Skin infections - Nanetti Flashcards

1
Q

Bacterial skin infections

A

Impetigo
Callulitis
Erysipelas
Follicu;itis
Furnucles/boils
Carbucles
Erysipelas
Necrotizing

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2
Q

What type of infection is folliculitis

A

staphylococcal

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3
Q

What is folluculitis

A

inflam of hair follicles - Sty for eyelashes

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4
Q

Aetiology

A

S.aureus infections - not infectious
or
yeast infec

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5
Q

clincial presentation of folluculitis

A

small, ref, pus-filled pimples hair follicles (face, neck, tighs)

Itching and tenderness in area

Bactiera spread into the dermis

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6
Q

Examples of deep folliculitis - infec spread to dermis

A

furuncles/boils

Carbucles

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7
Q

Furuncles or boils (deep folliculitis)

A

Painful, larger, swollen bump with a central core
Infection spreads in the dermis attracting neutrophils  pus
Pus is sealed by an abscess  limiting infection

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8
Q

Carbuncles (deeper folliculitis)

A

Cluster of connected furuncles or one furuncle not walled off
larger and deeper in dermis or hypodermis

s.aureus > can reach bloodstream > sepsis

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9
Q

Erysipelas

A

in upper dermis

S. pyogenes enters the skin through breaks - NOT S.aureus.
It spreads quickly and it is more likely to reach lymph/blood vessels

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10
Q

clinical pres of erysipelas

A

Well-defined, raised, and shiny red rash  Face, legs, arms.
Sharp borders, often with raised margins
Fever, chills and nausea

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11
Q

Cellulitis

A

deep dermis - subcutaneous tissue

aetiology = Streptococcus pyogenes or S.aureus  most common
others involved (Streptococcus groups C and G)

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12
Q

clinical pres of cellulitis

A

Commonly in one extremity of lower limbs, or face/trunk
Dark-red/purplish, swollen, warm, tense skin (with fluid)
The redness is less clearly defined than in erysipelas

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13
Q

Necrotizing fasciitis (flesh-eating disease)

A

severe infection in subcutaneous tissues and below (deep fascia)

strep pyogenas, s.aureurs

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14
Q

Clinical manifestations & pathogenesis
of necrotixing fasciitis

A

Strept A release proteolytic enzymes to penetrate into the subcutaneous tissues and below
Severe pain, swelling, and erythema. Rapid progression.
Skin changes, including blistering, necrosis. Fever & malaise
It may completely destroy the tissue, requiring amputation/surgery

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15
Q

treatment for Superficial localised impetigo

A

Topical Hydrogen peroxide (H₂O₂) 1% cream
aspecific biocide  Generating free radicals  destroy bacterial cell components

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16
Q

Superficial widespread impetigo

A

Topical antibiotics - fusidic acid or mupirocin (if fusidic acid resistance

Mechanism: Inhibition of the protein synthesis – bacteriostatic effect

17
Q

Bullous impetigo or patients with Non-bullous at risk of complications
Mild deeper infections (cellulitis/erysipelas)

A

Oral antibiotics
Flucloxacillin – as 1st line (500mg to 1g QDS – 5/7 days). Co‑amoxiclav if near the eyes
Clarithromycin or erythromycin (macrolides) as alternative first line - penicillin allergy

18
Q

Intravenous antibiotics

A

Intravenous Cefuroxime or Ceftriaxone (cephalosporins)
Or oral Co‑amoxiclav or oral clindamycin (lincosamine)

19
Q

Methicillin-resistant Staphylococcus aureus (MRSA)

A

Staph. aureus strains resistant to methicillin and other β-lactam antibiotics

20
Q

beta lactams high ____ MIC values to MRSA compared to MSSA

A

higher

21
Q

MRSA strains possess mecA gene, encoding for a transpeptidase that has _____ affinity for β-lactams

A

low

22
Q

Treatment for severe MRSA (or suspected):

A

Intravenous vancomycin or teicoplanin
glycopeptide inhibitors of the cell wall
or linezolid (protein synthesis inhibitor)

23
Q

low-risk HPV
e.g. HPV-6, 11

A

Ano-genital warts

24
Q

cancer types
(cervix, neck, anus)

A

High-risk
HPV-16, 18, 31, 45

25
Q

Cutaneous HPV

A

Cutaneous warts

26
Q

Warts/verrucae - Manifestations
- curtaneous

A

Benign solitary or multiple skin growths caused by cutaneous HPV
Grainy, cauliflower-like and slightly raised growths
On the hands, feet or on the sole of feet (verrucae/plantar warts)
Usually self-limiting, but can be embarrassing

27
Q

Wart spreading

A

They can spread though skin contact and sexually (genital warts).
HPV can be transmitted from contaminated surfaces (broken and/or wet).
HPC can survive for a long time on surfaces (swimming pool)

28
Q

Cutaneous wart formation

A

HPVs enter the broken skin

HPVs infect basal cells of the epidermis and establish persistent infection

Viruses encode viral oncogenes that stimulate cell division

Keratinocytes cannot mature or differentiate properly

29
Q

What are the treatment options for warts?

A

Topical salicylic acid - long treatment

AND/OR cryotherapy using liquid nitrogen (−196°C)
Thermal injury in the lesions to induce necrotic destruction of HPV-infected keratinocytes

30
Q

Herpes

A

prim. infec = develop lesions as cold sores - short lives

31
Q

How is Varicella zoster virus (VZV) caused?

A

agent of chickenpox (initial infection) and shingles (reactivation after latency)

32
Q

Treatement for herpes

A

Topical OTC acyclovir 5% cream for cold sores or genital herpes (4-6 times/day)
Reduce length of infection if administered within 24h from the initial symptoms (tingling on the lips)

33
Q

Oral treatments (acyclovir or prodrugs)

A

severe herpes infections and shingles, or infections in neonatal, elderly or immunocompromised patients (risk complications)
Antiviral therapy should start within 48-72 hours of the onset of shingles rash

34
Q

Fungal skin infections

A

Superficial/cutaneous dermatomycoses/tinea
Involve epidermidis stratus
Affecting trunk, feet, scalp, nails, groin areas

Subcutaneous mycoses
Involves dermis and subcutaneous tissue - Rare

35
Q

Dermatomycoses

A

Trunk, arms and legs – ringworm
Feet – athlete’s foot
Groin area - jock itch
Nails - onychomycosis

36
Q
A