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| CASE REPORT |
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| Year : 2019 | Volume
: 8
| Issue : 2 | Page : 147-150 |
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Post renal transplant pulmonary nocardiosis - A case report
Akhil Purushothaman Rajeswari, Gullipalli Prasad, Ramesh Chandra Vyasam, Bura Naga Raja Ramesh, Gunnam Sireesha, Athota Sam, Revu Praveen, Kondari Sai Sundeep, Kanala Sai Harisha
Department of Nephrology, Andhra Medical College, Visakhapatnam, Andhra Pradesh, India
| Date of Submission | 03-Mar-2019 |
| Date of Acceptance | 13-Apr-2019 |
| Date of Web Publication | 30-Jul-2019 |
Correspondence Address:
Dr. Gullipalli Prasad
37-10-129/2/2, Ayyappa Nagar, Visakhapatnam - 530 007, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_38_19
Nocardiosis is a rare opportunistic infection caused by an aerobic actinomycete, producing either local or disseminated disease. It is a systemic infection that usually begins in the lungs and has high predilection for brain, skin and subcutaneous tissues. It commonly affects solid organ transplant recipients on immunosuppressive drugs. The incidence of nocardiosis in solid organ transplant recipients is about 0.6%. In India, nocardiosis was reported in 1.4% of renal transplant recipients. We report a case of pulmonary nocardiosis in a postrenal transplant recipient. Patient presented with features suggestive of pneumonia not responding to antibiotics. Initial sputum gram stain and AFB was negative. Chest radiograph showed right parahilar non-homogenous opacity, and CT chest revealed right parahilar, and subcarinal adenopathy. Bronchoscopy was done which showed purulent secretion from right 6th bronchial segment and AFB stain of broncho alveolar lavage fluid, showed weak acid fast filamentous bacteria, suggestive of nocardiosis. Patient was treated with antibiotics imipenem and co-trimoxazole. Patient responded well to treatment and pneumonia was resolved.
Keywords: Atypical pneumonia, hilar lymphadenopathy, opportunistic infection, pulmonary nocardiosis, renal transplant
How to cite this article:
Rajeswari AP, Prasad G, Vyasam RC, Ramesh BN, Sireesha G, Sam A, Praveen R, Sundeep KS, Harisha KS. Post renal transplant pulmonary nocardiosis - A case report. J NTR Univ Health Sci 2019;8:147-50 |
How to cite this URL:
Rajeswari AP, Prasad G, Vyasam RC, Ramesh BN, Sireesha G, Sam A, Praveen R, Sundeep KS, Harisha KS. Post renal transplant pulmonary nocardiosis - A case report. J NTR Univ Health Sci [serial online] 2019 [cited 2023 Mar 22];8:147-50. Available from: https://www.jdrntruhs.org/text.asp?2019/8/2/147/263636 |
| Introduction | |  |
Nocardiosis is a rare opportunistic infection caused mainly by nocardia asteroids, less commonly nocardia farscinia, nocardia braziliensis and nocardia nova.[1] Nocardiosis is a systemic infection usually starts in the lungs and has high predilection for brain, skin and subcutaneous tissues. Pulmonary nocardiosis often presents with pneumonia not responding to antibiotics with rapid deterioration of graft function and significant mortality. It is commonly seen in solid organ transplant recipients on immunosuppressive drugs. The incidence of nocardiosis in solid organ transplant recipients is about 0.6%, highest in lung transplant recipients (3.5%)[2], and around 0.2% in renal transplant recipients. In India, nocardiosis was reported in 1.4% of renal transplant recipients,[3] most common species being nocardia steroids. Inhalation and inoculation are the two main routes of transmission of the bacteria. Intense immunosuppression is the commonest predisposing factor.[4]
We report here a case of pulmonary nocardiosis in a kidney transplant recipient that was treated successfully with imipenem and cotrimoxazole.
| Case Report | | |
A 38-year-old female presented with complaints of fever, of one month duration, along with cough and expectoration. Fever was high grade intermittent and associated with chills and rigor. Expectoration was yellow colored and mucopurulent in nature. There was no hemoptysis. She was diagnosed as having chronic kidney disease 6 years ago, and had undergone renal transplantation with live donor 2 years ago. She was given induction with anti thymocyte globulin and was on triple immunosuppressive therapy consisting of prednisolone (10 mg/day), tacrolimus (4 mg/day), and mycophenolate mofetil (2 g/day). She was non diabetic and was maintaining her blood pressures without any antihypertensives. Her graft function was normal for one year post transplant, then gradually deteriorated, and serum creatinine started rising and maintained around 3.5 mg/dl. But renal biopsy was deferred by the patient.
Physical examination recorded body temperature of 39°C, respiratory rate of 28 per minute, blood pressure was 130/80 mm Hg, with oxygen saturation maintaining at 97% in room air. General examination showed no evidence of pallor, icterus, cyanosis, clubbing, generalized lymphadenopathy or pedal edema. Systemic examination did not show any positive findings. Chest examination was unremarkable. Blood investigations showed hemoglobin of 13.8 mg/dl, a total WBC count of 17600, neutrophils 86%, lymphocytes 7% and ESR was 87 mm in first hour. Renal function showed blood urea of 121 mg/dl and serum creatinine of 6.2 mg/dl. Other blood investigations including liver function and serum electrolytes were normal. Chest radiograph showed nonhomogenous opacity in right parahilar region [Figure 1] and [Figure 2], Sputum gram stain and AFB were negative. CT chest [Figure 3] revealed consolidation, ground glass densities and alveolar opacities in right lower lobe and right upper lobe, along with pretracheal, right paratracheal and subcarinal lymphadenopathy – features suggestive of granulomatous or neoplastic etiology. So, video assisted bronchoscopy was done, which revealed purulent secretion from right 6th bronchial segment. BAL fluid showed weak acid fast branching filamentous elements, suggestive of nocardiosis. Patient was started on imipenem and cotrimoxazole empirically, and was continued for 2 weeks. | Figure 2: Chest x ray right lateral view showing consolidation of right middle lobe, hilar adenopathy
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 | Figure 3: HRCT chest axial view showing consolidation, ground glass densities and alveolar opacities in right lower lobe along with pretracheal and right paratracheal lymphadenopathy
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She improved clinically, fever and cough subsided. Serum creatinine was reduced to 3.8 mg/dl. Chest X-ray [Figure 4] done 4 weeks later revealed resolution of opacities. Patient was continued on TMP-SMX DS once daily.
| Discussion | | |
Nocardiosis is a rare disease, commonly seen in immunocompromised patients, especially solid organ transplant recipients.[5] The most common risk factor here is corticosteroid therapy and immunosuppressive drugs. In immunosuppressed patients, the incidence of nocardial infections is 0.4 to 3.6%.[6],[7] At the same time, the incidence in renal transplant recipient is 0.7 to 2.6%.[6],[8] The risk factors identified in a case control study of nocardiosis in solid organ transplant recipients are, high steroid intake, presence of cytomegalovirus disease and high median calcineurin inhibitor levels in the preceding 30 days [>15 ug/ml for tacrolimus and >300 ng/ml for cyclosporine].[1]
An observation by Carnet et al., in 933 transplant recipients between 1985 and 2002, receiving cyclosporine, showed only 2 cases of nocardiosis. He reported 4 cases out of 174 transplant recipients between 1996 and 2002, who were taking tacrolimus. He concluded as patients having tacrolimus-based immunosuppression is at increased risk for developing nocardiosis when compared to cyclosporine.[9]
Bilgarnia et al. and Flohr et al. reported two other cases of pulmonary nocardiosis. Both cases underwent re-transplantation, and preconditioning was done using plasmapheresis and rituximab. Post-transplant, these patients were maintained on mycophenolate mofetil, tacrolimus and steroids.[10],[11]
The present patient received induction treatment with ATG, and post-transplant, the patient was maintained with mycophenolate mofetil, tacrolimus and steroids. Nocardial infection is most common in first six months post-transplant period.[12] Rarely reported in the first month [13] or after the first year,[14] but the present case presented after two years post-transplant.
Most common clinical presentation of pulmonary nocardiosis is a sub-acute or chronic necrotizing pneumonia.[15] Typical presentation of pulmonary nocardiosis includes fever, cough, dyspnea, malaise, anorexia and chest pain.[16] Our patient also presented with fever, cough and breathlessness.
Pulmonary nocardiosis is usually diagnosed by sputum smears/sputum culture. There are no specific clinical or radiological feature suggestive of nocardiosis. So gram stain of sputum is the most important diagnostic tool of pulmonary nocardiosis.[17],[18] Multiple sputum specimens have to be examined as only one third them may show nocardia.[19] In the present case, initial sputum gram stain was negative. The BAL specimen showed weak acid fast branching filamentous suggestive of nocardiosis. Sputum culture revealed growth of nocardia asteroids.
Case studies showed that about 60-80% of nocardiosis in renal transplant patients is pulmonary nocardiosis and half of them have isolated lung involvement.[20] The present patient had an isolated pulmonary involvement without clinically evident dissemination. Pulmonary nocardial patients are at higher risk of systemic nocardiosis. It was suggested that 28-50% of pulmonary nocardiosis would develop disseminated nocardiosis (involving 2 or more organs).[21],[22],[23] So, high index of suspicion, early diagnosis and adequate treatment is the key in managing pulmonary nocardial infections. Nocardial infection is suspected in transplant recipients who are presenting with pulmonary symptoms and not responding to usual antibiotics.
Radiological patterns of pulmonary nocardiosis are not pathognomonic.[24],[25] Non-specific findings such as air space consolidation, presence of irregular nodular lesions, which may or may not associated with cavitation. Mediastinal and hilar lymphadenopathy was also described in pulmonary nocardiosis in around 15% of cases.[26],[27] The present case had multilobar involvement with airspace consolidation without cavitation. Also the patient had right paratracheal and subcarinal lymphnode enlargement.
Sulphonamides, especially cotrimoxazole, were used as a component of combined antimicrobial therapy. In our case, we have given cotrimoxazole along with imipenem initially. After 2 weeks, impanel was stopped and cotrimoxazole was continued. Patient improved symptomatically after 2 weeks of treatment. Radiological lesions started clearing after 3 weeks. Now, patient is continuing with cotrimoxazole.
Currently, there exists no routine single serodiagnostic test to identify patient with nocardial infection. Several cultures may be negative initially because of slow growth and variable colony morphology.[28] So specimens should be obtained by aggressive approaches in suspected cases, like bronchoscopic lavage, aspiration of abscess are valuable for diagnosis. In our case, we went ahead with bronchoscopic lavage culture and gram stain, as initial sputum culture and gram stain were negative.
So, in conclusion, high index of suspicion and aggressive investigation in a post renal transplant recipients can make an early diagnosis, adequate treatment and prevent dissemination of disease.
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.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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