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  Table of Contents    
CASE REPORT  
Year : 2019  |  Volume : 62  |  Issue : 2  |  Page : 329-331
Disseminated Nocardia farcinica infection presenting as a paravertebral abscess in a patient with systemic lupus erythematosus


1 Department of Infectious Disease and Clinical Microbiology, Merkezefendi State Hospital, Manisa, Turkey
2 Department of Infectious Disease and Clinical Microbiology, Ankara Numune Training and Research Hospital, Ankara, Turkey
3 Department of Medical Microbiology, Ankara Numune Training and Research Hospital, Ankara, Turkey
4 Department of Medical Microbiology, Ankara University Faculty of Medicine, Ankara, Turkey

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Date of Web Publication10-Apr-2019
 

   Abstract 


Disseminated Nocardia infections occur particularly in immunosuppressed hosts and are most often due to Nocardia farcinica, Nocardia nova, and Nocardia cyriacigeorgica. Here, we report an unusual case of disseminated N. farcinica infection presenting as a paravertebral abscess in a patient with systemic lupus erythematosus.

Keywords: Granulomatous, Nocardia farcinica, nocardiosis, paravertebral abscess

How to cite this article:
Ozen Y, Dokuzoguz B, Mumcuoglu I, Çelikbas AK, Karahan ZC, Özbay BO. Disseminated Nocardia farcinica infection presenting as a paravertebral abscess in a patient with systemic lupus erythematosus. Indian J Pathol Microbiol 2019;62:329-31

How to cite this URL:
Ozen Y, Dokuzoguz B, Mumcuoglu I, Çelikbas AK, Karahan ZC, Özbay BO. Disseminated Nocardia farcinica infection presenting as a paravertebral abscess in a patient with systemic lupus erythematosus. Indian J Pathol Microbiol [serial online] 2019 [cited 2019 Jul 22];62:329-31. Available from: http://www.ijpmonline.org/text.asp?2019/62/2/329/255804





   Introduction Top


Nocardia is an opportunistic pathogen which most commonly affects immunocompromised hosts. The predisposing factors are prolonged corticosteroid therapy, malignancies, organ transplantation, chronic lung disease, alcoholism, and diabetes mellitus.[1],[2] Dissemination to the central nervous system (CNS), cutaneous or subcutaneous tissue, joints, bones, eyes, kidney, and heart is the progression of the pulmonary involvement. Disseminated infections occur particularly in immunosuppressed hosts and are most often due to Nocardia farcinica, Nocardia nova, and Nocardia cyriacigeorgica.[2] Here, we report an unusual case of disseminated N. farcinica infection presenting as a paravertebral abscess in a patient with systemic lupus erythematosus (SLE).


   Case Report Top


A 24-year-old male with SLE presented with a 2-week history of low back pain. He was immunosuppressed with methylprednisolone 32 mg/day and mycophenolate mofetil (MMF) 2 g/day. When low back pain aggravated, he visited another hospital. The lumbar magnetic resonance imaging (MRI) revealed a 5.5 cm × 6 cm × 20 cm paravertebral abscess at Th11-L5. He had been operated for abscess evacuation and postoperative intravenous antibiotic therapy was initiated with ampicillin-sulbactam and amikacin. On the 2nd postoperative day, he was referred to our department for the evaluation and treatment of paravertebral abscess.

On admission, his body temperature was 36.2°C, blood pressure was 120/80 mmHg, heart rate was 70 beats/min, and respiration rate was 18 breaths/min. Auscultation of the lung showed clear lung sound without rhonchus or rale. There was no tenderness in the lower back. Findings from neurological examinations were normal. There was an erythematous plaque with papules on the right knee and an ecchymotic area below it [Figure 1].
Figure 1: Skin lesion of disseminated Nocardia farcinica infection

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The initial peripheral blood count revealed a white blood cell count of 18,200/mm3 (neutrophils 97.3%, lymphocytes 1.5%, and monocytes 1.2%), hemoglobin level of 10.4 g/dL, platelet count of 392,000/mm3, erythrocyte sedimentation rate of 72 mm/h, and C-reactive protein of 193 mg/L. Blood chemistry revealed a total protein level of 4.5 g/dL, albumin level of 2.3 g/dL, aspartate aminotransferase/alanine aminotransferase of 61/65 U/L, alkaline phosphatase of 82 IU/L, and blood urea nitrogen/creatinine of 36.4/1.14 mg/dL. An empiric antibiotic treatment was started with piperacillin-tazobactam and clindamycin.

Multiple nodules were seen on chest radiograph. Chest computed tomography (CT) showed mildly enlarged lymph nodes, bilateral pleural effusion, right-sided empyema, and multiple bilateral nodules, some of which presented cavitation. Although there were no neurological findings, an MRI of the brain was requested to look for cerebral involvement. MRI showed peripherally enhancing lesions in the left cerebellar hemisphere, right frontal region, and left parietal region with restricted diffusion. Fundus examination revealed bilateral macular infiltration. A punch biopsy was obtained from the lesion on the right knee [Figure 1]. Histopathological examination of skin biopsy revealed a dermal infiltration of histiocytoid cells staining positively for CD68, pointing toward granulomatous disease.

The paravertebral abscess was drained. Gram stain of the evacuated pus revealed Gram-positive filamentous bacilli with branching. The isolated strain was subjected to 16S rRNA sequence analysis that showed 100% match with N. farcinica 16S rRNA sequence. The result of antimicrobial susceptibility testing showed the isolate susceptible to linezolid, imipenem, ciprofloxacin, and trimethoprim-sulfamethoxazole (TMP-SMX).

Initial antimicrobial therapy was switched to intravenous linezolid (600 mg bid), imipenem (500 mg qid), and amikacin (1 g qd) according to the antimicrobial susceptibility patterns of N. farcinica.[3] Methylprednisolone was reduced to 4 mg by titration and MMF was discontinued.

Lumbar MR and chest CT were repeated during the 3rd week of treatment, which showed substantial resolution of the previously detected lesions. The patient was discharged with TMP-SMX and amikacin 6 weeks after admission. We planned a maintenance regimen of TMP-SMX treatment as long as immunosuppressive therapy continued.


   Discussion Top


Nocardia species are aerobic, catalase-positive, weakly acid-fast, fine right-angled branching filamentous Gram-positive bacteria belonging to Actinomycetales.[4] They are saprophytic bacteria which live in carbon-rich sources such as soil, decomposing organic matter, and aquatic environment.[5] There are more than ninety Nocardia species, many of which have been suspected of human disease. N. farcinica is an important member of Nocardia asteroides complex.[2],[3] The number of N. farcinica infections is increasing due to both the growing population of immunosuppressed hosts and improved techniques for the identification of the bacteria.[4]

Risk factors for nocardiosis are malignancies, diabetes mellitus, chronic pulmonary diseases, alcoholism, and medical immunosuppression. Organ transplant recipients are also at an increased risk of nocardiosis, especially among those who have high levels of calcineurin inhibitors, receipt of high-dose steroids, history of cytomegalovirus disease, older patient age, and longer length of stay in the Intensive Care Unit.[6],[7]

The most common site of infection is the lung because the major route of exposure being inhalation, and in decreasing order, skin and soft tissue, brain, joints or bones.[6] Endobronchial inflammatory masses, pneumonia, lung abscess, pleural effusion, empyema, and cavitary disease with contiguous extension to deep structures are the clinical manifestations of pulmonary nocardiosis. Radiological manifestations are cavitating nodules, pneumonic infiltrates, pleural effusions, and the “halo sign.”[2] About half of all cases of pulmonary disease also involve infections in regions outside the lungs.[8] The most common region of dissemination is the brain, followed by skin, eye, bone, kidneys, and heart. In our report, the primary site of nocardial infection was the lung. Disseminated infection spreads to paravertebral structures from the lung by contiguity and led to paravertebral abscess which is associated with pleura. However, it spreads through hematogen to brain, eye, and skin. For the diagnosis of disseminated nocardiosis, it is necessary to isolate and identify the organism through the evaluation of respiratory secretions, skin biopsies, or aspirates from deep collections. Culturing bacteria is difficult due to the slow growth of the organisms. Molecular identification by amplification of a portion of the genome with polymerase chain reaction, followed by 16S rRNA gene sequencing, is presently the most reliable method for identification of Nocardia species.[9],[10]

Successful treatment of paraspinal abscess as a part of disseminated nocardiosis requires appropriate antibiotic therapy and drainage of the abscess. Using three-drug regimen comprising of susceptible antibiotics for long term is recommended. Patterns of antimicrobial susceptibility have varied among Nocardia species. Unless TMP-SMX is the favored treatment for nocardiosis, N. farcinica shows a high rate resistance to TMP-SMX and optimal antibiotic treatment should be decided by antimicrobial susceptibility testing. It is generally susceptible to minocycline, amikacin, moxifloxacin, and imipenem.[2] In addition, linezolid is an additional option for the treatment of N. farcinica infection that show good activity against all the Nocardia species.[11]

Antibiotic treatment must be started intravenously and can be changed after 3–6 weeks by oral regimen due to clinical and radiological responses. Therapy has to be continued for 12 months if the CNS is involved. Furthermore, tracing patients for at least 1 year to detect late relapses is recommended.[12]


   Conclusion Top


Clinical course in N. farcinica infection is potentially lethal because of its high resistance to antibiotics and its tendency to disseminate. Empirical monotherapy with TMP-SMX may not be sufficient because of the specific drug pattern of N. farcinica, so that using a combination regimen of imipenem and amikacin may be a more likely initial treatment for nocardiosis.

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 Top

1.
Wilson JW. Nocardiosis: Updates and clinical overview. Mayo Clin Proc 2012;87:403-7.  Back to cited text no. 1
    
2.
Crossley KB, Peterson PK. Nocardia species: Origin. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and Practice in Infectious Diseases. 8th ed., Vol. 1. New York: Churchill Livingstone; 2015. p. 3830-41.  Back to cited text no. 2
    
3.
Brown-Elliott BA, Brown JM, Conville PS, Wallace RJ Jr. Clinical and laboratory features of the Nocardia spp. based on current molecular taxonomy. Clin Microbiol Rev 2006;19:259-82.  Back to cited text no. 3
    
4.
Park SD, Kim HJ, Jang IH, Uh Y, Kim J, Yoon KJ, et al. First report of Nocardia farcinica bursitis in a patient with diabetes mellitus. Ann Lab Med 2014;34:252-5.  Back to cited text no. 4
    
5.
Goodfellow M, Williams ST. Ecology of actinomycetes. Ann Rev Microbiol 1983;37:189-216.  Back to cited text no. 5
    
6.
Coussement J, Lebeaux D, van Delden C, Guillot H, Freund R, Marbus S, et al. Nocardia infection in solid organ transplant recipients: A multicenter European case-control study. Clin Infect Dis 2016;63:338-45.  Back to cited text no. 6
    
7.
Roth A, Andrees S, Kroppenstedt RM, Harmsen D, Mauch H. Phylogeny of the genus Nocardia based on reassessed 16S rRNA gene sequences reveals underspeciation and division of strains classified as Nocardia asteroides into three established species and two unnamed taxons. J Clin Microbiol 2003;41:851-6.  Back to cited text no. 7
    
8.
Filice GA. Nocardiosis. In: Niederman MS, Sarosi GA, Glassroth J, editors. Respiratory İnfections. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2001. p. 457-66.  Back to cited text no. 8
    
9.
Pelaez AI, Garcia-Suarez Mdel M, Manteca A, Melon O, Aranaz C, Cimadevilla R, et al. Afatal case of Nocardia otitidiscaviarum pulmonary infection and brain abscess: Taxonomic characterization by molecular techniques. Ann Clin Microbiol Antimicrob 2009;8:11.  Back to cited text no. 9
    
10.
Uhde KB, Pathak S, McCullum I Jr., Jannat-Khah DP, Shadomy SV, Dykewicz CA, et al. Antimicrobial-resistant Nocardia isolates, United States, 1995-2004. Clin Infect Dis 2010;51:1445-8.  Back to cited text no. 10
    
11.
Byrne E, Brophy BP, Perrett LV. Nocardia cerebral abscess: New concepts in diagnosis, management, and prognosis. J Neurol Neurosurg Psychiatry 1979;42:1038-45.  Back to cited text no. 11
    
12.
Geiseler PJ, Andersen BR. Results of therapy in systemic nocardiosis. Am J Med Sci 1979;278:188-94.  Back to cited text no. 12
    

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Correspondence Address:
Yeliz Ozen
Merkezefendi State Hospital, Izmir Street No: 288, Yunusemre/Manisa 45020
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_178_17

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