Lect 17 Flashcards

1
Q

clostridium species

  • gram status
  • oxygen?
A
  • gram postive bacilli
  • obligate anaerobes
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2
Q

pathogen that causes tetanus

A

clostridium tetani

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3
Q

pathogen that causes botulism

A

clostridium botulinum

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4
Q

clostridium tetani

  • gram status
  • spores have what appearance
A
  • gram positive
  • spores are terminal
    • tennis racket appearance
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5
Q

clostridium tetani toxin production is mediated by

A

plasmid-mediated

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6
Q

how is clostridium tetani transmitted

A
  • initial event is trauma which allows entery of spores
    • contaminated soil
    • or human/animal feces
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7
Q

what potent exotoxin does clostridium tetani release? what does it do?

A
  • tetanospasmin
    • absorbed by local nerve endings and transported through neurons
    • disruption of central motor control, autonomic function and NMJ
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8
Q

clinical presentation

  • lockjaw or trismus: spasm of masseter muscles
  • risus sardonicus: grimace
  • opisthotonos: arching of back
  • may lead to respiratory complications and cardiac complications -> usually causes death
A

clostridium tetani

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9
Q

prevention of clostridium tetani

A
  • routine immunization with tetanus toxoid
    • DTap and Td
  • Human tetanus immune globulin (HTIG) is recommended for passive immunization
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10
Q

DOC for clostridium tetani

A

penicillin plus antitoxin

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11
Q

clostridium botulinum

  • describes spores
A

spores are subterminal

  • give bacillus a distended shape
  • great heat resistance
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12
Q

describe toxins of clostridium botulinum

A
  • 8 serologically distinct botulinum toxins (A-G)
  • toxin is neurotoxic
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13
Q

clostridium botulinum can enter via what two mechanism

A
  1. wound botulism
  2. food poisoning: results from ingestion of neurotoxin in incompletely processed food that contains bacteria
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14
Q

what is infant botulism

A
  • results from germination of spores and multiplication of bacteria, along with release of neurotoxin
    • systemic effects are lethal (probable cause of sudden infant death)
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15
Q

how is clostridium botulinum diagnosed

A
  • confirmation is related to demonstration of toxin presence
    • fecal samples
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16
Q

treatment of clostridium botulinum

A
  • neutralization of toxin
    • abx typically not recommended
17
Q

explain basic features of Fungi

A
  • eukaryotic
  • consists of
    • Yeasts (unicellular)
    • molds
    • mushroons
18
Q

differentiate between Blastomyces and candida

A
  • Blastomyces: primary pathogens
  • candida: opportunistic pathogens
  • *any fungus capable at growing at 37 C is considered a potential pathogen
19
Q

cell membranes of fungi contain

A

ergosterol

20
Q

which type of fungi are unicellular

A

yeasts

21
Q

fungal cell wall is composed of what 4 major components

A
  1. Mannan
  2. PLM
  3. Chitin
  4. B-glucan
22
Q

what are function of secreted asparyl proteases (SAPs)

A

destroy host tissue at the site of infection

23
Q

Dimorphic fungi

A
  • are fungi that can reproduce as either a mycelial or a yeast-like state. Generally the mold form grows at 25° C, and the yeast-like pathogenic form at 37° C.
24
Q

Polyene antimycotics such as Amphotericin B and Nystatin have what MOA

A

interfere with ergosterol that is embedded in a fungal cell membrane

25
Q

MOA of Azoles

A
  • interfere with synthesis of new ergosterol
26
Q

MOA of Terbinafine

A
  • allylamine drug that blocks ergosterol biosynthesis in fungal cell membrane (by blocking squalene epoxidase)
27
Q

when is Terbinafine used

A

used in dermatophyte infections (parasitic fungal infections)

28
Q

route of administration of Terbinafine

A
  • topical
  • tablet: risk of hepatic toxicity
29
Q

MOA of Echinocandins (Echinocandin B)

A
  • inhibits the production of glucan in the cell wall
  • known as the “penicillin of antifungals”
30
Q

when is Echinocandins (Echinocandin B) used

A

systemic candidiasis and aspergillosis