Effects of viral respiratory disease education and surveillance on antibiotic prescribing.

BACKGROUND AND OBJECTIVES: We describe a partnership between family practice residency clinics and a state public health virology laboratory that has produced comprehensive viral respiratory disease education and surveillance. Family practice residents have been provided with education on respiratory viruses and the results of ongoing viral surveillance. The preliminary effects of this program on antibiotic prescribing by senior residents are evaluated in this paper. METHODS: We used a questionnaire to assess the acceptance by family practice residents of the educational component and the utility of ongoing viral surveillance. We used chart review to evaluate rates of antibiotic prescribing and the number of patients diagnosed per year with acute upper respiratory infection and acute bronchitis by senior residents in 1992 (preexposure) and 1996 (postexposure). RESULTS: By the third year of training, most residents (79%) reported receiving adequate training regarding common viral respiratory diseases. Moreover, residents reported that they were less likely to prescribe antibiotics to patients presenting with respiratory infections when provided with specific information on circulating viral pathogens. Antibiotic prescribing in the postexposure group was 68% lower for upper respiratory infection (URI) and 45% lower for a composite of URI and bronchitis. CONCLUSIONS: Education and monitoring of circulating respiratory viruses can result in familiarity with common disorders in primary care and reduce unnecessary antibiotic use.

Prolonged shedding of amantadine-resistant influenzae A viruses by immunodeficient patients: detection by polymerase chain reaction-restriction analysis.

Consecutive A (H3N2) influenza virus isolates from 2 influenza virus-infected immunodeficient patients treated with amantadine were examined using a novel polymerase chain reaction (PCR)-restriction analysis for resistance to this antiviral compound. The data indicate that immunodeficient patients may shed resistant viruses for prolonged periods and with different drug resistance mutations present at different times. This PCR-restriction technique allows rapid detection of amantadine- or rimantadine-resistant strains.

Adenovirus 21 infection in an isolated antarctic station: transmission of the virus and susceptibility of the population.

Natural dissemination of viral respiratory illness to susceptible men may occur with surprising difficulty. This was especially evident during a 1977 outbreak of adenovirus type 21 (Ad-21) at McMurdo Station, a US research base in Antarctica. The unique circumstances at McMurdo allowed 125 men from the US to join and intermingle with 75 men who had wintered for 6 months in complete isolation. For an additional 5-week (September 2 to October 4, 1977) isolation period, respiratory illness etiology and transmission were monitored in the combined population. A total of 89% of the population was susceptible (neutralizing antibody titer, less than 1:3) to Ad-21 but only 15.0% were infected. Illness spread very slowly (1.5 cases/100 persons/week) with no epidemic peak and was much less severe than Ad-21 outbreaks in other settings. The incidence of infection (17.3%) and illness (9.6%) was low even in men who had wintered over, with values very similar to those of the newcomers (13.9% and 8.9%, respectively). Thus, despite a harsh environment and frequent prolonged gatherings of susceptible personnel, even a respiratory virus type with known epidemic potential was surprisingly difficult to transmit.

The presence of hypodense eosinophils and diminished chemiluminescence response in asthma.

Although peripheral blood eosinophilia is a prominent feature of asthma, the contribution of eosinophils to asthma has yet to be fully comprehended. Furthermore, study of isolated eosinophil function in asthma has been complicated by difficult purification methods and, now, the presence of hypodense eosinophils. In our study, eosinophils were isolated from normal subjects and patients with asthma. Two principal evaluations were performed: (1) a comparison of the density-gradient profiles on peripheral blood leukocytes from normal subjects and patients with asthma and (2) a comparison of the chemiluminescence (CL) response with normal dense eosinophils from these two study groups. Granulocyte preparations were initially isolated from Ficoll-Hypaque gradients and were then applied to a continuous Percoll density gradient. In asthma, 40.8 +/- 5.8% of the peripheral blood eosinophils were hypodense (defined as a density less than 1.081 gm/ml), whereas normal subjects had only 9.1 +/- 1.9% of this subpopulation (p less than 0.01). Functional assessment of purified (greater than 90%) normal dense eosinophils was made by measurement of CL to opsonized zymosan particles and the soluble stimulus phorbol myristate acetate. In asthma, eosinophil CL to zymosan, but not phorbol myristate acetate, was significantly less. Differences in eosinophil CL between normal subjects and subjects with asthma did not correlate with the severity of airway obstruction or the peripheral blood eosinophil count. The reasons for the appearance of hypodense eosinophils and diminished metabolic activity in asthma are not established but raise the possibility that their presence represents previous eosinophil activation.

Enhanced eosinophil luminol-dependent chemiluminescence in allergic rhinitis.

Eosinophils were isolated from patients with seasonal allergic rhinitis, and their functional activity was evaluated by their luminol-dependent chemiluminescence (CL) response to opsonized zymosan and phorbol 12-myristate 13-acetate (PMA). We found that eosinophils from patients with allergic rhinitis produced a significantly greater CL response to opsonized zymosan than did normal cells. Eosinophils from both subjects with allergic rhinitis and control subjects were isolated to a purity of 95% and elicited peak values of 1,101, 901 +/- 133,708 cpm/5 X 10(5) cells (n = 7) and 417,278 +/- 25,910 cpm/5 X 10(5) cells (n = 5), respectively. The enhanced eosinophil CL to zymosan was found at times when the patients were maximally symptomatic with hay fever symptoms to ragweed pollen and again when they were asymptomatic. Eosinophils from these patients with allergic rhinitis also had enhanced CL to PMA (0.01 mcg/ml), but this increased activity was largely limited to times of hay fever symptoms. No correlation was found between enhanced eosinophil CL activity and the number of circulating eosinophils in allergic individuals. In contrast to the increased eosinophil activity, neutrophil CL to zymosan and PMA was similar in allergic and normal individuals throughout the study. These data provide evidence for the existence of enhanced oxidative metabolic function in eosinophils from patients with allergic rhinitis and raise the possibility that this particular activity is important in hay fever.

Comparison of superoxide generation and luminol-dependent chemiluminescence with eosinophils and neutrophils from normal individuals.

Although eosinophilia is found in many allergic and hypersensitivity diseases, the function of the eosinophil is not clearly established. To evaluate and characterize this function, anticoagulated blood from normal subjects was separated into purified populations of both eosinophils and neutrophils by a modified method for Percoll gradients. With this separation procedure, highly purified populations of eosinophils (95.0% +/- 2.1%) and neutrophils (97.2% +/- 0.4%) were obtained. Functional response of these two isolated granulocyte cell types was measured by luminol-dependent chemiluminescence (CL) and superoxide generation to opsonized zymosan and phorbol 12-myristate 13-acetate (PMA). Both the eosinophil and neutrophil peak CL response and superoxide generation to zymosan (1 mg), in the presence of autologous serum (10%), were identical. In contrast, when PMA (10(-4) to 10(0) micrograms/ml) was the stimulant, eosinophil CL was at least twofold greater than the neutrophil light emission (1,595,741 +/- 122,435 cpm/5 X 10(5) cells vs. 765,448 +/- 24,171 cpm/5 X 10(5) cells; n = 6). This same differential in responsiveness was seen in superoxide generation. Thus, under certain conditions the eosinophil's respiratory burst may be greater than that of the neutrophil, and this differential in metabolic activity may contribute directly to the eosinophil's inflammatory potential.

Role of serum in stimulation of polymorphonuclear leukocyte, luminol-dependent chemiluminescence by influenza A.

Granulocyte membrane perturbation activates oxidative metabolism with the release of highly reactive species (O2-, H2O2, OH., and 'O2) and emission of light (chemiluminescence (CL)). Using the CL response as a measure of oxidative metabolism, we assayed the effects of influenza A on the granulocyte respiratory burst. Human polymorphonuclear leukocytes (PMNs) were isolated by Ficoll-Hypaque cushioning and dextran sedimentation. The isolated PMNs were incubated with egg-grown influenza A (H3N2) virus, or a medium control, in the presence of 1 microM luminol and fresh autologous serum (10%). No light emission occurred during the incubation of PMNs with the medium control. Influenza A (33 to 50% egg-infective-doses (EID50):1 PMN) stimulated PMN light emission with a maximal response (48,386 +/- 10,764 cpm/10(6) PMN) occurring at 37 degrees CL was dependent on the virus dose with a diminished response (6,041 +/- 3,200 cpm/10(6) PMN) occurring at a lower infectivity of 10 EID50:1 PMN. Chemiluminescence responses were similar with infective and with noninfective virus particles (heat inactivated, 56 degrees C X 2 h). Fresh serum was necessary for the influenza virus to cause a CL response. A significant correlation (p less than 0.01) existed between the level of light emission and the hemagglutination-inhibiting (HI) antibody titer to influenza A of the autologous serum. Virus in the absence of detectable antibody did not stimulate CL. The virus-associated CL was completely inhibited if autologous serum was heated (56 degrees C X 30 min) or if the PMNs were pretreated with cytochalasin B (5 mcg/ml X 5 min). These findings suggest that influenza A-associated PMN CL requires antibody, complement, and phagocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)