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Year : 2013  |  Volume : 2  |  Issue : 2  |  Page : 133-135

Chest wall abscess caused by Nocardia asteroides

Departments of Microbiology and Chest Medicine, Columbia Asia Hospital, Yeshwanthpur and Hebbal, Bangalore, Karnataka, India

Date of Web Publication21-May-2013

Correspondence Address:
S Sreeja
No 10, 25 Feet Road, 4th Cross, Saraswathipuram Ulsoor, Bangalore, Karnataka
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We report a case of a postrenal transplant patient currently on immunosuppressive therapy, with an unusual presentation of pulmonary nocardiosis. The patient presented with a right-sided chest wall abscess. Pus was aspirated from the abscess and culture yielded pure growth of Nocardia asteroides. The patient responded well to surgical drainage and long term treatment with cotrimoxazole.

Keywords: Nocardia asteroides, postrenal transplant, pulmonary nocardiosis

How to cite this article:
Sreeja S, Udnur HB, Shiju M P. Chest wall abscess caused by Nocardia asteroides. J NTR Univ Health Sci 2013;2:133-5

How to cite this URL:
Sreeja S, Udnur HB, Shiju M P. Chest wall abscess caused by Nocardia asteroides. J NTR Univ Health Sci [serial online] 2013 [cited 2023 Jan 29];2:133-5. Available from: https://www.jdrntruhs.org/text.asp?2013/2/2/133/112348

  Introduction Top

Nocardiosis is caused by soil borne actinomycetes belonging to the genus Nocardia. Currently, the disease is on the rise primarily because of the increase in number of immunocompromised individuals due to human immunodeficiency virus infection and immuno­suppressive therapy during organ transplantation. [1] The reported overall incidence of nocardiosis among renal transplant patients ranges from 2% to 20%. [2] Pulmonary involvement is seen in 73-77% because the lungs are the primary portal of entry. [1],[3] About 25-50% of pulmonary nocardiosis may lead to extrapulmonary diseases. [1] Secondary hematogenous dissemination to chest wall is a rare occurrence. [4] We present a case of chest wall abscess secondary to pulmonary nocardiosis.

  Case report Top

A middle aged, male postrenal transplant patient on triple drug immunosuppressive therapy (Prednisolone, Azathioprine, and Cyclosporine) presented with pain and swelling on the right chest wall since 4 days. The swelling gradually increased in size and was associated with fever with chills and cough with minimal expectoration. He could not recollect any history of local trauma in the site. He is a known hypertensive and diabetic patient and had undergone renal transplantation 2 years back for chronic renal failure. Patient had a past history of receiving antitubercular drug therapy 1 year back for pulmonary tuberculosis (TB). The patient was hospitalized 2 months back for necrotizing pneumonia and was empirically treated for bacterial pneumonia. Sputum samples were negative for acid fast bacilli; therefore, a reactivation of pulmonary TB was temporarily ruled out. There was a partial response to amoxicillin-clavulanic acid combination. He presented again with history of cough with minimal yellowish white expectoration and right-sided pleuritic chest pain for 2 weeks. The pain was refractory to analgesics and a swelling developed 4 days back on the right chest wall which gradually increased to the present size. He also gave a history of swelling on the right thigh 1 week back which was diagnosed as an abscess and was surgically drained in a local hospital.

On physical examination the patient was febrile and had pedal edema. The pulse rate was 100 beats per minute and blood pressure 120/90 mm Hg. The respiratory rate was 26 breaths per min and oxygen saturation 96% in room air. On local examination the swelling was 3 × 4 cm size, circular, fluctuating and tender, situated on the right chest wall along the curvature of the fifth thoracic rib. Systemic examination including the respiratory system did not reveal any significant findings. The total leucocyte count was 18,600/mm 3 . The blood urea nitrogen was 49 mg/dL and serum creatinine 1.89 mg/dL. The chest X-ray and computed tomography scan [Figure 1] of the chest revealed old post-tubercular bronchiectasis with a cavity and pleural thickening. Ultrasound of the chest confirmed it as a chest wall abscess [Figure 2].
Figure 1: Computed tomography scan of the chest showing old post-tubercular bronchiectasis with a cavity and pleural thickening

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Figure 2: Ultrasound of the chest showing the abscess confined to the chest wall

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Two sputum samples that were sent for acid fast staining were negative. The patient refused bronchoscopy and therefore a bronchoalveolar lavage (BAL) could not be obtained. The pus was aspirated from the abscess and it was sent for culture and sensitivity and polymerase chain reaction for TB (TB-PCR). In view of the immune status of the patient in addition to routine Ziehl Neelsen (ZN) staining for tubercle bacilli, the pus was subjected to Modified ZN staining using 1% sulfuric acid. The microscopic examination of the modified ZN staining revealed scanty acid fast branching filaments morphologically resembling Nocardia [Figure 3]. After 48 hours of incubation at 37°C the blood agar plates showed dry chalky white, folded and wrinkled colonies of Nocardia species [Figure 4]. The isolate was sent for speciation and sensitivity to Kasturba Medical College, Mangalore and St Johns Medical College, Bangalore. The isolate was identified as Nocardia asteroides by standard biochemical tests like production of urease enzyme, negative hydrolysis test for adenine, casein, esculin, hypoxanthine, xanthine, tyrosine, and inability to utilize citrate.
Figure 3: Modified Ziehl Neelsen (×1000) staining showing acid fast branching fi laments of Nocardia

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Figure 4: Blood agar plate with dry chalky white colonies of Nocardia asteroides

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The isolate was sensitive to cotrimoxazole, erythromycin, ceftriaxone, ampicillin, linezolid, imipenem, gentamicin, and amikacin and resistant to tetracycline and ciprofloxacin. The TB-PCR of the pus was negative. The patient responded well with surgical drainage and cotrimoxazole therapy for 2 months. The pulmonary symptoms and the chest wall abscess subsided and the patient was put on 6 months cotrimoxazole maintenance therapy to prevent relapse.

  Discussion Top

Nocardia is an increasingly important opportunistic pathogen in immunosuppressed patients especially, solid organ transplant recipients. [5] In India the incidence of nocardiosis in renal transplant patients is 1.37%. The infection is most often caused by N. asteroides and predominantly it presents as pulmonary nocardiosis. [6] Secondary dissemination to central nervous system (CNS) and skin occurs in 40% cases of pulmonary nocardiosis. [5] Extrapulmonary lesions without the primary mode of access being identified have also been reported. [7]

But the diagnosis of nocardiosis especially, pulmonary nocardiosis is a challenge due to the following: (a) Nonspecific clinical presentation and in some cases lack of respiratory findings on examination. (b) Nonspecific or lack of radiological findings. [8] (c) The presence of easily diagnosed co-infections. [1] (d) Sputum smear may be negative. (e) BAL sample is necessary but high degree of suspicion is needed and a modified ZN stain using 1% sulfuric acid should be requested. (f) Nocardia colonies may take from 2 days to 4 weeks to grow.

The rate of mortality in pulmonary nocardiosis is 15-40% and increases with CNS involvement. [4] We were lucky that our patient had secondary cutaneous involvement and we were able to make a diagnosis and treat the patient on time. Cotrimoxazole is the drug of choice and it has to be given for 6-12 months to prevent relapse. Minocycline, amikacin, cephalosporins, imipenem and amoxicillin-clavulanic acid combination are used as an alternative or as an additional drug with cotrimoxazole. [9] Linezolid is the newer drug being evaluated for treatment of nocardiosis. [4] Delay in diagnosis affects the prognosis of the patient with nocardiosis. It is therefore imperative that practitioners have a high index of suspicion in evaluating patients who have compromised immunity and nocardiosis has to kept in mind as an important opportunistic pathogen.

  Acknowledgment Top

For confirmation of the isolate Mr. Prakash Peralam Yegneswaran Kasturba Medical College, Manipal, India.

  References Top

1.Mijares CC, Mendoza TM. Pulmonary nocardiois in renal transplant recipients. Phil J Microbiol Infect Dis 2001:144-152.  Back to cited text no. 1
2.Kayacan SM, Türkmen A, Aliº H, Imer M, Barlas O, Ecder ST, et al. Successful therapy combined with surgery for severe post-transplant nocardiosis. J Nephrol 2001;14:304-6.  Back to cited text no. 2
3.Wilson JP, Turner HR, Kirchner KA, Chapman SW. Nocardial infections in renal transplant recipients. Medicine (Baltimore) 1989;68:38-57.  Back to cited text no. 3
4.Moores LK. Unusual lung infections, Bronchiectasis and Cystic fibrosis. ACCP Pulmonary Medicine Board Review. 26 th ed. American College of Chest Physicians; 2012. p. 1-21   Back to cited text no. 4
5.Chapman SW, Wilson JP. Nocardiosis in transplant recipients. Semin Respir Infect 1990;5:74-9.  Back to cited text no. 5
6.John GT, Shankar V, Abraham AM, Mathew MS, Thomas PP, Jacob CK. Nocardiosis in tro pical renal transplant recipients. Clin Transplant 2002;16:285-9.  Back to cited text no. 6
7.Devi KR, Singh LR, Devi NT, Singh NS. Subcutaneous nocardial abscess in a post-renal transplant patient. Indian J Med Microbiol 2007;25:279-81.  Back to cited text no. 7
[PUBMED]  Medknow Journal  
8.Kramer MR, Uttamchandani RB. The radiographic appearance of pulmonary nocardiosis associated with AIDS. Chest 1990;98:382-5.  Back to cited text no. 8
9.Santamaria Saber LT, Figueiredo JF, Santos SB, Levy CE, Reis MA, Ferraz AS. Nocardia infection in renal transplant recipient: Diagnostic and therapeutic considerations. Rev Inst Med Trop Sao Paulo 1993;35:417-21.  Back to cited text no. 9


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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