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Mechanisms of Microbial Disease > Chapter 18 > Flashcards

Chapter 18 Flashcards

1
Q

Where are normal skin flora number higher?

A

In moist areas

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2
Q

How does shedding protect from viral skin infections?

A

Viruses cannot replicate in dead cells

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3
Q

What are the routes of skin infections?

A

Break of intact skin (infection from outside)
Skin manifestations of systemic infections
Toxin mediated skin damage (toxin in blood to skin)

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4
Q

What is staphylococcus aureus?

A

The most common skin pathogen, “swiss army knife” has virulence factors to counter almost every defence mechanism we have

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5
Q

What do staphylococcal skin infections cause?

A

Boils, abscesses to scaled skin syndrome, Toxic shock syndrome

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6
Q

What is the resistant form of staph aureus?

A

Methicillin resistant staph aureus

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7
Q

What is a boil?

A

A superficial infection of the hair follicle (folliculitis)

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8
Q

How does a boil progress?

A

Infection of the hair follicle multiplies and locally spread to cause an inflammatory reaction and an influx of neutrophils (pus), may drain inward and spread the bacteria

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9
Q

How is a boil treated?

A

Daring, antibiotics for severe infections (with fever)

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10
Q

Who will have recurrent infections of staphylococcus skin infections?

A

Nasal carriers will have recurrent infection

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11
Q

What happens in scalded skin syndrome?

A

The exfoliation toxin destroys the intercellular connections of the skin causing separation of the epidermis and large blisters

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12
Q

How is scalded skin syndrome treated?

A

Fluid replacement and antibiotics

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13
Q

What is Toxic Shock Syndrome?

A

Systemic infections from staph aureus that affect multiple organ systems

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14
Q

What are the symptoms of TSS?

A

Fever, hypotension, diffused red rashes and desquamation of the skin (limited to palms and soles of feet)

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15
Q

Why do tampons cause TSS?

A

The synthetic absorbent material holds lots of blood, which is the growth media for staph aureus (vaginal microflora) and produces toxins

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16
Q

What is the cause behind many streptococcal skin infections?

A

S. pyogenes

Group A streptococci

17
Q

What are some streptococcal skin infections?

A

Impetigo and erysipelas, cellulitis, necrotizing fasciitis

18
Q

How does impetigo occur?

A

Strep is acquired through contact with infected skin lesions and then it invades minor breaks in the skin, causing lesions. Deeper=lesions

19
Q

What is erysipelas?

A

An acute deeper infection of the dermis by strep. Can lead to bacteremia. Red rosy rash on face

20
Q

What does the virulence of GAS depend on?

A

Climate, humidity, race, trauma

21
Q

How is the s. pyogenes that infects the skin different from the one that infects the throat?

A

Subdivision of the species based on surface proteins (M proteins attached to PG)

22
Q

What is the incubation time for S. pyogenes skin infections?

A

24-48 hours post skin invasion

23
Q

What are the virulence factors of S. pyogenes?

A

Hyaluronidase and toxic products to facilitate its spread through the tissue

24
Q

What is the lysogenized strain of S. pyogenes? What does it do?

A

A strain that has been lysogenized by macrophages and now produces pyrogenic endotoxin causing a red rash

25
Q

What may S. pyogenes of the skin cause?

A

A toxic shock like syndrome

26
Q

What is cellulitis?

A

A diffuse inflammation and infection of the skin, deeper than erysipelas and originates from a superficial infection or following trauma
May have systemic features

27
Q

What are the systemic features that may occur with cellulitis?

A

Fever, malaise, headache, elevated white blood cell count

28
Q

How is cellulitis treated?

A

Use empirical antibiotic treatment until cause is known (most likely Gram + cocci)

29
Q

What causes cellulitis usually?

A

S. pyogenes, GAS

30
Q

What is necrotizing fasciitis?

A

A ‘flesh-eating disease’

Acute, highly toxic infection with a high mortality rate resulting from trauma to the skin

31
Q

What causes necrotizing fasciitis?

A

Often polymicrobial

Anaerobes, facultative anaerobes like S. pyogenes (don’t need oxygen)

32
Q

How do facultative anaerobes cause blisters?

A

They produce gas

33
Q

What causes gas gangrene?

A 
Clostridial sp (C. perfringens)
Anaerobes
34
Q

How does C. perfringens work?

A 
Contamination with spores
Produces lecithinase (like snake venom) which precipitates protein
35
Q

What are the clinical manifestations of gas gangrene?

A

Severe pain, edema, cellulitis, production of gas and foul-smelling purulent discharge

36
Q

How is gas gangrene treated?

A

Amputation, hyperbaric chamber (saturates with O2 to kill anaerobes) and antibiotics

37
Q

How can we tell if a pathogen is producing lecithinase?

A

Put sample on egg white media, put in antibodies against lecithinase which will bind and inactivate, stopping it’s precipitation of proteins.

Mechanisms of Microbial Disease (17 decks)

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