MICROBIOME

Introduction

The human microbiome or microbiota represents diverse viral, bacterial, fungal, and other species that live on and within us. They are part of us and we are part of this complex ecosystem. The human body contains >10 times more microbial cells than human cells. Microbial colonization of skin is denser in humid intertriginous and occluded sites such as axillae, anogenital regions, and web spaces of feet. An intact stratum corneum is the most important defense against invasion of pathogenic bacteria.

Resident flora of the skin

+The normal human skin is colonized by huge numbers of bacteria that live harmlessly as commensals on its surface and within its pilosebaceous follicles. The normal skin micriobiota is composed of aerobic cocci, aerobic and anaerobic coryneform bacteria, Gram-negative bacteria, and yeast. Four phyla – Actinobacteria, Firmicutes, Bacteroidetes and Proteobacteria – account for the vast majority of skin bacteria. These bacteria live as microcolonies on the surface and between the layers of the stratum corneum and in the infundibulum of the pilosebaceous units. In the uppermost layer of the stratum corneum, corynebacterium species are present. In the follicular canal of the pilosebaceous units, Propionibacterium species (anaerobic diphtheroids) are present in infrainfundibulum, coagulase- negative staphylococci (Staphylococci epidermidis) in the acroinfundibulum and Malassezia species of yeasts (also known as pityriasiform spp) are located near the ostium in the acroinfundibulum.

The role of the normal flora

The normal resident flora of the healthy skin helps to defend the skin against outside pathogens by bacterial interference or antibiotic production. Specifically, Staphylococci epidermidis, Propionibacterium acnes, corynebacteria and Malassezia spp. produce lipases and esterases that break down triglycerides of sebum to free fatty acids, leading to lower skin surface PH and thereby unfavorable growing conditions for skin pathogens such as Streptococcus pyogenes.

Pathophysiology

Intact skin is usually resistant to colonization or infection by S aureus or GABHS (group A beta hemolytic streptococcus).

The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. These fibronectin receptors are unavailable on intact skin; however, skin disruption may reveal fibronectin receptors and allow for colonization or invasion in these disrupted surfaces. Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment.

Any factor that causes disruption of skin can facilitate bacterial colonization or infection.

About 15-40 per cent of healthy humans are carriers of S. aureus, that is, they have the bacteria on their skin without any active infection or disease (colonization). The carrier sites are usually the nostrils and flexures, where the bacteria may be found intermittently or every time they are looked for.

GABHS colonization

If an individual is in close contact with others (eg, household members, classmates, teammates) who have GABHS skin infection or who are carriers of the organism, the normal skin of that individual may be colonized. Once the healthy skin is colonized, minor trauma, such as abrasions or insect bites, may result in the development of impetigo lesions within 1-2 weeks.

GABHS can be detected in the nose and throat of some individuals 2-3 weeks after lesions develop, although they do not have symptoms of streptococcal pharyngitis. This is because impetigo and pharyngitis are caused by different strains of the bacteria. Impetigo is usually due to pattern D strains, whereas pharyngitis is due to pattern A, B, and C strains.

Staphylococcus aureus colonization

Approximately 30% of the population is colonized in the anterior nares by S aureus. Bacteria can spread from the nose to healthy skin within 7-14 days, with impetigo lesions appearing 7-14 days later.

Approximately 10% of individuals are colonized with S aureus in the perineum and, more uncommonly, in the axillae, pharynx, and hands. Individuals who are permanent carriers serve as reservoirs of the infection for other people. S aureus often passes from one individual to another through direct hand contact, entering through broken skin created by cutaneous diseases.

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). In contrast, Group A Streptococci appear on normal skin first and then develop into skin lesions (approximately 10 days later), and then spread to the nose and throat of the same patient (after another 10 days). Thus, the sequence of spread of S. pyogenes in a given patient is from normal skin to lesions and eventually to the nose and throat. In contrast, the sequence of spread of S. aureus is from nose, to normal skin, to skin lesions.

Bacterial skin infection

Salient features

· Roughly 20% of outpatient dermatology visits are for bacterial skin infections

· Staphylococci and streptococci cause the majority of bacterial skin conditions, which range from common infections e.g. impetigo and cellulitis to multisystem disorders (e.g. toxic shock syndrome)

· An increase in the prevalence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) remains a concern

· Various systemic diseases and immunodeficiency states predispose patients to bacterial skin infections that can be severe and refractory to treatment

Gram-Positive Bacteria

Staphylococcal and Streptococcal Skin Infections

Bacterial infection of the skin, also called pyodermas, mostly produced by pus forming organism such as staphylococcus aureus or streptococci or both. Pyodermas are primary when involve the normal skin and secondary when involve the pre existing skin diseases. These bacteria can cause a variety of skin infections depending on the anatomic location of infections.

Primary pyodermas have a characteristic appearance and include:

Impetigo
Ecthyma
Folliculitis
Furuncle
Carbuncle
Sycosisbarbae
Erysepelas
Cellulitis

Empiric treatment of cutaneous staphylococcal and streptococcal infections in adults

Treatment duration is usually 7–10 days, depending on the severity and clinical response. Initial choice of antibiotic is dependent on known resistance patterns in a given community. Topical treatments for localized superficial infections (e.g. impetigo) include mupirocin 2% ointment/cream, retapamulin 1% ointment, or fusidic acid 2% cream. The contents of pustules or exudate (e.g. underlying a crust) should be sent for culture and sensitivities prior to beginning therapy. Systemic quinolones (other than delafloxacin) and macrolides are not optimal, as staphylococcal resistance is common and may develop rapidly. However, a topical quinolone, ozenoxacin 1% cream, is under development and has been shown in randomized controlled studies to be safe and effective for the treatment of impetigo. IV, intravenously; MSSA, methicillin-sensitive Staphylococcus aureus; MRSA, methicillin-resistant Staphylococcus aureus; PO, orally.

EMPIRIC TREATMENT OF CUTANEOUS STAPHYLOCOCCAL AND STREPTOCOCCAL INFECTIONS IN ADULTS
Streptococcal infection	· Dicloxacillin 500 mg PO four times a day · First generation cephalosporin · Nafcillin or oxacillin 1–2 g IV four times a day, if severe
Suspected MSSA infection e.g. impetigo requiring systemic treatment or non-purulent cellulitis	· First-generation cephalosporin, e.g. cephalexin 250–500 mg PO three or four times a day · Dicloxacillin 250–500 mg PO four times a day
Suspected MRSA infection e.g. furuncles/abscesses, purulent cellulitis, or infections that failed to respond to treatment with an antistaphylococcal β-lactam	· Doxycycline 100 mg PO two times a day^* · Trimethoprim–sulfamethoxazole 1 or 2 double-strength tablets PO twice a day^* · Clindamycin 300–450 mg PO four times a day
Other oral options · Minocycline^* · Linezolid^† or tedezolid^† · Delafloxacin^†
Intravenous options for severe disease · Vancomycin (first line) · Daptomycin · Telavancin, oritavancin, or albavancin · Teicoplanin · Ceftaroline or ceftobiprole^‡
Penicillin-allergic patients	· Clindamycin · Clarithromycin 250 mg PO two times a day
Additional special considerations	· Furuncle/abscess: incision and drainage (without packing) is a key component of successful treatment · If recurrent infections, address carrier state: 1. >Mupirocin 2% nasal ointment twice a day for 5 days 2. >Mupirocin 2% cream to major body folds (e.g. axillae, groin, inframammary) and umbilicus twice a day for 5 days 3. >Wash body with chlorhexidine or dilute bleach^** 2–3 times per week · Address fomites including sports equipment, keyboards, and remote controls · Consider close human contacts or pets as source of infection

EMPIRIC TREATMENT OF CUTANEOUS STAPHYLOCOCCAL AND STREPTOCOCCAL INFECTIONS IN ADULTS

Organism/situation

Suggested antibiotics

Streptococcal infection

· Dicloxacillin 500 mg PO four times a day

· First generation cephalosporin

· Nafcillin or oxacillin 1–2 g IV four times a day, if severe

Suspected MSSA infection

e.g. impetigo requiring systemic treatment or non-purulent cellulitis

· First-generation cephalosporin, e.g. cephalexin 250–500 mg PO three or four times a day

· Dicloxacillin 250–500 mg PO four times a day

Suspected MRSA infection

e.g. furuncles/abscesses, purulent cellulitis, or infections that failed to respond to treatment with an antistaphylococcal β-lactam

· Doxycycline 100 mg PO two times a day^*

· Trimethoprim–sulfamethoxazole 1 or 2 double-strength tablets PO twice a day^*

· Clindamycin 300–450 mg PO four times a day

Other oral options

· Minocycline^*

· Linezolid^† or tedezolid^†

· Delafloxacin^†

Intravenous options for severe disease

· Vancomycin (first line)

· Daptomycin

· Telavancin, oritavancin, or albavancin

· Teicoplanin

· Ceftaroline or ceftobiprole^‡

Penicillin-allergic patients

· Clindamycin

· Clarithromycin 250 mg PO two times a day

Additional special considerations

· Furuncle/abscess: incision and drainage (without packing) is a key component of successful treatment

· If recurrent infections, address carrier state:

>Mupirocin 2% nasal ointment twice a day for 5 days

>Mupirocin 2% cream to major body folds (e.g. axillae, groin, inframammary) and umbilicus twice a day for 5 days

>Wash body with chlorhexidine or dilute bleach^** 2–3 times per week

· Address fomites including sports equipment, keyboards, and remote controls

· Consider close human contacts or pets as source of infection

* Does not provide coverage of group A streptococci; if coverage of the latter is desired, a β-lactam should also be prescribed.

† Intravenous form also available.

** E.g. 0.5 cup of household bleach (6–8.25% sodium hypochlorite) in a full 40-gallon bathtub, or 0.5–1 teaspoon per gallon in a spray bottle.

Impetigo

Salient features

· Staphylococcus aureus and, to a lesser degree, group A β-hemolytic Streptococcus spp. are the major causes of impetigo

· Represents the most common bacterial skin infection in children

· Nasal carriers of S. aureus are at particular risk of developing impetigo

· Treatment decisions should consider resistance patterns of S. aureus

Introduction

Impetigo is a common, contagious, superficial skin infection that can present in non-bullous and bullous forms. The most common pathogen in both non-bullous and bullous impetigo is Staphylococcus aureus. Group A β hemolytic Streptococcus (Streptococcus pyogenes) represents another important cause of non-bullous impetigo. Overall, non-bullous impetigo accounts for approximately 70% of cases.

Epidemiology

Primary Impetigo frequently occurs in children (especially those <6 years of age), and worldwide it represents the most common bacterial skin infection in this group. Bullous impetigo is also common in the neonatal period. Adults most commonly acquire impetigo through contact with infected children. Impetigo is extremely contagious, spreading rapidly via direct person-to-person contact or through fomites. In temperate climates, peak incidence is in the summer months.

Predisposing factors include a warm ambient temperature, high humidity, poor hygiene, an atopic diathesis, skin trauma, and participation in contact sports (e.g. wrestling, football). Both S.aureus and S. pyogenes are found in the anterior nares of normal individuals (carriers). The transfer from here to the skin via rubbing, scratching or probing fingers is easy. Impetigo is extremely contagious, spreading from one individual to another by direct hand contact.

Pathogenesis

Intact skin is usually resistant to colonization or impetiginization, possibly due to absence of fibronectin receptors for teichoic acid moieties on S. aureus and group A Streptococcus. Infection typically occurs at sites of tiny defects such as from scratching (e.g. insect bites, atopic dermatitis), minor trauma (e.g. an abrasion, laceration or burn) or other skin infections (e.g. varicella). Disruption of the skin barrier allows the bacteria to adhere, invade and establish infection.

Bullous impetigo results from the local production of exfoliative toxins (ETA) by phage group II S. aureus at site(s) of cutaneous infection; hematogenous dissemination of the same toxins is the cause of staphylococcal scalded skin syndrome (SSSS). In both diseases, blister formation is mediated by exfoliative toxin A binding to the desmosomal protein desmoglein 1 and cleaving its extracellular domain, thus leading to acantholysis within the epidermal granular layer. S. aureus can be cultured from blister fluid, but not those of SSSS. Compared to non-bullous impetigo, the bullous form is more likely to develop on clinically intact skin, especially in intertriginous sites.

Clinical features

CHARACTERISTIC FEATURES OF BULLOUS AND NON-BULLOUS IMPETIGO
Epidemiology	· 70% of all cases of impetigo · Children most often affected	· Less common · Often occurs in the neonatal period, but children also affected
Clinical lesions	· Early: single 2–4 mm erythematous macule that rapidly evolves into a short-lived vesicle or pustule · Late: superficial erosion with a typical “honey-colored” yellow crust and rapid direct extension of infection to surrounding skin	· Early: small vesicles enlarge into 1–2 cm superficial bullae · Late: flaccid, transparent bullae measuring up to 5 cm in diameter; after rupture there is a collarette of scale, but no thick crust; usually little surrounding erythema
Distribution	· Face (around the nose and mouth) and extremities	· Face, trunk, buttocks, perineum, axillae, and extremities
Associated findings	· Mild lymphadenopathy may be present	· Usually no systemic symptoms but can be associated with weakness, fever, and diarrhea
Clinical course	· Usually a benign, self-limited process · Usually resolves within 2 weeks without scarring if untreated	· Usually resolves in 3–6 weeks without scarring if not treated
Complications	· In 5% of cases, non-bullous impetigo caused by Str. pyogenes (M protein types 1, 4, 12, 49, 55, 57, 60) results in acute post-streptococcal glomerulonephritis (APSG)^* · Risk of APSG is not altered by treatment with antibiotics · Impetigo has not been linked to a risk of rheumatic fever	· In infants/young children and adults with immunodeficiency or renal failure, exfoliative toxin may disseminate and cause staphylococcal scalded skin syndrome

CHARACTERISTIC FEATURES OF BULLOUS AND NON-BULLOUS IMPETIGO

Non-bullous impetigo

Bullous impetigo

Epidemiology

· 70% of all cases of impetigo

· Children most often affected

· Less common

· Often occurs in the neonatal period, but children also affected

Clinical lesions

· Early: single 2–4 mm erythematous macule that rapidly evolves into a short-lived vesicle or pustule

· Late: superficial erosion with a typical “honey-colored” yellow crust and rapid direct extension of infection to surrounding skin

· Early: small vesicles enlarge into 1–2 cm superficial bullae

· Late: flaccid, transparent bullae measuring up to 5 cm in diameter; after rupture there is a collarette of scale, but no thick crust; usually little surrounding erythema

Distribution

· Face (around the nose and mouth) and extremities

· Face, trunk, buttocks, perineum, axillae, and extremities

Associated findings

· Mild lymphadenopathy may be present

· Usually no systemic symptoms but can be associated with weakness, fever, and diarrhea

Clinical course

· Usually a benign, self-limited process

· Usually resolves within 2 weeks without scarring if untreated

· Usually resolves in 3–6 weeks without scarring if not treated

Complications

· In 5% of cases, non-bullous impetigo caused by Str. pyogenes (M protein types 1, 4, 12, 49, 55, 57, 60) results in acute post-streptococcal glomerulonephritis (APSG)^*

· Risk of APSG is not altered by treatment with antibiotics

· Impetigo has not been linked to a risk of rheumatic fever

· In infants/young children and adults with immunodeficiency or renal failure, exfoliative toxin may disseminate and cause staphylococcal scalded skin syndrome

* Associated with anti-DNase B and antistreptolysin O (ASO) antibodies.

Initially tiny, pinhead sized, tense, clear vesicles develop on erythematous background which evolves to non-bullous or Bullous impetigo.

In non-bullous impetigo, the initial vesicles rapidly become pustules which rupture so rapidly that it is seldom seen as such. The resulting erosion develops with marked exudation of pus that dries to form typical “honey-colored” thick crusted plaque with surrounding erythema that can enlarge to greater than 2 cm in diameter without central healing. The crusts eventually dry and separate to leave erythema, which fades without scarring within 2 weeks. In severe cases, there may be regional lymphadenitis with fever. The face, especially around the nose and mouth, and the limbs are the sites most commonly affected.

Bullous impetigo is characterized by the rapid progression of vesicles to flaccid bullae, which arise on areas of grossly normal skin and become much larger; a diameter of 2 cm is common. The contents are at first clear, later cloudy. As the bullae are superficial, they rupture and collapse within 2 to 3 days, forming shallow moist erosion that gives a more varnish-like appearance with collarette of scale, but no thick crust; but at times can form thin, brownish crusts. Central healing and peripheral extension may give rise to circinate lesions. Usually resolves in 3–6 weeks without scarring if not treated.

Distribution: more common in intertriginous sites.

While initially, only a few, small, asymmetrically scattered lesions are present, these rapidly coalesce. Patients tend to spread the infection with their hands, inoculating new spots as they scratch, and through the use of washcloths. The paranasal location may be explained by carriage of the bacteria in the nose and their spread through nasal discharge and sneezing.

Complications

In infants/young children and adults with immunodeficiency, exfoliative toxin may disseminate and cause staphylococcal scalded skin syndrome.

In 5% of cases, non-bullous impetigo that is caused by S. pyogenes (serotypes 1, 4, 12, 25 and 49) results in acute post-streptococcal glomerulonephritis (APSG). The latent period for development of nephritis after streptococcal pyoderma is 18–21 days. Post-streptococcal nephritis is a significant risk factor for chronic renal disease in later life.

Pathology

In non-bullous impetigo, small neutrophilic subcorneal pustules are present within the epidermis. Spongiosis frequently underlies the pustule. The upper dermis contains an intense infiltrate of neutrophils and lymphocytes. Gram-positive cocci are present within the pustules.

In bullous impetigo, there is cleavage of the upper epidermis, typically within the granular layer. Acantholysis mimicking pemphigus foliaceus may be observed. Relatively few inflammatory cells are present within the blister cavity, and a neutrophilic infiltrate is often found in the upper dermis. Gram-positive cocci may be evident.

Diagnosis

The diagnosis of impetigo is usually made clinically; exudate from beneath the crust or fluid from intact bullae can be sent for culture to confirm the diagnosis and determine susceptibility to antibiotics. Leukocytosis is seen in approximately half of patients with impetigo and regional lymphadenopathy is common.

Treatment

For healthy patients with a few superficial lesions and no systemic symptoms, topical mupirocin, retapamulin, or fusidic acid are used are often equally (if not more) effective than oral antibiotics. However, S. aureus can develop resistance to each of these agents. Treatment should also include washing the affected skin daily with disinfectants such as chlorhexidine, povidone–iodine or sodium hypochlorite and removing crusts, which can be facilitated by wet dressings. If a thick crust is present remove it by applying olive oil for 15-20 minutes. This will soften it so that it can be wiped off. Once the crust has been removed, apply topical antibiotic twice daily for 7–10 days. All close contacts and the patient should wash their hands with antibacterial soap to reduce onwards transmission.

If the impetigo is extensive, if there is a marked bullous component to the clinical picture or there is palpable lymphadenopathy then in addition give systemic antibiotics for 1 week. The choice of antibiotic will depend on local resistance patterns and any known antibiotic hypersensitivities of the patient. First line antibiotics include flucloxacillin (dicloxacillin), cephalexin, co‐amoxiclav, cloxacillin and clindamycin. Second line antibiotics include macrolides such as erythromycin and clarithromycin (macrolide resistance can be quite high) and co‐trimoxazole. Third line antibiotics include trimethoprim and tetracyclines. The risk of developing post-streptococcal glomerulonephritis following streptococcal impetigo is not affected by treatment and is greater with certain subtypes of Str. pyogenes. In contrast to pharyngitis, a link between streptococcal pyoderma and acute rheumatic fever has not been established. In patients with recurrent staphylococcal impetigo “decolonizing” the nares and skin should be done.

Ecthyma

Ecthyma is a deep form of untreated (neglected) non-bullous impetigo. Rather than spreading in the epidermis, the infection extends more deeply, penetrating the full thickness epidermis into the dermis producing a dirty ulcer with an adherent crust. It can be caused by a primary infection with Str. pyogenes or streptococcal super infection of a pre-existing ulceration or excoriated insect bite. Outbreaks of ecthyma have occurred among infantry units where skin trauma, poor hygiene, and crowded living conditions facilitate disease spread.

Clinical features

An initial vesiculo-pustule on an erythematous base is soon surmounted by a hard crust of dried exudates, which increases in size by peripheral accretion. The crust is removed with difficulty, to reveal a “punched-out” ulcer with a purulent base. The margin of the ulcer is indurated, raised, and a red edematous areola is often present. Healing occurs after about 4 weeks with scarring. Fewer than 10 lesions are typically seen, nearly always of the shins or dorsal feet of children, but new lesions may develop by autoinoculation.

CLINICAL FEATURES OF ECTHYMA
Clinical findings	• · Fewer than 10 lesions are typically seen, most commonly on the lower extremities · An initial vesiculopustule enlarges (0.5–3 cm in diameter) over the course of several days, and develops a hemorrhagic crust · The ulcer has a “punched-out” appearance and a purulent, necrotic base · Lesions are slow to heal and produce scarring
Risk factors	· Young age (children), lymphedematous limbs, poor hygiene, neglect (including the elderly), immunosuppression, scratching (e.g. of insect bites), trauma
Complications	· Lesions are often contaminated with staphylococci · Systemic symptoms and bacteremia are rarely seen · Cellulitis and osteomyelitis are extremely infrequent
Diagnosis	• · Clinical appearance · Culture of moist, purulent base; skin biopsy with deep-tissue Gram stain and culture occasionally required

This deeper form of non-bullous impetigo is due to a group A streptococcal infection.

Treatment

Improved hygiene and nutrition, and treatment of any other underlying diseases are important. The antibiotic chosen should be active against Streptococcus pyogenes, and Staphylococcus aureus. Necrotic infected adherent crust should be gently removed after soaking with a disinfectant and softening with an oily cream. Topical antibiotics such as fusidic acid and mupirocin can be applied twice daily to localized lesions. Oral antibiotics same as impetigo may be required for 1–2 weeks in the context of multiple lesions or immunocompromised vulnerable patients.

Bacterial folliculitis

Introduction

Folliculitis is defined histologically as the presence of inflammatory cells, within the wall and ostia of the hair follicle, creating a follicular-based pustule. The inflammation can be either limited to the superficial aspect of the follicle with primary involvement of the infundibulum or the inflammation can affect both the superficial and deep aspect of the follicle. Deep folliculitis can eventuate from chronic lesions of superficial folliculitis and this may ultimately result in scarring.

Epidemiology and pathogenesis

Folliculitis, furuncles, and carbuncles represent a continuum of severity of S. aureus infection.

Portal of entry: hair follicle, break in the integrity of skin.

Predisposing factors for staphylococcal folliculitis include occlusion, maceration and hyper hydration of the skin; shaving, plucking or waxing hair; use of strong topical corticosteroids; hot and humid weather; atopic dermatitis; and diabetes mellitus.

Clinical features

The appearance depends on the depth of follicular involvement.

Superficial folliculitis

(Bockhart’s impetigo) presents with multiple small, fragile, dome-shaped yellow pustules or crusted papules on an erythematous base occurs at the infundibulum (ostium or opening) of a hair follicle that are pierced by a central hair, although the hair may not always be visualized, often on the scalps of children and in the beard area, axillae, buttocks and limbs of adults. The lesions are frequently clustered and heal within 7–10 days without scarring.

Chronic folliculitis of the legs, caused by S. aureus, mainly affects young adult male farmers who work in wet soil condition. There is profuse eruption of superficial and deep follicular pustules on the thighs and lower legs that persists for many years and is resistant to treatment.

Deep Folliculitis

When the inflammation involving the entire length of the follicle along with the adjacent dermis, a focal follicular-centered dermal abscess results. When the condition occurs on the beard areas of the face, it is referred to as sycosis barbae, but if it occurs elsewhere, it is referred to as a furuncle or boil. A confluence of several furuncles results in a carbuncle.

Sycosis barbae

Definition

It is a subacute or chronic deep folliculitis involving the whole depth of the follicle and usually refers to disease in the beard area, sycosis barbae.

If the follicles are destroyed with clinically evident scaring then the term lupoid sycosis is applied. Folliculitis decalvans is essentially the same process involving the scalp. Many sites may be involved in the same individual.

Etiology

Commonly involves the follicles of the beard; most cases begin in the third or fourth decade. The infecting organism is Staph. aureus, the same phage type of which can be isolated from nose.

Pathology

In the early stage, one observes a perifollicular infiltrate largely composed of neutophils. The infiltrate develops into perifollicular abscess leading to destruction of hair follicles. Older lesions show perifollicular chronic granulomatous infiltrate (lymphocyte, plasma cells, histocytes and foreign body giant cells). The sebaceous gland, or the whole follicle, may be destroyed and replaced by scar tissue.

Clinical features

The essential lesion is an edematous, red, follicular papule and pustule, centered on a hair. The individual papules and pustules remain discrete, but at time they coalesce, to produce a raised plaque studded with pustules and crusts, which suggest the appearance of a ripe fig, which coined the term sycosis. The hairs are retained and there is no evident scarring.

In lupoid sycosis, the follicles are destroyed by scaring, and active papules and pustules fringe the advancing margin around a pink central atrophic scar, granulomatous inflammatory changes may give the papules a lupoid appearance.