Bacterial Infection of the Skin (Pyodermas) 2
Bacterial Infection of the Skin (Pyodermas) 2
(pyodermas)
Impetigo
• Impetigo is a contagious superficial (stratum
corneum) pyogenic infection of the skin.
• Two main clinical forms are recognized:
– non-bullous impetigo (or impetigo contagiosa)
– and bullous impetigo.
• Impetigo presents as either a primary
pyodermal of intact skin or a secondary
infection on pre existing skin condition.
Impetigo
• Impetigo rarely progresses to systemic infection,
although post streptococcal glomerulonephritis may
occur as a rare systemic complication.
• Impetigo occurs in individuals of all ages. However,
children younger than 6 years have a higher
incidence of impetigo than adults.
• Bullous impetigo is most common in neonates and
infants
Impetigo
• Causative agents
– Staphylococcus aureus.
• The non-bullous form is usually caused by
group Aβ streptococcus, in some
• geographical areas Staphylococcus aureus or
by both organisms together.
Impetigo
Clinical features
• Non-bullous impetigo:
– fragile vesicle or pustule that readily ruptures and
becomes a honey-yellow, adherent, crusted
papule or plaque and with minimal or no
surrounding redness and usually occurs on hands
and face unless secondary infection exists
(cellulites).
Impetigo
• Bullous impetigo:
– The characteristic lesion is a vesicle that develops
into a superficial flaccid bulla on intact skin, with
minimal or no surrounding redness. Initially, the
vesicle contains clear fluid that becomes turbid.
– The roof of the bulla ruptures, often leaving a
peripheral collarette of scale if removed; it reveals
a moist red base.
Impetigo
• Management
– Local management for small lesions: - Wash with
betadine solution or saline.
– Potassium permanganate 1 in 1000 solution
soaking twice a day until the pus exudates dry up.
– Gentian violet (GV) paint 0.5% apply BID.
– Topical antibiotics can be used, such as 2%
mupirocin, Gentamycine, Fucidic acid can be used
but costly.
Impetigo
• Systemic treatment: -
– for impetigo contagiosa, a single dose of benzathin penicillin
coupled with local care.
– Oral amoxacyllin or Ampicillin can also be used.
• For Bullous impetigo: - cloxacillin 500 mg po QID for 7 to 10 days.
In cases, with an allergy to penicillin, erythromycin can be given.
• The underlining skin conditions such as eczemas, scabies, fungal
infection, or pediculosis should be treated.
• Neglected impetigo becomes ecthyma, a superficial infection
which involves the upper dermis which may heal forming a scar..
Impetigo
Folliculitis
• Infection of the hair follicles.
• It occurs on hair bearing areas of the skin.
• Application of greasy substance such as Vaseline is a predisposition.
• Cause, staphylococcus aureus. However, fungi and virus can also
cause it.
• A furuncle is an acute, deep-seated, red, hot, tender nodule or
abscess that evolves around the hair follicle and is caused by
staphylococcus aureus.
• A carbuncle is a deeper infection comprised of interconnecting
abscesses usually arising in several adjacent hair follicles.
• Furuncle and carbuncle are common in obese, diabetic patients and
immunosuppressive conditions.
• Management of folliculitis
– Avoid greasy applications on the skin.
– Mupiricine topically can be used.
• Systemic antibiotics: -
– cloxacillin or erythromycin are choices of
treatment.
• For deep abscesses (furuncle and carbuncle)
incision and drainage is mandatory.
Folliculitis images
Cellulitis and Erysipelas
• Cellulitis is bacterial infection and inflammation of loose
connective tissue (dermis subcutaneous tissue)
• Erysipelas is a bacterial infection of the dermis and upper
subcutaneous tissue; characterized by a well-defined, raised
edge reflecting the more superficial (dermal) involvement
• Etiology
– Group A β hemolytic streptococcus.
– However, Staphylococcus aureus can also cause cellulites.
– In young children, Hemophilus influenza type B should be
considered as a possible etiology for cellulites especially of
the face (facial cellulitis).
• Clinical features
• The difference between the conditions is often times fluid
and more of academical.
• Except in mild cases, there is constitutional upset with fever
and malaise.
• Classical erysipelas starts abruptly and systemic symptoms
may be acute and severe, but the
• response to treatment is more rapid
• . Erythema, heat, swelling and pain or tenderness are
constant features in both. In erysipelas, the edge of the lesion
is well demarcated and raised, but in cellulitis it is diffuse.
• In erysipelas, blisters are common and severe cellulitis
may also show bullae or necrosis of epidermis and can
rarely progress to fasciitis or myositis. Lymphangitis and
lymphadenopathy are frequently associated with
cellulitis.
• Leg commonest site for cellulites. A skin break, usually a
wound even if superficial, an ulcer, or an inflammatory
lesion including interdigital fungal or bacterial infection,
may be identified as a portal of entry.
• Erysipelas may occur on the face or extremities and
usually accompanied by malaise and fever.
Complications
– fasciitis, myositis, subcutaneous abscesses, and septicemia.
– Pretibial cellulitis can result in osteomyelitis from contiguous spread.
– Post streptococcal glomerulonephritis
– If Lymphangitis is not treated properly, it can lead to lymphoedema.
Management
• Treat the fever and pain and elevate the affected part.
• Crystalline penicillin or procaine penicillin is the first line therapy and oral
Ampicillin or Amoxicillin may be used for mild infection and after the acute
phase resolves.
• The antibiotics should be continued for 10- 14 days.
Follow up:
• a) Response to the antibiotic
• b) For proper timing of surgical intervention.
Superficial fungal infection of
the skin
Superficial fungal infection of the skin
Dermatophytes
• Specifically Trichophyton, Epidermophyton and
Microsporum species, are responsible for most
superficial fungal infections.
• The term "Tinea" refers exclusively to
dermatophyte infections.
• Dividing infections into the body region most
often affected can help in identification of the
problem.
Tinea Capitis
• Dermatophytic infection of the head and scalp, usually found in infants,
children, and young adolescents.
• Most infections occur in preschool-aged children. Around puberty, sebum
production by sebaceous glands becomes active, and as a result, it tends
to disappear.
• Scaly patches on the scalp with variable degree of hair loss and
generalized scaling that resembles seborrhic dermatitis may occur on the
scalp.
• Cervical lymphadenopathy can occur when there is secondary bacterial
infection.
• Kerion is a form of Tinea capitis with accentuated inflammatory response.
It is boggy, nodular tender mass which may form pus.
• An unusual scaling reaction known as favus may give the scalp a waxy or
doughy appearance with thick crusted areas.
• Differential diagnosis (DDx)
– Seborrheic dermatitis, dandruff, scalp
– psoriasis, atopic dermatitis, scalp impetigo, and
alopecia areata The finding of large areas of
alopecia that have early pustule formation favors a
diagnosis of Tinea capitis over alopecia areata
• Investigation
– KOH preparation and look for the fungal elements
from skin scraping, nail or hair.
• Treatment
• Systemic therapy.
– Griseofulvin in a dose of 10-20 mg per kg for six weeks to 8weeks
is the first-line treatment of Tinea capitis.
– Ketoconazole 2-4mg per kg for ten days, itraconazole and
terbinafine (Lamisil) are good alternatives.
– Griseofulvin should be taken after fatty meal.
• Topical treatment ,
– Whitefield ointment is preferred in the absence of secondary
bacterial infection.
• Other family members should also be examined and treated.
Tinea capitis images
Tinea corporis
• Tinea corporis is dermatophytosis of the glabrous skin
of the trunk and extremities.
• Lesions are round, scaly patches that have a well
defined, enlarging border and a relatively clear central
portion.
• The active edge often contains follicular papules.
• Itching is variable and not diagnostic
• Tinea corporis can assume a giant size (Tinea
incognito) when steroids are applied for cosmetic
reasons or as a result of miss diagnosis.
• Differential Diagnosis (DDx) Lichen simplex chronicus, numular
eczema, atopic eczema, psoriasis, lichen planus.
• Investigation
– KOH from active edge of lesion.
– Culture for fungus only in doubtful cases if the KOH is negative.
• Treatment
– Small and single lesion can be treated with topical agents. Clotrimazole
1%,
– ketoconazole 2%, meconazole 1%. BID for two weeks
• Systemic:
– ketoconazole 2-4mg per kg of weight for 10 days.
– Itraconazole and fluconazole are choices if available.
– Griseofulvin is also effective for the treatment of Tinea corporis.
Tinea coporis images
Tinea pedis
• Tinea pedis is fungal infection of the feet and is usually
related to sweating and warmth, and use of occlusive
footwear. Men between 20 and 40 years of age are most
frequently affected.
• The infection often presents as white, macerated areas in
the 3rd or 4th toe webs. It may also present with a classic
pattern on the dorsal surface of the foot or as chronic dry,
scaly hyperkeratosis of the soles and heels. Itching is also
common with vesicular or hullous lesion.
• It is transmitted by direct contact or sharing of shoes,
towels or bath.
• Treatment
• Topical anti fungal creams or ointments applied regularly
for 4 - 6 wks.
• Systemic treatments provide better skin penetration than
most topical preparations,
– Itraconazole, terbinafine and griseofulvin are good choices for
oral therapy.
– Itraconazole and terbinafine are more effective than griseofulvin.
• Fluconazole is another option, especially in noncompliant
patients. ( once – weekly dosing)
• Personal hygiene (foot hygiene) is highly advised.
Tinea pedis
Tinea versicolor (Pityriasis versicolor)
• Common, benign, superficial cutaneous
(stratum corneum) fungal infection, at the
level of stratum corneum.
• Characterized by hypo pigmented or
hyperpigmented macules and patches with
faint scale on the chest and the back.
Pityriasis versicolor
Etiology: Malassezia furfur (Pityrosporon
ovale,)
– M furfur is a member of normal flora of the skin
found in 18% of infants and 90-100%of adults.
– Predisposing factors include
• genetic predisposition,
• warm, humid environments,
• excessive sweating,
• immunosuppression, malnutrition, and
Cushingdisease.
• Investigation
• The clinical presentation of Pityriasis versicolor is
distinctive, and the diagnosis is made without potassium
hydroxide (KOH) examination.
• Treatment
• Patients should be informed that it is caused by a normal
flora of the skin hence it is not transmitted and any skin
color alterations resolve within 1-2 months after
treatment.
• Recurrence is common if the patient is not given enough
dose of treatment..
• Effective topical agents include: Sodium thiosulphate solution,
selenium sulfide and azole, ciclopiroxolamine, and allylamine
antifungals.
• Topical azole antifungals (clotrimazole, ketoconazole meconazole)
can be applied every night for 2 weeks. Weekly applications of any
of the topical agents for the following few months may help
prevent recurrence.
• Systemic treatment is also effective and is often preferred by
patients because of convenience. Ketoconazole 200-mg daily for
10-days and as a single-dose 400-mg
• treatment, have comparative results. Oral therapy does not
prevent the high rate of recurrence, unless repeated on an
intermittent basis throughout the year.
Candidiasis
• Candida infections caused by yeast-like fungi.
• Candida albicans commonly occur in moist,
flexural sites.
• These fungi live on all surfaces of our bodies.
• Under certain conditions, they can become so
numerous that they cause infections,
particularly in warm and moist areas.
• The factors associated with increased colonization rates.
– Broad-spectrum antibiotics by compromising the mucocutaneous protective
bacterial flora
– Depressed cell-mediated immunity either acquired or congenital
– Diabetes mellitus
– Systemic corticosteroid treatment
– Hematological malignancies and solid tumors
– Severe traumas and burns
– Premature birth
• Three of every four women have at least one bout of vulvovaginal candidiasis
(VVC) during their lifetime.
• More than 90% of HIV positive patients experience oropharyngeal candidiasis
(OPC), and 10% have at least one episode of esophageal candidiasis.
• Candidal colonization is at the highest levels during the extremes of ages, in
neonates and people older than 65 years
Intertrigo:
• affects any site where the skin surfaces are in close proximity with warm and
moist environment.
• Pruritic rash that begins with vesiculopustules, which enlarge and rupture,
causing maceration and fissuring.
• Satellite lesions frequently are found that may coalesce and extend into larger
lesions.
Candida balanitis:
• Candida balanitis is acquired through sexual intercourse with a
partner who has vulvovaginal candidiasis.
• A patch resembling thrush appears on the glans and may spread
to the thighs, gluteal folds, buttocks, and scrotum.
Investigation
• Wet mount: for hyphae, pseudohyphae, or budding yeast cells.
• KOH smear: to demonstrate fungal elements.
Treatment
• Candida intertrigo - Topical azoles and polyenes, including clotrimazole,
miconazole, and nystatin, are effective.
• Keeping the infected area dry is important.
• Paronychia - the most important intervention is drainage followed by oral
antifungal therapy with either ketoconazole, fluconazole or itraconazole.
• Single daily dose of itraconazole taken for 3-6 months or a pulsed-dose
regimen that requires a slightly higher dose daily for 7 days, followed by 3
weeks off therapy. The cycle is repeated every month for 3-6 months.
Oropharyngeal candidasis (OPC): - Topical
(nystatin, clotrimazole, amphotericin B oral
suspension) or systemic oral azoles
(fluconazole, itraconazole, ketoconazole).
Vulvovaginal candidiasis – Azole suppository
or pessaries , in resistant case systemic
therapy for 10 days.
• Imidazole cream topically for 3 – 7 days with 1
dose of 150mg Fluconazole P.O.