pioderma 2013

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Pioderma

Dr. M. Izazi HP, SpKK

Departemen Ilmu Kesehatan Kulit dan

Kelamin Fakultas Kedokteran UNSRI/RSMHPalembang

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Pyodermas are infections in the epidermis, just below the

stratum corneum or in hair follicles.

Primarily caused by Staphylococcus aureus and group Astreptococcus.

cause a broad clinical spectrum of infection :

superficial pyodermas to invasive soft tissue infectionsdepending on : the organism

the anatomic location of infections

host factors

Pyodermas

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S. aureus permanently colonizes the anterior nares in 20 % of thepopulation.

Other sites of colonization : the axillae, perineum, pharynx, and hands.

Contributing factors: Immunosuppression, atopic dermatitis, pre-existingtissue injury, and inflammation.

Treatment: : change predisposing conditions, if possible

topical, oral, or parenteral antibioticsconsider local and current antimicrobial resistance patterns

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A. NON-BULLOUS IMPETIGO

Etiology :- Industrialized nations : most commonly caused by S. aureus

- developing nations : common cause by Group A streptococcus

> 70 % of pyoderma. Occurs in children & in adults.

Pathogenesis.

- Intact skin is usually resistant to colonization or impetiginization, possiblydue to absence of fibronectin receptors for teichoic acid moieties onS. aureus & group A streptococcus.

- In a typical sequence, S. aureus spreads from nose to normal skin

(approximately 11 days later) and then develop into skin lesions (after another 11 days).

- Conditions that disrupt the integrity epidermis a portal of entry include : insect bites, epidermal dermatophytoses, herpes simplex,

varicella, abrasions, lacerations, and thermal burns.

Impetigo

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Cutaneous Lesions

- Lesions commonly arise on the skin of the face(especially around the nares) or extremities after trauma

- Constitutional symptoms are absent

- The initial lesion is a transient vesicle or pustule that quickly evolvesinto a honey-colored crusted plaque (Ø can enlarge to > 2 cm)

- Surrounding erythema may be present

- Regional lymphadenopathy may be present > 90 % of patientswith prolonged, untreated infection

- Untreated, the lesions may slowly enlarge and involve new sites over several weeks

- In some individuals, lesions resolve spontaneously. In others, thelesions extend into the dermis, forming an ulcer (Ecthyma)

Differential Diagnosis :

Seborrheic dermatitis, Atopic dermatitis, Allergic contact dermatitis,

Epidermal dermatophyte infections, Tinea capitis, Herpes simplex,

Varicella, Herpes zoster, Scabies, Pediculosis capitis

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FIGURE . Staphylococcus aureus: Impetigo. Erythema and crusting on thenose (A), which can spread to involve the entire centrofacialregion (B).

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B. BULLOUS IMPETIGO

Three types of skin eruptions can be produced by phagegroup II S. aureus, particularly strains 77 and 55:

(1) bullous impetigo

(2) exfoliative disease (SSSS)

(3) nonstreptococcal scarlatiniform eruption

(staphylococcal scarlet fever)

All three represent varying cutaneous responses to

extracellular exfoliative toxins ("exfoliatin") types A and B

produced by these staphylococci

Exfoliative toxin A acts as a serine protease of

desmoglein 1, the desmosomal cadherin

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Cutaneous Lesions

commonly in newborn and older infants

characterized by : rapid progression of vesicles to flaccid bullae Bullae usually arise on areas of grossly normal skin

The Nikolsky sign (sheet-like removal of epidermis by shearingpressure) is not present

Bullae initially contain clear yellow fluid that subsequently becomesdark yellow and turbid, and their margins are sharply demarcated

without an erythematous halo The bullae are superficial 1-2 days rupture & collapse

thin, light-brown to golden-yellow crusts

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Laboratory Tests

- Gram stain of exudates : Gram-positive cocci in clusters

- culture from the contents of intact bullae : S. aureus phage group II

Histologically

- vesicle formation in the subcorneal or granular region

- occasional acantholytic cells within the blister

- spongiosis

- edema of the papillary dermis

- a mixed infiltrate of lymphocytes and neutrophils around blood

vessels of the superficial plexus

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Contact dermatitis, Bullous insect bites, Bullous tinea,

Bullous fixed drug reaction, Bullous drug eruption, SSS,Thermal burns, Pemphigus vulgaris, Bullous pemphigoid,Erythema multiforme, Dermatitis herpetiformis, herpes simplex,Varicella.

Prognosis and clinical course

- Untreated, invasive infection can complicate :

cellulitis, lymphangitis, and bacteremia, osteomyelitis, septic arthritis,pneumonitis, and septicemia.

- Exfoliatin production can lead to :

SSSS in infants and in adults immunocompromised or impaired renal function

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Treatment

mild to moderate cases : mupirocin ointment or cream, removal of crusts,

and good hygiene

Extensive cases systemic antibiotics :

- dicloxacillin (or similar penicillinase-resistant semi-syntheticpenicillin), 250 - 500 mg, PO qid, or

- erythromycin (in penicillin-allergic patient), 250 - 500 mg, PO qid

Treatment for 5 to 7 days (10 days if streptococci are isolated).

- azithromycin, PO (in adults 500 mg on the first day, 250 mg dailyon the next 4 days).

- amoxicillin plus clavulanic acid, 25 mg/ kg/day, tid [erythromycin-resistant S. aureus, commonly impetigo lesions of children]

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FIGURE . Bullous impetigo in a child.

Note blisters filled with cloudy fluid and lesions that

have ruptured, leading to erosions and crusting

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Treatments for Impetigo

T0PICAL SYSTEMIC

First line Mupirocin bid Dicloxacillin 250-500 mg PO qid for 5-7 days

Fusidic acid bid Amoxicillin plus clavu 25 mg/kg tid; 250-500 mg qidlanic acid; cephalexin

Second Azithromycin 500 mg x 1, then 250 mg daily for 4 days

line

(penicillin Clindamycin 15 mg/kg/day tid

allergy) Erythromycin 250-500 mg PO qid for 5-7 days

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Ecthyma Ecthyma is a cutaneous pyoderma characterized by thickly crusted erosions

or ulcerations

Lesion can evolve from a primary pyoderma or within a preexistingdermatosis or site of trauma.

usually a consequence of neglected impetigo and classically evolves inimpetigo occluded by footwear and clothing.

S. aureus and/or group A streptococcus can be isolated on culture.

Untreated staphylococcal or streptococcal impetigo can extend moredeeply, penetrating the epidermis, producing a shallow crusted ulcer

Ecthyma occurs most commonly on the lower extremities of children, or neglected elderly patients, or individuals with diabetes.

Poor hygiene and neglect are key elements in pathogenesis.

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The ulcer has :

- a "punched out" appearance when the dirty grayish-yellowcrust and purulent material are debrided.

- The margin of the ulcer is indurated, raised, and violaceous,and the granulating base extends deeply into the dermis.

Untreated ecthymatous lesions enlarge over weeks to months to adiameter of 2 to 3 cm or more.

The lesions are slow to heal, requiring several weeks of antibiotictreatment for resolution.

The complications :

- spread by autoinoculation or by insect vectors

- post-streptococcal sequela (glomerulonephritis)

Management of ecthyma is the same as for staphylococcal impetigo

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FIGURE Ecthyma. Multiple thicklycrusted ulcers on the leg

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Folliculitis

Folliculitis is a pyoderma that begins within the hair follicle

classified according : depth of invasion (superficial & deep), & microbialetiology

SUPERFICIAL FOLLICULITIS

Superficial folliculitis or follicular / Bockhart impetigo

- A small, fragile, dome-shaped pustule occurs at the infundibulum (ostiumor opening) of a hair follicle, often on the scalps of children and in thebeard area, axillae, extremities, and buttocks of adults

- cause by S. aureus

Periporitis staphylogenes refers to secondary infection of miliaria of theneonate by S. aureus.

Staphylococcal blepharitis is an S. aureus infection of the eyelids, presentingwith scaling or crusting of the eyelid margins, often with associatedconjunctivitis. The differential diagnosis includes seborrheic dermatitis androsacea of the eyelid.

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S. aureus folliculitis must be differentiated from :

- Three non-infectious, inflammatory, follicular disorders are morecommon in black men : S. aureus can cause secondary infection

+ pseudofolliculitis barbae, which occurs on the lower beard area;

+ folliculitis keloidalis or acne keloidalis nuchae, on the nape of the neck

+ perifolliculitis capitis, on the scalp

- Irritant folliculitis : exposure to mineral oils, tar products, & cutting oils

- Acne vulgaris

- drug-induced acneform eruptions- rosacea

- hidradenitis suppurativa

- acne necrotica of the scalp, and

- eosinophilic folliculitis of HIV disease

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DEEP FOLLICULITIS

Sycosis barbae : a deep folliculitis with perifollicular inflammation

in the bearded areas of the face and upper lip- If untreated : lesions may become more deeply seated and chronic

- treatment : with warm saline compresses and local antibiotics

(mupirocin or topical clindamycin) may be sufficient to

control infection.

More extensive cases require systemic antibiotic therapy

Lupoid sycosis : a deep, chronic form of sycosis barbae associated

with scarring, usually occurring as a circinate lesion

- A central cicatrix surrounded by pustules and papules gives theappearance of lupus vulgaris

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20

Figure 4. Bacterial folliculitis. A pustule pierced by a hair.

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Furuncles and Carbuncles

A furuncle or boil is a deep-seated inflammatory

nodule that develops around a hair follicle,

usually from a preceding, more superficial

folliculitis and often evolving into an abscess.

A carbuncle is a more extensive, deeper,

communicating, infiltrated lesion that develops

when suppuration occurs in thick inelastic skin

when multiple, closely set furuncles coalesce.

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FURUNCLES

- Furuncles arise in hair-bearing sites, particularly in regions subject tofriction, occlusion, and perspiration, such as the neck, face, axillae, and

buttocks.

- They may complicate pre-existing lesions such as atopic dermatitis,excoriations, abrasions, scabies, or pediculosis, but occur more often inthe absence of any local predisposing causes.

- systemic host factors is associated with furunculosis :obesity, blood dyscrasias, defects in neutrophil function(defects in chemotaxis associated with eczema and high levels of IgE,defects in intracellular killing of organisms as in chronic granulomatousdisease of childhood), treatment with glucocorticoids and cytotoxicagents, and immunoglobulin deficiency states.

- The process is often more extensive in patients with diabetes. Themajority of patients with problems of furunculosis appear to beotherwise healthy

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Cutaneous Lesions

- A furuncle starts as hard, tender, red folliculocentric nodule in hair-bearing skin that enlarges and becomes painful and fluctuant

after several days (i.e., undergoes abscess formation).

- Rupture occurs, with discharge of pus and often a core of necroticmaterial. The pain surrounding the lesion then subsides, and theredness and edema diminish over several days to several weeks.

- Furuncles may occur as solitary lesions or as multiple lesions insites such as the buttocks


- Cystic acne

- Kerion- Hidradenitis suppurativa

- Ruptured epidermal inclusion cyst Furuncular myiasis

- Apical dental abscess

- Osteomyelitis

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Figure 24.10 A

furuncle or aboil begins as a

tender, inflamed

nodule that

usually

becomes

fluctuant,points, and

ruptures.

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CARBUNCLES

A carbuncle is a larger, more serious inflammatory lesion with a

deeper base, characteristically occurring as an extremely painfullesion at the nape of the neck, the back, or thighs

Fever and malaise are often present, and the patient may appear quite ill.

The involved area is red and indurated, and multiple pustules soonappear on the surface, draining externally around multiple hair follicles.

The lesion soon develops a yellow-gray irregular crater at thecenter, which may then heal slowly by granulating, although the area

may remain deeply violaceous for a prolonged period.

The resulting permanent scar is often dense and readily evident.

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LABORATORY TESTS

Extensive furunculosis or a carbuncle may be associated with leukocytosis.

S. aureus is almost always the cause.

Histologic examination

furuncle shows a dense polymorphonuclear inflammatory process in the

dermis and subcutaneous fat

In carbuncles, multiple abscesses, separated by connective-tissue

trabeculae, infiltrate the dermis and pass along the edges of the hair

follicles, reaching the surface through openings in the undermined

epidermis.

The diagnosis is made on the basis of the clinical appearance.Confirms the diagnosis :

- Gram stain of pus : clusters of Gram-positive cocci

- Culture : isolation of S. aureus

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PROGNOSIS AND CLINICAL COURSE

The major problems with furunculosis and carbuncles are

bacteremic spread of infection and recurrence.

Lesions about the lips and nose raise the specter of spread via thefacial and angular emissary veins to the cavernous sinus.

Invasion of the bloodstream may occur from furuncles or carbunclesat any time, in an unpredictable fashion, resulting in metastaticinfection such as osteomyelitis, acute endocarditis, or brain abscess

Recurrent furunculosis is a troublesome process that may continue

for many years.

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TREATMENT

Simple furunculosis may be aided by local application of moist heat.

A carbuncle or a furuncle with surrounding cellulitis, or one withassociated fever, should be treated with a systemic antibiotic (as for impetigo)

- For severe infections or infections in a dangerous area, maximalantibiotic dosage should be employed by the parenteral route

. - If MRSA is implicated or suspected in serious infections :vancomycin (1.0 to 2.0 g intravenously daily in divided doses)

Antibiotic treatment should be continued for at least 1 week

- incision and drainage, when the lesions are large, painful, and

fluctuant

- draining lesions should be covered to prevent autoinoculation anddiligent hand washing performed

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Figure 24.11

Carbuncle on the

nape of a diabetic

man. This is a

staphylococcal

infection of several

contiguous hair

follicles.

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Abscess

Abscesses caused by S. aureus commonly occur in folliculocentric

infections : folliculitis, furuncles, and carbuncles.

Abscesses can also occur at sites of trauma, foreign bodies, burns,or sites of insertion of intravenous catheters.

The initial lesion is an erythematous nodule. If untreated, the lesionoften enlarges, with the formation of a pus-filled cavity

The initial and most important treatment of an abscess is incisionand drainage and antibiotic treatment as for furuncles

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31

FIGURE 7. Staphylococcus aureus abscess. A large painful abscess

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Erysipelas

Synonyms : st. anthony’s fire & ignis sacer

Erysipelas Is an acute beta-hemolytic group A streptococcal infection

of the skin involving the superficial dermal lymphatics

Cause by group A - hemolytic streptococcus (very uncommonly groupC or G streptococcus) and rarely caused by S. aureus

Group B – streptococcus is often responsible in newborn and may be

the cause of abdominal or perineal erysipelas in postpartum women

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Clinical features

- most frequent sites affected : face & legs

- prodromal symptoms : malaise, chills, high fever, headache, vomiting,& joint pains

- skin lesion may vary from transient hyperemia followed by slightdesquamation to intense inflammation with vesiculation & plegmon

- early stage : affected skin is scarlet, hot to the touch, brawny, swolleneruption begins as an erythematous patch & spreads by peripheralextension

A distinctive feature of the inflammation is advancing edge of the wallto the palpating finger (highly characteristic raised, indurated border)

- In some cases vesicles or bullae contain seropurulent fluid & mayresult in local gangrene

- Commonly with a polymorphonuclear leukocytosis of ≥ 20.000 / mm³

- Many cases : solely as an erythematous lesion without systemic

complaints

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Complications :

septicemia or deep cellulitis, more common in newborn & followingoperations on the elderly

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Predisposing causes :

- operative wounds

- fissures in the nares, auditory meatus, under the lobes of theears, anus or penis, & between or under the toes

- Any inflammation of the skin, especially is fissured or ulcerative,- abrasions or scratches, accidental scalp wounds, vaccination, &chronic leg ulcers


- contact dermatitis from plans, drugs, or dyes

- angioneurotic edema

- scarlet fever : widespread punctate erythema, never localized &edematous as erysipelas

- A butterfly pattern on the face may mimic lupus erythematosus

- ear involvement may suggest relapsing polychondritis- Acute tuberculoid leprosy of the face may look like erysipelasbut the absence of fever, pain, or leukocytosis

fever, pain, &

tenderness are

absent & itching issevere

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Treatment

- Locally, ice bags & cold compresses may be used

- Systemic penicillin is rapidly effective. Improvement in the general

condition occurs in 24 to 48 hours, but resolution of the cutaneouslesion may require several days

- treatment with antibiotics should be continued for at least 10 days -

- Erythromycin is also efficacious

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37

FIGURE 8. Erysipelas. There is painful, warm erythema of the

lower extremity with well defined borders.

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Cellulitis

Cellulitis is an infection of the deep dermis & subcutaneous tissue

caused most commonly by str.pyogenes & S. aureus.

Predisposition factor : lymphedema, alcoholism, DM, IV drug abuse, &

peripheral vascular disease.

Pathogenesis

- bacteria may gain access to the dermis via an external / a break inthe skin barrier (immunocompetent patient) or a hematogenous

route (immunocompromised patient)

- recurrent bouts of cellulitis may be caused by damage to the

lymphatic system (e.g. previous lymph node dissection, prior

episode of acute cellulitis

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Clinical features

- most common location : head & neck (children), extremities (adults)

- often preceded by systemic symptoms : fever, chills & malaise

- affected area : erythrma, warmth, pain, & swelling.

- the lesion usually has ill defined, non palpable borders. In severe

infections may occur : vesicles, bullae, pustules or necrotic tissue.

- the erythema rapidly become intense & spreads. The area become

infiltrated & pits on pressure. Sometimes the central part become

nodular & surmounted by a vesicle that ruptures & discharges pus &

necrotic material. Streaks of Lymphangitis may spread from the area

to the neighboring lymph glands.

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- complication (rare) : acute glomerulonephritis, lymphadenitis, &subacute bacterial endocarditis

recurrent cellulitis (damage to lymphatic vessel)

gangrene, abscesses, & sepsis

Pathology

- in dermis : infiltrate lymphocytes & neutrophils

edema & dilation of lymphatics & small blood vessels

in severe dermal edema may be seen subepidermal bullae

Laboratory examination

- diagnosis cellulitis usually clinical

- the leukocyte count is usually normal / slightly elevated

- culture & sensitivities should be obtained, if sign & symptom do notimprove after 24 – 36 hours of treatment : the primary site of infection,aspiration of the advancing edge, skin biopsy, or blood culture

- blood culture are almost always negative in immunocompetent host

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Treatment

- immobilization & elevation of the area affected

- application of wet dressing to area with bullae or exudate

- treatment should be targeted against Str.pyogenes & S.aureus- mild cases require a 10 days course of an oral antibiotic

- hospitalization & parenteral antibiotic : fasial cellulitis or seriously ill

(Intravenous penicillinase-resistant penicillins or first generation

cephalosporin are usually effective)

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FIGURE A. Cellulitis. The lower

extremity is swollen, erythematous, and

tender; there is blistering and crusting.

FIGURE B. Cellulitis after puncture trauma. The

forearm is swollen, erythematous, and tender;

there is abscess formation, blistering, and

crusting.

FIGURE C. Cellulitis arising at the site

of a surgical excision: Staphylococcusaureus. Note discharge of pus.

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Staphylococcal Scalded-Skin Syndrome (SSSS)

Synonyms : Ritter’s disease, pemphigus neonatorum

SSSS is a toxin-mediated epidermolytic disease characterized byerythema and widespread detachment of the superficial layers of theepidermis, resembling scalding

Onset : most common in neonates during first 3 months of lifeInfants and young children <5 years. Rare in adults

Etiology : S. aureus of phage group 2 (types 71 and 55), whichproduces exfoliative toxins A and B (ET-A and ET-B). Site of ET

production: purulent conjunctivitis, otitis media omphalitis, occultnasopharyngeal infection; bullous impetigo

Risk Factors : age <5 yearsadults: renal failure, systemic immunosuppression

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Pathogenesis

In newborns and infants, S. aureus colonizes nose, conjunctivae, or

umbilical stump with or without causing clinically apparent infection,producing ETs that are transported hematogenously to the skin

In bullous impetigo, ET is produced in impetigo lesion

Specific antistaphylococcal antibody, metabolic differences, or thegreater ability to localize, metabolize, and excrete in individuals >5 years

probably accounts for decreased incidence of SSSS with older age ET causes acantholysis and intraepidermal cleavage within the stratum

granulosum

More extensive epidermal damage is characterized by sloughing of superficial epidermis in SSSS

Healing occurs spontaneously in 5 to 7 days

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Clinical features

Localized Form (Bullous Impetigo)

- Intact flaccid purulent bullae, clustered. Rupture of the bullae results inmoist red and/or crusted erosive lesions. Lesions are often clustered in anintertriginous area

Generalized Form

- ET-induced changes : micromacular scarlatiniform rash or diffuse, ill-defined erythema and a fine, sandpaper appearance occur initially

- In 24 h, erythema deepens in color and involved skin becomes tender.Initially periorificially on face, neck, axillae, groins; becoming more widespreadin 24 to 48 h. Initial erythema and later sloughing of superficial layers of epidermis are most pronounced periorificially on face and in flexural areas onneck, axillae, groins, antecubital area, back (pressure points)

- With epidermolysis, epidermis appears wrinkled and can be removed bygentle pressure (skin resembles wet tissue paper) (Nikolsky's sign)

- In some infants, flaccid bullae occur. Unroofed epidermis forms erosionswith red, moist base. Desquamation occurs with healing

Mucous Membranes : Uninvolved

General Examination : possible low-grade fever, Irritable child & pain

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Differential Diagnosis : drug-induced TEN, Kawasaki's syndrome

Laboratory Examinations

- Gram's Stain : gram-positive cocci only at colonized site, not in

areas of epidermolysis- Bacterial Culture : S. aureus only at site of infection (i.e., site of

toxin production)—umbilical stump, ala nasi, nasopharynx,conjunctivae, external ear canal, stool. S. aureus is not recoveredfrom sites of sloughing skin or bullae

- Dermatopathology : Intraepidermal cleavage with splitting

occurring beneath and within stratum granulosum Diagnosis

Clinical findings confirmed by bacterial cultures

Course and Prognosis

Adequate antibiotic treatment : the superficially denuded areas heal in3 to 5 days associated with generalized desquamation in large sheetsof skin; there is no scarring.

Death can occur in neonates with extensive disease

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Management

Prophylaxis : prevent spread of toxigenic S. aureus in neonatal careunits

General Care- Hospitalization is recommended for neonates and young children,

especially if skin sloughing is extensive and parental compliancequestionable.

- Discharge home when significant improvement is apparent. If case ismild and home care reliable, children can be treated with oral antibiotic

Topical Therapy

- Baths or compresses for debridement of necrotic superficial epidermis.- Topical antimicrobial agents for impetigo lesions: mupirocin ointment,

bacitracin, or silver sulfadiazine ointment

Systemic Antimicrobial Therapy : See Table 1

Adjunctive Therapy

- Replace significant water and electrolyte loss intravenously in severecases

Antimicrobial agent Dosing

U ll f 7 14 dTable 1. Oral

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Usually for 7 – 14 days

Natural penicillin

Penicillin V

Penicillin G

Benzathine Penicillin G

250-500 mg tid/qid for 10 days

600.000 – 1,2 million U IM qd for 7 days

600.000 U IM for ≤ 6 years

1,2 million U IM for ≥ 7 years

Penicillinase- resistant penicillins

Cloxacillin

Dicloxacillin

NafcillinOxacillin

250 – 500 mg (adult) qid for 10 days

250 – 500 mg (adult) qid for 10 days

1.0-2.0 g IV q4h

1.0-2.0 g IV q4h

Aminopenicillins

Amoxicillin

Amoxicillin + clavulanic acid

Ampicillin

500 mg tid or 875 mg q12h

875/125 mg bid; 20 mg/kg per day tid for 10 days

250 – 500 mg (adult) qid for 7-10 days

Cephalosporins

Cephalexin

Cephradine

Cefaclor

Cefproxil

Cefuroxime axetil

Cefixime

250 – 500 mg (adult) qid for 10 days;

40-50 mg/kg per day (children) for 10 days


40-50 mg/kg per day (children) for 10 days

250 – 500 mg q8h250 – 500 mg q12h

250 – 500 mg q12h

250 – 500 mg q12-24h

Erythromycin group

Erythromycin ethylsuccinate

Clarithromycin

Azithromycin


40 mg/kg per day (children) for 10 days

500 mg bid for 10 days

500 mg on day 1, then 250 mg qd days 2 -5

Clindamycin 150 – 300 mg (adult) qid for 10 days ;

15 mg/kg per day (children) qid for 10 days

Tetracyclines

Minocycline

Doxycycline

Tetracycline


100 mg bid

250 – 500 mg qid

Miscellaneous agents

Trimethoprim-sulfamethoxazole

Metronidazole

Ciprofloxacin

160 mg TMP + 800 mg SMX bid

500 mg qid


Adapted from Wolff K, Johnson RA, Suurmond D. In. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology. New York:Mc Graw Hill, 2005;p598.

antimicrobial Agents for

Bacterial Infections

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Late stage of staphylococcal

scalded-skin syndrome

Generalized desquamation

with large sheets

Pictures of SSSS .

(A) erythema, more superficial blisters with

desquamation of large sheets.

B. Superficial erosions around the eye withunderlying denuded skin.

C. Characteristic crusting with superficial

erosions noted on face of this 10- month-old child

with SSSS.

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References

1. Craft N, Lee PK, Zipoli MT, Weinberg AN, Swartz MN, Johnson RA.

Superficial Cutaneous Infections and Pyodermas. In. Freedberg IM,

Eisen AZ, Wolff K, et al: eds. Fitzpatrick’s Dermatology in generalmedicine. 7th ed. New York : Mc Graw-Hill Book Co, 2008: 1649-709.

2. Wolff K, Johnson RA, Suurmond D. In. Fitzpatrick’s Color Atlas &

Synopsis of Clinical Dermatology. New York:Mc Graw Hill, 2005;p598

3. Halpern AV, Heymann WR. Bacterial diseases. In. Bolognia JL,Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. New York : Mosby

elsevier, 2008 :p. 1075-106

4. Odom RB , James WD, Berger TG. Andrews’ diseases of the skin. 9th

ed. Philadelphia : WB. Saunders Co, 2000

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Classification of Infectious Folliculitis

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Classification of Infectious Folliculitis

Bacterial folliculitis

· Staphylococcus aureusfolliculitis

· Periporitis staphylogenes

· Superficial (follicular or Bockhart impetigo)

· Deep (sycosis) [may progress to

furuncle (boil) or carbuncle]

· Pseudomonas aeruginosa folliculitis ("hot tub" folliculitis)

· Gram-negative folliculitis (occurs at the site of acne vulgaris, usually the

face, with long-term antibiotic therapy)

· Syphilitic folliculitis (secondary; acneform) Fungal folliculitis

· Dermatophytic folliculitis

· Tinea capitis

· Tinea barbae

· Majocchi granuloma

· Pityrosporum folliculitis · Candida folliculitis

Viral folliculitis

· Herpes simplex virus folliculitis

· Follicular molluscum contagiosum

Infestation

· Demodicidosis

Table 2 Organisms Antimicrobial Agents of Choice and Alternatives

7/29/2019 Pioderma 2013


Table 2. Organisms, Antimicrobial Agents of Choice, and Alternatives

Infecting Organism Antimicrobial Agent(s) of First Choice Alternative Antimicrobial Agents

Staphylococcus

aureus or epidermidis

Non-penicillinase producing Penicillin G or V A cephalosporin; clindamycin; vancomycin; imipenem;

a f luoroquinolone

Penicillinase-producing A penicillinase-resistant penicillin. PO: dicloxacillin,

cloxacillin. IV for severe infections; nafcillin, oxacillin

A cephalosporin; vancomycin;

amoxicillin/clavulanicacid; ticarcillin/clavulanic acid;

piperacillin/tazobactam; ampicillin/sulbactam;

imipenem; clindamycin; a fluoroquinolone

Methicillin-resistant Vancomycin ± gentamicin ± rifampin Trimethoprim-sulfamethoxazole; a fluoroquinolone;

minocycline; linezolid; quinupristin/dalfopristin

Streptococcu s pyogenes (group

A) and groups C and G

Penicillin G or V An erythromycin, clarithromycin, azithromycin; a

cephalosporin; vancomycin; clindamycin

Streptococcu s, group B Penicillin G or ampicillin A cephalosporin, vancomycin, an erythromycin

Streptococcu s pneumoniae

(pneumococcus)

Penicillin G or V A cephalosporin erythromycin; azithromycin;

clarithromycin; a fluoroquinolone; meropenem;

imipenem; trimethoprim-sulfameth-oxazole;clindamycin; a tetracycline

Penicillin-susceptible (MIC

<0.1 g/mL)

Penicillin G IV (12 million U/d for adults) or ceftriaxone

or cefotaxime

Levofloxacin; vancomycin; clindamycin

Penicillin-intermediate resistance

Penicillin-high level resistance

(MIC 2 g/mL)

Meningitis:

vancomycin + ceftriaxone or cefotaxime ± rifampin

Meropenem; imipenem; clindamycin

pioderma 2013

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