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38 Cards in this Set

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Clostridium
(general)
obligate anaerobic
gram positive rods
spore forming
catalase negative
oxidase negative
Clostridium botulinum
noninvasive, causing botulism (can be agent of bioterrorism)
Clostridium tentani
generally noninvasive (very limited invasion potential), causative agent of tetanus
Clostridium dificile
noninvasive, secreted toxin causing pseudomembranous colitis (a cause of antibiotic-mediated diarrhea)
Clostridium perfrigens
VERY INFASIVE PATHOGEN
gas gangrene
Clostridium septicum
invasive in malignancy
botulism toxin
cause of flaccid paralysis
exotoxins A and B
cause of diarrhea in pseudomembranous colitis due to Clostridium dificile
Alpha toxin
lecithinase which lysed host cell membrane; in combo with other degradative enzymes as the cause for "gas gangrene" due to Clostridium perfringens
Botulism
C. botulinum, gram positive with subterminal oval spores (not diagnostic for this species); soil organism; spores very resistant to physical and chemical agents; BOTULISM TOXIN IS VERY HEAT-LABILE; spores found in contaminated food, under anaerobic conditions...
Different types of botulism
1. food botulism found in canned vegetables
2. wound associated botulism
3. infant botulism (honey as a source...requires ingestion of spore)
Botulism toxin
EXTREMELY POTENT
HEAT LABILE (inactivated by boiling for 10 minutes)
not destroyed by stomach acid
7 types (A-G); A, B, and E are the most common
two subunit toxins (A and B)
Botulism toxin action
upon absorption in intestine, carried via blood to peripheral nerve synapses, acting as a neurotoxin...blocks release of ACh...flaccid paralysis, NO FEVER, NORMAL MENTAL STATUS
Botulisn clinical manifestations
weakness or flaccid paralysis of peripheral nerves including cranial nerves, symmetrical in distribution; dysphagia, diplopia, dry throat, dilated pupils, NO SENSORY DEFICIT
Diagnosis of botulism
usually a clinical diagnosis
do not rely on culturing the microorganisms; detecting botulism toxin in the serum, vomitus, or feces...detecting bacterial toxin in food with serological tests
EMG: electromyography...diminished action potential of the peripheral nerves...suggestive not diagnosic;
Therapy of botulism
removal of toxin from the stomach with lavage; treatment with antitoxin (from horse serum, toxin specifics A, B, and E); supportive care, may require respiratory support, 12% fatality rate
Prevention of botulism
canned food must be cooked (100 C for 10 minutes to inactivate the toxin)
Infant botulism
honey is common source of contamination; food contaminated with C. botulinum, toxin formed as a result of bacterial proliferation in gut; SYMPTOM IS MORE SUBTLE (constipation, weak head control (flaccid), cranial nerve deficit common; diagnosis: toxin in stool; treatment: supportive or new human antitoxin antibodies
Wound associated botulism
spores in soil contaminate wound, germinate and produce toxin; diagnosis by wound culture and demonstrated of toxin in serum
Clostridium tetanus
Clostridium tetani, gram positive rods, the only one with TERMINAL SPORE!!!!

the terminal spore is highly diagnosic
Clostridium tetanus: pathogenesis
non invasive, TOXIN MEDIATED DISEASE (caused by tetanus toxin, a NEUROTOXIN); only ONE SEROLOGICAL TYPE (remember botulism toxins have several serotypes)
C. tetanus toxin
A NEUROTOXIN; transported from the site of infection to peripheral and CNS nerves (affect anterior horn cells of spinal cord and on brain stem); toxin composed of 2 subunits (A and B), one subunit binds to neuronal ganglioside, the other subunit has the neurotoxin activity; inhibits release of neurotransmitters (glycine and GABA) resulting in spastic paralysis, CONVULSIVE CONTRACTIONS...locked jaw
C. tetanus clinical syndromes
violent muscle spasm, with the flexor muscle predominant; clenched teeth, neck, and back arched; NO FEVER AND NO SENSORY DEFICIT; involvement of respiratory muscles leads to respiratory failure; aspiration, dysphagia with oral pharyngeal involvement; complications may be pulmonary infections and respiratory problem
Treatment of C. tetanus
human tetanus immunoglobulin (only one anti-toxin); penicillin plus wound debridement (metronidazole if penicillin allergic); respiratory support; immunization with tetanus toxoid;

(theres a high fatality rate due to pulmonary complications and secondary infections)
Prevention of C. tetanus
immunization with three doses of tetanus toxoid in the first 6 months of life (remember that toxoid is toxin inactivated by formaldehyde); its given as DPT (diphtheria, pertussis, and tetanus vaccines); booster at 1 year and prior to school entry...booster every 10 years
Pseudomembranous colitis due to C. dificile enterotoxin
C. dificile, anaerobic, gram positive rod
C. dificile
COMMON CAUSE OF ANTIBIOTIC ASSOCIATED DIARRHEA due to toxin-mediated inflammation of the colon
Pathogenesis of C. dificile
antibiotic-induced suppression of normal flora - C. dificile would proliferate and synthesize two distinct toxins (exotoxins A and B)
Exotoxins of C. dificile
Exotoxin A: enterotoxin that binds to the gut receptor
Exotoxin B: cytotoxin, damaging colonic mucosa (bloody diarrhea), by ADP-ribosylating Rho, a GTP-binding protein

damage to the colon by exotoxin B leads to pseudomembrane formation
Diagnosis of C. dificile
history of antibiotic use (ampicillin, cephalosporins, and clindamycin); exotoxin B detected in the filtrate of stool samples; ELISA to detect toxins; stool culture for C. dificile (by itself is not very useful); sigmoidoscopy with visualization of pseudomembranes
Treatment of C. dificile
stop the offending antibiotics; treat with metronidazole or vancomycin

Prophylaxis: PRUDENT USE OF ANTIBIOTICS
Gas gangrene

histotoxic clostridia
invasive and rapidly progressive; primarily a surgical disease
Gas gangrene
many species of clostridia can cause gas gangrene (anaerobic gram + rod); CLOSTRIDIUM PERFRINGENS IS THE MOST COMMON; C. septicum, C. bifermentans, and C. ramosum (all anaerobes)
Hallmark of gas gangrene infections
TISSUE NECROSIS
Pathogenesis of gas gangrene
synthesize many toxins and enzymes which lyse host cells and tissues - thus accounting for tissue NECROSIS; lecithinase: ALPHA TOXIN - damage host cell membrane; collagenase; hyaluronidase (hyaluronic acid is a carb molecule in the host matrix); can grow RAPIDLY in anaerobic environment (deep penetrating wound or dead tissues); byproducts of anaerobic growth are GASES (H2 and CO2);
Clinical syndromes of gas gangrene
dependent on host anatomy: 1. cellulitis (superficial) 2. necrotizing cellulitis (invastion into dermis and underyling capillaries)
3. necrotizing faciitis
4. myositis or myonecrosis

may occur in the absence of open wound (eg penetrating but closed wound)

rarely with uterine infection (septic abortion) or GI lesion in lymphoma or leukemia
Diagnosis of gas gangrene
clinical mostly
CREPITUS (upon pressing the skin...due to gas in subcutaneous tissue and muscle)

DISCOLORATION and edema of the skin, extreme PAIN
Treatment of gas gangrene
SURGICAL - wound debridement

penicillin to kill remaining bacteria; hyperbaric oxygen in selected medical centers

outcome: may be rapidly fatal if left untreated