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Year : 2018 | Volume
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| Issue : 1 | Page : 141-142 |
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Nontuberculous mycobacterial empyema in an immunocompetent child |
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Ira Shah, Forum Shah
Department of Pediatrics, Pediatric TB Clinic, B. J. Wadia Hospital for Children, Mumbai, Maharashtra, India
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Date of Web Publication | 22-Mar-2018 |
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Abstract | | |
Nontuberculous mycobacterium (NTM) species are mycobacterial species other than those belonging to the Mycobacterium Tuberculosis complex and Mycobacterium leprae. There are very few reports of NTM in immunocompetent children causing empyema. In this article, we report a 9-year-old immunocompetent girl who presented with Mycobacterium avium-intracellulare empyema.
Keywords: Children, empyema, immunocompetent, nontuberculous mycobacteria
How to cite this article: Shah I, Shah F. Nontuberculous mycobacterial empyema in an immunocompetent child. Indian J Pathol Microbiol 2018;61:141-2 |
Introduction | |  |
Nontuberculous mycobacterium (NTM) species are mycobacterial species other than those belonging to the Mycobacterium tuberculosis complex and Mycobacterium leprae. NTM are generally free-living organisms that are ubiquitous in the environment. They are also called environmental mycobacteria and mycobacteria other than tuberculosis (TB).[1] There are about 100 different species of NTM.[2] Few species cause human disease of which the common ones are Mycobacterium avium, Mycobacterium kansasii, and Mycobacterium fortuitum.[1] Infections in humans with robust immune mechanisms are quite rare.[3] The spectrum of diseases caused by NTM range from pulmonary diseases including cavity, consolidation and bronchiectasis, lymphadenitis, skin, soft tissue, and injection site infections to disseminated disease in immunocompromised individuals.[4] There are very few reports of immunocompetent patients presenting with empyema.[5] In this article, we report a 9-year-old immunocompetent female patient who presented with M. avium-intracellulare (MAI) empyema.
Case Report | |  |
A 9-year-old girl presented with left-sided chest pain for 3 months. There was associated intermittent fever and cough for the past 2 weeks. There was no weight loss, night sweats, or contact with a patient having TB. She had no other illnesses in the past. On examination, weight was 23.3 kg. She had pallor, insignificant cervical adenopathy (1 cm × 0.5 cm). Respiratory system examination revealed decreased air entry in the left mammary, inframammary, and axillary areas. Rest of the systemic examination was normal. Investigations showed hemoglobin 8.3 g/dL, white cell count 4300 cell/cumm (polymorphs 63%, lymphocytes 33%, and eosinophils 3%), and erythrocyte sedimentation rate 145 mm at the end of 1 h. Liver function tests were normal. HIV ELISA was negative. Mantoux test and sputum for acid-fast bacillus (AFB) on smear were negative. Chest X-ray (CXR) revealed massive left-sided pleural effusion. On tapping of the pleural fluid, it was found to be pus. Pleural fluid contained proteins 3.4 mg/dL, glucose 54 mg/dL, and 1200 cells/cumm with 79% polymorphs. It did not show any AFB on smear. CT chest demonstrated left-sided large empyema with near total collapse of underlying lung. The child was taken up for thoracotomy and decortication and pus culture was sent for TB and bacterial culture. Bacterial culture did not grow any organism. The sample for TB culture was inoculated in both Mycobacteria Growth Indicator Tube 960 (MGIT 960) plus Löwenstein–Jensen medium. The patient was started on intravenous antibiotics but had no response and so four-drug antituberculous therapy (ATT) consisting of isoniazid (H), rifampicin (R), pyrazinamide (Z), and ethambutol (E) was added. TB MGIT 960 culture at the end of 3 weeks grew mycobacterium species which was confirmed to be NTM using an in-house ρ-nitro benzoic acid (PNBA) assay on MGIT 960 and further confirmed by the Food and Drug Administration approved ρ-nitro-α-acetylamino-β-hydroxypropiophenone (NAP) test on the BACTEC 460 TB system (BD Diagnostics, Sparks, MD, USA). The NTM isolated was further speciated using molecular methods. DNA was extracted using the standard CTAB-NaCl (cetyltrimethylammonium bromide-sodium chloride) method, and the 360 base pair (bp) region of the rpoB gene was amplified. Amplified products were further subjected to an in-house reverse line blot hybridization (RLBH) assay and restriction enzyme (RE) analysis. The species was confirmed to be MAI by sequencing the 360 bp amplified region of the rpoB gene. Immune workup in form of absolute CD4 (1455 cells/uL), CD8 (1104 cells/uL), CD19 (1254 cells/uL), CD16/56 (1003 cells/uL), and serum total IgG and IgM were normal. HIV ELISA was negative. ATT was modified and clarithromycin was added and pyrazinamide was stopped. A repeat CXR done after 2 months of therapy was normal. ATT is continued and the child is on regular follow-up.
Discussion | |  |
NTM are Gram-positive, acid-fast, and aerobic tubercle bacilli and are isolated from showerheads, bathroom, water distribution systems, soil, dust, milk, birds, and laboratory equipment.[6],[7],[8] The start of the 21st century has seen doubling of cases due to NTM as compared to 1990–1999.[9] This increased incidence has been attributed to showering, genetic mutations, climate changes, improved laboratory facilities, and nosocomial infections.[4] One of the most common NTMs causing infection in humans is MAI which was also isolated in our patient. Infection is through aerosol inhalation or through ingestion. Human-to-human transmission is rare.[8] MAI infections can cause varied pulmonary manifestations, lymphadenitis, skin infections, and disseminated disease. The pulmonary symptoms are usually vague and characterized by productive cough, dyspnea, hemoptysis, fever, weight loss, and malaise. Mantoux test may be weakly positive (5–10 mm).[6] Radiologically, cavities, consolidation, macro- and micro-nodules, and bronchiectasis are seen.[4] Pleural thickening and effusion is uncommon.[1],[8] In the immunocompromised patient, mediastinal involvement, unilateral interstitial infiltrates, segmental pneumonia, pleural effusion, and disseminated disease have been reported.[6] Our patient was HIV negative and had normal immunoglobulins and lymphocyte subsets. There have been only two reports of NTM in immunocompetent children causing empyema, both of which were due to Mycobacterium chelonae.[5] Diagnosis is made by inoculating on culture media. The identification of species is done using hybridization with specific probes and molecular biology techniques.[6]
The mainstay of NTM therapy is a minimum three-drug regimen of clarithromycin, rifampicin, and ethambutol for 1 year and the patient is culture negative. Streptomycin for the first 2–3 months of therapy may be considered for extensive disease.[8] Multidrug regimen enhances antimicrobial activity and prevents emergence of resistant strain. Although rifampicin decreases blood concentration of clarithromycin, studies have demonstrated superiority when rifampicin and clarithromycin are used concurrently.[10] The addition of isoniazid reduces failure of treatment/relapse rates for MAC.[11] Our patient was also treated with a multidrug regimen involving clarithromycin, isoniazid, rifampicin, and ethambutol. CXR after 2 months of treatment showed complete radiological clearance.
Conclusion | |  |
In patients with pleural effusion, the pleural fluid should be tested for mycobacteria on culture or PCR so that identification of species can be done and treatment can be tailored accordingly.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Katoch VM. Infections due to non-tuberculous mycobacteria (NTM). Indian J Med Res 2004;120:290-304. |
2. | Parrish SC, Myers J, Lazarus A. Nontuberculous mycobacterial pulmonary infections in Non-HIV patients. Postgrad Med 2008;120:78-86. |
3. | Holland SM. Nontuberculous mycobacteria. Am J Med Sci 2001;321:49-55. |
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5. | Wali S. Mycobacterium chelonae empyema with bronchopleural fistula in an immunocompetent patient. Ann Thorac Med 2009;4:213-5.  [ PUBMED] [Full text] |
6. | Baquero-Artigao F. Pediatric infections caused by nontuberculous mycobacteria. An Pediatr (Barc) 2005;62:458-66. |
7. | Ogawa K, Sano C. Strategies for Mycobacterium avium complex infection control in Japan: How do they improve the present situation? Kekkaku 2013;88:355-71. |
8. | Martins AB, Matos ED, Lemos AC. Infection with the Mycobacterium avium complex in patients without predisposing conditions: A case report and literature review. Braz J Infect Dis 2005;9:173-9. |
9. | Vu TT, Daniel SJ, Quach C. Nontuberculous mycobacteria in children: A changing pattern. J Otolaryngol 2005;34 Suppl 1:S40-4. |
10. | Kurashima A. Perspective of pulmonary MAC infection treatment. Kekkaku 2007;82:195-9. |
11. | Research Committee of the British Thoracic Society. First randomised trial of treatments for pulmonary disease caused by M avium intracellulare, M malmoense, and M xenopi in HIV negative patients: Rifampicin, ethambutol and isoniazid versus rifampicin and ethambutol. Thorax 2001;56:167-72. |

Correspondence Address: Ira Shah 1/B Saguna, 271/B St. Francis Road, Vile Parle (W), Mumbai - 400 056, Maharashtra India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/IJPM.IJPM_586_16

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This article has been cited by | 1 |
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| Keren Bachar, Tiberiu Shulimzon, Michael J. Segel | | Respiratory Medicine. 2022; 205: 107036 | | [Pubmed] | [DOI] | |
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