History
    He presented with fever,cough, and chillness one week after kidney transplantation fot chronic renal failure and hypertension. He received immune-suppression therapy with Azathioprine, Cyclosporin, and Prednisolone. Eight days after transplantation, acute borderline rejection developed and solumedrol pulse therapy wa performed.

Findings
* Frontal radiography (10 days after transplantation) showed several small nodules and bilateral pleural effusions.
* Frontal radiography (21 days after transplantation) showed increased number and size of nodules with ill-defined and irregular spiculated border on both lung fields and increased amount of pleural effusions.
* CT scan (21 days after transplantation) showed consolidation with surrounding ground-glass opacity in posterior segment of right upper lobe and multiple nodules with random distribution.
* Follow-up CT scan (40 days after transplantation) showed improved findings with decreased number and size of nodules and improved consolidation on right upper lobe. Note several nodules were replaced by smaller thin-walled cavitary lesions.

Discussion
    Nocardiosis is a rare infectious disease caused by nocardia species, which frequently involves patients with systemic disease such as diabetes, patients in corticosteroid therapy, organ transplantation recipients and immunocompromised patients. Nocardiosis in organ transplantation recipients occurs more frequently in patients with zathioprine/prednisolone
regimen than patients with cyclosporin/prednisolone regimen.  50-85% of nocardiosis is caused by Nocardia asteroides, which manifests as severe pulmonary infection or systemic infection. The causative organism is introduced via respiratory tract most frequently and the infection is localized to respiratory system in 75%. Skin and central nervous system are the
other frequent site of involvement.
    Pulmonary nocardiosis is caused by inhalation or aspiration of the organism from soil or water and cause suppurative response, granulomatous response or combination within the tissue involved. Infection begins as pneumonia in 75%,  and spread hematogenously in 50%. Clinical symptom is variable including fever above 38 0C, cough, weight loss and malaise.
Radiographically, consolidation, large irregular nodules, cavitation and pleural effusion are most frequent findings. Masses, reticular opacities and lymphadenopathy are also reported. CT findings consist of consolidation with internal low attenuation area (33%-80%). infiltration, cavitation (33%), one or multiple pulmonary nodules (83%), pleural effusion (50-80%) and chest wall extension (29-80%). In a immunocompromised host who is in corticosteroid therapy and shows these findings, pulmonary nocardiosis should be included in the differential diagnosis in addition to bacterial pneumonia, tuberculosis, fungal infection, actinomycosis, bronchogenic carcinoma, Cytomegalovirus pneumonia, and Pneumocystis
carinii pneumonia. Drug of choice is sulfisoxazole or trimethorprime-sulfamethoxazole. Amikacin, imipenem, and minocycline are also reported to be effective. Duration of therapy is 6-12 months usually. Drainage is necessary in cases of abscess formation.

References
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2. Julie A, Buckley AR, Padhani, and Janet EK. CT Features of Pulmonary Nocardiosis. J of Comput Assist Tomogr 1995;19(5):726-732
3. G. Pourmand SA, Jazaeri A, Mehrsai S, et al. Nocardiosis: Report of Four Cases in Renal Transplant Recipients. Transplant Proceed 1995;27(5):2731-2733
4. Yoon HK, Im JG, Ahn JM, Han MC. Pulmonary Nocardiosis: CT Findings. J of Comput Assist Tomogr 1995;19(1);52-55
5. Raj B, Uttamchandani GL, Daikos RR et al. Nocardiosis in 30 Patients with Advanced Human Immunodeficiency Virus Infection: Clinical Features and Outcome. Clinic Infect Dis 1994;18:348-353