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[An outbreak of Pseudomonas folliculitis in children--the first report on Pseudomonas folliculitis in Japan].

An outbreak of Pseudomonas aeruginosa folliculitis in 6 children occurred within 5 days after playing in a tiny vinyl pool. The follicular macular or pustular eruptions were mainly distributed on the trunk. No associated symptoms were seen. The causative Pseudomonas aeruginosa strain isolated from pustules of one case belonged to serogroup E, corresponding to O-11 (Difco). The rash subsided promptly and spontaneously. Furthermore, we have encountered another case of Psedomonas folliculitis caused by P. aeruginosa serogroup G, corresponding to O-6 (Difco). The maculopustular rash was distributed on the trunk and disappeared spontaneously as the cases mentioned above. The folliculitis of this baby were probably associated with the repeated use of family bath without changing water. In U.S. and Europe Pseudomonas folliculitis have been reported very frequently, but our cases were reported for the first time in Japan.

Child

Eosinophilic pustular folliculitis: fungal folliculitis?

Eosinophilic pustular folliculitis is a rare condition with no known cause. However, a fungal cause is suggested by (1) tinea-like annular lesions, (2) initial clinical consideration of fungal folliculitis in many reported cases, (3) an association with the acquired immunodeficiency syndrome, and (4) an association with scaly and vesiculopustular lesions of palms and soles. We report a case histologically identical to eosinophilic pustular folliculitis but in which hyphal fungal organisms were demonstrated in one of the involved hair follicles.

Adult

Human immunodeficiency virus-associated eosinophilic folliculitis. A unique dermatosis associated with advanced human immunodeficiency virus infection.

We studied 13 patients with human immunodeficiency virus (HIV) infection and a chronic pruritic folliculitis that was unresponsive to systemic treatment with bactericidal anti-staphylococcal antibiotics. The skin eruption was characterized by multiple urticarial follicular papules scattered on the trunk (100%), the head and neck (85%), and the proximal aspect of the extremities (62%). Absolute peripheral eosinophil counts were increased in six of 13 patients; a relative peripheral eosinophilia was present in 10 of 13 patients. Serum IgE levels were elevated in all seven patients tested (range, 88 to 9050 IU). Histopathologic features included a folliculitis with eosinophils. Pathogenic bacteria were not consistently found by routine bacterial skin cultures, cultures of skin biopsy specimens, or histopathologic evaluation. CD4 counts were decreased in all of the 12 patients tested (less than 300 cells per cubic millimeter) and were below 250 cells per cubic millimeter in 10 patients. A clinical response was noted to astemizole, to ultraviolet light in the B range, and to topical clobetasol propionate. These observations demonstrate that HIV-associated eosinophilic folliculitis is a unique HIV-related cutaneous disorder that is characterized by a culture-negative, chronic, pruritic folliculitis and a characteristic histopathologic picture. Of special importance, because it is associated with CD4 counts of less than 250 to 300 cells per cubic millimeter, eosinophilic folliculitis appears to be an important clinical marker of HIV infection and, particularly, of patients at increased risk of developing opportunistic infections. We suggest that the term eosinophilic pustular folliculitis (Ofuji's disease), previously used to describe this dermatosis in HIV-infected patients, should be discarded.

Acquired Immunodeficiency Syndrome

[Perforating folliculitis].

We report the case of a 20-year old male patient without significant familial or personal history who presented with a disseminated papular eruption on the abdomen, flanks and buttocks. The eruption was continual and proceeded by outbreaks, but it was not influenced by seasons. Physical examination of the skin, mucosae and skin appendages was otherwise normal. Histological examination showed all the criteria of perforating folliculitis as described by Mehregan and Coskey. On the basis of our case we would put perforating folliculitis back among the perforating dermatoses. The concept of this curious phenomenon is briefly reviewed; perforating folliculitis is part of the third group of the so-called primary forms. The clinical features are suggestive of the disease, with its small pigmented papules centred around a keratotic plug, forming a permanent disseminated eruption. Histology shows a granuloma facing a lateral perforation of the hair follicle, a pseudo-epitheliomatous epithelial hyperplasia and the presence of hair and keratin debris in the perforation. Various keratolytic treatments have been applied without success; retinoids have not been tried. The main diagnostic and nosological problem is Kyrle's disease. In view of clinical and histological data, many authors regard Kyrle's disease as a major form of perforating folliculitis. Pruritus, ascribed to an underlying illness in Kyrle's disease, is thought to increase the importance of the lesions. The specificity of perforating folliculitis is discussed, but it seems that side by side with secondary forms occurring in recognized diseases, there may be primary forms of perforating folliculitis. Dyskeratosis might be a cause of the perforation.

Adult

Experimental folliculitis with Pityrosporum orbiculare: the influence of host response.

The aetiology of the folliculitis associated with seborrhoeic eczema is unclear, though the yeast, Pityrosporum orbiculare has been implicated. P. orbiculare was applied under occlusion to normal forearm skin of patients with seborrhoeic eczema (SE), seborrhoeic eczema and folliculitis (SEF), and normal controls. There were significant differences in response to occlusion between the three groups. Those patients with previous clinical evidence of folliculitis (SEF) developed folliculitis at the site of occlusion more frequently than either of the other two groups (p less than 0.001), in whom only one patient developed skin changes. This difference was not explained by the response to occlusion alone, nor by natural carriage of yeasts. These results suggest that the yeast P. orbiculare is necessary for the development of folliculitis, but that the nature of the host response determines those patients prone to follicular inflammation.

Dermatitis, Seborrheic

Skin surface electron microscopy in Pityrosporum folliculitis. The role of follicular occlusion in disease and the response to oral ketoconazole.

The yeast Pityrosporum orbiculare is thought to cause the folliculitis associated with seborrheic eczema. However, a combination of mechanical and microbiological factors may be involved, with follicular occlusion leading to yeast overgrowth and folliculitis. Scanning electron microscopy was used to investigate this hypothesis. Skin biopsy specimens obtained from patients with Pityrosporum folliculitis were examined by scanning electron microscopy before and after oral ketoconazole therapy. Patients with active disease showed occlusion of noninflamed follicles, which resolved after ketoconazole treatment. Follicular occlusion was not present in biopsy specimens obtained from unaffected controls nor was it related to the presence of P orbiculare. These findings suggest that follicular occlusion may be a primary event in the development of this folliculitis, with yeast overgrowth a secondary occurrence. The beneficial effect of ketoconazole in this disease may be due to direct effects on the follicle.

Administration, Oral

Skin surface electron microscopy in Pityrosporum folliculitis. The role of follicular occlusion in disease and the response to oral ketoconazole.

The yeast Pityrosporum orbiculare is thought to cause the folliculitis associated with seborrheic eczema. However, a combination of mechanical and microbiological factors may be involved, with follicular occlusion leading to yeast overgrowth and folliculitis. Scanning electron microscopy was used to investigate this hypothesis. Skin biopsy specimens obtained from patients with Pityrosporum folliculitis were examined by scanning electron microscopy before and after oral ketoconazole therapy. Patients with active disease showed occlusion of noninflamed follicles, which resolved after ketoconazole treatment. Follicular occlusion was not present in biopsy specimens obtained from unaffected controls nor was it related to the presence of P orbiculare. These findings suggest that follicular occlusion may be a primary event in the development of this folliculitis, with yeast overgrowth a secondary occurrence. The beneficial effect of ketoconazole in this disease may be due to direct effects on the follicle.

Administration, Oral

Pityrosporum folliculitis in the Philippines: diagnosis, prevalence, and management.

Sixty-eight typical cases were studied to define the course of Pityrosporum folliculitis in a tropical setting. Contrary to reports in the literature, we found Pityrosporum folliculitis to be polymorphic. The "molluscoid" comedopapule was the most characteristic and common lesion, and it yielded consistently high spore counts. The face was commonly involved. To establish the diagnosis, we used direct microscopy of potassium hydroxide/Parker blue-black ink mounts of the lower poles of comedonal plugs. Pityrosporum folliculitis is common in the Philippines, although our adult controls had a low incidence of skin carriage of Pityrosporum orbiculare on the face compared with those reported in the West. Pityrosporum folliculitis coexisted with acne vulgaris in 56% of patients, and the addition of antimycotics to the acne regimen produced dramatic clearing of lesions.

Acne Vulgaris

Whirlpool-associated folliculitis caused by Pseudomonas aeruginosa: report of an outbreak and review.

An outbreak of folliculitis caused by Pseudomonas aeruginosa serotype O:7 occurred among the guests of a hotel in St. John's, Newfoundland, Canada, and the source of the infection was traced to the hotel whirlpool. Of 36 persons who used the whirlpool, 26 (72%) developed folliculitis within 1 to 5 days after exposure; the attack rate was significantly higher for children (90%) than for adults (50%). The rash characteristics were consistent with those of Pseudomonas folliculitis previously described (T. L. Gustafson, J. D. Band, R. H. Hutcheson, Jr., and W. Schaffner, Rev. Infect. Dis. 5:1-8, 1983). This is considered to be the first outbreak in which P. aeruginosa serotype O:7 has been incriminated. Published reports to date of outbreaks of Pseudomonas folliculitis associated with the use of whirlpools, hot tubs, swimming pools, etc., were reviewed.

Adolescent

Pseudomonas aeruginosa gram-negative folliculitis.

Three patients with sudden, unmanageable exacerbation of acne vulgaris were shown to have Gram-negative folliculitis due to Pseudomonas aeruginosa. In each patient, the source of the Pseudomonas proved to be an otitis externa infection. In contrast to previous cases of Gram-negative folliculitis due to Proteus, Escherichia coli, or Klebsiella, the anterior nares were not colonized. Treatment of the otitis externa and the Gram-negative folliculitis with acetic acid compresses and topical antibiotics led to prompt resolution without recurrence.

Acetates

[A classical form of eosinophilic pustular folliculitis--successful therapy with PUVA].

Eosinophilic pustular folliculitis was first defined by Ofuji et al. in 1970 [13]. It is reported most frequently in Japanese patients. It is characterized by the repetitive appearance of sterile papulopustular lesions that heal without scarring. Case reports from outside Japan frequently refer to ulcerating inflammation. We describe a classic form of eosinophilic pustular folliculitis in an European, and we show for the first time that the eosinophilic pustular folliculitis responds well to PUVA treatment.

Adult

[Diagnosis of oil-induced folliculitis].

Clinical, electrophysiologic and immunologic study of 113 patients with oil folliculitis was carried out. High electric resistance of hair follicles was established along with some immunologic shifts, i.e., a decrease of the general number of T-lymphocytes in peripheric blood and of the level of G and A immunoglobulins, an increase of the CIC content. On the basis of the obtained data clinical species of oil folliculitis characteristic of the initial and late disease stages were determined. A complex of clinical, electrophysiologic and immunologic signs aimed at raising accuracy and objectivity of oil folliculitis diagnosis was proposed.

Adolescent

Eosinophilic pustular folliculitis.

Eosinophilic pustular folliculitis is characterized by the spontaneous development of recurrent, sterile papules, pustules, and plaques on the face, trunk, arms, and occasionally the palms and soles. Although the large majority of the reported cases have occurred in Eastern Asians, most patients in the United States have been infants or men seropositive for human immunodeficiency virus. We describe a North American woman with eosinophilic pustular folliculitis who was neither seropositive for human immunodeficiency virus nor of Asiatic descent.

Adult

Treatment of gram-negative folliculitis with isotretinoin: positive clinical and microbiologic response.

Thirty-two patients with gram-negative folliculitis were treated with 0.47 to 1.0 mg/kg/day of isotretinoin. Serial microbiologic evaluations demonstrated rapid clearing of the face and nasal mucosa of gram-negative rods. The clinical response was rapid, complete, and induced prolonged remissions. Twenty-six of thirty-two patients developed Staphylococcus aureus nasal carriage by the end of the 20-week treatment course. Isotretinoin has decided advantages over previously reported therapies for gram-negative folliculitis.

Acne Vulgaris

Necrotizing lymphocytic folliculitis: the early lesion of acne necrotica (varioliformis).

Skin biopsy specimens from four patients who had recurrent bouts of lesions conforming to the clinical description of acne necrotica were studied. The pathologic findings were dominated by lymphocytic inflammation around centrally placed follicles evolving to follicular necrosis that extended to the perifollicular epidermis and dermis. Early lesions showed the development of multiple individual necrotic keratinocytes within the follicular sheath and adjacent epidermis with lymphocytic exocytosis. Later lesions showed more intense necrosis and scale crust obscuring the central target but were still dominated by a peripheral lymphocytic infiltrate. The early pathologic findings of acne necrotica (varioliformis) are represented by a necrotizing lymphocytic folliculitis and differ from the pattern seen in association with nonspecific excoriations, acute bacterial folliculitis, classic comedogenic acne, or acnitis.

Acne Vulgaris

Eosinophilic cellulitis and eosinophilic pustular folliculitis.

This report describes a patient with a drug reaction and histologic changes of both eosinophilic cellulitis and eosinophilic pustular folliculitis. We propose that some cases of eosinophilic pustular folliculitis, like eosinophilic cellulitis, may occur as a result of a hypersensitivity phenomenon.

Cellulitis

The ultrastructural histopathology of eosinophilic pustular folliculitis.

The follicular skin lesions of a patient with eosinophilic pustular folliculitis were investigated by electron microscopy. Pustules in the outer root sheath contained acantholytic keratinocytes with numerous microvilli and features of desmosomal cleavage. The infiltrating eosinophils and neutrophils exhibited autolytic or degenerative changes rather than degranulation. The aggregated tubulo-vesicular structures were associated with the debris of autolytic eosinophils. Multiple, tiny, bubble-like structures enclosed within a membrane were frequently seen in the intercellular space. The intercellular space of the outer root sheath was widened with decreased desmosomal adhesion between the keratinocytes, but no intracellular edema was detectable. The infiltrating lymphocytes, predominantly T-cells with convoluted nuclei, extended cytoplasmic processes to adjacent keratinocytes. Apposition of T-lymphocytes and Langerhans cells was noted. Some keratinocytes in the outer root sheath contained large, sebaceous lipid droplets. No obvious virus particles or other pathogenic agents were detected. It is possible that T-lymphocytes and other immunosurveillance cells are involved in the pathomechanism of eosinophilic pustular folliculitis.

Adult

Tufted-hair folliculitis.

A 21-year-old man presented with an erythematous pruritic plaque on the right parietal scalp of 2 years' evolution. Physical examination disclosed multiple bundles of hairs emerging from single dilated follicular openings. The disorder followed a relapsing and progressive course, in spite of several topical and systemic treatments. New tufts of hairs appeared in previously non-involved areas only after inflammatory changes occurred. The clinicopathological features, aetiological mechanisms and management of tufted-hair folliculitis are discussed. Tufted-hair folliculitis (THF) is a localized, inflammatory and exudative disease of the scalp characterized by a tufted appearance of the scalp hair, that may result in permanent and irreversible scarring alopecia. This condition was initially described by Smith and Sanderson in 1978 who coined the term THF to illustrate the phenomenon of multiple hairs emerging from single follicular openings. Only nine additional cases of THF have been reported elsewhere. We present herein a patient with recurrent and progressive THF resistant to several therapeutic strategies.

Adult