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ARTICLE IN PRESS
doi:
10.25259/IJDVL_960_2021

Destructive facial plaque with massive cervical lymphadenopathy

Departments of Dermatology, Venereology and Leprology, Chandigarh, India
Medical Microbiology, Chandigarh, India
Histopathology, Postgraduate Institute of Medical Education & Research, Chandigarh, India
Corresponding author: Dr. Vinay Keshavmurthy, Department of Dermatology, Venereology and Leprology, Postgraduate Institute of Medical Education & Research, Chandigarh, Chandigarh, India. vinay.keshavmurthy@gmail.com
Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Bakshi S, Sharma K, Keshavmurthy V, Chatterjee D, Dogra S. Destructive facial plaque with massive cervical lymphadenopathy. Indian J Dermatol Venereol Leprol doi: 10.25259/IJDVL_960_2021

A 32-years-old female with no known comorbidities presented with bilateral cervical lymphadenopathy and an erythematous plaque over the right side of face of three years duration. The patient did not recall any history of trauma prior to the onset of lesions. She had received anti-tubercular therapy twice in the past for six months each for suspected tuberculosis (based on cytology features) with little improvement. General examination revealed bilateral firm, non-tender, matted submandibular and cervical lymphadenopathy, the largest measuring 5×3 cm in size. Cutaneous examination revealed single well to ill-defined plaque with few satellite lesions involving the right side of the face and scalp with overlying erosions and yellowish crusting [Figure 1]. Computed tomography scan revealed multiple enlarged bilateral lymph nodes in neck at levels I-VI with homogeneous enhancement along with diffuse skin and subcutaneous tissue edema on the right side of face. Biopsies were obtained from the facial plaque [Figure 2A] and lymph node [Figure 2B].

Figure 1:: A 32-years-old female showing bilateral massive lymphadenopathy. An erythematous well to ill-defined plaque involving the right side of the face, extending to scalp, forehead, eyelids, cheeks and upper part of the neck with overlying erosions and yellowish crusting can be appreciated
Figure 2A:: Histopathology of section of skin shows multiple foci of necrotizing granulomas containing epithelioid histiocytes, Langhan's giant cells, and lymphocytic infiltrate in the dermis (H & E ×200)
Figure 2B:: Histopathology of section of lymph node showing numerous caseating epithelioid cell granulomas, causing its complete architectural effacement (H & E, ×200)

What is Your Diagnosis?

Diagnosis

Nontuberculous mycobacterial infection

Microscopic findings and laboratory investigation

On histopathological examination of the skin lesions and cervical lymph node, granulomatous inflammation with central caseous necrosis was seen. Acid-fast bacilli were observed on lymph node biopsy [Figure 3]. Mycobacterial cultures failed to grow the relevant organisms. Mycobacterium avium was identified in the lymph nodal tissue by polymerase chain reaction. On further investigations there was no evidence of an immunocompromised state; HIV serology was negative, T cell subsets were within normal range along with normal expression of interferon gamma receptor 1. Following 16 weeks of treatment with rifampicin 600 mg, clarithromycin 500 mg and minocycline 100 mg OD, there was significant improvement [Figure 4]. No adverse effects were observed.

Figure 3:: Section of lymph node showing acid-fast bacilli (Ziehl-Neelsen stain ×1000)
Figure 4:: Resolution of lymphadenopathy and healing of the facial plaque with scarring after treatment with rifampicin, clarithromycin and minocycline for 16 weeks

Discussion

Non-tuberculous mycobacteria also known as atypical mycobacteria or mycobacteria other than tuberculosis include mycobacterial pathogens other than Mycobacterium tuberculosis complex and Mycobacterium leprae. These include over 150 different species that are classified into rapidly growing and slowly growing mycobacteria.1

Mycobacterium avium complex encompasses many subspecies of slow-growing mycobacteria including Mycobacterium avium, Mycobacterium intracellulare and Mycobacterium chimaera. They are ubiquitous in the environment and are commonly found in soil and water sources. Mycobacterium avium complex infection is typically associated with pulmonary disease in an immunocompromised host, but there has been an increasing incidence of both pulmonary and extra-pulmonary infections (including skin and soft tissue infections, musculoskeletal infection, lymphadenitis and disseminated disease) in immunocompetent individuals.2

Skin and soft tissue infections caused by nontuberculous mycobacteria classically develop after traumatic injury, cosmetic procedures, or surgery, which can expose wounds to the soil, water, or medical devices contaminated with environmental mycobacteria. Cutaneous infections caused by the Mycobacterium avium complex can take the form of non-specific lesions including cellulitis, abscesses, folliculitis, pustules, ulcers, ecthyma-like lesions, nodules, infiltrated erythematous plaques, scaling plaques, verrucous ulcers, draining sinuses, sporotrichosis-like lesions, and panniculitis.

The clinical differentials of mycobacterial infection, lupoid leishmaniasis, deep fungal infection, Rosai-Dorfman disease, ulcerative sarcoidosis and Kikuchi disease were considered in our case which is further elaborated in Table 1. Diagnosis of non-tuberculous mycobacteria may be missed due to a lack of clinical suspicion and the difficulty in identifying the organisms by culture owing to very specific growth requirements in solid or liquid culture media. In such scenarios, a polymerase chain reaction may play an important role in identifying the organism as well as the species. However, the unavailability of laboratory facilities in resource-limited settings often leads to the treatment of these cases as drug-resistant tuberculosis.

Table 1:: Clinical differentials for the index case

Atypical mycobacterial infection

Deep fungal infection

Lupoid leishmaniasis

Rosai-Dorfman disease

Kikuchi disease

Etiology

Non-tuberculous mycobacteria

Chromoblastomycosis- Dematiaceous fungi

Blastomycosis- Blastomyces dermatitidis

Cryptococcosis-Cryptococcus neoformans

Leishmania tropica

Non-Langerhans cell histiocytosis

Necrotizing lymphadenitis of unknown cause

Epidemiology

No age or sex predilection, increased incidence in immunocompromised state

No age or sex predilection, increased incidence in immunocompromised state

No age or sex predilection,

most prevalent in Middle East and Afghanistan

Children and young adults, male predilection (Cutaneous form more common in female Asians)

Young adults, female predilection

Cutaneous features

Non-specific lesions including cellulitis, abscesses, folliculitis, pustules, ulcers, ecthyma-like lesions, nodules, infiltrated erythematous plaques, scaling plaques, verrucous ulcers, draining sinuses, sporotrichosis-like lesions, panniculitis

Papules or pustules progressing

to warty or vegetating, crusted plaques, ulcers, and hard infiltrated plaques or nodules

Brown red to brown yellow papules coalescing to form a plaque that appears close to the scar of an old lesion of cutaneous leishmaniasis

Slow growing, painless, nonpruritic nodules, plaques, or papules with colouration varying from yellow to red to brown

Facial erythema, eyelid edema, erythematous papules and plaques on face and trunk, leukocytoclastic vasculitis, urticarial or morbilliform rash

Extra-cutaneous features

Pulmonary disease, lymphadenitis, musculoskeletal infection, disseminated disease

Pulmonary disease, lymphadenitis, musculoskeletal infection, central nervous system, disseminated disease

Massive painless cervical lymphadenopathy, fever, night sweats, weight loss

Tender cervical lymphadenopathy, fever, weight loss, nausea, vomiting, hepatosplenomegaly

Histopathology

Tuberculoid granulomas with acid fast bacilli

Mixed granulomatous response with neutrophilic abscesses

Diffuse dermal granulomatous infiltrate composed of histiocytes, lymphocytes, giant cells and plasma cells

Amastigotes few in number or absent

Dense upper dermal histiocytic infiltration (Positive for S100, CD68, CD163, HAM-56) with scattered multinucleate giant cells and plasma cells.

Necrotic keratinocytes, karyorrhexis, vacuolar interface change, dermal lymphohistiocytic infiltrate and dermal papillary edema

Treatment

Combination of antibiotics including fluoroquinolones, macrolides, rifamycins, aminoglycosides depending on sensitivity results

Azoles, amphotericin B

Pentavalent antimonial compounds

Corticosteroids, sirolimus, chemotherapy,

Corticosteroids

Treatment for nontuberculous mycobacteria is species-specific. The recommended regimen for the treatment of skin and soft tissue infection caused by Mycobacterium avium complex includes a combination of three drugs: a macrolide (clarithromycin or azithromycin), ethambutol and rifamycin. The optimal duration of treatment is also unknown, but 6–12 months of treatment is usually recommended.3 Since our patient developed ocular toxicity secondary to previous courses of ethambutol, minocycline was employed as an alternative drug based on its effectiveness in pulmonary Mycobacterium avium complex infection.4

Acknowledgement

We are grateful to Dr Tarun Narang; Dr Megha Sharma and Dr Mayur Parkhi for their help in this article.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship

Nil.

Conflict of interest

There are no conflicts of interest.

References

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