Impetigo, folliculitis and skin abscess

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Impetigo is a contagious superficial epidermal infection caused by Staphylococcus aureus, group A Streptococcus or both. Non-bullous disease is most common; bullous disease reflects exfoliative staphylococcal toxin.

Folliculitis remains around the follicular opening, while furuncle and abscess extend deeper and collect pus. The practical distinction is source control: a drainable cavity is treated by incision rather than progressively broader antibiotics.

Treatment should be proportionate to extent, depth, systemic illness and transmission risk. Repeated topical antibiotic exposure selects resistance, so antiseptic treatment and short courses are deliberately preferred where appropriate.

Recurrent boils require a cause review: hidradenitis suppurativa, pilonidal disease, fistula, foreign material, diabetes, immune compromise, shared household transmission and staphylococcal carriage.

Key points

Non-bullous impetigo causes thin-walled vesicles or pustules that rupture into characteristic golden or honey-coloured crusts.
Bullous impetigo produces flaccid fluid-filled blisters from toxin-producing Staphylococcus aureus and usually needs oral treatment.
Folliculitis is a superficial pustule centred on a hair follicle; many limited cases improve with hygiene and removal of friction or occlusion.
A furuncle involves the deeper follicle, while a skin abscess is a tender fluctuant collection whose definitive treatment is incision and drainage.
For localised non-bullous impetigo, NICE first offers hydrogen peroxide 1% cream two or three times daily for five days when suitable.
If antiseptic is unsuitable, fusidic acid 2% three times daily for five days is a topical option; reserve mupirocin for suspected or confirmed fusidic-acid resistance.
For widespread non-bullous or bullous impetigo, flucloxacillin 500 mg four times daily for five days is NICE first-choice adult oral treatment.
Do not routinely combine topical and oral antibiotics for impetigo, and do not use antibiotics alone to treat a fluctuant abscess that needs drainage.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Impetigo pathogens

Staphylococcus aureus and group A Streptococcus infect disrupted superficial epidermis and spread readily through direct contact and scratching.

Follicular inoculation

Staphylococci enter follicles after shaving, friction and occlusion, while Pseudomonas follows contaminated warm-water exposure and yeast causes selected folliculitis.

Abscess-forming staphylococci

Staphylococcus aureus invades deeper follicular and dermal tissue, recruiting pus and forming a walled cavity, sometimes with community MRSA.

Barrier and host risk

Eczema, scabies, wounds, diabetes, immune compromise, crowding and close-contact sport increase bacterial entry, carriage and transmission.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Subcorneal toxin cleavage
Exfoliative staphylococcal toxins split desmoglein-mediated adhesion in superficial epidermis, producing flaccid bullae with little deep inflammation.
2
Superficial epidermal exudate
Bacterial replication and neutrophils form vesicles and pustules whose dried serum and debris create honey-coloured impetigo crust.
3
Follicular inflammation
Organisms and mechanical occlusion trigger a perifollicular neutrophilic response that remains superficial or extends into a painful furuncle.
4
Abscess encapsulation
Tissue necrosis and neutrophil debris liquefy into pus, while granulation tissue walls the collection off from antibiotic and immune penetration.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Non-bullous impetigo

Small vesicles or pustules rupture and leave adherent golden crusts, commonly around the nose, mouth and exposed extremities with minimal systemic illness.

Bullous impetigo

Flaccid superficial blisters enlarge and rupture to leave a varnish-like rim, reflecting local exfoliative-toxin production.

Follicular pustules

Small erythematous pustules each centred on a hair shaft support folliculitis from friction, shaving, occlusion or microbial overgrowth.

Drainable abscessRed flag

A tender fluctuant nodule with pointing, pus or an ultrasound-defined cavity indicates a collection needing incision and drainage.

Surrounding invasive diseaseRed flag

Spreading warmth, lymphangitis, fever, hypotension or disproportionate pain extends the problem beyond a simple superficial lesion.

Recurrent-site pattern

Repeated axillary, groin, inframammary or perineal nodules, tunnels and scars suggests hidradenitis rather than isolated bacterial boils.

Red flags requiring action

Pain out of proportion, bullae, anaesthesia, necrosis or crepitus suggests necrotising infection.
Painful eye movement, proptosis, ophthalmoplegia or visual change suggests orbital cellulitis.
Hypotension, confusion, tachypnoea or rapidly spreading erythema indicates invasive infection and possible sepsis.
A large, deep, recurrent or perineal abscess may reflect hidradenitis, fistula, foreign body or immune compromise.
Carbuncle, bacteraemia or persistent fever in diabetes or immune suppression lowers the threshold for admission.
Infants with widespread blistering or systemic illness require urgent paediatric assessment for staphylococcal toxin disease.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Full skin and anatomical examinationFirst step
Why
Define superficial versus deep disease, extent, drainable pus, lymphangitis and critical-site involvement.
Interpretation and limitations
Inspect under crust and around all lesions, palpate for fluctuance and examine eye, hand, perineum or joint function when nearby anatomy is threatened.
02
Swab of impetigo lesion
Why
Identify organism and resistance when disease recurs, worsens or fails initial treatment.
Interpretation and limitations
Routine sampling is unnecessary for a first typical episode; after cleaning crust, sample exudate and interpret carriage versus invasive clinical disease.
03
Deep pus culture
Why
Direct treatment after incision of a recurrent, severe, unusual or resistant-risk abscess.
Interpretation and limitations
Aspirated or operative pus is preferred to a superficial swab; drainage remains essential regardless of a later susceptible result.
04
Bedside ultrasound
Why
Distinguish cellulitis from an occult fluid collection and define depth before incision.
Interpretation and limitations
A discrete fluid cavity supports drainage; cobblestoning alone reflects oedema and does not prove bacterial cellulitis.
05
Blood cultures and systemic blood tests
Why
Assess bacteraemia, inflammation and organ dysfunction in fever, sepsis or immune compromise.
Interpretation and limitations
Routine blood tests are unnecessary for limited impetigo or folliculitis; systemic findings change setting and antimicrobial route.
06
Recurrence assessment
Why
Identify diabetes, immune compromise, hidradenitis, fistula, foreign body and household transmission.
Interpretation and limitations
Use glucose or HbA1c, HIV testing and imaging selectively from history and examination rather than applying a universal screening panel.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Herpes simplex

Grouped painful vesicles, recurrent same-site episodes and preceding prodromal tingling suggest cutaneous herpes viral infection rather than primary bacterial impetigo.

Eczema or contact dermatitis

Itch, scale, chronic distribution and exposure pattern may mimic impetigo, although scratching can add secondary bacterial crust.

Insect bites and scabies

Pruritic papules, puncta, burrows and affected contacts suggest infestation or arthropod reaction with possible secondary infection.

Hidradenitis suppurativa

Recurrent deep nodules, abscesses, draining tunnels and scars in characteristic flexural sites reflects chronic hidradenitis follicular inflammatory disease.

Ecthyma or necrotising infection

A deep punched-out ulcer or rapidly progressive severe pain with necrosis extends beyond uncomplicated superficial impetigo and requires urgent reassessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01LOCAL IMPETIGOUse antiseptic before antibioticFirst stepNon-bullous impetigo is localised and the patient is systemically well.

1Confirm the crusted superficial pattern and exclude herpes, eczema flare, ecthyma, cellulitis and bullous or widespread disease.
2Offer hydrogen peroxide 1% cream two or three times daily for five days when suitable and explain gentle crust cleansing and hand hygiene.
3If antiseptic is unsuitable, use fusidic acid 2% three times daily for five days, reserving mupirocin for fusidic-acid resistance risk.
4Review worsening or non-response and obtain a swab before changing treatment when feasible; do not add oral antibiotics routinely.

02WIDESPREADUse short oral therapyImpetigo is bullous, widespread or unsuitable for local treatment but there is no sepsis or deep infection.

1Assess transmission setting, immune status and systemic features and swab recurrent, outbreak-associated or treatment-resistant disease.
2AlternativeGive flucloxacillin 500 mg orally four times daily for five days when suitable, using a NICE allergy or pregnancy alternative when required.
3Do not simultaneously prescribe a topical antibiotic unless a specialist-supported separate indication exists.
4Give hygiene, laundry and exclusion advice and review promptly if blisters spread, fever develops or deeper skin becomes painful.

03ABSCESSIncise and drain pusExamination or ultrasound confirms a fluctuant skin abscess or carbuncle.

1Assess site, size, depth, neurovascular structures, analgesia and whether operating-theatre or specialist drainage is safer than bedside incision.
2Incise adequately, break loculations, drain and irrigate according to procedure practice and send pus culture for recurrent, severe or unusual disease.
3Use systemic antibiotics only when surrounding cellulitis, systemic illness, immune compromise, critical anatomy or local policy indicates them.
4AlternativeArrange packing or dressing review only as clinically necessary and reassess persistent pain or fever for inadequate drainage, deeper extension or an alternative diagnosis.

04RECURRENTFind the driver before decolonisingImpetigo or abscesses recur in the patient or household.

1Confirm the diagnosis and examine for hidradenitis, pilonidal sinus, eczema, tinea, foreign body, fistula and injection or shaving practices.
2Culture an active lesion and consider carriage-site sampling only through a local recurrent-staphylococcal pathway.
3Optimise skin care, wound covering, hand hygiene, laundry and non-sharing of towels and razors and treat relevant household cases.
4Use chlorhexidine and nasal decolonisation only after specialist or local-protocol selection, with a coordinated household plan when indicated.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

NICE first-choice topical antiseptic that avoids selecting resistance to a topical antibiotic.

Hydrogen peroxide 1% cream

Apply a thin layer two or three times daily for five days to localised non-bullous impetigo when the preparation is suitable.

Avoid contact with eyes and mucosa, stop for significant irritation and use another pathway for bullous, widespread, deep or systemically unwell disease.

Provides focused topical antistaphylococcal treatment for a small localised area under NICE guidance.

Fusidic acid 2% cream

Apply a thin layer three times daily for five days when localised non-bullous impetigo requires a topical antibiotic and antiseptic is unsuitable.

Avoid repeated or prolonged courses because resistance develops; obtain a swab for recurrence or failure and do not combine routinely with oral antibiotics.

NICE first-choice oral treatment for widespread or bullous disease targeting susceptible staphylococci and streptococci.

Flucloxacillin for impetigo

Give 500 mg orally four times daily for five days for widespread non-bullous or bullous impetigo in an adult.

Clarify immediate penicillin allergy, review liver disease and interactions and extend to seven days only after clinical review when response is inadequate.

NICE-listed oral alternative for widespread or bullous impetigo in a non-pregnant adult.

Clarithromycin allergy alternative

Give 250 mg to 500 mg orally twice daily for five days when penicillin allergy makes flucloxacillin unsuitable.

Review QT prolongation, liver disease and interactions including statins, warfarin and colchicine; use erythromycin when a macrolide is needed in pregnancy.

Treats surrounding or systemic infection when source control alone is insufficient for a drained abscess.

Abscess systemic antimicrobial

Use the local oral or intravenous skin-abscess regimen only after drainage, adjusted for cellulitis severity, MRSA risk, allergy, renal function and deep anatomy.

Do not substitute antibiotics for incision, obtain deep pus for recurrent or severe disease and narrow to culture while investigating unusual recurrence.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cellulitis and lymphangitis

Superficial infection can breach deeper dermis and spread with warmth, tenderness, proximal streaking and systemic illness.

Post-streptococcal glomerulonephritis

Nephritogenic streptococcal skin infection can trigger delayed immune-complex glomerular inflammation with haematuria, oedema, hypertension and acute kidney dysfunction.

Bacteraemia and metastatic infection

A deep staphylococcal abscess can seed the bloodstream, endocardium, bone and joints, especially during diabetes or clinically significant immune compromise.

Scarring and functional injury

Deep or poorly drained lesions near hand, eye or joint can destroy tissue and restrict movement or vision.

Household or institutional spread

Direct contact, shared towels and close living permit repeated impetigo and staphylococcal transmission without coordinated hygiene and case care.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review localised impetigo if it worsens or has not improved after the five-day course and reconsider diagnosis before repeating treatment.
Document number and distribution of lesions, new blistering, surrounding cellulitis, fever and household or institutional spread.
After abscess drainage review pain, cavity drainage, surrounding erythema, fever and function of nearby joint, hand or eye.
Check deep culture and resistance results and stop, narrow or change systemic treatment according to clinical need.
Monitor hepatic, renal, QT and interaction risks when systemic antibiotics are used in frailty or comorbidity.
For recurrent disease track sites, culture organisms, household cases and adherence to the selected cause-specific or decolonisation plan.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Crust colour is a useful clue

Golden adherent crust after superficial vesicle rupture supports non-bullous impetigo but eczema and herpes can become secondarily crusted.

Bullae imply toxin

Local exfoliative toxin splits superficial epidermis; systemic blistering and illness require assessment for staphylococcal scalded-skin syndrome.

Fluctuance changes the verb

Cellulitis is treated, but an abscess is drained; recognising a collection prevents ineffective antibiotic escalation.

Topical stewardship matters

Repeated fusidic acid exposure selects resistant staphylococci, so short restricted courses and antiseptic first use preserve activity.

Hot-tub folliculitis differs

Pseudomonas folliculitis after poorly chlorinated water often resolves with exposure avoidance and supportive care rather than routine antistaphylococcal therapy.

Recurrence may not be infection alone

Hidradenitis suppurativa produces tunnels and scarring that require dermatological disease control, not repeated incision and antibiotics alone.

11Common pitfallsFrequent interpretation and management errors.

01
Do not prescribe both topical and oral antibiotics routinely for impetigo.
02
Do not continue repeated fusidic acid courses without swabbing recurrent or failed disease.
03
Do not treat a fluctuant abscess with antibiotics alone when safe drainage is available.
04
Do not squeeze central facial lesions or overlook orbital symptoms near the eye.
05
Do not label recurrent axillary or groin nodules as simple boils without considering hidradenitis.
06
Do not use a positive carriage swab to justify indefinite decolonisation without a coordinated protocol.