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M202 > W24 Skin functions, microbiota and infections (GN) > Flashcards

W24 Skin functions, microbiota and infections (GN) Flashcards

1
Q

Physiology of the skin:
What are the Main general functions? (6)

A
  • The body’s largest organ
  • Mechanical barrier to heat, injury, UV lights and infections
  • Regulation of body temperature
  • Retention/excretion of water
  • Sensory detection
  • Synthesis of essential molecules
    (e.g. Vitamin D)
  • Outer waterproof covering of the body
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2
Q

What is the Structure of the skin?

A

Epidermidis - The outermost layer
* Varied thickness - 0.5 mm (eyelid) to 5 mm (heels)
* Composed mainly of keratinocytes

Dermis- Connective tissue containing:
* Elastin and collagen fibres (stretch & strength)
* Blood vessels and nerve terminations
* Hair follicles
* Sebaceous/sweat glands

Hypodermis/subcutaneous layer – not part of the skin
* Connect the skin to underlying bone and muscle
* Adipose tissue –resistance and thermal insulation

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3
Q

What are the 5 sublayers of the epidermis?

A
  • Stratus corneum (outermost)
  • Stratum lucidum
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basale (deepest)
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4
Q

What are the main cells in the epidermis? (3) (no blood vessels)
What are their roles?

A
  • Keratinocytes ( ̃90%)
    -keratinisation (secreting a fibrous protein - keratin)
    -provide mechanical strength
  • Melanocytes ( ̃5%)
    -producing melanin = inducing skin pigmentation
  • Langerhans cells
    -Dendritic cell recognising threats, activating immunity
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5
Q

Keratinisation - summary
Multiple stages of keratinocyte cell differentiation:

Describe each layer: (5)
Which contains langerhans cells?
Which contains melanocytes?

A

1. S. corneum:
> 15 layers of fully keratinized squamous cells (waterproof coat) that are shed & replaced
2. S. lucidum (only present on the soles and palms):
Few layers of flattened/dead cells losing nucleus and organelles
3. S. granulosum
Cells produce keratin granules & release lipid (barrier function)
4. S. spinosum
Cells accumulate keratin precursor. It contains Langerhans cells.
5. S. basale
* Stem cells undergo mitosis forming undifferentiated keratinocytes that migrate. Melanocytes are present

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6
Q

Skin microbiota
What are the 4 microenvironments that human skin is categorised into?
Where are most microbes found?

A

Oily, moist, dry, foot

  • Most microbes reside in the outermost layers of the stratum corneum
  • Others in hair follicles and gland pores
  • Relatively stable over time (in a healthy individual)
  • Core residents are common in a population
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7
Q

What are skin resident species?

A
  • Permanent inhabitants of the skin
  • Crucial roles in maintaining skin health
  • Establish stable populations over time
  • Even after hygienic practises
  • If disturbed, they are re-established promptly
  • Unlikely to cause opportunistic infections
  • The commensal Staphylococcus epidermidis
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8
Q

What are Skin Transient species?

A
  • Temporary inhabitants of the skin (short
    duration)
  • Their contribution is not key
  • Can be easily removed by routine hygiene
  • Usually not pathogenic, but can cause
    opportunistic infections
  • Species acquired via environmental exposure
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9
Q

Skin normal microbiota –
What are the Major components? (3)

A
  1. Bacteria
    * Diphteroirds
    -Corynebacterium species
    -Cutibacterium acnes = May cause acne
    - Low virulence
    - Responsible for body odour
    * Staphylococci
    - Wide range of virulence
    - Staphylococcus epidermidis (low virulence – protection against infections)
    - S. aureus have low/high virulent strains
  2. Yeasts
    * Malassezia species
    -Harmless in healthy individuals
    - Malassezia furfur causing dandruff or interfere with pigmentation
  3. Viruses
    * Combination of viruses
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10
Q

Skin as a barrier for infections
What are the intrinsic characteristics of the skin in creating hostile conditions for pathogen colonisation? (6)

A
  1. Low pH (4.0 - 6.0)
  2. Low moisture content
  3. Nutrient poor
  4. Releasing antimicrobial molecules
  5. Constant exfoliation of cells
  6. Pathogenic colonization prevention
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11
Q

Skin as a barrier for infections:
-what does the body have in place to inhibit pathogen growth

Benefits of low pH, low moisture content and nutrient poor?

A
  1. Low pH (4.0 - 6.0)
    * Most bacteria have neutral optimum pH
    * Growth inhibited at low pH
  2. Low moisture content
    * High salt concentration = Hypertonic environment = High osmotic pressure
  3. Nutrient poor
    * Stratum corneum = source of only peptides and lipids
    * Sebaceous glands secrete Sebum = source of only lipids
    * Sweat glands secrete sweat = salt-laden (high osmotic pressure
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12
Q

Skin as a barrier to infections
Releasing antimicrobial molecules:
What is released? (2)

A
  • Antimicrobial peptides - AMPs
    -Produced by sweat & sebaceous glands
  • Effects = direct killing & immune activation
  • Lysozyme
    -Product by sweat glands
    -Bactericidal effect on Gram +ve only
    -Hydrolysing NAM-NAG bonds of a peptidoglycan chain of their cell wall
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13
Q

Skin as a barrier to infections
Constant exfoliation of cells:
Why is this important?

A

Removing transient bacteria = Less opportunity to colonise the niche

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14
Q

Skin as a barrier to infections:
What is Pathogenic colonization prevention?

A
  • Outcompeting pathogens for nutrients and binding sites (niches)
  • Modulating local immunity = Langerhans cells activation
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15
Q

Skin normal microbiota:
What is the specific role of Cutibacterium acnes?

A

Digest sebum triglycerides in fatty acids (energy source) and propionic acid (maintaining a protective low pH)

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16
Q

Skin normal microbiota:
What is the specific role of Staphylococcus epidermidis?

A
  • Inhibits S. aureus biofilm by secreting proteases
  • Induces keratinocytes to produce antimicrobial peptides
17
Q

Normal microbiota can cause opportunistic infections:

A
  • Cutibacterium acnes
  • Can trigger inflammation = acne vulgaris
  • Staphylococcus epidermidis
  • Low virulent if confined to the epidermidis
  • It forms biofilms on plastic catheters - it
    may cause catheter- associated UTIs
18
Q

Mechanisms of skin opportunistic infections:

A
  1. Cuts, lesions, changes in barrier permeability
    -Microbiota can access the dermis and blood vessels
  2. Dysbiosis (microbiota alteration)
    -Opportunity for opportunistic pathogen to outgrow
    -Causes: metabolic diseases (e.g., diabetes), topical antibiotic treatments (encouraging fungal growth), inflammation

3.** Co-infections/immune deficiency**
-Within an infection, microbiota species can amplify tissue damage

19
Q

Bacterial Skin pathogens

A

Bacterial Skin pathogens:
* Staphylococcus & Streptococcus (Gram +ve) the most frequent in skin infections
* Also, Pseudomonads (i.e. Pseudomonas dermatitis), Gram -ve

Staphylococcus aureus = mostly involved in skin infections
* Minor component in the nose and skin (4 %) microbiota

Microscopic identification
* Gram staining Gram positive (purple stained)
* Morphology spherical (cocci)
* Arrangements grape-like clusters (Staphylo)
* Colonies on Agar shining golden yellow

20
Q

S. aureus virulence factors

A
  • S.aureus pathogenic strains express a range of virulence factors:
  • Proteolytic enzymes to invade tissues
  • Lipases, proteases, Hyaluronidase (breaking down proteoglycans in the dermis)
  • Factors to evade host defences
  • Coagulase = Induces blood clotting, evading phagocytosis
  • Proteins that neutralise AMPs
  • Capsule: hindering cellular antigens to avoid immune recognition
  • Cause host damage by producing different exotoxins
  • Exfoliatins - causing blistering of the skin
  • Toxic shock syndrome toxin = exacerbated inflammatory response = shock syndrome
21
Q

Streptococcus pyogenes virulence factors
( for info)

A

Distinct Strep A strains with different virulence factors:
* Proteolytic enzymes to invade tissues
-Hyaluronidase breaking down proteoglycan in the dermis
-Streptokinase - enzyme that dissolves blood clots
* Factors to evade host defences
-M protein on the fimbriae - evades phagocytosis
-Capsule made by hyaluronic acid (host component)  not targeted by immune cells
* Cause host damage by producing different exotoxins
-Streptolysins O and S, that lyse red blood cells and neutrophils
-Pyrogenic exotoxin  exacerbated inflammatory response  shock syndrome

22
Q

What are examples of bacterial skin infections?

A

Impetigo
Folliculitis
Furuncles/boils
Carbuncles
Erysipelas
Cellulitis
Necrotising fascitis

23
Q

Impetigo:
Causef by which bacteria?
2 clinical manifestations?

A
  • Affect superficial layer of the skin
  • Rash not painful, but may be itchy
  • Typical in children = face, arms, legs
  • Highly contagious = direct contact

Aetiology = mostly caused by S.aureus
* Primary infection = affecting healthy skin
* Secondary infection = after cuts or skin lesions (e.g. due to chickenpox or eczema)

Two clinical manifestations
* non-bullous impetigo – most common
* bullous impetigo (only S.aureus)

24
Q

Describe Non-bullous impetigo:

A

Thin-walled vesicles or pustules that rupture quickly
* Leaking pus forming brownish/honey crusts
* S.aureus and/or Streptococcus pyogenes involved

25
Q

Describe Bullous impetigo:
Appearance?
Where is it found on the body?
When they rupture?
Type of bacteria?

A
  • Larger and fluid-filled blisters/bullae (>1cm)
  • On the trunk, buttocks, extremities
  • Their rupture leaves a flat, yellow/varnish crust.
  • ONLY S. aureus = strains producing exfoliatin toxins
    -Exfoliatins penetrates the unbroken skin by disrupting its barrier
26
Q

What are the Bullous impetigo complications – S.aureus
(2)

A
  • Staphylococcal Scalded skin syndrome (in newborns)
  • S.aureus strains releasing exfoliatin B = causing skin blistering
  • Toxin can spread in the tissue and extend the lesion
    Clinical manifestations:
  • Initial erythematous rash resembling scalded skin = large bullae that rupture
  • Resulting in a widespread painful skin peeling

Staphylococcal Toxic shock syndrome
* S.aureus strains release toxic shock syndrome (TSS) – superantigen toxin
* Induces an over-activation inflammatory cells = cytokines storm
Clinical manifestations (life-threatening)
* Rapid onset of fever, rash, hypotension, shock with multiorgan involvement

M202 (72 decks)

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