(Photo: The New York Times)
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Make a specific influenza diagnosis for upper respiratory infection symptoms
On a frigid February morning Wilbur Wilfred Wallace (Fred) woke up and had an onset of chills. At first he thought this sensation was the consequence of the cold weather however he noted that he also had a stuffed nose and a mild sore throat. In addition he felt extremely fatigued in spite of having a good night of sleep after taking Ambien CR.
Fred is a 27-year-old male who drives a taxicab in New York City and picks up at least fifteen fares per day driving throughout the five boroughs. He lives with his wife and 80 year - old mother in law. He went to work on the day the illness symptoms started but returned home after lunch because he began to feel a dull pain in his back. Fred took over the counter (OTC) medications containing pseudoephedrine and acetaminophen throughout the remainder of the afternoon and into the evening. However the next morning he felt worse, was now coughing and when he took his temperature it was 102.2 o F. The ill feeling with temperature prompted him to travel by city bus to his physician's office.
On examination Fred's physician noted that his patient had a productive cough, was febrile, and was complaining of substernal pain as well as muscle ache. A rapid test of a throat swab for Group A Streptococcus was negative. A test of a nasal swab by a rapid antigen test indicated an acute influenza type A virus infection.
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The "QuickVue Influenza A + B Test".
This test allows for the rapid, qualitative detection of influenza type A and type B antigens directly from a nasal swab, nasal wash, and / or nasal aspirate specimens. The test is intended as an aid in the rapid differentiation of acute influenza type A and Type B virus infection.
A chest x-ray was normal, there was no respiratory distress and the WBC count was also normal. However Fred was now complaining of burning in his eyes, pain with eye motion, and photophobia. He also developed a headache and his sore throat was now severe.
One week after Fred's office visit a tissue culture isolation analysis of the nasal sample was completed and laboratory stock antisera were used to characterize the high titer virus as H1N1, strain A/New Caledonia/20/99. By this time the illness had resolved although Fred was still suffering from fatigue and would not drive his taxicab. His wife was now having symptoms of upper respiratory illness and his elderly mother in law was also complaining of a mild sore throat. The physician advised that his mother in law come in to the office and get a prescription for the drug amantidine.
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Example of a Hemagglutination assay used to determine the virus concentration from the tissue culture isolate.
Seven different samples of influenza virus, numbered 1 through 7 at the left, were serially diluted as indicated at the top, mixed with chicken red blood cells (RBC), and incubated on ice for 1 to 2 hours. Wells in the bottom row contain no virus. Agglutinated RBCs coat wells evenly, in contrast to nonagglutinated cells, which form a distinct button at the bottom of the well. The HA titer, shown at the right, is the last dilution that shows complete hemagglutination activity.
(From Fields Virology, 4th ed, Knipe & Howley, eds, Lippincott Williams & Wilkins, 2001, Fig. 2-8)
Internet Links - Virology:
QUESTIONS
and ANSWERS:
1. How is influenza transmitted among susceptible individuals and what is a typical pathogenic course of the infection?
ANSWER 1.
2. How is an influenza infection diagnosed vs. other respiratory viral infections (in particular the common cold)?
ANSWER 2.
3. What are the complications associated with an influenza virus infection?
ANSWER 3.
4. Why is it necessary for repeated influenza vaccinations and what makes people susceptible to repeated influenza infections?
ANSWER 4.
5. What are the major treatment and prevention methods for influenza? Who should be treated by these methods?
ANSWER 5.
6. What additional animal species can be infected by influenza virus and in what way does this affect the epidemiology of the illness?
ANSWER 6.
Appendix
Spanish Flu Epidemic: How (and How Not) to Battle Flu: A Tale of 23 Cities - New York Times
April 17, 2007
How (and How Not) to Battle Flu: A Tale of 23 Cities By NICHOLAS BAKALAR
When the Spanish flu reached the United States in the summer of 1918, it seemed to confine it to military camps. But when it arrived in Philadelphia in September, it struck with a vengeance.
By the time officials there grasped the threat of the virus, it was too late. The disease was rampaging through the population, partly because the city had allowed large public gatherings, including a citywide parade in support of a World War I loan drive, to go on as planned. In four months, more than 12,000 Philadelphians died an excess death rate of 719 people for every 100,000 inhabitants.
The story was quite different in St. Louis. Two weeks before Philadelphia officials began to react, doctors in St. Louis persuaded the city to require that influenza cases be registered with the health department. And two days after the first civilian cases, police officers helped the department enforce a shutdown of schools, churches and other gathering places. Infected people were quarantined in their homes.
Excess deaths in St. Louis were 347 per 100,000 people, less than half the rate in Philadelphia. Early action appeared to have saved thousands of lives. Scientists are still studying the 1918 pandemic, the deadliest of the 20th century, looking for lessons for future outbreaks - including the possibility that H5N1, the avian influenza virus, could mutate into a form spread easily from human to human. This month, researchers published two new studies in The Proceedings of the National Academy of Sciences comparing public-health responses in cities like St. Louis and Philadelphia. Using mathematical models, they reported that such large differences in death rates could be explained by the ways the cities carried out prevention measures, especially in their timing. Cities that instituted quarantine, school closings, bans on public gatherings and other such procedures early in the epidemic had peak death rates 30 percent to 50 percent lower than those that did not. "It had been received wisdom that these interventions didn't work," said Dr. Richard Hatchett, the lead author of one of the studies, "because they looked at the variability between cities and concluded that there was some other factor than the interventions that caused the differing outcomes. "That we were able to go back and ask the right questions," Dr. Hatchett said, "is a function of a lot of modeling work that we did previously." Dr. Hatchett, who is a researcher at the National Institutes of Health, said the findings might hold lessons for the 21st century. "When multiple interventions were introduced early, they were very effective in 1918," he said, "and that certainly offers hope that they would be similarly useful in an epidemic today if we didn't have an effective vaccine."
A two-week difference in response times, according to the researchers, is long enough for the number of people infected in an influenza epidemic to double three to five times.
Dr. Martin Cetron, director for global migration and quarantine at the federal Centers for Disease Control and Prevention in Atlanta, found reason for optimism in the study results.
"The thing I find encouraging about the Hatchett paper," he said, "is that when you look back to 1918, you find that those who used nonpharmaceutical measures effectively were able to mitigate the impact of the severe pandemics, and this is consistent with some of the 21st-century simulation models." The second study, in the same issue of The Proceedings, suggests that in one sense preventive measures can be too effective. In an influenza epidemic, a certain number of people survive the illness and are immune to reinfection. As these numbers increase, the epidemic fades.
But an effective prevention program without a vaccine can leave enough people uninfected and still susceptible to the virus to start the epidemic again as soon as the controls are lifted. This is what happened in St. Louis. On Nov. 14, 1918 - in high spirits three days after the armistice that ended the war, and with influenza cases declining - the city reopened schools and businesses. Two weeks later, the second wave of the epidemic struck, this time with children making up 30 percent to 40 percent of the infections. Controls were immediately reinstituted.
The study examined the course of the epidemic in 23 cities: San Francisco, St. Louis, Milwaukee and Kansas City, Mo., had the most effective prevention programs, and time was of the essence. If restrictions were introduced too late or lifted too early, success rates declined substantially. Neil Ferguson, a co-author of the second study and a professor of epidemiology at Imperial College London, explained in a telephone interview that the most successful interventions were in communities where the political and health authorities broadly agreed on what needed to be done and got significant cooperation from the public.
The key, Dr. Ferguson said, is to tune an imperfect intervention perfectly so that a single peak of minimal size is the result. Although no cities succeeded in doing this, those that got closest, like St. Louis, carried out early interventions before the first peak, and then reinstituted them when transmission rates began to rise again.
What these results mean for a future epidemic is not clear. "If avian flu became a pandemic tomorrow," Dr. Ferguson said, "we would start a crash program to make a vaccine."
But he added that rigid preventive measures like quarantines, mandated mask wearing and widespread business closings would still need to be put in place. "What our study shows," he continued, "is that interventions even without a vaccine can be effective in blocking transmission. What's much less certain is whether society is prepared to bear the costs of implementing such intrusive and costly measures for the months that would be required to manufacture a vaccine."
Copyright 2007 The New York Times Company
Flu triggers heart attacks, study shows:
Reuters Wed Apr 18, 2:07 PM ET
Influenza can trigger deadly heart attacks, researchers said on Wednesday in a study that supports what experts have long believed -- flu can kill people even if they do not die directly from the flu.
Their report shows that the seasonal virus can worsen heart disease and that deaths from heart attacks and heart disease are far more common during flu season.
This can add up to 90,000 extra deaths a year in the United States alone, said Dr. Mohammad Madjid of the University of Texas-Houston, who led the study.
Writing in the European Heart Journal, the researchers said their findings add to a growing list of reasons why people should get annual flu shots. They also said people with heart disease should stick to their medications religiously.
"Our research has shown that influenza epidemics are associated with a rise in coronary deaths," Madjid said in a statement. "This calls for more intensive efforts to increase the vaccination rate in people at risk of coronary heart disease.
"This may be especially important in an influenza pandemic when we would expect to see high mortality among the elderly and those suffering from heart problems or who have multiple coronary risk factors," he said.
Flu viruses change every year and several are usually circulating in any given season, making the risk of flu high for most people.
"Between 10 and 20 percent of people catch flu every year and I have estimated that we can prevent up to 90,000 coronary deaths a year in the (United States) if every high-risk patient received an annual flu vaccination," Madjid said.
Madjid and colleagues at the Influenza Research Institute in St. Petersburg, Russia, studied autopsy reports on people who died from heart disease in that city from between 1993 and 2000.
"This was a population where only a small minority were receiving flu vaccines or statin drugs, so this enabled us to see what happened naturally in the absence of these medicines," Madjid said.
They found that 11,892 people died from heart attacks and 23,000 died from chronic heart disease.
Deaths from heart attacks increased by a third in flu epidemic weeks compared to non-epidemic weeks and the chances of dying from chronic heart disease increased by a tenth.
"This study shows that flu is an important trigger of heart attacks because flu is a severe infection, with high incidence rates and is readily preventable." Madjid said.
"If people can recognize that the flu vaccine has specific cardioprotective effects, then high-risk people will be more likely to make sure that they receive the influenza vaccine every year."
