A family outbreak of gastroenteritis involving three adults and three children is described in which diarrhoea and vomiting were the main clinical features. One infant died in whom no pathogens could be detected in either small or large intestinal postmortem samples. Stool samples from two symptomatic siblings contained rotaviruses as demonstrated by electron microscopy. Both of these faecal samples were negative when assayed in a group A specific rotavirus enzyme-linked immunosorbent assay (ELISA) and subsequent genomic analysis of these rotaviruses was suggestive of group C rotavirus. Serological evidence showed that these atypical rotaviruses were members of serogroup C. Other atypical rotaviruses in faecal samples from sporadic cases in symptomatic children were detected over a similar time period and location. These had electrophoretic RNA profiles similar to those in the family outbreak. Furthermore, seroepidemiological studies detected group C rotavirus antibody in blood donors resident in the location of the family outbreak.
Summary:Over a 3-month period, four patients who had received unrelated donor (UD) bone marrow transplants (BMT) presented with severe mucocutaneous herpes simplex virus (HSV) infection while receiving acyclovir (ACV) prophylaxis. Sensitivity testing of the isolates revealed three to be acyclovir-resistant and in one patient the infection was also characterised by a marked failure to respond to foscarnet (phosphonoformic acid). The emergence of ACV-resistant HSV infections in themselves is a new and challenging problem, and yet a far greater problem will become evident if these infections develop resistance to non thymidine kinase dependent therapy. Keywords: acyclovir-resistant herpes simplex virus infections; bone marrow transplantation Herpes simplex virus (HSV) reactivates in 70-80% of seropositive recipients of allogeneic transplants, causing haemorrhagic mucocutaneous lesions which can add substantially to the morbidity of BMT. These infections are preventable with prophylactic acyclovir (ACV).1,2 The mode of action of acyclovir includes phosphorylation by viral thymidine kinase (TK) and then its incorporation into the viral DNA, thus terminating extension of the DNA chain. Resistance is usually due to loss of TK expression (TK−) and a correlation exists between the frequency with which resistant viruses are isolated and the degree of immunosuppression in the host.3,4 ACV-resistant HSV infections causing clinical problems in BMT patients have previously been documented, 5 as have resistant herpes virus infections generally. 6 We present a review of four patients who had received unrelated donor bone marrow transplants for the treatment of haematological malignancies and presented over a 3-month period between July and September 1995. They each had serological evidence of previous HSV infection at the time of transplant (complement fixing titres ranging from 24-64) and all four developed recurrent HSV lesions while receiving ACV prophylaxis. The standard regimen for ACV prophylaxis in UD BMT at the time was commenced at day −4 and continued until 6 months post-transplant, but was prolonged in the case of active graft-versus-host disease (GVHD). In patients at risk of cytomegalovirus (CMV) reactivation, the ACV was commenced at 500 mg/m 2 intravenously (i.v.) three times per day until day 30 and then changed to an oral dosage (200 mg five times per day). In those patients not deemed at risk for CMV, ACV was given orally throughout. The implications of the emergence of resistance in this population of immunosuppressed patients will be further discussed. Case reportPatient A, an 8-year-old girl with biphenotypic leukaemia developed mouth ulcers, culture positive for HSV-1, 5 days post-transplant (isolate A, day +5). She was changed from her oral ACV prophylaxis to high-dose intravenous ACV (10 mg/kg three times daily) for 2 weeks, to which she responded and was then converted back to oral therapy (400 mg × 5/day). However, on developing diarrhoea a week later the mouth ulcers recurred and on this occasion they...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.