Renal transplant with bronchiolitis obliterans organizing pneumonia (BOOP) attributable to tacrolimus and herpes simplex virus (HSV) pneumonia.

BACKGROUND: Solid organ transplants (SOTs) may be complicated by a wide variety of infectious and noninfectious pulmonary disorders. Transplant patients receive immunosuppressive drugs to prevent rejection, but these drugs also predispose them to infection. Because immunosuppressive therapy impairs T-lymphocyte function, ie, cell-mediated immunity, such therapy, not surprisingly, predisposes patients to intracellular pulmonary pathogens. Community-acquired pneumonia (CAP) in patients with SOT usually involves one of the common typical or atypical bacterial CAP pathogens infecting immunocompetent hosts. The most frequent intracellular CAP pathogens in SOTs during immunosuppressive therapy are viral, eg, cytomegalovirus (CMV), respiratory syncytial virus (RSV), and herpes simplex virus (HSV). In addition, intracellular fungal pathogens are also common in patients with SOTs during immunosuppressive therapy, eg, Pneumocystis (carinii) jiroveci pneumonia (PCP). In addition, a variety of noninfectious disorders are not uncommon in patients with SOTs, including bronchiolitis obliterans organizing pneumonia (BOOP). Bronchiolitis obliterans organizing pneumonia may be associated with a variety of infectious agents, or may be attributable to drugs, including some immunosuppressive agents.
METHODS: The clinical approach to CAP in patients with SOTs may be based on the appearance of the chest x-ray (CXR) or chest computed tomography scan, combined with the degree of hypoxemia (ie, the A-a gradient). Patients with SOTs and with a normal or nearly normal CXR and a high degree of hypoxemia (A-a gradient, >35) most often have an early viral pneumonia, eg, CMV or early PCP. If the CXR reveals bilateral patchy interstitial infiltrates and severe hypoxemia, the differential diagnosis is limited to moderate or severe viral pneumonia or PCP. Patients with SOTs and presenting with diffuse infiltrates and mild to moderate hypoxemia (A-a gradient, <35) are usually prone to noninfectious disorders, eg, congestive heart failure, pulmonary embolism, or drug-induced pneumonias. In patients with SOTs and CAP with focal or lobar infiltrates, the distribution of pathogens is the same as in immunocompetent hosts, ie, either a bacterial or atypical CAP pathogen. CASE REPORT AND
CONCLUSION: A renal transplant patient developed bilateral patchy interstitial infiltrates with severe hypoxemia during hospitalization. The most likely differential diagnostic possibilities included PCP and BOOP. Bronchoalveolar lavage was performed to rule out PCP, and indicated cytopathic effects diagnostic of HSV pneumonia. Lung biopsy pathology confirmed the diagnosis of BOOP. In reviewing the patient's medications, we surmised that tacrolimus may have caused BOOP. The tacrolimus was discontinued, and the patient received acyclovir for HSV pneumonia.