Afghani Women say the United States Military should get out of Afghanistan. That is the position of the Revolutionary Association of the Women of Afghanistan. They claim that the struggle against the warlords and Taliban is complicated by the presence of the NATO forces led by the USA. The CIA and other US agencies are funding the various factions of warlords instead of helping Afghani civil society. Before the 1980’s Afghanistan had a civil society that functioned. It is similar to Lebanon in that regard another country that was wracked with civil war for decades.
The world is drowning in shit. Humans creating factory farms that concentrate so many animals together that they become shit factories. Producing much more waste than can be used as fertilizer. They also are pumped full of antibiotics and some of them have been genetically modified to the point that they cannot even survive in the environment. Turkeys sold commercially are unable to survive outside of the factory farm. Meat sold in America, the result of factory farming is becoming more and more industrial and it is now the number one cause of air pollution. water pollution and global warming in the world. This is from the author of “Eating Animals”. Johnathan Safran Foer. He became a vegetarian convert after his wife gave birth to their son and he investigated the source of foods.
There is no way to produce enough meat ethically, or according to traditional methods to feed the entire population the amount of meat we consume at this time. That is largely the result of the fast food industry consuming vast quantities of dead animals. This is an industry that is based on force feeding massive amounts of adulterated meats to the populace. The result is food that is not nutritionally sound, that causes dangerous diseases such as swine flu and is the cause of massive amounts of pollution.
Some diseases originate in these industrial food sources, others are from more primitive sources such as the Chinese practice of keeping fowls, fish and humans in close proximity in a semi tropical environment with overcrowding. But the interesting question is, if this is true what can be done to avoid it and if it is true why now and not before. The flu, something that we are familiar with has sources that may ore may not be understood.
This is a brief history from Natural News.com
“412 BC – Major epidemic of a disease (which, although not called influenza, probably was influenza) recorded by Hippocrates.
1357 AD – The term, “influenza,” from the Italian word meaning “influence,” was coined. Popular belief at that time blamed the development of flu on the influence of the stars.
1485 – “Sweating sickness,” a flu-like malady, sickens hundreds of thousands of people in Britain. The Lord Mayor of London, his successor and six aldermen die. The Royal Navy cannot leave port due to the sickness of sailors. Doctors prescribe tobacco juice, lime juice, emetics, cathartics and bleeding as treatments for the disease.
1580 – First recorded influenza pandemic begins in Europe and spreads to Asia and Africa.
1700s – Influenza pandemics in 1729-1730, 1732-1733, 1781-1782.
1781 – Major epidemic causing high mortality among the elderly spreads across Russia from Asia.
1830 – Major epidemic causing high mortality among the elderly spreads across Russia from Asia.
1831, 1833-1834 – Influenza pandemics hit.
1847-1848 – Influenza sweeps through the Mediterranean to southern France and then continues across in Western Europe.
1878 – A disease causing high mortality in poultry becomes known as the “fowl plague.” Fowl plague is now called HPAI avian influenza.
1889-1890 – The “Russian flu” spreads through Europe and reaches North America in 1890.
1900 – Major epidemic.
1918-1919 – The “Spanish Flu” circles the globe (though some experts think it may have started in the U.S.). Caused by an H1N1 flu virus, it is the worst influenza pandemic (and subsequently, epidemic) to date. There are more than half a million U.S. deaths; worldwide death estimates range from 20 million to 100 million. According to Web MD, “The pandemic comes before the era of antibiotics — which are now essential in treating the secondary bacterial infections that often kill flu-weakened patients — so it’s difficult to say whether this flu would have the same dreadful impact in the modern world. But it is a very frightening disease, with very high death rates among young, previously healthy adults.”
1924 – The first outbreak of HPAI avian influenza — bird flu — in the U.S. It does not spread among humans.
Late 1920s – Richard Shope shows that swine influenza can be transmitted through filtered mucous, implying that influenza is caused by a virus.
1933 – Sir Christopher Andrewes, Wilson Smith and Sir Patrick Laidlaw isolate the first human influenza virus.
1940 – Frank Macfarlane Burnet grows influenza on a laboratory growth system (embryonated chicken eggs).
1941 – George K. Hirst discovers that influenza causes hemagglutination of red blood cells, thus providing a new method of assaying for the virus
1955 – Sir Christopher Andrewes, along with Burnet and Bang, coins the term “myxovirus” for the influenza family.
1957-1958 – The “Asian Flu” causes the second pandemic of the 20th century. Caused by an H2N2 virus, it begins in China and kills one million people worldwide, including 70,000 Americans.
1968-1969 – The “Hong Kong Flu” causes the last flu pandemic. It was caused by an H3N2 virus and killed some 34,000 Americans. The relatively low death toll is thought to have been due to two factors. First, the virus contained the N2 protein humans had been exposed to before. Second, an H3 virus circulated around the turn of the century, giving some immune protection to elderly people who had caught the flu back then.
Mid-1970s – Researchers realize that enormous pools of influenza virus continuously circulate in wild birds.
1976 – Swine flu breaks out among a handful of soldiers stationed at Fort Dix, N.J. One dies. It’s an H1N1 virus, and health officials worry that they are seeing the return of the 1918 H1N1 Spanish Flu pandemic. As the virus is circulating among U.S. pigs, President Gerald Ford calls for a crash vaccination program. Despite delays, a vaccine is made and a quarter of the U.S. population is inoculated. There were 25 deaths from a rare paralytic complication of the vaccination (Guillain-Barre syndrome). Nobody else died of swine flu, which never caused an epidemic.
1977 – Mild Russian influenza epidemic occurs.
1983 – The second HPAI outbreak occurs in the U.S. Caused by an H5N2 virus, it does not spread among humans. However, this severe poultry epidemic strikes chickens, turkeys and guinea fowl in Pennsylvania and Virginia. It is finally brought under control after the destruction of 17 million birds.
1988 – Wiley, Wilson and Skehel determine the location of the antigenic sites on the hemagglutinin molecule by X-ray crystallography.
1996 – HPAI H5N1 bird flu is isolated from a farmed goose in Guangdong, China.
May 1997 – The first person known to catch H5N1 bird flu dies in Hong Kong. The virus has been causing an epidemic among poultry in the city.
November-December 1997 – There are 18 new human cases of H5N1 bird flu in Hong Kong, 12 with direct contact with infected poultry. Six people die. Officials destroy 1.4 million chickens and ducks.
Jan. 5, 2003 – Health authorities in Vietnam inform the WHO office in Hanoi of an outbreak of severe respiratory illness in 11 previously healthy children hospitalized in Hanoi, with the most recent hospital admission on Jan. 4. Seven cases were fatal and two patients remain critically ill. A 12th case, a sibling of one of the Hanoi cases, died of a respiratory illness in a provincial hospital.”
The site then has an explosion of information on deaths from Bird flu in particular.
This is an article from last spring about Swine Flu mix with Bird Flu.
“Expert Warns Of Swine Flu-Bird Flu Mix
(CBS/AP) Bird flu kills more than 60 percent of its human victims, but doesn’t easily pass from person to person. Swine flu can be spread with a sneeze or handshake, but kills only a small fraction of the people it infects.
So what happens if they mix?
This is the scenario that has some scientists worried: The two viruses meet - possibly in Asia, where bird flu is endemic - and combine into a new bug that is both highly contagious and lethal, and can spread around the world.
Scientists are unsure how likely this possibility is, but note that the new swine flu strain - a never-before-seen mixture of pig, human and bird viruses - has shown itself to be especially adept at snatching evolutionarily advantageous genetic material from other flu viruses.
“This particular virus seems to have this unique ability to pick up other genes,” said leading virologist Dr. Robert Webster, whose team discovered an ancestor of the current flu virus at a North Carolina pig farm in 1998.
The current swine flu strain - known as H1N1 - has sickened more than 2,350 people in 26 countries. While people can catch bird flu from birds, the bird flu virus - H5N1 - does not easily jump from person to person. It has killed at least 258 people worldwide since it began to ravage poultry stocks in Asia in late 2003.”
Here is the information about the source of the current swine flu. Pig farms in North Carolina, not Mexico. But the current outbreak may have begun in Mexico where agribusiness has fewer regulations to worry about.
This is from a Wikepedia article about Swine Influenza.
“Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs, there is an informal surveillance network in the United States that is part of a world surveillance network.
Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930. For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997–1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2. In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm.
The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic. As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza.[ However, direct transmission from pigs to humans is rare, with only 12 cases in the U.S. since 2005. Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned.
Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year.”
This is from an interesting article from the CDC on the origins of the 1918 pandemic. Although it is fairly technical it is not above the level of an attentive reader and should be of interest.
“1918 Influenza: the Mother of All Pandemics
Jeffery K. Taubenberger* and David M. Morens†
*Armed Forces Institute of Pathology, Rockville, Maryland, USA; and †National Institutes of Health, Bethesda, Maryland, USA
The “Spanish” influenza pandemic of 1918–1919, which caused ≈50 million deaths worldwide, remains an ominous warning to public health. Many questions about its origins, its unusual epidemiologic features, and the basis of its pathogenicity remain unanswered. The public health implications of the pandemic therefore remain in doubt even as we now grapple with the feared emergence of a pandemic caused by H5N1 or other virus. However, new information about the 1918 virus is emerging, for example, sequencing of the entire genome from archival autopsy tissues. But, the viral genome alone is unlikely to provide answers to some critical questions. Understanding the 1918 pandemic and its implications for future pandemics requires careful experimentation and in-depth historical analysis.
An estimated one third of the world’s population (or ≈500 million persons) were infected and had clinically apparent illnesses (1,2) during the 1918–1919 influenza pandemic. The disease was exceptionally severe. Case-fatality rates were >2.5%, compared to <0.1% in other influenza pandemics (3,4). Total deaths were estimated at ≈50 million (5–7) and were arguably as high as 100 million (7).
The impact of this pandemic was not limited to 1918–1919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics.
In 1918, the cause of human influenza and its links to avian and swine influenza were unknown. Despite clinical and epidemiologic similarities to influenza pandemics of 1889, 1847, and even earlier, many questioned whether such an explosively fatal disease could be influenza at all. That question did not begin to be resolved until the 1930s, when closely related influenza viruses (now known to be H1N1 viruses) were isolated, first from pigs and shortly thereafter from humans. Seroepidemiologic studies soon linked both of these viruses to the 1918 pandemic (8). Subsequent research indicates that descendants of the 1918 virus still persists enzootically in pigs. They probably also circulated continuously in humans, undergoing gradual antigenic drift and causing annual epidemics, until the 1950s. With the appearance of a new H2N2 pandemic strain in 1957 ("Asian flu"), the direct H1N1 viral descendants of the 1918 pandemic strain disappeared from human circulation entirely, although the related lineage persisted enzootically in pigs. But in 1977, human H1N1 viruses suddenly "reemerged" from a laboratory freezer (9). They continue to circulate endemically and epidemically.
Thus in 2006, 2 major descendant lineages of the 1918 H1N1 virus, as well as 2 additional reassortant lineages, persist naturally: a human epidemic/endemic H1N1 lineage, a porcine enzootic H1N1 lineage (so-called classic swine flu), and the reassorted human H3N2 virus lineage, which like the human H1N1 virus, has led to a porcine H3N2 lineage. None of these viral descendants, however, approaches the pathogenicity of the 1918 parent virus.
Trying To Understand What Happened
By the early 1990s, 75 years of research had failed to answer a most basic question about the 1918 pandemic: why was it so fatal? No virus from 1918 had been isolated, but all of its apparent descendants caused substantially milder human disease. Moreover, examination of mortality data from the 1920s suggests that within a few years after 1918, influenza epidemics had settled into a pattern of annual epidemicity associated with strain drifting and substantially lowered death rates. Did some critical viral genetic event produce a 1918 virus of remarkable pathogenicity and then other critical genetic event occur soon after the 1918 pandemic to produce an attenuated H1N1 virus?
In 1995, a scientific team identified archival influenza autopsy materials collected in the autumn of 1918 and began the slow process of sequencing small viral RNA fragments to determine the genomic structure of the causative influenza virus (10). These efforts have now determined the complete genomic sequence of 1 virus and partial sequences from 4 others. The primary data from the above studies (11–17) and a number of reviews covering different aspects of the 1918 pandemic have recently been published (18–20) and confirm that the 1918 virus is the likely ancestor of all 4 of the human and swine H1N1 and H3N2 lineages, as well as the "extinct" H2N2 lineage. No known mutations correlated with high pathogenicity in other human or animal influenza viruses have been found in the 1918 genome, but ongoing studies to map virulence factors are yielding interesting results. The 1918 sequence data, however, leave unanswered questions about the origin of the virus (19) and about the epidemiology of the pandemic.
When and Where Did the 1918 Influenza Pandemic Arise?
Before and after 1918, most influenza pandemics developed in Asia and spread from there to the rest of the world. Confounding definite assignment of a geographic point of origin, the 1918 pandemic spread more or less simultaneously in 3 distinct waves during an ≈12-month period in 1918–1919, in Europe, Asia, and North America (the first wave was best described in the United States in March 1918). Historical and epidemiologic data are inadequate to identify the geographic origin of the virus (21), and recent phylogenetic analysis of the 1918 viral genome does not place the virus in any geographic context (19).
Although in 1918 influenza was not a nationally reportable disease and diagnostic criteria for influenza and pneumonia were vague, death rates from influenza and pneumonia in the United States had risen sharply in 1915 and 1916 because of a major respiratory disease epidemic beginning in December 1915 (22). Death rates then dipped slightly in 1917. The first pandemic influenza wave appeared in the spring of 1918, followed in rapid succession by much more fatal second and third waves in the fall and winter of 1918–1919, respectively (Figure 1). Is it possible that a poorly-adapted H1N1 virus was already beginning to spread in 1915, causing some serious illnesses but not yet sufficiently fit to initiate a pandemic? Data consistent with this possibility were reported at the time from European military camps (23), but a counter argument is that if a strain with a new hemagglutinin (HA) was causing enough illness to affect the US national death rates from pneumonia and influenza, it should have caused a pandemic sooner, and when it eventually did, in 1918, many people should have been immune or at least partially immunoprotected. "Herald" events in 1915, 1916, and possibly even in early 1918, if they occurred, would be difficult to identify.
The 1918 influenza pandemic had another unique feature, the simultaneous (or nearly simultaneous) infection of humans and swine. The virus of the 1918 pandemic likely expressed an antigenically novel subtype to which most humans and swine were immunologically naive in 1918 In summary, its origin remains puzzling.
Were the 3 Waves in 1918–1919 Caused by the Same Virus? If So, How and Why?
Historical records since the 16th century suggest that new influenza pandemics may appear at any time of year, not necessarily in the familiar annual winter patterns of interpandemic years, presumably because newly shifted influenza viruses behave differently when they find a universal or highly susceptible human population. Thereafter, confronted by the selection pressures of population immunity, these pandemic viruses begin to drift genetically and eventually settle into a pattern of annual epidemic recurrences caused by the drifted virus variants.
In the 1918–1919 pandemic, a first or spring wave began in March 1918 and spread unevenly through the United States, Europe, and possibly Asia over the next 6 months . Illness rates were high, but death rates in most locales were not appreciably above normal. A second or fall wave spread globally from September to November 1918 and was highly fatal. In many nations, a third wave occurred in early 1919 (21). Clinical similarities led contemporary observers to conclude initially that they were observing the same disease in the successive waves. The milder forms of illness in all 3 waves were identical and typical of influenza seen in the 1889 pandemic and in prior interpandemic years. In retrospect, even the rapid progressions from uncomplicated influenza infections to fatal pneumonia, a hallmark of the 1918–1919 fall and winter waves, had been noted in the relatively few severe spring wave cases. The differences between the waves thus seemed to be primarily in the much higher frequency of complicated, severe, and fatal cases in the last 2 waves.
But 3 extensive pandemic waves of influenza within 1 year, occurring in rapid succession, with only the briefest of quiescent intervals between them, was unprecedented. The occurrence, and to some extent the severity, of recurrent annual outbreaks, are driven by viral antigenic drift, with an antigenic variant virus emerging to become dominant approximately every 2 to 3 years. Without such drift, circulating human influenza viruses would presumably disappear once herd immunity had reached a critical threshold at which further virus spread was sufficiently limited. The timing and spacing of influenza epidemics in interpandemic years have been subjects of speculation for decades. Factors believed to be responsible include partial herd immunity limiting virus spread in all but the most favorable circumstances, which include lower environmental temperatures and human nasal temperatures (beneficial to thermolabile viruses such as influenza), optimal humidity, increased crowding indoors, and imperfect ventilation due to closed windows and suboptimal airflow.
However, such factors cannot explain the 3 pandemic waves of 1918–1919, which occurred in the spring-summer, summer-fall, and winter (of the Northern Hemisphere), respectively. The first 2 waves occurred at a time of year normally unfavorable to influenza virus spread. The second wave caused simultaneous outbreaks in the Northern and Southern Hemispheres from September to November. Furthermore, the interwave periods were so brief as to be almost undetectable in some locales. Reconciling epidemiologically the steep drop in cases in the first and second waves with the sharp rises in cases of the second and third waves is difficult. Assuming even transient postinfection immunity, how could susceptible persons be too few to sustain transmission at 1 point and yet enough to start a new explosive pandemic wave a few weeks later? Could the virus have mutated profoundly and almost simultaneously around the world, in the short periods between the successive waves? Acquiring viral drift sufficient to produce new influenza strains capable of escaping population immunity is believed to take years of global circulation, not weeks of local circulation. And having occurred, such mutated viruses normally take months to spread around the world.
At the beginning of other "off season" influenza pandemics, successive distinct waves within a year have not been reported. The 1889 pandemic, for example, began in the late spring of 1889 and took several months to spread throughout the world, peaking in northern Europe and the United States late in 1889 or early in 1890. The second recurrence peaked in late spring 1891 (more than a year after the first pandemic appearance) and the third in early 1892 (21). As was true for the 1918 pandemic, the second 1891 recurrence produced of the most deaths. The 3 recurrences in 1889–1892, however, were spread over >3 years, in contrast to 1918–1919, when the sequential waves seen in individual countries were typically compressed into ≈8–9 months.
What gave the 1918 virus the unprecedented ability to generate rapidly successive pandemic waves is unclear. Because the only 1918 pandemic virus samples we have yet identified are from second-wave patients (16), nothing can yet be said about whether the first (spring) wave, or for that matter, the third wave, represented circulation of the same virus or variants of it. Data from 1918 suggest that persons infected in the second wave may have been protected from influenza in the third wave. But the few data bearing on protection during the second and third waves after infection in the first wave are inconclusive and do little to resolve the question of whether the first wave was caused by the same virus or whether major genetic evolutionary events were occurring even as the pandemic exploded and progressed. Only influenza RNA–positive human samples from before 1918, and from all 3 waves, can answer this question.
What Was the Animal Host Origin of the Pandemic Virus?
Viral sequence data now suggest that the entire 1918 virus was novel to humans in, or shortly before, 1918, and that it thus was not a reassortant virus produced from old existing strains that acquired 1 or more new genes, such as those causing the 1957 and 1968 pandemics. On the contrary, the 1918 virus appears to be an avianlike influenza virus derived in toto from an unknown source (17,19), as its 8 genome segments are substantially different from contemporary avian influenza genes. Influenza virus gene sequences from a number of fixed specimens of wild birds collected circa 1918 show little difference from avian viruses isolated today, indicating that avian viruses likely undergo little antigenic change in their natural hosts even over long periods (24,25).
One possible explanation is that these unusual gene segments were acquired from a reservoir of influenza virus that has not yet been identified or sampled. All of these findings beg the question: where did the 1918 virus come from?
In contrast to the genetic makeup of the 1918 pandemic virus, the novel gene segments of the reassorted 1957 and 1968 pandemic viruses all originated in Eurasian avian viruses (26); both human viruses arose by the same mechanism—reassortment of a Eurasian wild waterfowl strain with the previously circulating human H1N1 strain. Proving the hypothesis that the virus responsible for the 1918 pandemic had a markedly different origin requires samples of human influenza strains circulating before 1918 and samples of influenza strains in the wild that more closely resemble the 1918 sequences.
Why did so many young healthy persons die?
One theory that may partially explain these findings is that the 1918 virus had an intrinsically high virulence, tempered only in those patients who had been born before 1889, e.g., because of exposure to a then-circulating virus capable of providing partial immunoprotection against the 1918 virus strain only in persons old enough (>35 years) to have been infected during that prior era (35). But this theory would present an additional paradox: an obscure precursor virus that left no detectable trace today would have had to have appeared and disappeared before 1889 and then reappeared more than 3 decades later.
Could a 1918-like Pandemic Appear Again? If So, What Could We Do About It?
In its disease course and pathologic features, the 1918 pandemic was different in degree, but not in kind, from previous and subsequent pandemics. Despite the extraordinary number of global deaths, most influenza cases in 1918 (>95% in most locales in industrialized nations) were mild and essentially indistinguishable from influenza cases today. Furthermore, laboratory experiments with recombinant influenza viruses containing genes from the 1918 virus suggest that the 1918 and 1918-like viruses would be as sensitive as other typical virus strains to the Food and Drug Administration–approved antiinfluenza drugs rimantadine and oseltamivir.
However, some characteristics of the 1918 pandemic appear unique: most notably, death rates were 5–20 times higher than expected. Clinically and pathologically, these high death rates appear to be the result of several factors, including a higher proportion of severe and complicated infections of the respiratory tract, rather than involvement of organ systems outside the normal range of the influenza virus. Also, the deaths were concentrated in an unusually young age group. Finally, in 1918, 3 separate recurrences of influenza followed each other with unusual rapidity, resulting in 3 explosive pandemic waves within a year’s time. Each of these unique characteristics may reflect genetic features of the 1918 virus, but understanding them will also require examination of host and environmental factors.
Until we can ascertain which of these factors gave rise to the mortality patterns observed and learn more about the formation of the pandemic, predictions are only educated guesses. We can only conclude that since it happened once, analogous conditions could lead to an equally devastating pandemic.”
I edited out some of the purely technical sections but even so it is a tough read and essentialy the article asks more questions than it answers. We know that these viruses exist in animal populations. They transfer over to human populations through a system of transference that is not well understood. The majority of cases seem to come from Asia but the record from the 1918 pandemic seem to show the American military base of Fort Riley, Kansas as an early source in the spring of 1918.
This is from an article on the flu By Molly Billings
“The origins of this influenza variant is not precisely known. It is thought to have originated in China in a rare genetic shift of the influenza virus. The recombination of its surface proteins created a virus novel to almost everyone and a loss of herd immunity. Recently the virus has been reconstructed from the tissue of a dead soldier and is now being genetically characterized. The name of Spanish Flu came from the early affliction and large mortalities in Spain (BMJ,10/19/1918) where it allegedly killed 8 million in May (BMJ, 7/13/1918). However, a first wave of influenza appeared early in the spring of 1918 in Kansas and in military camps throughout the US. Few noticed the epidemic in the midst of the war. Wilson had just given his 14 point address. There was virtually no response or acknowledgment to the epidemics in March and April in the military camps. It was unfortunate that no steps were taken to prepare for the usual recrudescence of the virulent influenza strain in the winter. The lack of action was later criticized when the epidemic could not be ignored in the winter of 1918 (BMJ, 1918). These first epidemics at training camps were a sign of what was coming in greater magnitude in the fall and winter of 1918 to the entire world.
The war brought the virus back into the US for the second wave of the epidemic. It first arrived in Boston in September of 1918 through the port busy with war shipments of machinery and supplies. The war also enabled the virus to spread and diffuse. Men across the nation were mobilizing to join the military and the cause. As they came together, they brought the virus with them and to those they contacted. The virus killed almost 200,00 in October of 1918 alone. In November 11 of 1918 the end of the war enabled a resurgence. As people celebrated Armistice Day with parades and large partiess, a complete disaster from the public health standpoint, a rebirth of the epidemic occurred in some cities. The flu that winter was beyond imagination as millions were infected and thousands died. Just as the war had effected the course of influenza, influenza affected the war. Entire fleets were ill with the disease and men on the front were too sick to fight. The flu was devastating to both sides, killing more men than their own weapons could.”
What is worse factory farming or intensive farming in hot humid climates? One is modern and has only been a factor in recent decades. The other has been around for thousands of years and is only intensified by the increased population and the speed of communications. We cannot avoid contact in the modern world but we can seek to eradicate the sources of disease in these manners.
A) Eating a mainly vegetarian diet.
B) Ending Factory Farming of livestock,
C) Stricter implimentation of approved sanitary regimes,
D) Reducing population concentrations of animals and humans.
E) Limiting Fast Food diets and stricter health standards for restaurants including manditory paid sick leave for employees.