Cutaneous infections of the head and neck

Cutaneous infections of the head and neck

Facial Plast Surg Clin N Am 11 (2003) 165 – 173 Cutaneous infections of the head and neck Michael Shapiro, MD, Victoria P. Werth, MD* Department of D...

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Facial Plast Surg Clin N Am 11 (2003) 165 – 173

Cutaneous infections of the head and neck Michael Shapiro, MD, Victoria P. Werth, MD* Department of Dermatology, University of Pennsylvania Health System, 2 Rhoads Pavilion, 34th & Spruce Streets, Philadelphia, PA 19104, USA

Impetigo Impetigo (Fig. 1), a superficial cutaneous bacterial infection, is one of the more common infections of the face. The nonbullous form was originally named ‘‘impetigo faciei contagiosa’’ by Kaposi in 1895 [1]. Localization to the perioral and nares regions is common because these areas are frequently the targets of trauma [2]. Staphylococcus aureus is the most commonly isolated agent in the nonbullous form, though group A b-hemolytic Streptococcal infections might also be seen [3]. Characteristically, 2- to 4-mm, erythematous macules evolve into vesicles or pustules, which quickly rupture to leave ‘‘honey-colored’’ yellow, crusted exudates [4]. Disease risk factors include varicella, insect bites, abrasions, lacerations, and burns [5]. Regional lymphadenopathy [6] and leukocytosis are common [7]. The bullous variant is invariably caused by S. aureus, it does not favor the face, and it is usually seen in neonates. Superficial fragile bullae rupture, leaving annular erosions with a collarette of scale. Complications include osteomyelitis, septic arthritis, pneumonia, septicemia [6], cellulitis, and acute poststreptococcal glomerulonephritis [8]. Poststreptococcal glomerulonephritis is caused by nephrogenic strains of group A b-hemolytic Streptococcus.

Erysipelas Erysipelas, which is usually caused by group A b-hemolytic Streptococcus [9], classically involves * Corresponding author. E-mail address: [email protected] (V.P. Werth).

the face. Recently, however, most cases have occurred on the lower extremities [10,11]. Young, elderly, and immunocompromised hosts are most susceptible, especially in the summer [12]. After several days of incubation, fevers, chills, malaise, and nausea develop. Subsequently, an erythematous, shiny, tense, warm plaque with a sharply demarcated, edematous border appears. On the face, the plaque often extends to cover an entire cheek, with involvement of the upper lip and eyelids. A tender submandibular lymph node is often present. Portals of entry include perle`che or rhagades of nostrils or external canthi, bites, and excoriated dermatoses [13]. Local and systemic complications are rare [9].

Actinomycosis More rare bacterial infections include cervicofacial actinomycosis and rhinoscleroma. Actinomyces israelii, the usual causative agent in actinomycosis, is a slow growing, branching, gram-positive bacteria. Aggregates of mycelial-type filaments form sulfur granules, which appear yellow in pus [14]. These normal constituents of mouth flora produce infection after tooth extraction or other oral surgical procedures (often in patients with neglected dental care), jaw fractures, puncture wounds, and molar tooth eruptions [15]. Chronic lesions present as painful, slowly enlarging, fluctuant nodules with reddish-purple discoloration of the overlying skin. Acute presentations of painful, suppurating, pyogenic infections with sinus tract formation to the skin or oral mucosa and an increased incidence of systemic symptoms might be observed [16]. Untreated disease produces ‘‘woody’’ fibrosis and a ‘‘lumpy jaw,’’ the latter finding resulting

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M. Shapiro, V.P. Werth / Facial Plast Surg Clin N Am 11 (2003) 165–173

Fig. 1. Impetigo.

from coexistent scarring and sinus tract formation. Infection is characteristically unimpeded by anatomic barriers and thus can localize to any tissue or structure of the upper and lower jaw. The mandible might be affected most frequently [17].

(termed a Buruli ulcer) [23]. Excision of preulcerative lesions is curative [24]. Head and neck disease occurs more commonly in young children [25]. Mycobacteria avium intracellulare is observed on the legs of immunocompromised hosts during disseminated infection. Recently, however, rosacea-like lesions in two immunocompetent brothers were noted [23,26]. Contact with Mycobacteria marinum following a minor injury in contaminated water, fish tanks, fisheries, and swimming pools produces a bluish-red nodule or pustule that ulcerates or forms a suppurating abscess on the face and elsewhere [21,27]. Mycobacteria kansasii, a photochromogen-like M. marinum, typically causes pulmonary disease. Skin lesions are seen in immunosuppressed subjects. The presentation of one case resembled rhinophyma [28]. Mycobacteria scrofulaceum and Mycobacteria avium might be the etiologic agents that are responsible for the majority of chronic cervicofacial adenitis in children. Examination reveals unilateral submandibular and submaxillary nodes and mild neck pain [29].

Rhinoscleroma Tuberculosis Rhinoscleroma, which is caused by Klebsiella rhinoscleromatis, occurs in isolated regions that are afflicted with crowding and poor sanitation. Direct, prolonged contact with mucous membrane secretions is required for transmission. The exudative disease stage is characterized by nasal congestion and frontoethmoidal headaches. Symptoms persist for months, and ultimately epistaxis, dyspnea, and a fetid nasal secretion can be observed [18,19]. The infiltrative stage follows, in which painless, red or waxy infiltrative lesions occur in the nasal septum and lower nasal fossa, producing obstruction. Laryngeal infiltration can result in voice changes, and soft palate anesthesia can occur [19,20]. Monstrous deformities are seen in the tumoral stage. Progressive lower nasal fossae disease eventuates in invasion of the nasal tip and alae, upper lip, and gums with partial or total nasal obstruction (which can be fatal). Progressive laryngeal disease destroys the patient’s ability to speak. Squamous cell carcinomas might develop [19].

Cutaneous tuberculosis (TB) is a rare manifestation of Mycobacteria tuberculosis infection. The three most common forms are scrofuloderma, TB verrucosa cutis, and lupus vulgaris (LV; Fig. 2). LV, the most frequently observed form, is a paucibacillary disease that is seen in patients with a moderate to high degree of immunity, usually secondary to a previous or concurrent mycobacterial infection [30,31].

Atypical mycobacteria Extremities, rather than the head and neck, are the most frequent sites for atypical mycobacterial infections [21]. Mycobacteria ulcerans infection occurs in warm climates [22] following minor injury, resulting in painless, subcutaneous swelling that progresses to a shallow necrotic ulcer with undermined edges

Fig. 2. Lupus vulgaris.

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Cooler body sites (eg, face, neck, and ears) are favored [31 – 33], as are buccal, nasal, and conjunctival mucosa [34]. LV lesions appear as red to orange papules or nodules that exhibit an ‘‘apple-jelly’’ hue under diascopy. Peripheral extension over many years leaves an atrophic central plaque. Ultimately, destruction and malignancy can develop (with squamous cell carcinomas seen most frequently) [35]. Establishing the diagnosis by culture, Fite stains, or polymerase chain reaction (PCR) analysis is challenging given the paucibacillary nature of LV lesions [36].

Leprosy Hansen’s disease, or leprosy (Figs. 3, 4), is caused by Mycobacteria leprae after an incubation period of 2 to 5 years or more. Transmission occurs through airborne droplets from the nasal mucosa or upper airways [37,38]. Most patients in the United States have lived in endemic areas of Asia, Africa, and Latin America, although leprosy is also endemic in Texas, Louisiana, and California [39]. M. leprae preferentially affects cooler areas of the body such as the face. Paucibacillary or tuberculoid leprosy, which is seen in patients with a vigorous cellular immune response, presents with erythematous or purplish, sharply demarcated plaques on the face and other areas. Lesions are characteristically hairless, dry, and hypoesthetic. Cutaneous nerves in proximity of the

Fig. 4. Borderline leprosy.

lesions, such as the greater auricular nerve, might be infiltrated and thickened [40]. Bilateral, symmetrical macules, papules, and nodules characterize multibacillary or lepromatous leprosy, which is seen in patients with a poor cellular immune response. The scalp is usually spared, but the nasal mucosa might be involved, leading to stuffiness, discharge, epistaxis, and nasal cartilage destruction. Loss of teeth might result from oral involvement. Diffuse infiltration and thickening of the skin can produce ‘‘leonine facies’’ over the face, ears, cheeks, nose, and eyebrows [41]. Loss of eyebrow hair (at the lateral margins first) or madarosis might be observed [37]. Ocular involvement can occur [40]. Seventh cranial nerve damage can prevent adequate eye closure, or lagophthalmos, resulting in corneal desiccation and increasing the risk of secondary infection [41]. Diagnosis of all forms of leprosy is made by clinical examination and skin biopsies (where acid-fast bacilli can be detected). Sensory loss might be difficult to appreciate in early facial lesions because of the rich innervation of this region [41].


Fig. 3. Adult male with leprosy; from Seoul, Korea.

Fungal infections of the face and scalp include Tinea capitis, Tinea barbae, Tinea faciale (Fig. 5), and sporotrichosis. In the Tinea diseases, the causative dermatophytes invade and remain in the stratum


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Fig. 5. Tinea faciale.

corneum [42]. Examination (usually of preadolescent children) reveals scaling, black dots, pustules, crusting, alopecia, abscesses, pruritus, and pain [43]. Transmission occurs by person-to-person contact and fomites. The three forms of T. capitis are ectothrix, endothrix, and favus. In ectothrix, hyphae fragment into arthroconidia outside the hair shaft with cuticle destruction. In endothrix, arthroconidia penetrate the hair shaft without cuticle destruction. Favus, which is seen rarely in the United States, exhibits a combination of arthroconidia, air spaces, and fragmented hyphae within the hair shaft [44], leading to the development of cup-shaped, yellow crusts around hairs and ultimately cicatricial alopecia. More than 90% of T. capitis in the United States is caused by endothrix infections, which are caused by Trichophyton tonsurans [43]. Microsporum canis is the second most commonly isolated organism [44], and Trichophyton schoenleinii is usually implicated in favus [45]. T. barbae is a superficial fungal infection of the male coarse-hair-bearing beard and mustache, predominantly through exposure to animals such as cows and dogs in rural areas. The most common dermatophytes are the zoophilic organisms Trichophyton mentagrophytes and Trichophyton verrucosum [46]. Clinically, nodular and boggy kerion-like lesions are seen, often on the chin, neck, and maxillary or submaxillary areas, with sparing of the upper lip [46]. Other forms include a superficial eruption resembling a bacterial folliculitis and a circinate, spreading, vesiculopustular eruption with central scaling [47]. The dimorphic fungus Sporothrix schenckii produces sporotrichosis. S. schenckii is ubiquitous in soil, sphagnum moss, decaying vegetation, and animals such as birds, dogs, horses, armadillos, and rats [48,49]. Infection occurs after inoculation with sharp

objects that harbor the spores such as thorns, straw, hay, and animal claws [50], although cheek-to-cheek transmission between a mother and a child has been reported [51]. Individuals at highest risk include florists, gardeners, forestry workers, miners, laboratory personnel, veterinarians, and pet owners [49]. Lymphocutaneous, fixed cutaneous, and disseminated forms of the disease are recognized. The lymphocutaneous pattern is most common and is characterized by a linear lymphangitic pattern of ulcerative nodules. The face is a frequent site of fixed cutaneous disease [50]. Children are more likely to present with this form of sporotrichosis, whereas adults usually exhibit lymphocutaneous lesions [52 – 54]. Fixed cutaneous sporotrichosis can exhibit ulcerative, verrucous, acneiform, or erythematous nodules and plaques [50]. A presentation mimicking facial cellulitis has been observed [55]. These lesions can persist for years until treated [48], and they likely represent a high degree of host immunity [49]. Definitive diagnosis is made by fungal cultures. Perle`che, from perle`cher or ‘‘to lick thoroughly with the tongue’’ in French, refers to inflammation and fissuring that leads to soggy, white, angular lesions of the corners of the mouth. Candida albicans overgrowth often occurs. The elderly and riboflavin[56] and zinc-deficient [57] individuals are predisposed. In old age, increasing skin laxity produces redundant creases that form an intertriginous zone. Edentulousness also deepens these crevices, leading to saliva accumulation and maceration [58].

Viral diseases Human papilloma virus Cutaneous viral infections of the head and neck include the human papilloma virus (HPV), human simplex virus (HSV), and varicella zoster virus (VZV). HPV produces verruca vulgaris (common warts; Fig. 6), verruca plana (flat warts), and filiform warts. Filiform warts commonly affect the face. Verruca plana appear as 2- to 4-mm, slightly elevated, flat-topped papules, whereas filiform warts display grouped, finger-like projections. Small, soft, pink or white papules of the buccal, gingival, or labial mucosa, tongue, and hard palate can occur. Other oral manifestations include focal epithelial hyperplasia [59] and oral condyloma acuminata [60,61]. Mastication of warts might result in their spread to the oral mucosa and lips. HPV genotypes have been associated with squamous cell carcinoma of the skin and possibly with cancers of the lip,

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Fig. 8. Labial herpes simplex virus.

Fig. 6. Periocular verruca vulgaris.

especially in immunosuppressed renal transplant recipients [62]. Herpes simplex More than 85% of adults worldwide have serologic evidence of herpes simplex virus (HSV-1) exposure, which is the causal agent in recurrent oral-facial ‘‘cold sores’’ or ‘‘fever blisters’’ (Figs. 7, 8) [63]. Primary infection can be asymptomatic or associated with a fever and a sore throat. Painful vesicles and erosions appear on the tongue, palate, gingiva, buccal mucosa, and lips and can coalesce to form plaques with a gray membrane surface [64]. The virus lies dormant in the trigeminal ganglion until reactivation by triggers such as sunlight, stress, fatigue, surgery, and other perioral trauma [65]. One-third of adults suffer from recurrent oro – facial infections [66]. Itch-

Fig. 7. Herpes simplex virus.

ing and burning on the vermilion border of the lips herald recurrent episodes. Erythematous papules then appear that vesiculate, ulcerate, crust over, and heal in 8 to 9 days [64]. Perioral cutaneous surgery, chemical peels, dermabrasion, and laser resurfacing can precipitate severe, widespread HSV reactivation with scarring. Prophylactic antiviral therapy is recommended for all patients undergoing perioral cutaneous procedures— including patients who do not have a history of prior HSV—because subclinical latent infections and de novo infections occur commonly [67 – 69]. Herpes zoster Varicella (chickenpox) usually occurs in childhood. The virus is highly contagious between the 2 days preceding the rash and when crusting has occurred [70]. Waves of pruritic vesicles arising on an erythematous base (described as ‘‘dew drops on rose petals’’) develop on the face and scalp and spread caudally. Low-grade fever and malaise can occur. New lesions arise as older ones become pustular, hemorrhagic, and crusted, thus characteristically producing the simultaneous appearance of lesions in various stages. Secondary bacterial infections can occur [71]. Adult infections might result in VZV pneumonitis and other complications [72]. More than 90% of adults demonstrate serologic evidence of previous infection with VZV, and up to 20% of individuals have disease reactivation later in life (eg, herpes zoster or shingles) [73]. Latent infection persists in dorsal ganglion cells. The incidence of herpes zoster increases with age and in immunocompromised states (Fig. 9) [74]. Onset is heralded by fever, malaise, headache, and neuralgias (including itching, tingling, burning, and severe pain). Grouped vesicles on an erythematous base appear in a dermatomal distribution. These vesicles become pustular


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and perioral and intra- and periocular lesions are seen [84,85]. The disease is self-limited in immunocompetent hosts [83]. In HIV patients, treatment-refractory disease is seen [86]. Molluscum contagiosum never enters a latent state.


Fig. 9. Varicella zoster virus.

and hemorrhagic, and ultimately crust in 7 to 10 days. Fifteen percent of cases involve the trigeminal ganglion [75]. Herpes zoster involves the ophthalmic division of the trigeminal nerve in 7% of patients [76]. In one third of these patients, the nasociliary portion of the ophthalmic nerve is affected, as evidenced by vesicles on the sides and tip of the nose [77]. Lid damage, conjunctivitis, uveitis, and ultimately blindness can ensue [70]. In the Ramsay-Hunt syndrome, geniculate ganglion involvement produces lesions on the pinna, auditory canal, and tongue. It also causes Bell’s palsy, tinnitus, deafness, and vertigo [76]. Other complications include postherpetic neuralgia and central nervous system infection. HSV and VSV are diagnosed through clinical evaluation, Tzanck smear looking for multinucleated giant cells [78], culture, and direct fluorescent antibody testing.

Molluscum contagiosum Molluscum contagiosum (Fig. 10) is a poxvirus that infects children, sexually active young adults, patients with atopic diatheses, and immunocompromised patients (including those with malignancies, organ transplant recipients, and HIV infection) [79]. Transmission occurs through close skin-to-skin contact and fomites in children, and during sexual encounters in adults [80]. The distinctive flesh-totranslucent colored, dome-shaped, umbilicated papules appear on the face, trunk, and extremities of children [81] and on the abdomen and genitalia of young adults [80]. A facial predilection is observed in HIV-seropositive patients, in whom disfiguring, giant lesions measuring up to 1.5 cm can occur [82]. Adjoining lesions can also be seen on bearded sites because of autoinoculation during shaving [83]. Intra-

Lesions of primary syphilis, which are caused by Treponema pallidum, develop 3 to 5 weeks after exposure, usually in the genital region [87]. The classic Hunterian chancre is a round or oval, sharply demarcated papule with a rolled border and an eroded surface [88]. It is firm, rubbery, and painless. The frequency of extragenital lesions is increasing. Two thirds of extragenital chancres occur above the neck, with half of these found on the lips and 10% on the tongue, tonsils, pharynx, and oral mucosa [89]. Regional lymphadenopathy is common within 2 weeks of the appearance of the chancre. It occurs in the submental and preauricular chains when oral lesions are present [90]. Secondary syphilis arises 4 to 10 weeks after the onset of primary syphilis [90]. A flu-like prodrome, lymphadenopathy in occipital and posterior cervical chains and elsewhere, iritis, and other ocular findings might accompany the frequently observed cutaneous secondary syphilids [91]. Macules arise on the trunk and spare the face but can spread there as they become more papular or annular in configuration (Fig. 11) [88]. Pustules are seen in less than 2% of cases, but they are most common on the face and scalp [92]. Reddish-copper colored, firm, scaly papules on the face have been described as ‘‘nickel and dime spots’’ [93]. The hairline might become involved in a crown distribution, termed corona veneris [90]. Irregular, ‘‘moth eaten,’’ nonscarring

Fig. 10. Molluscum contagiosum.

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Fig. 11. Secondary syphilis.

alopecia might be seen infrequently at the margins of the scalp and in the beard and eyebrows. Mucous membrane disease is also common. The most common lesion is the syphilitic sore throat, which is seen in 15% to 30% of cases [94]. Raised, slightly lobular papules called condyloma lata, and mucous patches, which are asymptomatic round or oval macerated slightly elevated erosions covered by a gray or pearly membrane, can be seen on the tongue, oral mucosa, lips, and throat. Grouped mucous patches on the soft palate or fauces form an elongated ulceration known as a ‘‘snail track ulcer’’ [95]. Raised and fissured mucous patches at the labial commissures are called ‘‘split papules’’ [90]. Finally, hypopigmented neck patches, termed leucoderma colli or ‘‘collar of Venus,’’ can be seen, often in dark-complexioned women [95]. Secondary syphilids resolve spontaneously within 3 to 12 weeks, but they might recur in the subsequent 5 years. The patient then enters the asymptomatic latent stage. One third of these patients go on to develop systemic, cutaneous, noduloulcerative, or gummatous tertiary syphilis [96]. Gummas can be seen on the buccal surface, larynx, pharynx, and tongue, where they can result in chronic interstitial glossitis with loss of normal papillae [91]. Infiltration of the floor of the nose or roof of the mouth can lead to perforation of the hard palate, and nasal deformities caused by septal destruction can be seen [95]. Diagnosis is achieved by clinical examination, darkfield microscopy, and serologic venereal disease research laboratory (VDRL) and rapid plasma reagin (RPR) testing.

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