Kingdom: Bacteria Phylum: Firmicutes Class: Clostridia Order: Clostridiales Family: Clostridiaceae Genus: Clostridium
Clostridium
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Gram + rods, Obligate anaerobes Spore formers Pathogenic Clostridium
C.perfringens,
C. difficile,
C. tetani C. botulinum.
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Clostridium perfringens
Ubiquitous, Anaerobic, Gram-positive, Spore-forming Bacillus Contaminant of meat and poultry foods Double zone of hemolysis Crepitus Non motile. Resistant to high temperatures
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Double zone of hemolysis Clostridium perfringens
Courtesy by CDC
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Virulent factors
Spore forming nature Less generation time Exotoxins alpha, beta , theta and epsilon Invasiveness: proteases, collagenases, phospholipase, and DNAse
Enterotoxin
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Alpha Toxin:
LecithinaseHydrolyzes lecithin and sphingomyelin destructs RBC's, and WBC's. Partial hemolysis
Beta Toxin:
Cytotoxin, responsible for necrotizing enteritis
Theta Toxin:
O2-labile beta-hemolysis small zone. Toxic to heart muscle, leading to myocarditis as a cardiac complication
Epsilon: Unknown function
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Enterotoxin:
Released upon sporulation and lysis of a vegetative cell
CPE gene on chromosome resistant to heat
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Epidemiology
1.4% of American retail food are positive C. perfringens type A is most common food poisoning Third most common cause of food poisoning in the United Kingdom
and the United States
Inoculation on Trauma or a recent surgical wound gas gangrene
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Food poisoning
Spores are resistant to cooking
Gas Gangrene
Inoculation of spores on wounds
Pathogenesis
Damage to muscle, and reduced blood flow and low PH anaerobic condition
Changes in to vegetative forms when food cooled down
Vegetative forms produce Enterotoxin
Spores vegetative forms , , , toxins released
Ingestion leads to diarrhea
Gas gangrene
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Metabolize carbohydrates CO2 and H2 Crypitus
Clinical features
Food poisoning:
TYPE-A. Found in meats, gravy.
8-16 hours after meal. Water diarrhea, no perforation, resolves spontaneously.
No fever.
Heating doesn't prevent it.
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Gas gangrene: 1-10 days incubation Severe pain, pressure and heaviness hemorrhagic bullae, Fever Drainage from the tissues, foul-smelling brown-red or bloody fluid Crepitus air in skin Intravascular coagulation Complications - blood pressure (hypotension), kidney failure, coma, and finally death. Cellulitis. Endometritis.
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Gas gangrene
Courtesy by CDC
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Diagnosis:
Specimens blood, feces, and exudate.
Clinically
Obligate anaerobe
Spore forming
Egg-Yolk Agar - Lecithin is present to test for Lecithinase activity.
Blood Agar culture- double layer of hemolysis
Non-motile.
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Treatment
Treatment:
Clean and debride wounds for prevention
Antibiotics - penicillin, intermittent hyperbaric oxygen treatment.
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Just to show oxygen chamber
Clostridium tetani
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Clostridium tetani
Clostridium tetani tetanus.
Gram+ bacillus, ubiquitous. Spore forming drum stick appearance.
C.Tetani as Drum stick
150 cases occur annually in the U.S
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Virulent Factor
Tetanus toxin (tetanospasmin):AB toxin
Heat labile, potent, antigenic exotoxin, A toxin - lethal B toxin Binding B unit Binds to Ganglioside receptors retrograde transport A unit inhibits GABA & Glycerin from inhibitory neurons Spasms.
Epidemiology:
Spores are ubiquitous in the soil and introduced through puncture wounds 150 cases occur annually in the U.S Neonatal mortality in Bangladesh, 112 of 330 infant deaths were due to tetanus.
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Tetanus toxin
Courtesy by W.W.Norton & Company
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C. Tetani spores in wounds
Pathogenesis
Skeletal Muscle spasms Masseter Lock Jaw or Trismus
low O2, low blood flow in wounds A unit Inhibits GABA & Glycerin Vegetative forms release A unit endocytosised and retrograde transport to inhibitory neurons
Tetanus Toxin AB toxin
A unit Inhibits GABA & Glycerin B unit Bind to Ganglioside receptors
B units Bind to Ganglioside receptors on Nerve cellsDr.Aravind
opisthotonos
Clinical Features
2-4 weeks incubation Less incubation period- wounds near to cranial nerves Masseter muscle- lockjaw- Trismus Minor stimulus- severe spasms Spasms of respiratory (increase mortality) and pharyngeal muscles Dysphagia Back muscles get effected Opisthotonus sweating, hyperthermia, cardiac arrhythmias Neonates & elderly- increase mortality
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Diagnosis
Only a few organisms in the lesions. Diagnosis is clinical -- not by microbial isolation Strict Anaerobe Drum stick appearance
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Treatment & prevention
Antitoxin - Given prophylactically if someone is potentially exposed
(has a puncture wound) and has not been vaccinated within 5 years.
Treatment: To someone who has never been vaccinated, the antitoxin
is given in one arm, and a vaccine is given in the other arm, simultaneously. Vaccine Given against the O-Antigen in cell wall.
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Clostridium Botulinum
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Gram-positive spore forming rod.
large anaerobe Serotypes: A- G
Only types A, B, E affect humans.
Motile
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Virulent Factor
Botulin Exotoxin:
Phage-mediated, heat labile toxin No persistent antibody to the toxin AB toxin:
A unit Inhibits Acetylcholine neurotransmitter release at Neuromuscular junction B unit Binding.
Ingestion of toxin Blood stream Neuromuscular junction Inhibits acetylcholine at presynaptic terminals Flaccid paralysis.
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Epidemiology: Usually found in alkaline foods, consumed without heating old canned foods or self-canned foods No Person to person transmission Honey based foods to infants
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Pathogenesis: Contaminated food toxin absorbed in duodenum and jejunum
blood steam and reaches presynaptic terminals blocks acetyl choline
neurotramitters flaccid paralysis.
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Clinical syndromes
Adult botulism or Food Botulism Infant Botulism Wound Botulism
Adult botulism 18-36 hours incubation weakness, dizziness and dryness of the mouth. Nausea and vomiting may occur. Neurologic features soon develop, including blurred vision, inability to swallow, difficulty in speech, descending weakness of skeletal muscles and respiratory paralysis.
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Infant Botulism: Infant at risk up to 1 year of age. Cause: Ingestion of spores, usually in unpasteurized honey. Constipation, dysphagia, poor food intake, respiratory paralysis, death
Wound Botulism: Rare, similar clinical presentation as food botulism
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Diagnosis:
Stool Toxin Test
Food stuffs- toxin test Serological tests of blood & intestinal contaminants
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Treatment
Ventilatory Support Administer antitoxin.
Gastric Lavage to wash out any unabsorbed toxin.
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No Honey Sweetie
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CLOSTRIDIUM DIFFICILE
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Gram (+) Rod, Spore-former
Obligate anaerobe
Motile
Endogenous Infection: Spores that were otherwise silent become
activated when normal flora is depressed by antibiotics.
Exogenous Infection: Nosocomial infection in the hospital.
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Virulent factors
Exotoxin A:
Protein that damages the intestinal mucosa. It attracts PMN's and causes them to degranulate, resulting in more damage.
Exotoxin B:
AB-Toxin that disrupts the cytoskeleton of enterocytes.
Fragment-A gets inside with the help of a host-cell protease. Mechanism of damage unknown.
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Epidemiology Endogenous Nosocomial
Prolonged use of antibiotics, Elderly are at greatest risk
Gastrointestinal surgery, serious underlying illness, immunocompromised, are at risk.
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Pathogenesis:
Usage of antibiotics diminish normal flora of GIT C.Difficile
sporulation after antibiotic therapy vegetative forms produce toxin
diarrhea and pseudo membrane enterocolitis. Antibiotic Leads AAD Ampicillin, clindamycin, cephalosporin's.
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Clinical features:
Diarrhea, nausea, vomiting, blood in stools, fever, leukocytosis
*Pseudomembranous enterocolitis due to B toxin- can destroy cellsdeath
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Diagnosis:
Stool toxin test
ELISA
Gas Liquid Chromatography
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Treatment:
Treatment has a high relapse rate. Discontinue broad-spectrum antibiotic therapy. Replace lost fluid and electrolytes. Vancomycin (some resistance has shown) or metronidazole is used when necessary.
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Hurts Buddy
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