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Approach to the patient with pustular skin lesions

Approach to the patient with pustular skin lesions
Literature review current through: Jan 2024.
This topic last updated: Nov 09, 2023.

INTRODUCTION — Pustules are skin lesions formed by a collection of leukocytes (predominantly neutrophils) within the epidermis or superficial dermis. Pustular skin lesions can be infectious or inflammatory and should be differentiated from vesicular eruptions. A thorough history, examination of the distribution, and evolution of pustules on the skin provide clues to generate a differential diagnosis. Targeted testing (eg, skin biopsy, microscopic examination, microbiologic testing) can help confirm the diagnosis.

The diagnosis and differential diagnosis of pustular skin disorders in adults and adolescents will be reviewed here. Pustular lesions in newborns and infants are discussed separately. (See "Vesicular, pustular, and bullous lesions in the newborn and infant".)

DIAGNOSTIC APPROACH

Patient history and clinical examination — A thorough history should be obtained for every patient presenting with pustular skin lesions. Emphasis should be placed on the timing of lesion onset and progression, prior skin conditions, possible infectious exposures, new medications, and recent procedures.

The clinical examination should assess a localized or generalized distribution pattern of pustules and evaluate for systemic symptoms (eg, fever, generalized lymphadenopathy, fatigue, and arthritis).

Skin swabs for suspected infectious pustules — Infection should be excluded in all patients with pustules [1,2]. Infectious pustules may develop as the result of bacterial, viral, or fungal agents. The initial infectious process may be primarily a skin infection (typically localized to one or a few areas) or systemic (lesions typically diffusely distributed).

In the patient with suspected infectious pustular lesions, unroof the pustule with a #10 scalpel or gauge 26 needle and collect a swab for:

Gram stain and bacterial culture – Gram stain can provide an easy clue to the diagnosis of bacterial infection. A bacterial culture should be performed to confirm the diagnosis. (See "Office-based dermatologic diagnostic procedures", section on 'Gram stain'.)

Potassium hydroxide preparation – A potassium hydroxide (KOH) preparation can confirm a fungal etiology. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

Tzanck smear – A Tzanck smear can identify viral pustules (herpes simplex virus [HSV] or varicella-zoster virus [VZV]). (See "Office-based dermatologic diagnostic procedures", section on 'Tzanck smear'.)

Scabies preparation – Scabies can be excluded via a mineral oil scabies preparation in the right clinical context. (See "Office-based dermatologic diagnostic procedures", section on 'Scabies preparation'.)

'Sterile' pustules — On skin swab, inflammatory pustules will exhibit only inflammatory cells and neutrophils. These are termed "sterile pustules" and help tailor the differential diagnosis away from infectious processes. Lesions may be localized to a single area, such as the face (suggesting acne, rosacea, or perioral dermatitis), or generalized (suggesting acute generalized exanthematous pustulosis [AGEP] or generalized pustular psoriasis).

A skin biopsy is the next diagnostic step for patients presenting with a generalized eruption of sterile pustules. Histopathologic examination may reveal inflammatory cells and additional dermal and epidermal changes that favor a specific diagnosis, while tissue cultures will fail to grow organisms.

DIFFERENTIAL DIAGNOSIS

Infectious pustules

Infectious folliculitis — Infectious folliculitis is a common, superficial infection of hair follicles that clinically manifests with pinpoint pustules centered around hair follicles (picture 1A-B) [3]. The initiating event is often a physical or chemical injury to the skin, including:

Shaving, plucking, or waxing hair

Friction from tight garments

Applying medications to the skin

Occupational contact with oils

Using hot tubs

Infectious folliculitis can be bacterial, viral, or fungal [4-6]. It can develop anywhere on the body except the palms and soles.

Bacterial folliculitis (picture 1A, 1C-D) can be identified by Gram stain and culture of a superficial pustule. The most common causative bacterial organisms include Staphylococcus aureus and Pseudomonas aeruginosa ("hot tub folliculitis") [7,8]. (See "Infectious folliculitis", section on 'Bacterial folliculitis' and "Approach to Gram stain and culture results in the microbiology laboratory".)

Fungal folliculitis (eg, Pityrosporum folliculitis) often presents with pruritic pustules on the face and upper body (picture 2). Fungal spores can be identified within the follicular lumen by potassium hydroxide (KOH) preparation [6]. Most patients with Pityrosporum folliculitis report worsening with heat or humidity [9]. (See "Infectious folliculitis", section on 'Fungal folliculitis'.)

Viral folliculitis (eg, herpetic folliculitis) is rare, occurring predominantly in patients who are immunocompromised. Diagnosis may require polymerase chain reaction (PCR) assay or viral culture. (See "Infectious folliculitis", section on 'Viral folliculitis' and "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection", section on 'Tests to confirm the diagnosis'.)

Dermatophyte infection — Dermatophyte infections are superficial fungal infections primarily caused by species derived from the genera Microsporum, Trichophyton, and Epidermophyton. Cutaneous manifestations include red, annular, scaly patches and plaques, often studded with pustules, that occur on any area of the scalp or body (picture 3).

Microscopic examination of skin scrapings in a 10% or 20% KOH solution showing long, septate, branching hyphae (picture 4) confirms the diagnosis [1].

Scabies — Scabies infections of the skin may present with pustules, papules, nodules, or vesicles (picture 5). Lesions are characteristically distributed to the volar wrists, elbows, axillae, umbilicus, genitals, breasts, and interdigital web spaces [2]. (See "Scabies: Epidemiology, clinical features, and diagnosis".)

A mineral oil preparation can be completed in the clinic by scraping the base of a pustule with a scalpel and spreading the scrapings onto a slide, which can reveal eggs, mites, or scabietic feces (picture 6) [2]. Dermoscopic examination shows a dark, triangular shape that represents the head of the mite within a burrow ("delta wing" sign) (picture 7A-B).

Herpes simplex — Herpes simplex virus (HSV) infection may present with grouped pustules on an erythematous base, characteristically on the orolabial (picture 8) or genital mucosa [1]. HSV may also present with localized clusters of pustules on the perianal, perineal, or genital skin. Patients with altered innate and adaptive immunity are at higher risk for HSV infections [10]. Herpes virus establishes latency in neurons and can cause primary disease as well as reactivation.

The diagnosis of HSV infection can be established by unroofing a vesicle and performing a Tzanck smear. However, because Tzanck smears cannot distinguish HSV from varicella-zoster virus (VZV), a PCR test should also be performed for accurate diagnosis. (See "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection", section on 'Tests to confirm the diagnosis'.)

Varicella — VZV causes primary varicella (chickenpox) and herpes zoster (shingles). Lesions of primary varicella may include disseminated pustules or vesicles in varying stages of evolution (picture 9A-C). Zoster presents with grouped pustules or vesicles extending along a dermatome and is often preceded by acute neuralgia (picture 10A-B). (See "Clinical features of varicella-zoster virus infection: Chickenpox" and "Epidemiology, clinical manifestations, and diagnosis of herpes zoster".)

Unroofing a pustule or vesicle and completing a Tzanck smear will reveal acantholysis, multinucleate keratinocytes, keratinocyte ballooning, and nuclear margination [1]. This test is the most sensitive and specific when performed on early lesions. A PCR test should be performed to confirm the diagnosis of VZV infection [1]. (See "Diagnosis of varicella-zoster virus infection".)

Disseminated gonococcal infection — Bacteremic spread of Neisseria gonorrhea can lead to systemic manifestations, including the tenosynovitis-dermatitis syndrome (triad of dermatitis, tenosynovitis, and polyarthralgias without purulent arthritis) and purulent arthritis syndrome without associated skin lesions [11]. (See "Cutaneous manifestations of gonorrhea", section on 'Disseminated gonococcal infection'.)

The tenosynovitis-dermatitis syndrome presents with polyarthralgias, tenosynovitis, and purpuric pustules on the distal extremities (picture 11A-B). The cutaneous lesions are thought to be the result of bacterial embolization and microabscess formation [12].

Urine or mucosal nucleic acid amplification test (NAAT) and blood cultures can help confirm the diagnosis. (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents", section on 'Diagnostic techniques'.)

Secondary syphilis — Secondary syphilis is the result of systemic dissemination of Treponema pallidum. Symptoms begin between 3 and 10 weeks following initial exposure with papulosquamous or pustular, generalized skin lesions [13]. Copper-colored papules on the palms and soles (picture 12), condylomata lata, and mucus patches in the mouth can also suggest the diagnosis. Central nervous system involvement during secondary syphilis should be considered, as it is often asymptomatic. Other common constitutional symptoms include headache, fatigue, malaise, lymphadenopathy, and hepatosplenomegaly. (See "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV".)

If performed, a biopsy of a cutaneous lesion shows variable features, including irregular acanthosis, necrotic keratinocytes, plasma cells, superficial neutrophils, and endothelial edema [14]. Diagnostic testing to confirm the diagnosis of syphilis is discussed in detail separately. (See "Syphilis: Screening and diagnostic testing".)

Mpox — Monkeypox virus is a deoxyribonucleic acid (DNA) virus that causes mpox (previously called monkeypox), a systemic illness characterized by vesicular and pustular skin lesions, mouth and throat ulcerations, fevers, myalgias, headache, respiratory distress, and lymphadenopathy [15]. Skin lesions develop early in the disease course and commonly affect the face and anogenital skin (picture 13) [16]. Skin lesions progress from umbilicated papules to pustules before crusting over [16]. Monkeypox virus transmission generally occurs via direct contact with skin lesions or bodily fluids, and symptoms typically last between two and four weeks [15]. (See "Epidemiology, clinical manifestations, and diagnosis of mpox (monkeypox)".)

A diagnosis of mpox can be made with PCR testing for orthopoxvirus DNA from the swab of a skin lesion. Serologic testing can be used to support the diagnosis if viral testing is not available.

If performed, a biopsy of a skin lesion may reveal epidermal necrosis, ballooning keratinocytes with basophilic "halo," eosinophilic intracytoplasmic inclusions (Guarnieri bodies), multinucleated giant cells, and a mixed inflammatory infiltrate with neutrophil exocytosis [17].

Inflammatory pustules

Localized

Acne vulgaris — Acne vulgaris presents with papules and pustules on the face, chest, and back (picture 14A-B). Open and closed comedones can provide additional support for this clinical diagnosis. Acne is a chronic inflammatory condition of the pilosebaceous unit triggered by bacterial colonization with Cutibacterium acnes, abnormal keratin turnover, increased sebum, and subsequent inflammation [18]. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris".)

Acneiform eruptions — Acneiform eruptions localized to the face may be seen in rosacea (picture 15A-B) or perioral dermatitis (picture 16A-D). (See 'Rosacea' below and 'Perioral (periorificial) dermatitis' below.)

Frequently, acneiform eruptions represent adverse reactions to drugs, including:

Corticosteroids – Generalized acneiform eruptions can be associated with systemic and topical corticosteroids and typically present with numerous monomorphic pustules on the face and back (picture 17A-B).

Targeted anticancer drugs – Acneiform eruptions are predominantly associated with epidermal growth factor receptor (EGFR) inhibitors, human epidermal growth factor receptor 2 (HER2) inhibitors, mitogen-activated protein kinase kinase (MEK) inhibitors, and mammalian target of rapamycin (mTOR) inhibitors [19]. Eruptions from targeted molecular anticancer drugs exhibit numerous pustules and papules without comedones that are accompanied by burning, pruritus, or xerosis (picture 18A-B) [19]. (See "Acneiform eruption secondary to epidermal growth factor receptor (EGFR) and MEK inhibitors".)

Other medications – Other medications that cause acneiform eruptions include antipsychotic drugs, antituberculosis drugs, vitamin B supplements, antifungals, hydroxychloroquine, naproxen, and mercury [20-23].

'Sterile folliculitis' — Folliculitis from physical or chemical irritants can present with sterile pustules (see 'Infectious folliculitis' above). These may develop in a localized or generalized fashion and may occur on any skin areas with hair follicles. Sterile, inflammatory folliculitis is a diagnosis of exclusion, and infectious folliculitis should be excluded first.

Rosacea — Rosacea is a chronic inflammatory dermatosis that may present with pustules and inflammatory papules on the face and neck (picture 15A-B). Recurrent episodes of flushing and erythema resulting in persistent facial redness, telangiectasias, and phymatous change are described. Exposure to temperature changes, alcohol, hot food or beverages, and spicy food are often reported as triggers. A subset of patients have ocular involvement, including photophobia, dryness, conjunctivitis, or blepharitis [24]. (See "Rosacea: Pathogenesis, clinical features, and diagnosis".)

Perioral (periorificial) dermatitis — Perioral (periorificial) dermatitis presents with papules and pustules distributed around facial orifices, often accompanied by erythema and scaling (picture 16A-E). Patients frequently report irritation, burning, and pruritus. Perioral dermatitis predominantly affects young females but can affect patients of any age or sex. There is often sparing of the skin immediately surrounding the vermilion border of the lips (picture 16E) [25,26]. Perioral dermatitis is thought to be triggered by topical irritants, such as skin care products, dental hygiene products, or topical corticosteroids. A KOH preparation can help exclude Candida, which may contribute to the lesions. (See "Perioral (periorificial) dermatitis".)

Miliaria — Eccrine miliaria is colloquially known as "heat rash" or "prickly heat" and occurs from occluded sweat glands and ducts. There are three types of miliaria: crystallina, rubra, and profunda. (See "Miliaria".)

Miliaria crystallina commonly affects neonates and presents with 1 to 2 mm superficial vesicles filled with sweat (picture 19A-C), which correlates with intra- or subcorneal neutrophilic vesicles on histopathology.

In miliaria rubra, the occlusion of the eccrine gland is deeper, resulting in inflammatory papules and pustules (miliaria pustulosa) that are not centered on hair follicles (picture 20A-D). Histology of miliaria rubra exhibits parakeratosis and epidermal spongiosis overlying eccrine glands.

Miliaria profunda results from deeper occlusion of eccrine glands at the dermal-epidermal junction and presents clinically with firm, skin-colored nodules (picture 21). Dermoscopy can provide a helpful clue to this diagnosis by revealing large, white globules with dark halos [27]. A punch biopsy will confirm the diagnosis.

Diffuse

Eosinophilic pustular folliculitis — Eosinophilic pustular folliculitis (EPF) is a chronic recurrent sterile folliculitis of unknown etiology characterized by a papulopustular eruption that predominantly affects seborrheic areas, including the face, chest, upper back, and arms. There are several variants of EPF, including:

The classic form of EPF (Ofuji disease) occurs in otherwise healthy young adults and is predominantly reported in East Asian populations [28,29].

EPF of infancy. (See "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Eosinophilic pustular folliculitis of infancy'.)

Immunosuppression-associated EPF, including:

Human immunodeficiency virus (HIV)-associated eosinophilic folliculitis, classified as an acquired immunodeficiency syndrome (AIDS)-defining illness in patients with HIV infection. It is characterized by 2 to 3 mm pruritic papules and pustules often accompanied by excoriations (picture 22A-B). (See "HIV-associated eosinophilic folliculitis".)

EPF associated with hematologic malignancies [30,31].

Bone marrow- or solid organ transplantation-associated EPF [32,33].

Drug induced – Rare cases of EPF have been associated with drugs [34-36].

The diagnosis of EPF can be challenging. A biopsy is required to confirm the diagnosis. Histology shows a heavy infiltration of the outer root sheath and sebaceous gland of eosinophils, with scattered mononuclear cells and neutrophils.

Acute generalized exanthematous pustulosis — Acute generalized exanthematous pustulosis (AGEP) is a severe cutaneous drug reaction with systemic symptoms. The most common causative agents include beta-lactam antibiotics, other antimicrobials, anticonvulsants, calcium channel blockers, and intravenous contrast media [37]. The median time from medication initiation to AGEP onset is three days but may be as short as 24 hours. (See "Acute generalized exanthematous pustulosis (AGEP)".)

Patients present with a generalized eruption of 1 to 2 mm pustules on an erythematous base, often accompanied by fever, leukocytosis with neutrophilia, and mild eosinophilia; liver or renal complications are uncommon but may occur [37]. The eruption often begins in flexural areas, evolves quickly to involve the trunk and extremities (picture 23A-C), and resolves with desquamation [37]. A biopsy revealing neutrophils in the stratum corneum and epidermis confirms the diagnosis.

Pustular psoriasis — Pustular psoriasis is characterized by psoriasiform papules and plaques, often studded with pustules. Patients may report pre-existing psoriasis. Reported triggers for pustular psoriasis may include infections, pregnancy, medications, stress, and withdrawal of systemic steroids [38]. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis" and "Dermatoses of pregnancy", section on 'Pustular psoriasis of pregnancy'.)

Pustular psoriasis frequently affects the palms and soles (picture 24A-B) and is called acrodermatitis continua of Hallopeau when pustules involve the fingers, toes, and nails (picture 25A-B). Annular generalized pustular psoriasis presents with annular lesions with peripheral pustules (picture 26). Generalized (von Zumbusch type) pustular psoriasis (picture 27A-B) may develop rapidly and is often accompanied by systemic symptoms, including arthritis, ocular inflammation, elevated inflammatory markers, neutrophilia, hypocalcemia, and elevated liver enzymes [38]. As the pustules evolve, they may form brown or yellow scale or crust at sites of prior involvement [38].

Pyoderma gangrenosum — Pyoderma gangrenosum is a rare inflammatory skin disorder with an estimated prevalence of 5.8 patients per 100,000 adults in the United States [39]. More than one-half of pyoderma gangrenosum cases arise in association with an underlying systemic disease, most commonly inflammatory bowel disease, inflammatory arthritis, and hematologic disorders [39]. (See "Pyoderma gangrenosum: Pathogenesis, clinical features, and diagnosis".)

Pyoderma gangrenosum typically presents as a tender nodule or pustule that rapidly progresses to a painful ulcer with characteristic violaceous, inflammatory borders and an undermined or overhanging border of residual epidermis that may appear gray, dusky, or necrotic (picture 28A-B). The ulcerative subtype is the most common morphologic variant, although bullous, vegetative, pustular, and peristomal forms of pyoderma gangrenosum also exist. The development of new lesions after minor skin trauma (pathergy) occurs in 20 to 30 percent of patients [40].

The histopathology of pyoderma gangrenosum classically shows a pandermal infiltrate predominantly composed of neutrophils with associated dermal edema. Appropriate history and laboratory testing should be aimed at investigating a potential underlying systemic disease [41]. Tissue culture should be performed to rule out infection.

Sweet syndrome (acute febrile neutrophilic dermatosis) — Sweet syndrome (acute febrile neutrophilic dermatosis) is an inflammatory skin reaction accompanied by systemic symptoms. Cutaneous lesions are characterized by the abrupt onset of tender pustules, papulonodules, or bullae. Lesions predominantly involve the head, neck, and arms (picture 29A-B) [42]. Major diagnostic criteria include the abrupt onset of skin lesions and histopathologic evidence of a dense neutrophilic infiltrate without leukocytoclastic vasculitis [42]. Sweet syndrome is associated with malignancies, specifically hematologic malignancies, infections, autoimmune diseases, immune deficiency, and inflammatory bowel disease [42]. (See "Sweet syndrome (acute febrile neutrophilic dermatosis): Pathogenesis, clinical manifestations, and diagnosis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Rosacea (The Basics)")

SUMMARY AND RECOMMENDATIONS

Approach to the diagnosis – The approach to a patient with pustular lesions centers around a thorough history, clinical examination, and select laboratory tests. History should include lesion timing of onset and progression, prior skin infections or infestations (eg, herpes simplex virus [HSV], varicella-zoster virus [VZV], dermatophytosis, scabies), and possible new infectious exposures. A discussion of new medications or recent procedures may provide clues to the diagnosis. Infection should be excluded in all patients with pustules. (See 'Diagnostic approach' above.)

Infectious pustules – Infectious pustules may develop as the result of bacterial, viral, or fungal agents. Unroofing a pustule with a scalpel or needle and completing a Gram stain and bacterial culture can demonstrate an underlying bacterial etiology. A potassium hydroxide (KOH) preparation with fungal culture can confirm a fungal infection. A Tzanck smear can help identify HSV/VZV infections; however, polymerase chain reaction (PCR) testing is required for accurate diagnosis. Scabies can be excluded via a mineral oil scabies preparation in clinic. (See 'Skin swabs for suspected infectious pustules' above.)

Inflammatory pustules – Inflammatory pustules will exhibit only inflammatory cells and neutrophils on microscopic examination of skin swab. These are termed "sterile pustules" and help tailor the differential diagnosis away from infectious processes. A skin biopsy is often required for accurate diagnosis. Tissue cultures will fail to grow organisms. Histology will reveal inflammatory cells without evidence of infectious agents and additional dermal and epidermal changes that can provide clues to the correct diagnosis. (See 'Inflammatory pustules' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Beth G Goldstein, MD, and Adam O Goldstein, MD, MPH, who contributed to earlier versions of this topic review.

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References

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