Folliculitis Causes and Treatment
Clinically, dissecting folliculitis of the scalp is characterized by peri-follicular pustules, nodules, abscesses and sinus that progressively evolve into scarring alopecia. The clinical picture is often complicated by a keloid tendency 4, 9, 15, 23 . The course of the disease is chronic and relapsing. Squamous cell carcinoma may arise in chronic relapsing lesions and has a recognized metastasizing potential. Death from metastatic carcinoma has been described in one patient 9 .
Histological changes in established HS. a Chronic folliculitis - dense lymphocytic infiltrate around hair follicle. b (i) Acute and chronic inflammatory cells around apocrine glands - low power. (ii) Acute and chronic inflammatory cells around apocrine glands - high power. c Pus in follicle. d Sinus tract formation. e Scarring around hair follicle Fig. 4.4 a-e. Histological changes in established HS. a Chronic folliculitis - dense lymphocytic infiltrate around hair follicle. b (i) Acute and chronic inflammatory cells around apocrine glands - low power. (ii) Acute and chronic inflammatory cells around apocrine glands - high power. c Pus in follicle. d Sinus tract formation. e Scarring around hair follicle
The term follicular occlusion disease refers to a possible common pathogenic mechanism of occlusion of sebaceous or apocrine glands, and diseases included in this term are listed in Table 6.1. An association of these disorders has been described in several patients, suggesting that a causal relationship may be found rather than mere co-occurrence. It has therefore been suggested that the association of HS, acne conglo-bata (AC) and dissecting folliculitis of the scalp should be named follicular occlusion triad. Acne tetrad includes pilonidal cyst in addition to the three aforementioned components. The actual evidence in favour of such aggregation is however predominantly morphological.
Follicular hyperkeratosis with plugging and dilatation of the hair follicle is seen as an early event in HS. The follicular epithelium may proliferate or may be destroyed. Inflammation is frequently not apparent in early lesions but peri-folliculitis will ensue and the inflammatory infiltrate embraces neutrophils, lymphocytes and histiocytes. Early lesions may show acute inflammation involving the apocrine gland and duct but this is not always apparent and would appear to be a rare primary event 7 . In a study of 36 patients apocrinitis was present in only 5 11 . Fig. 4.3 a-d. Early lesions in hidradenitis suppurativa. a Acute HS - lower power. b Follicular plugging. c Folliculitis - dense collection of neutrophils around hair follicle. d Acute folliculitis in HS Fig. 4.3 a-d. Early lesions in hidradenitis suppurativa. a Acute HS - lower power. b Follicular plugging. c Folliculitis - dense collection of neutrophils around hair follicle. d Acute folliculitis in HS
The microbial spoilage of cosmetics has been reported in the literature for many years 1-3 . One of the first reported incidents 4 is the death by tetanus of four babies in New Zealand in 1946, the vector being a contaminated talcum powder. The same vector was the source of two other cases of tetanus in an English hospital 5 . Since the 1960s, cases of cosmetic-induced infections were described in parallel with the awareness of the problem for topical drugs 6-12 . The isolated organisms were Gram-negative bacteria from the genus Klebsiella, Enterobacter, Serratia, and Pseudomonas 13,14 . The organism Pseudomonas aeruginosa, a particularly virulent hospital pathogen transmitted by eye cosmetics, led to cases of infections and even blindness 15-20 , or folliculitis from sponges 21 . Studies were then conducted to evaluate the importance of the problem 2229 and to investigate the primary contaminating sources such as raw materials, personnel, water, and packaging, as well as secondary...
Hindle et al. treated seven patients with a combination therapy of clindamycin (300 mg twice daily) and rifampicin (300 mg twice daily) for a 10-week period 25 . Three patients did not tolerate the combination, two because of diarrhea associated with Clostridium difficile, and three of them responded well and remained clear at 12 months. The combination of rifampi-cin and clindamycin was also successfully used for two other chronic and difficult-to-treat conditions folliculitis decalvans 45 and acne ke-loidalis nuchae 25 . Clindamycin is a lincos-amide antibiotic active against Gram-positive cocci (except enterococci) and most anaerobic bacteria 52 . Rifampicin is a broad spectrum antibacterial agent that inhibits the growth of the majority of Gram-positive bacteria as well as many Gram-negative microorganisms 55 . It is highly active against both Staphylococcus aureus and coagulase-negative staphylococci. Rapid emergence of resistance when the drug was used alone has limited the use...
Lead to colonoscopy, as the presence of gastrointestinal endoscopic lesions and granulomas on biopsy establishes the diagnosis of CD. Conversely, there is a need for a systematic search for acne, folliculitis, and HS skin lesions in CD patients, particularly when a steroid treatment is planned.
The pilosebaceous unit is an important site of skin infections such as acne vulgaris, folliculitis, furunculosis, and carbunculosis. A common pathogen associated with infections in the pilosebaceous unit is P. acnes. Although acne vulgaris is not an infectious disease, the role of P.
Despite this, we have seen the benefit of UVB 311nm phototherapy in HIV-infected patients with extreme pruritus associated with papular dermatoses or eosinophilic folliculitis, resistant to all other therapies. As long as these patients were under the protection of HAART, UV therapy caused no observable worsening of the immune status.
The exact cause of the rupture of the follicle is not established, although a lymphocytic inflammatory infiltrate appears to be present in early lesions (see Chap. 4). There is some evidence of infundibular epithelial hyperproliferation as well. In older lesions, sinus tract formation predominates the histopathology. It is speculated that the introduction of follicular material into the dermis as well as secondary colonization of sinus tracts cause flares of HS. These mechanisms suggest that HS can be classified as a folliculitis of unknown origin affecting the deeper end of the hair follicle and not involving the sebaceous glands. The polymicrobial colonization
The clinical characteristics of HS, i.e., deep-seated lesions and topography, are very specific and the hallmark of the disease however, they are not explained by the histological pictures which form the main evidence for establishing a connection with acne and the so-called follicular obstruction diseases. Exceptional case reports of an association of HS with dissecting folliculitis of the scalp, acne conglobata, large epithelial cysts and pilonidal cysts have focused attention on a possible common mechanism shared by these diseases and their grouping together under the term follicular obstruction diseases. Some case reports of an association with Dowling-Degos pigmentation of the flexure also point to a follicular obstruction. In spite of these anecdotal reports, the prevalence of acne in HS patients is identical to the prevalence in controls. The rarity of these reports and the Table 9.1. Similarities and differences between acne vulgaris, acne conglobata, hidradenitis suppurativa...
In 1956, Pillsbury, Shelley and Kligman coined the term follicular occlusion triad for the common association of acne conglobata, HS and dissecting folliculitis of the scalp. They proposed that the pathological event unique to each disease was follicular hyperkeratinization 19 . All three diseases, HS, acne conglobata and dissecting folliculitis, represent chronic, recurrent deep-seated folliculitis resulting in abscesses followed by sinus tract formation and scarring. In an actively inflamed lesion the sinus contains hairs surrounded by neutrophils, granulation and scar tissue (Fig. 4.7). In an end-stage lesion there is scarring with patchy inflammation, which may track down a healed sinus at the site of a destroyed hair follicle.
HS is clearly a follicular disease located to restricted areas of the body. The pathogenic process in the hair follicle may be elucidated from histology, and appears to be rupture of the deeper parts of the follicle, with spillage of the fol-licular contents into the dermis and subsequent inflammation (see Chap. 4). The exact cause of the rupture is however not established. So even if HS can be classified as a folliculitis, just as acne vulgaris, this classification does not aid our understanding significantly, and additional aspects of the diseases must therefore be considered.
I began to develop what I initially called acne and now know to be HS quite a number of years ago, probably when I was in my late 20s (I'll be 35 tomorrow). It began as very small cysts or pimples in my groin area or on my buttocks that initially would go away in a few days. I mentioned it briefly to a few doctors and was simply told I had ingrown hairs or folliculitis or it was from wearing jeans most of the time. Over the years, the frequency, size, and duration of them increased to the point where they became so