**2. Bacterial infections of scalp**

There are several types of infections of the scalp including chronic scalp folliculitis [SF], folliculitis decalvans [FD], tufted folliculitis [TF], acne nuchae keloidalis [ANK] and dissecting

cellulitis [DCS]. These infections have similar features like chronic scarring folliculocentric pustules localised to the scalp. Many of these conditions show the presence of *Staphylococcus aureus* [SA] and response to antibiotic therapy [1].

#### **2.1. Scalp folliculitis**

Folliculitis is a pyoderma that begins within the hair follicle. It is classified according to the microbial aetiology, including bacteria, viruses and fungi, as well as many other non-infectious ones. The most seen folliculitis of scalp are *Staphylococcus aureus* [*S. aureus*] folliculitis, Herpes simplex virus folliculitis and dermatophytic folliculitis [Tinea capitis]. Some of the predisposing factors are hyperhidrosis, maceration, friction, overweight, medications such as corticosteroids and halogenated compounds, as well as occlusive hair care products and topical hydrocarbons, such as oils and tars. In addition, immunodeficiencies such as HIV/AIDS and diabetes mellitus are also predisposed to folliculitis [2].

*S. aureus* is the most common cause of folliculitis. The major cause is either contagion or autoinoculation from a carrier focus, usually nasal or perianal region. The typical lesion of folliculitis is a small inflamed, dome-shaped papule or pustule which can be drained spontaneously. Both pruritus and pain can be seen. Systemic symptoms, such as fever or lymphadenopathy, may occur when the involvement is widespread. Biopsy is rarely needed to distinguish between fungal or viral folliculitis. Biopsy shows neutrophils in the dermis and follicular wall damage. Many of the patients may carry *S. aureus*, so nasal and perineal cultures should be taken. Other forms of folliculitis can be identical in appearance, so this possibility should always be taken into consideration. Treatment options include topical antibiotic or disinfectant solutions such as mupirocin cream, triclosan [2%] or chlorhexidine [1%] and antistaphylococcal systemic antibiotics [1, 2].

#### **2.2. Folliculitis decalvans**

Folliculitis decalvans [FD] is a rare type of cicatricial alopecia and was first described by Quinquaud in 1881 [3]. It is an inflammatory disease characterised by follicular pustules and haemorrhagic crusting, leading to scarring hair loss. Although in most patient FD started in the vertex, other sites such as the occipital or midscalp area may also be affected. At the periphery of lesion, follicular pustules continue to form. Tufting of hairs may be seen [4]. Clinically, the majority of the patients were generally healthy, without any systemic symptoms or any signs of immunosuppression. Although the exact cause remains unknown, *S. aureus* is usually cultured from these pustules [5]. The disease shows a chronic and relapsing course. Histologically, early lesions show dense perifollicular inflammatory infiltrates consisting mostly of neutrophils. In later stages, follicular rupture, lymphocytes, histiocytes and plasma cells are seen, as well as perifollicular and interstitial dermal fibrosis [6, 7]. Differential diagnosis of FD consists of follicular degeneration syndrome or central centrifugal scarring alopecia.

As FD is usually associated with infection of *S. aureus* [5, 6], systemic antibiotics are the mainstay of disease [e.g., cephalexin, minocycline, tetracycline, clindamycin, rifampicin, ciprofloxacin]. Because of its high lipid solubility, and it is said to be the best antistaphylococcal antibiotic, rifampicin has been successfully used in combination with various other antibiotics [5, 7]. Rifampicin is not recommended for lone use. Rifampicin 300 mg b.i.d and clindamycin 300 mg b.i.d is the preferred regimen. Shampooing with antibacterial wash products and topical corticosteroids may also be useful. Varying results have been reported after treatment with prednisolone, isotretinoin, human immunoglobulin and more recently biologics [e.g., infliximab and adalimumab] [8, 9], neodymium: yttrium aluminium-garnet [Nd:YAG] laser [10] and photodynamic therapy [PDT] [11]. There is very limited evidence that FD can be treated with dapsone, minoxidil or radiation therapy [12].

### **2.3. Tufted hair folliculitis**

cellulitis [DCS]. These infections have similar features like chronic scarring folliculocentric pustules localised to the scalp. Many of these conditions show the presence of *Staphylococcus* 

Folliculitis is a pyoderma that begins within the hair follicle. It is classified according to the microbial aetiology, including bacteria, viruses and fungi, as well as many other non-infectious ones. The most seen folliculitis of scalp are *Staphylococcus aureus* [*S. aureus*] folliculitis, Herpes simplex virus folliculitis and dermatophytic folliculitis [Tinea capitis]. Some of the predisposing factors are hyperhidrosis, maceration, friction, overweight, medications such as corticosteroids and halogenated compounds, as well as occlusive hair care products and topical hydrocarbons, such as oils and tars. In addition, immunodeficiencies such as HIV/AIDS

*S. aureus* is the most common cause of folliculitis. The major cause is either contagion or autoinoculation from a carrier focus, usually nasal or perianal region. The typical lesion of folliculitis is a small inflamed, dome-shaped papule or pustule which can be drained spontaneously. Both pruritus and pain can be seen. Systemic symptoms, such as fever or lymphadenopathy, may occur when the involvement is widespread. Biopsy is rarely needed to distinguish between fungal or viral folliculitis. Biopsy shows neutrophils in the dermis and follicular wall damage. Many of the patients may carry *S. aureus*, so nasal and perineal cultures should be taken. Other forms of folliculitis can be identical in appearance, so this possibility should always be taken into consideration. Treatment options include topical antibiotic or disinfectant solutions such as mupirocin cream, triclosan [2%] or chlorhexidine [1%] and antistaphy-

Folliculitis decalvans [FD] is a rare type of cicatricial alopecia and was first described by Quinquaud in 1881 [3]. It is an inflammatory disease characterised by follicular pustules and haemorrhagic crusting, leading to scarring hair loss. Although in most patient FD started in the vertex, other sites such as the occipital or midscalp area may also be affected. At the periphery of lesion, follicular pustules continue to form. Tufting of hairs may be seen [4]. Clinically, the majority of the patients were generally healthy, without any systemic symptoms or any signs of immunosuppression. Although the exact cause remains unknown, *S. aureus* is usually cultured from these pustules [5]. The disease shows a chronic and relapsing course. Histologically, early lesions show dense perifollicular inflammatory infiltrates consisting mostly of neutrophils. In later stages, follicular rupture, lymphocytes, histiocytes and plasma cells are seen, as well as perifollicular and interstitial dermal fibrosis [6, 7]. Differential diagnosis of FD consists of follicular degeneration syndrome or central centrifu-

As FD is usually associated with infection of *S. aureus* [5, 6], systemic antibiotics are the mainstay of disease [e.g., cephalexin, minocycline, tetracycline, clindamycin, rifampicin, ciprofloxacin].

*aureus* [SA] and response to antibiotic therapy [1].

and diabetes mellitus are also predisposed to folliculitis [2].

**2.1. Scalp folliculitis**

200 Hair and Scalp Disorders

lococcal systemic antibiotics [1, 2].

**2.2. Folliculitis decalvans**

gal scarring alopecia.

Tufted hair folliculitis [THF] was first described by Smith and Sanderson in 1978 [7]. It is characterised by scarring bacterial folliculitis of the scalp associated with multiple bundles of hair emerging from a single dilated follicular orifice in a 'doll's hair' pattern. Infection with *S. aureus* is thought to be initial causative factor [13]. Tufting of hair is caused by clustering of adjacent follicular unit due to a fibrosing process and to retention of telogen hairs within a dilated follicular orifice [14]. The patients were 20–60 years old, the peak incidence occurring in 30 years [4]. It affects male more frequently than female.

Clinically, it presents erythematous, infiltrated plaque of cicatricial alopecia and enlarged follicular openings with tufts containing 20–30 apparently normal hair shafts (**Figure 1**). The lesions are usually found in the occipital and parietal areas [8]. Frequently reported subjective symptoms are pruritus, pain and scales adherent to the scalp and hair. Regional lymph node enlargement [occipital, pre- or retroauricular] may also be noticed [9]. *S. aureus* is most often cultured from the lesions [10]. Underlying differences in follicular anatomy or host response may be responsible for the lesion [15]. Histopathological studies reveal scarring with perifollicular inflammation of plasma cells, lymphocytes and neutrophils around the upper portions of the follicles sparing at the hair root level. Multiple hairs are seen emerging from a single follicular opening (**Figure 2**) [13].

**Figure 1.** Cicatricial alopecia with tufted folliculitis.

**Figure 2.** Dermoscopic image of the scalp with tufted folliculitis characterised by multiple hairs emerging from one single dilated follicular orifice.

THF may be seen with dissecting cellulitis of the scalp, folliculitis decalvans, acne keloidalis, Melkersson-Rosenthal syndrome and hidradenitis suppurativa [16]. In some case reports it has been described that tufted folliculitis in association with medication use, specifically with cyclosporine and lapatinib [17, 18]. Differential diagnosis consists of folliculitis decalvans, folliculitis keloidalis nuchae, kerion celsi, dissecting cellulitis of scalp, trichostasis spinulosa, follicular lichen planus and relapsing staphylococcal folliculitis [19].

The course of THF is chronic and the patient may experience intermittent flares and remissions. Treatment of this relapsing condition is notoriously difficult. As *S. aureus* is the initial causative agent, systemic antibiotics including ciprofloxacin, erythromycin, flucloxacillin and amoxicillin/clavulanic acid are regarded the standard therapy. Rifampicin and nadifloxacin have been proven as more effective than other therapeutic modality to control the pustular phase of the disease, of the best antibiotics active against *S. aureus*, as well as to prevent possible recurrences [4, 20]. Rifampicin can be used with a dose of 450 mg twice per day for 4 weeks or 600 mg daily for 10 weeks [20, 21]. Recently, a case of tufted hair folliculitis being treated with trastuzumab, a selective HER2 inhibitor, has been reported [22]. Good results with excision of the areas of scarring have also been described [13, 15].

#### **2.4. Acne keloidalis nuchae**

Acne keloidalis nuchae [AKN] is a chronic scarring folliculitis characterised by fibrotic, keloidlike papules and plaques on the occipital scalp and posterior neck. The term acne keloidalis was given to this condition in 1872 by Bazin [23].

Early AKN lesions are seen as mildly pruritic papules and pustules arranged in irregularly linear groups just below the hairline. With continued inflammation or infection the papules tend to coalesce and form hypertrophic scars or keloids that may be painful and disfiguring (**Figures 3** and **4**). In advanced cases, abscesses and sinus tracts with purulent discharge may develop [24, 25]. Actually AKN is not a form of acne vulgaris and unlike true acne vulgaris, comedones are not a feature of AKN. It is very common in individuals of African descent. Its prevalence ranges from 1 to 16% and the male to female ratio is at least 20:1. The probable onset age of AKN is 15–25 years and reduces after 55 years of age [26].

**Figure 3.** Acne keloidalis nuchae. Papules are seen below the hairline.

THF may be seen with dissecting cellulitis of the scalp, folliculitis decalvans, acne keloidalis, Melkersson-Rosenthal syndrome and hidradenitis suppurativa [16]. In some case reports it has been described that tufted folliculitis in association with medication use, specifically with cyclosporine and lapatinib [17, 18]. Differential diagnosis consists of folliculitis decalvans, folliculitis keloidalis nuchae, kerion celsi, dissecting cellulitis of scalp, trichostasis spinulosa,

**Figure 2.** Dermoscopic image of the scalp with tufted folliculitis characterised by multiple hairs emerging from one

The course of THF is chronic and the patient may experience intermittent flares and remissions. Treatment of this relapsing condition is notoriously difficult. As *S. aureus* is the initial causative agent, systemic antibiotics including ciprofloxacin, erythromycin, flucloxacillin and amoxicillin/clavulanic acid are regarded the standard therapy. Rifampicin and nadifloxacin have been proven as more effective than other therapeutic modality to control the pustular phase of the disease, of the best antibiotics active against *S. aureus*, as well as to prevent possible recurrences [4, 20]. Rifampicin can be used with a dose of 450 mg twice per day for 4 weeks or 600 mg daily for 10 weeks [20, 21]. Recently, a case of tufted hair folliculitis being treated with trastuzumab, a selective HER2 inhibitor, has been reported [22]. Good

Acne keloidalis nuchae [AKN] is a chronic scarring folliculitis characterised by fibrotic, keloidlike papules and plaques on the occipital scalp and posterior neck. The term acne keloidalis

Early AKN lesions are seen as mildly pruritic papules and pustules arranged in irregularly linear groups just below the hairline. With continued inflammation or infection the

follicular lichen planus and relapsing staphylococcal folliculitis [19].

results with excision of the areas of scarring have also been described [13, 15].

**2.4. Acne keloidalis nuchae**

single dilated follicular orifice.

202 Hair and Scalp Disorders

was given to this condition in 1872 by Bazin [23].

**Figure 4.** Acne keloidalis nuchae. Papules and hypertrophic scars are noticed on the occipital region.

The exact aetiology of AKN is unclear but it is associated with several factors including androgen excess, chronic mechanical trauma such as close haircuts and chronic rubbing of the area by clothing stimulating an inflammatory reaction, secondary bacterial infection, mast cell density and medications such as antiepileptic drugs or cyclosporine [24, 26–28].

Histological studies show evidence of follicular and perifollicular infiltrate at the upper onethird of the hair follicle in early lesions, whereas more advanced lesions reveal disrupted hair follicles, a foreign-body reaction with granulomatous inflammation and fibrotic dermis [25, 29]. Differential diagnosis of AKN consists of the other chronic scarring folliculocentric pustules localised to the scalp.

First step in treatment is patient education. It should be advised that the patient should avoid from mechanical irritation from clothing for prevention. Prognosis becomes good if the treatment begins at early stage. However, once major scarring develops, therapy is more difficult and morbidity is increased. If pathogenic microorganism with culture are identified, appropriate antibiotics should be prescribed. Conventional treatment modalities usually involve use of topical, intralesional or systemic steroids in combination with retinoids and/or oral antibiotics such as doxycycline or minocycline to decrease inflammation. Oral isotretinoin of 20 mg daily may be used alone or in combination with topical fusidic acid and oral cefadroxil [500 mg twice daily for 2 weeks] to treat the patient [30]. Other treatment options are cryotherapy and targeted ultraviolet B [290–320 nm] phototherapy. Combination of cryotherapy and intralesional steroid may help to reduce the size and firmness of papules and nodules [31]. Radiation therapy and intralesional 5-fluorouracil are alternative treatment strategies for refractory cases [32]. Recently, laser treatment such as CO2 laser, 1064-nm Nd:YAG laser, 59-nm pulse dye laser [PDL] and 810-nm diode laser have been used which allow for 82–95% improvement in one to five sessions [33]. Patients who present with big fibrotic nodules would benefit most from surgical excision. Excision with primary closure may be used for excellent cosmetic results for the management of extensive cases of AKN [23, 28, 34].
