Skin infections and infestations Flashcards
Name 5 bacterial skin infections
Impetigo Folliculitis Cellulitis Erysipela Syphilis
Describe impetigo
- bacterial or viral
- what age group
- causative organism
Highly contagious and common bacterial infection of the skin that causes superficial blistering
typically occurs in children
Staph aureus or strep progenies
Treatment of impetigo
- if superficial/limited infection
- if widespread lesions
Topical antibiotics
Oral antibiotics
Describe folliculitis
- what is it
- causative organism
Infection of hair follicle
usually by staph aureus
Clinical features of folliculitis
erythematous papules or pustules around hair follicles
Clinical features of folliculitis
Erythematous papules or pustules around hair follicles
Treatment of folliculitis (2)
Antibacterial soap/washes
Topical antibiotics
Only oral antibiotics if acute and severe
Risk factors of folliculitis (3)
Trauma from shaving
Topical steroids
Diabetes
What is erysipelas + where does it usually affect +what condition is it similar to
Infection of the dermis (superficial cellulitis with lymphatic involvement); usually lower legs and face
Cellulitis but cellulitis affects deeper layers of the skin
Erysipelas (infection of the dermis) is mostly caused by what organism
Group A streptococci (Strep pyogenes)
Key clinical feature of erysipelas (superficial cellulitis) + others
Raised erythematous lesions (plaques) sharply demarcated from uninvolved skin (i.e. well defined margins)
Hot, swollen, sore skin
Fever/chills
Biochemical finding in erysipelas and cellulitis
Elevated WBC
Treatment of erysipelas
Oral antibiotics - penicillin
What is cellulitis + causative organisms
Infection of the deep dermis and subcutaneous tissue caused most commonly by Str.pyogenes and S.aureus
Risk factors of cellulitis (3)
Open wound/ulcer
Lymphoedema
IV drug abuse
Cardinal signs of inflammation are seen in cellulitis - name these
rubor (erythema), calor (warmth), dolor (pain) and tumor (swelling
Distinct skin difference between erysipelas and cellulitis
Cellulitis lesions have ill-defined, non-papable borders whereas erysipelas lesions are raised and palpable and well demarcated next to normal skin
Treatment of cellulitis
Antibiotics
What is syphilis + causative organism
sexually transmittedinfection(STI) caused by thebacteriaTreponema pallidum
Clinical features of cellulitis
Erythema with indistinct borders
Hot, red, swollen skin
Fever
Clinical features of
- primary syphilis
- secondary syphilis
- tertiary syphilis
Primary
- initially macule –> papule –> ulcerates into a chancre (painless ulcer) in the genital area or mouth
- may get unilateral lymphadenopathy of nodes close to the ulcer
Primary syphilis often manifests as what but can go unnoticed by patients
Painless genital/mouth ulcers (chancres)
Clinical features of secondary syphilis
- NON ITCHY diffuse rash - macules/papules on trunk/palms/soles
- flu like symptoms - fever, malaise
Clinical features of tertiary syphilis (after a long latent period)
neurological impairment
solitary granulomatous lesions (gummas)
cardiovascular problems
Treatment of syphilis
Intramuscular penicillin injection
Herpes simplex virus 1 affects where compared to herpes simplex virus 2
HSV1 affects mouth and lips area –> oral herpes (herpes labialis)
-but can also affect genitals
HSV2 affects genitals –> genital herpes
How is HSV transmitted
Through mucosal surfaces or breaks in the skin
Clinical features of HSV infection
- oral
- genital
Oral herpes
- SINGLE painful ulcer along the lip starting as vesicle –> ulcer
- tingling/burning before lesion fully developed
Genital herpes
- MULTIPLE painful ulcers that start as vesicles and progress to ulcers, then crusted lesions
- dysuria in women
- tingling/burning before lesion fully developed
Oral v genital herpes - which usually has more lesions
genital; oral usually just one lesion
Investigations of HSV infection
Viral swab –> viral culture
Viral swab –> HSV PCR
HSV type specific antibodies
Following primary infection with HSV, what happens
Latent stage - allows the virus to evade the immune system and cause lifelong infection by reducing the number of genes expressed and downregulation of the expression of major histocompatibility complex class I antigens on the surface of the infected cells