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MCIM 224 > 23 Bacterial Pathogens II - Skin and Soft Tissue Infections, GI Infections > Flashcards

23 Bacterial Pathogens II - Skin and Soft Tissue Infections, GI Infections Flashcards

1
Q

The skin is dry and salty. What kinds of bacteria can survive these conditions?

A
  1. Staphylococcus
  2. Streptococcus
    (both gram pos)
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2
Q

Purpose of surface layer of skin?

A

Physical barrier against microbes

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3
Q

This bacteria is part of the normal flora of skin and nasal passages in 10-15% of ppl.

A

Staphylococcus aureus (gram pos)

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4
Q

How do S. aureus bacteria cause skin infections?

A
  1. They migrate down hair follicles into sebaceous glands
  2. They multiply
  3. Inflammation occurs
  4. WBCs are recruited
  5. Small pus-filled abscesses form
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5
Q

How can S. aureus skin infections present themselves on the skin?

A
  1. Folliculitis > small red bumps involving a SINGLE follicle per bump
  2. Furuncles (“boils”) > when infection of a single follicle spreads to nearby tissues (redness, swelling, +/- pain)
  3. Carbuncles > when several furuncles merge
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6
Q

Reservoirs: How many people are asymptomatic carriers of S. aureus?

Where does S. aureus tend to reside?

A

10-15% of ppl

S. aureus tends to reside on the SKIN and in the NASAL PASSAGES

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7
Q

Transmission: How can S. aureus be transmitted?

A
  1. Direct contact
  2. Fomites (objects/surfaces that can carry an infection)
  3. Respiratory droplets
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8
Q

Prevention: How can S. aureus be prevented?

A
  1. Good hand hygiene (esp. after nasal contact and esp. around elderly pts)
  2. Chlorhexidine > “de-colonize” pts
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9
Q

Treatment: How can S. aureus that has infiltrated the skin be treated?

A
  1. Surgically drain furuncles/carbuncles of pus

2. Antibiotics

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10
Q

Describe “scalded skin syndrome” (How it’s caused, and what its characterized by)

A

Caused by some strains of S. aureus

S. aureus produces “exfoliatin” toxin > this exotoxin destroys the material holding the epidermis to the dermis > S. aureus grows at site of infection > toxin is released into blood and spreads further

It’s characterized by redness and soft blisters that cover 20-100% of the body.

The skin peels away > wet, scalded-looking area remains > looks like a burn

This is a potentially fatal disease

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11
Q

Who is most susceptible to scalded skin syndrome?

A

Children < 2 years old

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12
Q

How to treat scalded skin syndrome? (3)

A
  1. Protective isolation
  2. Antibiotics
  3. Removal of dead skin tissue
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13
Q

Besides scalded skin syndrome, what other diseases can be caused by Staph. aureus?

A
  1. Endocarditis
  2. Bacteremia
  3. Pneumonia
  4. Osteomyelitis
  5. Toxic shock syndrome
  6. Gastrointestinal distress
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14
Q

T or F: All strains of S. aureus cause all diseases.

A

F

Not all strains cause all diseases

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15
Q

Biggest concerns w/ S. aureus? (2)

A
  1. Increased numbers of methicillin-resistant strains of S. aureus (MRSA)
  2. Increasing rates of “community-acquired” MRSA
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16
Q

About how many Staph. aureus infections are now caused by MRSA strains?

A

~60%

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17
Q

What’re ‘enteric’ bacteria?

A

Bacteria who use water/food to cause GI infections

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18
Q

Differentiate b/w food poisoning and food infections:

A

Food poisoning: Occurs when a TOXIN is consumed w/ food/water > rapid onset of symptoms

Food infections: Occurs when LIVE BACTERIA are consumed w/ food/water > slower onset of symptoms

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19
Q

How many hours does it take to show symptoms of…

  1. food poisoning?
  2. food infection?
A
  1. 4-6h

2. 18-24h

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20
Q

Name of S. aureus exotoxin that causes food poisoning?

A

Enterotoxin A

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21
Q

How will heating food help w/ Staph aureus colonization? Why might this not be enough to make the food safe?

A

Heating food to 100ºC WILL kill S. aureus, but it DOES NOT destroy the toxins that it produces (Enterotoxin A)

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22
Q

How long does it take to recover without treatment from an affliction by enterotoxin A of S. aureus?

A

~18 hours

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23
Q

How does enterotoxin A cause diarrhea, nausea, and vomiting?

A

Diarrhea: toxin acts on gut epithelial cells > fluid absorption is prevented

Nausea/vomiting: toxin stimulates gut receptors

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24
Q

How to prevent Staph. aureus contamination in food?

A
  1. Proper refrigeration

2. Known carriers of S. aureus should be careful when handling food

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25
Q

What’s the “enterohemorrhagic” strain of E. coli?

What does ea. component of the strain designation mean?

A

O157:H7

O157: Type of LPS “O” side chain
H7: Type of flagella antigen

26
Q

Is E. coli O157:H7 ingestion considered to be a food infection or food poisoning?

A

Food infection

27
Q

Where does E. coli O157:H7 usually reside?

A

Intestinal tract of cattle

28
Q

Anything contaminated with WHAT can potentially lead to an infection with E. coli O157:H7?

A

Cow feces (since E. coli O157:H7 resides in its intestinal tract)

29
Q

Pathogenesis of E. coli O157:H7 infection?

A

E. coli attaches to gut epithelia via pili > they multiply > they release exotoxins (Verotoxin) > these toxins damage intestinal tract lining by killing the epithelial cells > bloody diarrhea (among others)

30
Q

Symptoms of E. coli O157:H7 infection?

When do they get better?

A
  1. Nausea
  2. abdominal cramping
  3. BLOODY diarrhea

Symptoms get better after 5-7 days

31
Q

How’s E. coli O157:H7 diagnosed?

A
  1. Look for tell-tale signs (e.g. bloody diarrhea)

2. Stool culture

32
Q

How should E. coli O157:H7 be treated?

How should it NOT be treated? Why?

A

Treated w/ fluid replacement therapy

Do not treat w/…

  1. antidiarrheals > prolongs E. coli stay in gut
  2. antibiotics > bacteria release more verotoxin when they die > worse symptoms
33
Q

Possible rare complication of E. coli O157:H7?

A

Hemolytic Uremic Syndrome

34
Q

What is Hemolytic Uremic Syndrome?

A

A rare complication of E. coli O157:H7 infection

-Verotoxin enters blood > RBCs destroyed + kidney damage

35
Q

2 ways E. coli O157:H7 is controlled?

A
  1. vaccination of cattle who act as reservoirs

2. clean/cook food adequately

36
Q

Diff b/w the toxin of S. aureus and E. coli O157:H7?

A

The Enterotoxin A of S. aureus is not destroyed by cooking, but the toxin of E. coli IS destroyed by cooking.

37
Q

Diff b/w O157 and K12 strains of E. coli? (2)

A 
O157 = pathogenic
K12 = non-pathogenic

O157 has ~200 extra genes not found in K12

38
Q

Name of bacteria that cause cholera?

A

Vibrio cholerae

39
Q

How does Vibrio cholerae gets transmitted?

A

via fecal-contaminated water

40
Q

V. cholerae gram stain and shape?

A

Gram -ve, curved rod

41
Q

How do V. cholerae cause symptoms?

A

Attach to intestinal wall via pili and adhesion proteins > produce exotoxin during growth > causes hypersecretion of water and ions from gut cells into intestinal tract > severe diarrhea

42
Q

T or F: V. cholerae exotoxin and the exotoxin of E. coli O157:H7 are similar in that they both damage the gut epithelia, causing similar symptoms.

A

F

E. coli exotoxin causes epithelial damage, but V. cholerae’s exotoxin does not cause epithelial damage

43
Q

T or F: The cholera bacteria invades the gut’s epithelial cells.

A

F

44
Q

What happens to the blood of a person infected w/ cholera?

A

Increases in viscosity

45
Q

Therapy req’d for inds with cholera?

A

Oral rehydration therapy

46
Q

4 ways to prevent cholera?

A
  1. Water purification
  2. Reduce chances of contact b/w drinking water and sewage
  3. Don’t eat raw foods washed in contaminated water
  4. Get the Dukoral vaccine
47
Q

For how long does the cholera vaccine protect you?

A

Up to two years

48
Q

Who should get the cholera vaccine?

A

Ppl traveling to high-risk areas

49
Q

Most common virulence factor that cause gastrointestinal infections?

A

Bacterial exotoxins

50
Q

T or F: Diagnosis based on symptoms alone is often enough to identify the bacterial species that cause gastrointestinal infections

A

F

Need to do cultures for bacterial identification

51
Q

Gram stain and bacterial shape of helicobacter pylori?

A

Gram neg
Rod
(also a motile bacterial species)

52
Q

How many ppl carry H. pylori as part of their normal flora?

A

80%

53
Q

Where do H. pylori tend to be found?

A

Mucosal lining of stomach and upper GI tract

54
Q

What enzyme is produced by H. pylori?

A

Urease

55
Q

What does urease do? How does this benefit H. pylori?

A

It breaks down urea to ammonia and CO2 > neutralizes stomach acids > allows H. pylori to survive

56
Q

How does H. pylori cause stomach ulcers?

A

Bacteria attaches to mucosal layer’s epithelial cells in stomach > causes localized inflammation > immune cells arrive > stomach epithelial and mucus-producing cells are destroyed > stomach gets exposed to gastric acid > ULCERS

57
Q

How to diagnose H. pylori?

A

Invasive: Endoscopic biopsy > culture

Non-invasive: “Urea Breath Test”

58
Q

How does the Urea Breath Test work?

A

Ingest soln w/ isotope carbon-labeled urea > urea gets converted to CO2 and NH3 by H. pylori > CO2 is breathed out can get detected

59
Q

What did old stomach ulcer therapies assume?

A

That stomach ulcers were caused by excessive stomach acid

60
Q

Current therapies for stomach ulcers that’re understood to be caused by H. pylori?

A

Antibiotics + acid-suppressing drugs

MCIM 224 (25 decks)

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