Journal of Clinical and Experimental Transplantation
Open Access

Bacterial

In heart transplant patients, bacterial infections have similar clinical manifestations commonly observed in other patient populations. However, clinical signs could also be subtle or absent (e.g., afebrile). They’re the foremost frequent sort of infections during this setting, reaching up to 50% of all infections. The foremost common is pulmonary infections followed by bacteremias, mediastinal, and skin infections. Staphylococcus aureus-predominantly methicillin-resistant can cause SSTI, ventilator-associated pneumonia, mediastinitis, CRBSI, other sorts of bacteremia, and osteomyelitis. In contrast, coagulasenegative Staphylococcus is more commonly related to CRBSI. Among Gram-negative bacteria, Pseudomonas aeruginosa is common, usually of pulmonary origin. Escherichia coli are the first causal organism of UTIs. Extended-spectrum β-lactamase (ESBL)-producing Klebsiella pneumoniae, Escherichia coli, Klebsiella oxytocin, and Citrobacter freundii also are found in 2.2% of heart transplant recipients.

Myocardia species are well recognized as an opportunistic pathogen during this setting. Although relatively rare in heart transplant recipients (frequency 90 days) has been more recently recognized related to receipt of sirolimus in conjunction with tacrolimus for refractory rejection or cardiac allograft vasculopathy. The foremost common clinical presentation for aspergillosis includes fever, cough, and single or multiple pulmonary nodules. Extra pulmonary manifestations include spondylodiscitis, infective endocarditis, mediastinitis, endophthalmitis, and brain and cutaneous abscesses. Dissemination tends to affect the CNS during a good proportion of the cases. Mucormycosis is that the second most frequent mold affecting heart transplant recipients. Macro, along side other non-Aspergilla’s molds (e.g., Scedosporium, Ochroconis gallopava), are related to disseminated infections, CNS involvement, and poorer outcomes. Pneumocystis jiroveci (PCP) although with a marked reduction in incidence with the introduction of universal prophylaxis is still a big pathogen and cases may occur late after heart transplant. Cryptococci’s, although infrequent among SOT patients, has its higher incidence in heart transplant recipients. Usually, its manifestations present late and affect the lungs and therefore the CNS predominantly. Histoplasmosis and coccidioidomycosis occurred typically within the first year after transplant. Antigenuria was the foremost sensitive diagnostic assay in SOT for histoplasmosis. Finally, Candida infections are a crucial explanation for morbidity and mortality also. Rate of colonization is above within the general population.

Viral

CMV infection is of critical importance among SOT. In heart transplant recipients, CMV has been inconsistently related to cardiac allograft vasculopathy. Furthermore, CMV results in upregulation of pro-inflammatory cytokines, increase procoagulant response, left ventricular dysfunction, allograft rejection, and a rise of opportunistic infections. The best risk for developing CMV disease is CMV-negative recipients of CMV-positive organs (D+/R−), followed by D+/R+ and D−/R+. A clinical report estimated that the speed of infections in heart transplant ranges between 9% and 35%, and disease is present in around 25% of patients. The clinical manifestations aren’t unique to heart transplant recipients and include a CMV syndrome (fevers, myalgia, arthralgia, malaise, leukopenia, and thrombocytopenia). CMV-associated end-organ injury during this setting includes most often pneumonitis and gastrointestinal disease. Other manifestations comprise myelosuppression, hepatitis, and pancreatitis. In contrast to the high frequency observed in AIDS patients, chorioretinitis in heart transplant patients is comparatively rare.

Chronic hepatitis without an identifiable cause should prompt testing for hepatitis E virus (HEV). Chronic HEV infection results in the rapid development of fibrosis. HEV testing should be through with RNA PCR thanks to a delay within the antibody response. We recommend decreased immunosuppression and ribavirin therapy for 3 months.

Parasitic

Cardiac transplant itself is one the predictors for development of toxoplasmosis. Other associated risk factors include negative serum status before transplant, diagnosis of cytomegalovirus (CMV) infection, and high-dose prednisone. Toxoplasmosis are often transmitted by the donor heart (D+/R−, especially during the primary 3 months) or can reactivate from the recipient (>3 months). Most of the infections developed during the primary 6 months post-transplant and are predominantly primary infections. About 22% of infected patients had a disseminated infection carrying an estimated 17% mortality. Toxoplasmosis can manifest otherwise with myocarditis, encephalitis, pneumonitis, or chorioretinitis. Diagnosis requires identification of tissue cysts surrounded by an abnormal inflammatory response, detection of Toxoplasma DNA in body fluids by PCR, or positive Toxoplasma-specific immunohistochemistry in affected organs. Posttransplant serological tests aren’t helpful for diagnosis and should be misleading since results may change or not any matter the presence of toxoplasmosis. The well-liked treatment regimen may be a combination of pyrimethamine with sulfadiazine.