W24 Skin infections (GN) Flashcards
What is Folliculitis? (Staphylococcal infection)
Aetiology:
S. aureus infections - the most common cause. Not infectious.
Or yeast infection (e.g., Malassezia) or irritation from shaving/friction
Clinical Presentation:
Small, red, pus-filled pimples around hair follicles (face, neck, thighs).
Itching & tenderness in the area
Bacteria can spread into the dermis and cause deep folliculitis
What are the 2 types of Deep folliculitis ?(staphylococcal infections)
- 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, deeper areas of inflammation (nodules). Usually, with fever
* The infection is deeper in the dermis or hypodermis
-S.aureus can reach the bloodstream = sepsis (rare
Streptococcal skin infections
What is Erysipelas?
Clinical manifestation?
Infection in the epidermis - 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
- Well-defined, raised, and shiny red rash= Face, legs, arms.
- Sharp borders, often with raised margins
- Fever, chills and nausea
What is Cellulitis?
Clinical manifestation?
Infection in the deep dermis - subcutaneous tissue
Aetiology
- Streptococcus pyogenes or S.aureus = most common
- others involved (Streptococcus groups C and G)
Clinical manifestations
* 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
- The infection can spread along tendons and muscles or sepsis
What is Necrotizing fasciitis? (flesh-eating disease)
Aetiology?
Clinical manifestations & pathogenesis?
- Severe infection in subcutaneous tissues and below (deep fascia)
- Streptococcus pyogenes, S.aureus = most common
Clinical manifestations & pathogenesis
* 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
Bacterial skin infections - treatment options
what are the prevention measures?
Treatment for Superficial localised impetigo?
Prevention
* Good hygiene - reduce the spread/transmission
Topical Hydrogen peroxide (H₂O₂) 1% cream
aspecific biocide = Generating free radicals = destroy bacterial cell components
Bacterial skin infections - treatment options
Treatment of Superficial widespread impetigo?
Mechanism?
Topical antibiotics - fusidic acid or mupirocin (if fusidic acid resistance)
Mechanism: Inhibition of the protein synthesis – bacteriostatic effect
Coverage: against Gram+ (Staphylococci, including MRSA, Streptococci)
Bacterial skin infections (mild to severe) treatments?
- Bullous impetigo or patients with Non-bullous at risk of complications
- Mild deeper infections (cellulitis/erysipelas)
Severe skin infections
- 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)
Hospital referral for which patients?
Severe infections
Widespread impetigo
Immune compromised
Facial cellulitis
bullous impetigo in babies (<1 year)
Patients at risk of complications
What is Methicillin-resistant Staphylococcus aureus (MRSA)?
MRSA = Staph. aureus strains resistant to methicillin and other β-lactam antibiotics
- MRSA strains particularly associated with cellulitis
* β-lactams display higher MIC values to MRSA compared to MSSA (Methicillin-sensitive S. aureus)
* MRSA strains possess mecA gene, encoding for a transpeptidase that has low affinity for β-lactams
Treatment for severe MRSA (or suspected):
Intravenous vancomycin or teicoplanin glycopeptide inhibitors of the cell wall
or linezolid (protein synthesis inhibitor)
Viral Diseases of the Skin
What are examples of Viruses and major skin diseases? (4)
Papilloma viruses (HPV) :
* Warts/Verrucae
* Different cancer types
Herpes simplex (HSV-1 & HSV-2)
Cold sores (HSV-1)
Genital herpes (HSV-2)
Varicella zoster virus (VZV)
* Chicken pox (primary infection)
* Shingles (reactivation)
Others with skin rash*
Measles
Rubella
Etc (roseola)
- Mild and highly contagious with characteristic skin rash:
Measles (small raised red-brown blotchy rash) and rubella (red-pink spotty rash)
can be prevented by the MMR vaccine
No specific antiviral drugs are available
Human papilloma viruses (HPV)
2 types?
> 200 HPV genotypes - different infections
1. Cutaneous HPV
- infecting skin cells
e.g. HPV-1, 2
=Cutaneous warts
- Mucosal HPV
infecting internal lining epithelial cells
* low-risk HPV
e.g. HPV-6, 11
=Ano-genital warts
* High-risk
HPV-16, 18, 31, 45
= cancer types
(cervix, neck, anus)
Cervical screening smear test to detect the HPV genotype and precancerous cells
HPV vaccines are available to prevent infections from high-risk genotypes
What are Cutaneous warts?
How do warts spread?
Warts/verrucae - Manifestations
* 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
- Ano-genital warts are caused by low-risk mucosal HPV
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)
What is the pathophysiology of Cutaneous wart formation? (4)
- 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
Warts – treatment options for cutaneous warts?
Treatments cutaneous warts - affected area only
* Topical salicylic acid - long treatment
Keratolytic agent = gradual lyse keratinocytes in the lesion and reduce the wart thickness
- AND/OR cryotherapy using liquid nitrogen (−196°C)
- Thermal injury in the lesions to induce necrotic destruction of HPV-infected keratinocytes
- Ablative therapy (e.g. surgery, laser treatment) to remove the lesion
Warts – treatment options for ano-genital warts – (information only)
Topical Podophyllotoxin cream = antimitotic agent to block the cell division within the wart
Topical Imiquimod cream = immune stimulator to kill infected cells in the lesion
Herpes virus infection and reactivation
HSV-1 primary infection and recurrent reactivations develop lesions known as cold sores
painful, short-lived vesicles that occur near the outer red margin of the lips
HSV-1 latency is established in the trigeminal nerve ganglia
Infections & physical (i.e. UVA) and hormonal (e.g. emotional stress, menstruation) stress triggers the HSV-1 reactivation
Varicella zoster virus (VZV)
What does it cause?
- Varicella zoster virus (VZV) is the causative agent of chickenpox (initial infection) and shingles (reactivation after latency)
Initial infection (chickenpox) and viral latency
Reactivation (shingles or zoster)
Antiviral Chemotherapy for Herpesvirus infections?
- 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
Viral polymerase inhibitors
(Nucleoside analogues – Obligate terminators)
What are examples? (3)
- Acyclovir
- Famciclovir (Acyclovir prodrug)
- Valaciclovir (Acyclovir prodrug)
VZV Prevention - Incidence of VZV infections can be reduced through vaccination
Fungal skin infections
Superficial/cutaneous dermatomycoses/tinea?
Subcutaneous mycoses?
What do they involve?
Involve epidermidis stratus
Affecting trunk, feet, scalp, nails, groin areas
Involves dermis and subcutaneous tissue - Rare
What is Dermatomycoses?
- Skin microbiota equilibrium is essential to avoid fungal infections
- Microbiota dysbiosis favours fungal overgrow = superficial dermatomycoses (tinea)
Trunk, arms and legs – ringworm
Feet – athlete’s foot
Groin area - jock itch
Nails - onychomycosis
- Spread by person/animal-person contact or by sharing contaminated objects (spores)
- Rare subcutaneous mycoses = Rare fungal microbes can invade the dermis
Treatment of dermatomycoses
What is used?
- Localised fungal infections are usually treated with topical OTC antifungals
- Treatment must last 1-2 weeks after the disappearance of infection signs avoid drug resistance
- Imidazole cream/shampoo 1st choice for ringworm/athlete’s foot
E.g. 2% miconazole, 1% clotrimazole, 1% ketoconazole
Ergosterol synthesis inhibitors (unique plasma membrane component) - Alternatives – allylamines (e.g. terbinafine cream) ergosterol synthesis inhibitor
- Referral and systemic therapy for disseminated, scalp infections and severe onychomycosis
