digoxin and Pneumonia--Pneumococcal

Pulmonary affections in patients with legionellosis are the main ones. The affections of the heart, gastrointestinal tract and other organs and systems are less frequent. Some characteristic features of the legionellosis clinical process in the case described are indicated. The torpid process of chronic bronchitis, the two-phase pattern of the disease, dyspnea at 3-4 month intervals, intermissions, edema and failure of complex therapy with antibiotics and cardiac glycosides provided a tentative diagnosis of Legionella pneumonia with affection of the myocardium. The importance of early serological diagnosis (enzyme immunoassay) was shown. A new approach to the treatment of legionellosis with cefuroxime was of interest.

Topics: Atrial Fibrillation; Cefuroxime; Cephalosporins; Digoxin; Drug Therapy, Combination; Female; Humans; Legionnaires' Disease; Middle Aged; Myocarditis; Pneumonia, Pneumococcal

Normal CD-1 mice were administered digoxin (4 micrograms/kg/24 h) and infected with type 3 Streptococcus pneumoniae in order to assess the effects of the cardiac glycoside on the chemotactic responsiveness of peripheral blood neutrophils and the mobilization of granulocytes from storage pools. The chemotactic responses to autologous zymosan-activated serum (C5a) by neutrophils obtained from uninfected digoxin-treated and control animals were similar; comparable observations were made with circulating granulocytes isolated from animals at 24 or 48 h after intratracheal challenge with 5 x 10(5) colony-forming units (cfu) of bacteria. However, at 4 and 6 h after intratracheal pneumococcal challenge, the number of immature neutrophils in the peripheral blood was significantly lower in the glycoside-treated animals versus controls; at 24 and 48 h, these differences were not apparent. Following the intravenous inoculation of pneumococci, the number of circulating immature neutrophils was also found to be significantly lower at 4 and 24 h in animals given the cardiac glycoside versus controls. We conclude that digoxin disrupts host defense in experimental pneumococcal pneumonia and bacteremia by impairing the mobilization of neutrophils.

Topics: Animals; Chemotaxis, Leukocyte; Digoxin; Female; Germ-Free Life; Leukocyte Count; Mice; Neutrophils; Pneumonia, Pneumococcal

Digoxin was administered to normal CD-1 mice (4 micrograms/kg per 24 hr), and the mice were inoculated intratracheally with Streptococcus pneumoniae in order to assess the effects of the cardiac glycoside on pulmonary antibacterial mechanisms. Digoxin-treated animals experienced a worse survival rate than did controls (19 of 50 versus 33 of 50; P less than .01). When challenged with a high inoculum (1 X 10(6) cfu), animals given the glycoside demonstrated a significant impairment in their capacity to clear viable pneumococci from the lungs; the depression in pulmonary clearance was associated with a marked attenuation in the ability of digoxin-treated mice to recruit granulocytes and macrophages into the bronchoalveolar spaces. Following low inoculum challenge (1 X 10(5) cfu), animals treated with the cardiac glycoside exhibited an inefficient pulmonary clearance and a blunted macrophage influx. At clinically relevant concentrations, digoxin demonstrated no effect on the in vitro pneumococcidal activity of resident murine alveolar macrophages. We conclude that digoxin can disrupt host defense against pneumococcus by impeding the normal inflammatory response to organisms deposited into the lower respiratory tract.

Topics: Animals; Digoxin; Ethanol; Female; Inflammation; Kinetics; Lethal Dose 50; Leukocyte Count; Lung; Macrophages; Mice; Neutrophils; Pneumonia, Pneumococcal; Streptococcus pneumoniae