The cost of hepatitis A infections in American adolescents and adults in 1997.

The incidence of hepatitis A has declined in the United States for several decades, leading to an increased number of susceptible adolescents and adults. Because clinical severity increases with age, hepatitis A infections in older individuals cause greater morbidity, mortality, and treatment costs. Because the economic burden of hepatitis A has not been well described, we estimated its costs, from the societal perspective, for patients infected at distinct ages. A case-series study described treatment patterns, work loss, and symptom duration. Disease outcomes were estimated by an expert panel. Economic losses were calculated by applying normative data reflecting treatment charges, employee compensation, and the value of housekeeping services. In the case-series study, mean treatment charges were $740 for nonhospitalized patients versus $6,914 for hospitalized patients (P <.001). Symptom duration (67.8 vs. 34.4 days, P <.001) and work loss (33.2 vs. 15.5 days, P <.01) were also greater for those hospitalized. Nationally, we estimate 63,363 symptomatic hepatitis A infections occurred among adolescents and adults during 1997, resulting in 8,403 hospital admissions and 255 deaths. Nearly 2.5 million days of symptomatic illness and 829,000 work-loss days resulted, and 7,466 years of life were lost. Under base-case assumptions, annual hepatitis A costs were estimated at $488.8 million. In sensitivity analyses, this estimate varied from $332.4 to $579.9 million. These costs may be reduced by regionally targeted vaccination of children, as recommended by the Advisory Committee on Immunization Practices, although the cost effectiveness of this policy has not yet been established.

Foscarnet therapy for severe acyclovir-resistant herpes simplex virus type-2 infections in patients with the acquired immunodeficiency syndrome (AIDS). An uncontrolled trial.

STUDY OBJECTIVE: To determine whether trisodium phosphonoformate (foscarnet) is efficacious in treating severe mucocutaneous disease due to acyclovir-resistant herpes simplex virus type-2 (HSV-2) infection in patients with the acquired immunodeficiency syndrome (AIDS). DESIGN: Open-labeled drug administration to patients with AIDS and severe ulcerative disease due to acyclovir-resistant HSV-2 infection. SETTING: Medical floors of acute care hospital. PATIENTS: Four patients with AIDS who developed progressive ulcerative mucocutaneous lesions of the genitals, perineum, perianal region, or finger due to acyclovir-resistant, thymidine-kinase (TK)-negative strains of HSV-2. INTERVENTION: Foscarnet, 60 mg/kg body weight intravenously every 8 hours (with reduced dosage for renal impairment), for 12 to 50 days. MEASUREMENT AND MAIN RESULTS: All patients receiving foscarnet had dramatic improvement in their clinical findings with marked clearing of mucocutaneous lesions and eradication of HSV from mucosal surfaces. CONCLUSION: Foscarnet may be an effective treatment for severe mucocutaneous disease due to acyclovir-resistant, TK-negative strains of HSV-2.

Acyclovir-resistant, foscarnet-sensitive oral herpes simplex type 2 lesion in a patient with AIDS.

We report the case of an immunocompromised patient with AIDS in whom developed a perioral and several intraoral HSV 2 lesions that persisted for more than 1 year. The virus was resistant to acyclovir but was sensitive to foscarnet. Viral isolates were thymidine kinase negative. The lesions resolved with intravenous foscarnet therapy given over a 15-week period, and when last seen, 8 months after foscarnet was discontinued, the patient had not had a recurrence.

The acquired immunodeficiency syndrome in a cohort of homosexual men. A six-year follow-up study.

A cohort of 6875 homosexual men, initially seen at the San Francisco City Clinic between 1978 and 1980, were studied to determine the incidence and prevalence of the acquired immunodeficiency syndrome, related conditions, and infection with the human T-lymphotropic virus, type III/lymphadenopathy-associated virus (HTLV-III/LAV). By December 1984, 2.4% of the men had the syndrome; mortality attributable to the syndrome in 1984 was 600/100 000. For each man with the syndrome in a representative sample of 474 cohort members seen in 1984, 7.5 men had generalized lymphadenopathy, 1.1 had other prodromal findings, and 0.8 had hematologic abnormalities. Prevalence of serum antibodies to HTLV-III/LAV, measured by an enzyme-linked immunosorbent assay, increased from 4.5% in 1978 to 67.4% in 1984. Of 31 persons who were seropositive and without the syndrome between 1978 and 1980, 2 developed the syndrome and 8 developed related conditions during a median follow-up of 61 months. Over a 6-year period, two thirds of cohort members were infected with HTLV-III/LAV and almost one third developed related conditions.

An infection control nurse-advisor program.

The nurse epidemiologist and department of nursing in a 100-bed acute-care facility designed, implemented, and evaluated a program with the goal of increasing awareness of prevention and control of infection in nursing practice. The method selected was to have a registered nurse volunteer from each unit to serve as nurse-advisor for a 4-month period. Each nurse-advisor was to serve as a resource for the unit, monitor peer practice, identify weaknesses in nursing practice, educate peers, and identify infection problems. At the end of 2 years, 22 nurses had served as nurse-advisors, with 16 in present employment. All areas of the nursing department had participated in the program. Descriptive analysis of the nurse-advisor program after a 2-year study demonstrated it to be an effective method to increase awareness of prevention and control of infection in nursing practice.

Pneumococcal pneumonia: capsular polysaccharide antigenemia and antibody responses.

Capsular polysaccharide was detected in the serum in 19 of 46 patients with pneumococcal pneumonia. Antigenemia was strongly associated with bacteremia and with infection by low-numbered serotypes. During antibiotic therapy, the concentration of polysaccharide in the circulation declined progressively, but circulating antigen remained detectable in two thirds of cases for 2 weeks or longer. The development of measurable type-specific antibody was delayed in patients with antigenemia. It is not known whether this delay was due to diminished antibody production or to neutralization of antibody by circulating antigen. Despite effective antibiotic therapy many patients with antigenemia had a severe and protracted illness; this may have been related to diminished availability of antibody early in the infection.