P. aeruginosa folliculitis is commonly associated with exposure to swimming pools, saunas, and hot tubs. Approximately 60% of pools and hot tubs may harbor this bacterium.6 Clinically, it is characterized by erythematous follicular papules and pustules that develop between 8h and 5 days (mean, 48h) after exposure to contaminated water7 (Fig. 1). It is often associated with pruritus and variable pain. Lesions typically appear in areas covered by swimwear, sparing the face and neck, as well as other occluded and apocrine-rich regions.1 This condition is generally self-limited, with spontaneous resolution within 7–14 days.3,8 In prolonged cases, cultures may be obtained, and treatment may include 2% acetic acid baths or topical therapies such as polymyxin B, tobramycin, gentamicin 0.1%, neomycin, benzoyl peroxide 5%–10%, chlorhexidine 0.5%–1%, or similar agents. In generalized or recurrent cases, oral fluoroquinolones such as ciprofloxacin may be prescribed.3,7,9

Fig. 1.

Pseudomonas aeruginosa folliculitis. Multiple monomorphic pustules with an erythematous base, intensely pruritic, located on the trunk and gluteal region, with marked clustering in the swimsuit area.

Green nail syndrome is a superficial nail infection characterized by green or blue-green discoloration of the nail plate10 (Fig. 2). Chronic proximal paronychia and distal-lateral onycholysis may also be present.10 Predisposing factors include frequent and prolonged water exposure, excessive detergent use, nail trauma, fungal coinfection, immunosuppression, nail psoriasis, and diabetes mellitus, among others.10 Diagnosis is clinical and confirmed by culture. Coinfection with dermatophytes is common, and fungal infection may facilitate P. aeruginosa colonization and overgrowth. Additionally, due to its fungistatic and/or fungicidal properties, P. aeruginosa may hinder fungal isolation in cultures.10,11 Management includes avoiding predisposing factors (moisture), trimming the nail, and topical application of 2% sodium hypochlorite, acetic acid, tobramycin, or gentamicin to the nail plate and cuticles for 1–4 months.3,12 Oral ciprofloxacin 500mg every 12h for 10 days may also be used.10,11

Fig. 2.

Green nail syndrome. Dark green discoloration involving the entire nail plate.

Superficial cutaneous infections include green foot syndrome (Fig. 3), intertrigo, ulcers, and hot foot syndrome, among others.13 These conditions are characterized by greenish discoloration, a sweet “grape juice-like” odor, and macerated or moth-eaten-appearing borders.3,14 They primarily affect moist areas such as interdigital spaces of the hands (Fig. 4) and feet, as well as intertriginous regions. Coinfection with dermatophytes and other bacteria is common.3,15,16 Diagnosis is based on microbiologic culture. Management includes debridement of macerated skin and the use of systemic antipseudomonal antibiotics combined with topical treatments.17,18

Fig. 3.

Pseudomonas aeruginosa infection of the feet (intertrigo). (A) Rounded ulcers with macerated (“moth-eaten”) borders, intensely painful, located in the interdigital spaces of all toes on both feet. (B) Wood lamp examination showing intense green fluorescence at the borders.

Fig. 4.

Pseudomonas aeruginosa infection of the hands. Cutaneous maceration and multiple rounded (“moth-eaten”), highly painful ulcers on both hands, with a 1-month duration. The patient had prolonged daily exposure of the hands to water.

Hot hand–foot syndrome is characterized by painful erythematous or purpuric nodules measuring 1–2cm on the palms and/or soles.19 It primarily affects children and may be accompanied by fever, malaise, and nausea.19,20 Histopathologic examination reveals a perivascular and perieccrine neutrophilic infiltrate extending into the subcutaneous tissue, with microabscess formation.19 Diagnosis is clinical, with exclusion of viral infections and eccrine hidradenitis, which is distinguished by neutrophilic infiltration of eccrine sweat glands and is typically triggered by cold exposure and mechanical stress.21 This condition is self-limited, resolving within 7–14 days. In highly symptomatic cases or in immunocompromised patients, anti-inflammatory agents and topical or systemic antipseudomonal antibiotics may be indicated.12,20,21

Infection of the external auditory canal (EAC) caused by P. aeruginosa is relatively common in both children and adults. A recent study of patients with otitis externa and media found that P. aeruginosa was the second most frequent causative agent (24.4%).22 Otitis externa (OE) is characterized by otalgia, local erythema, and swelling of the EAC, sometimes accompanied by greenish purulent discharge.12 Diagnosis is clinical and confirmed by microbiologic culture. Treatment includes removal of debris and topical antibiotics that preferably also cover Staphylococcus aureus, such as tobramycin, ofloxacin, or ciprofloxacin combined with dexamethasone. Systemic antibiotics may be required in selected cases.3,23

Malignant otitis externa is a deep infection of the EAC that may lead to osteomyelitis, mastoiditis, facial nerve palsy, sepsis, sigmoid sinus thrombosis, and death. Major risk factors include immunosuppression, HIV infection, diabetes mellitus, and advanced age.24 It presents as a rapidly progressive condition with severe otalgia, persistent otorrhea, auricular swelling, lymphadenopathy, and granulation tissue formation.25 Diagnosis is based on imaging studies and positive cultures.26 Management is multidisciplinary and requires hospitalization and intravenous empirical antibiotics.27 Surgical debridement is indicated in cases of necrosis.12

Perichondritis is a rare complication involving the auricular cartilage. It presents with edema, erythema, and pain of the auricle and may progress to localized abscess formation with risk of necrosis. Predisposing factors include local trauma, piercings, burns, surgical procedures, and immunosuppression.28 Diagnosis is clinical, and management includes systemic antibiotics and surgical debridement when necessary.29

These lesions are usually due to P. aeruginosa bacteremia, particularly in immunocompromised patients,30,31 although they may also occur in immunocompetent individuals.32,33 Diagnosis is confirmed by biopsy showing a neutrophilic infiltrate with lobular panniculitis32 and by microbiologic cultures of subcutaneous tissue. Treatment requires systemic antipseudomonal antibiotics.

Ecthyma gangrenosum (EG) is a severe infection classically described in immunosuppressed patients with bacteremia.34 Neutropenia is the main risk and prognostic factor,35 followed by lymphoproliferative disorders, malnutrition, diabetes mellitus, and extensive burns.36 Up to 74% of EG cases are caused by P. aeruginosa.37 A recent review showed that only 59% of patients presented with sepsis and that the classic triad of P. aeruginosa infection, sepsis, and immunosuppression was observed in only 19% of cases.37 In children, a recent retrospective study (n=17) found that most affected patients were immunosuppressed (14/17), with acute lymphoblastic leukemia being the most common cause; P. aeruginosa was isolated in 55%.38 EG initially presents as asymptomatic erythematous macules, most commonly in the anogenital region or extremities, which rapidly progress to painful vesicles and necrotic ulcers39 (Fig. 5). The most frequently affected areas are the gluteal/perineal region (57%), extremities (30%), trunk (6%), and face (6%).39 It is classically associated with fever, hypotension, and altered mental status.35,37 Histologically, a necrotizing hemorrhagic vasculitis with gram-negative bacilli in the medial and adventitial layers of deep vessels is observed.3 Diagnosis is based on clinical findings, local cultures, and blood cultures.3 Prompt treatment is essential, as mortality ranges from 10% to 70%.38 Some authors recommend combination IV antibiotic therapy with aminoglycosides (amikacin, gentamicin, tobramycin) and antipseudomonal penicillins (piperacillin–tazobactam, cefepime, ceftazidime, meropenem), along with surgical intervention when indicated.39,40

Fig. 5.

Ecthyma gangrenosum. Necrotic ulcers with an erythematous halo on the leg of an immunosuppressed patient.

P. aeruginosa is one of the main etiologic agents of superinfection in ulcers and burns.41,42 Antibiotic multidrug resistance has increased in recent years.43 Major risk factors include prolonged hospitalization, use of broad-spectrum antibiotics, prior P. aeruginosa infections within the unit, and extensive burn surface area.44 Diagnosis relies on high clinical suspicion, with greenish or yellowish discoloration serving as suggestive clues.12 Management includes debridement of necrotic tissue and systemic and/or topical antipseudomonal antibiotics.45,46

Necrotizing infections caused by P. aeruginosa are rare but associated with high mortality rates (≈30%) and may occur as part of polymicrobial infections.46 Risk factors include alcoholism, immunosuppression, and diabetes mellitus, among others.12 Clinically, they resemble other necrotizing infections, with necrotic areas, severe pain, and systemic symptoms. Management must be multidisciplinary and includes prompt surgical debridement and broad-spectrum combination intravenous antibiotic therapy.3,12