Pioderma

Dr. M. Izazi HP, SpKK

Departemen Ilmu Kesehatan Kulit dan

Kelamin Fakultas Kedokteran UNSRI/RSMH
Palembang
 Pyodermas
• Pyodermas are infections in the epidermis, just below the
stratum corneum or in hair follicles.

• Primarily caused by Staphylococcus aureus and group A

streptococcus.

cause a broad clinical spectrum of infection :

superficial pyodermas to invasive soft tissue infections
depending on : the organism
the anatomic location of infections
host factors
• S. aureus permanently colonizes the anterior nares in 20 % of the population.
Other sites of colonization : the axillae, perineum, pharynx, and hands.

• Contributing factors: Immunosuppression, atopic dermatitis, pre-existing

tissue injury, and inflammation.

• Treatment: : change predisposing conditions, if possible

topical, oral, or parenteral antibiotics
consider local and current antimicrobial resistance patterns
 Impetigo
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, possibly
due to absence of fibronectin receptors for teichoic acid moieties on
S. 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.
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 evolves
into a honey-colored crusted plaque (Ø can enlarge to > 2 cm)
- Surrounding erythema may be present
- Regional lymphadenopathy may be present > 90 % of patients with
prolonged, untreated infection
- Untreated, the lesions may slowly enlarge and involve new sites over
several weeks
- In some individuals, lesions resolve spontaneously. In others, the lesions
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
FIGURE . Staphylococcus aureus: Impetigo. Erythema and crusting on the
nose (A), which can spread to involve the entire centrofacial
region (B).
B. BULLOUS IMPETIGO

• Three types of skin eruptions can be produced by phage

group 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
• 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 shearing pressure)
is not present
– Bullae initially contain clear yellow fluid that subsequently becomes dark
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

• 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
• Differential Diagnosis :
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
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-synthetic
penicillin), 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 daily
on the next 4 days).
- amoxicillin plus clavulanic acid, 25 mg/ kg/day, tid [erythromycin-
resistant S. aureus, commonly impetigo lesions of children]
FIGURE . Bullous impetigo in a child.
Note blisters filled with cloudy fluid and lesions that
have ruptured, leading to erosions and crusting
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 qid
lanic 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
 Ecthyma
• Ecthyma is a cutaneous pyoderma characterized by thickly crusted erosions or
ulcerations

• Lesion can evolve from a primary pyoderma or within a preexisting dermatosis or

site of trauma.

• usually a consequence of neglected impetigo and classically evolves in impetigo

occluded by footwear and clothing.

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

• Untreated staphylococcal or streptococcal impetigo can extend more deeply,

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.

• The ulcer has :
- a "punched out" appearance when the dirty grayish-yellow
crust 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 a

diameter of 2 to 3 cm or more.

• The lesions are slow to heal, requiring several weeks of antibiotic

treatment 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

FIGURE Ecthyma. Multiple thickly
crusted ulcers on the leg
 Folliculitis
• Folliculitis is a pyoderma that begins within the hair follicle
classified according : depth of invasion (superficial & deep), & microbial etiology

SUPERFICIAL FOLLICULITIS

• Superficial folliculitis or follicular / Bockhart impetigo

- A small, fragile, dome-shaped pustule occurs at the infundibulum (ostium
or opening) of a hair follicle, often on the scalps of children and in the beard
area, axillae, extremities, and buttocks of adults
- cause by S. aureus

• Periporitis staphylogenes refers to secondary infection of miliaria of the neonate by

S. aureus.

• Staphylococcal blepharitis is an S. aureus infection of the eyelids, presenting with

scaling or crusting of the eyelid margins, often with associated conjunctivitis. The
differential diagnosis includes seborrheic dermatitis and rosacea of the eyelid.
• S. aureus folliculitis must be differentiated from :
- Three non-infectious, inflammatory, follicular disorders are more common 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
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 the
appearance of lupus vulgaris
Figure 4. Bacterial folliculitis. A pustule pierced by a hair.

20
 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.
FURUNCLES

- Furuncles arise in hair-bearing sites, particularly in regions subject to

friction, 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 in
the 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 granulomatous
disease of childhood), treatment with glucocorticoids and cytotoxic
agents, and immunoglobulin deficiency states.

- The process is often more extensive in patients with diabetes. The majority of
patients with problems of furunculosis appear to be otherwise healthy
• 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 necrotic

material. The pain surrounding the lesion then subsides, and the
redness and edema diminish over several days to several weeks.

- Furuncles may occur as solitary lesions or as multiple lesions in sites

such as the buttocks

• Differential Diagnosis :
- Cystic acne
- Kerion
- Hidradenitis suppurativa
- Ruptured epidermal inclusion cyst Furuncular myiasis
- Apical dental abscess
- Osteomyelitis
Figure 24.10 A
furuncle or a
boil begins as a
tender, inflamed
nodule that
usually
becomes
fluctuant,
points, and
ruptures.
CARBUNCLES

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

base, characteristically occurring as an extremely painful lesion 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 soon appear
on the surface, draining externally around multiple hair follicles.

• The lesion soon develops a yellow-gray irregular crater at the center,

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.

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
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 the facial
and angular emissary veins to the cavernous sinus.

• Invasion of the bloodstream may occur from furuncles or carbuncles at

any time, in an unpredictable fashion, resulting in metastatic infection
such as osteomyelitis, acute endocarditis, or brain abscess

• Recurrent furunculosis is a troublesome process that may continue for

many years.
TREATMENT

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

• A carbuncle or a furuncle with surrounding cellulitis, or one with

associated fever, should be treated with a systemic antibiotic (as for
impetigo)
- For severe infections or infections in a dangerous area, maximal
antibiotic 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 and

diligent hand washing performed
Figure 24.11
Carbuncle on the
nape of a diabetic
man. This is a
staphylococcal
infection of several
contiguous hair
follicles.
 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 lesion often

enlarges, with the formation of a pus-filled cavity

• The initial and most important treatment of an abscess is incision and

drainage and antibiotic treatment as for furuncles
FIGURE 7. Staphylococcus aureus abscess. A large painful abscess

31
 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 group C 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
• 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 slight
desquamation to intense inflammation with vesiculation & plegmon
- early stage : affected skin is scarlet, hot to the touch, brawny, swollen
eruption begins as an erythematous patch & spreads by peripheral
extension
A distinctive feature of the inflammation is advancing edge of the wall to
the palpating finger (highly characteristic raised, indurated border)
- In some cases vesicles or bullae contain seropurulent fluid & may
result in local gangrene
- Commonly with a polymorphonuclear leukocytosis of ≥ 20.000 / mm³
- Many cases : solely as an erythematous lesion without systemic complaints
• Complications :
septicemia or deep cellulitis, more common in newborn & following
operations on the elderly
• Predisposing causes :
- operative wounds
- fissures in the nares, auditory meatus, under the lobes of the
ears, 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

• Differential Diagnosis : fever, pain, &

- contact dermatitis from plans, drugs, or dyes tenderness are
- angioneurotic edema absent & itching is
severe
- 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 erysipelas
but the absence of fever, pain, or leukocytosis
• 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 cutaneous
lesion may require several days
- treatment with antibiotics should be continued for at least 10 days --
Erythromycin is also efficacious
FIGURE 8. Erysipelas. There is painful, warm erythema of the
lower extremity with well defined borders.

37
 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 in
the skin barrier (immunocompetent patient) or a hematogenous route
(immunocompromised patient)

- recurrent of cellulitis may be caused by damage to the lymphatic system

(e.g. previous lymph node dissection, prior episode of acute cellulitis)
• 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.
 - 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 not
improve 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
• 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)
FIGURE A. Cellulitis. The lower FIGURE B. Cellulitis after puncture trauma. The
extremity is swollen, erythematous, and forearm is swollen, erythematous, and tender;
tender; there is blistering and crusting. there is abscess formation, blistering, and
crusting.

FIGURE C. Cellulitis arising at the site

of a surgical excision: Staphylococcus
aureus. Note discharge of pus.
 Staphylococcal Scalded-Skin Syndrome (SSSS)

• Synonyms : Ritter’s disease, pemphigus neonatorum

• SSSS is a toxin-mediated epidermolytic disease characterized by erythema

and widespread detachment of the superficial layers of the epidermis,
resembling scalding

• Onset : most common in neonates during first 3 months of life Infants

and young children <5 years. Rare in adults

• Etiology : S. aureus of phage group 2 (types 71 and 55), which produces

exfoliative toxins A and B (ET-A and ET-B). Site of ET production: purulent
conjunctivitis, otitis media omphalitis, occult nasopharyngeal infection;
bullous impetigo

• Risk Factors : age <5 years

adults: renal failure, systemic immunosuppression
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 the greater
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
Clinical features

• Localized Form (Bullous Impetigo)

- Intact flaccid purulent bullae, clustered. Rupture of the bullae results in moist red
and/or crusted erosive lesions. Lesions are often clustered in an intertriginous 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 widespread in
24 to 48 h. Initial erythema and later sloughing of superficial layers of epidermis
are most pronounced periorificially on face and in flexural areas on neck,
axillae, groins, antecubital area, back (pressure points)
- With epidermolysis, epidermis appears wrinkled and can be removed by
gentle pressure (skin resembles wet tissue paper) (Nikolsky's sign)
- In some infants, flaccid bullae occur. Unroofed epidermis forms erosions with red,
moist base. Desquamation occurs with healing
• Mucous Membranes : Uninvolved
• General Examination : possible low-grade fever, Irritable child & pain
• 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 recovered
from 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 in 3 to
5 days associated with generalized desquamation in large sheets of skin;
there is no scarring.
Death can occur in neonates with extensive disease
Management
• Prophylaxis : prevent spread of toxigenic S. aureus in neonatal care
units
• General Care
- Hospitalization is recommended for neonates and young children,
especially if skin sloughing is extensive and parental compliance
questionable.
- Discharge home when significant improvement is apparent. If case is
mild 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 severe
cases
 Antimicrobial agent Dosing
Table 1. Oral
Usually for 7 – 14 days antimicrobial Agents for
Bacterial Infections
Natural penicillin 250-500 mg tid/qid for 10 days
Penicillin V 600.000 – 1,2 million U IM qd for 7 days
Penicillin G 600.000 U IM for ≤ 6 years
Benzathine Penicillin G 1,2 million U IM for ≥ 7 years

Penicillinase- resistant penicillins 250 – 500 mg (adult) qid for 10 days

Cloxacillin 250 – 500 mg (adult) qid for 10 days
Dicloxacillin 1.0-2.0 g IV q4h
Nafcillin 1.0-2.0 g IV q4h
Oxacillin

Aminopenicillins 500 mg tid or 875 mg q12h

Amoxicillin 875/125 mg bid; 20 mg/kg per day tid for 10 days
Amoxicillin + clavulanic acid 250 – 500 mg (adult) qid for 7-10 days
Ampicillin

Cephalosporins 250 – 500 mg (adult) qid for 10 days;

Cephalexin 40-50 mg/kg per day (children) for 10 days
250 – 500 mg (adult) qid for 10 days;
Cephradine 40-50 mg/kg per day (children) for 10 days
250 – 500 mg q8h
Cefaclor 250 – 500 mg q12h
Cefproxil 250 – 500 mg q12h
Cefuroxime axetil 250 – 500 mg q12-24h
Cefixime
Erythromycin group 250 – 500 mg (adult) qid for 10 days;
Erythromycin ethylsuccinate 40 mg/kg per day (children) for 10 days
500 mg bid for 10 days
Clarithromycin 500 mg on day 1, then 250 mg qd days 2-5
Azithromycin

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

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

Tetracyclines 100 mg bid for 10 days

Minocycline 100 mg bid
Doxycycline 250 – 500 mg qid
Tetracycline

Miscellaneous agents 160 mg TMP + 800 mg SMX bid

Trimethoprim-sulfamethoxazole 500 mg qid
Metronidazole 500 mg bid for 7 days
Ciprofloxacin

Adapted from Wolff K, Johnson RA, Suurmond D. In. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology. New York:Mc Graw Hill, 2005;p598.
Pictures of SSSS . Late stage of staphylococcal
scalded-skin syndrome
(A) erythema, more superficial blisters with
Generalized desquamation
desquamation of large sheets.
with large sheets
B. Superficial erosions around the eye with
underlying denuded skin.
C. Characteristic crusting with superficial
erosions noted on face of this 10- month-old child
with SSSS.
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
Infecting Organism
Staphylococcus
aureus or epidermidis
Non-penicillinase producing
Penicillinase-producing
Methicillin-resistant
Streptococcus
pyogenes (group A) and groups
C and G
Streptococcus, group B
Streptococcus pneumoniae
(pneumococcus)
Penicillin-susceptible (MIC
<0.1 g/mL)
Penicillin-intermediate resistance
Penicillin-high level resistance
(MIC 2 g/mL)
Antimicrobial Agent(s) of First Choice
Penicillin G or V
A penicillinase-resistant penicillin. PO: dicloxacillin,
cloxacillin. IV for severe infections; nafcillin,
oxacillin
Vancomycin ± gentamicin ± rifampin
Penicillin G or V
Penicillin G or ampicillin
Penicillin G or V
Penicillin G IV (12 million U/d for adults)
or ceftriaxone or cefotaxime
Meningitis:
vancomycin+ceftriaxone or cefotaxime ± rifampin
Other infections: varicomycin ±ceftriaxone
or cefotaxime; or levofloxacin
Alternative Antimicrobial Agents
A cephalosporin; clindamycin; vancomycin;
imipenem; a fluoroquinolone
A cephalosporin; vancomycin;
amoxicillin/clavulanicacid; ticarcillin/clavulanic acid;
piperacillin/tazobactam; ampicillin/sulbactam;
imipenem; clindamycin; a fluoroquinolone
Trimethoprim-sulfamethoxazole; a fluoroquinolone;
minocycline; linezolid; quinupristin/dalfopristin
An erythromycin, clarithromycin, azithromycin; a
cephalosporin; vancomycin; clindamycin
A cephalosporin, vancomycin, an erythromycin
A cephalosporin erythromycin; azithromycin;
clarithromycin; a fluoroquinolone; meropenem;
imipenem; trimethoprim-sulfameth-oxazole;
clindamycin; a tetracycline
Levofloxacin; vancomycin; clindamycin
Meropenem; imipenem; clindamycin
Quinupristin/dalfopristin; linezolid