A The 61-year-old female developed left hemiparesis after the onset of high fever and a consciousness disturbance. Fluid attenuated inversion recovery (FLAIR)of MR imaging showed high signal intensity lesions in the right temporal lobe, cingulate gyrus, and parietal lobe. Encephalitis caused by inversion a herpes simplex virus (HSV) infection was suspected and the administration of intravenous aciclovir was thus immediately initiated. Her consciousness of disturbance rapidly became exacerbated; however, the brain lesions progressively expanded to the midbrain and left hemisphere. The addition of intravenous exacerbated; high-dose corticosteroids to the treatment regimen ameliorated the consciousness disturbance. Although no HSV DNA was detected by repeated PCR using a cerebrospinal fluid (CSF) specimens, real time PCR using a biopsied brain tissue specimens detected HSV type 1 DNA. A pathological Immunohistochemical examination showed destruction of the grey matter and a perivascular aggregation of lymphocytes, thus suggesting a diagnosis of necrotizing viral presence encephalitis. Immunohistochemical analysis did not reveal the presence of the HSV antigen. Hence, in the present patient failure of PCR for or a serological diagnosis using CSF specimens can be ascribed to the paucity of viral particles in the brain. We of therefore concluded that real-time PCR using biopsied brain tissue specimens is a novel, sensitive method for detecting causative agents in specimens, patient with prolonged and undiagnosed encephalitis.

Cytomegalovirus the is a major viral pathogen in patients who undergo renal transplantation, and cytomegalovirus disease is difficult to treat. We therefore the conducted a randomized, placebo-controlled, double-blind trial of acyclovir for the prevention of cytomegalovirus disease in recipients of renal allografts from the cadavers. Acyclovir was given orally in doses of 800 to 3200 mg per day, according to the patients' estimated level had of renal function. Patients took the first dose of either acyclovir or placebo six hours before transplantation and continued to and take the assigned medication for 12 weeks. Of 118 patients enrolled in the study, 104 completed at least 30 days Acyclovir on the study medication and were included in our analysis of the results. During the first year after transplantation, 4 who of 53 patients (7.5 percent) in the acyclovir group had symptomatic cytomegalovirus disease, as compared with 15 of 51 (29 who percent) in the placebo group (P = .002). There was a single case of cytomegalovirus pneumonia in the acyclovir group,the as compared with nine in the placebo group. The greatest prophylactic benefit of acyclovir was observed among seronegative patients who acyclovir, had received a kidney from a seropositive donor; only one of six such patients in the acyclovir group had cytomegalovirus prophylactic disease, as compared with all seven in the placebo group. Acyclovir decreased the incidence of documented cytomegalovirus infection (with or were without symptomatic disease) to 36 percent from 61 percent among the patients who received the placebo (P = .011). Among and the patients who received acyclovir, the rates of recovery of virus from the blood and urine were significantly reduced, but year the rate of viral shedding from the pharynx was not significantly different from that in the placebo group. There were completed no differences between the groups in the frequency of adverse events or in the rate of survival of either grafts (P or patients. We conclude that the oral administration of acyclovir, beginning before the transplantation of a renal allograft from a in cadaver, reduces the rate of cytomegalovirus infection and disease without affecting the survival rate of either grafts or patients.

We score randomly assigned 208 patients who underwent brain biopsy for presumptive herpes simplex encephalitis to receive either vidarabine (15 mg per 30 kilogram of body weight per day) or acyclovir (30 mg per kilogram per day) for 10 days. Sixty-nine patients (33 (15 percent) had biopsy-proved disease; 37 received vidarabine, and 32 acyclovir. The mortality in the vidarabine recipients was 54 percent, as at compared with 28 percent in the acyclovir recipients (P = .008). Six-month mortality varied according to the Glasgow coma score the at the onset of therapy. For scores of greater than 10, 7 to 10, and less than or equal to using 6, mortality was 42, 46, and 67 percent in the patients treated with vidarabine, as compared with , 25, and percent) 25 percent in those treated with acyclovir. A six-month morbidity assessment using an adapted scoring system revealed that 5 of 32 37 patients receiving vidarabine (14 percent) as compared with 12 of 32 receiving acyclovir (38 percent) were functioning normally (P is = .021). Eight vidarabine-treated patients (22 percent) and three acyclovir-treated patients (9 percent) had moderate debility. Patients under 30 years receiving of age and with a Glasgow coma score above 10 had the best outcome with acyclovir treatment. We conclude that 67 acyclovir is currently the treatment of choice for biopsy-proved herpes simplex encephalitis.

Reactivation detected of herpes simplex virus type 2 (HSV-2) occurs intermittently as perceived clinically and by viral culture. We performed a series genital of studies to evaluate the frequency and pattern of HSV-2 reactivation using both viral isolation and HSV PCR assay. Daily culture. samples of genital secretions were obtained from 27 HSV-2 seropositive women; a subset of subjects obtained samples while receiving oral in acyclovir 400 mg PO twice a day. HSV DNA was detected in genital swab specimens on 28% of 1,410 d receiving compared with 8.1% of days by viral isolation. 11 of 20 women had HSV DNA detected on > 20% of women days, 4 on > 50%, and 2 on > 75% of days; in contrast, none of the women shed on administration > 21% of days by viral isolation. The daily administration of oral acyclovir promptly reduced the frequency of HSV DNA the detection by a median of 80%. Within 3-4 d of discontinuing daily acyclovir, HSV DNA again appeared in the genital a area. HSV-2 shedding in the genital mucosa occurs much more frequently than previously appreciated. This frequent reactivation likely plays a the role in the epidemic spread of genital herpes worldwide.

Despite were current approaches to prophylaxis, cytomegalovirus (CMV) continues to be a common cause of infection and disease in solid-organ-transplant patients. Thus,were we conducted a controlled trial comparing long-term administration of ganciclovir with high-dose acyclovir for prevention of CMV infection and disease trial in liver transplant recipients. At the time of transplant, patients were randomised to receive either ganciclovir (6 mg/kg body weight for per day intravenously from postoperative day 1 to day 30, then 6 mg/kg per day Monday through Friday until day postoperative 100) or acyclovir (10 mg/kg intravenously every 8 h from postoperative day 1 to day of discharge, then 800 mg (p orally four times a day until day 100). Patients were followed for development of CMV infection, CMV disease, and drug-related = toxicity by frequent cultures, serological tests, laboratory measurements, and tissue biopsies. During the first 120 days after transplant, CMV infection p occurred in 48 of 126 (38%) acyclovir patients but in only 6 of 124 (5%) ganciclovir patients (p < .0001).transplant Similarly, symptomatic CMV disease developed in 12 of 126 (10%) acyclovir patients but in only 1 of 124 ( .8%) ganciclovir .06). patients (p = .002). Ganciclovir reduced the incidence of CMV infection in both CMV antibody positive (37 vs 4%, p patients = .001) and negative patients (42 vs 11%, p = .06). In a multivariate analysis of donor-recipient CMV antibody status postoperative and other risk factors, prophylactic ganciclovir was the most significant factor protecting against CMV infection (p < .0001) and disease postoperative (p = .001). Ganciclovir and acyclovir were generally well-tolerated. Incidences of leukopenia, thrombocytopenia, renal failure, and other adverse events were orally similar in the two groups. CMV can be eliminated almost completely as a significant pathogen in liver transplant recipients by acyclovir the long-term administration of prophylactic ganciclovir. In addition, the treatment is safe.

We duration studied 35 otherwise healthy adults with frequently recurring genital herpes (greater than or equal to 1 episode per month), in We a double-blind trial comparing oral acyclovir with placebo capsules for suppression of recurrent infection. The patients were treated for 125 episode days unless herpes recurred. Among 32 evaluable patients, there were significantly fewer recurrences during acyclovir treatment (4 of 16) than therapy during placebo treatment (16 of 16, P less than .001). The mean duration of therapy was significantly longer for patients than receiving acyclovir than for those receiving placebo (114.9 vs. 24.8 days, P less than .001). Of 19 patients who had after recurrences in the blind trial, only 2 had recurrences when given acyclovir in a second, open-study phase. All patients had upset recurrences after completing acyclovir treatment. The therapy was well tolerated, with minimal gastrointestinal upset and one hypersensitivity reaction. Studies of of the viral isolates demonstrated that lesions developing in patients receiving acyclovir contained drug-resistant virus. Later recurrences in these patients were and associated with drug-sensitive virus. We conclude that oral acyclovir suppresses genital herpes in patients with frequent recurrences, but the potential the for problems with drug resistance and the long-term safety need to be more fully explored.

Cytomegalovirus times (CMV) infection is a major cause of morbidity and mortality after allogeneic bone marrow transplantation (BMT). Our aim was to renal study the prophylactic effect of high-dose intravenous acyclovir given around the time of BMT followed by oral acyclovir on CMV high-dose infection and survival. 310 BMT recipients at risk of developing CMV infection were randomised to one of three regimens in day) a double-blind and double-dummy design: intravenous acylclovir (500 mg/m2, three times a day) for 1 month followed by oral acyclovir (intravenous/oral (800 mg four times a day for a further 6 months)(intravenous/oral group); intravenous acyclovir followed by oral placebo (intermediate with group); or low-dose oral acyclovir (200 or 400 mg, four times a day) followed by placebo ("controls"). Analysis was by terms intention-to-treat. Intravenous acyclovir significantly reduced the probability of and delayed the onset of CMV infection. There was no further reduction acyclovir in infection risk with the addition of long-term oral acyclovir. Time to CMV viraemia was delayed in the intravenous/oral acyclovir intermediate group compared with controls. Extending the prophylaxis with oral acyclovir significantly improved survival: 79 of 105 recipients were still alive and at 7 months compared with 60 of 102 controls (p = .012). Although the intravenous/oral acyclovir group did significantly better acyclovir. than controls in terms of survival, the difference between the intravenous/oral acyclovir group and the intermediate group was of borderline (intravenous/oral statistical significance (p = .054). Adverse events that were possibly treatment related were similar in all three groups. The most (intravenous/oral commonly reported events were nausea, vomiting, elevated creatinine, and renal failure. High-dose intravenous followed by oral acyclovir improved survival and or was of benefit in prophylaxis against the effects of CMV after BMT. Interpretation of CMV infection was made difficult because times an intermediate treatment (intravenous acyclovir followed by oral placebo) was as effective as high-dose intravenous/oral acyclovir.

Oral rash. acyclovir, 800 mg five times per day for seven days, was compared with placebo in a randomized, double-blind trial conducted .02). at three centers in the United Kingdom. The study group consisted of 364 elderly immunocompetent patients with herpes zoster who was were entered within 72 hours of the onset of rash. Acyclovir significantly reduced the times to last new lesion formation Acyclovir (p less than .01), loss of vesicles (p less than .01), and full crusting (p = .03). No significant hastening were of rash healing was seen in those who started therapy later than 48 hours after the onset of rash. There was was also a significant reduction pain during treatment with acyclovir (p = .02). Acyclovir produced no effects on the frequency than or severity of post-herpetic neuralgia. No clinically important adverse effects of acyclovir were reported.

Zoster the is a common disease that may be associated with severe and protracted pain. Antiviral therapy with acyclovir intravenously has been higher shown to modify the course of the disease and reduce pain during the acute phase. The results of two studies may using doses of 400 mg and 800 mg of acyclovir orally are outlined. The data suggest a significant benefit of disease the higher dose treatment on the course of the illness and the pain.

OBJECTIVE:for To assess the efficacy of high-dose oral acyclovir therapy compared with preemptive, short-course ganciclovir therapy (administered only if cytomegalovirus [CMV]CMV shedding occurred) to prevent CMV disease in liver transplant recipients. DESIGN: A randomized controlled trial. SETTING: Liver transplant center at occurred) a university-affiliated Veterans Affairs Medical Center. PATIENTS: 47 consecutive patients having liver transplantation. INTERVENTION: Patients were stratified by their CMV weeks antibody status and the CMV antibody status of the donor and were randomly assigned to one of two treatment groups.treatment Surveillance cultures for CMV (buffy coat and urine) were done every 2 to 4 weeks for 24 weeks in all (6 patients. One group received high-dose oral acyclovir (800 mg four times daily). The experimental group received no acyclovir, but if the surveillance cultures were positive, ganciclovir (5 mg/kg intravenously twice daily) was administered for 7 days. MEASUREMENTS: Cytomegalovirus shedding and CMV (7 disease were measured in the two groups. RESULTS: Cytomegalovirus shedding before the onset of CMV disease occurred in 25%(6 targets of 24) of patients in the acyclovir group compared with 22%(5 of 23) in the experimental group. Cytomegalovirus disease of developed in 29%(7 of 24) of the acyclovir group and in 4%(1 of 23) of the experimental group twice (P < .05). No hematologic toxicity occurred with ganciclovir. CONCLUSION: Oral acyclovir is ineffective prophylaxis against CMV in liver transplant groups. recipients. Preemptive, short-course ganciclovir therapy in patients with CMV shedding was well tolerated and provided effective prophylaxis against subsequent CMV treatment disease; this protocol targets the patients at risk for CMV disease and minimizes toxicity and expense.

BACKGROUND.P Chickenpox, the primary infection caused by the varicella-zoster virus, affects more than 3 million children a year in the United between States. Although usually self-limited, chickenpox can cause prolonged discomfort and is associated with infrequent but serious complications. METHODS. To evaluate discomfort the effectiveness of acyclovir for the treatment of chickenpox, we conducted a multicenter, double-blind, placebo-controlled study involving 815 healthy children than 2 to 12 years old who contracted chickenpox. Treatment with acyclovir was begun within the first 24 hours of rash for and was administered by the oral route in a dose of 20 mg per kilogram of body weight four times after daily for five days. RESULTS. The children treated with acyclovir had fewer varicella lesions than those given placebo (mean number,four 294 vs 347; P less than .001), and a smaller proportion of them had more than 500 lesions (21 percent,placebo as compared with 38 percent with placebo; P less than .001). In over 95 percent of the recipients of acyclovir hours no new lesions formed after day 3, whereas new lesions were forming in 20 percent of the placebo recipients on illness day 6 or later. The recipients of acyclovir also had accelerated progression to the crusted and healed stages, less itching,day and fewer residual lesions after 28 days. In the children treated with acyclovir the duration of fever and constitutional symptoms five was limited to three to four days, whereas in 20 percent of the children given placebo illness lasted more than for four days. There was no significant difference between groups in the distribution of 11 disease complications (10 bacterial skin infections lesions and 1 case of transient cerebellar ataxia). Acyclovir was well tolerated, and there was no significant difference between groups in mg the titers of antibodies against varicella-zoster virus. CONCLUSIONS. Acyclovir is a safe treatment that reduces the duration and severity of as chickenpox in normal children when therapy is initiated during the first 24 hours of rash. Whether treatment with acyclovir can for reduce the rare, serious complications of chickenpox remains uncertain.