Common skin infections

and infestations
Dr. Thuzar Aung
Aim and objectives

 To know common cutaneous infections and infestations

 To recognize the clinical features of cutaneous bacteria, viral,
fungal and parasitic infections and infestations
 To discuss the basic treatment
 To decide the appropriate time for referral to dermatology
Bacterial infection
Impetigo
 Impetigo is a common and highly contagious superficial bacterial skin
infection.
 Two main presentations:
 Bullous impetigo, caused by a staphylococcal epidermolytic toxin
 Non-bullous impetigo which can be caused by either
Staphylococcus aureus or streptococci, or both together.
 All ages can be affected but non-bullous disease particularly
affects young children, often in late summer.
 Outbreaks - overcrowding and poor hygiene or in institutions.
 Widespread form can occur in neonates.
 Predisposing factors - minor skin abrasions and the existence
of other skin conditions, such as infestations or eczema.
Non-bullous impetigo

 Thin-walled vesicle  rapidly

ruptures and is rarely seen intact.
 Dried exudate, forming golden
crusting, arises on an erythematous
base.
 Bullous impetigo

 S. aureus strains that express

certain exfoliative toxins that
cleave desmoglein 1 in the
epidermis
 CF  clusters of thin-roofed bullae,
vesicles, and/or pustules
 Bullae initially contain clear yellow
fluid that subsequently becomes dark
yellow and turbid
 Site  face, scalp and limbs are commonly affected but other
sites can also be involved, particularly if there are predisposing
factors such as eczema.
 Lesions may be single or multiple and coalesce.
 Constitutional symptoms are uncommon.
Investigation
 Bacterial swab
Treatment
Treatment

 Localized cases – topical mupirocin or fusidic acid, removal of the

crusts with topical antiseptic and soap and water

 Wide-spread infection - systemic flucloxacillin or clarithromycin

 Strep. Pyogense - a serious complication glomerulo-nephritis (+) and

systemic antibiotics
 Scarring does not occur but there may be temporary dyspigmentation.
Staphylococcal scalded skin syndrome

 Serious exfoliating condition

 Occur predominantly in children, particularly neonates
 Caused by systemic circulation of epidermolytic toxins from a
Staph. aureus infection.
 Site - minor skin trauma, the umbilicus, urinary tract or
nasopharynx.
Clinical presentation

 Fever, irritability and skin tenderness

 Erythema usually begins in the groin
and axillae, and around the mouth.
 Blisters and superficial erosions
develop over 1–2 days and can
rapidly involve large areas, with
severe systemic upset.
Early SSSS
Late SSSS
 Ix  Bacterial swabs from primary sites of infection.
 Skin snip for histology
Management

 Systemic antibiotics and intensive supportive measures

 Bacterial swabs from nostrils, axillae and groins should be taken
from family members to exclude staphylococcal carriage.
 Although the acute presentation of SSSS is often severe, rapid
recovery and absence of scarring are usual, as the epidermal
split is superficial.
Toxic shock syndrome

 Fever, desquamating rash, circulatory

collapse and multi-organ involvement
 Caused by staphylococcal toxins and
early cases were thought to arise with
tampon use.
 Intensive supportive care and systemic
antibiotics are required.
Ecthyma

 Staph or Streptococci, or both

 Charaterized by adherent crusts overlying ulceration
 Most common sites  legs
 Predisposing factors  Poor hygiene, malnutrition and underlying skin
diseases such as scabies
 Commonly seen in drug abusers and minor trauma
 Mx  crust removal, Systemic and topical antibiotics
Folliculitis, Furuncles and Carbuncles

 Hair follicle inflammation

 Superficial, involving just the ostium of
the follicle (folliculitis)
 Deep (furuncles and carbuncles).
Superficial folliculitis

 The primary lesions are follicular pustules

and erythema.
 Caused by Staph. aureus, but can also be
sterile and caused by physical (traumatic
epilation) or chemical (mineral oil) injury.
Staphylococcal folliculitis
 Common in children
 Site - scalp or limbs.
 Pustules usually resolve without
scarring in 7–10 days but can
become chronic.
 In older children and adults,
they may progress to a deeper
form of folliculitis.
 Course  often self-limiting and may respond to irritant
removal and antiseptics.
 More severe cases may require topical or systemic antibiotics
and treatment of Staph. aureus carrier sites.
Deep folliculitis (furuncles and carbuncles)

Furuncle (boil)
 Acute Staph. aureus infection of the hair follicle, usually with
necrosis.
 Most common in young adults and males.
 Risk factors  Malnutrition, diabetes and HIV patients, chronic
Staph. aureus carriage in the nostrils and perineum, resistant strains,
such as MRSA, Friction caused by tight clothing
 Site  All body sites can be involved but neck, buttocks and
anogenital areas are commonly affected areas.
Clinical presentation

 Initially, an inflammatory follicular

nodule  pustular, fluctuant and
tender.
 Fever and mild constitutional upset.
 Lesions rupture over days to weeks,
discharge pus, become necrotic and
leave a scar.
Carbuncles

 If a deep Staph. aureus infection of a group of contiguous hair

follicles occurs  carbuncle
 Intense deep inflammation.
 Usually occurs in middle-aged men, often with predisposing
conditions such as diabetes or immunosuppression.
Clinical presentation

 Exquisitely tender nodule,

usually on the neck, shoulders or
hips, associated with severe
constitutional symptoms.
 Discharge, necrosis and scarring
 Ix  Bacterial swabs
 Treatment  anti-staphylococcal antibiotics, e.g. Flucloxacillin,
and sometimes incision and drainage.
 Cellulitis and erysipelas

Cellulitis Erysipelas
Inflammation of subcutaneous Bacterial infection of the dermis
tissue, due to bacterial infection and upper subcutaneous tissue
group A streptococci
Source of organism  ear infection, varicose eczema/ulcer or tinea pedis
Predisposing factors  Diabetes and immunosuppression
Malaise, fever and leucocytosis, and streptococcal serology
 Cellulitis Erysipelas
legs face
hot, painful, erythematous and oedematous
Blistering and may be haemorrhagic.
Regional lymphadenopathy is common.
typically ill defined well-defined edge due to its more
superficial level of involvement
 Treatment  intravenous flucloxacillin, with clarithromycin,
clindamycin
 Vancomycin as alternatives for penicillin-allergic patients.
 Milder cases  oral antibiotics.

 Cx lymphoedema, cavernous sinus thrombosis, sepsis and

glomerulonephritis.
Mycobacterial infections

 Mycobacterium leprae infection

 Mycobacterium tuberculosis
Mycobacterium leprae

 Infection may involve the skin and its manifestations will be

influenced by host immunity
 high levels of immunity  paucibacillary tuberculoid leprosy
 low immune resistance  multibacillary lepromatous leprosy.
 Hypopigmented or erythematous patches, with associated altered or
lost sensation, or skin thickening, nodules and infiltration should raise
suspicion of a diagnosis of leprosy. Lepromatous leprosy.

Tuberculoid leprosy
Mycobacterium tuberculosis.

 Skin - extrapulmonary site of involvement in tuberculosis,

usually due to infection with Mycobacterium tuberculosis.
 Skin manifestations depend on the route of infection, previous
sensitisation and host immunity.
 Cutaneous features
Lupus vulgaris Scrofuloderma
 Red–brown scarring  Skin changes overlying
inflammatory plaques due to lymph nodes or joints
direct skin inoculation; infected with tuberculosis
Tuberculids Erythema induratum (Bazin’s disease).
Investigation

 On diascopy, an ‘apple jelly’ appearance is typically seen,

indicating the granulomatous nature of skin involvement.
 Skin biopsy  Granulomas
 Culture of organisms
 PCR
 Investigation for pulmonary or other extrapulmonary sites.
 Reactivation of latent tuberculosis  patients receiving treatment
with immunosuppressants and biologic agents ( TNF-α antagonists
for conditions such as psoriasis) {screening and workup of such
patients prior to consideration of these therapeutic agents}
 Other mycobacterial skin infections

Mycobacterium marinum
 typically seen in those who clean tropical fish tanks.
 Sporotrichoid spread of granulomatous nodules from
the site of inoculation along lymphatics is typical
 Histology - granulomatous changes
 Resolution usually occurs with a prolonged course of
antibiotics such as doxycycline or minocycline.
 Resolution may also take place spontaneously or
after destructive therapies, such as cryotherapy.
Erythrasma

 Mild, chronic, localised, superficial skin infection caused by

Corynebacterium minutissimum (normal skin flora).
 Risk factors  Warmth and humidity
 Site  flexures and toe clefts.
 Asymptomatic or mildly itchy and lesions are well defined, red–
brown and scaly.
• Characteristic coral-pink fluorescence under Wood’s light .
 Microscopy and culture of skin scrapings can confirm the
diagnosis but are not usually needed if Wood’s light
examination is positive.
Treatment
 Topical azole (clotrimazole or miconazole) or fusidic acid
 Oral erythromycin can be used for extensive or resistant disease.
 Antiseptics can be used to prevent disease recurrence.
Pitted keratolysis

 Corynebacterium and Streptomyces spp.,

 Characteristic circular erosions (‘pits’) on the
soles.
 Usually asymptomatic and associated with
hyperhidrosis
 The bacterium can be identified in skin
scrapings
 Tx –1st line Fucidin ointment, imidazoles
 2nd line  Botulinum toxin
Viral Infections
Herpesvirus infections

Herpes simplex virus (HSV) 1 & 2

 HSV-1  mucocutaneous surfaces of head & neck
 HSV-2  genital mucosa, although there is overlap
 Acquired by “Inocultion of viruses” to mucosal surface.
 Infects sensory & autonomic neurons & causes latent infection
in the nerve ganglia.
 Primary infection is followed by episodes of reactivation
throughout life.
Clinical features
Primary
 Gingivostomatitis, pharyngitis or painful genital tract lesions.
 Associated with fever & regional LN.
 Recurrence

 Risk factors  Medical illness, menstration,

mechanical trauma, immunosuppression, stress, UV

 Oral mucosa – cold sore or herpes labialis

(prodromal hyperaesthesia is followed by rapid
vesiculation, pustulation and crusting).
 Genital – common cause of recurrent painful ulceration.
 Fingers – Paronychia, “whitlow”
Complications

 Eczema herpeticum – underlying

skin disease “eczema”
 Herpes keratitis  pain and blurring of vision
 HSV-1  viral encephalitis
 HSV-2  meningitis or transverse myelitis,
 HSV is implicated in the pathogenesis of Bell’s palsy.
 Immunocompromised hosts  oesophagitis, hepatitis,
pneumonitis, encephalitis, retinitis
 Neonatal HSV – associated with primary infection of mother
Skin lesions, hepatitis, pneumonitis, encephalitis.
Diagnosis
 Demonstration of virus in vesicular fluid by direct IF or PCR.
 HSV encephalitis  positive PCR in CSF
Management

 Therapy of localised disease must commence in the first 48 hours of

clinical disease (primary or recurrent); thereafter it is unlikely to influence
clinical outcome.
 Oral leasions  Topical acyclovir
 All severe manifestations should be treated, regardless of the time of
presentation
 Suspicion of HSV encephalopathy  immediate empirical antiviral
therapy
 Acyclovir reistance  foscarnet
Shingles (herpes zoster)

 After initial infection, VZV persists in latent form in the dorsal

root ganglion of sensory nerves and can reactivate in later life.
Clinical features

 Burning discomfort in the affected dermatome following

reactivation and discrete vesicles appear 3–4 days later.
 Thoracic dermatomes - most commonly involved
 Ophthalmic division of the trigeminal nerve
 vesicles may appear on the cornea  ulceration  blindness
Ramsay Hunt syndrome

 Geniculate ganglion involvement

 Facial palsy, ipsilateral loss of taste and
buccal ulceration + rash in the external
auditory canal.
Post-herpetic neuralgia

 Pain from shingles persists for 3 months or longer following

healing of the rash.
 More common with advanced age.
Management

 Early therapy with aciclovir or related

antivirals has been shown to reduce
both early- and late-onset pain,
especially in patients over 65 years.
Postherpetic neuralgia

 Amitriptyline 25–100 mg daily

 Gabapentin (commencing at 300 mg daily and building slowly to
300 mg twice daily or more) or
 Pregabalin (commencing at 75 mg twice daily and building up to
100 mg or 200 mg 3 times daily if tolerated).
 Capsaicin cream (0.075%) may be helpful.
 Glucocorticoids have not been demonstrated to reduce post-
herpetic neuralgia.
 Preventation

 Zoster vaccine  live attenuated vaccine

 It reduces the incidence of shingles and of post-
herpetic neuralgia.
 It is recommended in the UK for people aged
over 70 years.

 A recombinant vaccine is available in the USA.

Papillomaviruses & Viral warts

 DNA humanpapilloma virus (HPV)

 Transmission  direct virus contact, in living or shed skin
 HPV-16 & 18  SCC cervix, intraepithelial carcinoma of
genital skin
 Vaccinations(+)
Clinical features

 Initially - Smooth, skin-coloured papules  hyperkeratotoic &

warty
 Most common hands > face, genitalia, limbs
 Plantar warts (veruccae) – rough,  Mosaic warts – mosaic-like
horny rim, painful sheets of warts
 Plane warts – smooth, flat-  Facial warts – filiform
topped papules
 Genital warts – papillomatous & exuberant
Management

 Most viral warts  resolve spontaneously

 Treatments  destructive

 Salicylic acid or Salicylic/Lactic acid

combinations
 Wart paring
 Filiform facial warts  Cryotherapy

 Hand and foot warts  Salicylic acid wart paint

 Periungual and subungual warts  nail cutting and
electrodessication

 Other therapies  Topical formaldehyde, Glutaraldehyde,

Podophyllotoxin, Trichloroacetic acid, cantharidin, Topical or
systemic retinoids
 Intralesional bleomycin or interferon injections
 Imiquimod and PDT
Molluscum contagiosum

 DNA poxvirus
 Common in children, particularly with atopic dermatitis
 Immunosuppressed patients , HIV
 Dome-shaped, Umbilicated, skin-coloured papules with central punctum
 Multiple, sites of apposition (chest and inner arm)
Treatment

 Spontaneous resolution
 Topical salicylic acid, potassium hydroxide, podophyllin,
cantharidin, trichloroadetic acid, imiquimod
 Cryotherapy, Diathermy, Curettage, laser therapy
Cryotherapy
Curettage
Laser therapy
Orf

 Parapoxvirus skin infection

 Occupational risk for who work with sheep and goats
 Inoculation of virus into finger skin
 Inflammation & necrosis
 Resolves within 2-6 weeks
 No specific Tx is required unless there is secondary infections
Hand, foot and mouth disease

 Caused by enteroviruses (mainly coxsackievirus A16 and

enterovirus 71) and echoviruses.
 Children and occasionally adults
Clinical features

 Incubation period ~ 10 days.

 Relatively mild illness with fever and lymphadenopathy
 after an 2–3 days later  painful papular or vesicular rash appears
on palmoplantar surfaces of the hands and feet , oral lesions on the
buccal mucosa and tongue
 Papular erythematous rash may appear on the buttocks and thighs
 Antiviral treatment is not available, and management consists of
symptom relief with analgesics.
Fungal infections
 Superficial fungal infection: Dermatophytes & Yeasts

 Deep fungal infection: Chromomycosis & Sporotrichosis

 Soil origin  Geophilic

 Animal origin  Zoophilic
 Human skin  anthropophilic
 Dermatophyte infections (ringworm) – exteremely common

 Microsporum infect skin and hair

 Trichophyton infect skin, nail and hair
 Epidermophyton infect skin and nail
Diagnosis
 Skin scraping
 Hair pluckings
 Nail clippings from areas of disease activity

 Confirm the diagnosis by microscopy & fungal culture

Management
 Azoles (ketoconazole, miconazole)
 Triazoles (itraconazole, fluconazole)
 Triallylamines (terbinafine)

 Topical therapy  Terbinafine or miconazole

 Systemic (itraconazole, graseofulvin) therapy – scalp or nail
Tinea corporis

 Erythematous, annular & scaly

 Well-defined edge & central clearing

 Pustules (+) at active stage

 Asymmetrical & single/multiple

 Use of topical glucocorticoids worsen & increase disease extension 

Tinea incognito
Tinea cruris

 Trichophyton rubrum
 Itchy, erythematous plaques
 Groins and extend on to the thighs with raised active edge
Treatment
Tinea pedis

 “athlete’s foot”
 Caused by T. rubrum, T. interdigitale & Epidermophyton
floccosum
 Itchy rash b/t toes, with peeling, fissuring & maceration
Tinea capitis

 Scalp, most common in children

 Scalp inflammation & scaling with pustules & hair loss
Kerion

 Kerion is a boggy, inflammatory area of tinea capitis

 usually caused by zoophilic fungi T. verrucosum.
Onychomycosis

 Fungal infection of nail plate

 Yellow/brown nail discoloration, crumbling, thickening &
subungual hyperkeratosis.
 Asymmetry
 Toe nails are more commoly involved
 Candidiasis

 Superficial skin or mucosal infection caused by

Candidia albicans
 Predilection for warm & moist environments
 Napkin candidiasis in babies, Genital & Perineal
candidiasis, Intertrigo & Oral candidiasis
 Diagnosis – microscopy & fungal culture
 Topical or systemic antifungals – such as azoles
 Pityriasis versicolor

 Persistent superficial skin condition caused by Yeast –

Malassezia species (Malassezia globosa, M. sympadialis,
M. furfur)
 Warm & humid climates
 Scaly, oval macules usually
hypo/hyper-pigmented
Dx – microscopy
(spaghetti & meatballs hyphae)
 Tx – Selenium sulphide, ketoconazole shampoo,
topical/systemic azoles
Infestations
 Scabies

 Sarcoptes scabei
 Spreads by direct physical contact
 Scabietic burrow  a linear or curvilinear papule, caused by a burrowing
scabies mite
 Female mite burrows through the stratum corneum, laying eggs, eggs hatch
after 3 days into larvae, mature within about 2 weeks
Clinical presentation
 Pruritus
 irregular, tortuous and slightly scaly burrows
 sides of fingers, wrists, ankles and nipples, and genitalia
 form rubbery nodules
 small vesicles and papules with excoriations
 Secondary eczematisation
Management

 Topical treatment to affected individual and all asymptomatic

family members/physical contacts
 Malathion and permathrin, Crotamiton, benzyl benzoate and
10% sulphur ointment
 2 applications 1 week apart
 Heavy infestation  single dose of oral ivermectin
Benzyl benzoate (25% ointment)
 Rinsed off after 24hours
 CI – pregnant women and infants
 Advantages– effective and inexpensive
 Disadvantages – skin irritation
 Treat all family members & contacts

I. apply the lotion or cream to the entire body surface from the neck down
II. treat the face and scalp in infants, the elderly and the immuno-
suppressed
III. leave the lotion on for at least 8 hours and then wash off in the bath or
shower
IV. a repeat after 1 week
Head lice

 Pediculus humanus capitis

 Spread by direct head-to-head contact.
 C/F  itchness, secondary infection, cervical
lymphadenopathy
Treatment
 Treat affected individual and any affected household/school
contacts
 Topical dimeticone, permethrin, carbaryl or malathion – apply
twice at an interval of 7-10 days.
 Wet combing
 High-temperature washing of clothing and bedding
Body lice

 Live on clothing, feed on the skin.

 Poor hygiene and overcrowded conditions
Clinical features
 Itch, excoriations & secondary infection
Treatment
 Dry-cleaning and high-temperature washing of clothes.
 Heavy infestations  oral ivermectin
Pubic (crab) lice

 Sexually acquired and very itchy

Treatment
 Whole body treatment is required.
 Pubic hair may need to be shaved.
 Dry-cleaning & high-temperature washing of clothes.
 Heavy infestations  oral ivermectin
 Patients should be cleaned for STDs.