clostridium-difficile-infection-pathogenesis-and-clinical-findings

clostridium-difficile-infection-pathogenesis-and-clinical-findings

Antibiotics
I.e. Clindamycin,
fluoroquinolones
Poor cleaning
practices of:
Gastric Acid
Suppression
(↑ pH)
Susceptible Host
↑ Antibiotic
resistant strains
Health-Care Exposure
↑ C. diff spores
on hospital surfaces
Clostridium difficile (C. diff) Infection
Clostridium difficile
Infection of GI Tract
Release of toxin A and B
inactivates Rho GTPases in
colon cells
↑ colonocyte damage
Legend: Published March 30, 2019 on www.Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications thecalgaryguide.com
Authors:
Ryan Brenneis
Reviewers:
Yoyo Chan, Sean Doherty
Dr. Steve Vaughan*
* MD at time of publication
Inoculation of GI Tract
via fecal-oral route
Antacid Usage
ex) PPI, H2RA
Disruption of
GI microbiome
Contact exposure
to C. diff carriers
Co-morbidities
• Cirrhosis
• IBD
• Obesity
• Enteral Feeding
Recent
GI
Surgery
Chemotherapy
Demographics
• Old Age (> 65 y.o.)
• Caucasian
• Female > Male
Iatrogenic
Poor antibiotic
stewardship
Disruption of cytoskeleton
and tight junctions
Neutrophil chemotaxis
and activation
Diarrhea
Toxic
Megacolon
Abdominal
Cramps
Bloody
Stool
Abbreviations:
• PPI- Proton Pump Inhibitor
• H2RA- Histamine-2 Receptor Antagonist
• GI- Gastrointestinal
• y.o.- Years Old
• IBD- Inflammatory Bowel Disease
• GTPase- Guanine triphosphate
hydrolyzing enzyme
Colon cannot reabsorb
water effectively
Pseudomembranous
Colitis
Hypotension
Bowel
Perforation
Volume
Acute kidney injury Depletion
Equipment
Sanitization
Hand
hygiene
Environmental
exposure
Highly Infectious Pathogen
↑ Inflammation of colon
Muscle
Paralysis
Destruction of
nerve fibres
Breakdown of
membranes
Spores
persist in
GI tract
Recurrence