What Caused These Slightly Tender Papules and Nodules?

Patient Presentation

A 43-year-old woman presented with a mildly tender eruption on her chest and back, which developed over a 3-day period. She reported a mild concomitant myalgia but denied fevers or chills. On examination, there were multiple erythematous papules and nodules measuring from 5 mm to 2 cm in diameter, involving the trunk, buttocks and upper thighs. Some of the nodules were topped with pinpoint pustules. The lesions were mildly tender to palpation. No lymphadenopathy, splenomegaly or hepatomegaly were noted.

Diagnosis: Hot Tub Folliculitis

So-called “hot tub” folliculitis represents an infection of the pilosebaceous unit by Pseudomonas aeruginosa, most commonly as a result of exposure to contaminated bathing water.

The History of Pseudomonas and Hot Tub Folliculitis

Pseudomonas aeruginosa has long been known to cause cutaneous infections. Gessard initially described P. aeruginosa as a pathogen in 1882, when he linked the bacterium to wound infections that produced blue and green discoloration of soldiers’ bandages.¹ Since its initial recognition as a wound pathogen, P. aeruginosa’s spectrum of described cutaneous manifestations has expanded to include infections of otherwise intact skin: the “green-nail” syndrome, web space infections, otitis externa and ecthyma gangrenosum, among others.²

P. aeruginosa was not associated with a post-bathing eruption until nearly a century after its discovery, when McCausland and Cox linked the bacterium to an outbreak of folliculitis among users of a motel whirlpool in 1975.³ Over time, the number of recognized transmission modalities for Pseudomonas folliculitis has been expanded to include showers,⁴ contaminated loofah sponges,⁵ wetsuits,^6,7 water toys⁸ and leg depilation wax.⁹

More on Pseudomonas aeruginosa

Pseudomonas aeruginosa, an aerobic, motile, non-fermenting Gram-negative rod is ubiquitously found on moist surfaces. Two-thirds of clinical isolates produce pyocyanin pigment, resulting in characteristic blue-green colonies.¹⁰ Colonies grown on agar media are often noted to produce a fruity, grape-like odor. Pseudomonas has the ability to rapidly multiply in warm, nutrient-poor water, as well as to resist chlorination, which makes it a frequent constituent of bathing water flora. During infection, the bacterium derives its nutrients from products of tissue breakdown, mediated by the exotoxins elastase, alkaline phosphatase and phospholipase C.¹⁰

Epidemiology of Pseudomonas Folliculitis

Fifteen outbreaks of Pseudomonas folliculitis were reported to the Centers for Disease Control in 1999 through 2000, affecting a total of 161 individuals.11 Due to the generally mild nature of this condition, incidence is believed to be under-reported, rendering available figures imprecise.¹² There is a general consensus that an increasing number of cases are being reported with time, although it is uncertain whether this is due to a true increase in incidence or to improved detection.^13,14 Pseudomonas folliculitis is generally a community-acquired infection, although there have also been reports of nosocomial spread.¹⁵ Seasonal variation has been noted, with an increase in incidence during the winter months, possibly attributable to increased hot tub usage.¹²

Clinicopathologic Features of Pseudomonas Folliculitis

After exposure to a source of contamination, infected patients undergo an incubation period that averages 48 hours, but may range from 8 hours to 2 weeks. This is followed by the onset of a pruritic eruption involving mainly the trunk, buttocks, legs and arms. Characteristically, the head and neck are spared.¹⁶ The eruption rapidly progresses to papules with distinctive central pinpoint pustules; papules typically measure from 2 mm to 10 mm in diameter.¹⁷ Mature lesions are usually described as papulovesicles on an erythematous base. Systemic symptoms, including fever, fatigue, myalgia and tender lymphadenopathy variably and inconsistently accompany the eruption.

Serotype O-11 is implicated in about half of all outbreaks, with O-1, O-4, O-6, O-9 and O-10 being noted less frequently.^12,18 Patients with Pseudomonas folliculitis frequently experience other concomitant P. aeruginosa infections, such as mastitis, otitis externa, conjunctivitis and keratitis.^13,19,20 Urinary tract infections resulting from exposure to contaminated bathing water have also been described.²¹ Patients with open skin wounds may be at increased risk for invasive disease following exposure to contaminated water.

A case series supporting this hypothesis was recently reported in the Journal of the American Medical Association by Keene, et al., who identified contaminated water in an aerosolizer bottle as the source for a cluster of patients with post-ear piercing Pseudomonas chondritis.²² A newly described variant, dubbed the “Hot-Foot Syndrome” by Fiorillo and colleagues in the New England Journal of Medicine, presents with exquisitely painful nodular lesions in place of the papulovesicular eruption.²³

Pseudomonas is not a constituent of the normal skin flora, as it is poorly adapted to growth in a dry, acidic environment.²⁴ Pseudomonas folliculitis occurs only in situations where a pathogenic bacterial strain is introduced onto altered skin. Over-hydration of the stratum corneum compromises the skin’s natural barrier, increasing penetrance of the bacterium. Furthermore, warm environments facilitate infection by dilating skin pores that can serve as portals of entry. Even under these conditions, however, Pseudomonas is typically only capable of establishing a transitory colonization. During this brief period, the bacterium elaborates its exotoxins, which are believed to be the causative agents for the majority of folliculitis symptoms.²⁵ This transient colonization is consistent with the short duration and self-limited nature of symptoms, as well as with the difficulty noted in culturing Pseudomonas from lesions.

Factors related to risk of exposure include prolonged bathing time, which has been shown to directly increase risk of exposed individuals,²⁶ and bather load, which is postulated to increase the density of bacterial growth by providing more organic nutrients.²⁷ Occlusion by clothing is also theorized to increase the likelihood of colonization by trapping bacteria against the skin, which may explain the rash’s predilection for areas of the body covered by bathing attire.²⁴ All of these putative risk factors are consistent with the observation that children appear to have a higher attack rate than adults in any given epidemic, as children tend to have increased average bathing time and a relatively thinner stratum corneum.^{12, 28}

Differential Diagnosis

The diagnosis of Pseudomonas folliculitis is frequently missed, due to the variable nature of the skin lesions and the associated systemic symptoms. Sporadic cases are especially difficult to diagnose, as the appropriate history may not be elicited without a high index of suspicion.¹⁴

The differential diagnosis of Pseudomonas folliculitis is vast and encompasses many diverse maculopapular and vesicular diseases of the skin, including Staphylococcal folliculitis, impetigo, insect bites, scabies, varicella-zoster, herpes simplex, variola, contact dermatitis, follicular eczema, miliaria, papular sarcoidosis, swimmer’s itch and various fungal infections. A detailed history is essential to making an accurate diagnosis; most patients will report recent exposure to water or a wet environment, as was the case in our patient.

Although the classic form of Pseudomonas folliculitis involves a point-source epidemic due to contaminated recreational bathing equipment, an increasing number of non-recreational exposures have been reported. The latter are more likely to present as a chronic, recurring dermatitis, and may represent a special diagnostic challenge.²⁹ Two important physical findings that suggest Pseudomonas folliculitis are the rash’s characteristic distribution and the peri-follicular location of lesions. In cases involving fluorescein-producing strains of the bacterium, skin lesions may fluoresce yellow-green under a Wood’s lamp.³⁰ Patients may present with lesions in various stages of development, especially in cases where re-infection occurs due to continued exposure to the source of contamination. Diagnosis of Pseudomonas folliculitis is made on clinical grounds, as cultures are unreliable and not required. For public health reasons, however, it may be advisable to culture the presumed source of contamination.

Treatment, Prevention and Clinical Course

In immunocompetent patients, Pseudomonas folliculitis is a self-limited infection that spontaneously resolves within 7 to 14 days,³¹ although rare cases have been reported to last upward of 6 weeks.³² Post-inflammatory hyperpigmentation may persist for several months after resolution of the lesions.²⁴ In uncomplicated cases, both systemic and topical antibiotics are contraindicated, as they have not been proven to alter the natural history of this condition.^14,16 Complications requiring antibiotic therapy include immunocompromise, concomitant Pseudomonas infections in additional locations, and persistent cases.³³ Antibiotics of choice include third-generation oral cephalosporins and fluoroquinolones.

Preventative measures include identification of the source of Pseudomonas infection and sterilization thereof with 10% hypochlorite bleach.³⁴ For bathing water, the CDC recommends that chlorine, or preferably bromine, be continuously maintained at free residual levels of 3 ppm to 5 ppm, and that the pH be held between 7.2 and 7.8.³⁵ Contaminated bathing implements should be discarded, and new implements allowed to dry completely between uses, which may help prevent initial colonization by the bacterium.¹⁴

Prognosis

The prognosis of Pseudomonas folliculitis is excellent, with virtually all cases resolving spontaneously and without sequelae. Resolution without scarring is the rule.¹⁴ Rare cases have been described recurring for up to 3 months after initial exposure,³⁶ and these typically resolve with systemic antibiotic therapy. Systemic spread is not seen in the immunocompetent, although evolution into ecthyma gangrenosum has been described among immunocompromised patients.^37,38

Patient Presentation

A 43-year-old woman presented with a mildly tender eruption on her chest and back, which developed over a 3-day period. She reported a mild concomitant myalgia but denied fevers or chills. On examination, there were multiple erythematous papules and nodules measuring from 5 mm to 2 cm in diameter, involving the trunk, buttocks and upper thighs. Some of the nodules were topped with pinpoint pustules. The lesions were mildly tender to palpation. No lymphadenopathy, splenomegaly or hepatomegaly were noted.

Diagnosis: Hot Tub Folliculitis

So-called “hot tub” folliculitis represents an infection of the pilosebaceous unit by Pseudomonas aeruginosa, most commonly as a result of exposure to contaminated bathing water.

The History of Pseudomonas and Hot Tub Folliculitis

Pseudomonas aeruginosa has long been known to cause cutaneous infections. Gessard initially described P. aeruginosa as a pathogen in 1882, when he linked the bacterium to wound infections that produced blue and green discoloration of soldiers’ bandages.¹ Since its initial recognition as a wound pathogen, P. aeruginosa’s spectrum of described cutaneous manifestations has expanded to include infections of otherwise intact skin: the “green-nail” syndrome, web space infections, otitis externa and ecthyma gangrenosum, among others.²

P. aeruginosa was not associated with a post-bathing eruption until nearly a century after its discovery, when McCausland and Cox linked the bacterium to an outbreak of folliculitis among users of a motel whirlpool in 1975.³ Over time, the number of recognized transmission modalities for Pseudomonas folliculitis has been expanded to include showers,⁴ contaminated loofah sponges,⁵ wetsuits,^6,7 water toys⁸ and leg depilation wax.⁹

More on Pseudomonas aeruginosa

Pseudomonas aeruginosa, an aerobic, motile, non-fermenting Gram-negative rod is ubiquitously found on moist surfaces. Two-thirds of clinical isolates produce pyocyanin pigment, resulting in characteristic blue-green colonies.¹⁰ Colonies grown on agar media are often noted to produce a fruity, grape-like odor. Pseudomonas has the ability to rapidly multiply in warm, nutrient-poor water, as well as to resist chlorination, which makes it a frequent constituent of bathing water flora. During infection, the bacterium derives its nutrients from products of tissue breakdown, mediated by the exotoxins elastase, alkaline phosphatase and phospholipase C.¹⁰

Epidemiology of Pseudomonas Folliculitis

Fifteen outbreaks of Pseudomonas folliculitis were reported to the Centers for Disease Control in 1999 through 2000, affecting a total of 161 individuals.11 Due to the generally mild nature of this condition, incidence is believed to be under-reported, rendering available figures imprecise.¹² There is a general consensus that an increasing number of cases are being reported with time, although it is uncertain whether this is due to a true increase in incidence or to improved detection.^13,14 Pseudomonas folliculitis is generally a community-acquired infection, although there have also been reports of nosocomial spread.¹⁵ Seasonal variation has been noted, with an increase in incidence during the winter months, possibly attributable to increased hot tub usage.¹²

Clinicopathologic Features of Pseudomonas Folliculitis

After exposure to a source of contamination, infected patients undergo an incubation period that averages 48 hours, but may range from 8 hours to 2 weeks. This is followed by the onset of a pruritic eruption involving mainly the trunk, buttocks, legs and arms. Characteristically, the head and neck are spared.¹⁶ The eruption rapidly progresses to papules with distinctive central pinpoint pustules; papules typically measure from 2 mm to 10 mm in diameter.¹⁷ Mature lesions are usually described as papulovesicles on an erythematous base. Systemic symptoms, including fever, fatigue, myalgia and tender lymphadenopathy variably and inconsistently accompany the eruption.

Serotype O-11 is implicated in about half of all outbreaks, with O-1, O-4, O-6, O-9 and O-10 being noted less frequently.^12,18 Patients with Pseudomonas folliculitis frequently experience other concomitant P. aeruginosa infections, such as mastitis, otitis externa, conjunctivitis and keratitis.^13,19,20 Urinary tract infections resulting from exposure to contaminated bathing water have also been described.²¹ Patients with open skin wounds may be at increased risk for invasive disease following exposure to contaminated water.

A case series supporting this hypothesis was recently reported in the Journal of the American Medical Association by Keene, et al., who identified contaminated water in an aerosolizer bottle as the source for a cluster of patients with post-ear piercing Pseudomonas chondritis.²² A newly described variant, dubbed the “Hot-Foot Syndrome” by Fiorillo and colleagues in the New England Journal of Medicine, presents with exquisitely painful nodular lesions in place of the papulovesicular eruption.²³

Pseudomonas is not a constituent of the normal skin flora, as it is poorly adapted to growth in a dry, acidic environment.²⁴ Pseudomonas folliculitis occurs only in situations where a pathogenic bacterial strain is introduced onto altered skin. Over-hydration of the stratum corneum compromises the skin’s natural barrier, increasing penetrance of the bacterium. Furthermore, warm environments facilitate infection by dilating skin pores that can serve as portals of entry. Even under these conditions, however, Pseudomonas is typically only capable of establishing a transitory colonization. During this brief period, the bacterium elaborates its exotoxins, which are believed to be the causative agents for the majority of folliculitis symptoms.²⁵ This transient colonization is consistent with the short duration and self-limited nature of symptoms, as well as with the difficulty noted in culturing Pseudomonas from lesions.

Factors related to risk of exposure include prolonged bathing time, which has been shown to directly increase risk of exposed individuals,²⁶ and bather load, which is postulated to increase the density of bacterial growth by providing more organic nutrients.²⁷ Occlusion by clothing is also theorized to increase the likelihood of colonization by trapping bacteria against the skin, which may explain the rash’s predilection for areas of the body covered by bathing attire.²⁴ All of these putative risk factors are consistent with the observation that children appear to have a higher attack rate than adults in any given epidemic, as children tend to have increased average bathing time and a relatively thinner stratum corneum.^{12, 28}

Differential Diagnosis

The diagnosis of Pseudomonas folliculitis is frequently missed, due to the variable nature of the skin lesions and the associated systemic symptoms. Sporadic cases are especially difficult to diagnose, as the appropriate history may not be elicited without a high index of suspicion.¹⁴

The differential diagnosis of Pseudomonas folliculitis is vast and encompasses many diverse maculopapular and vesicular diseases of the skin, including Staphylococcal folliculitis, impetigo, insect bites, scabies, varicella-zoster, herpes simplex, variola, contact dermatitis, follicular eczema, miliaria, papular sarcoidosis, swimmer’s itch and various fungal infections. A detailed history is essential to making an accurate diagnosis; most patients will report recent exposure to water or a wet environment, as was the case in our patient.

Although the classic form of Pseudomonas folliculitis involves a point-source epidemic due to contaminated recreational bathing equipment, an increasing number of non-recreational exposures have been reported. The latter are more likely to present as a chronic, recurring dermatitis, and may represent a special diagnostic challenge.²⁹ Two important physical findings that suggest Pseudomonas folliculitis are the rash’s characteristic distribution and the peri-follicular location of lesions. In cases involving fluorescein-producing strains of the bacterium, skin lesions may fluoresce yellow-green under a Wood’s lamp.³⁰ Patients may present with lesions in various stages of development, especially in cases where re-infection occurs due to continued exposure to the source of contamination. Diagnosis of Pseudomonas folliculitis is made on clinical grounds, as cultures are unreliable and not required. For public health reasons, however, it may be advisable to culture the presumed source of contamination.

Treatment, Prevention and Clinical Course

In immunocompetent patients, Pseudomonas folliculitis is a self-limited infection that spontaneously resolves within 7 to 14 days,³¹ although rare cases have been reported to last upward of 6 weeks.³² Post-inflammatory hyperpigmentation may persist for several months after resolution of the lesions.²⁴ In uncomplicated cases, both systemic and topical antibiotics are contraindicated, as they have not been proven to alter the natural history of this condition.^14,16 Complications requiring antibiotic therapy include immunocompromise, concomitant Pseudomonas infections in additional locations, and persistent cases.³³ Antibiotics of choice include third-generation oral cephalosporins and fluoroquinolones.

Preventative measures include identification of the source of Pseudomonas infection and sterilization thereof with 10% hypochlorite bleach.³⁴ For bathing water, the CDC recommends that chlorine, or preferably bromine, be continuously maintained at free residual levels of 3 ppm to 5 ppm, and that the pH be held between 7.2 and 7.8.³⁵ Contaminated bathing implements should be discarded, and new implements allowed to dry completely between uses, which may help prevent initial colonization by the bacterium.¹⁴

Prognosis

The prognosis of Pseudomonas folliculitis is excellent, with virtually all cases resolving spontaneously and without sequelae. Resolution without scarring is the rule.¹⁴ Rare cases have been described recurring for up to 3 months after initial exposure,³⁶ and these typically resolve with systemic antibiotic therapy. Systemic spread is not seen in the immunocompetent, although evolution into ecthyma gangrenosum has been described among immunocompromised patients.^37,38