Epidemiology and clinical manifestations

Folliculitis is defined as inflammation of hair follicles. Therefore, this is a very nonspecific term which can apply to infectious folliculitis produced by bacterial or fungal infection, or to non-infectious from occlusion and friction. Bacterial folliculitis can occur in any population, and there is no predilection for gender, race, or age. Fungal folliculitis of anogenital skin is most common in adult men, particularly those with accompanying onychomycosis or tinea pedis. Irritant folliculitis of the vulva, mons, and medial thighs is especially common in women who shave, and in overweight individuals where friction, moisture, and persistent warmth are likely to produce irritant folliculitis.

Folliculitis is often an asymptomatic, cosmetic issue, but patients sometimes complain of mild irritation or itching. Folliculitis can be painful, especially in the uncommon case of folliculitis of the modified mucous membranes.

Folliculitis is manifested by scattered, red dome-shaped and crusted papules, pustules, or small, round erosions that are left as the pustules quickly rupture (Figures 20.1 and 20.2). Folliculitis occurs primarily on dry, keratinized skin, particularly the proximal, medial thighs due to friction, as well as on the buttocks. Folliculitis produced by Pseudomonas aeruginosa (hot-tub folliculitis) is manifested by papules that are usually larger and more tender, and pustules are less obvious. These are often prominent in the swimsuit distribution and skin folds.

Figure 20.1 Red papules and pustules on the buttocks are a very common manifestation of folliculitis.

Figure 20.2 Discrete red papules, crusts, and pustules are characteristic of folliculitis.

Folliculitis occasionally occurs on the modified mucous membranes, including the labia minora, where lesions often present as small papules with 1–2 mm superficial round erosions (Figure 20.3). Fungal folliculitis of genital skin occurs within plaques of tinea cruris and usually manifests as small nodules or crusts within red, scaling plaques on the proximal, medial thighs (Figure 20.4).

Figure 20.3 Shaving folliculitis is an irritant condition produced by short, stiff, sharp hair curling back into the skin.

Figure 20.4 Fungal folliculitis is characterized by papules, pustules, and crusts within an inflamed plaque of tinea cruris.

Differential diagnosis

Folliculitis is most often confused with inflamed mollusca contagiosa or insect bites (Figure 20.5). Keratosis pilaris and cutaneous Candida can occasionally mimic folliculitis as well (Table 20.1).

Figure 20.5 When inflamed, mollusca contagiosa are indistinguishable from folliculitis or furunculosis, but surrounding typical lesions generally allow for the correct diagnosis.

Table 20.1 Folliculitis

Laboratory and histology

Laboratory abnormalities are limited to cultures revealing the etiology of folliculitis, when it is infectious. A fungal preparation of a pustule roof shows branching hyphae, when the underlying cause is a fungal infection.

Histology is generally not performed, but at times a biopsy may be required for diagnosis. A biopsy shows an inflammatory infiltrate that includes neutrophils around the hair follicle, sometimes with rupture of the follicle. Bacterial folliculitis most often shows organisms just under the stratum corneum, although fungal folliculitis shows the dermatophyte within the stratum corneum. Special stains highlight the organisms. Occlusive folliculitis and acneiform folliculitis show no organisms.

Pathogenesis

As noted above, the pathogenesis depends upon the type of folliculitis. Bacterial folliculitis is almost always produced by Staphylococcus aureus. Occasionally, Pseudomonas aeruginosa causes bacterial folliculitis, usually in patients who have recently used an improperly maintained spa or hot tub. Fungal folliculitis is produced by dermatophytes sometimes self-inoculated from tinea pedis or with fungal folliculitis of the legs spread by shaving.

Irritant folliculitis can be produced by friction, occlusion of skin folds, and constant moisture of sweat or urine. Shaving also produces folliculitis when either the tops of hair follicles are irritated by the razor, or when the short, stiff, curly hair curves back into the skin to pierce it.

Management and prognosis

The treatment of folliculitis depends upon the cause. Bacterial folliculitis is treated according to cultures. Methicillin-resistant Staphylococcus aureus, even when community-acquired, is becoming increasingly prevalent, so that cultures are frequently indicated. Pseudomonas folliculitis clears whether or not antibiotic therapy is administered as long as the source of the organism is avoided. Patients with significant pain or constitutional symptoms generally benefit from ciprofloxacin or levofloxacin.

Fungal folliculitis requires oral therapy since topical medications do not penetrate follicles sufficiently. Options include griseofulvin 500 mg twice daily, terbinafine 250 mg daily, fluconazole 100–200 mg weekly, itraconazole 100 mg daily, or ketoconazole 200 mg daily until clear.

Irritant folliculitis generally responds at least partially and slowly to local care to manage friction and moisture. The chronic administration of antibiotics which exert nonspecific anti-inflammatory effects is useful as well. These include doxycycline 100 mg twice daily, clindamycin 150 mg twice daily, and minocycline 100 mg twice daily. Improvement requires several weeks and maximal improvement often requires 2 or 3 months.

Recurrence following therapy is common in all forms of folliculitis. When bacterial folliculitis recurs, the patient is likely to be a nasal carrier, and mupirocin ointment can be inserted in the nose two or three times daily for 1 week each month to eliminate this carrier state. Otherwise, intermittent treatment for recurrences is indicated.

Epidemiology and clinical manifestations

Genital herpes simplex virus infection occurs most often in younger, sexually active individuals. This is especially common in the adolescent and young adult age group, and it is seen most often in patients who report multiple sexual partners. More people are seropositive for HSV in the United States than Europe, and seropositivity is higher in the western world than in developing countries¹. About 17% of people in the United States show exposure to HSV type 2, and about 57.7% to type 1². Clinical disease is present in about 50 million people in the United States³.

Previously, acquisition of HSV infection was believed to occur primarily with sexual activity during an active outbreak. Now, asymptomatic shedding has been identified as a major factor in transmission of HSV infection. Shedding can be detected in asymptomatic women with a history of genital HSV infection on about 5% of days when no lesions are present⁴. In fact, most infections are transmitted during exposure in the absence of lesions. Clinical manifestations vary, with a primary episode classically appearing quite differently from a recurrent outbreak. First-episode HSV is usually subclinical (or unrecognized), but a true primary first episode typically exhibits widespread vesicles and erosions with only modest grouping of individual lesions (Figures 20.7 and 20.8). These occur on modified mucous membranes of the vulva, on the mucous membranes of the vagina and cervix, and on surrounding dry, keratinized skin. Vaginal and cervical involvement often cause an irritating, purulent vaginal discharge, as well as occasional discharge from the urethra and rectal mucosa. Patients report remarkable pain that sometimes prevents micturition, and swelling is often substantial. Bilateral lymphadenopathy is common, and some patients exhibit fever, myalgias, and headache. A primary outbreak generally requires about 2 weeks for complete evolution of blistering, crusting, and healing.

Figure 20.7 The vesicles of primary herpes simplex virus are diffuse rather than grouped; the central collapse of an otherwise intact vesicle is characteristic of a herpes (simplex or varicella-zoster) blister.

Figure 20.8 When occurring on thin, poorly keratinized skin, primary herpes simplex virus blisters are generally not appreciated, but rather appear as scattered, discrete, round erosions.

Most patients experience recurrences within the first year, which can be mild and occasional, or as often as two or three episodes per month. The frequency and severity of recurrences are less with infection produced by HSV type 1 than by type 2^5,6. With the progression of time, episodes usually become less frequent, less severe, and less painful. Most often, the first recognized episode is a recurrence following a subclinical primary infection.

Recurrent HSV infection is usually manifested by a prodrome of tingling, itching, or burning. This is quickly followed by red vesicopapules which progress into one or several plaques of clustered vesicles which erode into coalescing erosions (Figures 20.9 and 20.10). Often, this is one small plaque. In addition to blisters and round erosions, fissures can occur as a result of an HSV recurrence. Immunosuppressed women sometimes develop typical, ulcerative, chronic HSV infection.

Figure 20.9 Recurrent herpes simplex virus infection presents as grouped vesicles.

Figure 20.10 Clustered red papules and blister of recurrent herpes simplex virus infection.

Although patients usually describe pain with recurrent HSV lesions, it is usually far less disruptive and painful than a primary outbreak. Headache, fever, and myalgias are uncommon with recurrences. Recurrences usually last a total of about 3–5 days unless they are scrubbed, rubbed, or secondarily infected.

Differential diagnosis

Other causes of superficial, small, coalescing red papules and erosions include candidiasis, bullous impetigo, folliculitis, mollusca contagiosa, and very small aphthae (Table 20.2). A fixed drug eruption causes recurrent same-site erosions, although individual erosions are generally significantly larger than the small coalescing erosions of HSV infection. HSV can be differentiated by cultures, polymerase chain reaction (PCR) technique, or by biopsy. Positive serological tests only report previous exposure, not necessarily current infection.

Table 20.2 Herpes Simplex Virus Infection

Laboratory and histology

The most significant laboratory abnormality is a positive HSV culture or positive results on PCR for HSV. At times, particularly with a first-episode primary outbreak, patients exhibit leukocytosis.

Other laboratory abnormalities include positive serologies for HSV. Negative HSV serology is good evidence that a current eruption does not represent recurrent HSV infection.

A biopsy is an excellent means of nearly definitive, rapid diagnosis. Histology reveals ballooning degeneration of keratinocytes, where individual epidermal cells coalesce into very large multinucleated cells. This finding is only seen with the herpetic blisters of HSV, varicella, or herpes zoster.

Pathogenesis

HSV infection is produced by DNA double-stranded viruses which are members of the Herpesviridae family. There are two types of HSV: type 1, most often found on the lip; or type 2, most often found on the genitalia. However, the two types are seen increasingly in both areas, possibly due to the prevalence of oral–genital sexual activity.

The virus is introduced into the basal layer of the epidermis, either by friction and trauma, or by happenstance of exposure over a break in the epithelium.

Therapy and prognosis

HSV infection cannot be cured, but it can be controlled very well, and outbreaks can be nearly eliminated with ongoing suppressive oral antiviral therapy. Topical therapy generally produces statistically but not clinically significant amelioration of disease. First-episode, primary HSV infection is best treated with any of several oral antiviral therapies (Table 20.3).

Table 20.3 Treatment for Primary Genital Herpes Simplex Virus Infection³

Recurrent HSV infection can be managed several ways, again orally (Table 20.4). First, if patients experience mild or only occasional recurrences, the individual may choose no treatment. Otherwise, patients can take an oral antiviral medication immediately with the onset of the prodrome, often preventing the outbreak. Patients with frequently recurrent outbreaks, those with recurrences not prevented by immediate therapy, and those with a psychological need to eliminate as many symptoms as possible benefit from daily suppression (Table 20.5). Immunosuppressed patients often require daily suppression to prevent either very frequent outbreaks or chronic HSV erosions and ulcers (Figure 20.11). Unfortunately, immunosuppressed patients have a slight risk for resistant HSV infection that is uncontrolled with currently available antiviral therapies. Foscarnet is sometimes useful in that event. The advent of effective therapy for the acquired immunodeficiency syndrome has significantly decreased the frequency of resistant HSV infection.

Table 20.4 Treatment for Recurrent Genital Herpes Simplex Virus Infection³

Table 20.5 Schedules for Suppression of Genital Herpes Simplex Virus Infection³

Figure 20.11 Herpes simplex virus infection in immunosuppressed patients is often more aggressive, forming nonspecific ulcerations diagnosed by a high index of suspicion and confirmed on culture, polymerase chain reaction, or biopsy of the edge of the ulcer.

Reasons for treating and suppressing HSV, in addition to personal patient comfort, include decreasing the risk of transmission of the disease. The risk of transmission of infection to a regular partner has been estimated to be about 10% per year when couples only avoid sexual activity during a clinical outbreak⁷. Interestingly, this study showed that all seroconversions occurred in the female partner, suggesting that women are at higher risk than men. The addition of barrier protection and suppressive antiviral medication reduces but does not eliminate this risk. In one study, daily valacyclovir and famciclovir decreased shedding to 1.3% and 3.2% of days, respectively, with historical shedding rates at about 5%⁸.

Patient education and support are crucial. The manner of sexual transmission should be discussed. Patients should be advised of the phenomenon of asymptomatic shedding, and the risk of transmissibility in the absence of active lesions. Because the risk of infection can be only minimized but not eliminated, partners must be informed.

Women should be made aware that a very unlikely but important primary morbidity of HSV infection is perinatal transmission to a newborn. The majority of neonatal herpes occurs in the presence of a new primary first-episode HSV infection, rather than from a mother with known HSV who has a clinical recurrence at delivery. In addition, the sequelae for the infant are less severe for those with type 1 HSV than type 2. Although the risk of a transmission to a neonate is small, this is a disease with tragic consequences, and the mother and her obstetrician should be aware.

Epidemiology and clinical manifestations

Varicella is a classic childhood viral infection that occurs in nonimmunized individuals. Fortunately, since the relatively recent availability of the varicella vaccine, varicella has become uncommon. Herpes zoster occurs most often in older people as their immune system begins to wane, and the virus migrates from the ganglion, where it has lain dormant, to the skin, producing classic shingles. This occurs earlier in patients who are immunosuppressed for reasons other than age. Although a vaccine is now available for the prevention of herpes zoster, it is not yet widely used⁹.

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A Systematic Approach to the Dermatoses of Pregnancy The Papular and Pruritic Dermatoses of Pregnancy Atopic Eruption of Pregnancy Vulvar Dermatoses: the Eczematous Diseases Physiologic Skin Changes of Pregnancy of Vulvovaginal Disease

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