Repeated outbreaks of new pandemics are inevitable because of global trade and travel

It is often said that the only thing we can learn from history is that we can learn nothing. If you look back at the history of the global plague over the past century or so, you will find that this is not quite the case.
In the case of plagues, the truth is that plagues are always one step ahead of the human response.

A big part of the reason is the limitations of science.
During the Spanish pandemic of 1918, scientists stuck to the “germ theory” developed in the late 19th century and took a long time to realize that influenza was not caused by bacteria but by a virus, and identifying a pathogen and understanding its cause was not enough to control the spread of the epidemic.
The emergence of entirely new pathogens can quickly overturn established medical wisdom and undermine human confidence — something that happened again and again in the 20th century — and it means that the lack of effective information and treatment in the early stages of a pandemic can cause great alarm.
At the public policy level, we may not have formally acknowledged the limits of science until recently.
In February 2018, the world health organization added an unknown pathogen known as “unknown disease X” to its list of possible pandemic threats, acknowledging that “a currently unknown pathogen could one day cause a serious international pandemic.”

Social, political, economic and cultural factors can also greatly influence people’s response to the plague.
As long as there is bureaucracy, concealment and buck-passing are inevitable: during the 1918 pandemic, public health officials in New York exaggerated the flu’s impact on the German army for fear of affecting the war effort, while downplaying the American epidemic.
During the plague outbreak in Los Angeles in the 1920s, the authorities suppressed local media coverage for fear of damaging the city’s public image and economic interests.
Without knowledge of local culture and social behavior, international organizations have struggled to contain the epidemic: widespread distrust of foreigners and government elites has long kept ebola-stricken guineans from believing in the existence of ebola as a government or western conspiracy.
It is also bad to think that fighting the epidemic is a temporary success: the Brazilian government promised to spend heavily on improving sanitation in slums and providing medical assistance to local women in order to prevent the zika virus from disrupting the 2016 Olympics, but nothing happened after the games were over.

The most important factor is that human activity is upending the fragile balance between humans and viruses.
Urbanization and globalization have brought a large number of people together in a limited space, expanded the interactive boundary between human beings and nature (especially wild animals), accelerated the flow of people around the world, and created more and more favorable conditions for the expansion and spread of new pathogens.
From AIDS and SARS to ebola and zika, covid-19 is the latest example of a growing problem.

In the great human plague, Mark Honigsbaum, a British medical historian, presents people’s first reaction, panic, anxiety and coping strategies in the event of an outbreak of an unknown disease.
What can we learn from this history?
Be ever vigilant;
Do not think that a temporary victory is the end of the drama, the struggle between man and the plague will never end;
We should be realistic and not be blinded by ideology.
The current coronavirus outbreak has, so to speak, reinforced our impression of these lessons.

The great human plague: a global epidemic in a century by mark honisbaum. Translated by gu xiaoyang and li tong. Xin si culture. Citic publishing group. May, 2020

Preface: sharks and other predators (excerpt)

| gu xiaoyang li tong

Medical experts in the 19th century thought that by better understanding the social and environmental conditions that gave rise to infectious diseases, they could predict pandemics and thus — as the Victorian epidemiologist and hygienist William farr put it in 1847 — “eliminate panic.”
However, while advances in bacteriology led to the development of vaccines against diseases such as typhoid, cholera and plague, and fears of past pandemics receded, other diseases came on the stage and new fears replaced old fears.
Polio is a good example.
A month before sharks attacked swimmers on the jersey shore, a polio epidemic broke out near the shore in south brooklyn.
Investigators at New York’s health board immediately blamed the outbreak on recent Italian immigrants from Naples, who live in cramped, dirty apartments in an area known as “pig city.”
As polio cases rose, newspapers were filled with heartbreaking stories of babies dying or being paralysed, sparking an excessive panic and the flight of the rich (many new yorkers to the jersey shore).
Within weeks, the panic spread to neighboring states on the east coast, prompting quarantines, travel bans and forced hospitalizations.
These overreactions partly reflected the prevailing medical belief at the time that polio was a respiratory disease spread by coughing, sneezing and flies that grew in garbage.

In writing a history of polio, John r. Paul, an epidemiologist, described 1916 as “the culmination of quarantine and quarantine.”
By December 1916, when cooler weather began to subside, 27,000 cases and 6,000 deaths had occurred in 26 states, making it the world’s largest polio outbreak at the time.
In New York alone, 8,900 people became ill and 2,400 died, about one in every four children.

Polio spread so widely this time that it seemed as if americans were particularly susceptible to the disease.
But in fact, what most americans don’t know is that Sweden had a similar, terrifying outbreak five years ago.
During that outbreak, Swedish scientists repeatedly found polio virus in patients’ small intestine — an important step toward explaining the true cause and pathology of the disease.
The swedes also successfully cultured the virus in monkeys exposed to secretions from asymptomatic patients, heightening suspicions among scientists that “healthy carriers” act as reservoirs of the virus between outbreaks.
However, America’s leading polio experts ignored these insights.
It wasn’t until 1938 that researchers at Yale university picked up a study by Swedish scientists showing that polio was frequently detected in the feces of asymptomatic carriers, and that the virus could survive in untreated sewage for up to 10 weeks.

Today, it is recognized that in the era before the polio vaccine, the best way to avoid crippling the disease was to acquire immunity by getting infected once in early childhood, when serious complications are less likely to occur.
In this respect, dirt is an ally of mothers, and exposing babies to water and food contaminated with polio is a sensible strategy.
By the end of the 19th century, most children from poor immigrant communities had acquired immunity in this way.
Instead, it is children from new middle-class families and affluent neighborhoods who are most at risk.
Such was the case with franklin delano Roosevelt, the 32nd President of the United States, who remained uninfected as a teenager and did not catch the disease until 1921, when he was 39, while vacationing on campobelo island in new Brunswick.

How scientific knowledge of viruses and other infectious pathogens has sometimes blinded medical researchers to these ecological and immunological insights, or to an impending pandemic, is discussed in this book.
In the 1880s, German bacteriologist Robert Koch and French bacteriologist Louis Pasteur proved that tuberculosis was a bacterial infection and developed vaccines against anthrax, cholera and rabies, thus initiating the “germ theory” of the disease.
Ever since, scientists and public health officials who rely on their experimental techniques have dreamed of defeating the microbes that spread infectious diseases.
However, while medical microbiology and all related disciplines, such as epidemiology, parasitology, zoology, and most recently molecular biology, offer new ways to understand the spread and spread of new pathogens and enable clinicians to identify them, in many cases these sciences and techniques remain elusive.
It is sometimes argued that microbes are mutating and evolving all the time, and that scientific research cannot keep up with the speed of their genetic drift and the change in transmission patterns, but there is more to it than that.
Medical researchers tend to cling to particular paradigms and theories about the causes of disease, ignoring the threat posed by known and unknown pathogens.

Take influenza, the main character in chapter 1.
When the so-called “Spanish flu” appeared in the summer of 1918, near the end of world war I, most doctors thought it was little more than an old flu.
Doctors agree that the pathogen is unlikely to kill young people, let alone soldiers heading to the allied front in northern France.
They think like that, in part because of academic authority, Koch protege Richard dissemination, phil has suggested that influenza is transmitted by a tiny gram-negative bacteria, therefore, have been trained by German laboratory method of American scientists developed the prevention of influenza bacillus vaccine is only a matter of time, just as they develop vaccines to prevent cholera, diphtheria, typhus.
But pfeiffer and those who believed his method were wrong: influenza isn’t caused by a bacterium, it’s caused by a virus.
The virus is too small to be recognized under a normal light microscope.
In addition, ceramic filters were used to separate common bacteria from the nose and throat of flu patients, but the virus could pass through the filter directly.
Some researchers had begun to suspect that influenza might be caused by a “filleable pathogen,” but it would be years before pfeifer’s error was corrected and the viral etiology of influenza took over.
During that time, a lot of research time was wasted, and millions of young people died of the flu.

However, simply identifying the pathogen and understanding the cause of the disease is not enough to control the epidemic.
Although infectious pathogens may be necessary for disease, they are not sufficient.
Microbes interact with our immune systems in many ways, and when infected with the same pathogen, some people fall ill, while others are left unscathed or slightly unwell.
In fact, many bacteria and viruses can remain dormant in tissues and cells for decades before being reactivated by external events.
An external event may be a co-infection with another microbe, or a sudden attack of external stress on the body’s system, or weakening of the immune system as a result of aging.
What’s more, if we focus only on pathogenic microorganisms, we may miss the big picture.
Ebola virus may, for example, is one of the most deadly pathogens known to man, but only in deforestation causes a decline in the tropical rain forest, bat (presumably is virus between epidemic outbreaks of animal hosts) was kicked out of the nest, or humans to kill infected with the virus and eat them, the risk of the ebola virus is spreading to people.
And only when unsanitary practices in hospitals lead to the spread of a blood-borne infection can it spread to the wider community and spread to cities.
In this context, it is important to remember the point made by George Bernard shaw in the doctors’ dilemma: “the microbes that are characteristic of a disease are not necessarily the cause of it.”
In fact, if we apply shaw’s words today, we can say that almost all infectious diseases have broader environmental and social causes.
Only by fully considering the ecological, immune and behavioral factors of the emergence and spread of new pathogens can we have a relatively full and complete understanding of these microorganisms and their association with disease.

To be fair, there have always been medical researchers who have focused on studying our complex interactions with microbes in greater detail.
At the height of the antibiotic revolution 50 years ago, for example, Rene dubois, a researcher at the Rockefeller institute for medical research, criticised short-term technological solutions to medical problems.
At the time, most of his colleagues believed that there was no question that humans would conquer infectious diseases and that common pathogens would soon be eradicated.
Dubow, who isolated the first commercial antibiotic in 1939, was a professional, but he was alert to the prevailing hubris of the medical profession.
Dubois likens humans to “sorcerers’ apprentices,” suggesting that medical science has unleashed “potentially destructive forces” that could one day overturn the dream of a medical utopia.
“Modern humans believe that they have almost complete control of the natural forces that shaped human evolution in the past, and that they are now in control of their biological and cultural destinies,” he writes.
But that may be an illusion.
Like all living things, humans are part of an extremely complex ecosystem, linked through countless links to all its components.”
Dubow also suggests that getting rid of disease is a “fantasy” in which “nature will fight back in some unpredictable way at some unpredictable time.”

In the 1960s, however, despite the popularity of dubois’ work with the American public, his warnings about the impending end of the world of disease were largely ignored by his scientific peers.
As a result, shortly after dubeau’s death in February 1982, the centers for disease control and prevention (CDC) used the acronym “AIDS” to describe an unusual autoimmune disease that had popped up in the Los Angeles gay community and was spreading to other people.
The disease caught the medical community off guard.
But actually, the CDC shouldn’t be surprised, because something similar happened six years ago, in 1976.
A group of a luxury hotel to attend the American legion convention in Philadelphia veterans of the outbreak of SARS, when epidemiologists scrambling to try to find out the pathogenesis of “killer” in Philadelphia, the public into a panic, the first to the centers for disease control and prevention of epidemic disease detection personnel were confused, until a microbiologist identified pathogens – eosinophilic lung legionella, a growth in humid environments, such as the hotel’s cooling tower of tiny bacteria).
That same year, the panic was not only about legionnaires’ disease, but also about a new strain of swine flu that suddenly appeared at a U.S. army base in New Jersey — an emergency that caught the centers for disease control and prevention and public health officials off guard, eventually vaccinating millions of americans unnecessarily.
A similar situation occurred in 2003, when an elderly Chinese professor of nephrology checked into the Beijing international hotel in Hong Kong, triggering a cross-border outbreak of a severe respiratory disease.
The disease was originally thought to be caused by the H5N1 bird flu virus, but we now know that the pathogen was a novel coronavirus related to SARS.
In that case, a pandemic was averted through precise microbiological testing and unprecedented information sharing and collaboration among groups of scientists.
But that was a fluke, and since then we’ve had more outbreaks of pandemics that didn’t get the diagnosis right in the early stages.

The book will describe these events and what happened, and why we do our best to anticipate and prepare for pandemics, only to be caught off guard.
The history of some of these epidemics is well known to readers, such as the ebola scare of 2014-16 or the AIDS scare of the 1980s;

Others, such as pneumonic plague in Mexico’s Los Angeles area in 1924, or the “parrot fever” that swept the United States a few months after the Wall Street crash, may be less well known.
But whether or not they are familiar to the public, these pandemics reveal how quickly the emergence of new pathogens can overturn medical common sense, and how, in the absence of laboratory knowledge, effective vaccines and therapeutic drugs, pandemics have an extraordinary power to cause unease, panic and alarm.

Instead of dispelling panic, more medical knowledge and surveillance for infectious diseases may sow new fears and focus people too much on the threat of a pandemic they have never heard of before.
As a result, just as lifeguards now scour the ocean for dorsal fins in hopes of alerting swimmers, the world health organisation regularly monitors reports of unusual disease outbreaks on the Internet and detects viral mutations that could cause the next pandemic.
To some extent, this heightened vigilance is justified, but it comes at a price: perpetual anxiety about the next pandemic.
We are repeatedly told that the question is not whether the end of the world will happen, but when.
In this febrile atmosphere, it is no wonder that public health experts sometimes make the mistake of pressing the panic button when it is not necessary;
Or, as in the case of the ebola outbreak in west Africa, simply misread the threat.

It’s true that the media plays a role in these processes — nothing captures our attention like fear, after all — but while round-the-clock cable news channels and social media feed the unease, panic, and stigma associated with infectious disease outbreaks, journalists and bloggers are largely just media.
I believe that by alerting us to new sources of infection and defining certain behaviors as “risky,” medical science — and especially epidemiology — is the ultimate source of these unreasonable and often biased judgments.
While there is no doubt that a better understanding of the epidemiology and etiology of infectious diseases has greatly improved our ability to cope with pandemics, and that advances in medical technology have greatly improved human health and well-being, it is important to recognize that this knowledge is breeding new fears and anxieties.

Discussed in this book each epidemic depict different aspects of this process, the book also describes in each case, an epidemic disease outbreaks of how shaken the dominant paradigm and scientific paradigm of medicine confidence, emphasized at the expense of disease inducement to search at the expense of a wider range of ecology, the dangers of relying too much on a particular technology.
Based on a sociological and philosophical analysis of the construction of scientific knowledge, I will argue that what was “known” before the emergency has been proved wrong. These “known” things are: water towers and air-conditioning systems (in the case of legionnaires’ disease) do not pose a risk to hotel guests or to doctors and patients in hospitals;
Ebola does not spread in west Africa. It does not spread to big cities.
Zika is a relatively harmless mosquito-borne disease.
I also explained how, in each of these cases, the epidemic triggered a rethink of what is known and what is unknown, and how scientists and public health experts should avoid such epistemological blind spots in the future.

In discussing pandemics, this book also emphasizes that environmental, social and cultural factors play a key role in the changing patterns of disease prevalence and occurrence.
Looking back at dubow’s insights into pathogen ecology, I think that most diseases can be traced back to a disruption of the ecological balance, or to changes in the environment in which the pathogen habituates.
This applies especially to animal-borne diseases or zoonotic viruses, such as ebola, but also to symbiotic bacteria, such as streptococcus, which is a leading cause of community-acquired pneumonia.
The natural host of the ebola virus is now thought to be a fruit bat.
But while antibodies to the ebola virus have been found in various bats native to Africa, no live virus has ever been found in any bat.
The most likely reason is that, like other hosts and viruses linked by long evolution, the bat’s immune system quickly clears ebola from its bloodstream, but before it does, it passes on to another bat.
As a result, the virus circulates through bat populations without causing either to die out.
A similar process occurs with pathogens that have evolved to infect only humans, such as measles and poliovirus, which are first infected in childhood and usually cause only mild illness, after which the patient recovers and is immunized for life.
However, this immune equilibrium is often upset.
Disruption can occur naturally, for example, if a sufficient number of children are uninfected during childhood, resulting in a decline in herd immunity, or if the virus strain mutates suddenly (as often happens with influenza viruses), leaving people with little or no immunity, leading to the spread of new viruses.
In addition, this happens when we accidentally intervene between a virus and its natural host.
That’s probably what happened during the 2014 ebola outbreak, when children in the village of melendu teased a bat with a snout from a tree stump.
It is thought that something similar may have caused the transmission of HIV from chimpanzees to humans in Congo in the 1950s.
Tracing the exact origins of these epidemics is the subject of current research.
In the case of AIDS, there is no doubt that the beginning of the 20th century of steamboats on the Congo river and the construction of new roads and railways in colonial times were important contributors to the spread of AIDS, as were the greed of loggers and timber companies.
Social and cultural factors also play a role.
The virus probably would not have spread so widely and so quickly if there had been no venison and widespread prostitution around the railroad and lumber labor camps.
Similarly, without deep-rooted cultural beliefs and practices in west Africa, especially the observance of traditional funeral rituals and distrust of scientific medicine, ebola would not have developed into a major regional epidemic, much less a global health crisis.

The spread of ebola was caused by accidental human intervention in the virus and its natural host.
Photo credit: helo creative

But perhaps the most important reminder of medical history is the ancient link between epidemics and wars.
From Pericles in Athens in 430 BC, ordered the sea, in order to avoid since Sparta’s attack on the port city, has been regarded as the inventors of the deadly infectious disease outbreak of war (west Africa in 2014 or so, decades of civil war and armed conflict in Liberia and sierra leone health system is weak, lack of medical resources).
Although people still don’t know what causes the Athens plague pathogen, perhaps never know (cause of the plague disease may be anthrax, smallpox, typhus, and malaria), but there is no doubt that plague outbreaks of long wall behind the decisive factor is the Greek cities are crowded with more than 30 athenians and refugees from attica.
The crowded closed for the spread of the virus, if pathogens is virus, create the ideal conditions, will be turned into a charnel Athens (as thucydides’ tell us, because they have no house to receive the refugees from the countryside, “the heat, they were forced to squeeze in the sweltering huts, death there rampant”).
As a result, by the third epidemic in 426 BC, the population of Athens had shrunk by between a quarter and a third.

In the Athenian plague, for unknown reasons, the disease did not seem to affect the spartans, nor did it spread beyond the borders of attica.
But 2,000 years ago, cities and towns were isolated from each other, and people and pathogens spread far less between countries and continents.
Unfortunately, that is no longer the case today.
As a result of global trade and global travel, new viruses and their hosts continue to cross national borders and international time zones, where they encounter different ecological and immune environments.
The truest example came during world war I, when tens of thousands of young American recruits gathered at training camps on the east coast of the United States and then traveled back and forth between Europe and the United States, providing ideal conditions for the outbreak of the deadliest pandemic in history.

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