Archive for February 15th, 2008

Update: Influenza Activity — United States, September 30, 2007–February 9, 2008

This report summarizes U.S. influenza activity* since the beginning of the 2007–08 influenza season (September 30, 2007) and updates the previous summary (1). From September through early December, influenza activity remained low in the United States. Activity increased from early December through the end of the year and has continued to increase in January and February.

Viral Surveillance

During September 30, 2007–February 9, 2008, World Health Organization (WHO) and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States reported testing 94,502 specimens for influenza viruses, and 10,568 (11%) tested positive (Figure 1). Of these positive specimens, 8,889 (84%) were influenza A viruses, and 1,679 (16%) were influenza B viruses. A total of 2,299 (26%) of the influenza A viruses have been subtyped: 1,033 (45%) were influenza A (H1N1) viruses, and 1,266 (55%) were influenza A (H3N2) viruses. Although influenza A (H1N1) viruses predominated through mid-January, an increasing proportion of subtyped influenza A viruses are influenza A (H3N2) viruses. Influenza A (H3N2) viruses were reported more frequently than influenza A (H1N1) viruses during January 20–February 9. During the week ending February 9, H3N2 became the predominant virus for the season overall.

This season, more influenza A viruses than influenza B viruses have been identified in all regions. Among influenza A viruses, influenza A (H1N1) has predominated in the New England, Mid-Atlantic, West North Central, Mountain, and Pacific regions, and influenza A (H3N2) has predominated in the East North Central, South Atlantic, East South Central, and West South Central regions. This season, laboratory-confirmed influenza has been reported by the District of Columbia and 47 states from all nine surveillance regions.§

Antigenic Characterization

Since September 30, 2007, CDC has antigenically characterized 250 influenza viruses submitted by U.S. laboratories: 117 influenza A (H1N1), 65 influenza A (H3N2), and 68 influenza B viruses. One hundred seven (91%) of the 117 influenza A (H1N1) viruses were characterized as A/Solomon Islands/3/2006-like, the influenza A (H1N1) component of the 2007–08 influenza vaccine for the Northern Hemisphere and the 2008 influenza A (H1N1) component of the vaccine for the Southern Hemisphere; 10 (9%) of the 117 influenza A (H1N1) viruses were observed to have somewhat reduced titers with antisera produced against A/Solomon Islands/3/2006. Nine (14%) of the 65 influenza A (H3N2) viruses were characterized as A/Wisconsin/67/2005-like, the influenza A (H3N2) component of the 2007–08 influenza vaccine for the Northern Hemisphere. Fifty-three (81%) of the 65 influenza A (H3N2) viruses were characterized as A/Brisbane/10/2007-like, a recent antigenic variant that has evolved from A/Wisconsin/67/2005-like. A/Brisbane/10/2007-like virus is the recommended influenza A (H3N2) component for the 2008 Southern Hemisphere vaccine. Three (5%) of the 65 influenza A (H3N2) viruses were observed to have somewhat reduced titers with antisera produced against A/Wisconsin/67/2005 and A/Brisbane/10/2007.

Influenza B viruses currently circulating can be divided into two antigenically distinct lineages represented by B/Victoria/02/87 and B/Yamagata/16/88. Four (6%) of the 68 influenza B viruses characterized belong to the B/Victoria lineage of viruses. One virus with B/Victoria lineage, B/Malaysia/2506/2004, is the influenza B component of the 2007–08 influenza vaccine. Sixty-four (94%) of the 68 influenza B viruses belong to the B/Yamagata lineage of viruses.

Outpatient Illness Surveillance

For the week ending February 9, the percentage of outpatient visits for influenza-like illness (ILI)reported by approximately 1,400 U.S. sentinel providers in 50 states, Chicago, the District of Columbia, and New York City was 5.7%. This marks the seventh consecutive week that the percentage of outpatient visits for ILI exceeded the national baseline of 2.2%.** ILI was reported above region-specific baselines in all nine influenza surveillance regions. Also for the week ending
February 9, the percentage of outpatient visits for acute respiratory illness (ARI)†† reported by approximately 800 U.S. Department of Defense (DoD) and Department of Veterans’ Affairs (VA) BioSense§§ outpatient treatment facilities was 3.5%,¶¶ which was above the national baseline of 3.2% (Figure 2).

State-Specific Activity Levels

Until the week ending January 5, widespread*** influenza activity had not been reported in any state. During the week ending January 5, widespread influenza activity was reported in Colorado. The number of states reporting widespread activity has increased each week. For the week ending February 9, widespread activity was reported by 44 states, and regional activity was reported by five states (Figure 3).

Pneumonia and Influenza-Related Mortality

Pneumonia and influenza (P&I) was listed as an underlying or contributing cause of death for 7.6% of all deaths reported through the 122 Cities Mortality Reporting System for the week ending February 9. This percentage was above the epidemic threshold of 7.2% for the week††† and marked the fifth consecutive week that P&I deaths were above the epidemic threshold since influenza activity began rising in the United States (Figure 4).

Influenza-Associated Pediatric Hospitalizations

Pediatric hospitalizations associated with laboratory-confirmed influenza infections are monitored by two population-based surveillance networks, the Emerging Infections Program (EIP) and the New Vaccine Surveillance Network (NVSN). During November 4, 2007–January 26, 2008, the preliminary laboratory-confirmed influenza-associated hospitalization rate reported by NVSN for children aged 0–4 years was 0.73 per 10,000. During September 30, 2007–February 2, 2008, EIP sites reported a preliminary laboratory-confirmed influenza-associated hospitalization rate of 0.36 per 10,000 for children aged 0–17 years. For children aged 0–4 years, the rate was 1.0 per 10,000, and for children aged 5–17 years, the rate was 0.1 per 10,000.§§§

Influenza-Related Pediatric Mortality

As of February 9, a total of 10 pediatric deaths among children with laboratory-confirmed influenza had been reported to CDC through the National Notifiable Diseases Surveillance System for the 2007–08 influenza season. Ages of children who died ranged from 4 months to 14 years, with a median of 5.5 years. During the preceding three influenza seasons, the numbers of influenza-related pediatric deaths reported to CDC have ranged from 46 to 74.

Resistance to Antiviral Medications

During this influenza season, a small increase in the number of influenza viruses resistant to the neuraminidase inhibitor, oseltamivir, has been observed. Among the 350 influenza A and B viruses tested during the 2007–08 influenza season, 16 (4.6%) have been found to be resistant to oseltamivir. All of the oseltamivir-resistant viruses have been influenza A viruses (16 of 270, 5.9%). Of the resistant viruses, all are of the H1N1 subtype and have been determined to share the same genetic mutation that confers oseltamivir resistance. These 16 viruses represent 8.1% of the 198 influenza A (H1N1) viruses that have been tested, an increase from four (0.7%) of 588 influenza A (H1N1) viruses tested during the 2006–07 season. No resistance to oseltamivir has been determined among the 72 influenza A (H3N2) or the 80 influenza B viruses tested, and no antiviral resistance to zanamivir has been detected in any subtype. Adamantane resistance continues to be high; 87 (32%) of 271 influenza A viruses tested were resistant to adamantanes (i.e., amantadine or rimantadine), including 99% of influenza A (H3N2) viruses and 7.6% of influenza A (H1N1) viruses tested. Adamantanes are not recommended for the prevention or treatment of influenza this season because of the high rate of resistance among circulating influenza A viruses.

Editorial Note:

During October—December 2007, the United States experienced low but increasing levels of influenza activity. During January and early February, influenza activity increased more rapidly. For the week ending February 9, a total of 49 states reported either widespread or regional activity. During the most recent three influenza seasons (2004–05, 2005–06, and 2006–07), the number of states reporting regional or widespread activity peaked at 41–48 states. During this season, influenza virus isolates have been reported in all nine surveillance regions in the United States and, during the week ending February 9, 33% of specimens tested for influenza were positive. The peak percentage of specimens testing positive for influenza during the preceding three seasons ranged from 23% to 28%. During the week ending February 9, 5.7% of outpatient visits to sentinel providers were for influenza-like illness (ILI). The peak percentage of visits for ILI in the three previous seasons ranged from 3.3% to 5.4%.

Since 1977, influenza A (H1N1), influenza A (H3N2), and influenza B viruses have circulated globally. Each year’s influenza vaccine contains a virus representing each of these three distinct influenza virus groups. The three viruses selected to be included in this season’s vaccine were selected in February 2007 as the viruses that appeared most likely to be circulating during this influenza season (2). The degree of antigenic match between current influenza vaccine strains and the influenza viruses that are circulating this season will continue to be assessed as more viruses become available for analysis. To date, 91% of influenza A (H1N1) viruses sent to CDC for antigenic characterization were similar to A/Solomon Islands/3/2006, the influenza A (H1N1) component of the 2007–08 influenza vaccine. Although the majority of influenza A (H3N2) and influenza B viruses are not optimally matched, vaccination with the trivalent influenza vaccine continues to be recommended because the vaccine can provide partial protection against related strains and reduce the risk for influenza-related complications and deaths (3–6). In addition, the vaccine contains three strains, and communities can experience outbreaks with more than one strain of influenza in a given year.

Vaccination with trivalent influenza vaccines remains the best method for preventing influenza and its potentially severe complications. Although influenza activity is on the rise, vaccination during the current season still can provide benefit. Because persons require approximately 2 weeks after vaccination to develop immune response to vaccination, use of neuraminidase inhibitors for prevention of influenza in the 2 weeks after vaccination might be considered, especially for persons at high risk during a documented influenza outbreak (7).

Antiviral medications are an important tool for treatment of influenza and also can be used for prevention. Recent studies have identified a considerable protective effect of antiviral treatment against complications associated with influenza (8), including death among older adults hospitalized with laboratory-confirmed influenza (9). This season, a low level of resistance to the influenza antiviral drug oseltamivir among influenza A viruses (16 of 270 tested, 5.9%) has been detected. All 16 resistant viruses identified this season were of the influenza A (H1N1) subtype and share the same genetic mutation; this mutation is the most common mutation in this subtype that confers resistance to oseltamivir. Given the low level of resistance to oseltamivir, the finding of resistance only in influenza A (H1N1) viruses, and no resistance to zanamivir, these drugs continue to be recommended for the treatment and prophylaxis of influenza (10). Although recommendations for use of antiviral medications have not changed, enhanced surveillance for detection of oseltamivir-resistant viruses is ongoing and will enable continued monitoring for changing trends over time. In addition to vaccination and antivirals, other means of decreasing the spread and impact of influenza include frequent handwashing, staying home from work or school when ill, and covering the nose or mouth with a tissue when coughing or sneezing. Additional information is available at http://www.cdc.gov/flu/protect/habits.htm.

 

References

  1. CDC. Update: influenza activity—United States, September 30–December 1, 2007. MMWR 2007;56:1287–91.
  2. Recommended composition of influenza virus vaccines for use in the 2007–2008 influenza season. Wkly Epidemiol Rec 2007;82:69–73.
  3. Edwards KM, Dupont WD, Westrich MK, Plummer WD Jr, Palmer PS, Wright PF. A randomized controlled trial of cold-adapted and inactivated vaccines for the prevention of influenza A disease. J Infect Dis 1994;169:68–76.
  4. Nichol KL, Nordin JD, Nelson DB, Mullooly JP, Hak E. Effectiveness of influenza vaccine in the community-dwelling elderly. N Engl J Med 2007:357:1373–81.
  5. Shuler CM, Iwamoto M, Bridges CB. Vaccine effectiveness against medically attended, laboratory-confirmed influenza among children aged 6 to 59 months, 2003–2004. Pediatrics 2007;119:e587–95.
  6. Russell KL, Ryan MA, Hawksworth A, et al. Effectiveness of the 2003–2004 influenza vaccine among U.S. military basic trainees: a year of suboptimal match between vaccine and circulating strain. Vaccine 2005;23:1981–5.
  7. CDC. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2006;55(No. RR-10).
  8. Kaiser L, Wat C, Mills T, Mahoney P, Ward P, Hayden F. Impact of oseltamivir treatment on influenza-related lower respiratory tract complications and hospitalizations. Arch Intern Med 2003;163:1667–72.
  9. McGeer A, Green KA, Plevneshi A, et al. Antiviral therapy and outcomes of influenza requiring hospitalization in Ontario, Canada. Clin Infect Dis 2007;45:1568–75.
  10. CDC. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP), 2007. MMWR 2007;56(No. RR-6).

 

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Clinical Outcome of Patients With Upper-Extremity Deep Vein Thrombosis

 

by Munoz FJ,  Mismetti P, Poggio R, et al

 

Chest 2008; 133:143-148   

SUMMARY

Background: The significance and outcome of upper-extremity deep vein thrombosis (UEDVT) is not well-known due to the relative infrequency of the condition.  It has been believed that the condition is benign and self-limited. 

Objective: To determine the clinical characteristics and three-month outcome of patients who present with UEDVT.  Design: Prospective analysis based on data from the RIETE Registry.  This is an ongoing international (Spain, France, Italy, Israel, Argentina) registry of consecutive patients who have objectively-confirmed symptomatic pulmonary embolism (PE) or acute DVT.    

Population:  There were 11,564 DVT patients in the RIETE registry.  From this population, 512 (4.4%) were diagnosed with UEDVT and make up this study. 

Results: Clinically overt PE was present in 9% of those with UEDVT compared to 29% of those with lower extremity DVT (95% CI, 0.18 to 0.33).  For both groups, the 3-month outcome was similar.  38% of the UEDVT patients had cancer and 45% had catheter-related DVT (e.g. central lines, ports, peripheral lines, and pacemakers).  91% of the patients were initially treated with low-molecular-weight heparin (LMWH) which continued long-term for ¾ of them.  Three-quarter of those with no cancer were switched to oral agents.  At the 3-month follow-up, the cancer UEDVT patients when compared to the remaining UEDVT patients had an increased incidence of major [overt, requiring transfusions, or in enclosed body spaces] bleeding (4.1% vs 0.9%), recurrent venous thromboembolism (6.1% vs 2.8%) and deaths (22% vs 3/5%).  The 30 UEDVT patients who had a composite event (recurrent DVT, symptomatic PE, major bleeding) were significantly older, more likely to have cancer, and more likely to be symptomatic with PE. 

Conclusion:  UEDVT patients are more likely not to have overt PE compared to lower extremity DVT patients, but the 3 month outcome is the same for both groups.  Cancer UEDVT patients have the worse outcomes.  Comment:  This study supports the concept that UEDVT is a not a benign condition.  Once it’s diagnosed, then an active search for PE should be considered since oftentimes it’s occult.

“Perforated and Nonperforated Appendicitis: Defect in Enhancing Appendiceal Wall – Depiction with Multi-Detector Row CT”.

Tsuboi M, Takase K, Kaneda I, et al

Radiology 2008 January 246 141-148

SUMMARY

Background:  The approach is different when surgeons have to deal with a nonperforated appendicits compared to a perforated one.  Options for a perforated appendix may include antibiotics and/or drainage with or without interval surgery.  While single-section helical CT is becoming, arguably, the standard for diagnosing acute appendicitis, it has its limitations with regard to distinguishing a perforated appendix.  Can the use of the multi-detector row helical CT be more helpful with this particular problem? 

Objective: To evaluate the accuracy of multi-detector row helical CT with only IV contrast material for the diagnosis of perforated appendicitis. 

Design:  Retrospective analysis.  Population:  102 patients (60 male, mean age: 37.3 years, range: 4-82 years) with surgically- and pathologically-proven appendicitis. 

Interventions:  Case reports and CT findings were collated.  Two radiologists, blinded to the surgical and pathological findings, reviewed the multi-detector row helical CTs looking for evidence of perforation.  Imaging signs of perforation included appendiceal wall defects, abscess, phegmon, extraluminal air, and extraluminal appendicoliths. 

Results:  Of the 102 patients, 40 had a perforation.  An imaging abnormality was present in 38.  Two patients in the nonperforated group were falsely positive for a wall defect.  There were 2 false-negatives.  For multi-detector row helical CT diagnosing a perforated appendicitis, the sensitivity was 95%, the specificity was 96.8%, and the accuracy was 96.1%.  Among the 5 perforation findings, a defect in the enhancing appendiceal wall had the best diagnostic accuracy. 

Conclusion:  Multi-detector row helical CT with IV and without oral contrast material can accurately differentiate perforated appendicitis from nonperforated appendicitis. 

Comment:  Keep in mind that the total examination time including patient prep was under 15 minutes.