Sargassum algae

Clinical Presentation

Contact with skin can result in an exuberant erythematous, urticarial-like dermatitis (Figure 82-2).²⁶

FIGURE 82-2 Sargassum algae. An urticarial-like papular eczematous dermatitis from contact with Sargassum algae.

Treatment

Symptomatic treatment with oral antihistamines and topical corticosteroids is usually adequate (Tables 82-1 and 82-2).

TABLE 82-1 Potency Ranking of Topical Steroids

TABLE 82-2 Topical Antipruritics and Oral Antihistamines

Product (Brand Name, Manufacturer)	Description/Dosage
Topical
Pramoxine (Sarna Ultra, Stiefel)	1.0% pramoxine HCl, 0.5% menthol, 30% petroleum in a lotion base
Soothing relief cream (Neutrogena)	3% lidocaine (Xylocaine) in emollient cream
Hydrocortisone acetate (Pramosone cream, ointment, lotion, Ferndale)	Hydrocortisone acetate 1.0% and 2.5% with pramoxine HCl 1.0%
Oral
Fexofenadine (Allegra, Aventis)	60-mg tabs, capsules 1 PO tid or 180-mg capsule daily
Diphenhydramine (Benadryl, Parke-Davis)	25-mg capsule, 1 PO q 6 hr
Cetirizine hydrachloride (Zyrtec, Pfizer)	5-mg or 10-mg tab, 1 PO daily
	5 mg per tsp syrup, once or twice daily

Definition

L. majuscula (also known as Microcoleus lyngbyaceus) is finely filamentous and dark green or olive color. It grows in hairlike masses in clumps at depths of up to 30 m (100 feet) and is often found entangled with other algae in tide pools and reef flats.¹²⁶

Epidemiology and Risk Factors

Lyngbya is found throughout the Pacific and Indian Oceans and the Caribbean Sea. Strong currents and winds dislodge the algae from its normal habitat, fragment it, and carry it to the surf line. Dermatitis occurs only when the algae or its fragmented components are trapped beneath swimwear. On exiting the water, algae fragments are either washed off or dry out, rendering them harmless. Clinical manifestations may begin within minutes or hours of contact.

Pathophysiology

L. majuscula produces the dermatonecrotic toxins lyngbyatoxin A and debromoaplysiatoxin. Toxicity varies depending on season, type, and location of the algae.¹⁰⁵ Not every strain of Lyngbya is toxic. It is the potency and/or concentration of these toxins against the skin that determines the degree of cutaneous damage.

Clinical Presentation

Within minutes to hours, pruritus, burning sensations, and erythematous dermatitis develop in a swimsuit-patterned distribution. This is followed by varying degrees of blister formation, which ultimately may progress to epidermal and dermal necrosis (Figures 82-3 and 82-4). Additional symptoms can include periorbital edema, irritation of nasal mucosa, conjunctivitis, headache, and fatigue.⁶⁵ Symptoms last a few hours to days. Skin necrosis takes weeks to resolve. Anatomic locations typically are the genital, perineal, and perianal regions.

FIGURE 82-3 Rare and extreme example of superficial necrosis and inflammation secondary to dermonecrotic toxins of Microcoleus lyngbyaceus.

(Courtesy Edgar Maeyens, Jr., MD.)

FIGURE 82-4 Folliculitis in the bathing trunk area caused by Microcoleus lyngbyaceus.

(Courtesy Edgar Maeyens, Jr., MD.)

Differential Diagnosis

Differentiating Lyngbya dermatitis from “seabather’s eruption” and “swimmer’s itch” can be difficult.

Treatment

Treatment consists of prompt cleansing with copious amounts of soapy water to remove residual algae fragments. This is followed with two to three sequential isopropyl alcohol rinses and then application of a topical corticosteroid ointment (see Table 82-1). Severe dermatitis may require oral corticosteroids. If necrosis is present, wound care should include gentle debridement after warm saline compresses, followed by a combination of Biafine and triple antibiotic ointment two to three times a day until reepithelialization occurs. If difficulty with breathing occurs, this may be a systemic allergic response causing bronchospasm or early signs of anaphylaxis requiring antihistamines and epinephrine.

Sequelae

If diagnosed and treated promptly, no adverse sequelae occur. If diagnosis and therapy are delayed, skin necrosis will occur, resulting in possible secondary infection with severe scaring.

Prevention

Remove swimsuits and shower with soap on exiting the water. Avoid waters where algae densities are high or algae blooms exist. Swimsuits and swim gear must be machine washed to remove any residual algae fragments.

Definition

Ciguatera is the name given to a food-borne illness caused by consumption of fish contaminated with ciguatoxins (see Chapter 72). Dermatoses can occasionally be a feature of the illness. Ciguatera dermatitis is not diagnostic of ciguatera poisoning, because it is nonspecific and manifests with a wide range of clinical presentations.

Epidemiology and Risk Factors

Ciguatoxin accumulates in predator fish, such as grouper, snappers, amberjacks, and barracudas. Ciguatoxin is produced by dinoflagellates, such as Gambierdiscus toxicus.¹⁴² The toxin is heat-resistant, so cannot be destroyed by cooking. Ciguatoxin-producing dinoflagellates are localized to tropical waters of the Caribbean and Pacific. Ciguatoxin is found in hundreds of species of reef fish.

Pathophysiology

The precise pathophysiology of ciguatoxin dermatitis is unknown.

Clinical Presentation

Dermatologic manifestations of ciguatera poisoning include intense generalized pruritus associated with a diffuse, maculopapular eruption that can progress to bullae or desquamation (Figure 82-5). Other manifestations that have been reported include hair and nail loss, intense diaphoresis leading to dehydration, cyanosis, and urticaria.

FIGURE 82-5 Ciguatera dermatitis. Thirty-year-old male’s posterior hemithorax showing papules and rare blisters as a cutaneous manifestation of his ciguatera intoxication.

(Courtesy Edgar Maeyens, Jr., MD.)

Diagnostic Tests

No routine test exists to diagnose ciguatera dermatitis.

Treatment

There is neither a specific therapy nor an antidote for ciguatera poisoning. Treatment of cutaneous manifestations, as well as systemic ciguatera poisoning, is symptomatic and supportive.

Sequelae

No long-term cutaneous adverse effects have been reported.

Prevention

Avoid ingestion of fish likely to be ciguatoxic.

Definition

The genus Prototheca consists of nonpigmented algae from the family Chlorellaceae. Human and animal infections have been caused by an achlorophyllic mutant of the green algae Chlorella pyrenoidosa. Three species of Prototheca are recognized: Prototheca stagnora, P. wickerhamii, and P. zopfii. P. wickerhamii and P. zopfii are the pathogens most commonly implicated in human protothecosis.^21,42,77,139

Epidemiology and Risk Factors

Prototheca spp. are ubiquitous and have been isolated from fresh and marine water, streams, lakes, sewage treatment systems, tree slime, and soil. Infections usually occur after inoculation into skin following exposure to contaminated water or soil. Preexisting skin wounds facilitate entry of Prototheca. Person-to-person transmission has not been reported. The organism is of low virulence. Immunosuppressed persons or persons taking immunosuppressive medications are at increased risk of acquiring protothecosis.^74,83,139, The infection is usually localized in healthy individuals, but can disseminate in the immunocompromised.

Pathophysiology

Protothecae are unicellular, aerobic, spherical organisms without chlorophyll that have hyalin sporangia that reproduce asexually. They are unable to produce energy from photosynthesis and therefore exist as saprophytes.²¹ Protothecae are distinct from fungi and bacteria in size, morphology, and method of reproduction.

Histologically, organisms can be found within giant cells or lying freely in the dermis. Protothecae cells are round and contain two to eight tightly packed endospores in each cell or sporangium (Figure 82-6). Sporangia are described as being frambesiform (raspberry-like). The organism stains well with Grocott-Gomori methenamine silver nitrate, colloidal iron, and periodic acid–Schiff.⁵⁶

FIGURE 82-6 Protothecosis histology.

(Courtesy Edgar Maeyens, Jr., MD.)

Clinical Presentation

Clinical features of human protothecosis include:

1 Superficial cutaneous lesions

These manifest as papulonodules or verrucous plaques with or without ulcerations³⁹ (Figure 82-7). Bullous lesions may occur with subsequent rupture, drainage, and crusting.⁵⁶ Rarely, eczematous and cellulitis-like lesions occur.

FIGURE 82-7 Protothecosis of anterior leg.

(Courtesy Edgar Maeyens, Jr., MD.)

Mucosal

Lacoviello and colleagues reported a case of protothecosis of the esophagus, complicating prolonged endotracheal intubation.⁸²

In cases associated with a traumatic episode, the initial lesion is a tender, red papule or an asymptomatic nodule that enlarges and becomes pustular, then ulcerates. Purulent, malodorous, blood-tinged discharge may be present. Satellite lesions surrounding the primary lesion develop and frequently become confluent. Lesions can become verrucous and resemble chromomycosis. Regional lymph nodes may develop metastatic granulomas. Lesions extend centrifugally and occasionally disseminate. In the olecranon bursitis form, infection develops several weeks after an elbow injury and is localized to the bursa. Overlying sinus tracts may develop.

Differential Diagnosis

Differential diagnosis includes the following diseases: atypical Mycobacterium infection, chromoblastomycosis, pyoderma gangrenosum, deep fungal infection, blastomycosis-like pyoderma, and Majocchi’s granuloma.

Diagnostic Tests

Diagnosis of protothecosis can be made either by tissue biopsy or tissue culture. If uncertainty exists as to the exact nature of the organism, electron microscopy reveals a double-layered cell wall and no chloroplasts. These are features differentiating Prototheca from other algae.

Treatment

There is no defined pharmacologic protocol for eradication of Prototheca. Protothecosis shows no tendency to self-heal. It is a chronic and progressive disease.⁷⁰ Cutaneous lesions are cured with surgical excision. Amphotericin B has been used successfully.²⁹ Prolonged treatments with the algaecidal agents ketoconazole, itraconazole, fluconazole, and miconazole have been reported effective.^75,95,133

Definition

Pythiosis is a cutaneous/subcutaneous disease of humans and animals. The organism is found in tropical, subtropical, and temperate areas of the world. Although primarily a cutaneous and intestinal disease of animals (horses, cats, dogs, and cattle), it is now an emerging human pathogen.⁴⁷ Preferential ecologic niches are swampy environments, where the organism produces mobile biflagellate zoospores that are attracted chemotactically to traumatized human and animal tissues.⁷¹ The disease has been identified in the United States, Australia, Asia, South and Central America, and New Zealand.

Pathophysiology

The chemoattractants keratin and collagen from wounded skin attract P. insidiosum sporangia, which release biflagellated, mobile zoospores. Zoospores are attracted to hair and lacerated skin, where they encyst on contact. At the time of encystment in tissue, the flagellae detach and the zoospores become globose, forming germ tubes in 24 hours. Once attached, encysted zoospores secrete an amorphous material that acts as an adhesive substance.⁹⁷ Pythium species produce pectic and cellulolytic enzymes, macerating enzymes, and phytotic fungal products.⁴⁷ The role of these enzymes in production of the granulomatous response seen in human tissue is unknown.

Clinical Presentation

Cutaneous pythiosis typically begins as a pustule at the site of inoculation. The inflammatory response to the organism mimics cellulitis and eventuates in suppurative necrosis. Prototypically, the lower extremities are most frequently involved, but any cutaneous surface is vulnerable (Figures 82-8 and 82-9). Pythiosis can also progress to a systemic disease involving the vascular system, where it causes arterial occlusion.¹⁸

FIGURE 82-8 Human pythiosis. A pustule at the site of inoculation of Pythium insidiosum.

FIGURE 82-9 Human pythiosis. Suppurative necrotizing cellulitis of Pythium insidiosum infection.

Differential Diagnosis

Although not a true fungus, P. insidiosum has some morphologic characteristics in common with the order Zygomycetes. These similarities are best appreciated histologically. The fungi Zygomycetes are ubiquitous in nature, found in soil and decaying vegetation.

Hyphae of P. insidiosum species are broad, branched at right angles, usually nonseptate, and irregularly shaped with right-angled branching. They are described as ribbon-like (Figure 82-10, online).⁶ Fungi of the class Zygomycetes (e.g., Mucor, Rhizopus, and Absidia) are etiologic agents of a variety of infections in humans. Diseases caused by this group of fungi were formerly termed mucormycoses, but are now called zygomycoses.

FIGURE 82-10 Pythium insidiosum. Illustrations of Pythium insidiosum with right-angled branching, broad, nonseptate hyphae. These are microscopically similar to the Zygomycetes.

(Courtesy Jan Mucklestone.)

The spectrum of zygomycosis includes cutaneous, gastrointestinal, renal, central nervous system, pulmonary, and rhinocerebral infections.⁶ Cutaneous zygomycosis has been associated with burns, traumatic wounds, surgical wound infections, contaminated dressings, and intramuscular injections.⁶ Cutaneous zygomycosis begins with erythema and induration, gradually evolving into a necrotic ulcer virtually identical to pythiosis. It is believed that many cases of pythiosis have been misdiagnosed as therapeutically nonresponsive zygomycosis.

Diagnostic Tests

It is possible to culture pus, lesion exudate, or biopsy material on Sabouraud glucose or brain heart infusion agar. In 24 to 48 hours at 28° to 37° C (82.4° to 98.6° F), there appears a flat or submerged, colorless or white growth with short or no apparent aerial hyphae.⁷¹ Cotton blue dye–assisted microscopic examination shows broad, nonseptate, and/or sparsely septate hyaline hyphae.

Histopathologic examination of lesional tissue reveals broad, branched, and nonseptate or sparsely septate hyphae. The organism is best visualized with Gomori methenamine silver (GMS) or periodic acid–Schiff (PAS) stains. Microscopically, P. insidiosum resembles the hyphae of Zygomycetes (Figure 82-11, online).⁷¹ Fluorescein-labeled P. insidiosum antiglobulin and immunoperoxide procedures are specific for the organism in tissues.

FIGURE 82-11 Pythium insidiosum. Illustration of Aspergillus niger showing its septated branching hyphae contrasted with the nonseptated hyphal elements of Pythium insidiosum.

(Courtesy Jan Mucklestone.)

Serologic tests, such as enzyme-linked immunosorbent assay (ELISA) or immunodiffusion, are also diagnostic.¹⁷ In the absence of a positive culture, polymerase chain reaction and a species-specific DNA probe from ribosomal DNA complex have proven useful in identifying P. insidiosum.

Treatment

Little information exists on the efficacy of therapy. Whether a single agent or a combination of antimycotic agents can be curative has not been clearly established. Treatment results with conventional antimycotic medication, such as amphotericin B, have been contradictory. There are isolated case reports of successful treatment with various antimycotic agents, such as 5-fluorocytosine plus amphotericin B, or itraconazole and terbinafine for 1 year.¹⁴³

Prevention

Given that pythiosis occurs in animals and humans that frequent aquatic habitats harboring P. insidiosum, awareness of the potential for infection should prompt avoidance of aquatic environs such as ponds, marshes, and bodies of water rich in plants or decaying organic material. Cleansing of lacerations or abrasions acquired in such environments should be prompt and thorough. If a cutaneous wound exists prior to entry into a body of water, protective covering is recommended.

Definition

Aeromonas organisms are gram-negative, nonsporulating, facilitative, and aerobic bacilli. Formerly of the family Vibrionaceae, they have been reclassified as members of their own family, Aeromonadaceae. A. hydrophila have polar flagella.

Epidemiology and Risk Factors

Given their ubiquitous presence in fresh and brackish water along with their cytotoxic enterotoxins, prevention of access to open wounds is of utmost importance. Immunocompromised people more commonly develop serious complications, such as septicemia, meningitis, and pneumonia.

Pathophysiology

A. hydrophila is the cause of most Aeromonas soft tissue infections. Trauma or a preexisting open wound allows entry into the skin and soft tissues. Cellulitis develops within 8 to 48 hours and systemic signs are common. A. hydrophila possesses heat-stable enterotoxin (Cst) and heat-labile enterotoxin (Clt) genes that contribute to the organism’s toxicity.² A. hydrophila also produces hemolysins, aerolysins, and serine proteases, all of which contribute to its toxicity.³⁸

Clinical Presentation

Cellulitis may progress to focal, superficial, and cutaneous necrosis with purulent discharge (Figure 82-12), ecthyma gangrenosum–like cutaneous necrosis, fasciitis, myonecrosis, and osteomyelitis. On occasion, infections may be associated with gas production. Ecthyma gangrenosum and myonecrosis are uncommon and tend to occur in immunocompromised individuals.

FIGURE 82-12 Trauma-induced necrotic ulcer of the anterior leg of a fisherman caused by Aeromonas hydrophila.

(Courtesy Edgar Maeyens, Jr., MD.)

Differential Diagnosis

A. hydrophila cutaneous infections must be differentiated from streptococcal or Pseudomonas aeruginosa cellulitis, abscesses, and septicemia with ecthyma gangrenosum. Vibrio and Serratia species mimic both environmental exposures and cutaneous manifestations of Aeromonas infections. Presented with an individual who has cellulitis secondary to a water-related injury, one must consider Aeromonas and Vibrio species infections. In the rare gas-producing infections, evaluate for other gas-producing organisms, such as Clostridium species.

Diagnostic Tests

Culture the exudates and purulent material from wounds. Surgical samples of myonecrotic tissue should be cultured. Differentiation of Aeromonas from other gram-negative rods can be readily facilitated by culturing on blood agar containing ampicillin 10 or 30 µg/mL in a selective growth media or in Cefsulodin-Irgasan-Novobiocin agar.⁶⁶

Treatment

Aeromonas species are all usually sensitive to third-generation cephalosporins, carbapenems, and aztreonam. Fluoroquinolones are highly active against Aeromonas.¹³⁷ Pertinent disease-producing Aeromonas species are resistant to penicillin and ampicillin. Resistance to trimethoprim, sulfamethoxazole, and tetracycline are increasingly being reported.⁷⁸

Prevention

Do not enter any body of water with an open wound. If wounded while in fresh or brackish water, perform meticulous wound cleansing. A prophylactic course of fluoroquinolones should be considered.

Definition

C. violaceum is found in water and soil. It is capable of producing skin abscesses, sepsis and metastatic abscesses, and carries a mortality rate of greater than 50%. Mortality increases up to 75% to 80% for persons with septicemia or sepsis.^88,123,128

Epidemiology and Risk Factors

C. violaceum is found in water and soil. It is abundantly present in the tropics and subtropics. Greater than three dozen cases have been reported in the United States, almost all from the southeast, primarily Florida.^109,128 Infections occur primarily in the summer months. Cases have been reported from Africa, India, South America, and Australia.^44,93 C. violaceum infects humans through exposure of nonintact skin to contaminated water and soil or after ingesting contaminated food or water.

Physiology

C. violaceum is a facultative, anaerobic, elongated, gram-negative bacillus that is slightly curved and therefore resembles the vibrios. It produces purple pigment (violaceum), from which it derives its name. Violaceum protects the microorganism’s cell membrane from oxidation and peroxidation.⁹⁹ C. violaceum adapts well to either aerobic or anaerobic conditions because it has an efficient and flexible energy-generating metabolism. C. violaceum is also a reporter strain in quorum sensing.⁸⁷

Clinical Presentation

The initial symptom is inflammation of soft tissue with or without adenopathy. Clinically, this manifests as cellulitis. As the infection progresses, there is focal abscess formation. Untreated, cellulitis rapidly progresses to sepsis and metastatic abscesses (Figures 82-13 and 82-14). The entire infectious process can occur suddenly, leading to a life-threatening situation. It is not unusual for C. violaceum infection to present as sepsis with fever, pneumonia, and spleen, liver, and lung abscesses.⁹³

FIGURE 82-13 A minor abrasion while snorkeling led to this forearm infection with Chromobacterium violaceum.

(Courtesy Edgar Maeyens, Jr., MD.)

FIGURE 82-14 Chromobacterium violaceum. Lymphangitis of the forearm.

(Courtesy Edgar Maeyens, Jr., MD.)

Differential Diagnosis

The initial stages of infection may resemble staphylococcal or streptococcal cellulitis. Cutaneous ulcerations are similar to those of leishmaniasis, melioidosis, and ulceroglandular tularemia. Systemic infection with C. violaceum must be differentiated from melioidosis.

Treatment

While the optimal antibiotic therapy is not known, C. violaceum is typically susceptible to fluoroquinolones, tetracycline, gentamicin, imipenem, and trimethoprim–sulfamethoxazole. Aztreonam (Azactam), a product of C. violaceum, is a monobactam antibiotic active against gram-negative bacteria and most strains of chromobacterium.⁴⁵

Prevention

Avoid exposure to soil and/or stagnant or potentially contaminated water if there has been even a minor injury to the skin. If this is the situation, seek prompt medical attention at the first sign of cutaneous inflammation or purulence.

Definition

P. aeruginosa is a ubiquitous, modal, non-fermentative, primarily aerobic, gram-negative rod.^1,61 Ultrastructurally, P. aeruginosa possesses a polar flagellum and many surface pili. Virtually all strains produce an extracellular polysaccharide matrix necessary for biofilm formation.^118,135 It is a fastidious organism that survives extremes of temperature, under hostile conditions and with minimal nutritional support. It infects humans, other vertebrates, animals, and plants. The infection is often associated with moist conditions or environs. Pseudomonas skin infections can follow exposure to hot tubs, swimming pools, and whirlpools (Figures 82-15 and 82-16). P. aeruginosa is the most common cause of skin disorders in occupational saturation divers and can occur after recreational use of diving suits.^1,81

FIGURE 82-15 Pseudomonas aeruginosa. Primary infection of the penis in a young man with atopic dermatitis following hot tubbing.

(Courtesy Edgar Maeyens, Jr., MD.)

FIGURE 82-16 Pseudomonas aeruginosa. Primary infection of the forearm of a young man with atopic dermatitis following hot tubbing.

(Courtesy Edgar Maeyens, Jr., MD.)

Epidemiology

P. aeruginosa, although primarily a nosocomial pathogen, grows in a wide variety of environments with minimal nutritional components.¹⁰⁰ It is commonly found in soil, water, and plants, but healthy humans and animals can be colonized. Up to 7% of healthy humans carry P. aeruginosa on their skin and in their nasal mucosa and throat. As high as a 24% fecal carriage rate has been reported.¹⁰⁰

Pathogenesis

Healthy humans are resistant to Pseudomonas skin infection. It is only when barrier functions of the skin are disrupted that P. aeruginosa become invasive. Pseudomonas contains virtually all major classes of bacterial virulence systems and can potentially infect any body site. The virulence is in part determined by the status of host resistance, such as site of infection, comorbid conditions, and immune function. An example is ecthyma gangrenosum, which is cutaneous necrotizing vasculitis seen in persons with P. aeruginosa bacteremia (Figure 82-17).

FIGURE 82-17 Pseudomonas aeruginosa. Discrete foci of necrotizing vasculitis (ecthyma gangrenosum) caused by P. aeruginosa.

Definition

One of the more common types of cutaneous Pseudomonas infections is hot tub folliculitis, which is infection of the infundibuli of hair follicles by P. aeruginosa.

Epidemiology

This infection is seen most often following immersion in whirlpools or hot tubs, but can occur following swimming or scuba diving, both of which produce hyperhydration and maceration of the epidermis that predispose to Pseudomonas colonization and invasion. Numerous cases of “hot tub” or “whirlpool” dermatitis have been described.^32,120,140 Eruptions can also occur after use of heated recreational water sources, such as swimming pools, water slides, and communal bath tubs. Contaminated bath toys, loofah sponges, moisturizing creams, and diving suits have been implicated as fomites in cases of Pseudomonas folliculitis.^20,48,49,61

Pathophysiology

Histologically, an inflammatory response, primarily composed of polymorphonuclear leukocytes, surrounds and infiltrates the follicular epithelium. Clinically, this manifests as a pustule surmounting an erythematous papulonodule. Depending on the stage of evolution of this infection, purulence may or may not be present, and only inflammatory papulonodules can be in evidence (Figures 82-18 to 82-20). Histopathologically and microbiologically, this folliculitis rarely demonstrates the bacterium.

FIGURE 82-18 Hot tub folliculitis.

(Courtesy Edgar Maeyens, Jr., MD.)

FIGURE 82-19 Hot tub folliculitis.

(Courtesy Edgar Maeyens, Jr., MD.)

Figure 82-20 Hot tub folliculitis.

(Courtesy Edgar Maeyens, Jr., MD.)

Clinical Presentation

The eruption is perifollicular in distribution and appears within 48 hours of exposure. The eruption is most pronounced in areas covered by bathing garments, whereas the head and neck are spared unless submerged. Extent and severity of the eruption depend on the concentration of bacteria in the water source, duration of exposure time, presence or absence of preexisting skin disease, water temperature, and individual susceptibility. Pruritus and mild pain are common associated symptoms. Other symptoms include external otitis, conjunctivitis, tender breasts, enlarged and tender lymph nodes, fever, and malaise.^61,121 Serious infections arise in immunocompromised and debilitated individuals. Rapid progression to severe systemic disease, as manifested by hemorrhagic bullae, pneumonia, or septicemia, suggests immunosuppression.^46,53,117

Treatment

“Hot tub folliculitis” usually resolves spontaneously without therapy in 7 to 14 days. Keeping the skin dry and cool expedites resolution without formal therapy. Systemic infection is treated with either an aminoglycoside or ciprofloxacin.

Prevention

Prevention of P. aeruginosa infection requires either use of adequate disinfectant or avoidance of recreational closed-water systems and disinfection of reservoirs that are vehicles of transmission. Prompt drying of skin when exposed to wet, environmental conditions can prevent or at least minimize the degree of infection. Once colonization occurs, showering does not appear to prevent the disorder.¹²¹

Definition

Green nail syndrome is defined as greenish-black discoloration of the nail plate secondary to the combination of pigments, pyocyanin, and pyoverdin synthesized by the bacterium P. aeruginosa.

Pathophysiology

Hydration of paronychial skin, usually with entry into the epidermal barrier, predisposes to colonization with P. aeruginosa. Infection follows, producing erythema, edema, pain, and discoloration of the adjoining nail plate. If the course of injection is prolonged, the infection extends into the hyponychium, at which point onycholysis occurs.

Among the many virulent factors of P. aeruginosa are pyocyanin. Pyocyanin damages cells by producing hydrogen peroxide and superoxide. They also impart pigment to the nail plate and hyponychium. The typical discoloration of the nail plate seen in green nail syndrome is bluish-green and is the end point of the combination of two different pyocyanins (Figures 82-21 and 82-22). With loss of the epidermal barrier function in onycholysis, a polymicrobial infection may ensue.

FIGURE 82-21 Green nail syndrome. Acute purulent Pseudomonas aeruginosa paronychia with early pigment formation.

FIGURE 82-22 Green nail syndrome. Greenish-black discoloration of Pseudomonas onychia.

Risk Factors

Prolonged or frequent exposure to water, such as water sports, tending bar, and housecleaning predisposes individuals to Pseudomonas paronychia, especially if the nails and the cuticles are poorly manicured.

Clinical Presentation

Pain and swelling of paronychial tissues are the initial presentation. Occasionally, foci of purulence develop. If infection is not promptly treated, pigmentary changes within the nail plate appear and infection of the nail bed and matrix follow.

Differential Diagnosis

Without the pigmentary changes of the nail plate, diagnosis of P. aeruginosa as an etiologic agent is not clinically possible. Pseudomonal infection should be suspected if the patient has a history of abundant water exposure. Otherwise, consider as etiologies Staphylococcus spp., non-pseudomonal gram-negative organisms, or a polymicrobial infection.

Diagnostic Tests

Culture purulence if present. No additional tests are needed once the pigmentary changes occur.