The coinfection of tuberculosis (TB) and bacterial infection in the same bone is rare and has not been widely reported. Superadded bacterial infection in TB patients can lead to delayed diagnosis and inadequate treatment ^[1]. According to the 2017 World Health Organization report, 6.3 million new TB cases and 1.6 million deaths due to TB have been reported in 2016 ^[2]. In almost 75% of tuberculous osteomyelitis cases, Mycobacterium TB spreads  through hematogenous route ^[2]. Diagnosis of extrapulmonary TB, that constitutes of about 15–20% of TB, in immunocompetent patients is difficult due to atypical presentation ^[1]. TB abscess in immunocompetent hosts are seen very infrequently with involvement of spine in most cases ^[3]. Skeletal TB accounts for 1-3% of all TB      cases ^[4]. Brodie’s abscess is a sub-acute form of osteomyelitis, presenting as a collection of pus in bone ^[5]. The slow progress of tuberculous osteomyelitis, due to lack of significant elevations in the laboratory values and changes in the radiographic appearance, often leads to confusion with brodie’s abscess ^[2]. Sari et al. reported a case of a 65-yeer-old male with tuberculous osteomyelitis of distal tibia mimicking brodie’s abscess which was detected by TB-polymerase chain reaction (PCR) ^[2]. In this study, we present a case of coinfection of tuberculous osteomyelitis of tibia with Streptococcus agalactiae infection mimicking brodie’s abscess in a young immunocompetent patient.

A 24-year-old male of Asian origin came to our clinic with complaints of pain, swelling of left distal leg for the 2 weeks following blunt injury to right ankle. The patient had mild fever for 1 month with weight loss of 6 kgs over 3 months. His past medical history was insignificant. He had received Bacillus Calmette -Guérin vaccination and there was no history of recent contact with TB patients tenderness with local rise of temperature which was elicited at distal leg. The patient was afebrile at the time of presentation. Erythrocyte sedimentation rate and C-reactive protein were 12 and 18, respectively, with normal total white blood cell count. A plain X-ray of the left leg showed a well-defined lytic lesion at the distal metaphysis of tibia (Fig. 1). Magnetic resonance imaging reported as left tibia showing hypointense signals in T1 involving distal metaphysis extending to the subchondral region. On post- contrast study, there is abnormal enhancement in distal tibia with eccentric hypointensity and linear extension into the metaphysis. There is hyperintensity of adjacent soft tissues with thick-walled collection seen along the medial and posterior aspect of distal tibia with cortical breach on the posterior tibia cortex (Fig. 2). Intraoperatively, pus was noted to arise from distal tibia which was sent for microbiological and histopathological study (Fig. 3). The patient was taken up for distal tibia bone debridement and curettage. Culture-indicated growth of S. agalactiae and appropriate intravenous antibiotics were started. Bone biopsy result came after 10 days from initial washout and reported as necrotizing granulomatous lesion with Langerhans giant cells and mixed inflammatory cells suggestive of tuberculous osteomyelitis. On further imaging, computed tomography thorax revealed necrotic tuberculous mediastinal and hilar lymphadenopathy. The patient was treated with antitubercular treatment regime according to Indian tubercular society protocol (2 months- isoniazid 600 mg/week, rifampicin 450 mg/week, pyrazinamide 1500 mg/week, ethambutol 1200 mg/week , 4 months- isoniazid 600 mg/week, and rifampicin 450 mg/week). Antimicrobial therapy (Clindamycin + Cefazolin) was given for a period of 6 weeks for S. agalactiae infection. The patient was given below knee back slab for 4 weeks for soft- tissue healing and protective weight -bearing. Post-operative X-ray taken at follow-up showed no reactivation of infection (Fig. 4).

Tubercular and bacterial coinfection is uncommon in patients with preserved immunity. There are a few reports regarding the occurrence of TB with organisms such as Streptococcus pneumonia, Salmonella Typhi, and Streptococcus milleri ^[1]. However, TB osteomyelitis and bacterial coinfection within bone has not been reported in the literature. S. agalactiae is known to cause endocarditis, skin and soft- tissue infections, osteomyelitis, pneumonia, meningitis, and urinary tract infections ^[6]. Brodie’s abscess is known as a solitary lesion in the metaphyseal region and is characterized by the new bone formation around it. Tuberculous osteomyelitis can mimic many diseases clinically and radiologically such as brodie’s abscess, pyogenic infections, osteosarcoma, osteoid osteoma, osteoclastoma, and aneurysmal bone cyst ^[2]. Osteoporosis, bone lysis, sclerosis, and periostitis are seen in both tuberculous osteomyelitis and chronic pyogenic osteomyelitis and it is often difficult to differentiate the two conditions ^[7]. Making an accurate and timely diagnosis of brodie’s abscess is a challenge as patients remain afebrile often with unremarkable inflammatory markers and rarely exhibiting signs of systemic illness ^[8]. Vohra et al. reported about a case series of 28 patients with TB osteomyelitis and stated of six patients who exhibited clinical and radiological findings similar to chronic pyogenic osteomyelitis. To achieve rapid diagnosis and treatment, “culturing for every tumor and biopsy for every infection” should always be kept in mind ^[7]. In another study, Akgul noted that clinical, radiological, and laboratory findings of their tuberculous osteomyelitis case showed close similarity with subacute osteomyelitis ^[9]. Sari et al. reported a case of a 65-year-old male diagnosed with tuberculous osteomyelitis of tibia with similar clinical and radiological findings of that of brodie’s abscess ^[2]. Nijhawan et al. reported a case of a 64-year-old male with tuberculous osteomyelitis mimicking brodie’s abscess and these low virulence clinical cases can lead to delay in diagnosis and progressive bone destruction ^[10]. Arora et al. reported that three patients with concurrent TB and bacterial infection in pulmonary and extrapulmonary sites and antibiotics and anti-tubercular therapy were initiated, leading to improvement of the patient ^[1]. In all these studies, there was no superadded bacterial infection of bone along with mycobacterium TB which makes this case a rarity.

Tuberculous osteomyelitis mimicking brodie’s abscess is very rare. It is important to consider coinfection in osteomyelitis and it is essential to do TB-PCR and histopathological examination, along with bacterial and fungal culture of pus in subacute osteomyelitis for the early diagnosis and treatment.

Coinfection of tuberculous osteomyelitis with bacterial infection in the same bone has not been reported before, and thus, it is important to send pus sample for TB polymerase chain reaction test and histopathological examination, along with bacterial and fungal culture to determine the pathogens involved in all cases so that early treatment can be initiated. Brodie’s abscess can mimic as tuberculous osteomyelitis and to consider TB as one of the differentials in the diagnosis of subacute osteomyelitis.