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Adverse Occurrence type:
Very rare occurrence. In the clusters described here, two out of 5 recipients and 1 out of 2 recipients became infected. Serostatus and other details of all recipients were not mentioned hence difficult to assess.
Time to detection:
Ten days to signs and symptoms of hepatitis in liver recipient; less than 10 days to histological diagnosis in pre-implantation kidney and liver biopsy of donor organ.
Alerting signals, symptoms, evidence of occurrence:
Two sequential clusters linked by re-donation of transplanted kidney. Donor A (HSV-2 IgG positive, IgM negative and HSV DNA negative in blood) donated heart and lung, liver, kidney and kidney-pancreas. Heart-lung recipient who was seronegative for HSV received CMV prophylaxis and did not develop any HSV-related complications. The liver recipient had pre-existing HSV-1 and HSV-2 antibodies and received CMV prophylaxis; despite of all this, they developed extensive skin rash, fever, abdominal pain, hepatitis but responded to antiviral treatment. Simultaneous pancreas-kidney recipient suffered myocardial infarction (POD 1) and died on POD 9 (donor B). Following confirmation of brain death, the lungs and recently transplanted kidney were donated. Donor B's preimplantation kidney and non-utilised liver revealed features (coagulative parenchymal necrosis, nuclear inclusions) consistent with HSV-2 infection, confirmed by IHC. Both kidney and lung recipients were seropositive for HSV-1 and HSV-2 but developed HSV-2 viraemia and responded to pre-emptive treatment.
Demonstration of imputability or root cause:
Viral strains from 3 recipients were genotyped, with results showing high degree of similarity. This alone does not prove common source or donor imputability because there is high degree of homology between HSV strains circulating in certain geographical locations; molecular analysis has to be meticulous, comparing to other contemporaneous sequences. HSV-2 was demonstrated in the kidney (pre-implantation) and liver tissue (not transplanted) of donor B, proving donor-derived transmission of infection.
Suggest new keywords:
coagulative parenchymal necrosis; nuclear inclusion; skin rash; CSF; fever; hepatitis; liver transplant; kidney transplant; SPK transplant; nuclear inclusions
- Renal allograft re-use and herpetic re-infection. Setyapranata S et al. Nephrology. 20 Suppl 1:17-21, 2015 Mar. - Herpes simplex virus-2 transmission following solid organ transplantation: Donor-derived infection and transplantation from prior organ recipients. Transpl Infect Dis. 2017 Oct;19(5)
clone for kidney-pancreas; liver; kidney; both papers here refer to the same cluster.
Expert comments for publication:
Primary infection from the allograft causes clinical disease, it is frequently severe and associated with a poor outcome. In all available reports of possible donor-derived transmission of HSV infection, viraemia has not been demonstrated in donor blood; HSV is neurotropic, with existing evidence that viraemia can occur in debilitated individuals such as ICU patients. Negative PCR in donor's blood does not exclude possible donor-derived infection.