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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2000  |  Volume : 11  |  Issue : 4  |  Page : 583-586
Cerebral Nocardiosis in a Renal Transplant Recipient: A Case Report


Department of Nephrology, King Fahad Central Hospital, Gizan, Saudi Arabia

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   Abstract 

A 53-year-old renal allograft recipient developed nocardial cerebral abscess. It manifested clinically with encephalitis, polycythemia, convulsions, syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and a space-occupying lesion presenting as multiple ring shadows in the left fronto-parietal lobe on computerized tomography (CT scan) of the brain. The initial clinical presentation included an afebrile patient with headache, convulsions and altered sensorium with no lateralising neurological deficit. He deteriorated later and developed coma with right hemiplegia. Purulent material was drained through left frontal craniotomy, and the culture confirmed the presence of nocardial infection. Despite aggressive therapy, the patient died a few days later. We conclude that high degree of early suspicion, diagnosis and prompt treatment should be stressed.

Keywords: Cerebral nocardiosis, Renal transplantation.

How to cite this article:
Srinivas K V, Freigoun O S, Rabie A, Want MA, Bhakthavatsalam, Udayashanker. Cerebral Nocardiosis in a Renal Transplant Recipient: A Case Report. Saudi J Kidney Dis Transpl 2000;11:583-6

How to cite this URL:
Srinivas K V, Freigoun O S, Rabie A, Want MA, Bhakthavatsalam, Udayashanker. Cerebral Nocardiosis in a Renal Transplant Recipient: A Case Report. Saudi J Kidney Dis Transpl [serial online] 2000 [cited 2019 May 21];11:583-6. Available from: http://www.sjkdt.org/text.asp?2000/11/4/583/36647

   Introduction Top


Fungal infections are not uncommon in organ transplant recipients and typically present between 1-12 months following transplantation. [1],[2],[3]

In immunosuppressed patients, central nervous system fungal infections are characterized by subacute onset with subtle non-specific symptoms and signs, and often lack of associated systemic manifestations. [4] This necessitates a high degree of suspicion, thorough investigation and early institution of proper treatment. Surgical intervention and reduction of immuno­suppressive drugs may be required. Early diagnosis and treatment improves outcome. [5]


   Case Report Top


A 53-year-old renal allograft recipient was admitted to our hospital seven months post­transplantation with complaints of non­localizing, throbbing, generalized headache, tonic-clonic convulsions and altered sensorium of recent onset. He was receiving triple drug immunosuppression with cyclosporine, pred­nisolone and azathioprine. On admission, he was afebrile with high BP of 200/130 mm Hg. He was slightly confused, drowsy with bursts of incomprehensible speech. There was no sensory or motor deficit and no signs of meningeal irritation were evident. Conjunctivae were congested and fundus examination was normal.

Laboratory investigations showed elevated hemoglobin of 194 gm/L, leucocytosis 11,400 cells/pL, serum glucose of 11.3-13 mmol/L and severe hyponatremia at 102­108 mmol/L. Renal functions were within normal limits. Chest x-ray showed patchy consolidation of left lung base. The initial computerized tomography (CT) scan of the brain showed doubtful hypodense areas in left frontal lobe [Figure - 1]. Routine bacterial cultures were negative. Serum cytomegalo­virus (CMV) antibody titers were normal. Lumber puncture was not done as the patient refused to consent for it.

At this stage, he was managed with anti­hypertensive medications, antibiotics, fluid restriction, diuretics and intravenous saline infusions. Patient showed a subtle but definite clinical improvement. He decided against medical advice only to be readmitted two weeks later in a comatose state with a clear right-sided hemiplegia.

Repeat CT scan showed multiple ring shadows in the left fronto-parietal lobe, larger in size compared to earlier scans with severe brain edema, gross midline shift and a fresh hypodense lesion in brain stem.

Left frontal craniotomy was performed, abscesses were drained with enucleation. Pus smear showed gram positive weakly acid fast, branching  Nocardia asteroides Scientific Name Search  species. The patient was managed with intravenous mannitol, trimithoprim/sulfa­methoxazole and a decrease of the immunosuppressive drugs. Unfortunately his clinical condition deteriorated and he became ventilator dependent. He expired in the intensive care unit three days later.


   Discussion Top


There are between 500-1000 new cases of nocardiosis diagnosed annually in the USA. [6] Nocardial infection occurs through inhalation of fungal spores. In about 85% of these cases infection is caused by Nocardia asteroides, the remaining 15% are caused by  Nocardia brasiliensis Scientific Name Search is and Nocardia caviae. [7] Patients receiving steroids and/or chemotherapy, are highly susceptible. There is increased incidence of nocardiosis in patients suffering from bronchial asthma, malignancy or chronic pulmonary granulo­matous conditions. [8]

In organ transplant recipients, the non­specific and subtle clinical presentation delays a definite diagnosis and institution of prompt treatment, thereby often resulting in increased morbidity and mortality. [9]

The clinical manifestations of nocardiosis are extremely variable. [7] It usually presents as a respiratory illness with fever, malaise and unproductive cough. Lung lesions may present as diffuse fibrino-purulent pneumonia, resembling bacterial processes, or as single/multiple abscess cavities. [5] Patients can develop skin abscesses and joint infections. In about 20% of patients, infection may spread to the brain and manifest as well-defined localized abscess cavities. [10] Rarely, the cerebral lesions may be in the form of meningoencephalitis resulting in a more chronic clinical picture with headache, confusion and lethargy without well-defined localizing signs. [11]

Our patient had initial localized encepha­litis affecting frontal lobes presenting as abnormal behavioral pattern, convulsions and syndrome of inappropriate anti-diuretic hormone secretion. There was no focal neurological deficit and nuchal rigidity was absent. Later, with spread of the infection, he became comatosed and hemiplegic. In early stages, CT scan of the brain may show well-developed focal or diffuse lesions, which aid in the diagnosis.

Most cases of cerebral nocardiosis are fatal. [12] Therapy is initiated with intravenous trimithoprim/sulfamethoxazole and continued with oral therapy using one double strength tablet of the same medication twice a day. Minocycline is the best-established alternative oral drug and should be given in doses of 100-200 mg twice a day. [13] Amikacin, the best-established alternative drug for parental use, can be given in doses of 5-7.6 mg/kg every 12 hours. [14]

Response may be slow and therapy must be continued for at least one year in transplant recipients receiving immunosup­pressive agents to avoid relapses. [5]

Development of fever and headache in a transplant recipient, with CT scan of the brain showing circumscribed localized/ diffuse lesions should alert the treating nephrologist to thoroughly investigate and aggressively manage these patients. Delayed diagnosis and therapy carries poor prognosis.


   Acknowledgment Top


We thank Ms. Regina Stephen for typing this manuscript.

 
   References Top

1.Arduino RC, Johnson PC, Miranda AG. Nocardiosis in renal transplant recipients undergoing immunosuppression with cyclosporine. Clin Infect Dis 1993;16:505-­12.  Back to cited text no. 1  [PUBMED]  
2.Pourmand G, Jazaeri SA, Mehrsai A, Kalhori S, Afshar K. Nocardiosis: report of four cases in renal transplant recipients. Transplant Proc 1995;27(5):2731-3.  Back to cited text no. 2    
3.Reddy SS, Holley JL. Nocardiosis in a recently transplanted renal patient. Clin Nephrol 1998;50(2):123-7.  Back to cited text no. 3    
4.Hooper DC, Pruitt AA, Rubin RH. Central nervous system infection in the chronically immunosuppressed. Medicine 1982;61:166-88.  Back to cited text no. 4  [PUBMED]  
5.King CT, Chapman SW, Butkus DE. Recurrent nocardiosis in a renal transplant recipient. South Med J 1993;86:225-8.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Beaman BL, Burnside J, Edwards B, Causey W. Nocardial infections in the United States, 1972-1974. J Infect Dis 1976;134:286-9.  Back to cited text no. 6  [PUBMED]  
7.Curry WA. Human nocardiosis. A clinical review with selected case reports. Arch Intern Med 1980;140:818-26.  Back to cited text no. 7    
8.Palmer DL, Harvey RL, Wheeler JK. Diagnostic and therapeutic considerations in Nocardia asteroides infection. Medicine Baltimore 1974;53:391-401.  Back to cited text no. 8  [PUBMED]  
9.Bach MC, Adler JL, Breman J, et al. Influence of rejection therapy on nocardial infections in renal transplant recipients. Lancet 1973;1:18.  Back to cited text no. 9    
10.Frazier AR, Rosenow EC 3d, Roberts GD. Nocardiosis. A review of 25 cases occurring during 24 months. Mayo Clin Proc 1975;50:657-63.  Back to cited text no. 10    
11.Clinical neurology. AB Baker & Associate editor: LH Baker, Revised edition, Harper & Row Publishers 1982;(2)18:94-96.  Back to cited text no. 11    
12.Filice GA, Simpson GS. Management of nocardial infections, current clinical topics in infections diseases. Remington JS, Swartz MN (eds), New York, McGraw-Hill, 1984;5:49-64.  Back to cited text no. 12    
13.Petersen EA, Nash ML, Mammana RB, Copeland JG. Minocycline treatment of pulmonary nocardiosis. JAMA 1983;250: 930-2.  Back to cited text no. 13  [PUBMED]  
14.Wallace RJ Jr, Steele LC, Sumter G, Smith JM. Antimicrobial susceptibility patterns of nocardia asteroides. Anti­microb Agents Chemother 1988;32:1776-­9.  Back to cited text no. 14    

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Correspondence Address:
K V Srinivas
Department of Nephrology, King Fahad Central Hospital, P.O. Box 204, Gizan
Saudi Arabia
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PMID: 18209349

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    Abstract
    Introduction
    Case Report
    Discussion
    Acknowledgment
    References
    Article Figures
 

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