A Rare Case of Brodie’s Abscess in HIV Patient Caused by Mycobacterium kansasii

We report a rare case of Brodie’s abscess caused by Mycobacterium kansasii (M. kansasii). Our patient is a 39-year-old male who presented with right foot pain a month after a new diagnosis of HIV infection. X-ray and MRI were done, and the diagnosis of Brodie's abscess was confirmed. Surgical debridement was done, and bone cultures grew M. kansasii after five weeks. Brodie’s abscess is a subacute form of osteomyelitis usually caused by Staphylococcus. Some other bacteria have been implicated in several case reports. To best of our knowledge, this is the first case of Brodie's abscess caused by M. kansasii. M. kansasii is the atypical mycobacteria causing infections in immunocompromised hosts as in HIV patients with low CD4 count. M. kansasii is usually associated with lung infections with rare extrapulmonary manifestations as in our case.


Introduction
HIV patients with low CD4 count are prone to infections with atypical mycobacteria like Mycobacterium kansasii (M. kansasii). The incidence of M. kansasii infections in HIV patients may be as high as 532 per 100,000 population per year as compared to the general population where incidence is 0.5 per 100,000 population. M. kansasii often causes lung infections similar to Mycobacterium tuberculosis. Most HIV patients with infection with M. kansasii are associated with advanced immunosuppression with CD4 count <50 cells/μL. However, patients with comorbid lung pathology may get an infection at a higher CD4 count. Disseminated disease is uncommon in immunocompetent hosts, but it has been associated with HIV patients due to immunosuppressed state. Skeletal infections are rare with mycobacteria even in HIV patients. Musculoskeletal involvement usually happens after trauma or steroid injection causing monoarticular septic arthritis or tenosynovitis. Some cases of osteomyelitis associated with M. kansasii have been reported in immunocompromised patients. These usually involved the spine and skull. We present a case of a young HIV patient with Brodie's abscess of tibia caused by M. kansasii. To the best of our knowledge, it is the first case of Brodie's abscess caused by this M. kansasii reported in the literature.

Case Presentation
A 39-year-old male with HIV on antiretroviral therapy (ART) presented to a primary care physician with non-traumatic right ankle pain for about one-month duration. He was diagnosed with HIV about one month ago and ART (bictegravir 50 mg daily, emtricitabine 200 mg daily, and tenofovir alafenamide 25 mg daily) was initiated soon afterward. The last CD4 count about one month ago was 82 cells/μL (reference range 431-1,623 cells/μL). A right ankle X-ray ( Figure 1) showed a 20-mm lesion in the distal tibia diaphysis concerning for 1 1 Open Access Case osteomyelitis with a Brodie's abscess due to aggressive periosteal reaction.

FIGURE 1: X-ray of the right ankle
A 20-mm lesion seen in the distal tibia diaphysis was highly concerning for osteomyelitis with a Brodie's abscess given the aggressive periosteal reaction.
MRI of the right lower leg ( The patient was afebrile. Inflammatory markers were elevated: C reactive protein 2.5 mg/L (normal <1 mg/L), erythrocyte sedimentation rate was 26 mm/hr (normal 0 to <15 mm/hr), and white blood cell count 13.9 K/μL (normal 4.5-12 K/μL). The patient underwent surgery with debridement and irrigation. Initial cultures were negative. He was started on broad-spectrum antibiotics (sulfamethoxazole-trimethoprim DS 800-160 mg two tablets two times a day and amoxicillin-clavulanate 875-125 mg one tablet two times a day) and discharged home on postoperative day 6. Pathology showed granulomatous osteomyelitis highly suspicious for tuberculosis (TB). Acid-fast bacilli (AFB) and Grocott's methenamine silver (GMS) stains were negative. QuantiFeron®-TB Gold Plus test was positive (reference -negative). He had no evidence of lung TB on a chest X-ray. Given high suspicion for TB osteomyelitis, he was started on four-drug antitubercular therapy (rifabutin 300 mg daily, isoniazid 300 mg daily, ethambutol 1,200 mg daily, pyrazinamide 1,500 mg daily, and pyridoxine 50 mg daily), and broadspectrum antibiotics were discontinued. His ART regimen was modified to avoid drug interactions. His ART regimen was changed to abacavir 600 mg daily, dolutegravir 50 mg daily, and lamivudine 200 mg daily. About five weeks later, his bone cultures came back positive for M. kansasii. His regimen was adjusted according to sensitivities (rifabutin 300 mg daily, isoniazid 300 mg daily, ethambutol 1,200 mg daily, and pyridoxine 50 mg daily were continued, and pyrazinamide was discontinued). He was advised to continue with medications for nine months.

Discussion
Brodie's abscess was first reported by Sir Benjamin Brodie in 1832 [1]. It is subacute osteomyelitis associated with the accumulation of pus. Onset is usually insidious, and systemic signs and symptoms of infection are usually lacking [2]. Hematogenous spread often causes seeding of bacteria in the bone. Trauma has been implicated as a cause in some cases. Brodie's abscess is usually located in the metaphysis of the tubular bones of the lower extremity. Tibia is the most common bone to be infected [3]. Less frequently, it can happen in other tubular bones or in the diaphyseal region as in our case. Brodie's abscess is a contained infection surrounded by sclerotic bone, and this is the cause for little systemic response.
The patient usually presents with pain. A physical exam may reveal swelling and tenderness. As the onset is slow and it does not have obvious symptoms, diagnosis is often delayed by weeks and even months. Imaging is considered the gold standard for diagnosis of Brodie's abscess. Xrays are often done first and may reveal solitary lesion in the intramedullary region with welldefined sclerotic margins [4]. MRI often follows plain films and is highly sensitive for diagnosing Brodie's abscess. It may show 'penumbra sign' which is a typical four-layered target appearance: a center, an inner ring, an outer ring of fibrotic reaction, and a peripheral halo of bone marrow edema [5].
It is frequently treated by surgical debridement followed by antibiotics. Culture and tissue debridement play a crucial role in identifying the causative organism. Staphylococcus aureus (30%-60%) accounts for most of the infections causing Brodie's abscess. Other common pathogens are coagulase-negative Staphylococcus, Pseudomonas, and Klebsiella. About 25% of the cultures are negative and no organism can be identified [6].

Additional Information Disclosures
Human subjects: Consent was obtained by all participants in this study.

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