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64 Cards in this Set
- Front
- Back
C. perfringens type A: how acquired
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exogenously acquired more commonly than endogenously
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C. septicum
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endogenously acquired
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C. Perfringens type A and C. septicum Histotoxic group: tissue infections
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cellulitis, myonecrosis, gas gangrene, fasciitis
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Enterotoxigenic group: gastrointestinal disease
C. perfringens type A |
clostridial foodborne disease (8-24 hrs after ingesting large numbers of organisms on contaminated meat products; spores germinate and enterotoxin is produced)
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Enterotoxigenic group: gastrointestinal disease: C. perfringens
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necrotizing enteritis; beta toxin
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C. difficile: how acquired
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endogenously acquired or exogenously acquired person-to-person
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C. difficile: disease
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antibiotic-accociated diarrhea, antibiotic-associated pseudomembrane colitis
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Tetanus: C-tetani neurotoxin
How acquired? |
exogenously acuired
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C. tetani disease
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generalized, cephalic, localized, neonatal (contaminated umbilical stump)
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Botulism
C. botulinum neurotoxin How acquired? |
exogenously acquired
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Botulism disease
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foodborne intoxication (1-2 days incubation), infant (ingestion of spores in honey), wound (similar to foodborne symptoms, longer incubation)
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How do spores form? Why necessary?
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Clostridium endospores form under adverse environmental conditions. They are a survival mechanism.
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Describe spore shapes of most Clostridium
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Most Clostridium species, including C. pergringens and C. botulinum have ovoid subterminal (OST) spores
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Described C. tetani spores
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C. tetani have round terminal (RT) spores; tennis racket
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Human disease associated with C. diff
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antibiotic-associated diarrhea, pseudomembranous colitis
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Human disease associated with C. perfringens
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Soft tissue infections (cellulitis, suppurative myositis, myonecrosis, gas gangrene), food poisoning, enteritis, necroticans, septicemia
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Morphology and Physiology of C. perfringens
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large, gram-positive, rectangular bacilli, spores rarely seen in vitro, non-motile, rapid spreading growth
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Pathogenicity determinants of C. perfringens
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Four major letal toxins and an enterotoxin, six minor toxins and neuraminadase
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C. perfringens type A
Pathogenicity Determinants |
alpha toxin responsible for histotoxic and enterotoxigenic infections in humans
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Lab ID of C. perfringens
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Rapid growth, gas from glucose fermentation, double zone of hemolysis (beta and alpha)
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Lab ID of C. perfringens
Stormy fermentation |
Coagulation of milk due to large amounts of lactic acid and gas from lactose
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Lab ID of C. perfringens
Nagler reaction |
Lecithinase (alpha-toxin; phospholipase) hydrolyzes phospholipids in egg yolk agar around streak
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Diagnosis/Treatment of C. perfringens
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Surgical debridement of necrotic tissue, penicillin G in high doses, hypobaric chamber
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Epidemiolgy of C. perfringens
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Ubiquitous in soil, water, and intestinal tract of humansDisease from exogenous or endogenous exposure
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Double zone of hemolysis
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Seen when C. perfringens plated on BAP: innter beta hemolysis: theta toxin, outher alpha-hemolysis: alpha toxin
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Neuraminidase
Virulence Factor of C. perfringens |
alters cell surface ganglioside receptors; promotes capillary thrombosis
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Major Virulence Factors of C. perfringens
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alpha-iota toxins are all lethal toxins
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Minor Virulence Factors of C. perfringens
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delta-nu
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Enterotoxin
Virulence Factor of C. perfringens |
Alters membrane permeability
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Antigenic structure of C. tetani
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flagella (H), somatic (O), and spore antigens
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Pathogenicity Determinants of C. tetani
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plasmid-mediated A-B neurotoxin (tetanospasmin): blocks release of inihibitory neurotransmitters
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Lab ID of C. tetani
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resistance to heat, motility and toxin
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Diagnosis/Treatment/Preventrion
C. tetani |
Clean wounde (debridement), control spasps, metronidazole, passive immunity: vaccination, antitoxin
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Epidemiology of C. tetani
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Ubiquitous: spores found in most soils and can colonize gastrointestinal tract of humans and animals.
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Diseases of C. tetani
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generalized tetanus: most common
cephalic tetanus: high mortality localized or wound tetanus: good prognosis neonatal tetanus: high mortality |
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Diagnosis of tetanus
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Based on clinical presentation:
microscopy and culture have poor sensitivity; neither tetanus toxin nor antibodies are typically detected |
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Treatment, prevention and control
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Debridement, antibiotic therapy, passive immunitation w/ antitoxin globulin and vaccination w/ tetanus toxoid
Prevent: vaccine |
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Generalized tetanus
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Bulbar and paraspinal muscles involved (trismus/lockjaw, risus sardonicus); invovles autonomic nervous sys
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Cephalic tetanus
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primary infection in head, particularly ear; isolated: cranial nerves (7th); poor prognosis
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Localized tetanus
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involves muscles in area of primary injury; infection can precede generalized disease; favorable prognosis
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Neonatal tetanus
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generalized disease in neonates; infection originates from umbilical stump; poor prognosis in infants who are nonimmune
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C. botulinum
physiology and structure |
gram positive, spore-forming bacillus, strict anaerobe, fastidious, seven distinct toxins
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Virulence of C. botulinum
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Spore formation, botulinum tosxin (prevents release of neurotransmitter acetylcholine), binary toxin
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Epidemiology of C. botulinum
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Ubiquitous; human disease assoc w/ toxins A, B, E, F
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Diseases of C. botulinum
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foodborne botulism, infant botulism (most common), wound botulism
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Diagnosis of Botulism
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Confirmed by isolatiing the org or detecting the toxin in food products or pt's feces or serum
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Tx, prevention and control of botulism
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Admin metronidazole or penicilin, store foods in fridge (4degC), heat food 20 mins at 80degC--toxin is heat-labile
infant botulism: don't allow to eat honey when less than 1 year old |
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C. diff virulence factors
Enterotoxin (toxin A) |
produces chemotaxis; induces cytokine production with hypersecretion of fluid; hemorrhagic necrosis
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C. diff virulence factors
Cytotoxin (toxin B) |
induces depolymerization of actin with loss of cellular cytoskeleton
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C. diff virulence factors
Adhesin factor |
Mediates binding to human colonic cells
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Spore formation
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Permits organism's survival for months in hospital environment
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Diagram of antibiotic associated colitis notes
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pseudomembranous "plaque", area of epithelial destruction
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Treatment, Prevention and Control of C. diff
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Implicated antibiotic discontinued, tx w/ vancomycin in severe case, relapse common b/c spores not affected by antibiotics
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Diagnosis of C. diff
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Isolate org or detect cytotoxin or enteroxin in pt's feces
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Diseases of C. diff
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Asymptomatic colonization, antibiotic-associated diarrhea, pseudomembranous colitis
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Physiology and Structure of C. diff
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gram-positive, spore-forming bacillus, strict anaerobe
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Epidemiology of C. diff
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Ubiquitous, colonizes intestines of healthy ppl, exposure to antibiotics causes overgroth of cC. diff; spores found in hospital rms of infected pts
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Treatment of C. botulinum
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ventilatory support & trivalent (A, B, E) antitoxin binds free toxin in bloodstream; gastric lavage; care in home canning
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Antigenic structure of C. botulinum
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four groups (I-IV), seven antigenically distinct botulinum toxins (types A-G)
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Pathogenicity Determinants
C. botulinum |
Lethal foodborne intoxication w/ toxin types A, B, E, or F
toxin A: neurotoxin |
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Pathogenicity
C. botulinum Mode of action: A-B toxin |
Binds specific receptors on peripheral cholinergic nerve endings (neuromuscular juctions) where it blocks release of presynaptic acetylcholine (excitatory neurotransmitter) blocking muschle stimulation & resulting in flaccid paralysis
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Early disease
C. botulinum |
nausea, vomiting, weakness, lassitute (lack of energy), dizziness, constipation
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Late disease
C. botulinum |
double vision, difficulty in swallowing and speaking
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Final stage of disease
C. botulinum |
death due to respiratory paralysis
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