Bloodstream infections (BSIs), which represent the failure of the immune system to contain infection at a focal site and consequent disseminated disease, are a major cause of morbidity and mortality. The frequency of these infections, their epidemiology, and the invading organisms have changed in parallel with the evolution of medical care, particularly with the emergence of an increasingly ill and immunocompromised population of hospitalized patients who are often heavily dependent on medical support and indwelling devices. Currently, slightly more than 50% of BSIs are hospital acquired [1, 2].
With the development of potent antistaphylococcal b-lactam agents, Staphylococcus aureus gave way to gram-negative bacilli, often Enterobacteriaceae, as the predominant nosocomial pathogens in the 1970s. Nearly 75% of nosocomial infections were caused by gram-negative bacilli. However, by the early 1980s, a change in the spectrum of nosocomial pathogens was apparent, and gram-positive cocci began to reemerge as predominant nosocomial pathogens. The greater role of gram-positive cocci as causes of nosocomial BSIs continues and is a nationwide phenomenon.
It is interesting to take a more detailed look at the epidemiology and clinical significance of BSIs caused by gram-positive cocci. The time to onset of bacteremia varies depending on the infecting organism. Nosocomial bacteremia caused by viridans streptococci and S. aureus occurs earlier during hospitalization than does bacteremia caused by gram-negative bacilli, Candida, and enterococci. The average time to onset of bacteremia caused by streptococci and S. aureus is »2 weeks after the start of hospitalization. Gram-negative bacilli, Candida, and enterococci are encountered in blood cultures on average a week or so longer after the start of hospitalization. The mean time to onset of bacteremia caused by coagulase-negative staphylococci is »19 days after the start of hospitalization.
Organisms causing nosocomial BSIs vary depending on the location of patients within the institution. Coagulase-negative staphylococci are more likely to be isolated from cultures of blood specimens from patients in intensive care settings, whereas viridans streptococci and S. aureus are more commonly isolated from ward patients. Enterococci are isolated with similar frequency from patients in both settings. BSIs caused by viridans streptococci are associated with neutropenia and are commonly observed in patients on the hematology and oncology services. Crude mortality rates among patients with BSIs caused by these gram-positive cocci range from 17% to 32%; the lowest mortality rates are associated with coagulase-negative staphylococci, and the highest mortality rates have been noted among patients with enterococcal bacteremia.
Resistance to many of the antibiotics used to treat infections caused by gram-positive cocci is now commonplace in the isolates associated with nosocomial BSIs. In the SCOPE study, 80% of 3908 coagulase-negative staphylococci causing BSIs were resistant to methicillin and other b-lactam antibiotics, as were 29% of 1928 S. aureus isolates. Resistance to vancomycin was noted in 18% of all enterococci. Within the enterococci, resistance was notably segregated to Enterococcus faecium; among this species, the frequency of resistance to vancomycin was 50%, and that of resistance to ampicillin was 80%.
Although antibiotic resistance clearly limits therapeutic options for treating enterococcal infections, it is not clear whether resistance to vancomycin in infecting enterococci is associated with increased mortality. This lack of effect on mortality could be because vancomycin-resistant enterococci have intrinsically low virulence or because of the presence of more outcomedefining comorbid conditions in patients who develop infections with the resistant organisms.
