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Exacerbations of chronic bronchitis may be caused by a variety of bacterial and viral agents. There is ample documentation of a role for Hemophilus influenza, Streptococcus pneumonia, Mycoplasma pneumoniae, influenza A and B viruses, and several other respiratory viruses in causing these exacerbations. Because of the lack of frequency of exacerbations (once every 20 to 78 weeks) and the wide range of pathogens, trials of prophylaxis with antibiotics have been difficult to conduct. Controlled trials conducted since the 1950s have shown mixed results, some demonstrating a reduction in the number of exacerbations and others failing to show efficacy. Of the antibiotics used, tetracycline seemed the most effective. Both the pneumococcal polysaccharide and killed influenza virus vaccines have been suggested for patients with chronic bronchitis. The antiviral drug amantadine has been recommended when vaccine cannot be used. This reviewer concludes that prophylactic antibiotics should be used in selected patients with one or more exacerbations yearly using a drug such as tetracycline. A one-time dose of pneumococcal vaccine and the annual use of killed influenza vaccine are also reasonable. During an influenza A epidemic, amantadine should be considered for unvaccinated patients. Future studies should study intermittent v chronic prophylaxis with cheap but appropriate antibiotics (chosen for their microbial spectrum), and should test newer antiviral vaccines and antiviral drugs as they become available.

A Brucella melitensis infection involved three persons. The infections were acquired by contact with a culture suspension that had been spilled during a laboratory exercise. One of the patients had only indirect contact with the spilled culture, probably contact with contaminated fomites. Another of the patients developed a clinical remission before treatment with antibiotics and relapsed after six months. This patient also had a positive bone marrow culture when blood cultures were negative. The type of antibody response persisting in the sera of convalescents was studied by treating the sera with mercaptoethanol and rabbit antihuman IgM sera. In the patient who relapsed, IgG antibody predominated, whereas IgM persisted for over two years in the patient without relapsing disease.

Using an enzyme-linked immunosorbent assay for measuring IgG-, IgA-, and IgM-class antibodies to pneumococcal capsular polysaccharides, we studied responses of debilitated patients 71 to 95 years of age (average, 85 years) in nursing homes to 14-valent pneumococcal vaccine. A control group consisting of normal adults 23 to 41 years of age (average, 27 years) was used for comparison. Normal adults at 28 days postvaccination showed rises in IgG-, IgA-, and IgM-class antibodies to nearly all capsular polysaccharides. The IgG- and IgA-class antibody responses of the elderly patients did not differ significantly from those of the normal adults in most instances. IgM-class responses of the elderly subjects were poor and were significantly lower than those of the control group for six of 14 serotypes. Overall, these studies demonstrate that elderly patients, like healthy younger adults, mount a polyclonal antibody response to pneumococcal polysaccharide vaccine.

An outbreak of serious infections caused by Streptococcus pyogenes occurred in a nursing home for elderly patients. The outbreak began in mid-winter and continued for 12 months. Thirteen residents and two nurses had infections. Severity of infection was worse in residents, who developed sepsis, necrotizing fasciitis, cellulitis, septic arthritis, pneumonia, and conjunctivitis; in contrast, the nurses had pharyngitis only. Six of thirteen residents required acute hospital care, and the index case died with sepsis. Typing of S. pyogenes was done in 13 of 15 cases, and the same serotype (M-non-typable, T-25) was found. Control measures consisted of identifying all patients with infections, obtaining cultures, and providing prompt treatment. Patients in nursing homes are highly susceptible to serious infections with S. pyogenes.

All employees, including physicians, of a 450 bed hospital were monitored for puncture wounds from contaminated needles over a four-year period. Five hundred seventy-nine incidents were reported. Nurses were involved in 66% of instances, housekeeping 16%, laboratory workers 10%, physicians 4% and x-ray technicians 4%. Many puncture wounds were avoidable, suggesting the need for ongoing employee education. In 67% of the injuries blood from the patient in whom the needle had been used was tested for HBsAg; 1% of those tested were positive. In such instances, employees were given immune globulin. These data indicate that needle puncture wounds are a frequent problem for hospital workers, and carry a risk for transmitting hepatitis B. Efforts to prevent such injuries are needed.

In early 1974, seventeen children were treated for Reye syndrome. Thirteen of these were studied for laboratory evidence of concomitant viral infection. Influenza B/Hong Kong was isolated from the pharynx in four of nine 1974 cases tested. One child had just recovered from varicella. Adenovirus type 2 and respiratory syncytial virus were isolated from two additional patients. Serologic tests for influenza suggested concomitant or recent influenza B infection in ten of 13 of 1971 cases. During February 1975, six children were treated for this syndrome. Influenza A/Port Chalmers was recovered from three in six 1975 cases, and all six showed significant antibody rises to influenza A. These studies suggest that influenza viruses provide a trigger mechanism for the development of Reye syndrome in susceptible children.

After a local epidemic of A/USSR influenza, immunologic parameters related to influenza A/USSR/90/77 (H1N1) virus were studied in four age groups: elderly persons (greater than or equal to 64 years), healthy adults (20-44 years), children (six to 13 years), and neonates (who served as controls). Sera from the first three groups had nearly equivalent titers of hemagglutination-inhibiting antibody (geometric mean titers, 1:8-1:11), which were greater than those in cord blood of neonates. Lymphocyte proliferation responses to influenza A/USSR viral antigens among study groups were similar, with mean stimulation ratios (to whole virus) of 4.2-5.4; neonatal cord blood samples were unresponsive (stimulation ratio, 1.1). In contrast, the magnitude of antibody-dependent cellular cytotoxicity against baby hamster kidney target cells infected with influenza A/USSR virus was significantly greater with lymphocytes from adults and elderly persons (P less than 0.05) than with those from children.

The peripheral blood lymphocyte response and hemagglutination inhibition antibody titers were measured in nine adults before and after immunization with a killed split influenza virus vaccine. Cord blood lymphocytes were tested with the influenza antigen to exclude a nonspecific mitogenic effect. All of the subjects demonstrated preexisting antibody titers and antigen recognition by lymphocytes prior to immunization. The in vitro lymphocyte response after vaccination parallels the humoral antibody response to influenza antigen.

Children receiving smallpox, measles, and yellow fever vaccines simultaneously at separate sites responded adequately to all three vaccines. In those children, 9 months of age and older, who received these three vaccines in addition to diphtheria-pertussis-tetanus vaccine, there was a decrease in measles seroconversion rates from 89% to 70%. Possible interactions between live and killed vaccines should be considered when the administration of multiple antigens is planned.