All episodes of bloodstream infection in patients admitted to a Norwegian university hospital in 1974-1979 and in 1988-1989 were analyzed; altogether, there were 1,447 episodes involving 1,286 patients, and 54.3% of all episodes were hospital-acquired. The incidence of bloodstream infection increased between the two periods studied from 4.26/1,000 admissions to 8.71/1,000. Crude mortality rates were 27.6% and 18.8% and attributable mortality rates were 12.3% and 6.9% in the first and second periods, respectively. Patients > 60 years of age accounted for more than half of the bloodstream infections; mortality in this group was significantly higher than that among younger patients (31.4% vs. 13.9%). The frequency of isolation of Enterobacteriaceae decreased from 48% in the first period to 34% in the second, while the rate of isolation of coagulase-negative staphylococci increased from 6.5% to 16.9%. The shift in etiology may be explained in part by the occurrence of significantly more bloodstream infections related to intravascular devices, endocarditis, and skin and wound infections and of significantly fewer episodes related to abdominal or genitourinary disease in the second than in the first period. Almost all isolates of Enterobacteriaceae were susceptible to newer cephalosporins and aminoglycosides. In 1974-1979, 96 (69.1%) of 139 patients with septic shock died; in 1988-1989, the figure was 35 (52.2%) of 67 patients (P = .019). Clinical factors predictive of an adverse outcome were septic shock (odds ratio for first/second period, 12.7/4.6), intensive care treatment (not significant/10.6), malignant disease (4.6/2.6), any underlying disease (4.2/not significant), diabetes mellitus (3.6/not significant), age of> 60 years (not significant/3.0), and pulmonary source of infection (not significant/2.8).
During the period 1973-1984, 72 patients with infective endocarditis (IE) were hospitalized in the medical department, Bergen University Hospital. The male/female ratio was 1.25/1, the mean age 55.3 years. 35 infections were caused by streptococci, 18 by staphylococci, 6 by other microorganisms and in 13 cases no causal organism was found. Only 13 patients had rheumatic heart disease. The overall mortality was 35%, and the mean age of the patients who died was 65 years. The case fatality rates for staphylococcal and streptococcal endocarditis were 61 and 24% respectively. In the period 1973-1978 the case fatality rate was 50% compared to 26% during 1979-1984. The proportion of patients with culture-negative endocarditis was reduced from 31 to 11% from the first to the second half of the study and the percentage of patients who received antibiotics before diagnosis decreased from 81 to 58%. Valve replacement was performed in 4 patients with staphylococcal and 15 with streptococcal infections. Seven cases (mean age 73.4 years) were diagnosed at necropsy; 3 with staphylococcal infections. With increased clinical awareness of IE, liberal use of blood cultures, better diagnostic tools and earlier surgical intervention, especially in staphylococcal infections, a further reduction in mortality should be possible.
Chemiluminescence (CL) production by polymorphonuclear leukocytes (PMNLs) was examined in 63 patients with bacterial infections and 63 healthy controls. The production was significantly higher in the patients (mean +/- standard error = 134.5 +/- 5.0 X 10(3) cpm) than in the controls (118.9 +/- 2.5 X 10(3) cpm; p less than 0.05). In 38 patients CL values were within the normal range and in 19 patients above. CL production below that of any control occurred in 6 patients: 3 (of 4) with staphylococcal endocarditis, 2 (of 4) with pneumococcal meningitis and 1 with salmonella septicaemia and osteomyelitis. PMNL hexose monophosphate shunt activity as measured by glucose metabolism correlated with CL production. Patients with low CL production more often had large numbers of juvenile and immature myeloid cells in the peripheral blood than patients with normal or high CL values. 3/6 patients with low CL values died, 2/38 with normal and 0/19 with high values. Directed and spontaneous PMNL migration was examined in 39 of the 63 patients with bacterial infections. 13 patients had PMNLs with higher directed and 16 with higher spontaneous migration capacity than their corresponding controls. The remaining patients had PMNLs with lower migration capacity. 2 of the 39 patients died. Each had PMNLs with low migration capacity. CL production by PMNLs was examined in 16 patients with viral infections and 16 healthy controls. The production was significantly lower in the patients (mean +/- standard error = 105.5 +/- 6.6 X 10(3) cpm) than in the controls (129.1 +/- 5.3 X 10(3) cpm; p less than 0.01). 15 patients had lower values than their corresponding controls. The PMNL migration capacity was also lower in the patients. These findings indicate that the majority of patients with bacterial infections have PMNLs with normal or increased function. However, some patients have reduced PMNL function and this reduction may contribute to a fatal outcome of the disease. Patients with viral infections usually have reduced PMNL function.
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