C. Diff Flashcards

1
Q

What is c. diff?

A

An organism first described in 1935
➢ It was isolated from feces of normal infants and
named Bacillus difficilis due to difficulty of isolation
➢ Recognized as a pathogen in 1970s
➢ Gram-positive, spore forming bacteria
➢ Anaerobic, motile. Show optimum growth on blood agar
Rod-shaped bacteria
➢ Under SEM, they appear as long, irregular
cells with a bulge at their terminal ends
➢ Present in 2–5% of the healthy adult population

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2
Q

Under stress it produces

A

Under stress, C. difficile cells produce spores that
can resist extreme conditions that other bacteria
cannot tolerate

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3
Q

How does it spread?

A

➢ Diarrhoea is an efficient method of spreading
spores of C. difficile

➢ Spores can be spread by hands that touch contaminated surfaces

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4
Q

Risks of CDI

A

Previous hospitalisation
➢ Underlying disorder
➢ Age (>65 years)
➢ Use of antibiotics (+++)

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5
Q

Pathogenesis of C. Diff

Two Toxins

A

Enterotoxin (Toxin A):

  • Cytotoxin (Toxin B):
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6
Q

What does cytotoxin do?

A

Aggravate inflammation

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7
Q

What does enterotoxin do?

A

Toxin A binds to the brush border of the intestine
causing inflammation via recruitment of neutrophils.
This leads to the disruption of cell-cell junctions
resulting in watery Diarrhoea.

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8
Q

Symptoms of C. Diff?

A

Watery smelling Diarrhoea, greater than 3 times per 24 hours, lower
abdominal pain, low grade fever, nausea…
* Inflammatory Diarrhoe

Pseudomembranous colitis: Fulminant colitis,
Diarrhoea, diffuse abdominal pain, fever, abdominal
distention, marked leucocytosis…
It is an invasive disease that can cause sepsis,
bowel perforation and toxic megacolon.

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9
Q

Definition of CDI

A

A case definition of CDI should include the presence of clinical symptoms
(usually Diarrhoea) and a stool test result positive for C. difficile toxins, or
colonoscopy findings demonstrating pseudomembranous colitis

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10
Q

Sequence of events leading to C. Diff?

A

Alteration of the normal gut flora
➢ Nosocomial infection by C. difficile
➢ Growth and production of toxins
➢ Tissue damage by toxin A, exacerbated by toxin B
➢ Diarrhoea and colitis

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11
Q

How do we diagnose C. Diff?

A

Presence of toxins: Nucleic Acid Amplification Tests (NAATs) (such as
PCR)
➢ Glutamate Dehydrogenase (GDH) screening test for C. difficile (lower
sensitivity than NAATs)
➢ ELISA can be performed to reinforce results of the previous tests
➢ Visualisation of the pseudomembranes

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12
Q

Management and Treatment of C-Diff

A

Infection control
Antimicrobrial therapy and surgery

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13
Q

How do we provide infection control?

A

Rapid diagnostic testing
➢ Patient isolation
➢ Chlorine-releasing agents or a sporicidal product, gaseous hydrogen
peroxide and, more recently, UV decontamination!

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14
Q

How do we provide antimicrobiral therapies/surgery?

A

Antimicrobial therapy and surgery
➢ In about 20 % of patients with CDI, infection resolves within 2-3 days
of discontinuing the antibiotic that the patient is taking.
➢ Metronidazole, Vancomycin
➢ Fidaxomicin
➢ Abdominal colectomy (Fulminant CDI)!!
➢ Faecal microbiota transplantation (FMTh

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15
Q

What measures do we use to reduce incidences?

A

Accurate and rapid diagnosis
➢ Appropriate treatment option
➢ Implementation of enteric precautions for symptomatic patients
➢ Reinforcement of hand disinfection
➢ Reinforcement of environmental disinfection
➢ A restrictive antibiotic policy

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