Clostridium perfringensClostridium tetani Clostridium botulinumClostridium difficile Clostridium...
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Transcript of Clostridium perfringensClostridium tetani Clostridium botulinumClostridium difficile Clostridium...
Clostridium perfringens Clostridium tetani
Clostridium botulinum Clostridium difficile
Clostridium septicum
ANAEROBIC, SPORE-FORMINGGRAM-POSITIVE BACILLI
Clostridium perfringens
Causes two distinct diseases:
Gas gangrene
Food poisoning
Clostridium perfringens
Pathogenesis
Present in soil, water and sewage, and as a normal resident of the gastrointestinal tract
Spore formation enables the organism to survive in the environment
Clostridium perfringens
Clostridium perfringens
Pathogenesis
Alpha toxin: A phospholipase C (lecithinase) lyses erythrocytes, platelets, leukocytes and
endothelial cellsincreased vascular permeabilitymassive hemolysis and bleedingtissue destructionhepatic toxicitymyocardial dysfunction
Clostridium perfringens
phosphatidylcholine
Clostridium perfringens
Pathogenesis
Beta toxin necrotic lesions in necrotizing enteritis
Epsilon toxin increases vascular permeability
Iota toxin ADP ribosylating lethal toxin, necrotic activity, increases vascular permeability
Enterotoxin released during spore formation in the small intestine, disrupts ion transport
Clostridium perfringens
Zone of complete hemolysis caused by theta toxin
Wider zone of partial hemolysis caused by alpha toxin
Clostridium perfringens
Transmission
Exogenous exposure (soil, food, trauma, surgery) is more common than endogenous spread
Vegetative cells are part of the normal flora of the colon and vagina
Clostridium perfringens
Clinical syndromes
Myonecrosis (gas gangrene)Life-threatening diseaseMuscle necrosis, shock, renal failureDeath frequently within 2 days of onsetGas generated by the metabolic activity of the rapidly dividing bacteria
Clostridium perfringens
Clinical syndromes
Cellulitis: Necrosis of the skin layer (subcutaneous gas)
Fasciitis: Infection of the fascia, suppuration, gas
Food poisoning: Abdominal cramps and watery diarrhea
Necrotizing enteritis: Bloody diarrhea, shock and peritonitis
Clostridium perfringens
Clostridialcellulitis followingcompound fractureof the tibia
Clostridium perfringens
Treatment and control
Rapid treatment is essentialsurgical debridement high-dose penicillin G therapy
Proper wound care and use of prophylactic antibiotics can prevent infections
Clostridium tetani
Causes tetanus (lockjaw) Small, motile, spore-forming bacillus
Frequently stains negative
Terminal spores give the appearance of a drumstick
Clostridium tetani
Gram stain withterminal spores
Clostridium tetani
PathogenesisTetanospasmin
Synthesized as an A-B toxin
B chain binds to a receptor on neuronal membranes
Clostridium tetani
PathogenesisTetanospasmin
“A” chain (zinc endopeptidase)Localizes in vesicles in presynaptic
nerve terminals of inhibitory synapses
Causes the excitatory synaptic activity to be unregulated
Leads to spastic paralysis
Clostridium tetani
Pathogenesis
TetanolysinOxygen-labile hemolysinInhibited by serum cholesterol
Spore formation
Clostridium tetani
Transmission
In fertile soil and the GI tract of many animals and humans
> 1 million cases worldwide (mortality rate 20-50%)Half the deaths occurring in neonatesAssociated with minor trauma
skin break with contaminated splinter or nail Germination of spores favored by necrotic tissue
and poor blood supply
Clostridium tetani
Clinical syndromes
Generalized tetanus (trismus or lockjaw) risus sardonicus: "smile" due to sustained
contraction of the facial musclesDrooling, sweating, persistent back spasmsCardiac arrythmias, fluctuations in blood
pressure, hyperthermia, dehydration High mortality rate
Clostridium tetani
Clostridium tetani
Risus sardonicuscaused bysustained spasmsof the massetermuscles
Clinical syndromes
Localized tetanus: Involvement of muscles in area of primary injury. Prognosis favorable
Cephalic tetanus: Cranial nerves. Very poor prognosis
Neonatal tetanus: Via umbilical stump. Very poor prognosis when mothers are not immune
Clostridium tetani
Treatment and control
Debridement of the primary woundMetronidazole or penicillin GHuman tetanus immunoglobulinVaccination with tetanus toxoid
Three doses of tetanus toxoid and a booster every 10 years
Clostridium tetani
Pathogenesis
Botulinum toxinSimilar to tetanus toxin, but inhibits
cholinergic synaptic transmissionBinary toxin
Two components that combine to disrupt vascular permeability
Spore formation
Clostridium botulinum
Clostridium botulinum
Transmission and clinical syndromes
Foodborne botulismHome-canned foodsWeakness and dizziness 1-2 days laterBlurred vision, dry mouth due to
anticholinergic effect of the toxinConstipation and abdominal pain
Clostridium botulinum
Transmission and clinical syndromes
Progressive diseaseWeakening of peripheral muscles (flaccid
paralysis)Respiratory paralysisComplete recovery months to years
(regeneration of paralyzed nerve endings)
Clostridium botulinum
Transmission and clinical syndromes
Infant botulismIngestion of spores in food (contaminated
honey)Colonization of the GI tractInitial symptoms: constipation, weak cry,
failure to thrive
Clostridium botulinum
Transmission and clinical syndromes
Wound botulismDue to infection of woundsGI symptoms less severeOther symptoms identical to foodborne
disease
Clostridium botulinum
Treatment and control
Ventilatory supportLavageMetronidazole or penicillin therapyBotulinum antitoxin against toxins A, B and EPreventing spore germination by maintaining foods
in acid pH and at 4oCNo honey for children younger than 1 year
Clostridium botulinum
Antibiotic-associated gastrointestinal diseases
Can cause life-threatening pseudomembranous colitis
In soil, water and sewage
Clostridium difficile
Pathogenesis
Antibiotics (clindamycin and ampicillin) can alter the normal enteric flora and enable the overgrowth of relatively resistant C. difficile
Disease develops if the organism develops in the colon and produces toxins
Clostridium difficile
Pathogenesis
Enterotoxin (toxin A)
Causes hypersecretion of fluid (watery diarrhea) and hemorrhagic necrosis
Clostridium difficile
Pathogenesis
Cytotoxin (toxin B)ADP-ribosylates the GTP-binding protein
RhoInduces depolymerization of actinCauses damage to the colonic mucosa,
leading to pseudomembrane formation
Clostridium difficile
Pathogenesis
Adhesin factorMediates binding to human colonic cells
HyaluronidaseHydrolytic activity
SporesSurvival for months in a hospital environment
Clostridium difficile
Clinical syndromes
Diarrhea, associated with pseudomembranes (yellow-white plaques) on the colonic mucosa
Found in the GI tract of about 3% of the general population and up to 30% of hospitalized patients
The most common nosocomial cause of diarrhea
Clostridium difficile
Clostridium difficile
Antibioticassociated colitis
Plaques of fibrin,mucus andinflammatory cells
Antibioticassociated colitis
Plaque
Intact intestinalepithelium
Clostridium difficile
Treatment and control
Discontinuation of the implicated antibiotic
Therapy with metronidazole or vancomycin
Resistant spores can be a major source of nosocomial outbreaks
Clostridium difficile
Treatment and control
In patients with occult colon cancer, acute leukemia and diabetes
It can spread into tissues and proliferate, causing death within a few days of initial symptoms
Clostridium septicum