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Universidad de Valencia, Facultad de Medicina, Valencia, Spain" "etiqueta" => "l" "identificador" => "aff0060" ] 12 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Universitario San Juan de Alicante, Alicante, Spain" "etiqueta" => "m" "identificador" => "aff0065" ] 13 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Universitari General de Catalunya, Quirón salud, Barcelona, Spain" "etiqueta" => "n" "identificador" => "aff0070" ] 14 => array:3 [ "entidad" => "Servicio de Anatomía Patológica. Hospital Universitario Virgen Macarena, Sevilla, Spain" "etiqueta" => "o" "identificador" => "aff0075" ] 15 => array:3 [ "entidad" => "Servicio de Dermatología, Fundación Instituto Valenciano de Oncología, Valencia, Spain" "etiqueta" => "p" "identificador" => "aff0080" ] 16 => array:3 [ "entidad" => "Departamento de Dermatología, Hospital de San Pablo, Coquimbo, Chile" "etiqueta" => "q" "identificador" => "aff0085" ] 17 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Fundación Jiménez Díaz, Madrid, Spain" "etiqueta" => "r" "identificador" => "aff0090" ] 18 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Universitario de Salamanca, Salamanca, Spain" "etiqueta" => "s" "identificador" => "aff0095" ] 19 => array:3 [ "entidad" => "Servicio de Anatomía Patológica. Hospital Universitario Son Espases, Palma de Mallorca, Spain" "etiqueta" => "t" "identificador" => "aff0100" ] 20 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Clínico Universitario de Santiago, Santiago de Compostela, Spain" "etiqueta" => "u" "identificador" => "aff0105" ] 21 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Universitario de Cruces (Barakaldo), Vizcaya, Spain" "etiqueta" => "v" "identificador" => "aff0110" ] 22 => array:3 [ "entidad" => "Servicio de Anatomía Patológica del Hospital Universitario La Paz, Madrid, Spain" "etiqueta" => "w" "identificador" => "aff0115" ] 23 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital Universitario El Bierzo, Ponferrada, Spain" "etiqueta" => "x" "identificador" => "aff0120" ] 24 => array:3 [ "entidad" => "Servicio de Anatomía Patológica, Hospital de La Reina, Ponferrada, Spain" "etiqueta" => "y" "identificador" => "aff0125" ] 25 => array:3 [ "entidad" => "Unidad de Investigación, Instituto de Investigación Biomédica de A Coruña (INIBIC), Universidad de A Coruña, A Coruña, Spain" "etiqueta" => "z" "identificador" => "aff0130" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Granulomas en dermatopatología: principales entidades. Parte II" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig0030" "etiqueta" => "Figure 6" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr6.jpeg" "Alto" => 912 "Ancho" => 1405 "Tamanyo" => 666931 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0030" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Sarcoidosis. A, Epithelioid granulomas occupying the superficial and mid dermis with few peripheral lymphocytes (H&E, original magnification ×20). B, Epithelioid granulomas composed of cells with abundant eosinophilic cytoplasm (H&E, original magnification ×100). C, Silica particle (arrow) in a sarcoid granuloma (H&E, original magnification ×200). D, Schaumann body (arrow) (H&E, original magnification ×400). E, Asteroid body (H&E, original magnification ×2400). H&E indicates hematoxylin-eosin.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Granulomas are among the most common findings in dermatopathology. They are also the most variable, not just because of their morphologic characteristics, but also because of their etiology and clinical and prognostic significance.</p><p id="par0010" class="elsevierStylePara elsevierViewall">The aim of this 2-part article is to provide an overview of the main diseases that produce granulomas observed in skin biopsy specimens. In the first part, we looked at different types of granulomas and giant cells (e.g., foreign body granulomas) and some of the most representative diseases that cause granulomas of the skin, including metabolic, neoplastic, and autoimmune diseases.</p><p id="par0015" class="elsevierStylePara elsevierViewall">In the second part of this review, we look at other types of granuloma-producing diseases, including infections.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Granuloma Annulare</span><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Granuloma annulare (GA) is a relatively common immune-related granulomatous skin disease of multifactorial etiology. It can be localized or generalized, affects patients of all ages, and is associated with systemic diseases. It is a chronic inflammatory condition that is generally slow to resolve.</p><p id="par0025" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> GA usually presents as localized or generalized papules, erythematous plaques, or annular nodules with a predilection for the extremities (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A).<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Lesions sometimes present as subcutaneous or linear nodules with a perforating ulcerative appearance. Localized forms, in particular papules and subcutaneous lesions, are more common in children and young people, while generalized forms are more common in adults and older patients. Generalized GA can occur in association with various diseases, notably diabetes mellitus, hyperlipidemia, autoimmune diseases, immunodeficiency, hematologic diseases, and, on occasions, cancer. Different morphologic forms of GA in the same patient are not uncommon.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology</span>. Histology shows one or more areas of collagen degeneration with irregular contours, often in the dermis, surrounded by a granulomatous inflammatory reaction (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>B).<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> The inflammatory infiltrate is composed of palisading macrophages, epithelioid cells, fibroblasts, lymphocytes, and occasional eosinophils. Plasma cells are not present. A basophilic interstitial matrix formed by deposits of acid mucin and/or hypereosinophilic collagen is observed in the center. Colloidal iron is useful for detecting interstitial mucin, as this may be present in very small amounts. Dense perivascular lymphocytic crowns are also observed (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>C). Elastolysis, and consequently elastolytic granulomas, are not seen in GA. The pronounced degeneration of collagen in perforating GA produces necrotic tissue that is eliminated by hair follicles. Subcutaneous GA may masquerade as a rheumatoid nodule, but can be distinguished by the presence of mucin. There have been rare reports of sarcoid-like GA. GA is the result of an autoimmune inflammatory reaction mediated by CD4<span class="elsevierStyleSup">+</span> type 1/17 T helper cells, which activate macrophages (M2) and fibroblasts, triggering the production of acid mucin, metalloproteases, and proinflammatory cytokines, which alter the interstitium and produce collagen degeneration. GA is sometimes associated with impaired innate immunity.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Actinic Granuloma and Annular Elastolytic Giant Cell Granuloma Annulare</span><p id="par0035" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> The terms <span class="elsevierStyleItalic">actinic granuloma</span><a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> and <span class="elsevierStyleItalic">annular elastolytic giant cell granuloma annulare</span> (AEGCG)<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5–7</span></a> refer to similar, if not identical, elastolytic granulomatous lesions. While actinic granuloma often refers to lesions located in sun-exposed areas with significant actinic damage, AEGCG is used to describe to similar lesions in non-sun-exposed areas or as an umbrella term to describe both actinic lesions and lesions in non-sun-exposed areas. Because annular lesions are not always present, the term <span class="elsevierStyleItalic">elastolytic giant cell granuloma</span> has been proposed.<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5,8</span></a> Some authors have suggested that AEGCG may be a photoinduced variant of GA, but agreement is lacking.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Actinic granuloma and AEGCG occur in middle-aged adults, with no clear predilection for men or women.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Actinic granuloma presents as papules that generally converge to form annular lesions (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>A). AEGCG, in turn, is characterized by large annular plaques with raised borders and an atrophic center located (according to the strict definition of these entities) in non-sun-exposed areas. There have been reports of reticular and generalized variants and papules that do not evolve to form annular lesions.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> The clinical course is variable, with some lesions resolving spontaneously and others showing resistance to treatment (topical corticosteroids; pimecrolimus; cryotherapy; psoralen with UV-A; oral chloroquine or hydroxychloroquine; systemic corticosteroids, cyclosporine, or clofazimine; fumaric acid; dapsone; tranilast; and isotretinoin).<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Both actinic granuloma and AEGCG are histologically characterized by dermal granulomatous lesions with multinucleated giant cells (mostly foreign body giant cells with large numbers of nuclei) and signs of multifocal elastophagocytosis (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>B-E). Mucin deposits, palisading, and necrobiosis are generally not observed.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> There may be a predominance of nonmultinucleated histiocytes or even sarcoid-type granulomas. There have also been reports of a trizonal histologic pattern,<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a> with a giant cell component typically located at the raised erythematous border, a surrounding area of elastosis without an inflammatory component, and a central atrophic area with a marked reduction or absence of elastic fibers. There may be a variable lymphocytic component.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Morbihan Disease</span><p id="par0050" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Morbihan disease is a rare disease of unknown etiopathogenesis first described in 1957 by the French dermatologist Robert Degos in a farmer in Morbihan, Brittany.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> Morphologic findings include perilymphatic and intralymphatic granulomas.</p><p id="par0055" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Morbihan disease is more common in men aged between 40 and 60 years. It is associated with rosacea in 26% of cases<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> and there have been isolated reports of an association with lupus miliaris disseminatus faciei.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> It follows a chronic, recurrent course characterized by symmetric erythema and solid edema involving the upper two-thirds of the face (forehead, glabella, eyelids, nose, and chin) (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>). Although Morbihan disease is generally asymptomatic, its aesthetics can cause psychosocial disorders, and severe periorbital edema can cause visual field loss. Diagnosis is by exclusion. The differential diagnosis should include lupus erythematosus, dermatomyositis, and chronic actinic dermatitis.</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0060" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> The morphologic findings on histology are quite nonspecific (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>A), and include dermal interstitial edema (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>B), vascular ectasia, perifollicular fibrosis, a perivascular and perifollicular lymphohistiocytic inflammatory infiltrate (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>C) with neutrophils (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>D) and in some cases mast cells, sebaceous gland hyperplasia, and epithelioid granulomas, which are mainly perilymphatic and intralymphatic<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">12–14</span></a> but can be perifollicular. The histologic differential diagnosis should include other more common granulomatous diseases, notably, granulomatous rosacea, lupus miliaris disseminatus faciei, granulomatous periorificial dermatitis, anogenital granulomatosis, sarcoidosis, and Melkersson-Rosenthal syndrome. Most of these entities can be ruled out by integrating clinical and other histologic findings. Finally, although the etiology and pathogenesis of Morbihan disease remain to be elucidated, proposed mechanisms include an imbalance between lymph production and drainage, a loss of capillary and lymph vessel wall integrity associated with chronic inflammation, and alterations to dermal lymphatic vessels as a result of perilymphatic epithelioid granulomas.</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Sarcoidosis</span><p id="par0065" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Sarcoidosis is a multisystem disease of unknown etiology histologically characterized by noncaseating sarcoid granulomas in several organs, such as the lungs, lymph nodes, skin, and spleen.</p><p id="par0070" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Skin lesions in sarcoidosis are classified as specific or nonspecific. Specific lesions include granulomas, which are clinically highly variable and frequently consist of macules, papules, and plaques of varying shapes and sizes.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> The lesions sometimes arise in scars or at sites of trauma (e.g., tattoos, surgery, laser therapy, venipuncture)<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> (<a class="elsevierStyleCrossRef" href="#fig0025">Fig. 5</a>). Red-violaceous plaques in the center of the face, a manifestation known as <span class="elsevierStyleItalic">lupus pernio</span>, are characteristic of sarcoidosis. Nonspecific lesions do not have granulomas and include erythema nodosum, calcifications, prurigo, and erythema multiforme.</p><elsevierMultimedia ident="fig0025"></elsevierMultimedia><p id="par0075" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> The most characteristic histologic finding in sarcoidosis is the presence of "naked" sarcoid granulomas, which are noncaseating epithelioid granulomas surrounded by a small number of peripheral lymphocytes (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>A,B). They are usually located in the reticular dermis, and occasionally extend into the subcutaneous tissue. The epidermis may have a normal appearance, but sometimes shows atrophy, hyperplasia, or ulceration.<a class="elsevierStyleCrossRefs" href="#bib0075"><span class="elsevierStyleSup">15–18</span></a> Other less characteristic findings are perifollicular and perineural granulomas, tuberculoid granulomas, focal fibrinoid necrosis, dermal mucin, lichenoid damage, and vasculitis.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16,17</span></a> Intracytoplasmic inclusions (Schaumann bodies and asteroid bodies) may be occasionally observed, but while characteristic, they are not pathognomonic.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">17,18</span></a> Schaumann bodies are concentric, basophilic lamellar structures formed by calcium and proteins (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>D), while asteroid bodies are spiculated radial eosinophilic structures that appear to be formed by cytoskeletal filaments (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>E). Observation of foreign bodies in the granulomas (e.g., silica particles) is not uncommon<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16,18</span></a> (<a class="elsevierStyleCrossRef" href="#fig0030">Fig. 6</a>E) and has given rise to the concept of silica granulomas, which are thought to occur in patients with sarcoidosis who are more predisposed to the formation of granulomas in response to the accidental implantation of silica particles in the dermis.<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">19–21</span></a></p><elsevierMultimedia ident="fig0030"></elsevierMultimedia></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Interstitial and Palisaded Neutrophilic Granulomatous Dermatitis</span><p id="par0080" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Interstitial and palisaded neutrophilic granulomatous dermatitis is an entity, or rather a reactive histologic pattern, that is usually observed in systemic diseases, mostly of an autoimmune nature.</p><p id="par0085" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> It is a self-limiting condition that starts with symmetric, erythematous annular lesions, papules and nodules, or plaques,<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,22,23</span></a>mainly located on the extensor surface of the extremities and trunk.<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,24</span></a> It occurs in association with other conditions such as arthralgia and pruritus,<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> and is observed in autoimmune diseases,<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,22,25</span></a> such as lupus erythematosus, inflammatory bowel disease, rheumatoid arthritis,<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> granulomatosis with polyangiitis,<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> and certain hematologic malignancies, such as leukemia, multiple myeloma, and Hodgkin lymphoma.<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">25,28</span></a> Its association with drugs is unclear.<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3,22</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Histology shows a diffuse, superficial and/or deep dermal inflammatory infiltrate under a normal epidermis,<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> with central palisading neutrophils and histiocytes around an area of degenerated collagen with scant mucin (<a class="elsevierStyleCrossRef" href="#fig0035">Fig. 7</a>A,B). Other findings include karyorrhexis with variable leukocytoclastic vasculitis<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> and occasional eosinophils.<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">23,26</span></a></p><elsevierMultimedia ident="fig0035"></elsevierMultimedia></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Granulomas Caused by Deep Mycoses</span><p id="par0095" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> The deep mycoses are deep skin infections caused by fungi. Skin infection can occur by direct inoculation (e.g., trauma, wound infection) or spread from other organs, such as the lungs or central nervous system.</p><p id="par0100" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Skin lesions caused by deep fungal infections can be highly variable depending on the species involved, and include macules, papules, plaques, pustules, nodules, scars, areas of panniculitis, intertrigo, and tumors, with or without ulceration. Some lesions may even acquire a verrucous appearance that can be quite pronounced. Fungi can sometimes be eliminated through lesions in the form of particles visible to the naked eye (e.g., “sulphur" granules in the case of eumycetoma).<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> Certain infections in addition to sporotrichosis can produce a clear sporotrichoid pattern, characterized by linearly distributed lesions along the course of the lymphatic vessels (<a class="elsevierStyleCrossRef" href="#fig0040">Fig. 8</a>). Other infections can result in somewhat more characteristic lesions, such as keloid lesions in lobomycosis or molluscum-like lesions in coccidioidomycosis. The clinical presentations are so varied that infections such as histoplasmosis have been called <span class="elsevierStyleItalic">fungal syphilis</span>.</p><elsevierMultimedia ident="fig0040"></elsevierMultimedia><p id="par0105" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> The fungi responsible for the deep mycoses are distinguished by their morphology and size (<a class="elsevierStyleCrossRef" href="#fig0045">Fig. 9</a>).<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a> The main agents that affect humans are shown in <a class="elsevierStyleCrossRef" href="#fig0045">Fig. 9</a>, which includes <span class="elsevierStyleItalic">Prototheca</span>, an alga, for comparative purposes. Infections caused by pigmented fungi are easily identifiable (chromoblastomycosis, phaeohyphomycosis, and alternariosis). Most fungi responsible for the deep mycoses are easily identifiable by hematoxylin-eosin staining as they have distinctive appearances, sizes, and shapes (<a class="elsevierStyleCrossRefs" href="#fig0050">Figs. 10–12</a>), but special techniques are sometimes needed for better visualization. The most widely used stains are periodic acid-Schiff (PAS) and Grocott. Some fungi (e.g., <span class="elsevierStyleItalic">Lacazia</span>) are birefringent under polarized light.</p><elsevierMultimedia ident="fig0045"></elsevierMultimedia><elsevierMultimedia ident="fig0050"></elsevierMultimedia><elsevierMultimedia ident="fig0055"></elsevierMultimedia><elsevierMultimedia ident="fig0060"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">Several fungi trigger the formation of intense antibody deposits, visualized as a crown of eosinophils radiating around the fungus. This phenomenon is known as the <span class="elsevierStyleItalic">Splendore-Hoeppli phenomenon</span> (<a class="elsevierStyleCrossRef" href="#fig0065">Fig. 13</a>).</p><elsevierMultimedia ident="fig0065"></elsevierMultimedia><p id="par0115" class="elsevierStylePara elsevierViewall">Deep skin fungal infections are usually accompanied by a suppurative granulomatous response (abscess formation), with fungi usually observed in the center of the granuloma (suppurative area). Suppurative granulomas are not pathognomonic, as they are seen in other types of infections (e.g., those caused by atypical mycobacteria or <span class="elsevierStyleItalic">Tularemia</span> species). Sarcoid and caseating necrotizing granulomas may also be observed, making it less likely to suspect a fungal infection. Some fungi (such as <span class="elsevierStyleItalic">Coccidioides</span>) can induce a background mucinous response.</p><p id="par0120" class="elsevierStylePara elsevierViewall">Hyperplasia of the overlying epidermis, sometimes with a verrucous appearance, is quite common. Fungi may be eliminated through the skin. Granulomas may not always form in immunocompromised individuals, who show a predominantly neutrophilic response and are more prone to spread of the infection.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Mycobacterial Infections</span><p id="par0125" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Mycobacterial infections are caused by organisms of the genus <span class="elsevierStyleItalic">Mycobacterium</span>. The classic distinction is between <span class="elsevierStyleItalic">Mycobacterium tuberculosis</span>, responsible for tuberculosis, and non-tuberculous mycobacteria, which are grouped in the atypical category. Leprosy, which is caused by <span class="elsevierStyleItalic">Mycobacterium leprae</span>, is considered in a separate section in this article.</p><p id="par0130" class="elsevierStylePara elsevierViewall">Cutaneous tuberculosis is uncommon and accounts for less than 2% of extrapulmonary forms of tuberculosis. Its incidence, however, has increased together with that of other forms of tuberculosis in relation to human immunodeficiency virus (HIV) infection and an increase in multidrug-resistant strains. Nontuberculous mycobacteria are a large, heterogeneous group of ubiquitous opportunistic pathogens. Their incidence is difficult to estimate, although it appears to be increasing in both immunosuppressed and immunocompetent individuals.<a class="elsevierStyleCrossRefs" href="#bib0155"><span class="elsevierStyleSup">31–34</span></a> The main causes of cutaneous tuberculosis are <span class="elsevierStyleItalic">Mycobacterium marinum</span> (swimming pool granuloma), <span class="elsevierStyleItalic">Mycobacterium fortuitum-chelonae</span> complex, and <span class="elsevierStyleItalic">Mycobacterium ulcerans</span> (Buruli ulcer), which is extremely rare in our setting.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">34</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Cutaneous tuberculosis is characterized by 2 types of lesions<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">35–39</span></a>: true tuberculosis (linked to the presence of bacilli in lesions and a direct consequence of infection) and tuberculid lesions (a hypersensitivity reaction to antigens from the mycobacteria). It is usually classified according to the mode of acquisition, which can be exogenous (inoculation causing tuberculous chancre or tuberculosis verrucosa cutis) or endogenous, occurring by contiguity (scrofuloderma, tuberculosis cutis orificialis, and some cases of lupus vulgaris) or hematogenous spread (lupus vulgaris [<a class="elsevierStyleCrossRef" href="#fig0070">Fig. 14</a>A], miliary tuberculosis, and tuberculous gumma). Tuberculids include erythema induratum, papulonecrotic tuberculid, and lichen scrofulosorum.<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">36–39</span></a></p><elsevierMultimedia ident="fig0070"></elsevierMultimedia><p id="par0140" class="elsevierStylePara elsevierViewall">The clinical appearance of lesions caused by atypical mycobacteria is very broad and in many cases does not help establish a diagnosis (<a class="elsevierStyleCrossRef" href="#fig0075">Fig. 15</a>A). <span class="elsevierStyleItalic">M marinum</span> infections develop 1 to 2 weeks after sustaining a wound in an aquatic environment and often spread in a sporotrichoid-like pattern.<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">34,35,40</span></a><span class="elsevierStyleItalic">M fortuitum-chelonae</span> infections are the result of wound contamination, following, for example, surgery, injections, mesotherapy, or acupuncture.<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">35,40</span></a> Outbreaks have been described in association with the use of contaminated tattoo ink.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p><elsevierMultimedia ident="fig0075"></elsevierMultimedia><p id="par0145" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> All cutaneous forms of <span class="elsevierStyleItalic">M tuberculosis</span> infection are characterized by the presence of tuberculoid granulomas (<a class="elsevierStyleCrossRef" href="#fig0070">Fig. 14</a>B), which consist of aggregates of epithelioid macrophages and Langhans giant cells, variable degrees of central caseous necrosis, and abundant peripheral lymphocytes. The granulomas do not always show necrosis or suppuration, and, depending on the host’s immune status, there may even be predominant necrosis and an almost inexistent granulomatous response.<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">36,39,42</span></a> Diagnosis is based on identification of the microorganisms involved, as morphologic findings are not diagnostic. Microorganisms can be detected histopathologically, using Ziehl-Neelsen staining, for example, but this is positive in less than 5% of cases, as skin lesions usually have a low bacterial burden, and a minimum of 1000 to 10 000 colon-forming units per milliliter are normally required for detection.<a class="elsevierStyleCrossRefs" href="#bib0215"><span class="elsevierStyleSup">43,44</span></a> Alternative techniques include microbiological techniques such as smears, culture, and polymerase chain reaction (PCR) analysis of paraffin-embedded biopsy tissue. The main entity to consider in the differential diagnosis, apart from other granulomatous infections, is sarcoidosis, which can be distinguished by the absence of necrosis and peripheral lymphocytes.</p><p id="par0150" class="elsevierStylePara elsevierViewall">Erythema induratum is essentially a form of lobular panniculitis characterized by granulomatous inflammation and small vessel vasculitis within the lobules. Papulonecrotic tuberculids involve extensive dermal necrosis with areas of granulomatous inflammation and vasculitis.<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">36,37</span></a></p><p id="par0155" class="elsevierStylePara elsevierViewall">In the category of atypical mycobacteria, <span class="elsevierStyleItalic">M marinum</span> infection histologically resembles a granulomatous inflammatory reaction that is normally confined to the dermis and often shows central suppuration and secondary epidermal changes.<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">32,33</span></a><span class="elsevierStyleItalic">M fortuitum-chelonae</span> lesions show varying degrees of acute inflammation followed by the formation of granulomas, which are generally poorly defined. In some cases, aggregates of bacilli will be seen in areas of suppuration (<a class="elsevierStyleCrossRef" href="#fig0075">Fig. 15</a>B). These changes are nonspecific and are also observed in infections caused by other species that are less likely to affect the skin.<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">33,44</span></a></p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Leishmaniasis</span><p id="par0160" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Leishmaniasis is caused by flagellate parasites of the <span class="elsevierStyleItalic">Leishmania</span> genus and is usually transmitted by sandfly bites. The main reservoirs are wild or domestic mammals, particularly dogs.</p><p id="par0165" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Leishmaniasis can be cutaneous, mucocutaneous, or visceral. The clinical forms are highly variable and depend on the characteristics of the parasite, the vector, the host’s immune response, and the location of the lesions.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a> Cutaneous leishmaniasis (usually confined to the face, scalp, arms, or other exposed areas) presents as a self-limiting, slow-growing, hard, crusted papule (<a class="elsevierStyleCrossRef" href="#fig0080">Fig. 16</a>). Disseminated cutaneous forms occur in immunosuppressed individuals. There are also recurrent forms and post kala-azar dermal leishmaniasis. Mucocutaneous leishmaniasis, which is mostly caused by <span class="elsevierStyleItalic">Leishmania braziliensis</span>, causes lesions involving the oral and nasopharyngeal mucosa. With the exception of dark pigmentation, skin involvement is rare (5%) in visceral leishmaniasis (kala-azar), in which parasites are distributed throughout the reticuloendothelial system, causing fever, hepatosplenomegaly, and severe systemic disease.</p><elsevierMultimedia ident="fig0080"></elsevierMultimedia><p id="par0170" class="elsevierStylePara elsevierViewall">Several of the more than 20 <span class="elsevierStyleItalic">Leishmania</span> species that are potentially pathogenic to humans tend to show visceral tropism (e.g., <span class="elsevierStyleItalic">Leishmania donovani</span> and <span class="elsevierStyleItalic">Leishmania infantum</span>), but the majority show tropism for the skin or mucocutaneous surfaces. Exclusive cutaneous involvement may be seen in infections caused by <span class="elsevierStyleItalic">L infantum</span>, the predominant species in Spain and the western Mediterranean basin.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Histologic findings are correlated with clinical presentation and immune response. In patients who mount a poor immune response, histology typically shows innumerable amastigotes and abundant histiocytes, but no other inflammatory cells. Immunocompetent patients tend to have small or moderate numbers of amastigotes, in addition to granulomas, and, on occasions, necrosis.</p><p id="par0180" class="elsevierStylePara elsevierViewall">In acute forms of leishmaniasis, histology shows a dense, diffuse, predominantly histiocytic dermal infiltrate together with abundant lymphocytes and plasma cells. The epidermis may show marked hyperplasia, with hyperkeratosis or pseudoepitheliomatous changes. In other cases, atrophy or ulceration will be seen.</p><p id="par0185" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Leishmania</span> amastigotes (the intracellular form of the parasite) are predominantly observed at the intracytoplasmic level. They can be clearly visualized by staining with hematoxylin-eosin, or, when inside macrophages, Giemsa. They may also be observed in cytological smears obtained by scraping, touch imprint, or fine needle aspiration. Their bodies are round or oval and measure 2 to 5 μm in diameter. They show a peripheral enhancement pattern corresponding to the kinetoplast and are typically arranged at the periphery of the cytoplasm (<a class="elsevierStyleCrossRef" href="#fig0085">Fig. 17</a>, box A). Electron microscopy can distinguish between the nucleus, kinetoplast, and internal flagellum (<a class="elsevierStyleCrossRef" href="#fig0085">Fig. 17</a>, box B).<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a> They are not encapsulated and therefore stain negative for PAS and Grocott, distinguishing them from <span class="elsevierStyleItalic">Histoplasma capsulatum.</span> The promastigote form (which is longer, larger, and has an external flagellum) is confined to the intestine of the vector and is therefore not seen in lesions.</p><elsevierMultimedia ident="fig0085"></elsevierMultimedia><p id="par0190" class="elsevierStylePara elsevierViewall">In more chronic forms of leishmaniasis, confluent, poorly defined, epithelioid granulomas with a disordered appearance (messy granulomas)<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> are observed and usually occupy the full thickness of the dermis (<a class="elsevierStyleCrossRef" href="#fig0090">Fig. 18</a>A). Additional findings include Langhans giant cells, an increased number of plasma cells, and a decreased number of amastigotes, such that they may be difficult to discern. Amastigotes tend to be located in the uppermost areas of the dermis, at the subepidermal level (<a class="elsevierStyleCrossRef" href="#fig0085">Fig. 17</a>).</p><elsevierMultimedia ident="fig0090"></elsevierMultimedia><p id="par0195" class="elsevierStylePara elsevierViewall">Recurrent leishmaniasis shows confluent non-necrotizing epithelioid granulomas in which it is very difficult or even impossible to identify amastigotes. Other cells present are lymphocytes, plasma cells, and eosinophils.</p><p id="par0200" class="elsevierStylePara elsevierViewall">Immunohistochemistry is a useful diagnostic aid when there are few parasites. Monoclonal anti-Leishmania antibodies exist,<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a> but they are not widely available and their use is not standardized. Staining for CD1a with clone MTB1 may also be helpful, as it is positive for amastigotes, possibly due to transfer from Langerhans cells. CD1a preferentially stains amastigotes in the upper dermis, with less intense patterns observed in the deeper layers.<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a> Not all <span class="elsevierStyleItalic">Leishmania</span> species, however, show positive results. In addition, other clones of the same antibody may be negative. PCR is the most sensitive method for detecting <span class="elsevierStyleItalic">Leishmania</span> species, with a sensitivity rate of close to 100%.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a></p><p id="par0205" class="elsevierStylePara elsevierViewall">In diffuse cutaneous leishmaniasis, the dermis is diffusely occupied by macrophages that do not form granulomas and clear cytoplasm containing innumerable amastigotes (<a class="elsevierStyleCrossRef" href="#fig0090">Fig. 18</a>A). Lymphocytes and plasma cells are scarce, while epidermal changes are variable.</p><p id="par0210" class="elsevierStylePara elsevierViewall">The histologic differential diagnosis is broad and depends on the form of presentation. It must include other granulomatous diseases and depends on the correct identification of amastigotes. The dense inflammatory infiltrate can cause confusion with lymphoma. Intracellular parasites are also observed in rhinoscleroma, histoplasmosis, inguinal granuloma, and blastomycosis, each with distinct morphologic and staining characteristics. Established or chronic <span class="elsevierStyleItalic">Leishmania</span> lesions present abundant plasma cells, requiring the exclusion of secondary or tertiary syphilis. Epidermal hyperplasia can sometimes mimic squamous cell carcinoma. Other granulomatous diseases, such as lupus vulgaris, leprosy, and sarcoidosis should also be considered in the histologic differential diagnosis.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a></p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Diseases Caused by Parasites</span><p id="par0215" class="elsevierStylePara elsevierViewall">Granulomas secondary to parasite infestations account for up to 16.7% of all granulomas, and include, among others, schistosomiasis and granulomas secondary to hydatid cysts.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> In the section on helminth infections, we have included infections caused by trematodes (schistosomiasis, paragonimiasis, and fascioliasis), nematodes (cutaneous larva migrans, onchocerciasis, filariasis, gnathostomiasis, loiasis, dracunculiasis, strongyloidosis, ascariasis, streptocerciasis, dirofilariasis, and trichinosis) and cestodes (sparganosis, cysticercosis, and echinococcosis). The focus is on infections in which histology typically shows granulomas.</p><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Cutaneous Schistosomiasis</span><p id="par0220" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Cutaneous schistosomiasis is an endemic infection in tropical and subtropical regions caused by species of the genus <span class="elsevierStyleItalic">Schistosoma</span>, which are commonly found in snails. The infection is transmitted by contact with contaminated water. Of the 5 species that can affect humans, the 3 most common are <span class="elsevierStyleItalic">Schistosoma hematobium</span> (located in Africa and the Middle East and responsible for urinary schistosomiasis), <span class="elsevierStyleItalic">Schistosoma japonicum</span> (located in Japan and Southeast Asia), and <span class="elsevierStyleItalic">Schistosoma mansoni</span> (more common in Africa, South America, and the Caribbean).</p><p id="par0225" class="elsevierStylePara elsevierViewall">Skin lesions are associated with anthropophilic <span class="elsevierStyleItalic">Schistosoma</span> parasites, that is, parasites whose larval form (cercaria) can pierce the skin, producing adult worms that mate and release eggs to the exterior through the intestine or bladder. These skin lesions can be classified as <span class="elsevierStyleItalic">1</span>) bilharziasis cutanea tarda, which is a granulomatous reaction to adult worms and eggs; <span class="elsevierStyleItalic">2</span>) hypersensitivity reactions (cercarial dermatitis or swimmer's itch); or <span class="elsevierStyleItalic">3</span>) transient cutaneous responses to the release of eggs into the bloodstream (not involving intralesional parasites), with fever, urticaria, and sometimes, purpura (<a class="elsevierStyleCrossRef" href="#fig0090">Fig. 18</a>B).<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a> Swimmer's itch may also be caused by anthropophilic schistosomes, which, unable to mature and complete their life cycle in humans, die in the skin, producing a local inflammatory reaction only (<a class="elsevierStyleCrossRef" href="#fig0090">Fig. 18</a>C). In this next section, we will focus on cutaneous schistosomiasis (bilharziasis), which is typically granulomatous.</p><p id="par0230" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Schistosomiasis presents as papillomatous papules or plaques that can mimic genital warts associated with human papillomavirus infection.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> If detected, it is important to rule out parasites in the bladder and intestine.</p><p id="par0235" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Although papillomatosis and parakeratosis may be observed, the most characteristic histologic finding is a granulomatous inflammatory infiltrate with eosinophils and plasma cells around <span class="elsevierStyleItalic">Schistosoma</span> eggs. <span class="elsevierStyleItalic">S hematobium</span> eggs have a terminal spike, S <span class="elsevierStyleItalic">mansoni</span> eggs have a lateral spike, and <span class="elsevierStyleItalic">S japonicum</span> eggs have no spikes. In the case of swimmer's itch, the presence of nonpathogenic metacercariae unable to survive triggers a more intense reaction, producing greater spongiosis and a denser eosinophilic and neutrophilic infiltrate (<a class="elsevierStyleCrossRef" href="#fig0090">Fig. 18</a>C).</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Onchocerca Infections</span><p id="par0240" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition. Onchocerca</span> infections are a group of infections caused by nematodes (roundworms) of the <span class="elsevierStyleItalic">Filarioidea</span> genus with a threadlike body and a mouth surrounded by papillae. They are usually transmitted by mosquitoes. In this section, we will review the subcutaneous forms, which include onchocerciasis and loiasis or eye worm. Onchocerciasis, which is caused by <span class="elsevierStyleItalic">Onchocerca volvulus</span> and transmitted by blackflies of the <span class="elsevierStyleItalic">Simulium</span> genus, is characterized by the formation of granulomas.</p><p id="par0245" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation</span><span class="elsevierStyleBold">.</span> Onchocerciasis produces significant xerosis and signs of premature skin aging, accompanied by intense itching, isolated smooth-surfaced papules and hyperkeratotic macules, leopard skin (areas of depigmented and repigmented skin), and subcutaneous nodules called <span class="elsevierStyleItalic">onchocercomas</span>, which tend to arise on bony prominences.</p><p id="par0250" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Microfilaria may be observed in the skin, alongside edema, myxoid deposits, dilated lymph vessels, and an inflammatory neutrophilic and eosinophilic infiltrate. Histologic examination of an onchocercoma will show numerous organisms surrounded by a granulomatous inflammatory infiltrate (<a class="elsevierStyleCrossRef" href="#fig0090">Fig. 18</a>D). This infiltrate is usually separated from the thick cuticle of the filaria by a retraction artifact caused by the presence of phagocytes unable to attach themselves to the cuticle.</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Gnathostomiasis</span><p id="par0255" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Gnathostomiasis is an emerging parasitic disease caused by the third-stage larvae (L3) of nematodes of the genus <span class="elsevierStyleItalic">Gnathostoma</span> (order Spirurida), which have a complex life cycle involving a first intermediate host, a copepod, which is ingested by fish and freshwater amphibians, in which L2 parasites develop into L3 larvae capable of movement. From these second intermediate hosts, they can pass into dogs, cats, or pigs, where they trigger the formation of granulomas in the mucosa of the gastrointestinal tract. L1 aquatic larvae will then be eliminated in stools and ingested by copepods, where they will continue their cycle. Gnathostomiasis is more common in areas where fish or amphibians are consumed raw (e.g., sushi or ceviche).</p><p id="par0260" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation</span>. <span class="elsevierStyleItalic">Gnathostoma</span> parasites cannot complete their life cycle in humans, so once ingested, they travel through the mesenteric plexus to the subcutaneous tissue, where they cause migratory panniculitis. A history of eating raw fish and observation of tissue or peripheral blood eosinophilia are highly suggestive of gnathostomiasis.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> Migratory panniculitis may also be seen in subcutaneous toxocariasis, loaiasis, and even <span class="elsevierStyleItalic">Strongyloides stercoralis</span> infection, cutaneous larva migrans and, exceptionally, in association with ectopic migrating flukes such as <span class="elsevierStyleItalic">Fasciola hepatica</span> and <span class="elsevierStyleItalic">Paragonimus</span> species.</p><p id="par0265" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Although granulomas may form around <span class="elsevierStyleItalic">Gnathostoma</span> larvae (<a class="elsevierStyleCrossRef" href="#fig0095">Fig. 19</a>A), histology typically shows eosinophilic infiltrates of varying intensity, intermixed with lymphocytes, neutrophils, histiocytes, and even plasma cells (<a class="elsevierStyleCrossRef" href="#fig0095">Fig. 19</a>B). The worms may sometimes be found in the deep dermis or panniculus adiposus and have a diameter of approximately 200 to 300 μm.</p><elsevierMultimedia ident="fig0095"></elsevierMultimedia><p id="par0270" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Differential diagnosis. Gnathostoma</span> worms are similar in size to <span class="elsevierStyleItalic">Spirometra</span> worms, which cause sparganosis if ingested in raw meat or fish or if present in water or topical products applied to the skin. The larvae, which are white, flat and have a scalloped appearance, can live in the stomachs of carnivorous mammals, from where they may migrate to the skin, producing nodules that measure between 0.5 and 5 cm and resemble lipomas or fibroids. The incubation period is between 6 and 11 days.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> These nodules can open to the surface, allowing the larvae to escape. Histology often shows a granulomatous reaction around the larvae, which are easy to distinguish from <span class="elsevierStyleItalic">Gnathostoma</span> larvae, as they lack genital and intestinal structures and have a loose central stroma and discontinuous smooth muscle fibers.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> A palisaded granulomatous reaction with mucin, similar to that observed in GA, has been reported in sparganosis. Unlike in other parasitic diseases, surgical removal of the worm is common. Identification of the larvae is diagnostic.<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a></p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Dirofilariasis</span><p id="par0275" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Dirofilariasis is caused by nematodes of the genus <span class="elsevierStyleItalic">Dirofilaria</span>; the larvae of these nematodes are transmitted by mosquito bites and can affect the lung (<span class="elsevierStyleItalic">Dirofilaria immitis</span>) and other organs, including the skin (<span class="elsevierStyleItalic">Dirofilaria repens</span>).<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a></p><p id="par0280" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> The cutaneous manifestations of <span class="elsevierStyleItalic">Dirofilaria repens</span> are single or multiple erythematous nodules with a soft consistency caused by the degeneration of immature larvae, triggering a foreign body granulomatous reaction, with palisaded granulomas, necrobiotic collagen, and a mixed inflammatory infiltrate comprising eosinophils, plasma cells, lymphocytes, and histiocytes.</p><p id="par0285" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> The histologic findings of dirofilariasis are similar to those of necrobiosis lipoidica, although in serial tissue sections, it is common to see spaces in the upper area of the subcutaneous tissue with cuticular striations and spines and a central area with filarial viscera.<span class="elsevierStyleSup">59</span></p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Strongyloidiasis</span><p id="par0290" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Strongyloidiasis is primarily a gastrointestinal parasitic disease but it can affect the skin. Skin lesions are more common in immunosuppressed patients and are clinically relevant as they are the most common purpuric lesions observed in hyperinfestations and are associated with a poor prognosis.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a></p><p id="par0295" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Cutaneous strongyloidiasis can present as fast-moving larva currens (5–15 cm/h) or purpuric macules that converge centrifugally to form larger lesions in the abdominal and thigh areas.</p><p id="par0300" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology. Strongyloides</span> larvae can be detected in capillaries or among collagen fibers in the reticular dermis and may be surrounded by an inflammatory granulomatous infiltrate, although this is rare and has been attributed to the death of the larvae.<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">61</span></a></p><p id="par0305" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Differential diagnosis.</span> Cutaneous larva migrans, which occurs following the penetration of <span class="elsevierStyleItalic">Ancylostoma braziliense</span> into the skin, produces a characteristic, linear, serpentine lesion that follows the trajectory of the larva, which advances several centimeters a day. Histology does not normally show granulomas, but rather spongiosis and a lymphocytic inflammatory infiltrate rich in eosinophils. <span class="elsevierStyleItalic">Strongyloides</span> L3 larvae are similar in size to <span class="elsevierStyleItalic">Ancylostoma braziliense</span> larvae (about 3 keratinocytes), but the former are typically found in the dermis, while the latter, although less common, are typically found in the epidermis.<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">62</span></a> Size is useful for differentiating <span class="elsevierStyleItalic">Strongyloides</span> larvae from L3 <span class="elsevierStyleItalic">Gnathostoma</span> larvae, which with a diameter of 200 to 300 μm, are considerably larger.</p></span><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Cysticercosis</span><p id="par0310" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Cysticercosis is an infectious disease caused by the larval stage of <span class="elsevierStyleItalic">Taenia solium</span>. It is particularly concerning when it affects the central nervous system. It is estimated that 2% of seizure emergencies in developing countries are caused by this infection.</p><p id="par0315" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> Cutaneous cysticercosis presents as subcutaneous nodules (a single nodule or < 10) in 88% of cases.<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">63</span></a> The nodules are mainly located on the trunk and contain a yellowish liquid.</p><p id="par0320" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> When larvae are present, histology will show a cystic cavity surrounded by a vesicular wall. The lumen, which is scalloped in appearance, contains round nodular structures that correspond to invaginated scolices.<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">63</span></a> Granulomas are more common following rupture of the cyst.</p></span><span id="sec0085" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Echinococcosis or Hydatid Disease</span><p id="par0325" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Echinococcosis, or hydatid disease, is caused by larval stages (metacestodes) of parasites of the genus <span class="elsevierStyleItalic">Echinococcus</span>.</p><p id="par0330" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> As in cysticercosis, echinococcosis cysts can clinically masquerade as an infundibular cyst or lipoma<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">64</span></a> and tend to grow at a rate of 1 mm to 5 cm a year.</p><p id="par0335" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> Hydatid cysts have 3 main layers: an outer layer, the pericyst, formed by host cells; a middle layer; and a thick, translucent inner germinal layer, from which the scolices arise.<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">64</span></a> Since the lesions lack an epithelial lining, but contain multiple layers of elongated epithelioid histiocytes, they are pseudocysts. Histiocytes may stain positively with CD68, and lymphocytes and eosinophils are usually present. Cyst rupture leads to a granulomatous inflammatory reaction with fibrosis and multinucleated histiocytes, neutrophils, eosinophils, and, on occasions, leukocytoclastic vasculitis.</p></span></span><span id="sec0090" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Leprosy</span><p id="par0340" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Definition.</span> Leprosy is a chronic infection caused by the obligate intracellular parasites <span class="elsevierStyleItalic">Mycobacterium leprae</span> and <span class="elsevierStyleItalic">Mycobacterium lepromatosis.</span> It predominantly affects the skin, upper respiratory tract, and peripheral nerves. It is still endemic in many countries, including India, Indonesia, and Brazil. Most cases in Europe are imported.<a class="elsevierStyleCrossRefs" href="#bib0325"><span class="elsevierStyleSup">65,66</span></a></p><p id="par0345" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Clinical presentation.</span> The clinical forms of leprosy range from tuberculoid or paucibacillary leprosy at one end of the spectrum (few lesions and a competent immune system) to lepromatous or multibacillary leprosy at the other (numerous lesions and a deficient immune system).<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">67</span></a> In between lies indeterminate leprosy, which, depending on the patient's immune system, can progress to tuberculoid or lepromatous leprosy.</p><p id="par0350" class="elsevierStylePara elsevierViewall">Indeterminate leprosy manifests as 1 or more hypopigmented or erythematous macules, while tuberculoid leprosy presents as 1 or more well-demarcated erythematous-brownish plaques with a loss of sensation (<a class="elsevierStyleCrossRef" href="#fig0100">Fig. 20</a>A). Lepromatous leprosy, in turn, is a systemic disease that mainly presents with skin manifestations consisting of abundant, poorly demarcated plaques or nodules with pronounced diffuse infiltration and a progressive loss of sensation. In between are various dimorphic (borderline) lesions, with intermediate manifestations and lesions that are often annular (<a class="elsevierStyleCrossRef" href="#fig0100">Fig. 20</a>B).<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">68</span></a> Histoid leprosy is a rare nodular variant. Finally, there are a series of lepra reactions that represent acute episodes within this slow-progressing disease. Type I reactions are type IV hypersensitivity reactions, while type II reactions are the result of immune complex vasculitis.</p><elsevierMultimedia ident="fig0100"></elsevierMultimedia><p id="par0355" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Histopathology.</span> In indeterminate leprosy, histology shows a slight lymphohistiocytic infiltrate surrounding vessels, appendages, and nerves. Tuberculoid leprosy is characterized by non-necrotizing epithelioid granulomas with multinucleated giant cells and numerous lymphocytes; the infiltrate is often "sausage-shaped", as it follows the course of nerves and appendages. It does not normally contain bacilli (<a class="elsevierStyleCrossRef" href="#fig0105">Fig. 21</a>). The infiltrate in lepromatous leprosy contains some lymphocytes, but it is predominantly a nodular or diffuse dermal histiocytic infiltrate under a Grenz zone (<a class="elsevierStyleCrossRef" href="#fig0110">Fig. 22</a>A). The histiocytes, which are S-100 positive, have a broad granular cytoplasm, which in more advanced lesions is foamy; the nerves are usually intact in early-stage lesions, but in later stages they may show concentric fibrosis. The appendages are not visible. Histology shows large numbers of bacilli, which often form amphophilic groups called <span class="elsevierStyleItalic">globi</span> (<a class="elsevierStyleCrossRef" href="#fig0110">Fig. 22</a>B).<a class="elsevierStyleCrossRefs" href="#bib0325"><span class="elsevierStyleSup">65,67,68</span></a> Borderline forms show features in between those observed in tuberculoid and lepromatous leprosy (<a class="elsevierStyleCrossRef" href="#fig0110">Fig. 22</a>C). Histoid leprosy is characterized by predominantly spindle-shaped nodules formed by histiocytes containing numerous bacilli.<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">67</span></a></p><elsevierMultimedia ident="fig0105"></elsevierMultimedia><elsevierMultimedia ident="fig0110"></elsevierMultimedia><p id="par0360" class="elsevierStylePara elsevierViewall">Type I (reversal) reactions are characterized by a lymphocytic-granulomatous infiltrate around neurovascular bundles. Type II reactions (erythema nodosum leprosus), in turn, consist of leukocytoclastic vasculitis alongside other findings of leprosy, including globi. Lucio phenomenon is a variant of a type II reaction that consists of significant inflammation with arterial thrombi, infarctions, and abundant microorganisms.<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">68</span></a></p><p id="par0365" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Mycobacterium leprae</span> complex bacteria are gram-positive, acid-fast bacilli that can be detected with Fite or Ziehl-Neelsen staining and PCR.<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">65</span></a></p></span><span id="sec0095" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Funding</span><p id="par0370" class="elsevierStylePara elsevierViewall">No funding was received for this study.</p></span><span id="sec0100" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Conflicts of Interest</span><p id="par0375" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:18 [ 0 => array:3 [ "identificador" => "xres1591550" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1430022" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1591551" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1430021" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Granuloma Annulare" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Actinic Granuloma and Annular Elastolytic Giant Cell Granuloma Annulare" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Morbihan Disease" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "Sarcoidosis" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Interstitial and Palisaded Neutrophilic Granulomatous Dermatitis" ] 10 => array:2 [ "identificador" => "sec0035" "titulo" => "Granulomas Caused by Deep Mycoses" ] 11 => array:2 [ "identificador" => "sec0040" "titulo" => "Mycobacterial Infections" ] 12 => array:2 [ "identificador" => "sec0045" "titulo" => "Leishmaniasis" ] 13 => array:3 [ "identificador" => "sec0050" "titulo" => "Diseases Caused by Parasites" "secciones" => array:7 [ 0 => array:2 [ "identificador" => "sec0055" "titulo" => "Cutaneous Schistosomiasis" ] 1 => array:2 [ "identificador" => "sec0060" "titulo" => "Onchocerca Infections" ] 2 => array:2 [ "identificador" => "sec0065" "titulo" => "Gnathostomiasis" ] 3 => array:2 [ "identificador" => "sec0070" "titulo" => "Dirofilariasis" ] 4 => array:2 [ "identificador" => "sec0075" "titulo" => "Strongyloidiasis" ] 5 => array:2 [ "identificador" => "sec0080" "titulo" => "Cysticercosis" ] 6 => array:2 [ "identificador" => "sec0085" "titulo" => "Echinococcosis or Hydatid Disease" ] ] ] 14 => array:2 [ "identificador" => "sec0090" "titulo" => "Leprosy" ] 15 => array:2 [ "identificador" => "sec0095" "titulo" => "Funding" ] 16 => array:2 [ "identificador" => "sec0100" "titulo" => "Conflicts of Interest" ] 17 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2021-03-20" "fechaAceptado" => "2021-04-05" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1430022" "palabras" => array:5 [ 0 => "Granuloma" 1 => "Giant cells" 2 => "Langhans cells" 3 => "Touton giant cell" 4 => "Xanthogranuloma" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1430021" "palabras" => array:5 [ 0 => "Granuloma" 1 => "Célula gigante" 2 => "Célula de Langhans" 3 => "Célula de Touton" 4 => "xantogranuloma" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0115" class="elsevierStyleSimplePara elsevierViewall">Part 2 of this series on granulomatous diseases focuses on skin biopsy findings. Whereas the first part treated noninfectious conditions (metabolic disorders and tumors, among other conditions), this part mainly deals with various types of infectious disease along with other conditions seen fairly often by clinical dermatologists.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0120" class="elsevierStyleSimplePara elsevierViewall">Ésta es la segunda parte de una serie dedicada a la patología granulomatosa en la biopsia cutánea. Mientras que en la primera parte hablamos, entre otras, de algunas condiciones metabólicas y tumorales, esta segunda parte abordará fundamentalmente patología infecciosa de diversos tipos, junto con otras condiciones relativamente frecuentes en las consultas de dermatología.</p></span>" ] ] "NotaPie" => array:2 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Aróstegui Aguilar J, Diago A, Carrillo Gijón R, Fernández Figueras M, Fraga J, García Herrera A, et al. Granulomas en dermatopatología: principales entidades. Parte II. Actas Dermosifiliogr. 2021. <span class="elsevierStyleInterRef" id="intr0005" href="https://doi.org/10.1016/j.ad.2021.04.001">https://doi.org/10.1016/j.ad.2021.04.001</span></p>" ] 1 => array:2 [ "etiqueta" => "☆☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0010">This article is an initiative of the Dermopathology Research Group of the Spanish Academy of Dermatology and Venereology (AEDV) and the Spanish Pathology Society (SEAP). All the authors contributed equally to this work, regardless of the order of their surnames.</p>" ] ] "multimedia" => array:22 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 2176 "Ancho" => 905 "Tamanyo" => 765050 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A, Granuloma annulare. An arm showing several erythematous annular plaques with a slightly raised border and clear center. B, Skin showing 2 areas of collagen degeneration and interstitial changes in the reticular dermis surrounded by a band-like inflammatory infiltrate. The superficial dermis and epidermis are preserved. Note also the perivascular lymphocytic crowns and diffuse increase in fibroblast density (hematoxylin-eosin, original magnification ×40). C, Note the central area of disordered collagen accompanied by acid mucin deposits and surrounded by an infiltrate of macrophages, palisading epithelioid cells, fibroblasts, lymphocytes, and occasional eosinophils. Dense perivascular lymphocytic crowns without vasculitis are visible (hematoxylin-eosin, original magnification ×200).</p>" ] ] 1 => array:8 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1797 "Ancho" => 1505 "Tamanyo" => 917666 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Granuloma annulare. A, Large erythematous annular plaques with a raised border in a sun-exposed area. B, Panoramic histologic view showing an inflammatory infiltrate in the reticular dermis. C-E, Higher-magnification view showing a granulomatous lesion with numerous multinucleated giant cells and elastophagocytosis without palisading, increased mucin, or necrobiosis (hematoxylin-eosin, original magnification ×40 [B], ×400 [C,D], ×600 [E]).</p>" ] ] 2 => array:8 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 813 "Ancho" => 905 "Tamanyo" => 137776 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0015" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Morbihan disease. Erythematous-edematous lesion on the forehead. gr3.</p>" ] ] 3 => array:8 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 1152 "Ancho" => 1405 "Tamanyo" => 491931 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0020" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Morbihan disease. A, Panoramic image showing dermal edema with a perifollicular and interstitial inflammatory infiltrate (H&E, original magnification ×20). B, Detail of pronounced dermal edema together with dilated vessels (H&E, original magnification ×100). C, Perivascular lymphohistiocytic infiltrates (H&E, original magnification ×200). D, Detail of several polymorphonuclear neutrophils in the infiltrate (H&E, original magnification ×400). H&E indicates hematoxylin-eosin.</p>" ] ] 4 => array:8 [ "identificador" => "fig0025" "etiqueta" => "Figure 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 425 "Ancho" => 905 "Tamanyo" => 85642 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0025" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Sarcoidosis. Erythematous papules on both eyebrows after a tattoo (photo courtesy of Dr JF Mir-Bonafé).</p>" ] ] 5 => array:8 [ "identificador" => "fig0030" "etiqueta" => "Figure 6" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr6.jpeg" "Alto" => 912 "Ancho" => 1405 "Tamanyo" => 666931 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0030" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Sarcoidosis. A, Epithelioid granulomas occupying the superficial and mid dermis with few peripheral lymphocytes (H&E, original magnification ×20). B, Epithelioid granulomas composed of cells with abundant eosinophilic cytoplasm (H&E, original magnification ×100). C, Silica particle (arrow) in a sarcoid granuloma (H&E, original magnification ×200). D, Schaumann body (arrow) (H&E, original magnification ×400). E, Asteroid body (H&E, original magnification ×2400). H&E indicates hematoxylin-eosin.</p>" ] ] 6 => array:8 [ "identificador" => "fig0035" "etiqueta" => "Figure 7" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr7.jpeg" "Alto" => 1372 "Ancho" => 900 "Tamanyo" => 601900 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0035" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">A, Interstitial granulomatous dermatitis. Palisading histiocytes around an area of ​​necrosis with neutrophils (hematoxylin-eosin, original magnification ×100). B, Interstitial granulomatous dermatitis. Detail of neutrophils dissecting an area of degenerated collagen (hematoxylin-eosin, original magnification ×100).</p>" ] ] 7 => array:8 [ "identificador" => "fig0040" "etiqueta" => "Figure 8" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr8.jpeg" "Alto" => 1205 "Ancho" => 905 "Tamanyo" => 109695 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0040" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Sporotrichoid pattern. Lesions distributed along the course of a lymphatic vessel (photo courtesy of Dr Fernando Cabo, Dermatology Department, Hospital Universitario de Ourense, Spain).</p>" ] ] 8 => array:8 [ "identificador" => "fig0045" "etiqueta" => "Figure 9" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr9.jpeg" "Alto" => 1164 "Ancho" => 2508 "Tamanyo" => 367638 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0045" "detalle" => "Figure " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Schematic representation of main forms of fungi causing deep skin mycoses in humans. The alga <span class="elsevierStyleItalic">Prototheca</span> has been included for comparative purposes.</p>" ] ] 9 => array:8 [ "identificador" => "fig0050" "etiqueta" => "Figure 10" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr10.jpeg" "Alto" => 1795 "Ancho" => 1505 "Tamanyo" => 862097 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0050" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Deep skin mycosis. A, Aspergillosis (H&E, original magnification ×600). B, Blastomycosis (H&E, original magnification ×600). C, Coccidioidomycosis (H&E, original magnification ×600). D, Cryptococcosis (mucicarmine, original magnification ×200). E, Chromoblastomycosis (H&E, original magnification ×600). F, Phaeohyphomycosis (H&E, original magnification ×600). H&E indicates hematoxylin-eosin.</p>" ] ] 10 => array:8 [ "identificador" => "fig0055" "etiqueta" => "Figure 11" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr11.jpeg" "Alto" => 1607 "Ancho" => 1505 "Tamanyo" => 816915 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0055" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Deep skin mycoses. A, Fusariosis (H&E, original magnification ×400). B, Histoplasmosis (H&E, original magnification ×600). C, Lobomycosis (H&E, original magnification ×600). D, Mucormycosis (periodic acid-Schiff, original magnification ×200). E, Protothecosis (H&E, original magnification ×600). F, Paracoccidioidomycosis (H&E, original magnification ×600). H&E indicates hematoxylin-eosin.</p>" ] ] 11 => array:8 [ "identificador" => "fig0060" "etiqueta" => "Figure 12" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr12.jpeg" "Alto" => 1795 "Ancho" => 1505 "Tamanyo" => 1036253 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0060" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Deep skin mycosis. A,B, Rhinosporidiosis (A: H&E, original magnification ×400; B: Grocott, original magnification ×400). C, Sporotrichosis (H&E, original magnification ×600). D, Alternariosis (PAS × 600). E,F, Eumycetoma (PAS × 200 [E] and ×600 [F]). H&E indicates hematoxylin-eosin; PAS, periodic acid-Schiff.</p>" ] ] 12 => array:8 [ "identificador" => "fig0065" "etiqueta" => "Figure 13" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr13.jpeg" "Alto" => 917 "Ancho" => 905 "Tamanyo" => 144612 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0065" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Splendore-Hoeppli phenomenon. Note the radiating crown-shaped eosinophilic deposit surrounding a <span class="elsevierStyleItalic">Sporotrichum</span> organism (hematoxylin-eosin, original magnification ×1000).</p>" ] ] 13 => array:8 [ "identificador" => "fig0070" "etiqueta" => "Figure 14" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr14.jpeg" "Alto" => 872 "Ancho" => 1305 "Tamanyo" => 330586 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0070" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0070" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">Mycobacterium tuberculosis</span>. A, Lupus vulgaris lesion on the nasal dorsum (most common location) in a patient with pulmonary tuberculosis. Note the erythematous plaque formed by several papules and the characteristic apple jelly appearance observed by diascopy (Photograph courtesy of Dr Sánchez-Aguilar). B, Histologic appearance of a typical tuberculosis lesion: granulomas with central caseous necrosis and abundant peripheral lymphocytes (hematoxylin-eosin, original magnification ×40).</p>" ] ] 14 => array:8 [ "identificador" => "fig0075" "etiqueta" => "Figure 15" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr15.jpeg" "Alto" => 1353 "Ancho" => 905 "Tamanyo" => 198822 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0075" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0075" class="elsevierStyleSimplePara elsevierViewall">Example of <span class="elsevierStyleItalic">Mycobacterium chelonae</span> infection. A, Painful, suppurative nodular lesions with superficial ulcers and crusting (photo courtesy of Dr Rodríguez Blanco). B, <span class="elsevierStyleItalic">M</span> <span class="elsevierStyleItalic">chelonae</span> infection. Microorganisms sometimes tend to form clusters in areas of suppuration, where they can be demonstrated by Ziehl-Neelsen staining (Ziehl-Neelsen, original magnification ×1000).</p>" ] ] 15 => array:8 [ "identificador" => "fig0080" "etiqueta" => "Figure 16" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr16.jpeg" "Alto" => 680 "Ancho" => 905 "Tamanyo" => 93594 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0080" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0080" class="elsevierStyleSimplePara elsevierViewall">Cutaneous leishmaniasis (Oriental button). Shiny erythematous plaque with perilesional edema and a central crust (photograph courtesy of Dr Ana Martin-Santiago, Dermatology Department, Hospital Universitario Son Espases, Palma de Mallorca, Spain).</p>" ] ] 16 => array:8 [ "identificador" => "fig0085" "etiqueta" => "Figure 17" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr17.jpeg" "Alto" => 1672 "Ancho" => 1255 "Tamanyo" => 450999 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0085" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0085" class="elsevierStyleSimplePara elsevierViewall">Leishmaniasis. Subepidermal granulomatous infiltrate with atrophy of the epidermis. Abundant <span class="elsevierStyleItalic">Leishmania</span> amastigotes in the upper dermis (H&E, original magnification ×200). A, 2-μm intracellular amastigotes with peripheral enhancement and a tendency to align along the periphery of the cytoplasm (marquee sign) (H&E, original magnification ×1000). B, Transmission electron microscopy image (×8000) showing the nucleus (blue arrow), the kinetoplast (white arrow), and inner flagellum (yellow arrow). H&E indicates hematoxylin-eosin.</p>" ] ] 17 => array:8 [ "identificador" => "fig0090" "etiqueta" => "Figure 18" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr18.jpeg" "Alto" => 1396 "Ancho" => 1505 "Tamanyo" => 771452 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0090" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0090" class="elsevierStyleSimplePara elsevierViewall">A, Chronic form of leishmaniasis. Confluent, poorly defined, epithelioid granulomas with a disordered appearance (messy granulomas)<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> that usually occupy the full thickness of the dermis (hematoxylin-eosin, original magnification ×20). B, Vulvar bilharziasis cutanea tarda. Area of the reticular dermis showing an epithelioid granuloma with central necrosis around 7 round or oval structures. One of these, the most intact, has a lateral spicule, which is characteristic of <span class="elsevierStyleItalic">Schistosoma hematobium. C,</span> Swimmer’s itch due to cercariae. This is not a granulomatous reaction. Note the 3 longitudinal fragments of cercariae (species not identifiable) close to the eccrine glands and surrounded by a lymphohistiocytic infiltrate with numerous eosinophils. D, Onchocercoma. Note the granulomatous infiltrate with neutrophils and sclerosis, as well as several giant foreign body cells around the cross section in 3 areas. Note also the characteristic retraction artifact around the thick eosinophilic cuticle of the 3 filariae.</p>" ] ] 18 => array:8 [ "identificador" => "fig0095" "etiqueta" => "Figure 19" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr19.jpeg" "Alto" => 1472 "Ancho" => 905 "Tamanyo" => 542018 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0095" "detalle" => "Figure 1" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0095" class="elsevierStyleSimplePara elsevierViewall">Gnathostomiasis. A, Granulomatous reaction to larvae (H&E, original magnification ×20). B, Nonspecific infiltrates rich in eosinophils (H&E, original magnification ×100). H&E indicates hematoxylin-eosin.</p>" ] ] 19 => array:8 [ "identificador" => "fig0100" "etiqueta" => "Figure 20" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr20.jpeg" "Alto" => 1342 "Ancho" => 905 "Tamanyo" => 319562 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0100" "detalle" => "Figure 2" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0100" class="elsevierStyleSimplePara elsevierViewall">Leprosy. A, Erythematous, well-demarcated tuberculoid leprosy on the left temple of a young Paraguayan man. B, Dimorphic leprosy. Disseminated erythematous macules, some with an annular shape, on the legs of a middle-aged Filipino woman with dimorphic leprosy.</p>" ] ] 20 => array:8 [ "identificador" => "fig0105" "etiqueta" => "Figure 21" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr21.jpeg" "Alto" => 666 "Ancho" => 1255 "Tamanyo" => 337986 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0105" "detalle" => "Figure 2" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0105" class="elsevierStyleSimplePara elsevierViewall">Leprosy. Image of tuberculoid leprosy specimen from the patient in <a class="elsevierStyleCrossRef" href="#fig0100">Fig. 20</a>A showing a “sausage-shaped” lymphohistiocytic infiltrate along the course of the neurovascular bundles (H&E, original magnification ×20). The lower left inset shows epithelioid granulomas surrounded by lymphocytes (H&E, original magnification ×100). The lower right inset shows a nerve in the center of the granuloma (H&E, original magnification ×100). H&E indicates hematoxylin-eosin.</p>" ] ] 21 => array:8 [ "identificador" => "fig0110" "etiqueta" => "Figure 22" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr22.jpeg" "Alto" => 2162 "Ancho" => 905 "Tamanyo" => 821965 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0110" "detalle" => "Figure 2" "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0110" class="elsevierStyleSimplePara elsevierViewall">A, Lepromatous leprosy. Image showing a sheetlike histiocytic infiltrate under a Grenz zone (H&E, original magnification ×40). B, Higher magnification view showing numerous foamy histiocytes and multinucleated giant cells with globi in their cytoplasms (H&E, original magnification ×200). The lower left inset shows numerous bacilli stained using the Job-Fite technique; some of these are grouped into globi in the macrophages (Job-Fite, original magnification ×200). C, Dimorphic leprosy. Biopsy specimen from the patient in <a class="elsevierStyleCrossRef" href="#fig0095">Fig. 19</a>B, with a superficial and deep perivascular and periadnexal inflammatory infiltrate (H&E, original magnification ×20), composed of lymphocytes and histiocytes, as shown in the lower right inset. 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Year/Month | Html | Total | |
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