Spanish flu

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The Spanish Flu Pandemic, also known as La Grippe, was an unusually severe and deadly strain of avian influenza, a viral infectious disease, that killed some 25 million to 50 million people worldwide in 1918 and 1919. It is thought to have been one of the most deadly pandemics so far in human history. It was caused by the H1N1 type of flu virus, which is similar to bird flu of today, mainly H5N1 and H5N2.

The Allies of World War I frequently called it the "Spanish Flu." This was mainly because the pandemic received greater press attention in Spain than in the rest of the world, because Spain was not involved in the war and there was no wartime censorship. Spain did have one of the worst early outbreaks of the disease, with some 8 million people infected in May 1918. It was also described as "only the flu" or "the grippe" by public health officials seeking to prevent panic.

The Spanish flu might have contributed to the end of World War I. More United States soldiers died from the Spanish flu during World War I than from the war itself.

Geographic origin

Many infections with similar but milder symptoms were recorded in the spring of 1918, with sore throat, headaches, dizziness, and loss of appetite. It has been proposed that the earliest known cases were in Haskell County, Kansas, in January 1918. Several local men were inducted into the army at Fort Riley, Kansas, where on March 4, 1918, company cook Albert Gitchell reported to the infirmary with a temperature of 103°F (39.5°C). He was soon followed by Corporal Lee Drake and Sergeant Adolph Hurby. Within two days 522 men at the camp had reported sick. In the summer, infections became much more severe. In August 1918 the more deadly version broke out simultaneously in three disparate locations — Brest, France; Boston, Massachusetts; and Freetown, Sierra Leone. Many of the worst outbreaks of the "Flu" were among soldiers, both at the front lines and in camps far away which soon spread into civilian populations. Severe outbreaks often required hospitalization and even with the best of care, often one-third of those infected died.

Mutation theory

One prevailing theory hypothesizes that two primary mechanisms in genetics -- genetic drift and antigenic shift -- were involved in the creation of the virus strain found at Fort Riley. The fort bred its own swine and poultry for local consumption. Like the avian flu in Asian countries, poultry in the United States characteristically contract a certain strain of influenza. Swine also characteristically contract a specific strain of influenza; however, the two strains (one infecting avian species, the other infecting swine) can usually cross infect the opposite species. Occasionally, usually by chance, when the viruses cross infect from one species to another, one influenza strain can incorporate the other strain's properties and change drastically (so called "shift"). On the other hand, genetic drift is the random incorporation of mutations into the genome. Under bad circumstances the new influenza can kill half-or-more of the poultry and/or swine population, but what really concerns epidemiologists is genetic "shift", which is also theorized to have occurred at the fort. The strain that was jumping from swine to poultry or vice-versa jumped to humans (the genetic "shift") allowing the influenza that was confined to swine and poultry to become a human pathogen. At the same time, the new strain was highly infectious and deadly because humanity had never experienced such a strain of influenza.

Recently, scientists (see below) have reconstructed the virus, and the evidence gained from that reconstruction suggests that the virus jumped directly from birds to humans, without traveling through the swine. This does not eliminate the idea that the pandemic started with a Fort Riley cook, however; indeed, he could have been preparing chicken when he contracted the virus.

Effects of new strain

The strain was unusual in commonly killing many young and healthy victims, as opposed to more common influenzas which caused the bulk of their mortality among newborns and the old and infirm. People without symptoms could be struck suddenly and be rendered too feeble to walk within hours; many would die the next day. Symptoms included a blue tint to the face and coughing up blood caused by severe obstruction of the lungs. In further stages, the virus caused an uncontrollable haemorrhaging that filled the lungs, and patients would drown in their own body fluids.

Mortality in the fast-progressing cases was primarily from pneumonia, by virus-induced consolidation. Slower progressing cases featured secondary bacterial pneumonias while some suspect neural involvement led to psychiatric disorders in a minority of cases. Some deaths resulted from malnourishment and even animal attacks in overwhelmed communities.

Global mortality rate from the influenza was estimated at 2.5%–5% of the population, with some 20% of the world population suffering from the disease to some extent. The disease spread across the world killing twenty-five million in the course of six months; some estimates put the total of those killed worldwide at over twice that number, possibly as high as 100 million. An estimated 17 million died in India alone, with a mortality rate of about 5% of the population. In the Indian Army, almost 22% of troops who caught the disease died of it. About 28% of the population of the U.S. suffered from the disease, and some 500,000–675,000 died from it. Some 200,000 were killed in Britain and more than 400,000 in France. The death rate was especially high in indigenous peoples where some entire villages perished in Alaska and southern Africa. Fourteen percent of the population of the Fiji Islands died in a period of only two weeks while 22% of the population of Western Samoa died. By July of 1919, 257,363 deaths in Japan were attributed to influenza, giving an estimated Japanese mortality rate of 0.425%, much lower than nearly all other Asian countries for which data are available.

Social facts

While it usually only infected less than one-third of the population in most places and killed only a fraction of those infected, there were a number of towns in several countries where the entire population was wiped out. The only sizeable inhabited place with no documented outbreak of the flu in 1918–1919 was the island of Marajo at the mouth of the Amazon River in Brazil.

Many cities, states, and countries enforced restrictions on public gatherings and travel to try to stay the epidemic. In many places theaters, dance halls, churches and other public gathering places were shut down for over a year. Quarantines were enforced with little success. Some communities placed armed guards at the borders and turned back or quarantined any travellers. One U.S. town even outlawed shaking hands.

Even in areas where mortality was low, those incapacitated by the illness were often so numerous as to bring much of everyday life to a stop. Some communities closed all stores or required customers not to enter the store but place their orders outside the store for filling. There were many reports of places with no health care workers to tend the sick because of their own ill health and no able bodied grave diggers to inter the dead. Mass graves were dug by steam shovel and bodies buried without coffins in many places.

The social effects were intense due to the speed of the epidemic. AIDS killed 25 million in its first 25 years, but the Spanish flu may have killed as many in only 25 weeks beginning in September 1918.

The Spanish Flu vanished within eighteen months, and the actual cause was not determined at the time. It appears to have been an H1 virus type. (The outbreaks of bird flu in Hong Kong in 1997 and other parts of Asia since then are an H5 type.) The influenza virus was not understood by medical science at the time. Most of the contemporary effort was spent in an unsuccessful quest to find a vaccine to the supposed bacterial cause of the disease, Bacillus influenza. In fact this was only one of several causes of secondary pneumonia associated with the epidemic. Two much milder influenza pandemics followed the Spanish Flu: the Asian Flu in 1957, and the Hong Kong Flu in 1968.

It has been suggested that the stresses of combat, possibly combined with the effects of chemical warfare, may have weakened soldiers' immune systems thereby increasing their vulnerability to the disease and accelerating the process. Certainly the close quarters and mass movement of troops helped in its spread.

Bayer aspirin was just hitting the market in the U.S. at the time of the Spanish flu, but because Bayer was a German company, and World War I was happening at that time, many Americans distrusted it and thought that it was a form of germ warfare. This theory was even suggested by U.S. government officials. [1]

Notable victims

A number of notable people died in the epidemic, including:

Recent research

In February 1998, The Molecular Pathology Division of the US Armed Forces Institute of Pathology (AFIP) recovered samples of the 1918 influenza from the frozen corpse of a Native Alaskan woman buried for nearly eight decades in permafrost near Brevig Mission, Alaska. Brevig Mission lost approximately eighty-five percent of its population to the Spanish flu in November, 1918. One of the four recovered samples contained viable genetic material of the 1918 virus. This sample provided scientists a first hand opportunity to study the virus, which was inactivated with guanidinium thiocyanate before transport. This sample and others found in AFIP archives allowed researchers to completely analyze the critical gene structures of the 1918 virus. "We have now identified three cases: the Brevig Mission case and two archival cases that represent the only known sources of genetic material of the 1918 influenza virus," said Jeffery K.Taubenberger, MD, PhD, chief of the institute's molecular pathology division and principal investigator on the project.

In September 2000, Noymer and Garenne published a study that poses an ætiological theory explaining the unusual W-shaped mortality age profile of the virus. This profile is characterized by a mode in the 25–34-year age group. Usually, influenza has a U-shaped profile, being most deadly to the young and the old. Additionally, after the pandemic the difference in life expectancy between men and women decreased (women had a historically longer life expectancy). Noymer and Garenne have causally linked these two anomalies to an interaction with tuberculosis. They point out that it is a predominantly male disease and that it is a disease of young adulthood rather than old age.

In October 2002, the Armed Forces Institute of Pathology teamed up with a microbiologist from the Mount Sinai School of Medicine in New York. Together, they started to reconstruct the Spanish Flu. In an experiment, published in October 2002, they were successful in creating a virus with two 1918 genes. This virus was much more deadly to mice than other constructs containing genes from contemporary influenza virus. The experiments were conducted under high biosafety conditions at a laboratory of the US Department of Agriculture in Athens, Georgia.

In the February 6 2004, edition of Science magazine it was reported that two teams of researchers, one led by Sir John Skehel, director of the National Institute for Medical Research in London and another by Professor Ian Wilson of the Scripps Research Institute in San Diego had managed to synthesize the hemagglutinin protein responsible for the 1918 outbreak of Spanish Flu by piecing together DNA procured from a lung sample taken from the body of an Inuit woman buried in the Alaskan tundra and a number of preserved samples taken from American soldiers of the First World War. The two teams had analyzed the structure of the gene and discovered how subtle alterations to the shape of a protein molecule had allowed it to move from birds to humans with such devastating effects.

Wikinews has related news:

On October 5, 2005 researchers announced that the genetic sequence of the 1918 flu strain had been reconstructed using historic tissue samples[2]. The 2005 H5N1 bird flu strain spreading through Asia has some features of the 1918 strain but is so far not able to pass easily from human to human. [3]

On October 21, 2005 AVI BioPharma Inc. announced that some combinations of antisense drugs appeared to reduce the rate of genetic replication of the 1918 Spanish flu virus in laboratory experiments. This testing most certainly would have occurred at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) or possibly CDC in an enhanced level 3 or level 4 biosafety lab. [4] Additional experiments showed that a single mismatch within the targeted region of the virus caused less than a 10 percent loss of activity of the drug. This raises the possibility that a single antisense drug could potentially shut down multiple virus subtypes, including possibly the H5N1 bird flu, even if a mutation occurred in these highly conserved regions. [5] AVI BioPharma and the USAMRIID have previously announced positive results from testing an antisense compound against the Ebola virus. [6] Other antisense compounds are in clinical tests for Hepatitis C virus (HCV) at the Dept. of Veterans Affairs. [7]

Sources

  1. ^ Special report at Nature News: The 1918 flu virus is resurrected, Published online: 5 October 2005; | doi:10.1038/437794a. See: "Characterization of the 1918 influenza virus polymerase genes" by Jeffery K. Taubenberger, Ann H. Reid, Raina M. Lourens, Ruixue Wang, Guozhong Jin and Thomas G. Fanning in Nature (2005) volume 437 pages 889-893 doi:10.1038/nature04230. Also: "Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus" by Terrence M. Tumpey, Christopher F. Basler, Patricia V. Aguilar, Hui Zeng, Alicia Solórzano, David E. Swayne, Nancy J. Cox, Jacqueline M. Katz, Jeffery K. Taubenberger, Peter Palese and Adolfo García-Sastre in Science (2005) volume 310 pages 77-80. doi:10.1126/science.1119392
  • Terrence M. Tumpey, Adolfo García-Sastre, Andrea Mikulasova, Jeffery K. Taubenberger, David E. Swayne, Peter Palese, and Christopher F. Basler (2002) "Existing antivirals are effective against influenza viruses with genes from the 1918 pandemic virus". Proceedings of the National Academy of Sciences 99, 13849–13854.
  • Alfred W. Crosby (1990). America's Forgotten Pandemic: The Influenza of 1918. Cambridge University Press. ISBN 0521386950.
  • John M. Barry, (2004). The Great Influenza: The Epic Story of the Greatest Plague in History. Viking Penguin. ISBN 0670894737.
  • Leonard Crane, (2000). Ninth Day of Creation. Connection Books. ISBN 0967571294.
  • Andrew Noymer and Michel Garenne (2000). "The 1918 Influenza Epidemic's Effects on Sex Differentials in Mortality in the United States". Population and Development Review, 26(3):565–581.
  • Geoffrey W. Rice and Edwina Palmer (1993). "Pandemic Influenza in Japan, 1918–19: Mortality Patterns and Official Responses". Journal of Japanese Studies, 19(2):389–420.

See also

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