Abstract

Introduction: Cutaneous tuberculosis (CTB) is a rare form of extra-pulmonary tuberculosis that, when associated with late diagnosis, worsen the quality of life of the sick individuals. This report presents a case of late diagnosis of CTB. Unusual clinical manifestations retarded the correct tuberculosis diagnosis for more than a year. The immune response elicited by this type of tuberculosis as well as the factors that might contribute to the delay in diagnosis was evaluated and discussed. Methodology: Clinical evaluation and flow cytometric analyses of PBMC were realized for a case of CTB and a healthy individual as a control. Results: M. tuberculosis specific TCD8+ cell response was analyzed by flow cytometry and revealed positive cells for IL-17, IL-10, TGF-β and IDO. The CTB patient presented higher percentage of those cells when compared to a healthy donor. However, TCD8 cells positive for the important protective cytokine, IFN-γ was decreased in the CTB patient. Conclusion. The assessment of the M. tuberculosis specific TCD8+ immune response showed a regulatory/modulatory phenotype with a reduced IFN-γ response when compared to the healthy control that could have contributed to the CTB infection.

Highlights

  • Cutaneous tuberculosis (CTB) is a rare form of extra-pulmonary tuberculosis that, when associated with late diagnosis, worsen the quality of life of the sick individuals

  • When infection occurs by laboratory accident caused by clinical samples or M. tuberculosis cultures injected directly into the skin, the CTB clinical morphological variants are verrucosa cutis, lupus vulgaris or skin ulcers

  • The following antibodies (Abs) were used for surface and intracellular staining for flow cytometry: IFN- -FITC (BD Bioscience Pharmingen), IL-10-PE, IL-17-PE, CD8APC, TGF- -PE (IQ Products) and IDOFITC (Santa Cruz Biotechnology)

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Summary

Introduction

Cutaneous tuberculosis (CTB) is a rare form of extra-pulmonary tuberculosis that, when associated with late diagnosis, worsen the quality of life of the sick individuals. The assessment of the M. tuberculosis specific TCD8+ immune response showed a regulatory/modulatory phenotype with a reduced IFN- response when compared to the healthy control that could have contributed to the CTB infection. When infection occurs by laboratory accident caused by clinical samples or M. tuberculosis cultures injected directly into the skin, the CTB clinical morphological variants are verrucosa cutis (it manifests as a painless, solitary, purplish or brownish-red warty plaque that may extend peripherally causing central atrophy or form fissures that exude pus or keratinous material), lupus vulgaris (plaque type begins as discrete, redbrown papules that coalesce and form plaques with a slightly elevated verrucas border and central atrophy) or skin ulcers (chancres). A lymphatic or hematogenous disseminated miliary TB may cause CTB variants such as escrofuloderma (firm, painless, subcutaneous, red-brown nodules overlying an infected focus, which gradually enlarge and suppurate forming ulcers and sinus tracts that drain watery, purulent, or caseous material), lupus vulgaris (multiple, discrete, smooth 1 - 3 mm brown/red or brown-to-yellowish dome-shaped papules usually located on the face), and tuberculous abscesses (an inflammatory papule develops at the inoculation site and evolves into a firm, shallow, non-tender, nonhealing, undermined ulcer with a granulomatous base) as described before [2,7]

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