|Year : 2014 | Volume
| Issue : 1 | Page : 79-81
Mixed pulmonary infection in an immunocompromised patient: A rare case report
S Qureshi1, A Pandey1, TR Sirohi2, SR Verma3, V Sardana1, C Agrawal1, AK Asthana1, M Madan1
1 Department of Microbiology, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh, India
2 Department of Medicine, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh, India
3 Department of Radiology, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh, India
|Date of Submission||20-May-2013|
|Date of Acceptance||10-Oct-2013|
|Date of Web Publication||4-Jan-2014|
Department of Microbiology, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Patients who are immunocompromised are predisposed to a variety of common and uncommon pulmonary infections. We report a case of mixed pulmonary infection by drug resistant tuberculosis with a nocardiosis in a 49-year-old man who was a known case of chronic obstructive pulmonary disease, on prolonged corticosteroid use with diabetes mellitus. Chronic use of corticosteroids is a predisposing factor for opportunistic infections, such as nocardiosis or tuberculosis. Since such a mixed infection is rare, maybe a combined approach to therapy early in the course of disease would be effective in such cases.
Keywords: corticosteroid, immunocompromised, Nocardia, tuberculosis
|How to cite this article:|
Qureshi S, Pandey A, Sirohi T R, Verma S R, Sardana V, Agrawal C, Asthana A K, Madan M. Mixed pulmonary infection in an immunocompromised patient: A rare case report. Indian J Med Microbiol 2014;32:79-81
|How to cite this URL:|
Qureshi S, Pandey A, Sirohi T R, Verma S R, Sardana V, Agrawal C, Asthana A K, Madan M. Mixed pulmonary infection in an immunocompromised patient: A rare case report. Indian J Med Microbiol [serial online] 2014 [cited 2020 Jan 26];32:79-81. Available from: http://www.ijmm.org/text.asp?2014/32/1/79/124330
| ~ Introduction|| |
Pulmonary nocardiosis is a serious, opportunistic infection affecting patients with a chronic obstructive pulmonary disease (COPD) or patients who are immunosuppressed.  It was observed that 60-90% of the patients had some underlying immunosuppressive condition such as chronic steroid use, solid organ transplantation, malignancy or human immunodeficiency virus (HIV) infection.  The presence of Nocardia on direct microscopic examination of potentially contaminated specimens, such as sputum, greatly increases the likelihood of the organism's role as an aetiologic agent. Chronic use of corticosteroids is a predisposing factor for opportunistic infections such as nocardiosis or tuberculosis.  The authors report a rare case of mixed pulmonary infection by a drug resistant tuberculosis with nocardiosis in a man who was a known case of COPD, on prolonged steroid use with diabetes mellitus. Since such a mixed infection is very rare, no strategy has yet been established to treat such cases. Perhaps a combined approach to therapy early in the course of disease would have been effective in such cases.
| ~ Case Report|| |
This paper reports a case of a 49-year-old male patient who presented with severe breathlessness and pain abdomen for 3 days, fever with night sweats since a week, productive cough with mucopurulent expectoration over 2 months. He was a known case of COPD on prolonged steroid use for a decade, a smoker for the past 20 years with diabetes mellitus on oral anti-diabetic drugs. Prior to the presentation to our hospital the patient was diagnosed as smear positive pulmonary tuberculosis (acid fast bacilli grade 3+) and was being treated by a private doctor for which he was receiving treatment with the first line anti-tubercular agents isoniazid, rifampicin pyrazinamide and ethambutol for almost 6 months. Howsoever, the patients relative were unaware regarding culture and sensitivity for Mycobacterium tuberculosis being performed, therefore it is difficult to pinpoint in this case if the patient was infected with a multidrug-resistant tuberculosis strain or did he acquire the resistance later. On clinical examination, the patient was thin built and emaciated. A characteristic steroid faces was a remarkable finding. His pulse rate was 148/min, blood pressure was 110/70 mm of Hg and the body temperature was 100°F. There was mild pallor, but no icterus, cyanosis, clubbing or pedal edema. Examination of the respiratory system revealed, respiratory rate was 28/min with oxygen saturation 85% and there was bilateral infra-clavicular and inframammary crepitations. His hemoglobin was 9.2 g%, total leucocyte count was 13,000/cu mm with differential leucocyte counts showing 95% of neutrophils and 5% of lymphocytes and erythrocyte sedimentation rate of 86 mm/h. The liver and kidney function tests were within normal range. Arterial blood gas analysis was suggestive of respiratory alkalosis. His fasting blood sugar was 310 mg/dl suggesting uncontrolled diabetes. Antibodies to HIV-1 and 2 were non-reactive. The chest radiograph posteroanterior view revealed bilateral multiple cavities of varying sizes and computed tomography scan revealed multiple cavitatory lesions with effusions. Abdominal radiograph was suggestive of paralytic ileus with a multiple air fluid levels. Gram stained smears of sputum showed branched, beaded, Gram-positive filaments morphologically resembling Nocardia spp. [Figure 1]. Modified Ziehl-Neelsen stained smears with 1% H 2 SO 4 as decolorizing agent showed acid fast filaments [Figure 2]. The sputum samples was also positive for acid fast bacilli with 3+ grading using 25% H 2 SO 4 as decolorizing agent, in spite of the patient being on anti-tubercular drugs for the past 6 months. A line probe assay (LPA), reverse hybridisation by genotype MTBDR plus performed directly on the sputum sample showed the presence of M. tuberculosis complex, which was resistant to isoniazid and rifampicin. The sample was also inoculated on BacT/alert 3D (bioMeriux) for culture of M. tuberculosis after decontamination (the culture was positive after 3 weeks of incubation). However, as we lost the patient the treatment outcome on follow-up could not be assessed.
|Figure 1: Gram stain of sputum showing Gram-positive branching filaments (×100)|
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|Figure 2: Modifi ed Ziehl-Neelsen staining with 1% sulphuric acid (×100)|
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Simultaneously, the sputum sample was cultured on blood agar, chocolate agar, Sabouraud's dextrose agar (SDA), Lowenstein-Jensen (LJ) medium. Chalky white colonies were observed on blood and chocolate agar plates after 48 h of aerobic incubation at 37°C [Figure 3]. The growth on LJ media was moist and glabrous while growth on SDA was observed as white waxy colonies without pigment. The growth was confirmed as Nocardia spp. by the presence of Gram-positive thin beaded and branching filaments which were acid fast, urease positive and non-utilization of lactose. Blood culture was sterile even after a week of aerobic incubation at 37°C. The antibiotic susceptibility of Nocardia spp. was performed by disc diffusion method, ,, which showed the isolate to be sensitive to gentamicin, co-trimoxazole, linezolid, amikacin, ciprofloxacin, but resistant to ampicillin, tetracycline and cephalosporins. Following this, diagnosis of a case of mixed pulmonary infection by M. tuberculosis and Nocardia spp. was made and the clinician was informed. Patient was started on additional treatment with co-trimoxazole (trimethoprim/sulfamethoxazole) and linezolid along with intravenous insulin and supportive treatment for COPD and paralytic ileus. Unfortunately, the patient's condition worsened in spite of starting culture sensitive antibiotics and succumbed to his illness within a day following diagnosis of mixed pulmonary infection.
|Figure 3: Chalk like white colonies on blood agar after 48 h of aerobic incubation at 37°C|
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| ~ Discussion|| |
India has a very high prevalence of tuberculosis both in healthy and compromised hosts, whereas, Nocardia infections are rare among normal population, with most infections occurring in immunocompromised patients, predominantly showing pulmonary involvement.  Pulmonary nocardiosis is usually community acquired due to the direct inhalation of Nocardia spp. from contaminated soil, while person-to-person transmission is rare. Tuberculosis also has similar clinical presentation however; person-to-person transmission is the only way in which the disease spreads.
Patients who are immunocompromised are predisposed to a variety of common and uncommon pulmonary infections. Most of the cases of nocardiosis present with non-specific respiratory symptoms such as cough, chest pain, dyspnoea and haemoptysis, mimicking tuberculosis.  About 5% of the patients with proven pulmonary tuberculosis were shown to have co-infection with Nocardia.  Chronic nocardiosis carries a mortality rate of 33% whereas, acute disease shows a mortality rate of 66-72%.  It has been reported that with the incidence of concomitant pulmonary tuberculosis the mortality increases,  similar finding has been observed in our case. Although nocardiosis resembles tuberculosis, the first line anti-tubercular drugs have no roles to play in its treatment.  Since a mixed infection is very rare, no treatment strategy has yet been established to treat such cases. Maybe a combined approach to therapy early in the course of disease would have been effective in such cases. Traditionally sulphonamides have been considered the treatment of choice. However, resistance to sulphonamides is increasingly recognised. Carbapenems and linezolid have been found to be uniformly active against all the pathogenic Nocardia spp. that affects human beings. Although broth microdilution is now the Clinical and Laboratory Standards Institute recommended method for antimicrobial susceptibility testing for the Nocardiae, other methods have also been evaluated and their tests include disk-diffusion, agar dilution, Etests and the BACTEC radiometric growth index method. Few correlation studies have, however, been performed with the broth microdilution method. ,,
Therefore, it is important to establish a definitive diagnosis early in the course of disease. It has been suggested that microscopic morphology can be suggestive enough to warrant empiric therapy for nocardiosis while awaiting culture results, especially in seriously ill patients and in those with impaired immunity.  Pulmonary nocardiosis is difficult to diagnose only on the basis of clinical and radiological findings. Molecular techniques, such as polymerase chain reaction (PCR), restriction enzyme analysis and 16S rRNA gene sequencing, have revolutionised the identification of Nocardia spp. These techniques are, however, restricted to referral laboratories.  In patients with tuberculosis and nocardiosis on radiological finding most commonly there is non-segmental, cavitating pneumonia, often with pleural effusion or empyema. The finding seen in this case is consistent with the established radiological evidence.  If only PCR was positive it could also have been dead bacillus. However, in LPA as we got a specific band for M. tuberculosis complex the chance of contamination is ruled out as in latter the band would not have been there.
The present case is reported with the aim to highlight the fact that once pulmonary tuberculosis is diagnosed, co-infection with Nocardia is never suspected unless and until there is a high index of suspicion or when the patient does not recover after completing the course of ant tubercular chemotherapy.
| ~ Conclusion|| |
pulmonary infection may be difficult to diagnose only on the basis of clinical and radiological findings as they are non-specific. Close collaboration between clinicians and microbiologists is required to include specific stains and cultures for early diagnosis of such rare mixed infection and rapid institution of specific therapy, especially in immunocompromised patients and to evaluate all the possible causes of pulmonary involvement for a better patient outcome.
| ~ References|| |
|1.||Aminzadeh Z, Darazam IA. Concomitant pulmonary nocardiosis and tuberculosis in a patient with rheumatoid arthritis: A new view point. Jundishapur J Microbiol 2012;6:91-4. |
|2.||Lerner PI. Nocardiosis. Clin Infect Dis 1996;22:891-903;904. |
|3.||Agrawal SM, Raut SS. Primary cutaneous disease due to Nocardia asteroides in an immunocompetent host. Indian J Pathol Microbiol 2011;54:185-6. |
|4.||Wallace RJ Jr, Steele LC. Susceptibility testing of Nocardia species for the clinical laboratory. Diagn Microbiol Infect Dis 1988;9:155-66. |
|5.||Collee JG, Miles RS. Watt B. Tests for identification of bacteria. In: Collee JG, Fraser AG, Marmion BP, Simmons A, editors. Mackie and MacCartney Practical Medical Microbiology. 14 th ed. Edinburgh: Churchill Livingstone; 1996. |
|6.||Anil K, Mehta A, Ghanshyam K, Madan M. Pulmonary and extrapulmonary tuberculosis along with pulmonary nocardiosis in a patient with human immunodeficiency virus infection. J Clin Diagn Res 2011;5:109-11. |
|7.||Powers CN. Diagnosis of infectious diseases: A cytopathologist's perspective. Clin Microbiol Rev 1998;11:341-65. |
|8.||Verghese SL, Madhavan HN, Sekar B. Isolation and characterisation of Nocardia from clinical specimens. J Indian Med Assoc 1996;94:58-9, 70. |
|9.||Reddy SS, Reddy KM, Saraswathi K. A rare case of pulmonary nocardiasis in an AIDS patient. Indian J Med Sci 2010;64:192-5. |
|10.||Martínez R, Reyes S, Menéndez R. Pulmonary nocardiosis: Risk factors, clinical features, diagnosis and prognosis. Curr Opin Pulm Med 2008;14:219-27. |
|11.||Padley S, Rubens MB. Pulmonary infections. In: Sutton D, editor. Textbook of Radiology and Imaging. 7 th ed., Vol. 1. London: Churchill Livingstone; 2003. p. 131-60. |
[Figure 1], [Figure 2], [Figure 3]