Stomach bug symptoms to know as norovirus cases are surging in the U.S.
Four 20th-century Flu Outbreaks
(Mental Floss) -- As panic mounts over the increasing number of swine flu cases, it looks like the world is ending, with a sniffle and sneeze -- again.
Doctors at work Wednesday in the Navy Hospital in Mexico City -- the epicenter of the swine flu outbreak.
But this certainly isn't the first time humanity has had to gird itself against the threat of pandemic. Here's a little background on some recent history's most terrifying pandemics:
The Spanish flu of 1918: Don't blame the Spanish
The absolute worst flu pandemic in recent memory was the so-called Spanish flu outbreak of 1918. Somewhere between 20 and 50 million people died from the Spanish Flu -- more than the number of people who died in World War I.
But don't blame the Spanish. In fact, the virus was likely spread by U.S. Soldiers shipped off to fight in World War I -- the first recorded case of the flu came on March 11, 1918, at Fort Riley, Kansas. Within a week, the virus had made the rounds through the unsanitary military base -- 522 men reported to the camp infirmary, all suffering from the same illness. 
The flu moved on from there, primarily through military channels, popping up all over the southern Eastern Seaboard, in California, and other states throughout the Union, infecting 28 percent of Americans. Military transport ships then became floating Petri dishes, incubating the disease and then releasing it on arrival in France. From there, the flu ravaged the rest of Europe, already in a weakened state after years of devastating war.Read soldier's letters about the disease
And this particular strain of the flu was terrifying -- sufferers often succumbed to total respiration failure within hours, essentially suffocating to death in the fluid that filled their lungs. Mental Floss: Catching up with the plague
It was also puzzling -- where most flu strains affected the weakest members of the population, the elderly, the very young, and people already ill of health, this flu largely affected healthy young people.
The fact that a war was on also contributed to the rapid spread of the virus, in part due to the fact that affected countries didn't acknowledge the pandemic. The Spanish flu got its name from the fact that Spanish papers were the first ones to report that millions of their people were dying from the flu; other countries, on both sides of the Allied and Central Powers lines and though similarly affected by the virus, kept mum for fear of revealing a weakness to the enemy.
Moreover, the war effort left the U.S. And other countries without sufficient medical care -- many trained doctors and nurses had gone to the front.
Waves of the virus broke on U.S. Shores, each time killing more and more people and prompting drastic measures. In Philadelphia, according to a contemporary New York Times article, courts were adjourned, theaters were closed, churches asked to suspend services, football games cancelled, even the sale of liquor prohibited.
The flu also inspired, much in the same way the plague allegedly inspired that "pocket full of posies" rhyme, a creepy schoolgirl jump rope rhyme:
"I had a little bird
And its name was Enza
I opened the window
And in-flew-Enza"
After spending several long months exhausting the population, the virus disappeared before it could even be isolated. It's been since identified as a "pure" avian virus, meaning that it adapted from a bird-based illness to possess the necessary features for easy human to human transmission.
The Asian flu of 1957: Science in action
By 1957, scientists had a better handle on the whole vaccine, immunology, epidemiology thing, so when the first cases of Asian Flu popped up in China in February 1957, they identified it quickly. But vaccines for the virus weren't available until August 1957, giving the disease several months to spread across the globe. By fall, every continent, every region had seen cases of the virus.
The virus killed more than 2 million people worldwide, 70,000 people in the U.S. Alone. In the first wave of the disease, which crossed the globe in the summer and fall of 1957, the illness also proved particularly virulent among school children, young adults, and pregnant women. In the second wave, which hit in the early part of 1958, elderly people were its victims.
Unlike during the Spanish flu pandemic, U.S. Medical personnel were somewhat more proactive in clamping down on the Asian flu outbreak.
Several major networks used the relatively new medium of television to quickly distribute information on how to deal with the flu: One program featured actors demonstrating symptoms of the flu, animated cartoons explaining how vaccinations work, and sober discussions of where the Asian flu came from and what could and could not be done about it ("the new miracle or wonder drugs," antibiotics, the program cautions, could not be used to treat the flu). Mental Floss: Epidemic vs. Pandemic: What's the difference?
Elsewhere, communities jumped into action: At the University of Illinois, for example, health officers set up 336 hospital cots in an ice rink to prepare for the "worst case scenario."
This virus petered out within a year, and while deadly, had little of the devastating effect of the Spanish flu.
Hong Kong flu-ey of 1968
This pandemic was considered more mild than the two that preceded it; around 1 million people are estimated to have died as a result to the pandemic, however, this flu spread more slowly than the previous two, perhaps owing to a resistance built up from the previous pandemic. The virus was first noticed in China in mid-July; by August, more than 500,000 cases in Hong Kong alone were reported.
The Hong Kong flu was also one of the many unfortunate side effects of the war in Vietnam: Though the virus was first spotted in China, soldiers returning from the Vietnamese front brought the disease home. In three months, the Hong Kong flu had made its way from California across America, proving lethal primarily for the elderly and young children. Europe and the UK were hit by the pandemic, but were largely unfazed: In the UK, for example, death from flu and flu-related illness was actually lower that year than it had been the previous year.
The first swine flu, 1976: The pandemic that wasn't
Scary as it is now, the first time swine flu appeared in the States was more of a whimper than a bang.
The virus first popped up in early February 1976, when a 19-year-old private at Fort Dix, New Jersey, reported to his superior that he felt ill and tired, although not so bad as to skip the training hike later that day. He died within 24 hours. It was echoes of the 1918 Spanish flu epidemic all over again.
An autopsy revealed that the young soldier had contracted swine flu; shortly after, other soldiers were admitted to the hospital with the same symptoms and officials soon found that 500 people at the base were infected with the virus, though they hadn't become ill.
Upon hearing about the potential pandemic, President Gerald Ford ordered the mobilization of a nationwide vaccination program, at a cost of $135 million in 1976 dollars -- that'd be roughly $505 million today. After the first reported infection in February, the virus laid low for the next few months.
In October 1976, health officials, armed with a vaccination and a healthy dose of scaremongering, took to the streets. Propaganda about the potential pandemic was more frightening than the actual thing and possibly even more frightening than the news reports this time around. Health officials tried hard to terrify the populace into getting flu shots with an ominous voice intoning "a swine flu epidemic may be coming" over images of people lying in hospital sickbeds. It worked: More than 40 million Americans, a quarter of the population, got their flu shots.
However, that may have not been the best idea -- while the flu itself only killed one person, the vaccine killed more than 30. Within two months after the mass inoculations began, 500 people came down with Guillain-Barré syndrome, a paralyzing nerve disease.
This, combined with the fact that the prophesied epidemic never really materialized, didn't exactly help Ford's flagging political career: While the dismal economic state probably had more to do with it, Ford lost re-election that year. Mental Floss: 11 memorable moments from forgotten presidential elections
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All About Influenza
Genetics Of The Influenza Virus
The name "influenza" is derived from the Latin word for "influence," and the pathogens that cause this disease are RNA viruses from the family Orthomyxoviridae. The genomes of all influenza viruses are composed of eight single-stranded RNA segments (Figure 1). These RNAs are negative-sense molecules, meaning that they must be copied into positive-sense molecules in order to direct the production of proteins.There are three basic types of influenza viruses: A, B, and C. Influenza B and C viruses only infect humans, so novel antigens are not introduced from other species. Only influenza A viruses infect nonhuman hosts, and a reassortment of genes can occur between those subtypes that typically infect animals and those that infect humans, resulting in antigenic shift and potential pandemics. Epidemics of seasonal influenza occur due to influenza A or B viruses.
As in all viruses, the genome of an influenza virus particle is encased in a capsid that consists of protein. The influenza A capsid (Figure 2) contains the antigenic glycoproteins hemagglutinin (HA) and neuraminidase (NA); several hundred molecules of each protein are needed to form the capsid. These proteins are the parts of the virus that are recognized as foreign by a host's immune system, thus eliciting an immune response. Because many different subtypes of the influenza A hemagglutinin and neuraminidase proteins exist, the human immune system is frequently challenged with new antigens. For example, point mutations in the HA and NA genes can lead to changes in antigenicity that allow a virus to infect people who were either infected or vaccinated with a previously circulating virus. This phenomenon is referred to as antigenic drift. In addition to humans, other animals can be infected with or serve as a reservoir for influenza, and outbreaks have been seen in poultry, pigs, horses, seals, and camels (Hayden & Palese, 1997). When a strain is named, the host (if not human), the location where the virus originated, the strain number, the year of isolation, and the HA/NA subtype are all included in the name.
Figure 2: Electron micrograph of influenza A virus particles.
The genome of influenza A viruses consists of eight single-stranded RNA segments, and the viral particle has two major glycoproteins on its surface: hemagglutinin and neuraminidase.
With the HA and NA genes, the influenza A genome contains eight genes encoding 11 proteins. These proteins include three RNA polymerases that function together as a complex required by the virus to replicate its RNA genome. Interestingly, these polymerases have been shown to have high error rates due to a lack of proofreading ability, which leads to high mutation rates in replicated viral genomes and therefore rapid rates of viral evolution. This high rate of mutation and evolution is one source of influenza virus genetic diversity. The influenza genome also encodes additional structural proteins necessary to form the capsid, the nucleoprotein (NP), and the proteins NS1 (nonstructural protein 1) and NS2/nuclear export protein (NEP), whose roles are still being investigated. Still other proteins encoded by the viral genome include membrane proteins M1 and M2 (which are needed for nuclear export and several other functions) and, of course, HA and NA (which play roles in viral attachment and release from host cells, respectively).Due to the segmented nature of the influenza genome, in which coding sequences are located on individual RNA strands, genomes are readily shuffled in host cells that are infected with more than one flu virus. For example, when a cell is infected with influenza viruses from different species, reassortment can result in progeny viruses that contain genes from strains that normally infect birds and genes from strains that normally infect humans, leading to the creation of new strains that have never been seen in most hosts. Moreover, because at least 16 different hemagglutinin subtypes and nine different neuraminidase subtypes have been characterized, many different combinations of capsid proteins are possible. Of these subtypes, three subtypes of hemagglutinin (H1, H2, and H3) and two subtypes of neuraminidase (N1 and N2) have caused sustained epidemics in the human population. Birds are hosts for all influenza A subtypes and are the reservoir from which new HA subtypes are introduced into humans (Palese, 2004).
Scientific Investigation Of The 1918 Flu
Despite recent advances in microbiology, early 20th-century scientists struggled to understand the source of the deadly 1918 influenza epidemic and how best to prevent it. Some thought it might develop from a germ planted by Germans trying to get an edge in World War I. Others tried to protect themselves from the flu by drinking noxious homemade elixirs. It was not until the late 1990s that researchers armed with the latest technology and a greater understanding of molecular biology were able to uncover some of the hidden mysteries surrounding the strain of influenza virus that triggered such a devastating epidemic in 1918.
In 1997, the Molecular Pathology Division of the Armed Forces Institute of Pathology (AFIP) identified genetic material from the 1918 influenza in the frozen remains of a Native Alaskan victim of the disease, buried for nearly 80 years in Brevig Mission, Alaska. AFIP scientists identified two more positive cases in formalin-fixed, paraffin-embedded tissue samples from the AFIP archives. Both archival cases were autopsies of U.S. Servicemen who died during the pandemic — the first in Fort Jackson, SC, the second in Camp Upton, NY. While all of the virus' genetic material – the RNA – was fragmented into tiny pieces, the scientists were able to use the latest molecular techniques to identify complete gene structures of the virus.
In 1999, the AFIP reported that after completely analyzing a critical gene from the 1918 influenza virus their researchers had determined that the 1918 virus apparently evolved in mammals, either humans or pigs, over a period of years before it matured into a virus strong enough to kill millions. Ann Reid, a molecular biologist with the AFIP and the main author of the study, told the Associated Press that the gene probably "was adapting in humans or in swine for maybe several years before it broke out as a pandemic virus." Reid added, "We can't tell whether it went from pigs into humans or from humans into pigs." Through this investigation, Reid was able to map a gene called the hemagglutinin, which is key to allowing the influenza virus to take hold. Reid reported that the hemagglutinin closely resembles mammal genes.
In 2005, researchers from the CDC, Mount Sinai School of Medicine, the Armed Forces Institute of Pathology and the U.S. Department of Agriculture successfully collaborated in sequencing and reconstructing the 1918 influenza virus. According to their research findings, the virus not only proved deadly to mammalian specimens, but also proved virulent against chicken embryos. The team, including Ann Reid and Jeffery Taubenberger, concluded that polymerase genes found in the 1918 reconstructed flu are more similar to those found in avian flu viruses than those found in other mammalian flu viruses. These findings have swung the scientific community pendulum back to attributing the 1918 influenza virus to an avian source rather than that of a swine. Since the publications of these findings, other members of the scientific community have debated and disputed these conclusions. It seems that despite advances in science and technology, many of the puzzles of the 1918 influenza virus may forever be clouded in mystery.
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