Previous studies of infections with influenza A in animal models have stressed the tropism of this virus for the upper respiratory tract. To assess the interaction of influenza A virus with human respiratory tissue, we maintained adenoids, consisting of ciliated epithelium with underlying lymphoid follicles, in organ culture. When the organ cultures were inoculated with wild-type influenza A/Alaska (H3N2), epithelial damage and migration of inflammatory cells from the follicles into the lamina propria were seen. Growth of the virus and ciliary damage in infected organ cultures from seronegative donors were significantly greater than that seen in organ cultures from seropositive donors. Adenoidal lymphocytes were then studied to determine which factors might modulate infectivity. Specific in vitro production of antibody to influenza A/Alaska was demonstrated by adenoidal lymphocytes from seropositive donors, whereas lymphocytes from seronegative donors did not produce antibody. The human adenoid organ culture provides an attractive model to study the pathogenesis of influenza A infections and the resultant local immune response.
Respiratory syncytial virus (RSV), a major respiratory pathogen of children, has been speculated to cause disease by immunologic mechanisms. Although circulating levels of complement (C) are normal during RSV infections, the role of C in respiratory tract secretion is unclear. Since epithelial cells of the respiratory tract of children infected with RSV express viral surface antigens, the ability of RSV infected human cells to activate C was studied. RSV infected human cells (HeLa) were found to activate both the classical and alternative C pathways as measured by the cleavage of native C3 into its breakdown products. Increased C activation occurred in the presence of antibody. Cytolysis of RSV infected cells was then studied using a chromium release assay. Both the classical and alternative C pathways in the presence of antibody participated in the lysis of RSV infected cells. The combined effects of activation of C and the lysis of RSV infected cells by C and antibody may contribute to the pathogenesis of disease.
Ke l'.1a n), St. Lou is University, St. Louis University Sch oo l of Medic ine , (;lennon Memorial Hospita l for Children, Department of Pediatrics/Adolescent Medicine, St. Louis , t10. S ingl e drug therapy with a broad spe ctrum antibiotic is a des irable o ption f or patient s with bone and joint infections of unkn own etiology. \ie initiated tre atment for 23 ch i ldren , ages 6 months-15 years (mean 6.5 years) with cefoxitin. The infecting organisms proved t o be Strep. pneumoniae-2, b-2, epidermidis, melaninogenicus, Mo raxella sp. and Ps. fluorescens-1 each. No agent was identified in 6 cases. lnitTaT clinical re sponse was good in21 cases (91 %). One primary re sis tant organism (Ps. fluorescens) and one cephalosporin-tol erant S. aureu s faile d to respond. A third child with infe ct ion due to H. Trif!Uenzae b developed meningitis after 3 days. These3, and 6 patients with neg at ive cultures, were drop ped from the study. All other patients did well and received x 15.7 days IV cefoxitin before swit ching to oral antimicrobials. Adverse reactions included allergic rash (1), mild eosinophilia (2) andmildelevation of SGOT (1). Cefoxitin was discontinued for reason of the ra s h ; all other reactions resolved when the drug was discontinued at the completion of therapy. Neutropenia (PMN <1000/mm3) was seen in 2 patients but resolved spontaneou s l y. Urinary reducing subs tance s wer e detected inS cases (22%). Cefoxitin ap pearstobe satisfactor y initial therapy for osteomyelitis an d sep tic arthriti s in pediatric patients; it should not be use d for infant s <2 years of age where H. influenzae b is suspected, due to the possible development of meningitis.
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