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Actinomycosis is an infectious disease caused by anaerobic gram-positive, non-spore forming bacteria of the genus Actinomyces that affects the oropharynx, digestive tract, and genitalia. Thoracic actinomycosis may affect the respiratory tract and the pleura, even extending to the chest wall. Pulmonary actinomycosis occurs in immunocompetent persons during the fourth and fifth decades of life, with greater prevalence in men, and is generally due to Actinomyces israelii or A meyeri. It is frequently misdiagnosed as primary or metastatic lung cancer or conventional lung infections (eg, tuberculosis). The accepted predisposing factors for bronchopulmonary actinomycosis are poor dental hygiene, alcoholism and various chronic debilitating diseases, hiatus hernia, and gastro-oesophageal reflux. We report an interesting case of pulmonary actinomycosis presenting with haemoptysis, associated with achlasia cardia, and treated as tuberculosis.
We decided to write this case:
A 17-year-old male student presented with a 4 week history of weight loss, malaise and loss of appetite. He denied any history of fever but 2 days later developed a massive bout of haemoptysis. Examination revealed signs of consolidation and a x-ray chest confirmed right upper lobe pneumonia. The patient received a course of antibiotics (cefuroxime and clarithromycin) and his sputum for acid fast bacillus (AFB) was repeatedly negative. Complete blood counts were normal and erythrocyte sedimentation rate (ESR) was 47 mm in the first hour. The haemoptysis stopped and the patient was discharged home. Three weeks later the patient came for a follow-up, and a repeat x-ray showed features of cavitation (fig 1). Computed tomography (CT) scan of the chest confirmed multiple cavities and pneumonic consolidation (fig 2), and an additional finding of a dilated oesophagus. Blood tests revealed a haemoglobin value of 13 g/dl and a total leucocyte count of 8.8/mm3 (normal 4.0–11.0); ESR was 124 mm in the first hour, and Mountoux test was negative. Bronchoscopy was undertaken and the bronchoalveolar lavage was negative for any abnormal cells and AFB. In view of the endemicity of tuberculosis in this part of the world, the persistent fever, weight loss and multiple cavitary lesions, antitubercular medication was started. The patient completed a 2 month course of the intensive treatment phase, but without any clinical and radiological improvement, so he was admitted for re-evaluation.
The patient’s history was again taken and was insignificant other than a failure to gain weight as compared to other siblings after the age of 14 years. In view of the dilated oesophagus on the CT chest scan, a barium oesophageal swallow was performed which revealed achalasia cardia (fig 3). An oesophago-gastroscopy also revealed a tight lower oesophageal sphincter and a dilated oesophagus with some food debris. The patient was referred for manometry and pneumatic dilatation of the achalasia and bronchoscopy was repeated. Bronchoalveolar lavage was sent for AFB staining and cultures. A israelii was stained on one of the lavage samples. The patient was started on amoxicillin-clavulanic acid and discharged for follow-up after 4 weeks. He showed subjective improvement and was advised to continue the same medication for 6–12 months. Meanwhile, he has undergone pneumatic dilatation for achalasia cardia, and is doing well and gaining weight.
Achalasia is a rare primary oesophageal motor disorder caused by degeneration or dysfunction of the inhibitory innervation of the oesophageal smooth muscle, resulting in incomplete relaxation of the lower sphincter and absent peristalsis in the oesophageal body.3 The presenting complaints at the time of diagnosis are dysphagia, postprandial and/or nocturnal regurgitation, weight loss, chest pain and cough. Pulmonary disease associated with achalasia is typically brought about by aspiration of contaminated matter from the dilated oesophagus into the respiratory tree.4
A israelii is a normal inhabitant in the oral cavity and upper intestinal tract of humans. It is believed that pulmonary actinomycosis occurs by aspiration of contaminated secretions from the oropharynx.5 Actinomycosis may appear as endobronchial or pleuroparenchymal disease, and bronchial foreign bodies (chicken and fish bones, grape seeds, beans, teeth, dental prostheses, alimentary material) or broncholiths may favour secondary colonisation by Actinomyces species.6
Pulmonary actinomycosis has been reported in patients with hiatus hernia and gastro-oesophageal reflux disease.1 There is one case report of achalasia cardia in association with pulmonary actinomycosis2 which has been misdiagnosed as lung malignancy. Our case is the second of its type, with haemoptysis as the presentation, which was treated initially as tuberculosis. Tuberculosis is a masquerader of pulmonary actinomycosis,7 as are fungal infections. In conclusion, the unusual presentation of achalasia cardia as haemoptysis, the misdiagnosis of pulmonary actinomycosis as tuberculosis, and association of achalasia cardia and pulmonary actinomycosis are reported here. A thorough workup is needed in such situations to avoid toxicity of antitubercular medications, lung resections and, importantly, patient morbidity and mortality.
We acknowledge the support provided by our directress postgraduate education and training Mdm Manal Karima and director patient sfety and quality advocacy Miss Fadwa Bawazir.
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.