.
3, 8
Figure 1. CT image of
pseudomembranous colitis
Endoscopy
Lower gastrointestinal endoscopy (e.g. sigmoidoscopy and colonoscopy) is not indicated for the investigation of suspected
CDI; however, it can be considered where there is uncertainty regarding the diagnosis.
In the setting of CDI, erythema and in
intraluminal pseudomembranes is diagnostic.
3, 8
Figure 2. Endoscopic image of
pseudomembranous colitis

Diagnosis

Diagnosis requires both the presence of clinical symptoms and con
The choice of enteric investigations varies by institution. Always check local microbiology policy before ordering
investigations.
Stool PCR is recommended as the sole investigation if there is institutional agreement on stool submission criteria whereby
samples should only be sent for new-onset diarrhoea without clear cause in patients not receiving laxatives.Where no pre-agreed institutional criteria are present, a multistep process including a combination of EIA and PCR is
recommended.
3, 9

Management

Acute management
All acutely unwell patients should be assessed and managed with an ABCDE approach.
Acute management for suspected CDI may include\:
Analgesia\: for abdominal pain
Antipyretics\: to manage fever
Intravenous (IV) \: to manage dehydration and correct electrolyte abnormalities
Antidiarrheals (e.g. loperamide) or drugs with antimotility properties (e.g. opioids) are not recommended acutely for
suspected CDI. Opioids can increase the risk of severe disease.
3
Contributing medications such as ongoing antibiotics and PPIs/H2 antagonists should be reviewed and stopped, if
possible.
Antibiotic therapy
For the acute management of CDI, NICE recommends the following antibiotics\:
3, 10
First line\: oral vancomycin 125 mg four times daily (QDS) for 10 days
Second line\: oral
Life-threatening CDI\: oral vancomycin 500 mg QDS + IV metronidazole 500 mg three times daily for 10 days
Vancomycin absorption
Vancomycin is poorly absorbed in the gastrointestinal (GI) tract and has an oral
bioavailability of \<10%. This is advantageous for the management of CDI as orally administered vancomycin remains
within the GI tract and acts topically upon C . d i
11
Surgical management
Surgical management is only indicated for life-threatening cases of CDI where there is fulminant colitis or complications
such as toxic megacolon or intestinal perforation.
3
Surgical opinion should be obtained at the earliest opportunity if complications are identi
to medical therapy and have worsening clinical features or rising lactate.
3
Recurrent CDI
CDI is prone to relapse and recurrence. Approximately 25% of patients who receive vancomycin for the
CDI will su
3
Relapsed CDI is de
Recurrent CDI is de
The investigative approach for relapsed and recurrent CDI is the same as for
For antibiotic therapy, NICE recommends\:
10
Relapsed CDI\: oral
Recurrent CDI\: oral vancomycin 125 mg QDS or oral
With specialist input, prolonged courses of treatment for up to 20 days can be considered to reduce the risk of further
recurrences.Complications
Noteworthy complications of CDI include\:
1, 3
Severe dehydration and electrolyte derangement
Sepsis and septic shock
Pseudomembranous colitis
Fulminant colitis
Toxic megacolon
Ileus
Intestinal perforation
Urinary tract infection (secondary to diarrhoea)

References

StatPearls. Clostridiodes diLINK].
UpToDate. Clostridiodes di
Available from\: [LINK].
BMJ Best Practice. Clostridiodes diLINK].
Curry S, Hecker M, O’Hagan J, et al. Natural History of C l o s t r i d i o i d e s d i
Acquisition of Carriage in Healthcare Settings\: A Prospective Cohort Study. C l i n i c a l I n f e c t i o u s D i s e a s e s . 2023 Mar 11;77(1)\:77–
83.
Czepiel J, Dróżdż M, Pituch H, et al. Clostridium di
I n f e c t i o u s D i s e a s e s . 2019 Apr 3;38(7)\:1211–21.
StatPearls. Pseudomembranous Colitis. Published in 2023. Available from\: [LINK].
Lawes T, Lopez-Lozano J, Reboot C, et al. E
molecular epidemiology of Clostridium di
L a n c e t I n f e c t i o u s D i s e a s e s . 2017 Feb;17(2)\:194–206.
UpToDate. Clostridiodes di
[LINK].
McDonald L, Gerding D, Johnson S, et al. Clinical Practice Guidelines for Clostridium di
2017 Update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America
(SHEA). C l i n i c a l I n f e c t i o u s D i s e a s e s . 2018 Feb 15;66(7)\:e1–48.
NICE. Clostridiodes diLINK].
StatPearls. Vancomycin. Published in 2023. Available from\: [LINK].
Image references
Figure 1. HellerhoLINK]. License\: [CC BY-SA 3.0].
Figure 2. Samir. P s e u d o m e m b r a n o u s c o l i t i s . Available from\: [LINK]. License\: [CC BY 3.0].

Reviewer

Dr Robert Laing
Consultant in Infectious Diseases and General Medicine

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Di
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