7. In diabetics without foot ulcers, cellulitis is most often due to Streptococcus and occasionally to Staphylococcus species.
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. aureus. Cellulitis due to anaerobes and gram-negative organisms in the absence of foot ulcers or similar lesions is distinctly unusual.
Another “pearl” about cellulitis: Group A strep cellulitis is often initially slow to respond to therapy. 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.
8. Quinolones are no longer highly reliable as empiric therapy against gram-negative infections.
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). Approximately 5–10% of E. coli are now quinolone resistant, and in some hospitals more than half of Pseudomonas aeruginosa are now quinolone resistant. 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.
9. VRE in the stool does not need to be treated.
The great majority of patients who test positive for VRE in a stool specimen never acquire an infection with VRE. 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.