Pediatric Tinea Versicolor Clinical Presentation

pHistory Questioning the patient with tinea versicolor about skin or systemic diseases, current therapy, and drug allergies provides guidance in selecting an appropriate therapy. The following are factors that may be used to guide therapy:

Other diseases, including renal disease, hepatic disease, and endocrine disease (eg, diabetes mellitus) History of HIV or other immunocompromising disorder, which can increase the severity of tinea versicolor Other skin disorders, including personal or family history of atopy or other eczematous conditions Current or recent topical or systemic therapy Drug allergies Seasonal variations in skin color Use of some body oils, which may supply additional nutrients to the M furfur Sweat associated with exercise, which may contribute to disease development and recurrence

Physical

Lesion characteristics o Skin lesions are either hypopigmented or hyperpigmented in various shapes, as the name implies. o Lesions are either macules or very superficial plaques with fine scale that may not be evident except upon close examination o Even when scale is not apparent, when the skin is wiped with a wet cloth and scraped for examination, it yields a surprising amount of dirty-brown keratin. If not, the areas of dyschromia may represent residual effects of previously treated tinea versicolor. o Occasionally, determining whether the lighter or darker skin is affected is difficult. o Lesions have relatively sharp margins and may be lighter or darker than the normal skin color. The lesions are frequently a light tan color in light-skinned individuals. o The color of lesions varies from individual to individual, but each individual's lesions are approximately the same color.

o o o o o

Lesions are evenly pigmented. The inflammatory border, relative central clearing, and erythema seen in most fungal infections are lacking. Small lesions are usually circular or oval. Confluent patches with scattered circular or oval macules around the edges are common. Other lesions may be large enough to cover most of the trunk. Lesions are usually asymptomatic but may be mildly pruritic. The pruritus is more intense when the patient is excessively warm. Residual hypopigmentation, without overlying scale, may remain for many months following effective treatment. These areas may become more apparent following sun exposure, causing the patient to incorrectly suspect that the infection has recurred.

Examples of findings in tinea versicolor are shown in the images below.

In patients with lighter skin color, lesions frequently are a light tan or salmon color.

Scale is frequently difficult to appreciate upon clinical examination.

This individual developed skin discoloration and mild itching every summer for the past few years. These patients should be instructed on the prophylactic use of topical therapy.

This superficial plaque of tinea versicolor is located in the right antecubital fossa of an adult. This appearance and distribution is uncommon but not rare. A potassium hydroxide (KOH) preparation confirmed the diagnosis.

Although tinea versicolor is uncommon in children in temperate climates, when it does occur, it is more likely to be atypical in distribution. This 7-year-old boy had areas of tinea versicolor across the forehead and both temples. He was in good health and lived in Washington state when he was diagnosed.

In some patients, the areas affected by tinea versicolor are not always obvious. In this patient, the abnormal areas are hypopigmented.

Some patients present with extensive tinea versicolor. This patient related that his discoloration had been present for more than 20 years. The light-colored areas on the abdomen are the normal areas of skin. Although topical therapy alone is usually effective, this patient may benefit from initial therapy with oral ketoconazole, followed by selenium sulfide applications in the shower 2-3 times a month.

Significant hyperpigmentation caused by a tinea versicolor infection.

Lesion distribution o The upper trunk is most commonly affected, but the lesions often spread to the upper arms, antecubital fossae, neck, abdomen, and popliteal fossae. o Lesions in the axillae, groin, thighs, and genitalia are less common. o Facial, scalp, and palmar lesions occur in the tropics but are rare in temperate zones o In some patients, tinea versicolor primarily affects the flexural regions, the face, or isolated areas of the extremities. This unusual pattern of tinea versicolor is seen more often in immunocompromised hosts and can be confused with candidiasis, seborrheic dermatitis, psoriasis, erythrasma, and dermatophyte infections. o Lesions that are imperceptible or doubtful are more visible using a Wood lamp in a darkened room.

Causes

M furfur is now the most commonly accepted name for the etiologic agent of tinea versicolor. Thus, P orbiculare, P ovale, and Malassezia ovalis are synonyms . M furfur is a dimorphic lipophilic organism that is cultured only in media enriched with C12-sized or C14-sized fatty acids. Malassezia is able to

exist in both yeast and mycelial forms, with yeast most commonly associated with saprofital form (P ovale). Historically, the name M furfur was used to designate the fungal pathogen of tinea versicolor before it is grown in culture. M furfur is not a dermatophyte, does not grow on dermatophyte test media (DTM), and does not respond to griseofulvin therapy. With the advent of DNA sequencing, numerous pathogenic and nonpathogenic species were found. Some of them appear to be more common in certain areas of the world, and some are more likely to be pathogenic in one area and not in another. Much of the confusion was resolved with the taxonomic revision in 1996, based on sequencing of the large-subunit rRNA and nuclear DNA of more than 100 isolates of Malassezia species.[2] The genus Malassezia was revised to include 7 species: Malassezia globosa, Malassezia sympodialis, M furfur, Malassezia slooffiae, Malassezia pachydermatis, Malassezia restricta, and Malassezia obtusa. The clinical significance of each of these species is under investigation. A study of the epidemiology of Malassezia yeasts associated with pityriasis (tinea) versicolor in Canada revealed the most frequently isolated species included M sympodialis, M globosa, and M furfur. One study found M globosa in 97% of patients with tinea versicolor; it was found alone in 60% of cases, was associated with M sympodialis in 29% of cases, and was associated with M slooffiae in 7% of cases.[2]M sympodialis and M slooffiae were found in similar percentages on clinically uninvolved skin of the trunk, whereas M globosa was not isolated at other sites. Thus, some authors suggest that M globosa in its mycelial phase is the causative agent of tinea versicolor.[3, 2]

Differentials

Cutaneous T-Cell Lymphoma Leprosy Nummular Dermatitis Parapsoriasis Pityriasis Alba Pityriasis Rosea Syphilis Vitiligo

Cutaneous T-Cell Lymphoma

Background

Cutaneous T-cell lymphomas (CTCLs) are the largest group of cutaneous lymphomas, representing 65% of all cutaneous lymphomas. The World Health Organization (WHO)/European Organization for Research and Treatment of Cancer (EORTC) classification (WHO-EORTC classification) is used to categorize CTCLs.[1, 2, 3] However, a substantial subset of T-cell primary cutaneous lymphomas remains that cannot be classified beyond the unspecified peripheral T-cell category, some of which may have an aggressive course.[4] Note the clinical images below.

Tumor-stage cutaneous T-cell lymphoma.

Middle-aged woman with mycosis fungoides showing ulceration and marked depigmentation of advanced disease. Mature T-cell and natural killer (NK) cell neoplasms according to the WHOEORTC classification are as follows:

Mycosis fungoides (MF): - Variants of MF (pagetoid reticulosis [localized disease], follicular, syringotropic, granulomatous variant), subtype of MF (ie, granulomatous slack skin (GSS) syndrome) Szary syndrome CD30+ T-cell lymphoproliferative disorders of the skin - Lymphomatoid papulosis, primary cutaneous anaplastic large cell lymphoma Subcutaneous panniculitislike T-cell lymphoma Primary cutaneous peripheral T-cell lymphoma (PTL), unspecified Subtypes of PTL (primary cutaneous aggressive epidermotropic CD8+ Tcell lymphoma [provisional], cutaneous gamma/delta-positive T-cell lymphoma (CGD-TCL) [provisional], primary cutaneous CD4+ small/medium-sized pleomorphic T-cell lymphoma [provisional]) Extranodal NK/T-cell lymphoma, nasal type - Variant (hydroa vacciniformialike lymphoma) Adult T-cell leukemia/lymphoma

Angioimmunoblastic T-cell lymphoma

CTCL, most commonly seen as MF, is a relatively common clonal expansion of T helper cells and, more rarely, T suppressor/killer cells or NK cells, that usually appears as a widespread, chronic, cutaneous eruption. MF itself is often an epidermotropic disorder characterized by evolution of patches into plaques and tumors composed of small- to medium-sized skin-homing T cells, some (or, rarely, all) of which have convoluted, cerebriform nuclei. Pagetoid reticulosis is a variant of MF and is characterized by the presence of localized patches or plaques with an intraepidermal proliferation of neoplastic T cells. The term pagetoid reticulosis should be restricted to the localized type (Woringer-Kolopp type) and should not be used to describe the disseminated type (Ketron-Goodman type). Generalized cases should probably be classified as aggressive epidermotropic CD8+ CTCL, CGD-TCL, or tumor-stage MF.[5] GSS syndrome is a rare subtype of CTCL characterized by the slow development of folds of lax skin in the major skin folds and, histologically, by an infiltrate of clonal T cells, with exceptionally large multinucleated giant cells sometimes showing inclusion of fragmented elastic fibers. Granulomatous CTCLs are rare, so limited data on the clinicopathological and prognostic features are available.[6] Patients with granulomatous MF and GSS display overlapping histologic features and differ clinically by the development of bulky skin folds in GSS. Szary syndrome (SS) has been defined historically by the triad of erythroderma, generalized lymphadenopathy, and the presence of neoplastic T cells (Szary cells) in skin, lymph nodes, and peripheral blood. Some authorities believe the diagnosis of SS should include one or more of the following[7] :

An absolute Szary cell count of least 1000/L Demonstration of immunophenotypical abnormalities (an expanded CD4+ T-cell population resulting in a CD4/CD8 ratio of more than 10:1; loss of any or all of the T-cell antigens CD2, CD3, CD4, CD5; or loss of both CD4 and CD5) Demonstration of a T-cell clone in the peripheral blood by molecular or cytogenetic methods

SS is an erythrodermic CTCL. Demonstration of a T-cell clone (preferably of the same T-cell clone in skin and peripheral blood) in combination with one of the aforementioned cytomorphological or immunophenotypical criteria has been suggested as minimal criteria for the diagnosis of SS, in order to exclude patients with benign inflammatory conditions simulating SS. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive T-cell neoplasm etiologically linked with the human T-cell leukemia virus 1 (HTLV-1). Cutaneous

lesions are usually a manifestation of widely disseminated disease, although a slowly progressive form that may only involve the skin may occur.[8] Subcutaneous panniculitislike T-cell lymphoma (SPTL) is a cytotoxic T-cell lymphoma characterized by the presence of primarily subcutaneous infiltrates of small, medium, or large pleomorphic T cells and many macrophages, predominantly affecting the legs and often complicated by a hemophagocytic syndrome.[9] At least 2 groups of SPTL with different histologies, phenotypes, and prognoses can be distinguished. Cases with an alpha/beta-positive T-cell phenotype are usually CD8+, are restricted to the subcutaneous tissue (with no dermal or epidermal involvement), and tend to run an indolent clinical course.[10, 11] The SPTL designation is only used for patients with an alpha/beta-positive Tcell phenotype, whereas those with a gamma/delta T-cell phenotype are now categorized as having CGD-TCL.[1, 2, 3, 11, 12] Extranodal NK/T-cell lymphoma, nasal type, is an Epstein-Barr virus (EBV) positive lymphoma of small, medium, or large cells, usually with an NK-cell, or, more rarely, a cytotoxic T-cell phenotype. The skin is the second most common site of involvement, with the nasal cavity/nasopharynx being the most common and the reason why it was once known as a lethal midline granuloma. Cutaneous involvement may be primary or secondary. Because both primary and secondary involvement are clinically aggressive and require the same type of treatment, distinction between the 2 cutaneous involvements seems unnecessary.[11, 13, 14] Primary cutaneous PTL, type unspecified, is the designation for CTCLs that do not fit into any of the better-defined subtypes of CTCL.[1, 2, 3] These include the 3 provisional entities described below, because primary cutaneous aggressive epidermotropic CD8+ cytotoxic T-cell lymphoma, CGD-TCL, and primary cutaneous small-medium CD4+ T-cell lymphoma can be separated out as provisional entities. The remaining diseases that do not fit into any of the betterdefined subtypes of CTCL are characterized as follows:

Primary cutaneous aggressive epidermotropic CD8+ cytotoxic T-cell lymphoma, a provisional entity, is characterized by a proliferation of epidermotropic CD8+ cytotoxic T cells and aggressive clinical behavior.[5] CGD-TCL is composed of a clonal proliferation of mature, activated gamma/delta T cells with a cytotoxic phenotype.[12, 15, 16] It may be primary or secondary cutaneous lymphoma. Primary cutaneous CD4+ small/medium-sized pleomorphic T-cell lymphoma is the diagnosis used when a predominance of small- to medium-sized CD4+ pleomorphic T cells are present without a history of patches and plaques typical of MF.[17]

For additional information from other eMedicine articles, see T-Cell Disorders, Mycosis Fungoides, and Lymphoma, Cutaneous T-Cell.

Pathophysiology
The primary pathophysiologic mechanisms for the development of cutaneous Tcell lymphoma (CTCL) (ie, mycosis fungoides [MF]) have not been elucidated. MF may be preceded by a T-cellmediated chronic inflammatory skin disease, which may occasionally progress to a fatal lymphoma. Karyotypic analysis of cutaneous and blood lymphocytes has shown several genetically aberrant T-cell clones in the same patient. A genotraumatic T cell is one with a tendency to develop numerous clonal chromosomal aberrations. Normal T lymphocytes show apoptosis during in vitro culturing, whereas genotraumatic ones have the ability to develop clonal chromosomal aberrations to become immortalized. This concept implies genetic instability followed by T-cell proliferation. Successive cell divisions of a genotraumatic T-cell clone may produce multiple and complex chromosomal aberrations. Some may reprogram the genotraumatic cells to apoptosis, whereas one or more may produce the phenotypic alterations of malignancy if not eliminated in vivo. Thus, one hypothesis is that the development of genotraumatic T lymphocytes is involved in the etiopathogenesis and the progression of MF. It would also predict that each patient would likely have a unique malignant clone, which, in fact, has been found to be the case. CTCL is a group of T-cell proliferative disorders. Primary cutaneous lymphomas require distinction from histologically similar primary nodal ones because their clinical behavior, prognosis, and therapy are often different. In addition, a difference often exists between primary cutaneous and nodal lymphomas in the presence of specific translocations.

Epidemiology
Frequency United States The incidence of cutaneous T-cell lymphoma (CTCL) is approximately 5 cases per million population per year. International Cutaneous T-cell lymphomas (CTCLs) account for 65% of cutaneous lymphomas. CTCLs have a worldwide distribution, with no well-identified increase in prevalence in any region. Some studies have identified an increase in prevalence

in industrial populations (eg, among workers who use machine cutting oils). ATLL is endemic in areas with a high prevalence of HTLV-1 infection, such as southwest Japan, the Caribbean islands, South America, and parts of Central Africa. ATLL occurs in 1-5% of seropositive individuals after more than 2 decades of viral persistence.[8] Nasal NK/T-cell lymphoma, which is associated with EBV infection, is more common in Asia, Central America, and South America. In the dermatology center of Professor Alsaleh in Kuwait, Arab males with MF outnumbered females by a 2:1 ratio.[18] The annual incidence rate in Kuwait was 0.43 case per 100,000 persons; this was found to be significantly higher among Arabs compared with non-Arab Asians. Race In the United States, cutaneous T-cell lymphoma (CTCL) is more common among Americans of sub-Saharan African lineage than those of European background, in a ratio of approximately 2:1. Sex Cutaneous T-cell lymphoma (CTCL) is more common in men in a ratio of approximately 2:1. Age Most patients with cutaneous T-cell lymphoma (CTCL) are middle-aged or elderly. Many patients have had a poorly defined form of dermatitis for many years prior to the onset of CTCL. In a significant proportion of cases, the onset of the disease, or of a dermatitic precursor of the disease, occurred in childhood. CTCL starting in children younger than 10 years is exceedingly rare and does not show a male predominance; one series even reported a strong female predilection. Similar to adult patients, however, most children present in stage IA or IB and have a good-to-excellent prognosis with treatment, although cases progressing to plaque, tumor-stage disease, and death have been reported. Some patients with limited MF are described as having Woringer-Kolopptype pagetoid reticulosis. These patients are usually middle-aged, with an age distribution in one series ranging from 13-68 years and a mean age of 55 years.

Leprosy
Background

Leprosy is a chronic infection caused by the acid-fast, rod-shaped bacillus Mycobacterium leprae. Leprosy can be considered 2 connected diseases that primarily affect superficial tissues, especially the skin and peripheral nerves. Initially, a mycobacterial infection causes a wide array of cellular immune responses. These immunologic events then elicit the second part of the disease, a peripheral neuropathy with potentially long-term consequences. The social and psychological effects of leprosy, as well as its highly visible debilities and sequelae (as seen in the image below), have resulted in a historical stigma associated with leprosy. To minimize the prejudice against those with leprosy, the condition is also known as Hansen disease, named after G.A. Hansen, who is credited with the 1873 discovery of M leprae. This mycobacterium grows extremely slowly and has not been successfully cultured in vitro.

Hands with Z-thumbs, clawing, contractures, and shortening of fingers due to repetitive injury and healing. Ho Chi Minh City, Vietnam. (Courtesy of D. Scott Smith, MD) In the 1990s, the World Health Organization (WHO) launched a campaign to eliminate leprosy as a public health problem by 2000. Elimination, as defined by the WHO, was defined as a reduction of patients with leprosy requiring multidrug therapy to fewer than 1 per 10,000 population. This goal was achieved in terms of global prevalence by 2002, but 15 of the 122 countries where leprosy was endemic in 1985 still have prevalence rates of greater than 1 per 10,000 population.[1] Although multidrug regimens have been used globally to cure nearly 14 million patients with leprosy since 1985, the number of new leprosy cases remained relatively unchanged from 1980 to 2000, ranging from 500,000-700,000 worldwide per year.[2] Access and delivery of antibiotics continues to be a problem in the most endemic nations. With the precise transmission mechanism of leprosy still unknown and a lack of an effective vaccine, leprosy will probably continue to pose an ongoing public health problem in the coming decades.

Pathophysiology

Leprosy can manifest in different forms, depending on the host response to the organism. Individuals who have a vigorous cellular immune response to M leprae have the tuberculoid form of the disease that usually involves the skin and peripheral nerves. The number of skin lesions is limited, and they tend to be dry and hypoesthetic. Nerve involvement is usually asymmetric. This form of the disease is also referred to as paucibacillary leprosy because of the low number of bacteria in the skin lesions (ie, < 5 skin lesions, with absence of organisms on smear). Results of skin tests with antigen from killed organisms are positive in these individuals. Individuals with minimal cellular immune response have the lepromatous form of the disease, which is characterized by extensive skin involvement. Skin lesions are often described as infiltrated nodules and plaques, and nerve involvement tends to be symmetric in distribution. The organism grows best at 27-30C; therefore, skin lesions tend to develop in the cooler areas of the body, with sparing of the groin, axilla, and scalp. This form of the disease is also referred to as multibacillary leprosy because of the large number of bacteria found in the lesions (ie, >6 lesions, with possible visualization of bacilli on smear). Results of skin tests with antigen from killed organisms are nonreactive. Patients may also present with features of both categories; however, over time, they usually evolve to one or the other (indeterminate or borderline leprosy). Interestingly, most individuals who are exposed to leprosy never develop the disease. Classification of leprosy: Leprosy has 2 classification schemas: the 5-category Ridley-Jopling system and the simpler and more commonly used WHO standard.

Ridley-Jopling: Depending on the host response to the organism, leprosy can manifest clinically along a spectrum bounded by the tuberculoid and lepromatous forms of the disease. Most patients fall into the intermediate classifications, which include borderline tuberculoid leprosy, midborderline leprosy, and borderline lepromatous leprosy. The classification of the disease typically changes as it evolves during its progression or management. The Ridley-Jopling system is used globally and forms the basis of clinical studies of leprosy. It may also be more useful in guiding treatment regimens and assessing risk of acute complications. Physical findings in each subtype are presented in the Clinical section. WHO system: The WHO recommends classifying leprosy according to the number of lesions and the presence of bacilli on a skin smear. This method is useful in countries where biopsy analysis in unavailable. o Paucibacillary leprosy is characterized by 5 or fewer lesions with absence of organisms on smear. Paucibacillary leprosy generally

includes the tuberculoid and borderline lepromatous categories from the Ridley-Jopling system. Multibacillary leprosy is marked by 6 or more lesions with possible visualization of bacilli on smear. Lepromatous leprosy, borderline lepromatous leprosy, and midborderline leprosy on the RidleyJopling scale are included in the multibacillary leprosy category.

Epidemiology
Frequency United States In the United States, an average of 150 cases are diagnosed each year. In 2004, 69 new cases of leprosy were detected and 131 total persons were reported to have the disease, according to the WHO. Most cases of leprosy in the United States are found in immigrants, although endemic foci exist in parts of Louisiana, Florida, and Texas along the Gulf of Mexico; in Mexican and Asian California populations; and in Spanish Americans in New York City. Around 85% of these detected leprosy cases involve patients who have lived in foreign countries, primarily Asia, Africa, and Latin America.[3] Based on genetic analysis studies, wild armadillos and many patients with leprosy in the southern United States are infected with the same strain of M leprae.[4] Leprosy may be a zoonosis in the southern United States because armadillos are a large reservoir for this disease. International According to WHO figures, the global registered prevalence of leprosy at the start of 2005 was 286,063 cases. Global annual detection rates have declined from 2001 to 2004, when 763,262 and 407,791 new cases were reported, respectively. Leprosy is still deemed a public health problem in 9 countries: Angola, Brazil, Central African Republic, Democratic Republic of the Congo, India, Madagascar, Mozambique, Nepal, and the United Republic of Tanzania. These countries account for 84% of reported cases. Furthermore, more than 94% of new cases of leprosy in Latin America are reported in Brazil.[1] Mortality/Morbidity Leprosy is rarely fatal, and the primary consequence of infection is nerve impairment and debilitating sequelae. According to one study, 33-56% of newly diagnosed patients already displayed signs of impaired nerve function.[5] According to estimates, 3 million people who have completed multidrug therapy

for leprosy have sustained disability due to nerve damage. Although both lepromatous leprosy and tuberculoid leprosy involve the skin and peripheral nerves, tuberculoid leprosy has more severe manifestations. Nerve involvement results in loss of sensory and motor function, which may lead to frequent trauma and amputation. The ulnar nerve is most commonly involved.

Damage in the following nerves is associated with characteristic impairments in leprosy: o Ulnar and median - Clawed hand o Posterior tibial - Plantar insensitivity and clawed toes o Common peroneal -Foot drop o Radial cutaneous, facial, and greater auricular nerves (may also be involved; as seen in the image below)

Patient with facial nerve palsy and contractures of the hand. Daloa, Ivory Coast. (Courtesy of D. Scott Smith, MD) Infiltration by bacteria may lead to destruction of nasal cartilage (lepromatous leprosy), ocular involvement, and diffuse thickening of the skin. Advanced cases of leprosy involve the loss of eyebrows and lashes, but these deformities are less common today. Worldwide, leprosy is considered the most common cause of crippling of the hand, which is caused by ulnar nerve involvement.[6] Peroneal nerve involvement can lead to foot drop, posterior tibial nerve involvement, and clawed toes.

Race Leprosy was once endemic worldwide, and no racial predilection is known. In the late 1800s, the incidence of leprosy in northern Europe and North America dropped dramatically, and the disease is now reported primarily in tropical areas. Sex Leprosy is generally more common in males than in females, with a male-tofemale ratio of 1.5:1. In some areas in Africa, the prevalence of leprosy among females is equal to or greater than that in males.[2]

Age Leprosy can occur at any age, but, in developing countries, the age-specific incidence of leprosy peaks in children younger than 10 years, who account for 20% of leprosy cases. Leprosy is very rare in infants; however, they are at a relatively high risk of acquiring leprosy from the mother, especially in cases of lepromatous leprosy or midborderline leprosy.

Nummular Dermatitis
Background
Nummular (meaning "coin-shaped") dermatitis is a form of eczema. Nummular dermatitis is characterized by round-to-oval erythematous plaques most commonly found on the arms and legs. Lesions often start as papules, which then coalesce into plaques with scale. Early nummular dermatitis lesions may be studded with vesicles containing serous exudate. They are usually very pruritic.

Pathophysiology
Nummular dermatitis is a condition confined to the skin. It has recently been classified as a form of atopic dermatitis. Little is known about the pathophysiology of nummular dermatitis, but it is frequently accompanied by xerosis. Dryness of the skin results in dysfunction of the epidermal lipid barrier; this may allow permeation of environmental allergens, which induce an allergic or irritant response.[1, 2] This is supported by one study that showed that elderly patients with nummular dermatitis had increased sensitivity to environmental aeroallergens compared with age-matched controls. This impaired cutaneous barrier in the setting of nummular dermatitis may also lead to increased susceptibility to allergic contact dermatitis to materials such as metals. Onset has been associated with medications. Onset of severe, generalized nummular lesions has been reported in association with interferon and ribavirin therapy for hepatitis C.[3, 4] Association with use of inhibitors of tumor necrosis factor has also been reported.[5] Onset has also been described in association with mercury in dental amalgams. Hypersensitivity to the metals in the mouth is posulated to be sufficient to drive an immune response that results in cutaneous nummular plaques.

Because of the intense pruritus associated with nummular dermatitis, the potential role of mast cells in the disease process has been investigated. Increased numbers of mast cells have been observed in lesional compared with nonlesional samples in persons with nummular dermatitis. One study identified neurogenic contributors to inflammation in both nummular dermatitis and atopic dermatitis by investigating the association between mast cells and sensory nerves and identifying the distribution of neuropeptides in the epidermis and upper dermis of patients with nummular eczema. Researchers hypothesized that release of histamine and other inflammatory mediators from mast cells may initiate pruritus by interacting with neural C-fibers. The research showed that dermal contacts between mast cells and nerves were increased in number in both lesional and nonlesional samples of nummular eczema compared with normal controls. In addition, substance P and calcitonin gene-related peptide fibers were prominently increased in lesional samples compared with nonlesional samples from patients with nummular eczema. These neuropeptides may stimulate release of other cytokines and promote inflammation.[6, 7, 8] Other research has demonstrated that mast cells present in the dermis of patients with nummular eczema may have decreased chymase activity, imparting reduced ability to degrade neuropeptides and protein. This dysregulation could lead to decreased capability of the enzyme to suppress inflammation.

Epidemiology
Frequency United States The prevalence of nummular dermatitis is 2 cases per 1000 people. Dermatitis (eg, atopic, asteatotic, dyshidrotic, nummular, hand) is one of the most common dermatologic conditions. International The incidence internationally is the same as it is in the United States. Mortality/Morbidity

Pruritus, often worst at night, may cause irritability, insomnia, or both. Secondary infection may result in lesions that ooze serosanguineous exudate. The most common organism revealed by culture is Staphylococcus aureus.

Generalized flares may require bed rest, oral antibiotics, a cool environment, systemic antibiotics, and/or systemic steroids. Increased contact sensitivity to environmental antigens (especially metals) could limit ability to tolerate those antigens, especially clothing, metal snaps, jewelry, dental amalgams or occupational exposure.

Race No racial predilection has been observed for nummular dermatitis. Sex Nummular dermatitis is more common in males than in females (see Age below). Age Nummular dermatitis has 2 peaks of age distribution. The most common is in the sixth to seventh decade of life. This is most often seen in males. A smaller peak occurs in the second to third decade of life, which is most often seen in association with atopic dermatitis. This is more often seen in females. It is uncommon in children.

Parapsoriasis
Overview of Parapsoriasis
Parapsoriasis describes a group of cutaneous diseases that can be characterized by scaly patches or slightly elevated papules and/or plaques that have a resemblance to psoriasishence the nomenclature. However, this description includes several inflammatory cutaneous diseases that are unrelated with respect to pathogenesis, histopathology, and response to treatment. Because of the variation in clinical presentation and a lack of a specific diagnostic finding on histopathology, a uniformly accepted definition of parapsoriasis remains lacking. In 1902, Brocq initially described 3 major entities that fit the description:

Pityriasis lichenoides (acuta and chronica) Small plaque parapsoriasis Large plaque parapsoriasis (parapsoriasis en plaque)

Pityriasis lichenoides (acuta and chronica) Pityriasis lichenoides variants describe scaly dermatoses with necrotic papules that are clinically and histologically different from parapsoriasis. These diseases generally are benign and undergo spontaneous resolution but, at times, may have a protracted course (see Pityriasis Lichenoides for further discussion). Large plaque and small plaque parapsoriasis Current terminology of parapsoriasis refers to 2 disease processes that are caused by T-cellpredominant infiltrates in the skin. These disease processes are large plaque parapsoriasis and small plaque parapsoriasis. As the nomenclature and description of the disease spectrum under the descriptive term parapsoriasis evolved, the primary focus has been on the distinction of whether the disorder progresses to mycosis fungoides (MF) or cutaneous T-cell lymphoma (CTCL). Small plaque parapsoriasis is a benign disorder that rarely if ever progresses. Large plaque parapsoriasis is more ominous in that approximately 10% of patients progress to MF/CTCL.[1] Controversy exists currently in the classification of large plaque parapsoriasis because some believe it is equivalent to the earliest stage CTCL, the patch stage.[2, 3, 4] The duration of parapsoriasis can be variable. Small plaque disease lasts several months to years and can spontaneously resolve. Large plaque disease is chronic, and treatment is recommended because it may prevent progression to CTCL. No clear etiology for small plaque or large plaque parapsoriasis is known, and no specific association has been made with contact exposure or infections. For more information, see the topic Psoriasis.

Pathophysiology of Parapsoriasis
The initiating cause of parapsoriasis is unknown, but the diseases likely represent different stages in a continuum of lymphoproliferative disorders from chronic dermatitis to frank malignancy of cutaneous T-cell lymphoma (CTCL). Small plaque parapsoriasis Small plaque parapsoriasis likely is a reactive process of predominantly CD4+ T cells. Genotypic pattern observed in small plaque parapsoriasis is similar to that observed in chronic dermatitis, and the pattern of clonality of T cells is consistent with the response of a specific subset of T cells that have been stimulated by an antigen. Multiple dominant clones can be detected by polymerase chain reaction

(PCR) of T-cell receptor gene usage, which supports a reactive process. Lymphocytes do not show histologic atypia to suggest malignant transformation. Southern blot analysis of T-cell receptor genes from parapsoriasis does not identify a dominant clone of T cells. Some physicians believe that small plaque parapsoriasis is an abortive T-cell lymphoma; however, no clear distinguishing evidence, such as genetic changes (eg, TP53 mutations) observed in other malignancies, exists to support this contention.[5] Nevertheless, a hint to the verity of this hypothesis is the recent identification of increased telomerase activity in T cells from CTCL at low-grade stages, high-grade lymphoma, and parapsoriasis, which is activity not exhibited in normal T cells. A better understanding is likely to develop from further molecular characterization.[6] Large plaque parapsoriasis Large plaque parapsoriasis is a chronic inflammatory disorder, and the pathophysiology has been speculated to be long-term antigen stimulation. This disorder is associated with a dominant T-cell clone, one that may represent up to 50% of the T-cell infiltrate. If the histologic appearance is benign, without atypical lymphocytes, classification of large plaque parapsoriasis is made. If atypical lymphocytes are present, many would classify such patients as having patch stage CTCL. Human herpesvirus type 8 has been detected in up to 87% of skin lesions of large plaque parapsoriasis. This is the first association of a specific infectious agent with large plaque parapsoriasis, and the significance is unclear. Further studies are important to determine the significance of this finding.[7]

Epidemiology of Parapsoriasis
There are no accurate statistics on the incidence and frequency of parapsoriasis, but digitate dermatoses may be underreported because of the lack of symptoms and subtle presentation. Patients may underreport the frequency of large plaque parapsoriasis when it is asymptomatic and subtle. Large plaque parapsoriasis may be greater than the reported incidence of mycosis fungoides (MF), which is approximately 3.6 cases per million population per year. Mortality has not been reported for small plaque parapsoriasis. Morbidity is limited to symptoms, which are minimal. For large plaque parapsoriasis, mortality may be associated with progression to MF (cutaneous T-cell lymphoma [CTCL]). The patch stage of MF represents the early stages of CTCL, and the 5-year survival rate is greater than 90%. Long-term survival is the same as that from a matched controlled population.[8]

Small plaque parapsoriasis is associated with male predominance. The male-tofemale ratio is 3:1. A slight asymmetry favoring male dominance for large plaque parapsoriasis may exist. For both small plaque parapsoriasis and large plaque parapsoriasis, presentation most frequently is in middle age; peak incidence is in the fifth decade of life.

Clinical Presentation
Patient history Onset of parapsoriasis is indolent. It develops from a few patches and becomes more visible over a protracted period of time. Additional lesions develop progressively in some individuals. Small plaque parapsoriasis can last months to several years; the disease often resolves spontaneously. Large plaque parapsoriasis is a chronic disorder that manifests in an indolent manner and progresses over many years, sometimes decades. It may progress to mycosis fungoides (MF), a cutaneous T-cell lymphoma (CTCL), after an indeterminate number of years. Large plaque parapsoriasis does not enter remission without treatment. Physical examination Lesions of small plaque parapsoriasis are well-circumscribed, slightly scaly, light salmon-colored patches that measure less than 5 cm in diameter and are scattered over the trunk and extremities. Digitate pattern is a distinctive form of small plaque disease that consists of palisading elongated fingerlike patches that follow the dermatome and are most prominently displayed on the lateral thorax and abdomen. (See the images below.)

Small plaque parapsoriasis. Small plaque parapsoriasis. Large plaque parapsoriasis manifests as faint erythematous patches with arcuate geographic borders. Each lesion often is greater than 6 cm in diameter. Lesions are scattered on the proximal extremities and the trunk and often show a bathingsuit distribution. Surfaces of the lesions have a faint red-to-salmon color; show flaky thin scales; and have an atrophic, cigarette-paper or tissue-paper, wrinkling quality. (See the image below.)

Large plaque parapsoriasis.

Diagnosis of Parapsoriasis
The differential diagnosis for parapsoriasis includes the following:

Contact Dermatitis, Allergic Cutaneous T-Cell Lymphoma Nummular Dermatitis Pityriasis Alba Pityriasis Lichenoides Pityriasis Rosea Psoriasis, Guttate Syphilis

Laboratory studies A complete blood cell count with differential should be performed, and a high lymphocyte count or the presence of Szary cells suggests mycosis fungoides/cutaneous T-cell lymphoma (MF/CTCL). Skin biopsy Skin biopsy with immunophenotyping analysis and gene rearrangement studies should be performed. Histologic findings Histopathology of small plaque parapsoriasis shows a mild superficial perivascular lymphocytic infiltrate with a nonspecific inflammatory infiltrate of CD4+ and CD8+ T cells. However, CD4+ T cells are predominant. The epidermis may show mild spongiosis, focal hyperkeratosis, scale crust, parakeratosis, and occasional exocytosis. Often, the pattern is not diagnostic and is nonspecific. Lymphocytes are small and do not show atypical features. In large plaque parapsoriasis, a superficial dermal inflammatory infiltrate consists predominantly of lymphocytes. Numerous lymphocytes abut the dermalepidermal junction and single lymphocytes can be observed in the epidermis. Lymphocytes are generally small and do not show atypical nuclei. Blood vessels are dilated, and melanophages can be present. The epidermis shows flattening of the rete ridges when epidermal atrophy is prominent on clinical examination. Acanthosis of the epidermis and irregular hyperkeratosis of the cornified layer are present. In contrast to small plaque parapsoriasis, spongiosis is absent. Gene rearrangement studies can assist in excluding MF or CTCL.

Treatment of Parapsoriasis
Parapsoriasis can be managed conservatively on the basis of symptoms, and often, topical treatment is effective. Small plaque parapsoriasis Small plaque parapsoriasis usually is asymptomatic. Treatment should be based on alleviation of symptoms associated with scaliness, and patients should be reassured of the benign self-limiting nature of the disease.

Emollients may be sufficient to treat scaliness; however, a trial of midpotency topical steroids (class 3-5) may lead to greater clinical responsiveness. Phototherapy is effective in treating lesions that are widely scattered. Broad- or narrow-band UV-B can be effective and can lead to remission.[9, 10] More recalcitrant presentations can be treated with psoralen and long-wave ultraviolet radiation (PUVA). Annual follow-up is recommended. An increase in the number of lesions, an increase in the size of lesions, or the development of induration or epidermal atrophy should prompt a repeat skin biopsy to consider a diagnosis of mycosis fungoides (MF) in evolution. Large plaque parapsoriasis Large plaque parapsoriasis should be treated, because treatment may prevent progression to MF (cutaneous T-cell lymphoma [CTCL]). Therapy includes midto high-potency topical steroids (class 2-4), topical nitrogen mustard, and topical carmustine (BCNU). Patients using topical treatment need follow-up every 2-3 months. Phototherapy with either broad- or narrow-band UV-B or PUVA can be effective in inducing remission. Phototherapy requires an evaluation to response after every 8-12 visits or monthly. Large plaque parapsoriasis requires closer follow-up than small plaque parapsoriasis. Follow-up frequency is determined by the treatment modality used. Follow-up every 6 months is recommended. Increasing number of lesions, increase in lesion size, or the development of induration or epidermal atrophy should prompt a repeat skin biopsy to consider a diagnosis of MF in evolution. If patients remit or do not desire treatment, follow-up is still recommended to assess for recurrence or progression. Consultations Consult with a dermatologist specializing in cutaneous lymphoma to coordinate medical care if progression to MF (CTCL) occurs. Complications Administration of topical chemotherapy agents may result in development of contact dermatitis.

Prognosis

Small plaque parapsoriasis may persist in a stable pattern for years to decades and then resolve spontaneously. A small number of cases may progress to mycosis fungoides (MF). Large plaque parapsoriasis remains indolent for many years. The disease may progress to cutaneous T-cell lymphoma (CTCL) with transformation of lymphocytes from benign small size to larger atypical lymphocytes. The 5-year survival rate, however, still remains high and is greater than 90%

Pityriasis Alba in Emergency Medicine

Background
Pityriasis alba is a term derived from the words scaly (pityriasis) and white (alba). Characteristic pityriasis alba is shown in the image below.

Note the characteristic, ill-defined, hypopigmented macules in this 6-year-old child with pityriasis alba. Debate exists as to the term extensive pityriasis alba (EPA), which some believe to be a confusing misnomer applied to a pathoetiologically different entity and has the proposed name of "progressive extensive hypomelanosis". EPA is believed to be a primary, acquired hypopigmentation observed in females aged 18-25 years of mixed ethnic origin; it is characterized by hypochromic, nonscaly macules developing on the back and abdomen, increasing in number and progressively coalescing over the whole trunk into larger patches surrounded by smaller welldefined macules. Although the single skin lesions of EPA do not differ substantially from those of pityriasis alba, consistent differences are as follows:[1]

A widespread and symmetric involvement of the trunk by numerous, round, nonscaly hypomelanotic patches without a preceding inflammatory phase and chronic in duration (This is as opposed to face predominance in pityriasis alba.) Histologic examination shows a decrease of epidermal melanin; spongiosis is absent. Ultrastructural studies suggested reduced number of active melanocytes and a decrease in number and size of melanosomes. No atopy and no associated pathologies or familial occurrences have been reported. The age of occurrence; the sex ratio (female preponderance) Widespread lesions of classical pityriasis alba can be observed in atopic dermatitis, but they should not be confused with the disorder described by Zaynoun as EPA.

Some authors believe EPA overlaps with another condition described "progressive and extensive hypomelanosis" in persons of mixed racial background and also reported as "progressive and confluent hypomelanosis of the melanodermic metis" or "creole dyschromia". The alternate name of "progressive extensive hypomelanosis" has been proposed.[1]

Pathophysiology
No known cause of pityriasis alba has been reported. Atopy and postinflammatory changes are leading current theories as to the origin of the lesions. Theories of origin include hypopigmentation secondary to pityriacitrin, a substance produced by Malassezia yeasts, that acts as a natural sunscreen. A large number of patients with pityriasis alba have a history of atopic disease. In addition, atopic patients are more prone to developing pityriasis alba.[2] Histology of biopsy studies show features including hyperkeratosis (33.33%), parakeratosis (40%), acanthosis (53.33%), spongiosis (80%), and perivascular infiltrate (100%).[2] However, these findings are not specific enough to make the diagnosis. Atrophic sebaceous glands were noted in almost half the cases in one study.[3] Anemia has been reported in up to 16% of patients.[2] This may be a coincidental finding, and the clinical relevance of anemia is not yet known. Ultrastructure studies note that despite a reduced pigment in lesional skin, there is no difference in melanocytes between lesional and nonlesional skin in the same patient, although this finding is still under debate. Degenerative changes in melanocytes and reduced keratonocyte melanosomes were also noted.[3] Overall, the defect is believed to be due to decreased melanin.

Epidemiology
Frequency United States Pityriasis alba is relatively common, occurring in up to 5% of children, but the exact epidemiology has not been described. Mortality/Morbidity Pityriasis alba is often an incidental finding on clinical examination and generally a self-limited asymptomatic disease that may resolve without intervention. Mortality is not associated with this condition. Cosmetic appearance may be of concern in extensive disease. Race Pityriasis alba does not seem to be more prevalent in any race; however, it is more obvious in dark-skinned individuals. Sex No sex predilection has been noted. A slight male predominance has been noted.[2] Age Pityriasis alba is most often noted in those younger than 20 years.

Pediatric Pityriasis Rosea

Background
Pityriasis rosea (PR) was first described by Camille Melchior Gilbert in 1860. The term pityriasis rosea means fine pink scale. It is a common skin disorder observed in otherwise healthy people, most frequently children and young adults. Pityriasis rosea manifests as an acute, self-limiting, papulosquamous eruption with a 6-week to 8-week duration. It may sometimes occur in atypical variants or may mimic other skin disorders, such as secondary syphilis.[1, 2, 39] Guidelines for diagnosing syphilis (and distinguishing the roseola from pityriasis rosea) have been established.[3]

Pathophysiology
The specific cause of the disorder remains unclear; however, its seasonal occurrence, clinical course, possibility of epidemic occurrence, presence of occasional prodromal symptoms, and infrequent likelihood of recurrences have all suggested an infectious viral etiology. The disease has been associated with recent upper respiratory infections. Increased incidence among groups with close physical contact (eg, families, students, military personnel) has been reported. A higher incidence among patients with decreased immunity (eg, pregnant women, bone marrow transplant patients) has also been noted. Additionally, ampicillin has been found to increase the distribution of the eruption; this phenomenon bears a striking resemblance to the effect of ampicillin on the rash of infectious mononucleosis. Finally, some immunological findings, including the presence of immunoglobulin (Ig)M directed against keratinocytes or the increase of Langerhans cells and CT4 T lymphocytes in the dermal infiltrate of patients with pityriasis rosea also support the pathogenetic role of a transmissible agent.[36] Many common infectious microorganisms have been considered (eg, influenza A, B, and H1N1; parainfluenza I, II, and III; Epstein-Barr virus; parvovirus B19; cytomegalovirus; herpesviruses 1, 2, and 8; Mycoplasma) and have been shown not to be causative. Recent reports using polymerase chain reaction (PCR) analysis have suggested a role for human herpesvirus (HHV)-7 and HHV-6 but this has not been confirmed in later studies.[4, 5, 6, 7, 34, 8, 9, 10, 11, 26, 29, 33, 37] Despite the prevailing opinion that pityriasis rosea is caused by an infectious agent, it does not appear to be very contagious; household contacts and schoolmates usually do not develop the disease. Pityriasis rosealike eruptions can also occur in association with many drugs. These include acetylsalicylic acid, barbiturates, bismuth, captopril, clonidine, gold, imatinib, isotretinoin, ketotifen, levamisole, metronidazole, omeprazole, Dpenicillamine, terbinafine, and Bacillus Calmette-Gurin or diphtheria vaccine. Anti TNF-alpha agents such as adalimumab and etanercept have also been implicated.[12, 35] Drug-induced pityriasis rosea often lasts longer than nondruginduced pityriasis rosea.

Epidemiology

Frequency United States An estimated frequency of 0.13-0.14% has been reported, with a 0.3-3% prevalence at dermatologic centers. International Pityriasis rosea accounts for approximately 2% of outpatient visits in dermatology. It is present worldwide and occurs year round, although it may be more common in the fall and spring. In some geographic areas, such as India, Malaysia, and Australia, it may be more frequent in the dry hot season. Mortality/Morbidity Pityriasis rosea is a self-limiting, benign disorder with a recurrence rate of less than 3%. It usually lasts for 6-8 weeks but can last as long as 3-6 months. Postinflammatory pigment changes are common, especially in black people. Bacterial superinfections are rarely observed. In pregnant women, it has sometimes been associated with miscarriage (if occurring within the first 15 wk of pregnancy), or premature delivery, neonatal hypotonia and hyporeactivity.[13] Race Pityriasis rosea shows no racial specificity, although black people may have more extensive or atypical disease. The lesions may show a dark hue and lack the erythematous component. Sex Pityriasis rosea occurs slightly more often in females than in males. The femaleto-male ratio is reported as 2:1 or 3:2 in the United States. Age Pityriasis rosea is observed in people of all age groups, although it is most common in persons aged 10-35 years. The youngest patient reported in the literature was aged 3 months, and the oldest was aged 85 years.

Syphilis

Background
Syphilis is an infectious venereal disease caused by the spirochete Treponema pallidum. Syphilis is transmissible by sexual contact with infectious lesions, from mother to fetus in utero, via blood product transfusion, and occasionally through breaks in the skin that come into contact with infectious lesions. If untreated, it progresses through 4 stages: primary, secondary, latent, and tertiary. Syphilis has a myriad of presentations and can mimic many other infections and immune-mediated processes in advanced stages. Hence, it has earned the nickname the great impostor. The complex and variable manifestations of the disease prompted Sir William Osler to remark, The physician who knows syphilis knows medicine. Many famous personages throughout history are thought to have suffered from syphilis, including Bram Stoker, Henry VIII, and Vincent Van Gogh. Since the discovery of penicillin in the mid-20th century, the spread of this once very common disease has been largely controlled, but efforts to eradicate the disease entirely have been unsuccessful.

Pathophysiology
Three genera of spirochetes cause human infection:

Treponema, which causes syphilis, yaws, and pinta Borrelia, which causes Lyme disease and relapsing fever Leptospira, which causes leptospirosis

The particular spirochete responsible for syphilis is Treponema pallidum. T pallidum is a fragile spiral bacterium 6-15 micrometers long by 0.25 micrometers in diameter. Its small size makes it invisible on light microscopy; therefore, it must be identified by its distinctive undulating movements on darkfield microscopy. It can survive only briefly outside of the body; thus, transmission almost always requires direct contact with the infectious lesion. S yphilis is usually classified into 4 stages: primary, secondary, latent, and tertiary. It can be either acquired or congenital. That is, it can be transmitted either by intimate contact with infectious lesions (most common) or via blood transfusion (if blood has been collected during early syphilis), and it can also be transmitted transplacentally from an infected mother to her fetus.

Acquired syphilis In acquired syphilis, T pallidum rapidly penetrates intact mucous membranes or microscopic dermal abrasions and, within a few hours, enters the lymphatics and blood to produce systemic infection. Incubation time from exposure to development of primary lesions, which occur at the primary site of inoculation, averages 3 weeks but can range from 10-90 days. Studies in rabbits show that spirochetes can be found in the lymphatic system as early as 30 minutes after primary inoculation, suggesting that syphilis is a systemic disease from the outset. The central nervous system (CNS) is invaded early in the infection; during the secondary stage, examinations demonstrate that more than 30% of patients have abnormal findings in the cerebrospinal fluid (CSF). During the first 5-10 years after the onset of untreated primary infection, the disease principally involves the meninges and blood vessels, resulting in meningovascular neurosyphilis. Later, the parenchyma of the brain and spinal cord are damaged, resulting in parenchymatous neurosyphilis. Go to Neurosyphilis for complete information on this topic. Regardless of the stage of disease and location of lesions, histopathologic hallmarks of syphilis include endarteritis (which in some instances may be obliterative in nature) and a plasma cellrich infiltrate. Endarteritis is caused by the binding of spirochetes to endothelial cells, mediated by host fibronectin molecules bound to the surface of the spirochetes. The resultant endarteritis can heal with scarring in some instances. The syphilitic infiltrate reflects a delayed-type hypersensitivity response to T pallidum, and in certain individuals with tertiary syphilis, this response by sensitized T lymphocytes and macrophages results in gummatous ulcerations and necrosis. Antigens of T pallidum induce host production of treponemal antibodies and nonspecific reagin antibodies. Immunity to syphilis is incomplete. For example, host humoral and cellular immune responses may prevent the formation of a primary lesion on subsequent infections with T pallidum, but they are insufficient to clear the organism. This may be because the outer sheath of the spirochete is lacking immunogenic molecules, or it may be because of downregulation of helper T cells of the TH1 class.[1, 2] Primary syphilis is characterized by the development of a painless chancre at the site of transmission after an incubation period of 3-6 weeks. The lesion has a punched-out base and rolled edges and is highly infectious. Histologically, the chancre is characterized by mononuclear leukocytic infiltration, macrophages, and lymphocytes. The inflammatory reaction causes an obliterative endarteritis. In this stage, the spirochete can be isolated from the

surface of the ulceration or the overlying exudate of the chancre. Whether treated or not, healing occurs within 3-12 weeks, with considerable residual fibrosis. Secondary syphilis develops about 4-10 weeks after the appearance of the primary lesion. During this stage, the spirochetes multiply and spread throughout the body. Secondary syphilis lesions are quite variable in their manifestations. Systemic manifestations include malaise, fever, myalgias, arthralgias, lymphadenopathy, and rash. Widespread mucocutaneous lesions are observed over the entire body and may involve the palms, soles, and oral mucosae. Most often, the lesions are macular, discrete, reddish brown, and 5 mm or smaller in diameter; however, they can be pustular, annular, or scaling. All such lesions contain treponemes. Of these, wet mucous patches are the most contagious. Histologically, the inflammatory reaction is similar to but less intense than that of the primary chancre. Other skin findings of secondary syphilis are condylomata lata and patchy alopecia. Condylomata lata are painless, highly infectious gray-white lesions that develop in warm, moist sites. The alopecia is characterized by patchy hair loss of the scalp and facial hair, including the eyebrows. Patients with this finding have been referred to as having a moth-eaten appearance. During secondary infection, the immune reaction is at its peak and antibody titers are high. Latent syphilis is a stage at which the features of secondary syphilis have resolved, though patients remain seroreactive. Some patients experience recurrence of the infectious skin lesions of secondary syphilis during this period. About one third of untreated latent syphilis patients go on to develop tertiary syphilis, whereas the rest remain asymptomatic. Currently, tertiary syphilis disease is rare. When it does occur, it mainly affects the cardiovascular system (80-85%) and the CNS (5-10%), developing over months to years and involving slow inflammatory damage to tissues. The 3 general categories of tertiary syphilis are gummatous syphilis (also called late benign), cardiovascular syphilis, and neurosyphilis. Gummatous syphilis is characterized by granulomatous lesions, called gummas, which are characterized by a center of necrotic tissue with a rubbery texture. Gummas principally form in the liver, bones, and testes but may affect any organ. Histological examination shows palisaded macrophages and fibroblasts, as well as plasma cells surrounding the margins. Gummas may break down and form ulcers, eventually becoming fibrotic. Treponemes are rarely visualized or recovered from these lesions. Cardiovascular syphilis occurs at least 10 years after primary infection. The most common manifestation is aneurysm formation in the ascending aorta, caused by

chronic inflammatory destruction of the vasa vasorum, the penetrating vessels that nourish the walls of large arteries. Aortic valve insufficiency may result. Neurosyphilis has several forms. If the spirochete invades the CNS, syphilitic meningitis results. Syphilitic meningitis is an early manifestation, usually occurring within 6 months of the primary infection. CSF shows high protein, low glucose, high lymphocyte count, and positive syphilis serology. Meningovascular syphilis occurs as a result of damage to the blood vessels of the meninges, brain, and spinal cord, leading to infarctions causing a wide spectrum of neurologic impairments. Parenchymal neurosyphilis includes tabes dorsalis and general paresis. Tabes dorsalis develops as the posterior columns and dorsal roots of the spinal cord are damaged. Posterior column impairment results in impaired vibration and proprioceptive sensation, leading to a wide-based gait. Disruption of the dorsal roots leads to loss of pain and temperature sensation and areflexia. Damage to the cortical regions of the brain leads to general paresis, formerly called general paresis of the insane, which mimics other forms of dementia. Impairment of memory and speech, personality changes, irritability, and psychotic symptoms develop and may advance to progressive dementia. The Argyll-Robertson pupil, a pupil that does not react to light but does constrict during accommodation, may be seen in tabes dorsalis and general paresis. The precise location of the lesion causing this phenomenon is unknown. Congenital syphilis Congenital syphilis, discussed briefly here, is a veritable potpourri of antiquated medical terminology. The treponemes readily cross the placental barrier and infect the fetus, causing a high rate of spontaneous abortion and stillbirth. Within the first 2 years of life, symptoms are similar to severe adult secondary syphilis with widespread condylomata lata and rash. Snuffles describes the mucopurulent rhinitis caused by involvement of the nasal mucosae. Later manifestations of congenital syphilis include bone and teeth deformities, such as saddle nose (due to destruction of the nasal septum), saber shins (due to inflammation and bowing of the tibia), Cluttons joints (due to inflammation of the knee joints), Hutchinsons teeth (in which the upper incisors are widely spaced and notched), and mulberry molars (in which the molars have too many cusps).

Tabes dorsalis and general paresis may develop as in adults, with 8th cranial nerve deafness and optic nerve atrophy as well as a variety of other ophthalmologic involvement leading to blindness being additional features. Go to Pediatric Syphilis for complete information on this topic.

Etiology
The cause of syphilis is infection with the spirochete T pallidum.T pallidum is solely a human pathogen and does not naturally occur in other species. T pallidum has, however, been cloned in Escherichia coli and has been used experimentally in rabbits. Transmission of T pallidum occurs via penetration of the spirochetes through mucosal membranes and abrasions on epithelial surfaces. It is primarily spread through sexual contact but can be spread by exposure to blood products and transferred in utero. T pallidum is a labile organism that cannot survive drying or exposure to disinfectants; thus, fomite transmission (eg, from toilet seats) is virtually impossible. Risk factors of syphilis include the following:

Unprotected sex, promiscuous sex, and intravenous drug use are the major risk factors. Health care workers are at occupational risk.

Epidemiology
United States statistics Since reporting began in 1941, the incidence of primary and secondary syphilis in the United States has varied. The incidence dropped from 66.4 cases per 100,000 in 1947 to 3.9 cases per 100,000 in 1956 following the introduction of penicillin. During the mid 1980s, however, this trend reversed. Increases in the use of intravenous (IV) drugs and crack cocaine, the exchange of sex for drugs, indiscriminate or anonymous sex, and the number of people with multiple sexual partners contributed to the turnaround. From 1986-1990, the rate of syphilis nearly doubled, reaching a peak of 53.8 cases per 100,000 population in 1990. After 1990, the incidence decreased again; there were 53,000 reported cases (11,387 primary and secondary cases) in 1996, compared with 113,000 cases (33,962 primary and secondary cases) reported in 1992. In 2000, the number of syphilis cases reported was at an all-time low, with rates falling to 2.1 cases per

100,000 population. Increased awareness, aggressive screening, and emphasis on primary prevention contributed to the decrease. Since 2000, however, the number of syphilis cases in the United States has slightly increased each year. The Centers for Disease Control and Prevention (CDC) reported that, from 2003-2004, the rate of primary and secondary syphilis increased 8%, from 2.5 to 2.7 cases per 100,000 population.[3] Preliminary 2007 syphilis data showed that the US rate of primary and secondary syphilis increased 12% between 2006 and 2007, from 3.3 to 3.7 cases per 100,000 population. A total of 11,466 cases were reported in 2007.[4] Most of this increase has been noted in men, particularly in men who have sex with men (MSM).[3] The overall cases reported in women decreased. More than 80% of cases were reported in the southern United States. Trends for congenital syphilis cases closely parallel those for acquired syphilis cases in women, namely, a decreased incidence over the past decade. International statistics Internationally, the prevalence of syphilis varies by region. Syphilis remains prevalent in many developing countries and in some areas of North America, Asia, and Europe, especially Eastern Europe. The highest rates are in South and Southeast Asia, followed closely by sub-Saharan Africa. The third highest rates are in the regions of Latin America and the Caribbean.[5] In some regions of Siberia, as of 1999, prevalence was 1300 cases per 100,000 population.[6] Age distribution for syphilis Syphilis is most common during the years of peak sexual activity. Most new cases occur in men and women aged 15-40 years. In 2007, the rate of primary and secondary syphilis was highest in people aged 25-29 years (8.9 per 100,000).[7] An age-based breakdown of syphilis can be found on the CDC Web site. The incidence of congenital syphilis has increased 3.7% from 2005-2006 after 14 years of decline in the United States (from 8.2 to 8.5 cases per 100,000 live births). Between 1996 and 2005, the yearly incidence of congenital syphilis decreased by an average of 14.1% (see the CDC Web site for more information). Sex distribution for syphilis Men are affected more frequently with primary or secondary syphilis than women. This difference has varied over time. Male-to-female ratios of primary and secondary syphilis increased from 1.6:1 in 1965 to nearly 3:1 in 1985. After, the ratio decreased, reaching a nadir in 1994-95.

Since 2002, the incidence of primary and secondary syphilis has risen 54% among men (from 3.7 per 100,000 in 2002 to 5.7 per 100,000 in 2006). Among women, the rates of primary and secondary syphilis remain lower. After a decade of declines, the overall prevalence of syphilis among females increased 11.1% between 2005 and 2006 (from 0.9 to 1 per 100,000). Males with primary and secondary syphilis outnumber females 6 to 1.[3] The recent increase in the male-tofemale ratio is largely attributable to the increased rate of disease among MSM. Studies of patients diagnosed with sexually transmitted diseases (STDs) demonstrate that men are screened for syphilis in emergency departments and health clinics more often than women. Although surveillance data based on risk behavior are not available, a separate CDC analysis suggests that approximately 64% of all adult primary and secondary syphilis cases in 2004 were among MSM, up from an estimated 5% in 1999. In 2007, 65% of new cases occurred in MSM, and there is a high rate of HIV co-infection.[7] Sex-based trends in syphilis can be found on the CDC Web site.[8] Prevalence of syphilis by race or ethnicity In the United States, syphilis is more prevalent among persons of minority race and ethnicity. Non-Hispanic blacks are at higher risk for syphilis than nonHispanic whites. In 1997, the reported incidence of syphilis among non-Hispanic blacks was 22 cases per 100,000 population. This was 44 times higher than the rate in non-Hispanic whites.[9] This ratio had declined to 8:1 by 2002, after implementation of a national plan to eliminate syphilis in the United States. Although the reported prevalence of syphilis is somewhat higher among blacks than other ethnic groups,[10] this rate has declined significantly in recent years. From 2000-2003, the primary and secondary syphilis rate declined from 12 cases per 100,000 population to 7.8 cases per 100,000 population in this ethnic group. In 2002, 49.8% of all reported cases were in blacks, compared with 39.2% of cases in 2003.[11] In 2004, the rate among blacks was 5.6 times higher than the rate among whites.[3] From 2005 to 2006, the incidence of primary and secondary syphilis increased in all racial and ethnic groups, with a 5.6% increase in non-Hispanic whites (from 1.8 to 1.9 per 100,000 population), 16.5% in African Americans (from 9.7 to 11.3 per 100,000 population), 12.5% among Hispanics (from 3.2 to 3.6 per 100,000 population), 18.2% among Asian/Pacific Islanders (from 1.1 to 1.3 per 100,000 population), and 37.5% among American Indian/Alaska Natives (from 2.4 to 3.3 per 100,000 population). Data can be found on the CDC Web site.

Prognosis
The morbidity of syphilis ranges from the relatively minor symptoms of the primary stages of infection to the more significant constitutional systemic symptoms of secondary syphilis and the significant neurological and cardiovascular consequences of tertiary disease. Since latent syphilis can persist for years or decades, the manifestations of tertiary syphilis often occur much later in life, causing significant morbidity. Although rarely seen by clinicians since the use of penicillin became widespread in the 1950s, the primary complications of syphilis in adults include neurosyphilis, cardiovascular syphilis, and gumma. Death resulting from syphilis continues to occur. One study found that of 113 recorded deaths resulting from sexually transmitted diseases, 105 were caused by syphilis, with cardiovascular and neurosyphilis accounting for the majority of these deaths. These figures have continued to increase since the emergence of the AIDS epidemic, since genital ulcer diseases (including syphilis) are cofactors for the sexual transmission of HIV. Additionally, untreated patients who are HIV seropositive have an increased risk for rapid progression to neurosyphilis and for its complications. In addition, patients with HIV are at greater risk for development or relapse of early symptomatic neurosyphilis for up to 2 years after treatment with intramuscular or intravenous penicillin. The morbidity and mortality of untreated syphilis must be estimated from the limited data available regarding its natural course. These data are largely from one retrospective study of autopsies and two prospective studies, most notably the famous Tuskegee Study of Untreated Syphilis in the Negro Male, which fell under serious ethical scrutiny in later years for exploiting a vulnerable patient population and not offering treatment for the disease when it became available after the study was underway. These data indicate that approximately one third of patients left untreated will develop late complications, with 10% of the total developing cardiovascular syphilis; 6%, neurosyphilis; and 16%, gummatous syphilis. Mortality rates in general are greater among those affected, and late complications appear to occur more commonly in men than in women.[12, 13] For patients diagnosed with either primary or secondary syphilis (without auditory/neurologic/ocular involvement), the prognosis is good following appropriate treatment. T pallidum remains highly responsive to the penicillins, and cure is likely. For patients diagnosed with tertiary syphilis, the prognosis is less sanguine. Twenty percent of untreated patients with tertiary syphilis die of the disease, although a significant number of patients demonstrate cure with antibiotic

therapy. With adequate treatment, 90% of patients with neurosyphilis have a clinical response. Overall prognosis for tertiary syphilis depends on the duration and extent of disease activity, along with prior attempts to treat the disease. For example, prognosis for advanced symptomatic disease in cardiovascular syphilis is poor, unless it is treated with high doses of IV penicillin. In contrast, in patients with neurosyphilis complicated by optic atrophy and blindness, the ability to regain vision remains poor despite attempts with high-dose penicillin. Congenital syphilis is the most serious outcome of syphilis in women. It has been shown that a higher proportion of infants are affected if the mother has untreated secondary syphilis, compared to untreated early latent syphilis. Since T pallidum does not invade the placental tissue or the fetus until the fifth month of gestation, syphilis causes late abortion, stillbirth, or death soon after delivery in more than 40% of untreated maternal infections.[14, 15] Neonatal mortality usually results from pulmonary hemorrhage, bacterial superinfection, or fulminant hepatitis. For patients who are pregnant and have early syphilis, it is likely that the mother will deliver a child not infected by syphilis (assuming the mother was treated appropriately).

Patient Education
Patients who abuse IV drugs should be advised to avoid sharing needles and to use clean needles. Needle exchange programs are in place in some areas; however, the establishment and existence of these programs remain controversial in many communities. It is also important to stress to patients the importance of compliance with their entire antibiotic course and follow-up visits. As with all STDs, patient education must stress the importance of safer sexual practices and the need for prompt medical evaluation of chancres and other symptoms of STDs. All patients diagnosed with an STD should be screened for HIV infection. Patients with syphilis should be counseled to notify their partners of infection and to inform them of the need to be treated. Information regarding management of sex partners infected with syphilis can be found at the CDC Web site. For patient education information, see the Sexually Transmitted Diseases Center and Pregnancy and Reproduction Center, as well as Sexually Transmitted Diseases, Syphilis, Birth Control Overview, and Birth Control FAQs.

Vitiligo
Background
Vitiligo is an acquired pigmentary disorder of the skin and mucous membranes, and it is characterized by circumscribed depigmented macules and patches. Vitiligo is a progressive disorder in which some or all of the melanocytes in the affected skin are selectively destroyed. Vitiligo affects 0.5-2% of the world population, and the average age of onset is 20 years.

Pathophysiology
Vitiligo is a multifactorial polygenic disorder with a complex pathogenesis. It is related to both genetic and nongenetic factors. Although several theories have been proposed about the pathogenesis of vitiligo, the precise cause remains unknown. Generally agreed upon principles are an absence of functional melanocytes in vitiligo skin and a loss of histochemically recognized melanocytes, owing to their destruction. However, the destruction is most likely a slow process resulting in a progressive decrease of melanocytes. Theories regarding destruction of melanocytes include autoimmune mechanisms,[1] cytotoxic mechanisms, an intrinsic defect of melanocytes, oxidant-antioxidant mechanisms, and neural mechanisms. Autoimmune destruction of melanocytes The autoimmune theory proposes alteration in humoral and cellular immunity in the destruction of melanocytes of vitiligo. Thyroid disorders, particularly Hashimoto thyroiditis and Graves disease; other endocrinopathies, such as Addison disease and diabetes mellitus; and alopecia areata; pernicious anemia; inflammatory bowel disease; psoriasis; and autoimmune polyglandular syndrome are all associated with vitiligo. The most convincing evidence of an autoimmune pathogenesis is the presence of circulating antibodies in patients with vitiligo.[2] The role of humoral immunity is further supported by the observation that melanocytes are destroyed in healthy skin engrafted onto nude mice injected with vitiligo patient sera.[3] In addition to the involvement of humoral immune mechanisms in the pathogenesis of vitiligo, strong evidence indicates involvement of cellular immunity in vitiligo. Destruction of melanocytes may be directly mediated by autoreactive CD8+ T cells. Activated CD8+ T cells have been demonstrated in perilesional vitiligo skin. In addition, melanocyte-specific T cells have been detected in peripheral blood of patients with autoimmune vitiligo.[4]

Intrinsic defect of melanocytes Vitiligo melanocytes may have an intrinsic defect leading to melanocyte death. These melanocytes demonstrate various abnormalities, including abnormal, rough endoplasmic reticulum and incompetent synthesis and processing of melanocytes. In addition, homing-receptor dysregulation has also been detected. Early apoptosis of melanocytes has also been suggested as a cause of reduced melanocyte survival; however, subsequent investigation found that the relative apoptosis susceptibility of vitiligo melanocytes was comparable with that of normal control pigment cells.[5] Disturbance in oxidant-antioxidant system in vitiligo Oxidant stress may also play an essential role in the pathogenesis of vitiligo. Studies suggest that accumulation of free radicals toxic to melanocytes leads to their destruction. Because patients with vitiligo exhibit a characteristic yellow/green or bluish fluorescence in clinically affected skin, this led to the discovery that the fluorescence is due to accumulation of 2 different oxidized pteridines. The overproduction of pteridines led to the discovery of a metabolic defect in tetrahydrobiopterin homeostasis in patients with vitiligo, which results in the accumulation of melanocytotoxic hydrogen peroxide.[6] Because oxidative stress has been suggested to be the initial pathogenic event in melanocyte degeneration, several studies have been conducted to evaluate this theory. Recent investigations set out to evaluate the role of oxidative stress by measuring levels of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) in lesional and normal skin of patients with vitiligo and in the skin of normal control subjects. They concluded oxidative stress is increased in vitiligo, as indicated by high levels of SOD and low levels of CAT in the skin of vitiligo patients.[7] Neural theory Case reports describe patients afflicted with a nerve injury who also have vitiligo have hypopigmentation or depigmentation in denervated areas. Additionally, segmental vitiligo frequently occurs in a dermatomal pattern, which suggests that certain chemical mediators are released from nerve endings that affect melanin production. Further, sweating and vasoconstriction are increased in depigmented patches of vitiligo, implying an increase in adrenergic activity. Finally, increased urinary excretion of homovanillic acid and vanilmandelic acid (neurometabolites) has been documented in patients with vitiligo. This may be a secondary or primary phenomenon.[8] In summary, although the ultimate cause of vitiligo is not completely known, this condition does not reflect simple melanocyte loss, but possible immunologic

alterations and other molecular defects leading to pigment cell destruction; however, melanocytes may be present in depigmented skin after years of onset and may still respond to medical therapy under appropriate stimulation. Genetics of vitiligo Vitiligo is characterized by incomplete penetrance, multiple susceptibility loci, and genetic heterogeneity.[9] The inheritance of vitiligo may involve genes associated with the biosynthesis of melanin, a response to oxidative stress, and regulation of autoimmunity.[10] Human leukocyte antigens (HLAs) may be associated, but not in a consistent manner. For example, HLA-DR4 is increased in blacks, HLA-B13 is increased in Moroccan Jews, and HLA-B35 is increased in Yemenite Jews. An association with HLA-B13 is described in the presence of antithyroid antibodies. A genome-wide association study of generalized vitiligo in an isolated European founder population identified that the group had significant association with single-nucleotide polymorphisms in a 30-kb LD block on band 6q27, in close vicinity to IDDM8, which is a linkage and an association signal for type I diabetes mellitus and rheumatoid arthritis. Only one gene, SMOC2, is in the region of association, within which SNP rs13208776 attained genome-wide significance for association with other autoimmune diseases and vitiligo.[11] The age of onset has a genetic component; in another genomewide association study, a quantitative locus for age of onset was found in the major histocompatibility complex class II region near a region associated with generalized vitiligo susceptibility.[12]

Epidemiology
Frequency United States In the United States, the relative rate of vitiligo is 1%. International Vitiligo is relatively common, with a rate of 1-2%. Approximately 30% of vitiligo cases occur with a familial clustering of cases.

Sex A female preponderance has been reported for vitiligo, but it is not statistically significant and the discrepancy has been attributed to an increase in reporting of cosmetic concerns by female patients. Age Vitiligo may appear at any time from birth to senescence, although the onset is most commonly observed in persons aged 10-30 years. Vitiligo rarely is seen in infancy or old age. Nearly all cases of vitiligo are acquired relatively early in life. The average age of onset for vitiligo is approximately 20 years. The age of onset is unlikely to vary between the sexes. Heightened concern about the appearance of the skin may contribute to an early awareness of vitiligo among females.

Pediatric Tinea Versicolor Workup

Laboratory Studies
The diagnosis of tinea versicolor is usually made based on clinical examination findings; however, the diagnosis is easily confirmed with microscopic examination of scales soaked in 10%-15% potassium hydroxide (KOH). See the images below.

Upon potassium hydroxide (KOH) examination, hyphae are visible and grow into strands within clumps of keratinocytes. Thick-

walled spores frequently occur in grapelike clumps. Individual spores and short stubby hyphae float in the clear areas between clumps of keratinocytes. Many of

the short hyphae are dystrophic. Mycelium strands and numerous spores observed on a potassium hydroxide (KOH) preparation of tinea versicolor. This combination is commonly referred to as "spaghetti and meatballs."

Microscopic examination o Microscopic examination demonstrates the characteristic thickwalled spherical or oval yeast forms and coarse septate mycelium, often broken up into short filaments. o This combination of mycelium strands and numerous spores is commonly referred to as "spaghetti and meatballs." o Liquid blue ink, methylene blue, or Swartz-Medrik stain can be added to the KOH preparation for better visualization of the causative organism. o Scales may also be removed using clear adhesive tape; they are then directly examined. The tape must be clear and is pressed several times over involved areas of skin. The tape is then lightly pressed, sticky side down, onto a microscope slide. A small drop of methylene blue or other appropriate stain is placed at the edge of the tape and allowed to run between the tape and the glass slide. Spores, often in grapelike clumps, and mycelium are easily seen.

See the image below. Clear adhesive tape can be pressed onto areas of tinea versicolor to collect hyphae and spores. The tape is then lightly pressed onto a glass slide, and a drop of methylene blue is placed at the edge of the tape. The methylene blue is allowed to run under the tape

staining Malassezia furfur. The spores and hyphae easily are seen against a background clutter of keratinocytes and glue. Cultures o M furfur is a dimorphic lipophilic organism, which is cultured only in media enriched with C12-sized to C14-sized fatty acids. It is not a dermatophyte, does not grow on DTM, and does not respond to griseofulvin therapy. o If inoculated into lipid-rich media, the scales of tinea versicolor show spherical yeasts that produce the mycelial phase of the normal flora yeast P orbiculare. Scales that show mycelium and clusters of oval yeasts on direct microscopy grow P ovale on culture. o Colonization by M furfur is especially dense in the scalp, the upper trunk, and the flexures. In patients with clinical disease, the organism occurs in both the filamentous (hyphal) and the yeast (spore) stage forms.

Imaging Studies

The disease does not require any imaging studies.

Other Tests

Wood lamp evaluation: Pityriasis versicolor showes blue-green fluorescence of macular dyschromic lesions if irradiated by ultraviolet light with wavelength of approximately 365 nm (black light). However, the test findings may be negative in individuals on antimycotic therapy of those who have recently showered because the fluorescent is water soluble.

Histologic Findings

The characteristic histological changes include hyperkeratosis, parakeratosis, and slight acanthosis with a mild perivascular inflammatory infiltrate in the upper dermis. The organism is usually present in the upper layers of the stratum corneum, and electron microscopy reveals invasion between and within the keratinized cells. M furfur is detected by hematoxylin and eosin (H and E) stain alone, although periodic acid-Schiff (PAS) or methenamine-silver staining facilitates detection.

Staging
Different rare clinical forms have been described as follows:

Papulous variant Erythematous and papulous variant in children Tinea versicolor with atypical localization on face Tinea versicolor with atypical localization on wrists Pityriasis versicolor alba

Pediatric Tinea Versicolor Treatment & Management

Medical Care
Tinea versicolor is easily treated, and skin color alterations usually resolve within a few months of treatment.[4] It does not leave any permanent scars or pigment changes. Topical therapy alone is indicated for most patients. Systemic treatment is indicated for extensive involvement, for recurrent infections, or when topical therapy has failed. Because treatment is relatively easy and recurrence is common, therapy must be as safe, inexpensive, and convenient as possible. A plan for prophylactic therapy should be discussed with all patients to reduce the high recurrence rate. Various regimens involve both topical and oral therapies.[5] The most common is varying regimens of selenium sulfide shampoo or lotion and oral therapy with ketoconazole.

Surgical Care
The disease does not require any surgical care.

Diet
Because studies indicate that tinea versicolor may associate with malnutrition the diet of patients have to be rational and not restrictive.

Activity
Activity limitations are not necessary. However, active patients who excessively perspire are more likely to develop recurrences.

Pediatric Tinea Versicolor Medication

Medication Summary
Tinea versicolor responds well to both topical and oral antimycotic therapies. Some patients prefer oral therapy because of convenience, while others prefer the safety of topical therapies. Many effective topical therapies are available without prescription and can be used for suppressive therapy or for treating recurrences without the need for a follow-up visit. Topical therapy alone is indicated for most patients. Systemic treatment may be indicated for patients with extensive involvement, those with recurrent infections, or those in whom topical therapy has failed.

Antifungal Agent, Topical

Class Summary Selenium sulfide is effective against M furfur; it also has cytostatic effects on the epidermis and follicular epithelium, thus reducing corneocyte production. Azole, allylamine and other antifungal creams are also highly effective mycocides against M furfur. View full drug information Selenium sulfide topical (Selsun Blue, Exsel, Head & Shoulders)

Available as shampoo or lotion in 1% or 2.5% concentrations. It is a safe and effective therapy that has been used for years. The principle advantages of selenium sulfide are its low cost, OTC availability, and convenient application. However, it is an irritant, and some patients report itching or eczema after overnight applications. It may also stain clothes and bedding. Lotion is preferred in children and patients with sensitive skin. View full drug information Clotrimazole topical (Lotrimin-AF, Canesten)

Imidazole broad-spectrum antifungal agent. Inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. View full drug information Econazole (Pevaryl, Spectazole)

Antifungal agent that is a water-miscible base consisting of pegoxol 7 stearate, peglicol 5 oleate, mineral oil, benzoic acid, butylated hydroxyanisole, and purified water. The color of the soft cream is white to off white and is for topical use only. Interferes with RNA and protein synthesis and metabolism. Disrupts fungal cell wall permeability, causing fungal cell death. Exhibits broad-spectrum antifungal activity against many gram-negative organisms. Effective in cutaneous infections. View full drug information Ketoconazole topical (Nizoral)

Imidazole broad-spectrum antifungal agent. Inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. View full drug information Oxiconazole (Oxistat)

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out and resulting in fungal cell death. View full drug information Ciclopirox (Batrafen, Loprox)

Interferes with synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells. View full drug information

Naftifine (Exoderil, Naftin)

Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease the synthesis of ergosterol, which, in turn, inhibits fungal cell growth. View full drug information Terbinafine topical (Lamisil)

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Use medication until symptoms significantly improve. Duration of treatment should be >1 wk, but not >4 wk. View full drug information Butenafine (Mentax)

Inhibits squalene epoxidation, which, in turn, causes blockage of ergosterol biosynthesis (an essential component of fungal cell membranes). Used topically for tinea (pityriasis) versicolor due to M furfur, tinea pedis (ie, athlete's foot), tinea corporis (ie, ringworm), and tinea cruris (ie, jock itch) due to Epidermophyton floccosum, Trichophyton mentagrophytes, Trichophyton rubrum, and Trichophyton tonsurans.

Antifungal Agent, Systemic

Class Summary Systemic azoles are highly effective against M furfur and are usually combined with topical antimycotics in severe cases. View full drug information Ketoconazole oral (Nizoral)

Both topical and systemic agent. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. Achieves excellent skin levels with minimal PO dosing. M furfur is eradicated by the presence of ketoconazole in outer skin layers. Tinea versicolor is extremely rare in small children; thus, do not treat children aged < 10 y with PO ketoconazole for tinea versicolor. View full drug information Fluconazole (Diflucan)

Synthetic PO antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. Has little affinity for mammalian cytochromes, which is believed to explain its low toxicity. Available as tabs for PO administration, as a powder for PO susp, and as a sterile solution for IV use. Has fewer adverse effects and better tissue distribution than older systemic imidazoles. Most commonly used in the treatment of candidiasis. View full drug information Itraconazole (Sporanox, Orungal)

Synthetic triazole antifungal agent that inhibits fungal cell growth by inhibiting the cytochrome P-450dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Pediatric Tinea Versicolor Follow-up

Further Inpatient Care
No Inpatients Care is needed.

Further Outpatient Care

Tinea versicolor tends to be associated with recurrences that must be properly treated.

Inpatient & Outpatient Medications

Some authors recommend prophylactic with varying regimens of selenium sulfide shampoo or lotion.

Transfer

Tinea versicolor is caused by M furfur, which is normally present on the skin surface and, therefore, is not considered a contagious disease. In past contaminated clothes and underwear were believed to play a role in disease transfer; however, climate factors, hyperhidrosis, sebum secretion, and genetic factors appear to be involved in disease pathogenesis.

Deterrence/Prevention

Tinea versicolor has a high recurrence rate and may require frequent prophylactic treatment with intermittent topical or oral therapy. Good personal hygiene may help limit recurrences. Specifically, patients should shower as soon as possible after participating in activities or exercise that produce significant perspiration.

Complications

The disease has benign course; however, it tends to have recurrences that must be properly treated. Some patients report for itching, burning and irritation of lesions. Severe depigmentation may cause significant psychological discomfort.

Prognosis

Prognosis is excellent. Although tinea versicolor is recurrent in some patients, the condition remains treatable.

Patient Education

Tinea versicolor is caused by a fungus that is normally present on the skin surface and, therefore, is not considered a contagious disease. The disease causes no permanent sequelae, and any pigmentary alterations resolve entirely within a few months of adequate treatment. Effective therapy is available. Recurrences are common, and prophylactic therapy may be required.