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The HSV-1 Rapid Test is a dual unit, membrane-based immunoassay for the qualitative determination, either in heparinized capillary whole blood taken by fingerstick or in serum, of circulating IgG antibodies specific for herpes simplex virus type 1 (HSV-1) which arise as a result of infection with HSV-1.
Here, we report two cases of acute hepatitis and FHF secondary to primary HSV type 1 infection following renal transplantation in the absence of any mucocutaneous manifestation. Fulminant hepatitis following primary herpes simplex virus infection in renal transplant recipients. Quantitative stability of DNA after extended storage of clinical specimens as determined by real-time PCR. Herpes simplex virus-associated acute liver failure: A difficult diagnosis with a poor prog­nosis.
Herpes simplex virus hepatitis: An analysis of the published literature and institutional case.
Primary herpes simplex virus type 2 infection as a cause of liver failure after liver trans­plantation. We report two cases of FHF secondary to primary HSV infection following deceased donor renal transplantation.
Both patients were seronegative for HSV 1 and HSV 2 immuno­globulin G (IgG) before transplantation, whereas the donor of patient 1 was HSV 1 IgG-positive but had no viremia and the donor of patient 2 was HSV-seronegative. The first patient was treated successfully with intra­venous (IV) acyclovir and immunoglobulin (IVIG). Patient 1 recovered with acyclovir and immunoglobulin whereas patient 2 did not respond and succumbed to death.
HSV­seronegative patients are potentially at risk of developing severe primary HSV disease following transplantation, particularly in the absence of routine anti-viral prophylaxis. Her pre-transplant serology showed the presence of specific IgG against Epstein-Barr virus (EBV) and varicella zoster virus (VZV), but not against cytomegalovirus (CMV), HSV 1 or HSV 2. Fol­lowing the transplant surgery, she was monitored twice-weekly for CMV DNA and weekly for EBV DNA in whole blood by polymerase chain reaction (PCR) assays and, according to the unit protocol, she was not given any anti-CMV prophylaxis.The patient received anti-CD25 monoclonal antibody for induction and prednisolone, tacro­limus and mycophenolate mofetil (MMF) for maintenance immunosuppression. Multiple blood cul­tures were negative and a computed tomo­graphy (CT) scan of her abdomen and pelvis did not demonstrate any intra-abdominal or pe­rinephric collection. Three days later, her ala­nine aminotransferase (ALT) and aspartate amino-transferase (AST) started to rise and she continued to rapidly deteriorate. This was as­sociated with an initial rise in white cell count and CRP, with an associated thrombocyto­penia. A triple-phase liver pro­tocol CT scan revealed multiple low-density lesions with-in the liver suggestive of micro­abcesses [Figure 1].


These are in keeping with micro abscesses.Click here to viewShe rapidly became hypoxic and encephalo­pathic and was transferred to the intensive care unit for ventilatory support. With worsening renal function, she became oliguric and re­quired continuous veno-venous hemofiltration (CVVHF).
A laparoscopic liver biopsy [Figure 2]A showed necrotic areas in the liver contai­ning inflammatory infiltrates with "glassy" nu­clei around the necrotic areas.
Some hepatocytes around the necrotic areas contain "glassy" nuclei, and there are occasional multinucleate cells. She had weekly renal transplant biopsy X 4, which correlated with acute tubular necrosis (ATN), and the im­munoperoxidase staining for HSV was nega­tive in all the biopsies. She made a good res­ponse to acyclovir, IVIG and the reduction of her immunosuppressive drugs.
Despite the ra­pid recovery of liver function tests and con­tinued IV acyclovir, her blood HSV PCR le­vels remained elevated [Figure 3]. However, she developed HSV 1-specific IgG 5 weeks after her initial primary HSV diagnosis and her HSV DNA in the blood eventually became un­detectable after 4 months. Rapid improvement in AST following treatment with IV aciclovir.Click here to viewCase 2A 59-year-old man with autosomal-dominant polycystic kidney disease, maintained on hemo­dialysis for 5 years, was admitted to the hospital for deceased donor renal transplantation. Standard immunosup­pression was commenced pre-operatively as with our first reported case.Post-operatively, the patient required inotropic support for 3 days in the intensive care unit as he became hypotensive during the operation and his blood pressure persistently dropped when trying to wean him off in the recovery room despite adequate intravenous infusion.
Bilateral basal lung collapse was noted on chest radiography and intravenous amoxicillin and clavulanic acid were continued post-ope­ratively.
Within the next 48 hours, he became acutely unwell; pyrexial and clinically septic, with deteriorating graft func­tion and a significant clotting diathesis. Hepatic CT and ultrasound demonstrated a liver with normal appearance, all vessels patent and no evidence of necrosis or infarction.
Pending repeat viral serology and PCR, empirical intravenous acy­clovir was commenced on day 13. On day 14, the patient became frankly encephalopathic, with profuse melena, and died later on the same day.The PCR detected high levels of HSV-1 DNA in the blood. Our evi­dence is therefore consistent with a primary HSV I infection causing hepatitis and fulmi­nant hepatic failure, but the source of infection remains unclear. Primary infection in neonates, pregnant women and immunosupressed patients can lead to FHF without skin lesions. In 1980, Eliot et al reported two additional fatal cases that occurred in renal transplant recipients; in their first case, there was evidence that the allograft might have been the source of infec­tion and in their second case, the patient was found to have disseminated infection from a genital ulcer and failed to respond to vida­rabine therapy, despite being started at an early stage of the clinical course.


Norvell et al in 2007 analyzed the published literature of her­pes simplex viral hepatitis. They found that most cases were first diagnosed at autopsy (58%) and, from all the reports, only 30% were immunosuppressed transplant patients. It remains unclear why one-quarter of the pa­tients who were considered immunocompetent progressed to FHF. The donor in the first case was HSV 1-seropositive and, therefore, the donor kidney itself could have been the source of HSV transmission.
However, this could not be confirmed as the donor was aviremic and, without a comparison of the two virus strains, other sources could not be ruled out. Koneru et al described two patients who received renal transplants from the same donor in 1988; both patients died from FHF secondary to HSV. The donor in our second case was reported as HSV 1 and 2-seronegative; the source of infection in this case remains unclear.
However, this is likely to be from exogenous sources on the ward.The clinical presentation in most cases in the literature is fever (98%), with absence of skin lesions (56%).
Hence, early clinical suspicion of HSV in a febrile patient is an important factor to improve the outcome. It was noticed that coagulopathy, thrombocytopenia and leuko­penia are common laboratory findings (more than 70% of the cases). However, most cen­ters do not have access to rapid molecular tests and, often, the diagnosis is made after the pa­tient has developed FHF.
It is clear that early diagnosis and, more importantly, clinical suspicion and early treat­ment are key features in improving patient survival. In the first patient who was successfully treated, cessation of all immunosuppre­ssion, apart from steroids and the addition of IVIG as part of the antiviral treatment, resulted in response to acyclovir without permitting transplant rejection.Routine CMV prophylaxis with valganciclovir offers partial protection against HSV. We routinely screen our patients for HSV IgG pretransplant and, following these two cases, now add valaciclovir prophylaxis for HSV-serone­gative patients.



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