Professional Documents
Culture Documents
Clostridium
Clostridium
Clostridium
Clostridium
Dr.Aravind
C. difficile,
C. tetani C. botulinum.
Dr.Aravind
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
Dr.Aravind
Courtesy by CDC
Dr.Aravind
Virulent factors
Spore forming nature Less generation time Exotoxins alpha, beta , theta and epsilon Invasiveness: proteases, collagenases, phospholipase, and DNAse
Enterotoxin
Dr.Aravind
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
Enterotoxin:
Released upon sporulation and lysis of a vegetative cell
Dr.Aravind
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
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
Gas gangrene
Dr.Aravind
Clinical features
Food poisoning:
No fever.
Heating doesn't prevent it.
Dr.Aravind
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.
Dr.Aravind
Gas gangrene
Courtesy by CDC
Dr.Aravind
Diagnosis:
Specimens blood, feces, and exudate.
Clinically
Obligate anaerobe
Spore forming
Egg-Yolk Agar - Lecithin is present to test for Lecithinase activity.
Treatment
Treatment:
Dr.Aravind
Clostridium tetani
Dr.Aravind
Clostridium tetani
Clostridium tetani tetanus.
Gram+ bacillus, ubiquitous. Spore forming drum stick appearance.
C.Tetani as Drum stick
Dr.Aravind
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.
Dr.Aravind
Tetanus toxin
Dr.Aravind
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
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
Dr.Aravind
Diagnosis
Only a few organisms in the lesions. Diagnosis is clinical -- not by microbial isolation Strict Anaerobe Drum stick appearance
Dr.Aravind
Dr.Aravind
Clostridium Botulinum
Dr.Aravind
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.
Dr.Aravind
Dr.Aravind
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
Dr.Aravind
Dr.Aravind
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.
Dr.Aravind
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
Dr.Aravind
Diagnosis:
Dr.Aravind
Treatment
Ventilatory Support Administer antitoxin.
Dr.Aravind
No Honey Sweetie
Dr.Aravind
CLOSTRIDIUM DIFFICILE
Dr.Aravind
Obligate anaerobe
Motile
Dr.Aravind
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.
Dr.Aravind
Pathogenesis:
Usage of antibiotics diminish normal flora of GIT C.Difficile
Dr.Aravind
Clinical features:
Diarrhea, nausea, vomiting, blood in stools, fever, leukocytosis
*Pseudomembranous enterocolitis due to B toxin- can destroy cellsdeath
Dr.Aravind
Dr.Aravind
Diagnosis:
Stool toxin test
ELISA
Gas Liquid Chromatography
Dr.Aravind
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.
Dr.Aravind
Hurts Buddy
Dr.Aravind