Herpes simplex virus 2 (HSV-2)

Donor A died of hypoxic ischaemic brain inlury with no evidence or history of recurrent HSV 2 infection. Retrospective testing revealed positive IgG, negative IgM and negative PCR for HSV 2. The liver recipient of donor A was investigated in the light of the fidings. Recipient had serological evidence of HSV 1and HSV 2 infection prior to transplant (positive IgG) and was also receiving Valganciclovir (VGCV) prophylaxis for CMV. Despite of these, there was viraemia, disseminated skin rash and hepatitis (ALT 236 U/L, AST 72 U/L, GGT 130 U/L). Interruption of prednisolone and IV aciclovir (ACV) were successful in controlling infection. The heart and lung recipient from donor A had no serological evidence of HSV infection prior to the transplant. Having received IV ganciclovir and human hyperimunoglobulin for prophylaxis of CMV mismatch, this recipient did not develop HSV 2 vireamia nor symptoms. It is not described whether serology was performed to check for seroconversion. The recipeint of the other kidney from donor A had a pre-transplant HSV 1 IgG positive but HSV 2 IgG negative result. He was receiving oral VGCV as CMV prophylaxis and did not develop any HSV symptoms. His post transplant HSV 2 serology is not mentioned. The kidney-pancreas recipient from donor A had an acute myocardial infarction with cardiac arrest on day 2 post transplant. Extended antimicrobial cover was introduced due to fever and negative bacterial cultures. Patient showed minimal neurological resposne despite weaning of sedation, progressive deterioration with increased inotrope requirements and died on day 9. Retrospective testing showed that this patient was seronegative for HSV before transpant and had high HSV 2 viral load in blood at time of death, consistent with primary HSV 2 infection. This patient went on to donate the transplanted kidney and lungs (donor B) before the herpetic infection was diagnosed. At retrieval, macroscopic fatty changes were noted in the liver and subsequent histology (coagulative parenchimal necrosis and nuclear inclusion) and PCR revealed HSV 2 infection. The biopsy of the kidney graft also revealed HSV 2 infection by immunohistochemical staining. The recipient of the re-transplanted kidney from donor B had been previoulsy infected with HSV 1and HSV 2 according to his serology results. Due to the suspicion of HSV 2 infection in the donor, he was started on VGCV; due to detectable viraemia, he was switched to IV ACV, with control. The bilateral lung recipient form donor B was seropositve for both HSV 1 and HSV 2 IgG pre-transplant. Because HSV 2 viraemia was detected on day +2 whilst on IV ganciclovir, VGCV 1gr tds was commenced, with resolution of viraemia.