Abstract
Tuberculous pleurisy and subsequent pleural thickening could be associated with recurrent tuberculous infection http://ow.ly/BLGK30aJjvI
To the Editor:
We read with great interest the paper by Petruccioli et al. [1] where the authors describe new prognostic tests and different approaches that can predict the progression from latent to active tuberculosis (TB). We have taken the opportunity to comment on this paper to describe a recent case of recurrent tuberculous infection in a patient with a long-lasting history of tuberculous pleurisy and secondary residual pleural thickening.
At the age of 33 the patient had suffered from a left tuberculous pleurisy treated by anti-TB therapy, including daily intramuscular streptomycin (15 mg·kg−1 for 2 months), daily oral rifampin (10 mg·kg−1 for 6 months) and daily oral isoniazid (5 mg·kg−1 for 6 months) combined with pleural drainage. At that time, Mycobacterium tuberculosis was isolated from sputum and pleural fluid. At the age of 46, the patient underwent examination for a blunt thoracic trauma and a chest radiograph showed a chronic left pleural effusion likely due to his previous pleurisy (figure 1a); however, no treatment was proposed.
At 65 years of age, the patient (a non-smoking man) presented with chest pain and dyspnoea. A chest radiograph showed an enlargement of the pleural collection (figure 1b) and a computed tomography (CT)-scan of the chest confirmed the presence of a calcifying pleurisy leading to a contralateral mediastinal shift and lung atelectasis (figures 1c and 1e). Bronchoscopy was negative, the patient was afebrile and blood gas examination showed oxygen tension (PO2) of 67 mmHg, carbon dioxide tension (PCO2) of 46 mmHg and oxygen saturation of 94%. Pulmonary function tests revealed a moderate restrictive pattern. White blood cell count was normal and C-reactive protein level was elevated (152 mg·L−1; range 0–5 mg·L−1), while a Quantiferon-TB test was negative. Considering his previous history and the actual respiratory symptoms, a chest tube was positioned and a brownish purulent effusion (600 mL) was drained which had an observed lymphocyte percentage of 88%. Its bacteriological examination revealed the presence of Streptococcus pyogenes, while testing for M. tuberculosis and other atypical mycobacteria gave negative results. Antibiotic therapy (with amoxicillin/clavulanic acid) and daily pleural lavages with saline solution were started, although the patient refused any more-aggressive surgical procedures. The drain was removed 8 days later and the patient was discharged with a C-reactive protein level of 4 mg·L−1 while antibiotics were continued for 3 weeks.
The patient was then not traceable for the next 2 years until they spontaneously presented to an outpatient clinic with a chest radiograph (figure 1d) identical to the very first radiograph (figure 1a). On this occasion the chest radiogram was performed as a preoperative control prior to inguinal hernia repair. The radiological findings shown in figure 1a and figure 1d illustrate well the chronic evolution of a tuberculous pleurisy. At the age of 76 (time of last follow-up), the patient was asymptomatic and in good condition, and no other pulmonary complications were reported.
We think that this case is an interesting example of recurrent tuberculous infection due to reactivation of TB in a patient who was previously “cured”. A serious infection by M. Tuberculosis was initially controlled by an adequate anti-TB therapy including streptomycin, rifampin and isoniazid as stated above. It seems likely that the antibiotics were able to decrease the total bacterial count to a minimum but were not able to completely eradicate the infection, which could justify the presence of a chronic pleural fluid with diffuse calcifications. A sort of immunological equilibrium was then reached by the patient and this was maintained until an unexpected superinfection occurred. We would like to hear Dr Petruccioli's opinion about this and whether it could be of any interest and value to screen the patient by tuberculin skin test, interferon-γ release assay, or by any other method they describe in their paper.
Our patient presented residual pleural thickening (RPT) due to chronic tuberculous pleurisy. Tuberculous pleurisy is the second most common form of extra-pulmonary tuberculosis, the first being lymphatic tuberculosis [2–4]. A definitive diagnosis of tuberculous pleurisy usually requires a mycobacterial culture of pleural fluid or a pleural biopsy. The diagnostic yield for a pleural effusion culture was found to range from 12 to 70% [2, 3]. In 2012, Ruan et al. [2] published a retrospective cohort study showing an effusion culture diagnostic yield of 63% that increased to 79% in combination with sputum cultures. They also observed that the lymphocyte percentage of pleural fluid was negatively associated with the probability of a positive effusion culture [2]. This may reflect our own findings, in which the pleural lymphocyte percentage was high and the culture for M. tuberculosis was negative. It has been shown that the drainage of pleural effusion, even in the early stages, does not prevent the development of RPT [3]. Lai et al. [5] have reported a randomised study comparing the efficacy of standard anti-TB treatment combined with pigtail drainage to standard anti-TB treatment only. They found that the addition of pigtail drainage was not clinically relevant and did not reduce the level of RPT. Our patient presented an evident RPT over a period of years, despite successful initial anti-TB treatment and numerous subsequent incidences of pleural drainage.
Acknowledgements
We would like to thank Petruccioli, Elisa (National Institute for Infectious Diseases “L. Spallanzani”, Rome, Italy) and co-workers for their comprehensive work on different tools for predicting the development of active TB from latent TB infection.
Footnotes
Conflict of interest: None declared.
- Received December 16, 2016.
- Accepted January 23, 2017.
- Copyright ©ERS 2017