Herpes-simplex-virus infection after renal transplantation

Montgomerie, John Z.; Becroft, D. M. O.; Croxson, M. C.; Doak, P. B.; North, J. D. K.

doi:10.1097/00007890-197010000-00014

Cited by 26 publications

(37 citation statements)

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“…Although in many human infections with HSV viraemia is not important, in neonatal infection (Bahrani et al, 1966;Arvin et al, 1982) and in immunosuppressed people (Montgomerie et al, 1969) it probably plays a significant role in the disease. Involvement of the adrenal gland and the possibility of damage in the cord should be borne in mind when considering explanations of nervous system dysfunction associated with HSV infections (Klastersky et aL, 1972;Craig & Nahmias, 1973;Shturman-Ellstein et al, 1976;Caplan et al, 1977;Oates & Greenhouse, 1978;White et al, 1984).…”

Section: Isolation Of Hsv From Adrenal Glands Of Female Mice After Inmentioning

confidence: 99%

Infection of the Adrenal Gland as a Route to the Central Nervous System after Viraemia with Herpes Simplex Virus in the Mouse

Hill¹,

Yirrell²,

Blyth³

1986

Journal of General Virology

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SUMMARYIntravenous inoculation of 4-week-old female NIH (inbred) mice with herpes simplex virus type 1 (HSV-1) strain P2C6 (defective in thymidine kinase) produced bilateral hind limb paralysis in nearly all animals by the 5th day after inoculation; very few mice died. In male mice the incidence and severity of paralysis was considerably lower than in females. The parental strain, CL(101), produced similar paralysis but all mice died by day 7. Observations on paralysis and death after intravenous inoculation are given for other strains of HSV-1 and HSV-2. By day 1 after inoculation of P2C6 significant virus replication had occurred in the adrenal glands but in none of the other organs tested. Titres of virus were similar in the adrenal glands of male and female mice. Histology of the adrenals showed most extensive replication in the cortex with some involvement of the medulla, particularly at the corticomedullary junction. By the 2nd and 3rd days, virus was detected in the lower thoracic spinal cord of both male and female animals but clearance was possibly quicker from males. Adrenalectomy proved that virus reached the cord via the adrenals. In the cord the infection was associated with bilateral demyelination in the ventral white matter as early as day 3.

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Section: Isolation Of Hsv From Adrenal Glands Of Female Mice After Inmentioning

confidence: 99%

Infection of the Adrenal Gland as a Route to the Central Nervous System after Viraemia with Herpes Simplex Virus in the Mouse

Hill¹,

Yirrell²,

Blyth³

1986

Journal of General Virology

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“…If not diagnosed in time, it may lead quickly to DIC and death. Sporadic case reports have described fulminant hepatitis in both immunocompromised [8][9][10][11][12][13] and normal hosts [14][15][16][17][18][19]. We present here 12 cases of herpes hepatitis from one institution that occurred in liver, heart, or kidney transplant recipients.…”

mentioning

confidence: 99%

Herpes Simplex Virus Hepatitis after Solid Organ Transplantation in Adults

Kusne

Schwartz

Breinig

et al. 1991

Journal of Infectious Diseases

151

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Twelve patients developed herpes simplex (HSV) hepatitis a median of 18 days after solid organ transplantation. This is earlier than cytomegalovirus hepatitis, which usually occurs 30-40 days after transplantation. Eight recipients (67%) died, and in seven, the diagnosis was made at autopsy or <48 h before death. Clinical manifestations associated with mortality were hypotension, disseminated intravascular coagulation (DIC), metabolic acidosis, gastrointestinal bleeding, and bacteremia. Laboratory abnormalities at diagnosis associated with mortality were high creatinine, low platelet counts, prolonged partial thromboplastin time, and a high percentage of band forms on the blood smear. Disseminated HSV disease was noted in four of six patients who had an autopsy and included involvement of lungs in three and the gastrointestinal tract in three. Five recipients developed DIC and all died. Pathologically, HSV hepatitis has two forms, focal and diffuse. All three patients with diffuse liver pathology died. However, three of seven with focal liver pathology survived with antiviral therapy, which suggests that early diagnosis and treatment may be lifesaving. None of these patients had received prophylactic acyclovir. It is possible that acyclovir prophylaxis may be able to prevent this disease.Herpes simplex virus (HSV) hepatitis is considered rare [1]. It has been observed most frequently as part of disseminated HSV in immunologically compromised patients or during pregnancy. Sporadic cases have been reported from this institution in renal transplant recipients and have ended fatally [2,3], as have most cases reported in the literature. Here we report 12 cases that occurred after solid organ transplantation over a 9-year period (1980)(1981)(1982)(1983)(1984)(1985)(1986)(1987)(1988). This series is large enough to allow us to determine the approximate frequency of HSV hepatitis in our transplantation population; to present the effect of viral dissemination, the nature of the liver pathology, and the range of clinical and laboratory characteristics of the disease; and to investigate prognostic factors. Materials and Methods DefinitionsCases of HSV hepatitis were diagnosed by laboratory, histologic, and clinical findings of one or more of the following in liver tissue from a biopsy or autopsy: isolation of HSV, positive immunoperoxidase staining for HSV antigen, or histology showing intranuclear inclusion bodies and pathology consistent with HSV lesions. In one case there was no liver tissue to examine, and the diagnosis was made by isolation of HSV from multiple sites outside the liver, including buffy coat, and clinical evidence of fulminant hepatitis. The histologic pattern of Laboratory methodsTissue specimens obtained by biopsy or at autopsy were examined after routine staining and processing for detection of HSV antigen by immunoperoxidase staining and, on occasion, processed for isolation of HSV. Other specimens obtained from transplant recipients for viral isolation included throat wash, urine, buffy co...

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“…Herpesviruses are known to be capable of reactivation, especially during immunosuppression (Rifkind, 1966;Kanich & Craighead, 1966;Montgomerie et al 1969) and this could explain the active CMV infections seen in this group without the need for re-infection to have occurred (Carlstrom, 1965;Anderson & Spencer, 1969). Kanich & Craighead (1966) did not find evidence of CMV infection in those renal transplant patients not given immunosuppressives.…”

Section: Discussionmentioning

confidence: 95%

“…varicella-zoster (Rifkind, 1966) and herpes simplex virus (Montgomerie et al 1969) and as herpesviruses are known to produce latent infection the possibility of reactivation arose (Kanich & Craighead, 1966). However, immunosuppression also leads to increased susceptibility to infections of many kinds, including primary CMV infections (Bodey, Wertlake, Douglas & Levin, 1965) so that the problem arose of the part played by the two sources of virus, reactivated endogenous virus (Kanich & Craighead, 1966) compared with fresh infection (Craighead, Hanshaw & Carpenter, 1967).…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus antibody production in renal transplant patients

Nagington

1971

Epidemiol. Infect.

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SUMMARYSera were examined from 50 patients on the renal transplant unit, Cambridge, for antibody against cytomegalovirus by complement fixation and by immunofluorescence for IgG and IgM antibodies.The incidence of antibody on admission was 84 % with a possible further 8 % so that nearly all had been infected at some time by CMV. 43 (86 %) patients showed evidence of active infection after admission, 39 by serology and four only from the examination of post-mortem material.Twenty-one patients produced IgM antibody and production was prolonged for years in patients that survived. Antibody production was related both to transplantation and admission to hospital.The evidence indicated that primary CMV infections were rare, that IgM antibody production was the result of active infection and that this could be attributed to reactivation without the need to invoke re-infection as the source although this type of patient is both susceptible and exposed to re-infection.

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Herpes-simplex-virus infection after renal transplantation

Cited by 26 publications

References 0 publications

Infection of the Adrenal Gland as a Route to the Central Nervous System after Viraemia with Herpes Simplex Virus in the Mouse

Infection of the Adrenal Gland as a Route to the Central Nervous System after Viraemia with Herpes Simplex Virus in the Mouse

Herpes Simplex Virus Hepatitis after Solid Organ Transplantation in Adults

Cytomegalovirus antibody production in renal transplant patients

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