Pan American Society for Clinical Virology

Newsletter

Volume 23 No. 1 March 1997

WWW Version


The Officers and councillors welcome suggestions and comments concerning the PASCV. It is intended that the Newsletter be a forum for exchange of views and information that will be beneficial to the membership. In particular, the experiences of members with reagents, techniques, and new products applicable to rapid viral diagnosis are solicited and will be published in the Newsletter.

The 1996-1997 Influenza Season - A View from the Benches

Danny L. Wiedbrauk, Ph.D.

William Beaumont Hospital, Royal Oak, Michigan 48073

Influenza moves rapidly throughout the population each winter, causing 10,000 to 40,000 excess deaths annually.1 In the virology laboratory, this observation means that the influenza season can be easy or difficult, depending upon a number of factors. My informal poll of selected laboratories indicates that the 1996-97 influenza season ranks as one of the ugliest in recent memory. In these laboratories, the influenza-associated workload was higher than it has been for the past five years. Virology laboratories were not the only ones who were caught short. Becton Dickinson ran out of Directigen® influenza A EIA kits again this year and some laboratories had to wait 2-4 weeks for their order to be filled.

Several factors have apparently contributed to the increased influenza workload. First, the A/Wuhan(H3N2)-like strain currently circulating in North America is different-enough from the A/Johannesburg(H3N2) vaccine strain that previous vaccinations may not provide protection from significant disease. Second, anecdotal information from several local physicians indicates that the circulating influenza A strain is particularly aggressive, causing significant and widespread illness. While the truth of this observation remains to be determined, this observation is circulating among local physicians and they are ordering more influenza tests. Finally, the recent recall of the Fluogen® trivalent vaccine has heightened the awareness of physicians and the lay public. Only 5-7% of the influenza-vaccinated population were given recalled vaccine lots.3

However, the publicity associated with this recall has significantly increased laboratory orders for influenza testing. With increased awareness of influenza and increased testing volumes comes an increased number of questions about influenza. Several of the most frequently asked questions (and our answers) are listed below.

Just when we thought we had this season under control, a number of laboratories began isolating influenza B. Maybe this isn't over yet!

How is the influenza season progressing?

The Centers for Disease Control and Prevention (CDC) report that regional influenza activity was first observed in Maryland in mid-October. Data from the CDC collaborating laboratories in the U.S. indicate that peak isolation rates were observed from November 17 through December 7, 1996.2 At that time, 99% of influenza viruses isolates were type A and 1% were type B. All the subtyped isolates were type A(H3N2) and were antigenically similar to the H3N2 strain that was included in the current vaccine (see below).2

What influenza strains are in the 1996-1997 vaccine?

The trivalent influenza vaccine prepared for the 1996-97 season included A/Texas/36/91-like (H1N1), A/Wuhan/359/95-like (H3N2), and B/Beijing/184/93-like influenza strains. The 1996-97 vaccine differs from the previous vaccine in that A/Wuhan/359/95 strain replaced the A/Johanesburg/33/94(H3N2) strain. To further confuse the issue, U.S. vaccine producers replaced the A/Wuhan/359/95-like and the B/Beijing/184/93-like viruses with the antigenically equivalent A/Nanchang/933/95/(H3N2) and B/Harbin/07/94 strains because these strains were easier to propagate in vitro.4,5 This change has caused some confusion in the medical and lay community.

Why was the influenza vaccine recalled? Which vaccine did we get?

In November, 1996, Parke-Davis (Parke-Davis Division, Warner Lambert Company, Morris Plains, NJ) voluntarily recalled 11 lots of Fluogen® trivalent influenza vaccine because the monitored quality of the A/Nanchang/933/95/(H3N2) hemagglutinin antigen had declined.3 The reason for this decline was not known. In investigating this problem, the CDC and the New York State Department of Health evaluated the antibody responses to the 1996-1997 vaccine among 86 residents of three nursing homes in New York who received the recalled vaccine and 86 residents from three other nursing homes who received vaccine produced by a different manufacturer. This investigation revealed that the residents who were given the recalled vaccine had significantly lower antibody titers to the A/Nanchang/933/95/(H3N2) strain than nursing home residents who received vaccine from another manufacturer 3. In addition, significantly fewer residents who received the recalled vaccine achieved hemagglutinin inhibition assay titers of >1:40 to the A/Nanchang/933/95(H3N2) compared with controls. The antibody titers to the A/Texas/36/91/(H1N1) and the B/Harbin/07/94 vaccine components were similar in both groups.

How effective is the influenza vaccine?

The protection offered by the influenza vaccine correlates with the development of hemagglutinin antibodies. In young adults, immunization provides 65 to 80% protection against illness caused by an influenza virus when there is a good match with the vaccine strain.5 Influenza vaccination is 30-70% effective in preventing hospitalization for pneumonia and influenza among elderly individuals who do not live in nursing homes or other long-term care settings. Unfortunately, the vaccine may be only 30-40% effective in preventing clinical illness in elderly residents of nursing homes. While the vaccine usually does not prevent disease in these individuals, the vaccine lessens the severity of disease and is 50-60% effective in preventing hospital admissions and 80% effective in preventing death from influenza-associated pneumonia5,6 Risk-benefit studies have consistently shown that the risk of death from influenza outweighs the potential for adverse vaccine reactions in all age groups.7,8 Despite its known benefits, current levels of immunization against influenza are approximately 30% for persons 65 years of age or older and 9-13% among adults who have high risk conditions.6

Are there rapid tests for influenza?

Laboratory detection of influenza virus can be accomplished using tube cultures, shell vial cultures, direct fluorescent antibody (DFA) methods 9, enzyme immunoassays (EIA) (influenza A only), and the polymerase chain reaction (PCR). Tube and shell vial cultures are not considered rapid tests because their turnaround times are 2-14 days and 1-2 days, respectively. Likewise, PCR tests, which have mean turnaround times of 24-48 hours, cannot be classified as rapid diagnostic tests for influenza.

Although commercial DFA and EIA methods are very specific (95-100% versus culture), they are not as sensitive as culture methods. Most DFA reagents for influenza virus detection have sensitivities of 85-95% compared with culture. DFA methods can detect influenza type A and B while rapid membrane EIA tests only detect influenza A. Rapid membrane EIA methods for influenza A have somewhat lower (75-90%) sensitivities compared with culture. Although membrane-based EIA tests are 5-15 times more expensive than DFA procedures, these low complexity tests can be performed by personnel who have significantly less training and expertise than is required for DFA tests. For this reason, rapid membrane assays are increasingly used in STAT laboratories, physician offices, and in situations were point-of-care testing is desirable. Like the rapid strep tests, EIA-negative specimens should be cultured to maximize the influenza detection rates. Follow-up cultures are important to minimize the spread of disease and its associated complications. In addition, hospitals and nursing homes who exclusively use rapid EIA methods to cohort patients with influenza and to identify nosocomial infections10 may miss a significant number of influenza infections.

Literature Cited

1. Gardner P, Schaffner W. Immunization of adults. N Eng J Med 1993; 328:1252-1258.
2. Centers for Disease Control. Update: Influenza activity - United States, 1996-97 season. MMWR 1996; 45:1102-1105.
3. Centers for Disease Control. Decreased antibody response to influenza vaccine among nursing-home residents who received recalled vaccine - New York, 1996. MMWR 1996; 45:1100-1102.
4. Centers for Disease Control. Update: Influenza activity - United States and worldwide, 1995-96 season, and composition of the 1996-97 influenza vaccine. MMWR 1996; 45:326-329.
5. Centers for Disease Control. Prevention and control of influenza: Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1996; 45:1-24.
6. American College of Physicians Task Force on Adult Immunization, Infectious Disease Society of America. Guide for adult immunization. Philadelphia, PA: American College of Physicians, 1990.
7. Office of Technology Assessment. Cost effectiveness of influenza vaccination. Washington, DC: Government Printing Office, 1981.
8. Nichol KL, Margolis KL, Wuorenma J, von Sternberg T. The efficacy and cost effectiveness of vaccination against influenza among elderly persons living in the community. New England Journal of Medicine 1994; 33:1778-784.
9. Wiedbrauk DL, Johnston SLG. Manual of Clinical Virology. New York, NY: Raven Press, 1993.
10. Serwint JR, Miller RM. Why diagnose influenza infections in hospitalized pediatric patients? Pediatric Infectious Disease Journal 1993; 12.


Deceased Member

by Dr.Richard L. Hodinka

Children's Hospital of Philadelphia

The fields of clinical microbiology and virology have suffered a great loss with the death of Philip A. Hanff on Dec. 9, 1996 at age 48. Phil was diagnosed with esophageal cancer in Nov. 1995 and succumbed to aggressive liver metastases found in Nov. 1996.

He was a native of Los Angeles, CA and earned an B.A. degree from the University of California, Riverside in 1970 and a Ph.D. from the University of California, Los Angeles in 1980. From 1975-1982, he completed two research postdoctoral fellowships at the University of California School of Medicine, Los Angeles, and from 1982-1984, finished his clinical microbiology postdoctoral fellowship in the clinical Microbiology-Immunology Laboratories at North Carolina Memorial Hospital on the campus of the University of North Carolina, Chapel Hill.

His career as a clinical microbiologist began in 1984 as Scientific Director of the Clinical Microbiology Laboratories at Beth Israel Deaconess Medical Center in Boston. He was an instructor in Pathology at the Harvard Medical School from 1984-1989 and was promoted to an Asst Professor of Pathology in 1989.

Phil was a member of the American Society for Microbiology since 1978 and was an active participant in the Pan American Society for Clinical Virology for the past 10 years. Phil also was an annual speaker for and helped initiate the panel on "Clinical Case Presentation and Discussion" which has been a successful component of the Clinical Virology Symposium in Clearwater since 1993. He served on editorial boards and was a guest reviewer for a number of journals. He was in constant demand as an invited speaker for numerous microbiology meetings and had many published contributions in clinical microbiology.

Phil directed an outstanding diagnostic microbiology lab and trained and supervised many technologists and medical scientists. He was an excellent researcher and clinical educator and was held with great esteem by his students, colleagues and peers. He had a quick wit, was always friendly and cooperative in his approach, and was compassionate and sensitive to the needs and emotions of people who worked with him. His informed opinions and advise were well respected. His wisdom and intellect went far beyond his chosen field of science. Phil was a tremendous asset to the fields of clinical microbiology and virology.

On a more personal note, I will always remember Phil through our annual gatherings at the Clinical Virology Symposium. Although this meeting is a platform for science, it also allows individuals to establish friendships that will remain forever. Many of us enjoyed Phil's company, as we dined with him, shared conversations during nightly beach walks, and played some "interesting" games of volleyball as time permitted. Since his passing, I have often reflected on the laughter and fun had by all.

Phil was a warm and caring person who was always attentive to his family and friends. He will be remembered often and will be dearly missed by his many colleagues, professional acquaintances, and friends. My deepest sympathy goes to his family.

Phil is survived by his wife, Jeni Yamada, and their three boys, Aaron, Jason and Adam. A memorial fund has been established on behalf of his widow and children. Contributions may be directed to:

The Philip A. Hanff Family Trust

c/o Department of Pathology

Beth Israel Deaconess Medical Center

330 Brookline Ave.

Boston, MA 02215