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