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Atopic Eczema Dermatitis Syndrome
Folliculitis - Cure Your Folliculitis
Hereditary forms of folliculitis, such as follicular eczema (generally classified under "atopic dermatitis"), and the deeper forms of inflammatory folliculitis that involve the entire follicular structure, such as folliculitis decalvans, occur most commonly in blacks. Folliculitis may also be seen as a secondary infection in conditions such as eczema, scabies, and excoriated insect bites. It is more commonly found in patients who are diabetic, obese, or immunocompromised.
Coagulates-positive Staphylococcus aureus is the responsible pathogenic bacterium in most cases of infectious folliculitis. Folliculitis may evolve into afuruncle (boil), which is a deep infection; a carbuncle refers to an aggregation of furuncles. The discussion in this article will be limited to the superficial forms of folliculitis.
PHYSICAL FINDINGS
A pustule or papule with a central hair is the primary lesion in folliculitis. Secondary lesions evolve from ruptured pustules and may consist of erosions, crusts, and darkly pigmented macules. The central hair shaft may not always be visible. Follicular lesions tend to exist in a gridlike pattern on hair-bearing areas of the body.
CAUSES AND
PRECIPITATING
FACTORS
Patients with conditions that reduce host resistance, such as diabetes or human immunodeficiency virus infection, are more likely to develop an infectious bacterial, viral, or fungal folliculitis. Folliculitis is more common in carriers of aureus, particularly nasal carriers. Infectious and inflammatory folliculitis may be seen in areas of skin subjected to:
-Repeated trauma (such as waxing, plucking, and shaving).
-Friction.
- Restrictive clothing, such as tight jeans.
- Excessive sweating.
Folliculitis is more commonly seen in the obese. Inflammatory folliculitis (follicular eczema) with episodic bacterial superinfection is more likely to occur in patients with atopic dermatitis.
STAPHYLOCOCCAL FOLLICULITIS
S aureus folliculitis is the most common type. It may occur in crops of pustules and/or papules on the scalp, thighs, legs, axillae, and inguinal areas. Folliculitis involving an eyelash is called a hordeolum, or sty. Similarly, folliculitis may affect a single nasal hair follicle and produce a tender erythematous papule or pustule within the nasal mucosa or near the tip of the nose.
OTHER FORMS OF FOLLICULITIS
Folliculitis is not always caused by S aureus. Other forms of folliculitis may be caused by organisms acquired in hot tubs or by irritation, friction, chemicals, steroids, or fungi. In addition, therapeutically recalcitrant folliculidities, such as the herpes simplex infections or eosinophilic pustular folliculitis, may be seen in patients with acquired immunodeficiency syndrome (AIDS).
HOT TUB FOLLICULITIS Pseudomonas folliculitis, which may be acquired from communal hot tubs, is caused by Pseudomonas aeruginosa infection. Although they have increased the incidence of folliculitis, hot tubs are often overlooked as a cause. Jacuzzis, therapeutic whirlpools ("whirlpool folliculitis"), public swimming pools, and the use of loofah sponges may also be a source of Pseudomonas infection. Pseudomonas folliculitis has recently been found to occur under diving suits and after wax depilation. Lesions of hot tub folliculitis consist of intensely pruritic or tender follicular papules and/or pustules that are most often found on the trunk (the area covered by a bathing suit). They occur one to three days after bathing in a hot tub, whirlpool, or public swimming pool.
Nonbacterial, or sterile, folliculitis can arise from physical or chemical irritation. Such irritants include leg waxing, leg shaving, axillary shaving, and hair plucking. Chemical depilatories, electrolysis, occlusive dressings, and excessive sweating can also contribute to this problem, as can wear tight jeans. Nonbacterial folliculitis may also be related to working conditions, such as the use of greases or oils, and to the application of various cosmetics. Bacteria, such as S aureus, are not infrequent secondary invaders
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Manifestations of Mucocutaneous Infection
Great variability exists in the clinical symptomatology of primary HSV-1 infections; asymptomatic infection is the rule rather than the exception. The incubation period ranges from 2 days to 12 days, with a mean of about 4 days. Primary HSV-1 infection results in oral shedding of virus in the mouth for as long as 23 days. Neutralizing antibodies appear between days 4 and 7 after the onset of disease, and levels of these antibodies peak in about 3 weeks.
Symptomatic disease in children is characterized by involvement of the buccal and gingival mucosa. The duration of illness is 2-3 weeks. Children with symptomatic primary infection are often unable to swallow liquids because of the associated pain. Lesions within the mouth evolve from vesicles to shallow ulcerations on an erythematous base before healing.
Submandibular lymphadenopathy is common in patients with primary gingivostomatitis but rare in those with recurrent infections. Other findings include sore throat and mouth, malaise, tender cervical lymphadenopathy, and an inability to eat. A clinical distinction should be drawn between intraoral gingival lesions, indicative of presumed primary infection, and lip lesions indicative of recurrent infections.
Pharyngitis is common, along with a mononucleosis-like syndrome, among patients with primary HSV infections that develop later in life. The differential diagnosis of HSV gingivostomatitis includes herpangina, candidal infections of the mouth, Epstein-Barr virus mononucleosis, lesions induced by chemotherapy or radiation therapy, and Stevens-Johnson syndrome.
The onset of recurrent orolabial lesions is heralded by a prodrome of pain, burning, tingling, or itching, which generally lasts for 6 hours and is followed by the appearance of vesicles. Vesicles appear most commonly at the vermilion border of the lip and persist on average for only 48 hours. The vesicles generally number three to five.
Lesions progress to the pustular or ulcerative and crusting stage within 72-96 hours, and healing is complete within 8-10 days. Pain is most severe at the outset and resolves quickly over 96-120 hours. The frequency of recurrences varies among individuals. Other cutaneous HSV-1 lesions occur.
Skin infections caused by HSV generally manifest as eczema herpeticum in patients with underlying atopic dermatitis. Lesions can be either localized, resembling herpes zoster, or disseminated. Infections of the digits, known as herpetic whitlow, are particularly common among medical and dental personnel.
The estimated incidence of herpetic whitlow is 2.4 cases per 100,000 population per year, and it is caused by HSV-1 or HSV-2. Disseminated cutaneous HSV infections have been reported among wrestlers. Other skin disorders associated with extensive cutaneous lesions include Darier’s disease and Se´zary syndrome. HSV infections of either type can trigger erythema multiforme.
Primary and secondary manifestations of infections sustained by herpes simplex viruses are among the most prevalent human maladies. The emergence of drug-resistant strains of HSV is a growing problem and represents a serious concern both in terms of clinical management and of viral ecology. Resistance to all major herpes treatments, such as acyclovir, vidarabine and foscarnet, has been increasingly observed, especially amongst those immuno-compromised.
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