| 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 Jul 17];11:583-6. Available from: http://www.sjkdt.org/text.asp?2000/11/4/583/36647
| Introduction|| |
Fungal infections are not uncommon in organ transplant recipients and typically present between 1-12 months following transplantation. ,,
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.  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. 
| Case Report|| |
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 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|| |
There are between 500-1000 new cases of nocardiosis diagnosed annually in the USA.  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 is and Nocardia caviae.  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. 
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. 
The clinical manifestations of nocardiosis are extremely variable.  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.  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.  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. 
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.  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.  Amikacin, the best-established alternative drug for parental use, can be given in doses of 5-7.6 mg/kg every 12 hours. 
Response may be slow and therapy must be continued for at least one year in transplant recipients receiving immunosuppressive agents to avoid relapses. 
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|| |
We thank Ms. Regina Stephen for typing this manuscript.
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K V Srinivas
Department of Nephrology, King Fahad Central Hospital, P.O. Box 204, Gizan
[Figure - 1]