Version May 2024
INTRODUCTION — Pseudomonas aeruginosa is one of the most commonly considered gram-negative aerobic bacilli in the differential diagnosis of gram-negative infections. Consideration of this organism is important because it causes severe and often fatal hospital-acquired infections, especially in immunocompromised hosts. Selection of antibiotic treatment for P. aeruginosa is complicated because it is often antibiotic resistant.
The clinical manifestations, diagnosis, and treatment of P. aeruginosa skin, soft tissue, and bone infections will be reviewed here.
The general principles of antimicrobial treatment of infections caused by P. aeruginosa, including antibiotic options and decisions on combination therapy, are discussed in detail elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections".)
The clinical manifestations and management of other P. aeruginosa infections and the epidemiology and pathogenesis of infection with this organism are also discussed separately.
●(See "Epidemiology, microbiology, and pathogenesis of Pseudomonas aeruginosa infection".)
●(See "Pseudomonas aeruginosa bacteremia and endocarditis".)
●(See "Pseudomonas aeruginosa pneumonia".)
CLINICAL SYNDROMES — P. aeruginosa can cause various specific clinical skin, soft tissue, and bone infections. Certain syndromes are classically or most commonly associated with P. aeruginosa, specifically. These include:
●Ecthyma gangrenosum
●Burn wound infections
●Folliculitis associated with hot tub exposures
●Foot infection following nail puncture injury
●Green nail syndrome
●Perichondritis following ear piercing or acupuncture
These are discussed in further detail below.
Additionally, P. aeruginosa can be involved in other general skin and soft tissue infections, such as cellulitis (particularly in neutropenic patients), postoperative infections, infections following trauma (particularly after injury in aquatic environments), and infections of chronic decubitus ulcers. P. aeruginosa osteomyelitis can result from direct invasion or hematogenous spread, especially in injection drug users. Inflammatory subcutaneous nodules (ie, panniculitis) due to P. aeruginosa in the absence of bacteremia or classic immunosuppression have been rarely reported [1]. Skull base osteomyelitis associated with malignant otitis externa is most commonly caused by P. aeruginosa and is discussed elsewhere. (See "Malignant (necrotizing) external otitis".)
As with other infections, P. aeruginosa soft tissue infections are often associated with worse outcomes than other pathogens. As an example, in a prospective study of 132 patients who received skin grafts for soft-tissue defects, P. aeruginosa was the most common etiologic microorganism in skin-graft loss due to infection (58 percent) [2]. Infections due to P. aeruginosa were more fulminant and were 4.2 times more likely to require reoperation that those caused by other organisms.
MANAGEMENT PRINCIPLES — In general, treatment of P. aeruginosa skin, soft tissue, and bone infections should include aggressive surgical debridement of any necrotic tissue and infected eschars, in addition to antibiotic therapy. Antibiotic options include beta-lactams, carbapenems, or fluoroquinolones that have antipseudomonal activity (table 1). In general, aminoglycosides should not be used as a single agent for infection at these sites.
Advanced beta-lactam beta-lactamase inhibitor combinations (such as ceftolozane-tazobactam, ceftazidime-avibactam) may also have a role in treating skin, soft tissue, and bone infections caused by multidrug-resistant and extensively drug-resistant P. aeruginosa infections if other agents are not feasible (eg, because of drug allergy) [3-5]. A recent study assessing the susceptibility of P. aeruginosa strains causing SSTIs that were isolated from 47 centers from various countries reported that 98.6 percent of strains were susceptible to ceftolozane-tazobactam, 98.3 percent were susceptible to ceftazidime-avibactam, and 98.3 percent were susceptible to imipenem-relebactam [6]. In fact, a recent systematic review showed that SSTIs caused by difficult-to-treat P. aeruginosa are the most common indication for off-label use of ceftolozane-tazobactam (37.7 percent) with a clinical success rate of 79.6 percent [7]. Additionally, most real-world experiences with ceftolozane-tazobactam have shown good clinical outcomes in the subset of patients with SSTIs due to P. aeruginosa [8,9]. Hence, novel antipseudomonal agents may soon be recommended as first-line therapy for difficult-to-treat P. aeruginosa SSTIs [10]. Although the fluoroquinolone delafloxacin has theoretical utility for polymicrobial soft tissue infections when coverage against both P. aeruginosa and methicillin-resistant Staphylococcus aureus (MRSA) is desired, we generally use other better established regimens pending further data on its use.
Specific antipseudomonal agents and doses are discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)
The usual duration of antimicrobial therapy for skin and soft tissue infection is 10 to 14 days; however, shorter courses may be acceptable if the clinical signs and symptoms of infection have resolved. Occasional patients will continue to have local signs of infection at the end of two weeks of treatment. We generally continue oral antibiotic therapy (if the isolate is susceptible) in these patients until resolution of all erythema has occurred. Routine bedside re-evaluation is essential and antimicrobial therapy should be reconsidered when other noninfectious causes are more likely and the Pseudomonas is felt to be a colonizer [11].
The usual duration of antimicrobial therapy for osteomyelitis is six weeks following surgical debridement. If the isolate is fluoroquinolone susceptible, therapy with oral ciprofloxacin (750 mg twice daily) can be used.
Specifics on the management of ecthyma gangrenosum, burn infections, folliculitis, infections following nail puncture, and green nail syndrome are discussed below.
ECTHYMA GANGRENOSUM — P. aeruginosa has been classically associated with a characteristic skin lesion called ecthyma gangrenosum (picture 1), which is most frequently described in the setting of bacteremia in immunocompromised patients. It results from perivascular bacterial invasion of the media and adventitia of arteries and veins with secondary ischemic necrosis. Ecthyma refers to an ulcerative lesion that extends through the epidermis and deep into the dermis and appears as a "punched-out" ulcer covered in crust surrounded by raised violaceous margins. Although ecthyma gangrenosum is not pathognomonic of P. aeruginosa infection, the presence of these lesions should immediately raise the high probability that P. aeruginosa is the causative organism. This is particularly important for critically ill patients who present with severe sepsis and require prompt antipseudomonal empiric antimicrobial therapy [12,13].
Epidemiology — Ecthyma gangrenosum is classically associated with P. aeruginosa sepsis and bacteremia in immunocompromised patients, including those with neutropenia or congenital immunodeficiencies (eg, Bruton agammaglobulinemia [14,15]) and those on immune modulating agents. It has been observed in approximately 1.3 to 3 percent of P. aeruginosa bacteremia cases [16]. In some cases, ecthyma has been described in patients who were subsequently discovered to have an immune deficit [17]. Furthermore, it has also been reported in healthy, immunocompetent patients without bacteremia or systemic infection. In such patients, ecthyma gangrenosum can present as localized skin lesions [16].
Lesions may occur after breakdown of mechanical defense barriers and local infection [18]. Diabetes and malnutrition have been identified as predisposing factors in patients without classic immunocompromise [18].
Pathogenesis — Ecthyma gangrenosum results from perivascular bacterial invasion of the media and adventitia of arteries and veins with secondary ischemic necrosis.
Pseudomonas produces several toxins that mediate the process of tissue degradation. Exotoxin A inhibits protein synthesis and elastase degrades elastin, thereby destroying the blood vessel wall support. Phospholipase C breaks down phospholipids in cell membranes and pyocyanin produces reactive oxygen species toxic to cells [18].
Clinical findings — The lesions of ecthyma gangrenosum (picture 1 and picture 2) commonly begin as painless red macules which rapidly evolve into areas of induration that develop into pustules and/or bullae. Ultimately, these become gangrenous ulcers. Ecthyma lesions typically progress rapidly (within 12 to 18 hours). The lesions may involve the skin or mucous membranes.
Although ecthyma gangrenosum can occur at any anatomic location, the anogenital and axillary areas are most commonly involved [16]. The gluteal and perineal areas are involved in 57 percent of cases, extremities in 30 percent, the trunk in 6 percent, and the face in 6 percent. Periorbital lesions are very rare but have been described.
Lesions may be single or multiple; in the latter case, they may be in different stages of development at any given point in time.
Biopsy of ecthyma gangrenosum lesions typically shows hemorrhagic necrosis, gram-negative bacilli, and damage to the media of arterial blood vessels [19].
Most patients have fever and may be systemically ill; however, ecthyma gangrenosum can occur in patients in the absence of fever or other constitutional signs.
Differential diagnosis — Ecthyma gangrenosum is not pathognomonic of P. aeruginosa infection. Identical lesions have been seen with systemic infection due to an array of common and uncommon bacterial, viral, and fungal pathogens [20]. Among bacterial pathogens, Pseudomonas stutzeri, Aeromonas spp, Stenotrophomonas spp, Citrobacter spp, methicillin-resistant S. aureus, and atypical mycobacteria have been described to cause ecthyma gangrenosum. Among fungal infections, Fusarium spp have been classically associated with ecthyma gangrenosum, and a few reports have described ecthyma gangrenosum-like lesions in immunocompromised patients with disseminated candidiasis [21,22]. It should be noted that when other pathogens are isolated from ecthyma gangrenosum lesions in addition to P. aeruginosa, the possibility of contamination should be considered.
In light of the broad microbial differential diagnosis, efforts to identify the causative pathogen in every patient are warranted. These are discussed below. (See 'Diagnosis and evaluation' below.)
Pyoderma gangrenosum may rarely be confused with ecthyma gangrenosum when it is evolving from a pustule or vesicle into a typical cutaneous ulcer. However, the lesions of pyoderma gangrenosum are not due to an infection, they are usually tender, and patients are typically not systemically sick. (See "Pyoderma gangrenosum: Pathogenesis, clinical features, and diagnosis".)
Diagnosis and evaluation — The diagnosis of ecthyma gangrenosum is generally made based on the characteristic clinical appearance of the lesions in the appropriate clinical setting. The presence of these lesions should immediately raise the possibility of bacteremia, particularly with P. aeruginosa, and should thus prompt the collection of blood cultures if not already performed. However, the absence of growth on blood cultures does not rule out the diagnosis of ecthyma.
A specific microbial diagnosis is important given that many different organisms can cause ecthyma gangrenosum, which is another reason for collecting blood cultures. Culture of exudates from an aspirate or swab of lesions is easy to perform and may identify a causative pathogen. If both blood cultures and cultures from skin exudates are negative, a biopsy of the lesion for pathology and bacterial, fungal, and mycobacterial cultures may be useful to exclude other etiologies. In fact, an early skin biopsy may be beneficial in immunocompromised hosts to rule out nonbacterial causative organisms like fungi that can be visualized on direct observation of specimens and require prompt antifungal treatment [23].
Treatment — Because of the typical involvement of P. aeruginosa, empiric antimicrobial therapy of a lesion suspicious for ecthyma gangrenosum should include an agent with antipseudomonal activity (table 1). The choice of agent should take into account the local epidemiology and resistance rates. In a recent retrospective study of pediatric patients with hematologic and solid organ malignancy and ecthyma gangrenosum, over 30 percent of the isolated strains were multidrug-resistant P. aeruginosa with one out of three isolates being resistant to piperacillin-tazobactam, highlighting the burden of antimicrobial resistance in this patient population [24]. In certain high-risk patients (eg, neutropenic or otherwise immunocompromised) and those with severe infections (eg, sepsis or septic shock), we favor the use of a combination antimicrobial regimen for initial empiric therapy. The rationale for the use of combination therapy is discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Role of combination antimicrobial therapy'.)
Once the causative organism and its susceptibility pattern are identified, directed therapy with a single active agent can be tailored to these results. Specific antimicrobial options for P. aeruginosa infections are discussed elsewhere (table 1).
Although not generally warranted for infections with limited involvement, surgical debridement to achieve source control and even skin grafting may be necessary in patients with severe or extensive skin [25].
Nonantibiotic alternative therapies have been considered to target biofilm formation, which plays an important role in P. aeruginosa proliferation and resistance to treatment in ecthyma gangrenosum [26].
BURN INFECTIONS — P. aeruginosa skin infection complicating burn injuries is a severe infection often associated with antibiotic resistance that warrants combination empiric therapy. These infections often have a poor outcome despite the use of appropriate antibiotic therapy [27,28].
Epidemiology — P. aeruginosa is one of the most commonly isolated organisms from burn patients, accounting for 57 percent of positive swab and tissue culture results in one study [29]. According to a systematic review and meta-analysis, P. aeruginosa is the most common causative organism among Gram-negative-associated burn wound infections and is an independent predictor of mortality [30]. Burn wound infection with P. aeruginosa occurs most commonly after the first week of hospitalization, highlighting the importance of infection prevention and control practices to reduce the risk of infection [31]. Rates of bacteremia due to P. aeruginosa vary by center. In one study of 5882 burn patients admitted to a burn center over a 25 year period, P. aeruginosa bacteremia occurred in 9 percent of cases [27]. The mortality rates in patients with and without bacteremia were 77 and 49 percent, respectively. In another study, bacteremia occurred in 7 percent of 1415 burn patients; 15 percent of these bacteremic patients were infected with P. aeruginosa (1 percent overall) [28].
Among children, factors associated with an increased risk of infection with P. aeruginosa include flame and inhalation burns, full thickness burns, and total body surface area involvement greater than 30 percent [32]. A retrospective analysis of P. aeruginosa bacteremia in children found that 7 percent of cases occurred in burn patients; mortality among burn patients was greater than oncology patients and other patients (40 versus 19 and 11 percent, respectively) [33].
Pathogenesis — Patients with extensive burns are considered to be immunosuppressed on the basis of altered neutrophil activity, T lymphocyte dysfunction, and imbalance in the production of cytokines [34-36]. Colonization of the burn eschar site with P. aeruginosa (up to 105 of bacteria per gram of tissue) is common. Burns destroy the physical barrier to tissue invasion; this in turn allows bacteria on the surface of the skin to invade into the dermis and enter the lymphatics along fibrous septae. After such invasion, organisms can proliferate in necrotic tissue and invade blood vessels, producing a secondary bacteremia.
Physical findings — Examination of the skin in patients with burn injuries complicated by P. aeruginosa infection typically reveals discoloration of the burn eschar, bleeding in the subcutaneous tissue, and degeneration of the granulation tissue. Healthy adjacent tissue may rapidly develop edema, hemorrhage, and necrosis, with new nodular lesions and eschars forming by centrifugal spread. Systemic signs and symptoms identical to those seen with other systemic bacterial infections are usually present.
Diagnosis — The diagnosis of P. aeruginosa infection in burn patients can be made through growth of the organism on quantitative cultures from a biopsy obtained from the burn skin as well as adjacent unburned tissue [37]. A colony count of 105 organisms per gram of tissue in the setting of consistent clinical findings is indicative of a burn wound infection, as opposed to simple colonization. The distinction between the varying levels of bacterial involvement in burn wound infections is discussed in detail elsewhere. (See "Burn wound infection and sepsis", section on 'Differential diagnosis' and "Burn wound infection and sepsis", section on 'Diagnosis'.)
Molecular testing with polymerase chain reaction (PCR) could be a useful tool to detect P. aeruginosa in burn wounds, but it is not widely available beyond research studies [38]. It provides rapid results and can distinguish P. aeruginosa from other Pseudomonas species and other gram-negative bacilli that might resemble P. aeruginosa through conventional diagnostic methods. Novel diagnostic tools, such as peptide nucleic acid fluorescent in situ hybridization (PNA-FISH) and matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry (MS), may accelerate bacterial identification and susceptibility testing and improve the time to appropriate antimicrobial treatment [39].
Antimicrobial resistance — A high rate of antibiotic resistance has been observed in burn patients with P. aeruginosa infections, and this affects decisions about empiric therapy. As an example, in a study of 70 P. aeruginosa isolates from patients in a burn center in Iran, 89 percent were resistant to ticarcillin-clavulanate, 76 percent to gentamicin and imipenem, and 20 percent to meropenem [40]. In another study from Rio de Janeiro, 71 percent of the 35 isolates of P. aeruginosa recovered from burn patients or burn unit environment were multidrug-resistant [41]. Another study from a burn center in Sweden reported that 26 percent of P. aeruginosa isolates from 1994 to 2012 were carbapenem-resistant [42].
Certain features may be associated with a greater likelihood of infection with resistant organisms. Risk factors for acquisition of imipenem-resistant P. aeruginosa were identified in a multivariate analysis of 133 patients (93 with imipenem-resistant and 40 with imipenem-sensitive P. aeruginosa) hospitalized in a burn unit in Turkey between July 2003 and November 2004 [43]. Independent risk factors included:
●Prior carbapenem use (odds ratio [OR], 7.4)
●Prior broad-spectrum antibiotic use (OR, 6.5)
●Length of hospitalization (OR, 3.6)
●Presence of imipenem-resistant P. aeruginosa in the unit (OR, 2.6)
●Previous presence of imipenem-sensitive P. aeruginosa in the patient (OR, 1.7)
Treatment — Treatment of P. aeruginosa burn wound infections involves aggressive surgical debridement of necrotic tissue and infected eschar, as well as systemic antimicrobial therapy.
For empiric therapy prior to the availability of susceptibility testing results in burn patients with serious P. aeruginosa wound infections, we suggest a combination of two antibiotics because of the high load of organisms and the likelihood of infection with or development of resistant organisms. Possible regimens include ceftazidime, cefepime, ciprofloxacin, aztreonam, or an antipseudomonal carbapenem each in combination with an aminoglycoside (tobramycin, amikacin, or gentamicin) (table 1). The rationale for combination therapy and discussion of aminoglycoside dosing are found elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Role of combination antimicrobial therapy' and "Dosing and administration of parenteral aminoglycosides".)
Once susceptibility testing results are available, directed therapy with a single agent guided by these results is preferable, if possible. Specific antimicrobial options for P. aeruginosa infections are discussed elsewhere (table 1). (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity' and "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotic selection'.)
When a skin and soft tissue infection with a carbapenem-resistant P. aeruginosa (CRPA) is suspected or documented, ceftolozane-tazobactam, ceftazidime-avibactam, imipenem-relebactam, and cefiderocol can be used [44]. The novel fluoroquinolones finafloxacin and delafloxacin also appear promising for the treatment of CRPA [45]
Treatment of multidrug-resistant pathogens, including P. aeruginosa, with bacteriophages is being evaluated in patients with burns and device-related infections. In one randomized study of 27 patients, a cocktail of topical bacteriophages was used to treat burn wounds infected with P. aeruginosa; half of those who received the bacteriophage cocktail had a reduced quantity of bacteria in the wound, although this was a lower proportion than those who received standard of care [46].
Management of the burn wound itself is discussed in detail elsewhere. (See "Overview of surgical procedures used in the management of burn injuries" and "Burn wound infection and sepsis", section on 'Treatment'.)
The mortality of P. aeruginosa burn wound infections and associated sepsis can be very high [27,28]. However, early diagnosis and prompt treatment of infections in the setting of burns, even those caused by P. aeruginosa, can be associated with a considerably lower mortality rate, nine percent in one series [47].
Prevention — Because of the higher rate of antimicrobial resistance and the associated difficulty in treating these infections, prevention of P. aeruginosa infections is an especially important strategy to reduce the burden of disease. Measures to decrease the incidence of infection by attempting to reduce the colonizing bacterial population have been used. These include cleaning, debridement, and dressing, as well as application of topical antimicrobials. The local and surgical management of burn wounds for prevention of infection is discussed in detail elsewhere. (See "Topical agents and dressings for local burn wound care" and "Burn wound infection and sepsis", section on 'Treatment'.)
Protection against subsequent P. aeruginosa infections through vaccination is under evaluation [48].
HOT TUB-ASSOCIATED ERUPTIONS — "Hot tub folliculitis and hot foot syndrome" are benign, self-limited skin lesions caused by P. aeruginosa that can occur following exposure to contaminated water.
P. aeruginosa folliculitis is typically associated with the use of spa pools, whirlpools, or exposure to inadequately chlorinated swimming pools and hot tubs [49,50]. Two outbreaks of P. aeruginosa folliculitis from hotel swimming pool and hot tub exposures were described in Colorado and Maine in 1999 and 2000; both facilities used offsite maintenance crews and free levels of chlorine were found to be low [50]. Additional risk factors that may increase the risk of hot-tub folliculitis include female sex, alterations of skin flora, length of hot-tub exposure, and underlying skin trauma [51].
P. aeruginosa folliculitis typically develops 8 to 48 hours after exposure to contaminated water. The eruption in P. aeruginosa folliculitis consists of tender and pruritic papules, papulopustules, or nodules (picture 3) [52-54]. Most patients have malaise and some have low grade fever (42 and 22 percent, respectively in the Colorado and Maine outbreaks noted above) [50]. Urticarial lesions on the trunk, extremities, hands, and feet have also been reported [52-55]. In one outbreak of folliculitis in Alaska among bathers in a contaminated hot tub, five of nine affected bathers had inflammation of Montgomery's follicles of the breast [56]. Longer periods of bathing and bathing later in the day were associated with an increased risk of disease.
A variation on this entity has been reported, consisting of tender erythematous nodules on the soles of the feet and labelled "pseudomonas hot foot syndrome" [55,57,58]. A group of 40 children developed these lesions within 40 hours of wading in a pool with a rough floor and were unable to bear weight on the affected areas; culture of the wading pool water grew abundant P. aeruginosa [57]. All patients recovered without specific antibiotic therapy. It is thought that hot hand-foot syndrome is more common in children due to their thinner epidermis of the palms and soles [59].
P. aeruginosa folliculitis and hot foot syndrome are self-limiting conditions that improve with removal of the exposure and symptomatic care. An oral fluoroquinolone (eg, ciprofloxacin) may be warranted for lesions that are persistent or cause significant discomfort. (See "Infectious folliculitis", section on 'Pseudomonal folliculitis'.)
INFECTION FOLLOWING NAIL PUNCTURE — P. aeruginosa osteochondritis, osteomyelitis, and septic arthritis following nail puncture wound to the foot is a well-described complication. This syndrome occurs predominantly in children with a history of wearing tennis shoes, [60] but it also occurs in adults as well [61]. The association with tennis shoes is possibly due to the moist inner sole of the shoe which would provide a suitable environment for growth of this organism [62]. In one study, P. aeruginosa was isolated from the sneakers of seven of eight children with documented P. aeruginosa osteomyelitis following a plantar puncture wound and from 4 of 33 pairs of randomly selected worn and discarded sneakers, but not from unworn shoes; the organism was most frequently isolated from the inner foam layer of the sneaker sole. Evaluation, management, and prevention of infections following puncture wound injury, including pseudomonal plantar puncture wound infections, are discussed in detail elsewhere. (See "Infectious complications of puncture wounds", section on 'Evaluation' and "Infectious complications of puncture wounds", section on 'Management' and "Infectious complications of puncture wounds", section on 'Prevention'.)
TOE WEB INFECTION — Gram-negative interweb foot impetigo is a relatively common disorder and is often bilateral [63]. Secondary cellulitis may occur.
The infection is commonly associated with the use of closed-toe or tight-fitting shoes and in individuals in whom strong physical exertion plays an important role in athletic, occupational, or recreational activities. Other predisposing factors include interdigital tinea pedis, eczema, hyperhidrosis, diabetes mellitus, and self-medication with topical antifungals, antibiotics, and glucocorticoids [63-68].
Gram-negative mixed bacterial infection, including with Pseudomonas species, may represent a mild secondary infection of tinea pedis. Among patients with mixed gram-negative interweb foot infection, P. aeruginosa appears to be the most commonly isolated pathogen [64].
No pathognomonic clinical presentation exists to differentiate gram-negative interweb foot infection from gram-positive or fungal infections. The condition initially presents as interdigital erythema with malodorous exudate, pain, and itching [64] but can progress to advanced stages of gram-negative infection with sepsis if left untreated [69]. For cases that are refractory to appropriate antibiotic therapy, the possibility of other processes, including eczematous dermatitis and malignancy, should be considered [67,70,71].
GREEN NAIL SYNDROME — Patients with chronic onycholytic toenails who have prolonged immersion exposure to fresh water may develop a characteristic green discoloration called the green nail syndrome [54,72,73] (picture 4 and picture 5 and picture 6). This is almost always a complication of onycholysis or chronic paronychia and is usually restricted to one or two nails. In addition to the fungi associated with the onycholysis, P. aeruginosa is generally isolated from the nail. The green color is due to accumulation of debris below the nail and the pigment pyocyanin adhering to the undersurface of the nail plate. Although clinical and dermoscopic findings are enough to diagnose green nail syndrome, some patients may require gram stain, culture, histopathology, or more advanced diagnostics to confirm the diagnosis [68].
Topical therapy is typically the first line treatment for this condition [74-76]. Many patients respond to two weeks of topical fluoroquinolones and antiseptic soaks. Such antiseptic measures include applying acetic acid or sulfacetamide in 50 to 70 percent ethyl alcohol, 4 percent thymol in chloroform, or Clorox diluted in 1:4 two to three times a day to the space to suppress the growth of P. aeruginosa [77].
In addition, the patient should be advised to avoid excessive immersion in hot water, even when wearing protective gloves. After washing, the nails should be dried thoroughly. In some cases, the use of a hair dryer is recommended to keep the nail plate-nail bed space as dry as possible. Thorough trimming should be repeated at intervals of four weeks until the normal nail regrows. Treatment of any underlying nail disease (eg, fungal infection, psoriasis) is indicated. (See "Onychomycosis: Epidemiology, clinical features, and diagnosis".)
Systemic antibiotics may be warranted in patients who do not respond to topical treatment. Because the appearance is relatively characteristic and there can be difficulty in obtaining adequate samples for culture, we start empiric oral antimicrobial therapy in such patients. Oral ciprofloxacin (500 to 750 mg PO BID) for a period of four weeks has been found to be effective [78]. If there is no improvement, then nail removal with cultures and sensitivity testing would be a reasonable next step.
PERICHONDRITIS OF THE EAR — P. aeruginosa perichondritis of the helix or tragus of the ear can occur after trauma, surgery, or burns, and a number of cases have been reported following piercing of the upper ear cartilage [79]. P. aeruginosa is more often isolated in suppurative perichondritis rather than nonabscess perichondritis [80]. This is discussed in detail elsewhere. (See "Pseudomonas aeruginosa infections of the eye, ear, urinary tract, gastrointestinal tract, and central nervous system", section on 'Perichondritis'.)
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: Bacterial folliculitis (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Clinical spectrum – Certain clinical syndromes are classically associated with P. aeruginosa. These include ecthyma gangrenosum, burn wound infections, infection following nail puncture, eruptions associated with hot tub exposures, green nail syndrome, and perichondritis of the ear. Additionally, P. aeruginosa can be involved in other more typical skin and soft tissue infections (eg, cellulitis), especially those in immunocompromised patients or following instrumentation or water exposure. (See 'Clinical syndromes' above.)
●Principles of management – In general, treatment of P. aeruginosa skin, soft tissue, and bone infections should include aggressive surgical debridement of any necrotic tissue and infected eschars, in addition to antibiotic therapy. Antibiotic options include beta-lactams, carbapenems, or fluoroquinolones that have antipseudomonal activity (table 1). Aminoglycosides should not be used as a single agent for infection at these sites. (See 'Management principles' above.)
●Ecthyma gangrenosum – Ecthyma gangrenosum is most commonly associated with bacteremia in immunocompromised hosts. The lesions begin as painless red macules which rapidly evolve into areas of induration that develop into pustules and/or bullae then ultimately become gangrenous ulcers (picture 1 and picture 2). (See 'Epidemiology' above and 'Clinical findings' above.)
The diagnosis of ecthyma gangrenosum is generally made based on the clinical appearance of characteristic lesions. Cultures of blood and lesion exudates may be informative. Otherwise, skin biopsy may be warranted. (See 'Differential diagnosis' above and 'Diagnosis and evaluation' above.)
Empiric antimicrobial therapy of a lesion suspicious for ecthyma gangrenosum should include an agent with antipseudomonal activity (table 1). Once the causative organism and its susceptibility pattern are identified, directed therapy with a single active agent can be tailored to these results. (See 'Treatment' above.)
●Burns – P. aeruginosa skin infection complicating burn injuries is associated with high mortality despite aggressive antibiotic therapy. Infected skin typically reveals discoloration of the burn eschar, bleeding in the subcutaneous tissue, and degeneration of the granulation tissue. Systemic signs and symptoms are usually present as well. (See 'Epidemiology' above and 'Physical findings' above.)
The diagnosis of P. aeruginosa infection in burn patients is confirmed by quantitative cultures from a biopsy of the burned skin, as well as adjacent unburned tissue. A colony count of 105 organisms per gram of tissue is significant. (See 'Diagnosis' above.)
For empiric antimicrobial therapy of burn patients with known or suspected P. aeruginosa infections, we suggest a combination of two intravenous antipseudomonal agents (Grade 2C). We initiate therapy with ceftazidime, cefepime, ciprofloxacin, aztreonam, or an antipseudomonal carbapenem plus an aminoglycoside (table 1). (See 'Treatment' above.)
●Infection following nail puncture – P. aeruginosa osteochondritis, osteomyelitis, and septic arthritis following nail puncture wound to the foot is a well-described complication. This syndrome occurs predominantly in children with a history of wearing tennis shoes. Evaluation, management, and prevention of pseudomonal puncture wound infections are discussed elsewhere. (See "Infectious complications of puncture wounds".)
●Other syndromes – Other conditions for which empiric antipseudomonal therapy is indicated include toe web infection, green nail syndrome, and infectious perichondritis of the ear. Hot tub-associated folliculitis and "hot foot syndrome" due to P. aeruginosa typically resolve without antibiotic therapy. (See 'Toe web infection' above and 'Green nail syndrome' above and 'Perichondritis of the ear' above and 'Hot tub-associated eruptions' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
