Bonnie Bean

Acyclovir Halts Progression of Herpes Zoster in Immunocompromised Patients

We conducted a placebo-controlled, double-blind study of acyclovir therapy for acute herpes zoster in immunocompromised patients. Of the 94 patients enrolled in the study, 52 had localized skin lesions at entry, and 42 had disseminated cutaneous zoster. A one-week course of intravenous acyclovir (1500 mg per square meter of body-surface area per day) halted progression of zoster in both groups, as determined by development or progression of cutaneous dissemination, development of visceral zoster, or proportion of cases deemed treatment failures. Significantly fewer patients treated with acyclovir within the first three days after the onset of exanthem had complications of zoster, as compared with patients treated with placebo (P = 0.02 by Fishers exact test), but acyclovir also stopped progression of zoster in patients treated after three days of rash (P = 0.05 by Fishers exact test). Acyclovir recipients with disseminated cutaneous zoster had a significantly accelerated rate of clearance of virus from vesicles, as compared with placebo recipients (P = 0.05 by the Breslow test).

Acyclovir therapy for acute herpes zoster.

31 adults took part in a randomised, placebo-controlled, double-blind trial of intravenous acyclovir therapy (500 mg/m2 intravenously 3 times daily for 5 days) for acute herpes zoster. Acyclovir reduced pain, decreased erythema, prevented the formation of new lesions, and healed skin faster than did placebo. The duration of viral shedding was also significantly shorter in acyclovir recipients (2 days versus 5 days). However, 6(35%) of 17 acyclovir recipients had recurrence of pain after the drug was discontinued, and acyclovir did not appear to affect post-herpetic neuralgia. Acyclovir therapy was associated with a transient rise in serum creatinine levels, and may have been related to nausea and vomiting. Intravenous acyclovir was effective therapy for acute herpes zoster but the ideal treatment regimen might be a lower daily dose given for a longer period.

ACYCLOVIR THERAPY FOR MUCOCUTANEOUS HERPES SIMPLEX INFECTIONS IN IMMUNOCOMPROMISED PATIENTS

11 of 24 immunocompromised patients with mucocutaneous herpes simplex virus (HSV) infections were given intravenous acyclovir in a randomised double-blind placebo-controlled study. Patients receiving acyclovir experienced no major adverse effects. The median times to cessation of new lesion formation, lesion crusting, lesion healing, cessation of pain, and termination of viral shedding were shorter in the acyclovir-treated group than in the placebo group. The time-to-event probability curves for the acyclovir and placebo groups were significantly different for cessation of pain (p=0.032) and termination of viral shedding (p=0.004). The median times to termination of viral shedding were also statistically different (p=0.045). Acyclovir seems to be a non-toxic and effective treatment for mucocutaneous HSV infections in immunocompromised patients.

Continuous infusion of high-dose acyclovir for serious herpesvirus infections.

Thirteen patients with herpesvirus infections who were unresponsive to at least 72 h of intermittent acyclovir administration received high-dose continuous infusion. Steady-state concentrations were maintained at between 20 and 98 mumol/liter. Of 12 patients who had continuous infusion for greater than 5 days, 7 (58%) resolved their infections, as determined by clinical and virologic parameters, suggesting that continuous infusion may succeed in some patients who do not respond to conventional therapy.

Influenza B: Hospital activity during a community epidemic

During a community epidemic of influenza B, surveillance throat cultures for influenza were collected from febrile adult patients and hospital employees on three medical wards to determine the frequency and source of influenza among hospitalized patients. Twenty-five cases of influenza B (18.5% of febrile patients) were identified; no clusters of influenza-like illness occurred. The attack rate on two wards was 4.6%. Peak hospital influenza incidence followed that in the community by 1-2 weeks. Twelve of the cases were community-acquired and 13 were nosocomial. 75% of community-acquired cases had three or more common influenza B symptoms, compared with only 39% of nosocomial cases. A viral etiology of fever was suspected clinically in one-half of the cases, but influenza was specifically suspected in only one case. Two ill culture-positive nurses were identified on the job but no asymptomatic carriers were found among ward personnel. We conclude that influenza B cases were present among hospitalized patients in the absence of recognizable clusters of disease and that patients with community-acquired illness as well as nursing personnel may have introduced influenza into the hospital. Influenza B may be difficult to diagnose clinically in hospitalized patients, but viral throat cultures performed in all suspected cases should identify many infected patients.

Progressive mucocutaneous herpes simplex infection due to acyclovir-resistant virus in an immunocompromised patient: Correlation of viral susceptibilities and plasma levels with response to therapy

Rapidly progressive disease due to acyclovir-resistant herpes simplex has not been described. We report such a case and detail successful patient management using viral sensitivities and plasma acyclovir levels to guide therapy. Response was correlated with plasma levels above those inhibiting viral growth by 50% (ID50) in vitro.

Acute Lymphatic Filariasis in an American Traveler

Acute lymphatic filariasis developed in an American traveling recreationally to Asia. The illness was characterized by fatigue, eosinophilia, and lymphedema of the arm and chest wall, but no lymphangitis, lymphadenitis, or pain. Complete resolution occurred over 1-2 years. We discuss this syndrome and describe the use of new diagnostic tests in its diagnosis and management.

Pharmacokinetics, protein binding, and predicted extravascular distribution of moxalactam in normal and renal failure subjects.

Ten normal subjects and ten patients with chronic renal failure requiring hemodialysis were given intravenous infusions of moxalactam ranging from 500 mg to 2 g. Serum and urine concentrations were measured for up to 12 h. Renal failure subjects were given doses both during and between hemodialysis treatments. Protein binding of moxalactam in both normal and uremic serum was determined by ultracentrifugation. The serum half-life in normal subjects was 2.1 and 2.3 h for the 1- and 2-g doses, respectively. The half-life of moxalactam in patients with renal failure was 13.9 h on the 500-mg dose and 13.3 h on the 1.0-g dose. During hemodialysis the serum half-life fell to 4.4 and 5.7 h, respectively. Moxalactam protein binding ranged from 52% in normal serum to 36% in renal failure patient serum. Unbound moxalactam appeared to distribute with the entire body water based on the serum pharmacokinetics and antibiotic serum protein binding determined in this study.