Did You Know?
1918-1919: Over 25 million people die
See updates at bottom -- September, 2001, May 2003.
The Bubonic Plague has been considered the ultimate killer among diseases. Epidemics in the 6th, 14th, and 17th centuries combined to kill an estimated 137 million people worldwide.
The mention of the name today sends shivers down the spines of many and there is little doubt that it is a terrible and deadly disease.
The death rate was 90% for those exposed to the bacterium. It was transmitted by the fleas from infected Old English black rats. The symptoms were clear: swollen lymph nodes (buboes, hence the name), high fever, and delirium. In the worst case, the lungs became infected and the pneumonic form was spread from person to person by coughing, sneezing, or simply talking. From the time of infection to death was less than one week.
The plague is considered to be the worst epidemic of all time, but it wasn't (not that we are downplaying the severity of the plague). At its worst, the bubonic plague killed 2 million victims a year. This is certainly a bad situation, but there is one that is worse. The pandemic (an epidemic that is spread worldwide) that killed at least 25 million people in one year (maybe 40 million before running it's course). A disease that is largely forgotten. A disease that occurred in the 20th century! You may be thinking AID's, Syphilis, or the dreaded Ebola.
All are wrong.
It was the influenza of 1918-1919, right after World War I (the war killed 9 million men in 4 years) This was no minor disease -- everyone on the planet was at risk. And it started in the United States.
In one year, nearly twenty million cases were reported in the United States, accounting for almost one million deaths. The cause is still unknown, but is believed to have been a mutated swine virus.
It all started on the morning of March 11, 1918 at Camp Funston, Kansas. A company cook named Albert Mitchell reported sick with typical flu-like symptoms -- low-grade fever, mild sore throat, slight headache, and muscle aches. Bed rest was recommended. By noon, 107 soldiers were sick. Within two days Camp Funston had 629 cases and many of them were gravely ill with severe pneumonia. Then reports started coming in from other military bases around the country. Thousands of sailors docked off the East Coast were sick. Within a week the disease was hitting such isolated places as Alcatraz.
Whatever the cause, it was clearly airborne. Within seven days, every state in the Union had been infected. Then it spread across the Atlantic. By April, French troops and civilians were infected. By mid-April, the disease had spread to China and Japan. By May, the virus had spread throughout Africa and South America.
The actual killer was the pneumonia that accompanied the infection. In Philadelphia, 158 out of every 1000 people died. 148 out of 1000 in Baltimore. 109 out of 1000 in Washington, D. C.
The good news (if there was any) was that the disease peaked within two to three weeks after showing up in a given city. It left as quickly as it arrived. The United States death toll was a total of 850,000 people, making it an area of the world that was least devastated by this virus.
In Nome, Alaska sixty percent of the Eskimo population was wiped out. 80-90% of the Samoan population was infected, many of the survivors dying from starvation (they lacked the energy to feed themselves). Luxury ocean liners from Europe would arrive in New York with 7% less passengers than they embarked with. The confined area of the ship was especially conducive to the spread of the disease.
In the end, 25 million people had died. Some estimates put the number as high as 37 million. Eighteen months after the disease appeared, the flu bug vanished and has never shown up again.
So what happened? Until recently, no one was really sure. In March of 1997, the news broke that researchers at the Armed Forces Institute of Pathology in Washington, D. C. had isolated genetic material from the virus. This was no easy task. The living virus is no longer around. It turns out that while conducting autopsies in 1918, Army doctors had preserved some specimens in formaldehyde. One of these jars contained the lungs of a 21 year old soldier that died on September 26, 1918. The researchers spent nearly two years extracting just seven percent of the genetic code, but the evidence gathered has provided a great wealth of information.
It appears that the virus passed from birds to pigs and then to humans. These are the deadliest of all viruses. The viruses tend to remain stable in the birds, but occasionally they infect pigs. Of course, the pig immune system kicks into action and the virus is forced to mutate to survive. Both the Asian flu (1957) and the Hong Kong flu (1968), which were not as deadly, mutated from pig viruses.
The scary part is that it could happen again -- and we're not prepared.
Mundus Novus Historiaź
Update -- September, 2001
The Charlotte Observer -- Medical Mystery
Hypothesis says human immune system wasn't ready for hybrid virus
By DAVID BROWN
An Australian research team believes it's found a clue to one of medicine's biggest mysteries -- why the Spanish flu virus of 1918 was so deadly.
Scientists at Australian National University in Canberra say a crucial gene in the 1918 virus arose from the recombination of genes in two pre-existing influenza viruses.
The resulting hybrid was different enough to catch most people's immune systems unprepared, which allowed it to spread rapidly.
"What we've in essence found is that a fairly significant change occurred immediately before the pandemic," said Mark Gibbs, a biologist at the university.
The quest isn't simply academic. Virologists and public health officials would like to be able to identify dangerous strains of influenza among the many variants emerging every year.
The explanation, which appears today in a paper in Science written by Gibbs and two colleagues, was greeted skeptically by other scientists.
Robert Webster, an influenza researcher who wrote a commentary in Science, called the proposal "definitely a stretch."
The Australian researchers used data from the partially reconstructed viral genes from three 1918 victims to make their argument.
The Spanish flu killed at least 20 million, and possibly as many as 40 million people in 1918 and 1919. What caused the virus to infect and kill so many people has puzzled virologists.
Influenza virus contains eight separate pieces of genetic "segments." There are numerous variations of each segment. Those variations account for the huge number of distinct flu viruses infecting people, chickens, geese, ducks, pigs, horses and other animals.
Two gene segments are especially important because they carry the directions for making the proteins hemagglutinin (HA) and neuraminidase (NA) that sit on the outside of the virus.
A global pandemic occurs when a virus appears carrying a new HA or NA gene, with the old one swapped out. This is called reassortment. Gibbs says the 1918 bug wasn't a reassortment, but something rarer: A new HA gene was formed by the cutting and splicing of two pre-existing HA genes -- called recombination.
Recombination has only been seen a few times in influenza virus, and some experts contend it's actually never been proved.
Update -- May, 2003
SARS scare reminiscent of 1918 flu pandemic
By LUKE SHOCKMAN
-- Donald Henderson knows history, and he is worried.
The doctor who led the international effort to eradicate smallpox said he's worried about history repeating itself, only on a much deadlier scale this time around.
In 1918, for reasons still unclear today, a new strain of flu - sometimes referred to as the Spanish flu - swept across the world, killing 20 million people.
Eighty-five years later, another virus is on the attack. SARS - severe acute respiratory syndrome - surfaced last fall in China, and so far has infected more than 7,800 people worldwide and killed more than 600.
That's a low death toll compared to the Spanish flu. But Henderson, who headed a team of international doctors who snuffed smallpox by the early 1980s, said it is not the death toll itself that concerns him with SARS - it is the percentage of people who die after contracting the virus.
The Spanish flu "had a death rate of about 1 or 2 percent, and SARS appears to be considerably higher," he said.
Much higher, in fact. Henderson and others caution that it is too early to say exactly what the death rate is because there are so many unknowns, but so far SARS appears to kill at least 5 percent to 15 percent of people it infects. If SARS somehow races through large populations similar to what the Spanish flu did ...
"We all consider this to be very, very worrisome," Henderson said. "There are those who've said we don't have many cases, or that we have more cases of AIDS. Well, true. But this has the potential for spread like HIV doesn't."
Now a professor at Johns Hopkins Bloomberg School of Public Health, as well as an adviser to U.S. Secretary of Health Tommy Thompson, Henderson doubts authorities will be able to eradicate SARS like he did with smallpox.
"If you get sick with smallpox, you are really sick and not inclined to fly. With SARS, you get a fever and a cough, but people with the disease, many of them are mobile, so the likelihood of transmission is much higher," he said.
Other public health authorities are more optimistic.
"We think we have a window of opportunity to get rid of this disease and put it back in the box," said Maria Cheng, a spokesman for the World Health Organization, based in Geneva.
Cheng said a vaccine might be developed in a year or two; others say it could take much longer. Even without a vaccine for SARS, she said, the disease can be contained. What happens with China, she said, is the big unknown.
China has been hit hard by SARS, with almost 300 killed and more than 5,200 infected. Authorities there initially covered up news of the disease, allowing the disease to spread rapidly. Even now, after improving its efforts, Cheng said China is still not providing enough information about SARS to international experts.
Last week, China's Supreme Court threatened execution of people who knowingly spread the disease by violating SARS quarantine laws. If China fails to contain SARS, Cheng agreed that chances for containing the virus dim for the very reasons Henderson pointed out.
Fortunately, SARS has not spread as quickly as the Spanish flu - yet - and the disease appears to have had little impact in the United States. Nationwide, there have been 350 suspected and probable cases, but no deaths.
Some public health experts have complained that SARS is getting too much attention, and the media are needlessly panicking the public.
Dr. David Baltimore, a Nobel Prize-winning vaccine research at the California Institute of Technology, wrote a guest editorial last month in The Wall Street Journal complaining of what he perceived as overreaction by the media and public toward SARS.
Dr. Jeffrey Koplan, who was director of the Centers for Disease Control and Prevention in Atlanta from 1998 until last year, disagreed.
"I don't think SARS has been overemphasized," he said. "Let him (Baltimore) see a room full of people on respirators."
While Koplan said he thinks all the attention SARS has been getting is appropriate, he said some of what's been reported is either inaccurate or misses the point.
Take the question of a vaccine, for example. While many experts, including those at the World Health Organization, suggest a vaccine might be developed within a year or two, Koplan scoffs at that.
"Forget it. If you have a vaccine in 10 years, consider yourself lucky," he said.
Current CDC officials say much the same thing.
What health officials need to focus on is a diagnostic test for SARS, Koplan said. For now, he said, authorities are trying to define SARS cases based on some rather shaky criteria, including whether you visited a country where SARS is present. But a definitive, cheap, quick test is needed soon, he said, so quarantine measures can be more efficient.
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