Methicillin-resistant Staphylococcus aureus (MRSA) has become a major nosocomial pathogen in many hospitals worldwide. Even more alarming, MRSA strains that are vancomycin intermediate-susceptible are isolated with increasing frequency, making therapy for staphylococcal infections even more difficult and prevention more important than ever. Spread of S. aureus in hospitals and infection control measures are reviewed. The major sources of S. aureus in hospitals are septic lesions and carriage sites of patients and personnel. Carriage often precedes infection. The anterior nares are the most consistent carriage site, followed by the perineal area. Skin contamination and aerial dissemination vary markedly between carriers and are most pronounced for combined nasal and perineal carriers. The principal mode of transmission is via transiently contaminated hands of hospital personnel. Airborne transmission seems important in the acquisition of nasal carriage. Infection control strategies include screening and isolation of newly admitted patients suspected of carrying MRSA or S. aureus with intermediáte resistance to vancomycin, implementation of an infection control program to prevent transmission of resistant strains between patients and hospital personnel, and institution of a proper antibiotic policy to minimize antibiotic resistance development. MRSA carriers should be treated with intranasal antibiotics, e.g. mupirocin, and skin disinfectants to eliminate carriage. Education of hospital personnel is essential. Improved knowledge about the best ways to ensure favourable infection control practices is needed. Active intervention against the spread of MRSA is important.
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).
Polymorphonuclear leukocytes of 18 patients during 19 episodes of active bacterial infection produced increased chemiluminescence (mean +/- standard error [SE], 56.3 +/- 4.4 X 10(3) cpm) when the production was compared to that of 29 uninfected controls (35.3 +/- 2.4 X 10(3) cpm; P less than 0.01). Chemiluminescence production remained increased with persistent infection but fell to the levels of controls with appropriate therapy. Phagocytic uptake as determined with radiolabeled bacteria was increased, and chemotactic responsiveness was markedly enhanced in the patients (mean index +/- SE, 260 +/- 51) when these responses were compared with those of controls (77 +/- 18). Chemiluminescence and chemotactic activity correlated in the patients with bacterial infection (r = 0.76), but one function did not appear to depend upon the intactness of the other. The ratio of cyclic guanosine 3',5'-phosphate to cyclic adenosine 3',5'-hosphate in the polymorphonuclear leukocytes of patients with infections (mean +/- SE, 0.102 +/- 0.0008) was also significantly higher than in controls (0.067 +/- 0.007). These data indicate that the polymorphonuclear leukocytes of the majority of patients with active bacterial infection are in an activated state both functionally and metabolically.
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