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68 Cards in this Set

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Taxonomic classifcation Clostridium spp? (6)
Kingdom - Bacteria
Phylum - Firmicutes
Class - Clostridia
Order - Clostridiales
Family - Clostridiaceae
Genus - Clostridium
Clostridium spp. characteristics? (6)
1. GPR - obligate anaerobic spore forming
2. Spore deforms cell
3. Spore variations to spp.
4. Flagella (+) (not C. perfringens)
5. Loci: soil + normaflora (i.e. gut, feces)
6. Lecithinase (+)
6. LT survival
7. Gas produces + high biochemical activity
Clostridium spp. are distinguished based on? (3)
Pathomechanism:
i. gas gangrene/histolytic - C. perfringens
ii. Neurotoxic - C. tetani + C. botulinum
iii. Enteric - C. difficile
Clostridium perfringens characteristics ? (6)
1. GPR - obligate anaerobe spore forming
2. Flagella (-)
3. Capsule (+)
4. Central spore, pear-shaped rod
5. Double hemolytic zone (blood agar)
6. High gas producer
C. perfringens VFs: EXOENZYMES? (3)
1. Collagenase
2. Hyaluronidase
3. DNAse
C. perfringens VFs: SURFACE MOLECULES?
Capsule (12 different capsular AGs)
C. perfringens VFs: EXOTOXINS (membrane damaging)? (5)
Nercotizing and hemolysing toxins
- alpha toxin (lecithinase, PLC --> *lysis)
- beta toxin (necrotizing)
- epsilon toxin (increases vascular permeability of GI)
- Iota toxin (*ADP-ribosylation of actin --> *necrosis)
Enterotoxin (*food poisoning, GI diseases)
What is a spp. specific variant of the Lecithinase rxn?
Nagler-reaction (target = C. perfringens)
Nagler-reaction?
- Egg yolk medium
- Antitoxin blocks lecithinase prod. via C. prefringens
- turbidity opalescence due to lecithinase prod.
- Egg yolk medium
- Antitoxin blocks lecithinase prod. via C. prefringens
- turbidity opalescence due to lecithinase prod.
Toxinogenic strains: C. prefringens?
Types: A-E
What are the most freq. causative agents of GAS GANGRENE? (2)
1. C. perfringens (most freq)
2. C. septicum
Pathogenesis: C. perfringens?
1. Endogenous infections (rare)
2. Exogenous infections - wound contaminated w/ spore-soil (1 cause)
3. AC, septic abortus (rare)
C. perfringens wound infection manifestations? (5)
1. Foul discharge
2. Malignant edema
3. Gas-phlegmone
4. Myositis
5. Cellulitis
Causes of endogenous C. perfringens infection? (4)
1. Colon surgery + carcinoma
2. Gut rupture
3. appendicitis perforata
4. Post-amputation
General symptoms: C. perfringens? (7)
1. Malaise
2. Hypotonia
3. Fever
4. Vomiting
5. Toxemis
6. Shock
7. Death
Necrotizing enterocolitis (NEC), caused by? (4)
1. C. perfringens, TYPE C, B-toxin producing
2. Prevention: Type C toxoid immunization
3. *necrotic lesions jejunum, bloody diarrhea, peritonitis
4. via pork meat
Incubation period: C. perfringens?
1-3 days
What strain of C. perfringens produces enterotoxin that causes FOOD POISONING?
TYPE A C. perfringens (via meat)
Type A C. perfringens causes?
FOOD Poisoning
- *watery diarrhea, abdominal cramps
- 9-15hr incubation
- Detect: enterotoxin in stool
- Diagnosis: 10^5 colonies/g cultivaiton
C. perfringens: DIAGNOSTICS? (7)
(usually clinically)
1. Sample - necrotic tissue
2. Microscopically (Gram)
3. Anaerobic cultivation
4. Blood agar (double hemolysis)
5. Nagler rxn
6. Gas chromatography
7. Phage typing
C. perfringens: PREVENTION? (4)
Wound cleansing:
- efface necrotized material
- rinse w/ H202
- hyperbaric 02 treatment
- amputation
C. perfringens: TREATMENT (antibiotics) (2)
High dose AB
1. Penicillin G +/- clindamycin
2. Imipenem or Cephalosporins (III) - SEVERE CASES
C. perfringens: TREATMENT (antitoxin)? (3)
Polyvalent antiserum (1 to neutralize existing toxins)
1. C. perfringens antitoxins
2. C. septicum antitoxins
3. C. novyi antitoxins
C. perfringens rod + spore shape?
C. tetani contains what type of spore?
Terminal spore
Terminal spore
C. tetani characteristics? (6)
1. GPR obligate anaerobe spore forming
2. Terminal spore
3. Peritrichous flagella + swarming
4. B-Hemolytic
5. Mild gas production
6. Neurotoxic
C. tetani virulence factor?
EXOTOXIN = tetanospasmin
Effect of C. tetani exotoxin tetanospasmin?
1. Enhances ACh effect --> *tetany
2. Exotoxin --> blocks inhibitory Renshaw interneurons from releasing GABA + glycine (CNS)
C. tetani loci? (3)
1. Soil + dust
2. Animal feces
3. Gut normaflora (sometimes)
C. tetani: port of entry? (5)
1.injury
2. burn + deep wounds
3. umbilical wounds
4. abortion
5. surgery, injections, ointments
(exogenous infections)
Incubation period: C. tetani?
4d-several weeks (LONG
Latency of spasms: C. tetani?
5-7d
Clinical findings: C. tetani? (7)
1. Lockjaw
2. Spasms
3. Hydrophobia
4. Respiratory dysfunciton
5. Opisthotonus (dorsal mm. sustained spasm)
6. Risus (facial mm. spasms)
7. Fully concious
Localized type of C.tetani?
Neonatal tetanus (entry: umbilical stump)
C. tetani: Diagnosis? (4)
1. Clinical symptoms
2. Anaerobic cultivation
3. Direct smear
4. Animal inoculation
C. tetani: PREVENTION?
DPTa (dipetheria, pertussis, tetanus, acellular)
- combined vaccine containing toxoid
- active immunization
C. tetani types of treatments? (4)
1. Symptomatic
2. Toxoid recall injection
3. Antitoxin
4. Antibiotics
C. tetani: Symptomatic therapy? (5)
1. Surgical debridement (no hyperbaric 02)
2. Cleansing wounds
3. Muscle relaxants
4. Sedation
5. Assisted ventilation
C. tetani: Toxoid recall injection therapy?
Toxoid vaccine + antitoxin iv
C. tetani: Antitoxin therapy?
Treat for those born before 1941, give before toxin is fixed in nerves
C. tetani: Antibiotic therapy?
Penicillin G
How do you treat elderly C. tetanus infected patients?
1. Toxoid vaccine (*slow immunity development)
AND
2. Antitoxic serum (to provide fast therapy)

(booster shot + antitoxic serum)
C. botulinum characteristics? (5)
1. GPR obligate anaerobe spore forming
2. Flagella (+)
3. Subterminal or central pore
4. High gas production
5. Loci: everywhere, maybe gut flora
C. botulinum: CULTIVATION?
Blood agar + anaerobic
C. botulinum virulence factors?
EXOTOXINS (A-H; A,B,E, F = human pathogens)
C. Botulinum exotoxin mech?
1. Neurotoxin (circ --> nerve endings --> *flaccid paralysis)
2. Heavy chain - binds motor endplate
3. Light chain - endocytosed --> cleaves SNAREs = block ACh vesicular release (no fusion)
Toxic dose of C. tetani and C. botulinum?
C. tetani = 0.0001 ug (mouse lethal dose)
C. botulinum = 1-2 ug lethal
C. botulinum antigens? (2)
1. Same O-AGs (somatic)
2. Different H-AGs (flagellar)
Pathogenesis: C. botulinum?
1. Toxicosis (foodborne botulism)
2. Wound botulism
3. Infant botulism
Toxicosis (foodborne botulism)?
meats/tin cans --> entry --> 3hrs to 1-2d latency --> gut absorbs toxin --> circulation = toxaemia
Neonatal botulism?
Spores in honey --> colonization in GI of infants < 1 year --> weakness, floppy baby, sudden death syndrome
Inhalation of botulism can be used as a?
Biological weapon
Clinical symptoms: C. botulinum? (5)
1. Double vision (initial symptom, due to brain nerves blocked)
2. Speech+swallow disorders
3. Ptosis (drooping lower eyelid)
4. Respiratory paralysis (-->*death)
5. Cardiac arrest
Diagnostics: C. botulinum?
Toxin detection w/ animal inoculation:
- food sample
- blood
- stool
C. botulinum: TREATMENT? (3)
1. Trivalent antitoxic serum (A, B, E) (-->*toxin neutralization)
2. Ventilation (100d, symptomatic)
3. Infants - pencillin 10-20MU/d
C. difficile characteristics? (6)
1. GPR obligate anaerobe spore forming
2. Motile
3. Central spore
4. Resistant to many antibiotics
5. Nosocomial pathogen (primarily)
6. gut normaflora
What is the most freq agent causing nosocomial diarrhea?
C. difficle
What does C. difficle cause? (2)
1. Pseudo-membranous colitis
2. Diarrhea
C. difficle virulence factors?
1. Enterotoxin - toxin A (-->*watery diarrhea)
2. Cytotoxin - toxin B (-->*colon wall destruction)
Pathogenesis: C. difficile
1. Endogenously - via gut normaflora (due to antibiotics effacing normaflora --> *overgrowth of C. difficle)
2. Exogenously - nosocomial infection --> *diarrhea
C. difficile: TREATMENT induced resistance?
PROLONGED TREATMENT resistance build up (i think)
1. Clindamycin
2. Cephalosporin
3. Fluoroquinolone
C. difficile: THERAPY?
1. Vancomycin
2. Metronidazole
3. Bacitracin
C. difficile: DIAGNOSIS?
1. endoscopy
2. CCFA, blood agar
3. Phage typing
4. Toxin detection (ELISA, latex agglutination,PCR)
What clostridum spp. is resistant to ethanol and soap needs to be used instead?
C. difficile
Which ribotype produces the binary toxin of C. difficile?
027 ribotype (A,B toxin with 027 = most lethal)
Dysbacteriosis?
disease caused by an imbalance of the normal flora
(i.e. C. difficile infections)
Category A bioterrorisim agents? (4)
1. B. anthracis
2. C. botulinum (toxin)
3. Yersinia pestis
4. Francisella tularensis
etc..
Category B bioterrorisim agents? (6)
1. Brucella spp.
2. Staphylococcus aureus (enterotoxin B)
3. E. coli (O57:H7)
4. V. cholerae
5. Shigella spp.
6. Salmonella spp.