Download Clostridium difficile

Clostridium
Dr.Batool
Clostridium difficile
1- Pathogen disease causing Pseudomembranous Colitis
2- Habitats (gastrointestinal tract of Humans and other animals, Soils,
Marine Sediments).
3- Target Area of Infection: Colon
4- The mortality rate is 1 to 2.5%.
Virulence factors:
1- Enterotoxin (Toxin A):
- Causing diarrhea: Protein toxin released by C. difficile in the
lower Intestine.
- Alters the permeability of the epithelial cells of the intestinal wall.
- Pore forming toxins, secreted by bacteria, form pores in cell
membranes causing cells death.
2- Cytotoxin (Toxin B).
- kill cells.
- Associated with inflammation.
Pathogenesis:
1- Toxigenic strains produce 2 large protein exotoxins that are
associated with virulence (Toxins A and B)
2- Mutants strains that do not make toxins A and B are not virulent.
3-Some strains make a third toxin known as Binary Toxin by itself, not
pathogenic may act synergistically with toxins A and B in severe colitis
(More common in animal strains).
C. difficile which secretes two types of toxin (A and B), which cause
disruption to the barrier function of the colonic mucosa. They are
cytotoxic to cells of the intestinal tract, B being about 1,000 times more
potent than A. Transmission of infection is via an indirect faeco-oral
route, through spores left on surfaces. The spores can survive for months
and patients can become carriers. The risk of colonization increases with
length of hospital stay.
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Clostridium
Dr.Batool
 Pseudomembranous colitis (PMC) is an acute, exudative colitis
usually caused by Clostridium difficile. PMC can rarely be caused
by other bacteria - eg, Staphylococcus spp. or enterotoxigenic
Clostridium perfringens, Campylobacter spp., Listeria spp.
and Salmonella spp.
 C difficile colonization results in a wide spectrum of clinical
conditions, including an asymptomatic carrier state; mild, selflimited diarrhea; pseudomembranous colitis; and fulminant colitis.
Most patients develop diarrhea during or shortly after starting
antibiotics. However, 25-40% of patients asymptomatic for 10
weeks after completing antibiotic therapy.
 PMC has emerged, particularly in recent years, as a major and
very expensive health care problem. Spores formed by the
organism are implicated in spread of infection and have
implications for hygiene and prevention of infection. C. difficile is
an anaerobic Gram-positive rod
Symptoms:
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Mild to moderate watery diarrhea that is rarely bloody.
Cramping abdominal pain
Anorexia and Malaise
Fever, especially in more severe cases.
Treatment:
1- C. difficile sometimes resolves in two to three days after you have
stopped taking antibiotics.
2- It can also be treated with other antibiotics, such as vancomycin and
Flagyle.
 The strain of C. difficile that produces a large amount of toxin is
harder to treat.
What increases my risk for acquiring C. difficile?
•Taking antibiotics
•Having surgery
•Being in a health care facility for an extended period of time
•Having serious, underlying illness
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Clostridium
Dr.Batool
•Advanced age
Role of Antibiotics:
• All antibiotics (including metronidazole and vancomycin) are
associated with CDI.
• High-risk group
– Clindamycin
– Cephalosporins/penicillins/beta-lactams.
– Fluoroquinolones.
• Alteration of normal colonic flora thought to favor growth of C.
difficile
Infection Control:
1- Wash hands with warm soap and water.
2- Mechanical removal of spores.
3- Alcohol does not kill spores
4- Stool is pre-treated with alcohol when growing C. difficile
5- Contact and barrier precautions
6- Antibiotic stewardship
Clostridium botulinum
1-Gram positive
2-Obligate anaerobic bacillus.
3-Motile.
4-Spores (ubiquitous, Resistant to heat, light, drying and radiation,
specific conditions for germination, anaerobic conditions, warmth (10-50
C),Mild alkalinity.
5- Clostridium botulinum is widely distributed in soil and contaminated
fruits and vegetables. Inadequate precautions in processing and handling
of a certain food will allow this organism to grow and produce one of the
most powerful exotoxins known.
Transmission:
1234-
Ingestion (organism, spores, neurotoxin)
Wound contamination
Inhalation
Person-to-person not documented.
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Clostridium
Dr.Batool
Virulence factors (exotoxin, neurotoxin):
There are seven antigenic varieties of toxin(A-G) are known:
1- A,B,E and F are the principle causes of human illness.
2- Type E predominantly with fish products.
3- Type C and D are associated with animal diseases.
Action of botulism toxin:
It is a neurotoxic protein. All of its types (A, B, and E) are made of heavy
and light chains linked by disulfide bonds. The heavy chain is thought to
bind the toxin to the motor nerve end.
The light chain blocks the calcium mediated release of acetyl choline.
The toxin acts by blocking the release of acetyl choline at synapses and
neuromuscular junctions causing flaccid paralysis.
Pathogenesis:
-Three forms are fatal and need to a medical emergency
-Incubation period: 12-36 hours
1- Wound Botulism
Organism enters wound  Develops under anaerobic conditions,
 From ground-in dirt or gravelIt does not penetrate intact skin
Associated with addicts of black-tar heroin.
2- Food borne Botulism
 Preformed toxin ingested from contaminated food(most common
from home-canned foods (green beans, beets, corn, garlic,
tomatoes; type A
 Improperly fermented fish (Alaska); type E
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Infant Botulism
Infants < 1 year old, 94% < 6 months old
Spores from varied sources
Honey, food, dust, corn syrup
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Clostridium
Dr.Batool
Diagnosis:- Demonstration of toxins in serum from the patient and
toxin may be found in left food.
Treatment:
1- Trivalent antitoxin(A,B,E,F toxin must be administrated
intravenously.
2- Adequate ventilation
These will reduce mortality rate from 65 % to below25%.
3- Infant botulism is recovered with supportive therapy alone.
Control:
1-Boiling of home canned food for 20 minutes to destroy the toxin.
2-Strict regulation of commercial canning.
3- Avoiding swelled canned food or that with suspected appearance or
odor.
References:
1- Jawetz, Melnick, & Adelberg’s.( 2013). Medical Microbiology (Twenty-Sixth Edition).
2- Kenneth Todar. (2008).Todar’s Online Textbook of Bacteriology
,University of Wisconsin.
3- Ray, C.G., ed. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill.
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