Anterior Chest Wall Tuberculosis Masquerading as a Chronic Parasternal Sinus in an Apparently Immunocompetent Adult: A Diagnostic Challenge in a Resource-Limited Setting

Abstract

Background

Anterior chest wall tuberculosis is an uncommon form of extrapulmonary tuberculosis that can mimic a chronic pyogenic abscess or chest wall mass. Its indolent presentation and absence of constitutional symptoms may delay diagnosis, particularly in resource-limited settings.

Case Presentation

A 22-year-old previously healthy male soldier presented with a progressively enlarging parasternal–xiphoid swelling and intermittent seropurulent discharge, without respiratory or constitutional symptoms. Examination revealed a minimally tender 5 × 2 cm fluctuant swelling with a draining sinus and localized skin changes. Thoracic computed tomography showed a 57 × 18 mm subcutaneous collection at the xiphoid level without demonstrated pleural or osseous involvement, alongside centrilobular nodules and a tree-in-bud pattern suggestive of pulmonary infection. Incision, drainage, and debridement were performed. Xpert MTB/RIF Ultra testing of a fluid specimen detected Mycobacterium tuberculosis complex at a low bacillary load, without rifampicin resistance detected. Histopathological examination was reported to show caseating granulomatous inflammation with multinucleated giant cells. Sputum testing was also positive for M. tuberculosis, supporting concomitant pulmonary tuberculosis. First-line antituberculous therapy was initiated. The wound was closed at the 14-day postoperative assessment. Following six months of treatment, the patient remained asymptomatic; follow-up computed tomography demonstrated resolution of the chest wall collection and regression of pulmonary abnormalities.

Conclusion

Chest wall tuberculosis should be considered in patients with persistent parasternal swelling or a draining sinus, even without constitutional or respiratory symptoms. Tissue sampling, molecular and histopathological evaluation, and assessment for concomitant pulmonary disease support timely diagnosis and appropriate treatment.

Introduction

Tuberculosis remains a major global public health challenge, particularly in low- and middle-income countries, where delayed diagnosis and limited access to molecular testing and specialist services contribute to ongoing morbidity and transmission. Although pulmonary tuberculosis is the predominant form, extrapulmonary tuberculosis accounts for approximately 15–20% of cases among immunocompetent individuals and may involve lymph nodes, pleura, bones, joints, and soft tissues.¹ Its nonspecific clinical manifestations frequently complicate timely diagnosis.

Chest wall tuberculosis is an uncommon manifestation of extrapulmonary tuberculosis, accounting for approximately 1–2% of all tuberculosis cases and less than 5% of osteoarticular tuberculosis.^2,3 It may involve the ribs, sternum, costochondral junctions, intercostal tissues, or adjacent subcutaneous structures. Proposed mechanisms include hematogenous dissemination, lymphatic spread, direct extension from adjacent infected structures, and reactivation of dormant bacilli.^2–4 Clinically, it often presents as a slowly enlarging, painless or minimally tender swelling, commonly termed a cold abscess, characterized by minimal local inflammatory signs.^3,4

The atypical presentation of chest wall tuberculosis creates diagnostic challenges because lesions may mimic chronic bacterial abscesses, infected epidermoid cysts, benign soft-tissue masses, or malignancy.^5,6 Chronic sinus formation and the absence of constitutional or respiratory symptoms may further delay recognition. Similar presentations have been documented in patients without known immunocompromising conditions, emphasizing the importance of considering tuberculosis in persistent chest wall lesions, particularly in endemic settings.^4–7

Computed tomography (CT) is valuable for characterizing chest wall collections and identifying associated pulmonary, pleural, lymphatic, or osseous involvement. However, imaging findings are not specific, and microbiological and histopathological investigations remain essential for diagnostic confirmation.^2,3,7 Molecular assays, including Xpert MTB/RIF Ultra, enable rapid detection of Mycobacterium tuberculosis complex and assessment of rifampicin resistance. Standard multidrug antituberculous therapy remains the cornerstone of management, while surgical drainage or debridement may be necessary for diagnostic sampling or treatment of selected lesions.^3,4

We report a young adult with no known immunocompromising condition who presented with an anterior chest wall tuberculous abscess masquerading as a chronic parasternal draining sinus, without constitutional or respiratory symptoms. The identification of concomitant pulmonary tuberculosis highlights the importance of evaluating the lungs even when the presenting complaint is confined to the chest wall. This case emphasizes the role of early tissue sampling, molecular testing, and integrated medical-surgical management in resource-limited settings.

Case Presentation

A 22-year-old previously healthy male soldier presented to the thoracic surgery outpatient clinic with a progressively enlarging swelling over the lower anterior chest wall in the parasternal–xiphoid region, accompanied by intermittent seropurulent discharge. He denied fever, chest pain, cough, night sweats, weight loss, or preceding trauma. The patient had received oral amoxicillin 500 mg every 8 hours for 14 days before presentation, without improvement. There was no known history of tuberculosis, diabetes mellitus, other immunocompromising conditions, or use of immunosuppressive medications. Preoperative HIV screening by enzyme-linked immunosorbent assay (ELISA) was negative, and random blood glucose was 119 mg/dL.

Examination revealed a soft, fluctuant swelling measuring approximately 5 × 2 cm, with a small draining sinus over the xiphoid region. The lesion was minimally tender, and the overlying skin showed localized dark discoloration and focal necrosis without marked erythema or increased local temperature. No cervical, supraclavicular, or axillary lymphadenopathy was detected, and the remainder of the systemic examination was unremarkable (Figure 1).

Figure 1.

Clinical appearance of the anterior chest wall lesion at presentation. Clinical photograph showing a localized swelling measuring approximately 5 × 2 cm over the lower anterior chest wall near the xiphoid region, with overlying skin discoloration and superficial scaling.

Other routine laboratory investigations were reportedly within reference limits. Non-contrast computed tomography (CT) of the thorax demonstrated a well-defined hypodense subcutaneous collection measuring 57 × 18 mm at the level of the xiphoid process, without adjacent rib or sternal destruction (Figure 2A and B). There was no mediastinal or hilar lymphadenopathy, pleural effusion, or pleural thickening. The CT also showed diffuse centrilobular ground-glass nodules with a tree-in-bud pattern in the left upper lobe and additional focal nodules in the right upper and lower lobes, raising suspicion for endobronchial spread of tuberculosis (Figure 2C). Atelectatic fibrotic bands were present in the right lower lobe, and a 2-cm subpleural bulla was noted in the left lower lobe.

Figure 2.

Baseline non-contrast chest computed tomography (ct). (A and B) Axial mediastinal-window images demonstrating a localized subcutaneous collection in the anterior chest wall at the xiphoid level, without evidence of adjacent osseous destruction. (C) Axial lung-window image showing centrilobular nodules with a tree-in-bud pattern, predominantly in the left upper lobe, suggestive of endobronchial spread of infection.

The initial working diagnosis was a chronic parasternal abscess. The patient underwent incision, drainage, and debridement. Intraoperative exploration revealed an abscess-containing cavity with a foramen-like tract at its base near the sternum; however, no direct communication with the pleural cavity or bone involvement was demonstrated. Purulent material and tissue specimens were obtained for microbiological and histopathological evaluation (Figure 3A and B).

Figure 3.

Intraoperative findings and diagnostic specimens from the anterior chest wall lesion. (A) Intraoperative photograph obtained during surgical drainage and debridement, demonstrating the exposed abscess cavity. (B) Photograph showing excised tissue specimens and aspirated material collected during surgical exploration for diagnostic evaluation. (C) Xpert MTB/RIF Ultra assay of anterior chest wall abscess fluid demonstrating Mycobacterium tuberculosis complex detected at a low bacillary load, with rifampicin resistance not detected.

Routine aerobic and anaerobic bacterial cultures yielded no growth, and conventional staining was inconclusive. Mycobacterial culture was unavailable because of institutional laboratory and biosafety limitations. Xpert MTB/RIF Ultra testing of the anterior chest wall abscess fluid detected Mycobacterium tuberculosis complex at a low bacillary load, with rifampicin resistance not detected (Figure 3C). Histopathological examination demonstrated caseating granulomatous inflammation with multinucleated giant cells and an accompanying histiocytic and lymphocytic infiltrate (Figure 4A and B). The concordant molecular and histopathological findings confirmed the diagnosis of an anterior chest wall tuberculous cold abscess. Sputum testing was also positive for Mycobacterium tuberculosis, confirming concomitant pulmonary tuberculosis.

Figure 4.

Histopathological findings of the anterior chest wall lesion. (A) Low-power hematoxylin and eosin (H&E)-stained section (×4) showing granulomatous inflammation involving the skin and underlying connective tissue. (B) Higher-power H&E-stained section (×40) demonstrating aggregates of epithelioid histiocytes admixed with lymphocytes and multinucleated giant cells.

The postoperative course was uncomplicated. A Hemovac drain was removed after the output became minimal, and the patient was discharged in stable condition. Standard first-line antituberculous therapy was initiated through the tuberculosis clinic in accordance with national treatment guidance. At the 14-day postoperative review, the wound had healed satisfactorily, and the sutures were removed (Figure 5).

Figure 5.

Postoperative clinical appearance of the anterior chest wall. Clinical photograph obtained at the 14-day postoperative follow-up, following suture removal, showing closure of the surgical incision with early raised scar formation.

At 6 months, the patient had completed antituberculous therapy and remained clinically asymptomatic. Follow-up contrast-enhanced thoracic CT demonstrated complete resolution of the anterior chest wall collection and regression of the previously observed tree-in-bud nodules and ground-glass opacities, with no residual chest wall collection or radiological evidence of active infection. A thin-walled air cyst was observed in the left lung (Figure 6A and B). The operative site had healed completely, with no recurrent swelling, sinus formation, discharge, or other clinical evidence of recurrence.

Figure 6.

Follow-up contrast-enhanced chest ct after completion of antituberculous therapy. (A) Axial lung-window image showing regression of the previously described pulmonary abnormalities and a thin-walled air cyst in the left lung. (B) Axial mediastinal-window image demonstrating resolution of the previously identified anterior chest wall collection.

Discussion

Anterior chest wall tuberculosis is an uncommon and frequently underrecognized manifestation of extrapulmonary tuberculosis. This case is clinically important because an apparently immunocompetent young adult presented with a chronic parasternal draining sinus and minimal inflammatory features, without constitutional or respiratory symptoms, despite microbiologically confirmed disease at both the chest wall and pulmonary sites. The initial impression of a chronic parasternal abscess illustrates how an indolent tuberculous lesion may be mistaken for a routine surgical infection when the diagnosis is based on appearance alone.

Chest wall involvement accounts for only a small proportion of tuberculosis and musculoskeletal tuberculosis, and its presentation is heterogeneous.^1,2 The typical lesion is a slowly enlarging, painless or minimally tender cold abscess with little erythema, warmth, or systemic inflammatory response.^3,4 As a result, chest wall tuberculosis may resemble a pyogenic abscess, infected cutaneous lesion, gynecomastia, benign soft-tissue tumor, or malignancy.^5,6 The focal skin necrosis and draining sinus in the present patient further increased the likelihood of an initial diagnosis of chronic bacterial infection, although the absence of pronounced tenderness, surrounding cellulitis, fever, and constitutional symptoms favored a chronic granulomatous process. Similar diagnostic delays have been described in isolated soft-tissue tuberculosis, in which definitive recognition often depends on tissue sampling rather than clinical examination alone.⁷

The coexistence of sputum-positive pulmonary tuberculosis strengthens the biological relationship between the pulmonary and chest wall lesions. Proposed mechanisms of chest wall involvement include direct extension from pleural or pulmonary disease, spread from regional lymph nodes, hematogenous dissemination, and reactivation of dormant bacilli within chest wall tissues.^2–4 In this patient, CT demonstrated tree-in-bud nodules and centrilobular ground-glass opacities compatible with endobronchial pulmonary spread, but no pleural effusion, pleural thickening, thoracic lymphadenopathy, or osseous destruction. Although a foramen-like tract was described near the sternum intraoperatively, direct communication with the pleural cavity or infected bone was not demonstrated. Lymphatic or hematogenous dissemination remains plausible; however, the precise route cannot be established from the available findings. This differs from reports of isolated chest wall disease without pulmonary involvement and highlights the importance of assessing the entire thorax even when the presenting complaint is confined to the chest wall.^8,9

Computed tomography was central to defining the anatomical extent of disease and identifying the otherwise clinically silent pulmonary component. The scan demonstrated a 57 × 18 mm subcutaneous collection at the xiphoid level, delineated the associated pulmonary abnormalities, and excluded rib or sternal destruction, pleural involvement, and mediastinal or hilar lymphadenopathy. CT is particularly valuable in chest wall tuberculosis because it can characterize the collection, reveal deep extension or sinus formation, identify bone and pleural disease, and guide the choice and extent of surgical intervention.^2,10 Nevertheless, CT appearances are not pathognomonic, and tuberculous collections may remain indistinguishable from pyogenic infection or neoplasia without microbiological or histopathological confirmation.^6,10

The diagnosis in this case was supported by concordant evidence from three sources. Xpert MTB/RIF Ultra testing of the abscess material detected Mycobacterium tuberculosis at a low bacillary load and showed no rifampicin resistance; histopathological examination demonstrated caseating granulomatous inflammation with multinucleated giant cells; and sputum testing confirmed concomitant pulmonary tuberculosis. Molecular testing is especially useful in extrapulmonary disease because these specimens are often paucibacillary and may be negative on smear microscopy, while culture may require several weeks.¹¹ However, the sensitivity of Xpert assays varies by specimen type, and a negative result does not exclude extrapulmonary tuberculosis when clinical and histopathological suspicion remains high.¹¹ In the present case, the agreement between molecular findings, characteristic histology, sputum positivity, compatible CT abnormalities, and subsequent treatment response provided strong diagnostic certainty.⁷

Standard multidrug anti-tuberculous therapy remains the cornerstone of management, whereas the role of surgery should be individualized according to lesion size, tissue necrosis, sinus formation, diagnostic uncertainty, structural involvement, and response to medical treatment.^3,12 Incision, drainage, and debridement were appropriate in this patient because the lesion contained purulent material, had developed a chronic draining sinus with focal skin necrosis, and required representative specimens for definitive diagnosis. The absence of rib, sternal, or pleural involvement supported a limited local procedure rather than radical chest wall resection. This proportional approach achieved source control and tissue diagnosis while avoiding unnecessary structural resection.

Published surgical series emphasize that incomplete treatment of diseased tissue may contribute to persistent drainage or recurrence. Sakuraba et al advocated complete excision of the abscess, with rib resection when involved, followed by anti-tuberculous chemotherapy.¹³ In a retrospective series of 68 surgically treated patients, complete excision, primary closure, and obliteration of residual dead space were associated with fewer postoperative complications, while adjunctive anti-tuberculous therapy was considered important for reducing recurrence.¹⁴ A larger series of 120 patients similarly reported favorable outcomes with systematic exploration, complete resection when necessary, cavity management, drainage, and anti-tuberculous medication.¹⁵ These data derive largely from retrospective surgical cohorts and should not be interpreted as requiring extensive resection in every case; surgery should remain tailored to radiological and intraoperative disease extent.

The patient had an uncomplicated postoperative course, satisfactory wound healing at 14 days, and complete clinical and radiological resolution after six months of anti-tuberculous therapy. Regression of the tree-in-bud nodules and ground-glass opacities, together with disappearance of the chest wall collection, supported treatment response at both pulmonary and extrapulmonary sites. Comparable favorable outcomes have been reported when appropriately selected surgical management is combined with effective anti-tuberculous therapy.^3,9 The absence of recurrent swelling, discharge, or sinus formation at six months is reassuring, although longer follow-up would provide greater confidence regarding late local recurrence.

This case has particular relevance to tuberculosis-endemic and resource-limited settings. Chronic chest wall swellings may be managed empirically as bacterial abscesses when access to advanced imaging, mycobacterial culture, or specialist pathology is restricted. Repeated antibiotic courses or drainage without microbiological and histopathological sampling may delay definitive therapy and, when pulmonary tuberculosis coexists, prolong community transmission. A pragmatic approach is to recognize the cold-abscess phenotype, evaluate the lungs and pleura with available thoracic imaging, and obtain adequate fluid and tissue for rapid molecular testing and histopathology. In this patient, CT, Xpert MTB/RIF Ultra, sputum testing, and histopathological examination provided sufficient diagnostic evidence without reliance on more resource-intensive modalities.

In conclusion, anterior chest wall tuberculosis should be considered in an apparently immunocompetent patient with a chronic parasternal swelling or draining sinus, even when constitutional and respiratory symptoms are absent. The simultaneous presence of sputum-positive pulmonary tuberculosis underscores the need to investigate beyond the local chest wall lesion. Early tissue acquisition, molecular confirmation, histopathological correlation, and appropriately selected combined medical-surgical management can prevent diagnostic delay, avoid unnecessarily extensive surgery, reduce ongoing transmission, and achieve complete resolution.

Limitations

This report is limited by its single-patient design and cannot establish the frequency, route of spread, or optimal surgical strategy for anterior chest wall tuberculosis. The exact anatomical pathway linking the pulmonary and chest wall lesions could not be determined because no definite pleural or osseous communication was demonstrated. The available record did not specify the exact method used for sputum confirmation, mycobacterial culture and phenotypic drug-susceptibility testing, comprehensive drug-susceptibility testing, or the detailed doses of the anti-tuberculous regimen. In addition, follow-up was limited to 6 months and may not exclude late local recurrence. Nevertheless, the concordant clinical, radiological, molecular, histopathological, and therapeutic findings provide strong support for the final diagnosis.

Conclusion

Anterior chest wall tuberculosis is an important diagnostic consideration in patients with a persistent parasternal swelling or draining sinus, including immunocompetent individuals without constitutional or respiratory symptoms. In this patient, the diagnosis was established through concordant molecular and histopathological findings from the chest wall lesion, while sputum positivity confirmed concomitant pulmonary tuberculosis. Thoracic imaging defined the extent of both disease sites and excluded pleural, lymph-node, and osseous involvement. Local drainage and debridement followed by standard anti-tuberculous therapy resulted in complete clinical and radiological resolution at 6 months. The case supports early sampling of atypical chronic chest wall lesions and integrated evaluation for pulmonary tuberculosis, particularly in endemic and resource-limited settings.

Funding Statement

No funding was received.

Abbreviations

CT, computed tomography; EPTB, extrapulmonary tuberculosis; H&E, hematoxylin and eosin; HIV, human immunodeficiency virus; MTB, Mycobacterium tuberculosis; RIF, rifampicin; TB, tuberculosis; Xpert MTB/RIF Ultra, Xpert MTB/RIF Ultra assay.

Data Sharing Statement

All data relevant to this case report are included in the article and its figures. Further de-identified clinical information is available from the corresponding author on reasonable request, subject to applicable confidentiality requirements.

Ethics Approval and Consent to Participate

Our institution does not require ethical approval for reporting individual case report.

Consent to Publish

Written informed consent was obtained from the patient for publication of this case report and all accompanying clinical images.

Author Contributions

SHA (corresponding author): Conceptualization, investigation, data curation, writing – original draft, and writing – review and editing. MMM: Writing – review and editing. MBI: Writing – review and editing. AAS: Writing – review and editing. All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that they have no competing interests.