Description

Tuberculosis (TB) remains an important public health problem with pulmonary TB being the most common form.1 However, there has been a significant rise in the extrapulmonary TB cases particularly in immunosuppressed patients. A woman in her third decade was admitted with reports of fever and right upper quadrant pain. The patient had underwent live-related renal allograft transplantation 2 months back with basic disease likely obstructive uropathy secondary to renal stone disease. She was maintained on triple immunosuppression with tacrolimus in a dose of 2 mg two times per day, methylprednisolone (7.5 mg/day) and mycophenolate mofetil (1 gm two times per day) with a stable post-transplant creatinine of 1 mg/dL. One month post-transplant, she developed extra pulmonary TB (pleural) and was started on levofloxacin-based antitubercular therapy (ATT), and mycophenolate mofetil was withheld. There was no history of TB in the pretransplant period and no history of contact exposure could be elicited. The patient and her donor were evaluated for latent TB pretransplant with history, chest X-ray and tuberculin skin testing as per our centre protocol that was normal. One month postinitiation of ATT, currently she presented with high-grade fever and right hypochondriac pain for 2 weeks duration. On examination, she was febrile with stable vitals and had tenderness in right hypochondrium. Laboratory evaluation revealed haemoglobin of 81 g/L, total leucocyte count of 5.8×10⁹/L, serum creatinine of 4.7 mg/dL, erythrocyte sedimentation rate of 60 mm/hour, total bilirubin of 0.8 mg/dL with aspartate transaminase of 13 U/L and alanine transaminase of 9 U/L. Urine analysis revealed field full of pus cells with sterile culture. Ultrasonography and CT abdomen revealed subcapsular perihepatic collection adjacent to the right lobe of liver measuring 2.1 cm with mild right-sided pleural effusion (figure 1A). Then 15 cc of pus was aspirated under ultrasound guidance and the patient was empirically started on meropenem and metronidazole. Routine bacterial culture of the pus was negative for bacteria/fungus, however, Ziehl-Neelson staining revealed >10 acid fast bacilli (AFB) per high power field (figure 1B) with Gene Xpert positive and no rifampicin resistance detected. Allograft biopsy was done in view of recent deterioration of renal function that revealed graft tubulointerstitial nephritis and no evidence of rejection. Urine for bacterial culture revealed no growth and was negative for PCR for Mycobacterium tuberculosis. The patient was continued on four drug ATT with isoniazid, levofloxacin, pyrazinamide and ethambutol. Intravenous meropenem was continued for 2 weeks. Gradually, serum creatinine shows a declining trend with nadir of 1.7 mg/dL at discharge. Repeat ultrasonography showed decrease in the size of liver abscess.

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Figure 1

(A) Axial contrast-enhanced CT demonstrates subcapsular perihepatic collection adjacent to the right lobe of liver. (B) Ziehl-Neelson staining of pus obtained from the abscess demonstrating nuerous acid fast bacilli stained in red against a background of pus cells.

TB is one of the leading infections in the renal transplant recipients in developing countries with a incidence in various studies varying from 10% to 15%.2 Renal allograft recipients have a high frequency of extrapulmonary TB presumably due to the chronic immunosuppression facilitating haematogenous spread to single or multiple non-pulmonary sites. It can occur either from donor kidney or from endogenous reactivation of latent TB infection or from acquiring new M. tuberculosis infection. Careful history of exposure and risk factors should be obtained in patients with high index of suspicion of TB. Tuberculin skin test and IFN-γ release assays are routinely used for screening for latent TB infection in donor and recipient prior to transplant.

Tubercular liver abscess in renal transplant recipients is rare and only few cases have been reported. It is usually secondary to primary pulmonary or gastrointestinal involvement and isolated hepatic involvement is rare. High-grade fever, right hypochondrial pain, hepatomegaly, loss of weight and appetite are the common clinical symptoms and signs of tubercular liver abscess. Diagnosis of tubercular abscess is difficult due to the low yield of Ziehl-Neelsen staining and long turn around time taken for tubercular cultures. Gene Xpert testing has a higher sensitivity as compared with AFB staining in diagnosis of extrapulmonary TB and may be used as replacement test of non-respiratory samples.3 The optimal duration of ATT in renal transplant recipients has not been defined clearly and varies from 9 to 18 months based on the regimens used.4 Rifampicin can induce metabolism of steroids and calcineurin inhibitors (CNIs) and increase the risk of rejection. Hence, close monitoring of drug levels is required and the dose of CNIs may have to be increased twofold to fivefold to overcome this effect. Levofloxacin-based non-rifampicin antituberculous therapy has shown to be equally effective in resource-limited settings.5 Percutaneous drainage and ATT remain the main treatment options of tubercular liver abscess.

Our patient presented with extrapulmonary TB (pleural and hepatic) early after renal transplant and was managed with levofloxacin-based ATT and percutaneous drainage. High index of suspicion and knowledge of unusual presentations of TB in solid-organ transplant recipients are required for early diagnosis and management to prevent morbidity and mortality.