No abstract

The objective of this practice guideline is to provide recommendations for the accurate diagnosis and optimal treatment of group A streptococcal pharyngitis in children and adults. The desired outcomes are prevention of acute rheumatic fever, prevention of suppurative complications, improvement of clinical symptoms and signs, reduction in transmission of group A bhemolytic streptococci to close contacts of patients, and minimization of potential adverse effects of inappropriate antimicrobial therapy. This statement is an update of the practice guideline published in 1997 [1] and takes into account relevant research published since that time. A major substantive change is the acceptance of negative results of rapid antigen detection testing (RADT) for exclusion of acute streptococcal pharyngitis, without the previously mandated confirmation with a negative culture result, provided certain criteria are met, as detailed below. Diagnosis. Acute pharyngitis is one of the most frequent illnesses for which pediatricians, internists, and other primary care physicians are consulted. Although the group A streptococcus is the most common

Two-hundred seventy-six volunteers completed a life stressor interview and psychological questionnaires and provided blood and urine samples. They were then inoculated with common cold viruses and monitored for the onset of disease. Although severe acute stressful life events (less than 1 month long) were not associated with developing colds, severe chronic stressors (1 month or longer) were associated with a substantial increase in risk of disease. This relation was attributable primarily to under-or unemployment and to enduring interpersonal difficulties with family or friends. The association between chronic stressors and susceptibility to colds could not be fully explained by differences among stressed and nonstressed persons in social network characteristics, personality, health practices, or prechallenge endocrine or immune measures.

Acute sinusitis can be classified into categories on the basis of several characteristics, including the immune status of the patient; infectious or noninfectious nature; occurrence in the community or hospital setting; and viral, bacterial, or fungal etiology (table 1). These categories are of both theoretical and practical importance for understanding the pathogenesis and clinical expression of the infection and for optimizing approaches to diagnosis and treatment. This review is confined to sinus infections of viral and bacterial etiology acquired in the community.

To further understand the biology of rhinovirus (RV), we determined whether IL-6 was produced during RV infections and characterized the mechanism by which RV stimulates lung cell IL-6 production. In contrast to normals and minimally symptomatic volunteers, IL-6 was detected in the nasal washings from patients who developed colds after RV challenge. RV14 and RV1A, major and minor receptor group RVs, respectively, were potent stimulators of IL-6 protein production in vitro. These effects were associated with significant increases in IL-6 mRNA accumulation and gene transcription. RV was also a potent stimulator of IL-6 promoter-driven luciferase activity. This stimulation was modestly decreased by mutation of the nuclear factor (NF)-IL-6 site and abrogated by mutation of the NF-B site in this promoter. An NF-B-DNA binding activity, mediated by p65, p50, and p52 NF-B moieties, was rapidly induced in RV-infected cells. Activator protein 1-DNA binding was not similarly altered. These studies demonstrate that IL-6 is produced during symptomatic RV infections, that RVs are potent stimulators of IL-6 elaboration, and that RV stimulation of IL-6 production is mediated by an NF-B-dependent transcriptional stimulation pathway. IL-6 may play an important role in the pathogenesis of RV infection, and NF-B activation is likely to be an important event in RVinduced pathologies. ( J. Clin. Invest. 1996. 97:421-430.)