Skin infections - Nanetti Flashcards
Bacterial skin infections
Impetigo
Callulitis
Erysipelas
Follicu;itis
Furnucles/boils
Carbucles
Erysipelas
Necrotizing
What type of infection is folliculitis
staphylococcal
What is folluculitis
inflam of hair follicles - Sty for eyelashes
Aetiology
S.aureus infections - not infectious
or
yeast infec
clincial presentation of folluculitis
small, ref, pus-filled pimples hair follicles (face, neck, tighs)
Itching and tenderness in area
Bactiera spread into the dermis
Examples of deep folliculitis - infec spread to dermis
furuncles/boils
Carbucles
Furuncles or boils (deep folliculitis)
Painful, larger, swollen bump with a central core
Infection spreads in the dermis attracting neutrophils pus
Pus is sealed by an abscess limiting infection
Carbuncles (deeper folliculitis)
Cluster of connected furuncles or one furuncle not walled off
larger and deeper in dermis or hypodermis
s.aureus > can reach bloodstream > sepsis
Erysipelas
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
clinical pres of erysipelas
Well-defined, raised, and shiny red rash Face, legs, arms.
Sharp borders, often with raised margins
Fever, chills and nausea
Cellulitis
deep dermis - subcutaneous tissue
aetiology = Streptococcus pyogenes or S.aureus most common
others involved (Streptococcus groups C and G)
clinical pres of cellulitis
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
Necrotizing fasciitis (flesh-eating disease)
severe infection in subcutaneous tissues and below (deep fascia)
strep pyogenas, s.aureurs
Clinical manifestations & pathogenesis
of necrotixing fasciitis
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
treatment for Superficial localised impetigo
Topical Hydrogen peroxide (H₂O₂) 1% cream
aspecific biocide Generating free radicals destroy bacterial cell components
Superficial widespread impetigo
Topical antibiotics - fusidic acid or mupirocin (if fusidic acid resistance
Mechanism: Inhibition of the protein synthesis – bacteriostatic effect
Bullous impetigo or patients with Non-bullous at risk of complications
Mild deeper infections (cellulitis/erysipelas)
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
Intravenous antibiotics
Intravenous Cefuroxime or Ceftriaxone (cephalosporins)
Or oral Co‑amoxiclav or oral clindamycin (lincosamine)
Methicillin-resistant Staphylococcus aureus (MRSA)
Staph. aureus strains resistant to methicillin and other β-lactam antibiotics
beta lactams high ____ MIC values to MRSA compared to MSSA
higher
MRSA strains possess mecA gene, encoding for a transpeptidase that has _____ affinity for β-lactams
low
Treatment for severe MRSA (or suspected):
Intravenous vancomycin or teicoplanin
glycopeptide inhibitors of the cell wall
or linezolid (protein synthesis inhibitor)
low-risk HPV
e.g. HPV-6, 11
Ano-genital warts
cancer types
(cervix, neck, anus)
High-risk
HPV-16, 18, 31, 45
Cutaneous HPV
Cutaneous warts
Warts/verrucae - Manifestations
- curtaneous
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
Wart spreading
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)
Cutaneous wart formation
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
What are the treatment options for warts?
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
Herpes
prim. infec = develop lesions as cold sores - short lives
How is Varicella zoster virus (VZV) caused?
agent of chickenpox (initial infection) and shingles (reactivation after latency)
Treatement for herpes
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)
Oral treatments (acyclovir or prodrugs)
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
Fungal skin infections
Superficial/cutaneous dermatomycoses/tinea
Involve epidermidis stratus
Affecting trunk, feet, scalp, nails, groin areas
Subcutaneous mycoses
Involves dermis and subcutaneous tissue - Rare
Dermatomycoses
Trunk, arms and legs – ringworm
Feet – athlete’s foot
Groin area - jock itch
Nails - onychomycosis
