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HSS1100 > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

There are __ medically important gram positive bacteria.

A

6

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2
Q

describe/ name the 6 important bacteria

A

2 cocci (staphylococci and streptococci)
4 rods (2 spore forming and 2 non spore forming)

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3
Q

Name the 2 spore forming, gram positive bacteria

A

Bacillus and Clostridium

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4
Q

describe the 2 spore forming, gram positive bacteria

A
  • releases exotoxins
  • biochemically different due to its use of oxygen
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5
Q

Bacillus is anaerobic or aerobic

A

aerobic

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6
Q

Cereus is anaerobic or aerobic

A

anaerobic

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7
Q

What are the 2 pathogenic species of Bacillus

A

B.anthracis, B. cereus

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8
Q
  • causes the disease anthrax
  • only bacteria with capsule made of protein (poly-D-glutamic acid)
    -prevents phagocytosis
A

Bacillus anthracis

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9
Q

who does anthrax infect?

A

herbivores such as cow and sheep or humans exposed to spores by direct contact with infected animals or soils

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10
Q

What condition is most optimal for B.anthracis

A

37 degrees Celsius, increased in CO2 and serum proteins

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11
Q

B. anthracis was used for
chemo treatment
chemical peel masks
biological terrorism
phagocytosis

A

biological terrorism

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12
Q

where is the B.anthracis plasmid encoded on

A

PXO1

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13
Q

What are the 3 proteins for B. anthracis

A
  • edema factor (EF): disrupts water homeostasis
  • protective antigen (PA): promotes entry of EF into phagocytic cells (similar to B subunit of A-B toxins)
  • lethal factor (LF): zinc metalloprotease that inactivate protein kinase
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14
Q

What are the 2 mandatory plasmids for bacterial virulence

A

PXO1 and PXO2

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15
Q

Antibiotics for B.anthracis

A

Antibiotics: penicillin, doxycyclin, ciprofloxacin or levofloxacin

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16
Q

What is the difference between B.cereus and B.anthracis

A

motile, non capsulated and resistant to penicillin

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17
Q

B. cereus effects of disease

A

food poisoning (nausea, vomiting and diarrhea) when spore are present in food, which survive initial cooking process

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18
Q

What do B. cereus do in food ? how do we stop germination?

A

They germinate in food and release enterotoxin. Food must be exposed to high temperature and/ or reirrigated in order to inactivate spores

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19
Q

2 types of enterotoxins are made

A

Heat- liable toxin (similar to cholera and LT from E. coli
1. Nausea, abdominal pain, diarrhea
2. Last usually 12-24 hours

Heat-stable toxin
1. Similar to S. aureus food poisoning
2. short incubation period
3. severe nausea and vomiting
4. Limited diarrhea

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20
Q

A patient presents w/ food poisoning (and examination of food reveals B. cereus) can antibiotics be given?

A

-antibiotic therapy will not alter the course of patient symptoms this is b/c its the preformed toxin that cause the food poisoning

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21
Q

What are Clostridium species?

A
  • Gram positive, spore forming rods, anaerobic
  • famous for botulism, tetanus, gas gangrene and pseudomembranous colitis
    -exotoxin are extra powerful; rapidly diagnose or patient dies
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22
Q

-produces lethal neurotoxin that causes rapidly fatal food poisoning
- neurotoxin blocks release of acetylcholine (Ach) from nerve terminals in autonomic nervous system

A

Clostridium botulinum

23
Q

flaccid muscle paralysis results (Clostridium botulinum)

A
  1. afebrile
  2. bilateral cranial nerve palsies
  3. double vision
  4. difficulty swallowing
  5. general muscle weakness (leads to sudden respiratory paralysis and death)
24
Q

What does Botulism result from? how to destroy spores?

A

-adult botulism result form eating smoked fished
-improperly prepared home canned vegetables. Properly cooking
-infant botulism associated to fresh honey contamination with spores

25
Q

How does improper canning allow for optimal growth of spores

A

anaerobic condition allowing for growth and synthesis of neurotoxin

26
Q

What happens during infant botulism?

A
  1. spores germinate and bacteria colonize infants intestinal tract
  2. neurotoxin release
  3. constipation for 2-3 days, followed by difficulty swallowing and muscle weakness (floppy baby)
27
Q

What is the treatment for Clostridium Botulinum

A

antitoxin, neutralizes unbound free neurotoxin in bloodstream

-intubation and ventilatory support until respiratory muscle resume activity

28
Q

-gram positive, spore forming, anaerobic
-skin trauma by an object with contaminated spores (step on a rusty nail)
-found in soil and animal feces

A

Clostridium tetani

29
Q

What happens once Clostridium tetani is in your wound

A

-will germinate as long as there is anaerobic conditions

30
Q

exotoxin in Clostridium tetani is called _________ and causes sustained contraction of skeletal muscle (tetany)

A

tetanospasmin

31
Q

where does tetanospasmin act on

A

inhibitory Renshaw cells interneurons (prevent release of GABA and glycine, which inhibit neurotransmitters)

32
Q

What happens after GABA and glycnine is released

A
  1. inhibitory interneurons allow motor neurons to send high frequency impulses to muscle cells (sustained tetany ensues)
33
Q

what are clinical presentation of tetanus include?

A

sever muscle spasms (trismus, aka lockjaw), grotesque grinning expressions (risus sardonicus)

34
Q

When is the mortality rate high in tetanus

A

once lockjaw is acheieved

35
Q

is there a vaccine for tetanus

A

humans are given formalin-inactivated toxin (tetanus toxoid) every 10 years as booster and is part of the DPT shot

36
Q

-gas gangrene
-mature in anaerobic conditions and produce gas
-common in soldier wounded in battle

A

Clostridium Perrigin

37
Q

What are the steps of cellulitis/wound infection

A

1.necrotic (dead) skin exposed to bacteria
2. bacteria grows and damages local tissue
3. palpitation reveals moist, spongy, crackling consitency to skin due to gas (creptius)

38
Q

clostridial myonecrosis

A

1.innoculated with trauma into muscle, secretes exotoxin destroying adjacent muscle
2.gas formation when are fermented from action of enzyme
3.CT scan will show pocket of gas within muscles and subcutaneous tissue
4.enzyme degrades muscle (gets thin, blackish fluid exuding skin)
5. atal unless identified and treated very early with hyperbaric oxygen and
antibiotics (such as penicillin), with removal of necrotic tissue

39
Q

clostridium difficile is more common than anthrax, tetanus, and botulism (T/F)

A

T

40
Q

what cause the growth of clostridium difficle

A

responsible for antibiotic-associated pseudomembranous enterocolitis
- arises from overuse of broad spectrum antibiotics (ampicillin, clindamycin, and
cephalosporins), which destroy normal intestinal flora

41
Q

what part of the body does C. difficile infect

A

the colon

42
Q

C.difficile What does toxin A cause? Toxin B? what are the symptoms

A

A. Diarrhea,

B. cytotoxic to colonic cells.

symptoms: Severe diarrhea, abdominal cramping and fever

43
Q

When would a doctor thing that C.difficile is a viable diagnoses

A

when patient develops diarrhea on antibiotics (toxin in stool confirms diagnosis)

44
Q

What is the treatment plan for C. difficile

A
  1. discontinue initial antibiotic regimen
  2. Administer metronidazole or vancomycin by mouth since they are not absorbed orally into bloodstream.
45
Q

What are the names of non-spore forming rods

A

Listeria monocytogenes and Cornyebacterium diphtheririae

46
Q

How many protective barriers can Listeria monocytogenes cross?

A
  1. blood-brain, gastrointestinal, and
    feto-placental
47
Q

Gram positive, non spore forming, crosses 3 protective barriers

-may leads to general malaise, meningitis, spontaneous abortions

A

general malaise, to meningitis to spontaneous
abortions (stillbirth) to death

48
Q

why is listeria monocytogenes considered a facultative intracellular organism

A

it can live outside or within cells

49
Q

what is not a problem for medical proffesionals when treating L. monocytogenes

A

antimicrobial resistance (treatments include ampicillin and trimethroprim-sulfamethoxazole)

50
Q

L. monocytogenes is a psychrophile what does this mean?

A

it survives in the refirgerator

51
Q

What does Corynebacterium diphtheriae do?

A

causes diphtheria
- colonizes the pharynx, forming a grayish pseudo membrane composed of fibrin, leukocytes,
necrotic epithelial cells and C. diphtheriae cells

  • from here, bacteria releases powerful exotoxin into bloodstream
  • exotoxin damages heart and neural cells by interfering with protein synthesis
52
Q

What is the 3 step treatment of Corynebacterium diphtheriae

A

Treatment consists of 3 steps
1- antitoxin to inactivate circulating toxin
2- penicillin or erythromycin to kill the bacteria
3- DPT vaccine (D = diphtheria)

53
Q

What is a unique way to get ride of C. diptheriae

A

lysogenized by a temperate bacteriophage

54
Q

Bacteriophage codes for diphtheria exotoxin, which contains two subunits. What are they called and what do they do?

A

Bacteriophage codes for diphtheria exotoxin, which contains two subunits. The B subunit
binds to target cells and allows A subunit to enter, and the A subunit blocks protein synthesis
(inactivates elongation factor EF2)

HSS1100 (12 decks)

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