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Box 12 Cambridge, DC The above information must wait on each other: You must think each treatment certain and the world quantity used, or a monohydrate of quantities ordered. Because vancomycin does not fully penetrate the lungs, it is necessary to constantly monitor blood levels of the drug, and even then the correlation between those levels and the amount of drug that reaches the lungs is unclear.

According to Kollef, there is no need to monitor blood levels with linezolid therapy, and there are fewer known side effects than with vancomycin. Kollef's team previously published the first two controlled studies comparing the two drugs in hospital-associated pneumonia. They randomly assigned patients to receive either linezolid or vancomycin.

In their current paper, the team combined data from those two studies and analyzed results from the patients who had ventilator-associated pneumonia.

Linezolid was about 15 percent more effective in eradicating the infection than vancomycin 49 percent versus 34 percent , and overall survival rates in this population were marginally better with linezolid compared with vancomycin. The most striking difference appeared when the team separately analyzed results from the subset of patients with MRSA.

In this group, linezolid was more than 40 percent more effective in curing the infection 60 percent were cured with linezolid compared to 22 percent with vancomycin. Patients treated with linezolid were more than 22 percent more likely to survive than those given vancomycin 84 percent survived with linezolid versus 62 percent with vancomycin.

They also will examine whether higher doses of vancomycin improve the drug's efficacy in this population. Often the alternative diagnosis is suspected based on blood cultures obtained prior to the patient receiving broad-spectrum antibiotics in the emergency room. In the last 3 months we have seen patients with liver abscesses, endocarditis, and osteomyelitis initially felt to have community-acquired pneumonia whose blood cultures initiated prior to antibiotic therapy revealed a pathogen that caused a search for an alternative source of infection.

The vast majority of patients only need 2 blood cultures from 2 sites 20 minutes apart before initiation of antibiotic therapy. Patients in whom common skin contaminants may easily be interpreted as pathogens such as patients with prosthetic heart valves should have 3 sets of blood cultures to aid in the interpretation of cultures that are positive for skin contaminants such as coagulase negative staph.

Diabetic patients who have infections related to foot ulcers or ischemic lesions require broad-spectrum antimicrobial therapy active against anaerobes, gram-positives, and gram-negatives.

However, diabetic patients who are not critically ill who are admitted with a clinical picture typical for cellulitis tend to be infected with the same pathogens as non-diabetic patients.

We frequently encounter diabetic patients who present with a clinical picture of an uncomplicated cellulitis without ulcers or other lower-extremity lesions and are treated with broader-spectrum antimicrobial therapy than is needed for cellulitis.

Broader therapy is often more expensive, and it puts patients at risk for more adverse effects such as CDAD. The great majority of patients with cellulitis have infection with group A strep and other streptococci, and less often S. Cellulitis due to anaerobes and gram-negative organisms in the absence of foot ulcers or similar lesions is distinctly unusual.

The local findings may take 3 or 4 days to show improvement and there actually may be slight worsening despite 1 or 2 days of appropriate antibiotics. This is believed to be related to toxins produced by group A strep and other local tissue factors.

Even if an antimicrobial is successful in eradicating strep, there are still toxins in the tissues that produce aggressive local findings. We often get consulted about patients with cellulitis who after 2 days of antimicrobial therapy may have some improvement in their fever curve and white blood cell count but have worsening of the local findings.

These patients almost never need a change in antimicrobial therapy, but need more time—and elevation. I was taught by one of my mentors of the importance of elevating an extremity when treating cellulitis.

My clinical experience has borne out this wisdom. In addition, patients with lower-extremity edema or venous insufficiency or venous stasis who present with cellulitis must have edema and stasis aggressively treated for the cellulitis to respond to antimicrobial therapy. Five years ago in Ohio, if a patient presented with pyelonephritis or a complicated UTI as a community-acquired infection, it was unusual for the causative pathogen to be quinolone resistant.

Quinolones such as ciprofloxacin could be used as empiric therapy for serious gram-negative infections with a great deal of confidence that the causative agent would be sensitive.

In the last 5 years we have seen a steady, progressive increase in resistance to quinolones in both community acquired and nosocomial infections 7,8. Seriously ill patients with infections that are likely due to gram-negative rods should not be treated empirically with quinolone monotherapy in most settings. Oral quinolones, due to their excellent oral bioavailability, continue to have in important role in treating gram-negative infections, but their use should be based on the results of a culture with antimicrobial susceptibility.

Patients who are colonized with VRE in the stool will clear colonization over several weeks or months if there is no antimicrobial pressure to select for VRE. Infectious disease clinicians spend a lot of time trying to allay the fear of patients and families who become extremely nervous due to isolation procedures for VRE. My usual approach is to tell the patients that the only reason they are in isolation is to prevent VRE from spreading to the very, very small group of patients who actually are susceptible to infection with VRE, such as liver transplant patients.

I tell the family there is almost no chance that healthy family members will develop a VRE infection and that the VRE bacteria is normally found as a natural part of the human intestinal flora. VRE is simply 1 strain that has particular resistance to antibiotics, making it difficult to treat when infection occurs, but it is not more pathogenic. Infection with VRE is relatively rare and with the possible exception of cystitis or bladder colonization there is an extremely low risk of any actual infection despite VRE colonization.

Uncomplicated cystitis due to VRE can usually be treated with nitrofurantoin. In the last 5 years in the United States, there has been a steady increase in MRSA infections in patients without traditional risk factors 9, Historically, clinicians have been concerned about MRSA in nursing home patients, patients in other long-term care facilities, injection drug users, and hospitalized patients.

In the last 5 years there have been increasing numbers of patients with MRSA with none of these risk factors. Often these patients present with a serious life-threatening S. It is now appropriate to give vancomycin empirically for patients who have serious illnesses due to suspected S.

As ID practitioners, we do not want to encourage overuse of vancomycin, and clinicians should quickly switch to other agents if the patient proves not to be infected with MRSA. While vancomycin is a useful drug, it is considered inferior to the beta-lactams for many infections, such as bone or joint infections, and should only be used in patients with documented or suspected MRSA, or patients intolerant of beta-lactams.

Several new drugs provide alternatives to vancomycin for MRSA, including linezolid and daptomycin. Both of these agents are more expensive and have not proven in clinical trials to be superior with the possible exception of linezolid for MRSA pneumonia.