Outcome after cardiac transplantation has improved considerably in recent decades, with 50% of patients surviving over 9 years.1
A consequence of this is an increase in the number of individuals in the community requiring long-term antirejection therapy, and an increased vulnerability to secondary infection.2
Post-transplant maintenance immunosuppression commonly comprises triple therapy, with an antiproliferative agent, such as mycophenolate mofetil or azathioprine, a calcineurin inhibitor such as ciclosporin or tacrolimus and a steroid such as prednisolone. It is often possible to taper or discontinue steroid therapy in patients on long-term immunosuppression with no features of acute rejection.2
Infectious complications after heart transplantation are common, with 0.6 episodes per patient occurring over a mean time of 4.5 years in a recently analysed cohort.3
Gram-positive bacteria, Cytomegalovirus, fungi, P jiroveci
and Nocardia have all been implicated.3
In one cohort study, the incidence of PCP up to 1 year after transplantation was 3.6%,4
although more recent studies have suggested that this incidence has fallen.3
Consequently, prophylaxis for PCP with trimethoprim-sulfamethoxazole in the immediate post-transplantation period has long been advocated.5
Late presentation of PCP after solid organ transplantation, however, appears to be substantially less common. After follow-up of 32 757 renal transplant recipients in the United States, the latest case of PCP observed was in the second year after transplantation.6
In heart transplant patients, the longest interval between transplantation and the development of PCP in one cohort study was 781 days.5
PCP is an opportunistic infection of the lung parenchyma caused by the fungus Pneumocystis jiroveci
. In patients without HIV it commonly presents with acute-onset respiratory failure and bilateral perihilar infiltrates on the plain chest radiograph.7
Confirmation of the diagnosis requires identification of the organism in a relevant sample, typically by induced sputum or BAL. Identification may be achieved by conventional or immunofluorescence antibody staining, or by PCR assay. Sensitivity and specificity for real-time PCR has been reported as 94–100% and 86–100%, respectively.8
Mortality from PCP in HIV-negative patients is between 30% and 60%.8
Among HIV-negative patients admitted to an intensive therapy unit, outcome is even poorer, with one study quoting a 1-year mortality of 80%.9
Treatment regimens for PCP typically comprise a combination of antimicrobials and corticosteroids. The first choice antimicrobial regime is trimethoprim-sulfamethoxazole (co-trimoxazole) in doses of 15–20 mg/kg and 75–100 mg/kg, respectively.8
Alternative therapies include pentamidine, primiquine plus clindamycin or atovaquone.8
Corticosteroids have been shown to reduce mortality in HIV-infected patients with an alveolar-arterial oxygen gradient greater than 35 mm Hg.7
There is less evidence for HIV-negative patients, but one study suggested adjunctive corticosteroids reduce the duration of mechanical ventilation and ICU stay.10
This is, to our knowledge, the first report in the literature of a case of PCP occurring over 8 years after cardiac transplantation. Indeed, the patient in question was at relatively low risk for PCP given the absence of a calcineurin inhibitor in his immunosuppressive regimen. We recommend, therefore, that physicians maintain a high degree of vigilance for the presence of PCP in patients who have undergone heart transplants, even if many years previously.
- Long-term survival after cardiac transplantation is improving.
- Patients with cardiac transplants are likely to make up an increasing proportion of patients treated in non-specialist centres.
- Physicians should maintain a high index of suspicion for Pneumocystis jiroveci pneumonia in patients presenting with respiratory symptoms after cardiac transplantation.