Endobronchial Actinomycosis – The Great Masquerader

Abstract

Actinomycosis is a rare infection caused by Gram-positive, facultative anaerobic bacteria of the Actinomyceataceae family. Pulmonary Actinomycosis has a strong clinical and radiological resemblance to tuberculosis, lung abscess, and lung cancer, leading to missed or delayed diagnosis. We present a case of an elderly male with a productive cough and weight loss with right upper lobe consolidation on imaging. Definitive diagnosis was by histopathology; drawing samples by fiber-optic bronchoscopy, broncho-alveolar lavage, and endobronchial ultrasound. Tuberculosis, fungal infection, and malignancy were ruled out. Diagnosis was confirmed by demonstration of filamentous colonies of Actinomyces on hematoxylin and eosin and Grocott-Gomori’s methanamine silver stain. The patient showed good clinical and radiological response to Penicillin therapy.

INTRODUCTION

Actinomycosis is an infection characterized by the formation of abscess, induration, sinus tracts, fistulae, and tissue fibrosis. It is caused by nonspore-forming, nonacid-fast, Gram-positive, facultative anaerobic bacteria of the Actinomyceataceae family, which are commensals of the oral cavity, intestinal tract, and female genital tract.[1] The hallmark of actinomycosis is the spread across tissue planes and formation of sulfur granules, which are actually the colononies of Actinomycetes. Actinomyces israelii, the main disease-causing species in humans, has predominant cervicofacial involvement (50%), whereas the abdominal, thoracopulmonary, pelvic, and central nervous systems are less affected.[2] Predisposing factors include diabetes mellitus, immunosuppression, malnutrition, and local tissue damage or inflammation (dental procedures, gingivitis, irradiation, osteonecrosis, and poor oral hygiene). Actinomycosis presents a diagnostic challenge as it clinically and radiologically mimics several other conditions, particularly malignancy and tuberculosis. We present a challenging case of endobronchial actinomycosis.

CASE REPORT

A 78-year-old male presented with productive cough, atypical chest discomfort, and unquantified weight loss with decreased appetite for 5 months. He was on regular treatment for hypertension, diabetes mellitus, and chronic kidney disease. He was a regular smoker (smoking index = 25) and did not consume alcohol. He denied fever, night sweats, or hemoptysis. His body mass index was 19.2Kg/m² with stable vitals. He had poor oral hygiene and nicotine stains. Bronchial breath sounds with few crackles were auscultated in the right scapular and mammary areas. There was no significant lymphadenopathy. Investigations revealed mild leukocytosis, erythrocyte sedimentation rate of 79, blood and sputum cultures were sterile, tests for tuberculosis and fungi were negative, viral markers were negative, and the peripheral blood smear did not show malignant cytology. Chest radiograph revealed consolidation in the right upper zone. Contrast-enhanced computed tomography (CT) chest showed right upper lobe (RUL) consolidation with heterogeneous enhancement, few bronchiectasis changes, and reactionary lymphadenopathy [Figure 1a-b]. Fiber-optic bronchoscopy revealed an irregular RUL endobronchial lesion with creamy colored material, partially obstructing the RUL [Figure 2]. Broncho-alveolar lavage (BAL) cytology revealed inflammatory cells with no malignant cells. Endobronchial ultrasound biopsy of the lesion revealed Actinomyces colonies within in inflammed bronchial mucosa on hematoxylin and eosin (H and E) staining [Figure 3]. Actinomyces spp were best visualized using the Grocott-Gomori’s methanamine (GGM) silver stain, confirming the diagnosis of endobronchial actinomycosis [Figure 4]. He was initially treated with intravenous penicillin for 6 weeks, followed by oral amoxycillin for 6 months, after which he showed good clinical and radiological response.

Figure 1.

CECT chest showing Rt upper lobe consolidation with areas of heterogenous enhancement marked by arrow in (a) and adjacent areas of bronchiectasis and fibrosis marked by arrow in (b)

Figure 2.

Irregular Rt upper lobe endobronchial lesion with creamy-coloured material, partially obstructing the Rt upper lobe segment in fiberoptic bronchoscopy

Figure 3.

Actinomycosis colonies(marked by arrow) seen within ulcerated and inflamed bronchial mucosa with fibrin deposits in H and E Stain(40x)

Figure 4.

Filamentous colonies of Actinomyces sp (marked by arrows) in Gomori’s silver stain

DISCUSSION

Pulmonary actinomycosis is a rare presentation of human actinomycosis infection. It has no predilection for age, race, season, or occupation,[2] but is 2–4 times more common in males.[2] Actinomyces spp are commensal flora of the oral cavity and intestinal tract.[1] Disease occurs almost exclusively by direct invasion into deeper tissues by mucosal breach and rarely by hematogenous spread.[3] Thoracic infections usually occur following aspiration of bacteria from the oropharynx, especially in patients with dental disease or poor oral hygiene, and rarely following esophageal perforation.[4] Other predisposing factors are diabetes mellitus, immunocompromised state, and local tissue damage.[3]

Actinomycosis is a polymicrobial infections where common bacteria, like other anaerobes, Streptococcus spp, etc., act like co-pathogens.[3] These copathogens assist in the spread of infection by inhibiting host defenses and reducing local oxygen tension. They spread across tissue planes, leading to a chronic, indurated, suppurative lesions often with draining sinuses and fibrosis. The purulent discharge contains sulfur granules representing colonies of Actinomycetes.

Pulmonary actinomycosis can mimic lung abscess, foreign body, malignancy, or granulomatous infections such as tuberculosis or nocardiosis; both clinically and radiologically.[5] The symptoms are nonspecific, like productive cough, shortness of breath, fever, chest pain, hemoptysis, and weight loss. Due to its indolent course, it can present in late stages as complications such as chest wall sinuses, superior vena cava syndrome, mediastinal involvement, pericarditis, and rarely esophageal perforations and vertebral involvement.[2] A CT scan is the most appropriate radiological tool for detecting cavitary lesions and lung masses.

Actinomycosis should be suspected in any patient presenting with indolent, constitutional symptoms and with fistulas, sinus tracts, and/or masses that are spreading to adjacent structures without regard to tissue planes. Definitive diagnosis requires isolation and identification of the pathogen on either culture or histopathology.[6,7] Pulmonary samples for diagnosing actinomycosis include those from fiberoptic bronchoscopy, especially for endobronchial disease, and culture of BAL washings or lung biopsy. All collected samples should be sent for Gram stain, acid-fast bacilli stain, aerobic and anaerobic culture, H and E staining, as well as special staining with GGM stain.[1,6,7] The presence, in pus or tissue specimens, of nonacid-fast, Gram-positive organisms with filamentous branching is very suggestive of actinomycosis.[6,7] Culture is more specific, but the diagnosis is confirmed by culture in < 50% of suspected cases.[6,7] On H and E staining, tissue sections reveal chronic inflammatory granulation tissue of Actinomyces colonies with infiltration by neutrophils, foamy macrophages, plasma cells and lymphocytes, and surrounding dense fibrosis. Actinomyces spp are best visualized using the GGM silver stain. If both microbiology and histology testing are negative for Actinomyces spp (particularly in the setting of prior antibiotic therapy) but actinomycosis is suspected based on the clinical presentation, molecular techniques or nuclear probes may be helpful in identifying the causative pathogen.[8]

Actinomycosis infection is sensitive to initial treatment with intravenous Penicillins for 4–6 weeks followed by 6–12 months of oral amoxycillin.[9] Doxycycline, clindamycin, erythromycin, and tetracyclines are alternatives in case of penicillin allergy. Response to therapy is measured by resolution of clinical symptoms and radiological clearance.

CONCLUSION

Endobronchial actinomycosis is a rare infection which requires a strong clinical suspicion and early diagnosis to prevent catastrophic complications. It poses a diagnostic challenge due to its resemblance to lung cancer, abscess, and tuberculosis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.