Updates: Resistant CMV During Empiric Therapy; High Rate of False-Negative Rectal Swabs for VRE?; Influenza 2002/2003
February 15, 2002 4 minutes read
Resistant CMV During Empiric Therapy
Source: Limaye AP, et al. J Infect Dis. 2002;185:20-27.
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Lung transplant patients are at significant risk for invasive CMV infection, and are frequent recipients of preventative ganciclovir therapy. Limaye and colleagues at the Fred Hutchinson Cancer Research Center in Seattle retrospectively assessed the frequency of ganciclovir-resistant (gan-R) CMV infection in a group of lung transplant patients who received pre-emptive ganciclovir therapy. Patients who were CMV seropositive (R+) (n = 34) or who received an organ from a seropositive donor (R-/D+) (n = 3) received pre-emptive pp65 antigen-directed ganciclovir therapy for at least 4 weeks or longer depending on their antigen levels. An additional 8 patients (D+/R-) received empiric ganciclovir prophylaxis (5 mg/kg daily) for 100 days post-transplantation, irrespective of their antigen levels or CMV DNAemia.
Invasive CMV disease occurred in 18 of 37 (48.6%) patients receiving antigen-directed pre-emptive ganciclovir therapy and 2 of 8 (25%) patients receiving prophylactic therapy. None of the D+/R- patients developed invasive CMV within 100 days of transplantation, but 34% did by 1 year. In contrast, 29% of R+ patients developed invasive CMV infection within 100 days of transplantation, and 60% developed CMV infection within 1 year, all of whom received empiric antigen-directed therapy. CMV isolates from 4 (9%) patients were gan-R, all of which contained the UL97 mutation. Interestingly, Gan-R was more frequent in D+/R- patients than in R+ patients (3 of 11 vs 1 of 34; P = .04). Fortunately, in patients receiving ganciclovir, mutations in the UL97 gene, which prevents phosphorylation of ganciclovir, are generally more frequent than those involving the DNA polymerase. Isolates that exhibit only the UL97 mutation remain sensitive to foscavir and cidofovir, neither of which requires phosphorylation.
High Rate of False-Negative Rectal Swabs for VRE?
Source: D’Agata EM, et al. Clin Infect Dis. 2002;34:167-172.
Rectal swab specimens for identifying patients with gastrointestinal colonization with vancomycin-resistant enterococci are standard procedure in many institutions. In order to increase the yield, the Hospital Infection Control Advisory Practices Committee recommends that such cultures be performed using selective media containing vancomycin, although this approach has never been validated. In this study, the results of rectal and skin swabs were compared with quantitative stool cultures in 13 patients with known VRE colonization or infection. Both rectal and skin swabs were plated on media containing 6 mg/mL of vancomycin; after 48 hours, skin swabs were subcultured to sheep blood agar. Two sites for skin swabs were selected—the anterior neck and the antecubital area, both commonly used for venipunctures.
The overall sensitivity of rectal swabs in the detection of VRE was only 58%, ranging from 0% for patients with low levels of VRE in stool (< 4.5 logs cfu/gram) to 100% in patients with heavier colonization (> 7.5 logs cfu/gram. Surprisingly, skin swabs were more likely to be positive, especially at lower levels of fecal colonization.
In patients receiving antimicrobials with anti-anaerobic activity, who are more likely to have higher levels of fecal VRE, rectal swabs are sufficiently sensitive. However, in patients who are no longer receiving antibiotics, who are more likely to have low-level fecal carriage, (see Clinical Briefs, March 1, 2001) rectal swabs may be falsely negative ~50% of the time. Although often considered "cleared" of their VRE from an infection control standpoint, these patients would still present a risk for transmission of VRE, especially if they are incontinent, diapered, or have diarrhea.
Influenza 2002/2003
Source: PHLS. Press Release, Feb. 6, 2002; ProMED-mail post, Feb. 7, 2002. www.promedmail.org.
Influenza experts, who meet annually to determine the composition of the following year’s influenza vaccine, are focused on a new strain of Influenza A virus (H1N2), which has been identified as causing human infection in Israel, England, and Egypt. This new subtype appears to contains a little bit of each of 2 influenza viruses that have been circulating in the human population for years, H1N1 and H3N2. Both the H1 hemagglutinin and the N2 neuraminidase of the new strain appear very similar to the corresponding parts of the existing subtypes. A similar reassortment occurred in China during the 1988/1989 flu season, although it did not spread farther at that time, and has also been found in swine for more than 10 years. This information provides an even more compelling reason to strive for maximal vaccine coverage of the elderly and high-risk patients next year.
Dr. Kemper, Clinical Associate Professor of Medicine, Stanford University, Division of Infectious Diseases; Santa Clara Valley Medical Center, is Associate Editor of Infectious Disease Alert.
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