Case Reports and Clinical Images

Recurrent Facial Cellulitis

Andrew Kapoor1*, Polly van den Berg2

1Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA, USA;

2Harvard Medical School, Boston, MA, USA

Corresponding Author: Andrew Kapoor:

Submitted: 30 March 2021; Accepted: 22 April 2021; Published: 9 March 2022

DOI: 10.22374/cjgim.v17i1.547

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A 72-year-old woman was presented to the hospital with progressive facial erythema and induration. Three months prior, she had sustained a minor head injury, and computed tomography (CT) of the head performed at the time demonstrated a small subdural and forehead hematoma. In the outpatient setting, she was treated with several courses of antibiotics for recurrent cellulitis secondary to her traumatic injury without any significant improvement. Given the progressive induration and the new onset diplopia, she presented to the hospital for evaluation (Figure 1A). An MRI of the head demonstrated a heterogeneously enhancing mass with central necrosis, extending from the left frontal scalp inferiorly along the neck with intracranial extension into the left orbit (Figure 1B). A core biopsy was performed, and a cytogenetic analysis by fluorescence in situ hybridization (FISH) revealed a MYC rearrangement without any rearrangements of BCL2 or BCL6. The in-situ hybridization for Epstein-Barr Virus (EBV) on tissue, and serologic HIV testing were negative. Immunostaining turned out positive for CD20, BCL6, MYC, and pathology was morphologically consistent with a diagnosis of Burkitt lymphoma (BL). A systemic chemotherapy was initiated with CODOX-M and IVAC along with radiation. Though the treatment resulted in significant clinical improvement, the patient died two months later from complications.

Figure 1. (A) Visualization of the rapidly enlarging facial mass at presentation demonstrating large areas of induration, skin necrosis, and left-sided proptosis. (B) Axial T1 weighted MRI image at the level of the orbits showing tumor invasion into the left orbit superiorly with intracranial extension. Also visible are areas of hypoattenuation indicative of central necrosis.

First described by Dennis Burkitt in 1958,1 BL is a rapidly progressive type of non-Hodgkin B cell lymphoma characterized by the rearrangement of the MYC oncogene resulting in cellular dysregulation and rapid cellular growth.2 There are three distinct clinical variants of BL which include: endemic, sporadic, and immunodeficiency-associated. Although classically thought of as EBV-related malignancies only seen in pediatrics, those from equatorial Africa, or in patients with AIDS, non-endemic (sporadic) Burkitt lymphoma accounts for 1-2% of adult lymphomas in North America and Europe.3 In North America, sporadic BL cases can often mimic more common conditions such as cellulitis or melanoma, resulting in diagnostic delays that may impact patient outcomes. Given its shifting epidemiology, BL should be considered in adults with rapidly enlarging masses even in the absence of typical epidemiologic risk factors like country of origin or HIV serostatus.

Conflicts of Interest

The authors have no competing interests or financial disclosures.


There were no funding sources supporting this submission.

Contributor’s statement

Both authors contributed equally to the clinical care and preparation of this manuscript along with its accompanying clinical images.


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2. Dave SS, Fu K, Wright GW, et al. Molecular diagnosis of Burkitt’s lymphoma. N Engl J Med. 2006;354(23):2431–42. 10.1056/NEJMoa055759

3. Blum KA, Lozanski G, Byrd JC. Adult Burkitt leukemia and lymphoma. Blood. 2004;104(10):3009–20. 10.1182/blood-2004-02-0405