1 Service de Transplantation Rénale 2 Service de Chirurgie Vasculaire 3 Service de Chirurgie Urologique 4 Service de Radiologie 5 Service de Médecine Interne et Maladies Infectieuses Hôpital Pellegrin Bordeaux France
Case report
A 50-year-old man with familial polycystic hepatorenal disease started chronic haemodialysis in 1994. His first kidney transplantation in 1994 was rapidly complicated by acute rejection and thrombosis of the graft vein, leading to his return to haemodialysis and graft removal 2 months later. A second kidney was grafted in the left iliac fossa in September 1999 with return of diuresis and recovery of complete renal function. Immunosuppressive therapy combined tacrolimus (FK506), mycophenolate mofetil, and methylprednisolone. When he was discharged 3 weeks later, his clinical, biological, and sonographic evaluations were normal.
Three weeks later (6 weeks post-transplantation), the patient was hospitalized for 4 days for an isolated fever (37.538°C). Blood cultures, polymerase-chain reaction search for cytomegalovirus and herpes simplex viruses, and serological assays for antibodies to Legionella, Salmonella, Aspergillus and Candida were negative. Urine bacteriological and virological analysis, and stool parasitological tests were also negative. Chest X-ray and graft Doppler sonography were normal. Apyrexia returned spontaneously.
Eight days later, the patient was readmitted with a high fever (39°C) and pain in the left iliac fossa. The graft was functioning well; bacteriological and virological analysis remained negative, but lymphopenia (400/mm3) with diminished CD4+ cell (100/mm3) without leukocytosis was noted. An abdominal computed tomography (CT) scan was carried out, showing an abscess at the lower pole of the graft, followed 4 days later, by a magnetic resonance imaging (MRI) angiography of the graft (Figure 1) and standard angiography (Figure 2
).
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Fever and pain in the left iliac fossa are related to perirenal infection. Vancomycin and imipenem were prescribed for suspected infection of a haematoma and apyrexia was obtained within 48 h. The MRI angiography (Figure 1) confirmed the presence of the perirenal abscess and showed an aneurysm of the graft artery at the level of its anastomosis with the left external iliac artery, which were confirmed by classical angiography (Figure 2
). We diagnosed a perirenal abscess and mycotic aneurysm in a renal transplant recipient.
Surgery was performed to drain the abscess, resect the aneurysm, and reattach the graft artery. The postoperative evolution was unremarkable. Graft function was preserved, pain and fever disappeared. Cultures of abscess, aneurysm wall, and intra-aneurysm thrombus specimens obtained during surgery grew to Nocardia nova (Figure 3) susceptible to ampicillin, imipenem, amikacin, erythromycin, and cefotaxime, but resistant to trimethoprimsulphamethoxazole, minocycline, ciprofloxacin and tobramycin. Vancomycin was stopped, and intravenous imipenem (1.5 g/day) was continued alone for 8 weeks with good tolerance. It was replaced by oral roxithromycin (300 mg/day), prescribed for 7 months, for a total antibiotic treatment of 9 months. A chest radiographs and cerebral MRI eliminated the possibility of secondary localizations. MRI angiography of the graft 3 months after surgery was normal. At present, 8 months after CT diagnosis, the patient has normal renal function and is doing well.
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The role of cellular immunity in host defence is well known and takes place in two phases: local macrophages and polymorphonuclear leukocytes inhibit the bacteria, then specific T cells destroy them. The elevated incidence of this type of infection in transplant recipients and HIV-infected individuals is explained by the preponderant role of cellular immunity. The role of humoral immunity is unknown.
Nocardiosis, an opportunistic infection caused by Nocardia, affects renal transplant recipients at an incidence estimated at 25%, depending upon the series [1,3,4,7]. Nocardia infections have two particular characteristics: the ability to spread to all organs and the tendency to relapse and progress despite appropriate therapy. The clinical manifestations are diverse and non-specific. Pulmonary involvement is the revealing sign for 80% of the cases and central nervous system involvement, usually by secondary dissemination, remains an indicator of poor prognosis with morbidity/mortality exceeding 75% [1,2,4]. Cutaneous involvement (abscess, ulceration, pyoderma) is primary in more than 90% of the patients, with secondary lymphangitis and mycetoma when chronic. Even though skin symptoms are secondary to haematogenic dissemination in only 2% of the cases, cutaneous involvement should be considered secondarily and the search for a deep focus, specifically the brain, is mandatory. To a lesser degree, the infection affects the retinae, joints, and heart, and, more rarely, the pancreas, liver and spleen. Several retroperitoneal or psoas abscesses have been reported.
Sulphonamides remain the reference treatment, especially trimethoprimsulphamethoxazole [4]. The efficacy of other antibiotic classes have been demonstrated, but several cases of resistance to tetracyclines and/or sulphonamides have been reported, as in our patient. Alternative agents (amikacin, imipenem, third-generation cephalosporins, minocycline, etc.) are successful in treating patients with nocardiosis. Nocardia nova susceptibility to antibiotics varies but remains constant for ampicillin and erythromycin. No clinical data determined the superiority of this agents over sulphonamides, either alone or in combination. The recommended duration of treatment is 6 months but can be extended to 12 months for immunocompromised patients or when there is cerebral involvement. This type of infection seems to occur less frequently in centres that prescribe anti-pneumocystosis prophylaxis with trimethoprim-sulphamethoxazole. In our renal transplantation unit, although such prophylaxis is not used, it was the first case of proven nocardiosis in a series of 1550 renal transplant recipients.
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