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    Journal List J Clin Aesthet Dermatol v.2(10); Oct 2009 PMC2923933 J Clin Aesthet Dermatol. 2009 October; 2(10): 19–27. PMCID: PMC2923933 A Practical Case Report and Review for the Dermatologist Amylynne Frankel, MD, Carolin Penrose, MD, and Jason Emer, MD Author information ► Copyright and License information ► This article has been cited by other articles in PMC. Abstract Mycobacterium tuberculosis is a worldwide, problematic, communicable pathogen that has increasingly been regarde
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    Journal List    J Clin Aesthet Dermatol    v.2(10); Oct 2009    PMC2923933 J Clin Aesthet Dermatol. 2009 October; 2(10): 19  – 27. PMCID: PMC2923933  A Practical Case Report and Review for the Dermatologist  Amylynne Frankel, MD, Carolin Penrose, MD, and Jason Emer , MD    Author information ►  Copyright and License information ►     This article has been cited by other articles in PMC.   Abstract  Mycobacterium tuberculosis  is a worldwide, problematic, communicable pathogen that has increasingly been regarded as a notable, serious infection in the United States. The underlying basis of this recent epidemic is dependent on such factors as the association of tuberculosis (TB) with the human immunodeficiency virus (HIV) epidemic, increased immigration from endemic countries, and the transmission of TB in crowded settings, such as healthcare facilities, prisons, and homeless shelters.1 – 4 Most often TB is an airborne transmissible disease with skin manifestations presenting as a result of hematogenous spread or direct extension from a latent or active foci of infection. However, primary inoculation may occur as a direct introduction of the mycobacterium into the skin or mucosa of a susceptible individual by trauma or injury. Increased risk of acquiring disease occurs with HIV infection, intravenous drug abuse, diabetes mellitus, immunosuppressive therapy, malignancies, end-stage renal disease, and infancy. Cutaneous tuberculosis (CTB) is frequently elusive as it mimics a wide differential diagnosis and also evades microbiological confirmation despite recent advances in sophisticated techniques.5 Although rare, given its  worldwide prevalence, it is important for clinicians to recognize the many clinical variants of CTB to prevent missed or delayed diagnoses. Go to:   Case Report  A 24-year-old Hispanic woman presented with a painful lesion on her right buttock that began during her pregnancy four years prior. The lesion appeared as a large, reddish-brown, scaly plaque with well-defined  borders and central atrophic changes covering the entire surface of the right buttock (Figure 1). The lesion was tender and warm with notable   expression to light touch of purulent material through multiple fissures along the periphery. The patient reported no other symptoms, such as fever, chills, cough, or fatigue. On physical examination, vital signs were  within normal limits, the skin demonstrated no other significant changes, and the patient had no notable lymphadenopathy. On history, the patient reported the skin lesion had progressively increased over the past four years. She had been previously diagnosed with psoriasis and  was treated with multiple topical therapies, including salicylic acid and potent topical corticosteroids without any relief. Further, the patient reported having a similar lesion (which was on her neck) as a child that  was surgically removed in Mexico. She had been Bacille Calmette-Guérin (BCG)-vaccinated in the past. Figure 1    Large, reddish-brown, scaly plaque covering the entire surface of the right buttock Serum QuantiFERON®-TB Gold (QFT-G; Cellestis Inc.,Valencia, California) testing was performed along with tissue cultures and skin  biopsy with histological analysis. Histopathology of the plaque showed pseudoepitheliomatous hyperplasia and neutrophilic microabscesses in the epidermis. The dermis contained a mixed neutrophilic and granulomatous infiltrate (Figures 2 and and3).3). Acid-fast bacillus   (AFB) staining showed rare elongated acid-fast structures suggestive of TB infection (Figure 4). Culture from lesional tissue   grew  Mycobacterium tuberculosis  and serum QFT-G testing was positive. The patient was referred to infectious disease to rule out active TB infection. Sputum cultures were negative and a chest x-ray showed no active pulmonary disease. Figures 2 and 3   Histology demonstrating pseudoepitheliomatous hyperplasia and neutrophilic microabscesses in the epidermis and a mixed neutrophilic and granulomatous infiltrate in the dermis (H&E, low and medium powers) Figure 4    Staining showing elongated acid-fast structures  A diagnosis of CTB was made based on the patient’s history, clinical picture, and diagnostic testing. Although an explicit classification of CTB could not be specified, lupus vulgaris (LV) and tuberculosis verrucosa cutis (TVC) are two variants of CTB that have been shown to occur in a previously sensitized individual, and her diagnosis was assumed to be one of these two variants. The patient was treated by infectious disease  with multidrug TB therapy (pyrazinamide, rifampin, ethambutol, and isoniazid) resulting in lesion clearance at three months. Currently, the patient remains free of tuberculous disease. Go to:  Discussion CTB describes dermatological manifestations of TB involving the skin,  which can be caused by  Mycobacterium tuberculosis, Mycobacterium bovis , and the BCG vaccination. These lesions can be acquired exogenously or endogenously, although the former is significantly less common. TB is one of the most common, rampant infectious diseases in underdeveloped countries, and the number of cases in industrialized countries has increased in recent years as a result of the increased incidence of HIV infection and increasing multidrug resistance. 6   Although CTB is reported as less than one percent of all cases of TB, it is important for practitioners to consider this infection  when faced with a suggestive clinical picture. 7  Early classification of CTB was based on lesion morphology. As knowledge of the disease increased, it became apparent that although lesions appeared clinically similar, their development, progression, and prognosis were different. Tappeiner and Wolff proposed the most widely accepted classification based on the route of infection (Table 1). 5,8  Exogenous inoculation occurs after the direct inoculation  of   Mycobacterium tuberculosis  into the skin of a person who is susceptible to infection. This leads to TVC, tuberculosis chancre, and some cases of LV. Endogenous infection occurs in patients who were previously infected either by lymphatic spread, hematogenous spread, or contiguous extension. Lymphatic spread is seen occasionally in LV. Hematogenous spread is seen in acute miliary TB, metastatic TB abscess (gummatous TB), papulonecrotic tuberculid (PNT), and LV. Contiguous extension is seen in scrofuloderma and orificial tuberculosis. Table 1 Two differing classifications of tuberculosis  An additional classification system designed to enhance the Tappeiner and Wolff system included further distinction based on bacterial load. This system is extremely similar to Ridley and Jopling’s desc ription of  Mycobacterium leprae   in Hanson’s disease. In the multibacillary forms, a plethora of mycobacteria can easily be identified on histological examination utilizing the Ziehl-Neelsen staining (AFB) method and culture. In the paucibacillary forms, sparse bacilli are seen on histological examination and culture isolation of mycobacteria is the exception rather than the rule. 1   Go to:  Multibacillary Forms Primary inoculation TB (tuberculous chancre) typically follows a penetrating injury that results in the direct introduction of mycobacterium into the skin or mucosa of an individual with no previous TB infection. Within 2 to 4 weeks, an inflammatory papule develops at the inoculation site and evolves into a firm, shallow, non-tender, nonhealing, undermined ulcer with a granulomatous base (Figure   5). 3,5,9  Painless, regional lymphadenopathy is frequently apparent around   the time a tuberculin skin test (TST) converts to positive. Figure 5 
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