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Is Omicron Mother Nature’s Variant?
July 8, 2022 - 11:27 am

In January, Chinese virologists isolated the virus that causes Covid-19. Earlier this month, a team of virologists gave this new virus a new name: SARS-CoV-2.

To do so, they had to move the virus to the head of a very, very long line.

In recent years, scientists have discovered that the world of virus diversity — what they sometimes call the virosphere — is unimaginably vast. They have uncovered hundreds of thousands of new species that have yet to be named. And they suspect that there are millions, perhaps even trillions, of species waiting to be found.

“Suffice to say that we have only sampled a minuscule fraction of the virosphere,” said Edward Holmes of the University of Sydney in Australia.

With the discovery of viruses in the late 1800s, scientists soon recognized that different species caused different diseases — rabies and influenza, for example. Later, virologists learned how to recognize new kinds of viruses by growing them in labs, where subtler biological features emerged.

After decades of this painstaking work, virologists have officially named 6,828 species of viruses; the figure includes 1,000 or so that will be formally accepted in the next few weeks by the International Committee on the Taxonomy of Viruses. That’s a paltry count when you consider that entomologists have named 380,000 species of beetles alone.

But in recent years, virologists have changed the way they hunt. Now they look for bits of genetic material in samples — water, mud, blood — and use sophisticated computer programs to recognize viral genes.

Matthew Sullivan, a virologist at Ohio State University, has used this method to search for viruses that infect life in the ocean. He and his colleagues analyzed genetic material in seawater collected on a scientific voyage around the world. Some genes belonged to species already known to science. But many were new. In 2016, Dr. Sullivan and his colleagues reported over 15,000 viruses, each representing a new species.

That was more than twice as many species as all the previously identified viruses. And with that, Dr. Sullivan thought he and his colleagues had pretty much finished off the diversity of viruses in the sea. But they went on collecting more water, and invented new ways to search it for the genetic material of viruses. In 2019, they reported finding a total of 200,000 species.

“I’ve stopped saying, ‘We’re done,’” Dr. Sullivan said.

Other researchers are discovering thousands of new viruses as well. “Right now, we are in the exponential phase,” said Dr. Jens H. Kuhn, the lead virologist at the Integrated Research Facility at Fort Detrick in Maryland. “If someone gives me a million dollars and I go out and sample sea cucumbers, I will present you with 10,000 new viruses.”

Formally describing a new virus remains a time-consuming task. When Chinese researchers isolated the Covid-19-causing virus earlier this year, they found that it had a distinctive crown of proteins. This hallmark told them that the virus belonged to the coronavirus family, which contains 39 known species. The World Health Organization used this finding to give the disease its name — Coronavirus Disease 2019, or Covid-19 for short.

To determine just what kind of coronavirus they were dealing with, virologists sequenced its genes. The virus was genetically similar to the one that caused the SARS outbreak in 2002. In March, the International Committee on Taxonomy of Viruses declared that the two viruses belonged to the same species. The virus that caused SARS is known as SARS-CoV. So they called the Covid-19-causing virus SARS-CoV-2.

The viruses that infect humans are the best understood of all. But only about 250 species of viruses choose us as their host — “an insignificant fraction of the virosphere infect humans,” Dr. Holmes said.

While hundreds of thousands of new species still await their own names, virologists believe that far more await discovery. Dr. Holmes estimates that the viruses infecting animals, plants, fungi and protozoans (a group called eukaryotes) number 100 million species.

Bacteria and other single-celled microbes belong to a group called prokaryotes. In a paper published on March 4 in Microbiology and Molecular Biology Reviews, Dr. Kuhn and his colleagues argued that there are, at minimum, 100 million species of viruses that infect prokaryotes.

But some researchers suspect there are many more species of prokaryotes in the world — which would mean many more species of viruses. The true figure might be as high as 10 trillion.

For each of those species, scientists will have to figure out how it is related to other viruses. That is far harder to determine for viruses than for familiar life-forms like animals and plants.

Scientists who study animals and plants can rely on the tried and true classification system first established by Carl Linnaeus in the 1700s. Our species belongs to the class Mammalia, for instance, and, above that, the animal kingdom. Virologists have struggled to figure out the classes and kingdoms of the virosphere. Part of the problem is that viruses have a penchant for trading genes with other species, making it hard to draw bright lines between groups of them.

And very often, a new virus simply makes no sense. An extreme example came to light in February when scientists searching for viruses in a lake found a new one they named Yaravirus. Of Yaravirus’s 74 genes, 68 are unlike any ever found in any virus.

In recent years, Dr. Kuhn and his colleagues have sought to tame this chaos. They have developed what they call a “megataxonomy” to classify viruses that seems to work. The team sorted viruses based on whether they carried one or more of a few “hallmark genes.” They also looked for groups of species that trade genes among each other, and less so with other groups.

“A coherent account of the global organization of the virus world is now within reach,” they wrote in their new paper. Dr. Kuhn, in an interview, said, “We were all a bit surprised this system is so logical in the end.”

Dr. Kuhn and his colleagues submitted their system to the taxonomy committee, and he said it would likely be accepted soon. Still, the megataxonomy is far from complete. Yaravirus, for instance, still floats on its own, lonely and unclassifiable.

Some researchers are skeptical about the megataxonomy. Dr. Holmes thinks it is too soon to attempt one, given that researchers have found so few viruses. “Why build something so rigid when it may just fall as we sample more?” he asked. Dr. Kuhn argues that it’s worth starting to build a system, even if it needs to be adjusted later.

Making sense of the virosphere is not just an intellectually challenging puzzle, Dr. Kuhn said. At Fort Dietrick, he runs experiments on some of the world’s most dangerous viruses, such as Ebola and SARS-CoV-2. A better understanding of the virosphere could help him and his colleagues come up with ways to combat these threats and others we don’t even know about yet.

“We have to understand what is out there,” he said.

The Fight Over Inoculation During the 1721 Boston Smallpox Epidemic
The Fight Over Inoculation During the 1721 Boston Smallpox Epidemic
May 20, 2022 - 8:35 am

On a November day in 1721, a small bomb was hurled through the window of a local Boston Reverend named Cotton Mather. Attached to the explosive, which fortunately did not detonate, was the message: “Cotton Mather, you dog, dam you! I’ll inoculate you with this; with a pox to you.’’ This was not a religiously motivated act of terrorism, but a violent response to Reverend Mather’s active promotion of smallpox inoculation. The smallpox epidemic that struck Boston in 1721 was one of the most deadly of the century in colonial America, but was also the catalyst for the first major application of preventative inoculation in the colonies. The use of inoculation laid the foundation for the modern techniques of infectious diseases prevention, and the contentious public debate that accompanied the introduction of this poorly understood medical technology has surprising similarities to contemporary misunderstandings over vaccination.

The Boston Epidemic
For over a year, from the spring of 1721 until winter 1722, a smallpox epidemic afflicted the city of Boston. Out of a population of 11,000, over 6000 cases were reported with 850 dying from the disease. Of a series of seven epidemics in the region during the 1700s, this was the most deadly [2]. Though tragic, the 1721 epidemic led to a major milestone in the history of vaccination and smallpox eradication. The use of inoculation during this epidemic, and the heated debate that arose surrounding the practice, was one of the first major applications of inoculations in western society, paving the way for Edward Jenner to develop smallpox vaccination by the end of the century.

The Disease and Early Inoculation
Smallpox is an ancient disease caused by the Variola virus. This virus exists in two main forms: Variola major, which historically has a mortality rate of around 30%, and the less severe Variola minor with a mortality rate around 1% [3]. Variola major is predominantly transmitted either by direct or indirect contact with the respiratory droplets from an infected individual [4]. The natural pathogenesis of Variola major begins with the infection of the mucous membrane of the upper respiratory system, then invasion of the bloodstream, and eventually the skin, producing the classical presentation of smallpox pustules and signifying that the patient has become infectious. Death can result from toxins in the blood, blood clots, and septic shock [5].

Inoculation against smallpox is believed to have been practiced in China as far back as 1000 CE, and is reported to have been common in India, Africa, and Turkey prior to its introduction into western societies in the 18th century [1]. In China the practice was to blow dried and ground Variola scabs into the nostrils of the patient. In Turkey, however, the technique of inoculation involved inducing a less serious form of the smallpox disease by exposing an incision to the Variola pus [6]. The latter is the procedure that was eventually brought to England and colonial America. The idea was based on the basic observation that those who survived smallpox, moderate or severe, were significantly less likely to contract the disease again. By deliberately inducing an acute smallpox infection through a small localized wound, a healthy person was more likely to survive the infection than if they had acquired the disease naturally through aerosolized viral particles. Smallpox vaccination, as developed by Edward Jenner in the late 1700s, worked on the same principle but differed in that the viral source was the less dangerous cowpox disease (Table 1) [7]. Today, smallpox vaccination uses the Vaccinia virus to induce immunity, and the principle of vaccination has been applied to battling numerous other infectious diseases.

Introducing Inoculation to the West
Although inoculation was already common in certain parts of the world by the early 18th century, it was only just beginning to be discussed in England and colonial America. Cotton Mather is largely credited with introducing inoculation to the colonies and doing a great deal to promote the use of this method as standard for smallpox prevention during the 1721 epidemic. Mather is believed to have first learned about inoculation from his West African slave Onesimus, writing, “he told me that he had undergone the operation which had given something of the smallpox and would forever preserve him from it, adding that was often used in West Africa.’’ After confirming this account with other West African slaves and reading of similar methods being performed in Turkey, Mather became an avid proponent of inoculation [8]. When the 1721 smallpox epidemic struck Boston, Mather took the opportunity to campaign for the systematic application of inoculation. What followed was a fierce public debate, but also one of the first widespread and well-documented uses of inoculation to combat such an epidemic in the West.

The Outbreak in Boston
On April 22, 1721, a British ship arrived in Boston Harbor. On board, one of the sailors had begun to exhibit symptoms of smallpox. He was quickly quarantined, but several more members of the crew soon fell ill with the disease. An outbreak of the disease spread quickly through the city [1]. As the epidemic worsened, Cotton Mather reached out to the medical community of Boston, imploring them to use the inoculation method. One physician, Zabdiel Boylston, heeded his call, but most other doctors were hostile to the idea. At the forefront of the anti-inoculation contingency was one of Boston’s only physicians who actually held a medical degree, Dr. William Douglass. The arguments against inoculation were varied, ranging from disagreement on religious grounds to scientific uncertainty. While many argued that inoculation violated divine law, by either inflicting harm on innocent people or by attempting to counter God’s specific will, the main argument that Douglass made was that inoculation was untested and seemingly based on folklore. Douglas feared that unchecked use of inoculation would only quicken the spread of disease throughout the city [8].

By modern standards, this argument seems highly sensible. The use of a poorly researched medical technique, particularly one as potentially hazardous as intentionally exposing healthy people – including children – to smallpox, would be highly unethical today. To many professional Boston physicians, inoculation must have appeared as unscientific as other contemporary treatments such as bleeding and purging, which were still common practice during the early 18th century.

But as the epidemic began to diminish in early 1722, Mather and Boylston had collected surprisingly thorough data that made a clear argument for the effectiveness of inoculation (Figure 1). Boylston, who had personally inoculated some 287 people, recorded that of those inoculated only 2% had died. In comparison, the mortality rate of the naturally occurring disease during that year was 14.8% [1].

Although inoculations were themselves a risky practice and carried a not-insignificant health risk, this data demonstrates that inoculations were significantly less fatal than the naturally occurring virus. Ultimately, this helped to disprove the opposition’s fear that such a technique would only facilitate the spread of disease. Mather and Boylston’s advocacy and observations resulted in what was actually one of the earliest clinical trials on record, and the use of both experimental and control groups to demonstrate the effectiveness of inoculation significantly aided the adoption of the practice [1,9].

Smallpox continued to be a significant health threat throughout the 18th and 19th centuries, and part of the 20th, but the introduction and success of inoculation in the early 1700s, followed later by the much safer vaccination method developed by Edward Jenner, steadily reduced the threat the disease posed until its eradication in 1980 (Figure 2) [10].

Then and Now
The debate over the use of inoculation, particularly apparent during the 1721 epidemic in Boston, still bears relevance today. Modern vaccination campaigns, most notably targeting the eradication of polio, continue to face violent opposition in many parts of the world where the disease is still present, particularly in Pakistan, Afghanistan, and Nigeria [11]. Just this past November four polio vaccination workers were killed in Pakistan [12]. Even in the United States, outbreaks among groups of unvaccinated individuals have risen in the past decade, a trend that is often attributed to the spread of misinformation regarding the potential risks, contents, and mechanism of vaccination [13,14]. The story of the 1721 Boston Smallpox epidemic, and the controversy that accompanied the introduction of inoculation by Dr. Boylston and Cotton Mather, exemplifies how opposition to inoculation and then vaccination has been present for as long as the practices themselves. Although there is still a great deal of work to be done in the fight against infectious diseases and enclaves of opposition remain, the effectiveness and benefit of vaccination has been clearly demonstrated over many decades of systemic application that began with the work of Mather and Boylston [15].

Matthew Niederhuber is a Research Assistant in the Silver Lab in Department of Systems Biology at Harvard Medical School.

References
[1] Best, M. Neuhauser, D. and Slavin, L. “Cotton Mather, you dog, dam you! I’l inoculate you with this; with a pox to you”: smallpox inoculation, Boston, 1721. Quality and Safety in Health Care 2004.13:82-83.

[2] Henry E. H. Experience in Massachusetts and a Few Other Places with Smallpox and Vaccination. Boston Medical Surgical Journal 1921. 185:221-228.

[3] Centers for Disease Control and Prevention: “Smallpox Disease Overview” http://emergency.cdc.gov/agent/smallpox/overview/disease-facts.asp

[4] World Health Organization: “Frequently asked questions and answers on smallpox” http://www.who.int/csr/disease/smallpox/faq/en/

[5] Behbehani, Abbas. The Smallpox Story: Life and Death of an Old Disease. Microbiological Reviews 1983. 47.4:455-509.

[6] U.S. National Library of Medicine: “Smallpox: A Great and Terrible Scourge” http://www.nlm.nih.gov/exhibition/smallpox/sp_variolation.html

[7] Riedel, S. Edward Jenner and the history of smallpox and vaccination. Baylor University Medical Center Proceedings 2005. 18.1:21-25.

[8] Buhr, S. To Inoculate or Not to Inoculate?: The Debate and the Smallpox Epidemic of 1721. Constructing the Past 2000. 1:61-67.

[9] Boylston, Z. An Historical Account of the Small-pox Inoculated in New England, Upon All Sorts of Persons, Whites, Blacks, and of All Ages and Constitutions: With Some Account of the Nature of the Infection in the Natural and Inoculated Way, and Their Different Effects on Human Bodies: with Some Short Directions to the Unexperienced in this Method of Practice / Humbly Dedicated to Her Royal Highness the Princess of Wales. Boston: 1730.

[10] World Health Organization: “Smallpox” http://www.who.int/csr/disease/smallpox/en/

[11] Bhutta, Z. Infectious disease: Polio eradication hinges on child health in Pakistan. Nature 2014. 511:285-287.

[12] Yousafza G. “Militants kill four polio workers in Pakistan.” Reuters 26 Nov. 2014.

[13] Omer, S. et al. Vaccine Refusal, Mandatory Immunization, and the Risks of Vaccine-Preventable Diseases. New England Journal of Medicine 2009. 360:1981-1988.

[14] Wang, E. et al. Nonmedical Exemptions From School Immunization Requirements: A Systematic Review. American Journal of Public Health 2014. 11:62-84.

[15] Scully, T. The Age of Vaccines. Nature 2014. 507:S2-S3.

Source: Harvard University

Spike in child hepatitis cases linked to common virus
Spike in child hepatitis cases linked to common virus
April 22, 2022 - 8:10 am

By Meredith Wadman
Health Reporter at Science

 

Puzzled scientists are searching for the cause of a strange and alarming outbreak of severe hepatitis in young children, with 74 cases documented in the United Kingdom and three in Spain. Clinicians in Denmark and the Netherlands are also reporting similar cases. And in the United States, the Centers for Disease Control and Prevention (CDC) said late yesterday it is investigating nine cases in Alabama.

Viruses can cause hepatitis, an inflammation of the liver, but otherwise-healthy children rarely become seriously ill. As of 12 April, none of the U.K. or Spanish children have died, but some are very sick: All have been admitted to hospitals and seven required liver transplants, six of them in the United Kingdom, according to a World Health Organization (WHO) statement issued today. Two of the nine affected children in Alabama have required liver transplants, the state’s Department of Public Health announced this afternoon.

The leading theory is that an adenovirus, a family of viruses that more typically cause colds, is the culprit—up to half of the sickened children in the United Kingdom tested positive for such a virus, as did all the children in Alabama. But so far, the evidence is too thin to resolve the mystery, researchers and physicians say.

“This is a severe phenomenon,” says Deirdre Kelly, a pediatric hepatologist at Birmingham Children’s Hospital in the United Kingdom. “These [were] perfectly healthy children … up to a week ago.” Not all the news is bad, however. “Most of [the children] recover on their own,” Kelly notes.

“This should be taken seriously,” WHO’s Regional Office for Europe wrote in an emailed statement. “The increase is unexpected and the usual causes have been excluded.”

Scottish investigators first identified the outbreak on 31 March, when they alerted Public Health Scotland to a cluster of 3- to 5-year-olds admitted to the Royal Hospital for Children in Glasgow in the first 3 weeks of March. Each was diagnosed with severe hepatitis of unknown cause. Typically, Scotland sees fewer than four such cases annually, the investigators wrote in a paper published yesterday. But there have been 13 cases in Scottish children as of 12 April, all but one in March and April.

Kelly, who works at one of England’s three centers for pediatric liver disease and transplantation, says that since the start of this year, her unit has seen 40 cases of childhood hepatitis of uncertain cause. Over the same January to April period in 2018, her unit saw only seven such children.

Most of the U.K. children are 2 to 5 years old, according to a statement issued on 8 April by the UK Health Security Agency. The European Centre for Disease Prevention and Control issued a public alert on 12 April about the U.K. outbreak, noting that vomiting and jaundice—yellowing of the skin and the whites of the eyes—are common symptoms.

Early hypotheses about what might be making the children sick included a toxic exposure from food, drinks, or toys, but suspicion now centers on a virus. None of the U.K. or Spanish kids had the hepatitis A, B, C, or E viruses, typical infectious causes of the disease. But a handful of children tested positive for SARS-CoV-2 infection shortly before or upon hospital admission; none had received a COVID-19 vaccine. In addition, as many as half had adenovirus, a common virus passed by respiratory droplets and from touching infected people or virus on surfaces. It can cause vomiting, diarrhea, conjunctivitis, and cold symptoms but rarely causes hepatitis.

“The leading hypotheses center around adenovirus—either a new variant with a distinct clinical syndrome or a routinely circulating variant that is more severely impacting younger children who are immunologically naïve,” the Scottish investigators wrote.

Isolation of the youngest children during the pandemic lockdown may have left them immunologically vulnerable because they haven’t been exposed to the multiplicity of viruses, including adenoviruses, that typically attend toddlerhood. “We are seeing a surge in typical childhood viral infections as children come out of lockdown, [as well as] a surge in adenovirus infections”—but can’t be sure that one is causing the other, says Will Irving, a clinical virologist at the University of Nottingham.

Researchers continue to study other possibilities. For example, the immunological effects of a prior episode of COVID-19 might have left children more vulnerable to infection or the illness could be a long-term complication of COVID-19 itself. An unidentified toxin has also not been ruled out.

All the cases might not have a single cause, cautions Jim McMenamin, an epidemiologist who heads the infection service of Public Health Scotland. “It’s awfully important that we ensure we are looking for everything, that we are not confining ourselves to saying this is simply one viral cause.”

In the United States, CDC is helping the Alabama Department of Public Health investigate nine cases of hepatitis in children ranging in age from 1 to 6 years old and who also tested positive for adenovirus. The cases have occurred since October 2021, Kristen Nordlund, a CDC spokesperson, wrote in the statement emailed to ScienceInsider last night.

“CDC is working with state health departments to see if there are additional U.S. cases, and what may be causing these cases,” she wrote. “Adenovirus may be the cause for these, but investigators are still learning more—including ruling out the more common causes of hepatitis.”

Wes Stubblefield, a district medical officer with the Alabama Department of Public Health, said in an interview today that the most recent case in Alabama occurred in February, and that five of the nine children tested positive for adenovirus-41, a strain that commonly causes gastroenteritis.

Meanwhile, in Spain, the government of the Madrid region announced on 13 April that three regions—Madrid, Aragón, and Castilla-La Mancha—had each reported a case of severe hepatitis of unknown origin in young children. One child has received a liver transplant.

Physicians at major pediatric liver centers in the Netherlands and Denmark told ScienceInsider yesterday they are seeing similar trends. “There are children that are very sick and have been referred for transplantation,” says Ruben de Kleine, a pediatric liver transplant surgeon at University Medical Center Groningen. “We have assessed a similar number of kids for transplantation within the first 4 months of 2022 [to what we] normally do in a whole year.”

At Copenhagen University Hospital, too, “we have more cases with [acute liver failure] than we normally have,” says pediatric hepatologist Marianne Hørby Jørgensen. No children there have needed transplants.

Hørby Jørgensen and de Kleine both stress that parents should not panic. To date, clinicians have identified small numbers of cases in their countries where, combined, more than 230,000 infants are born each year.

The enigma of the 1889 Russian flu pandemic – a coronavirus?
The enigma of the 1889 Russian flu pandemic: A coronavirus?
March 11, 2022 - 6:23 pm

Since the Renaissance, the world has faced multiple influenza pandemics, punctuated by lulls lasting a few decades. “Influenza” has been defined by the sudden onset of respiratory signs with fever and high contagiousness in the population. In the 19th century, several pandemics originating in the East were reported, including 1831–1833, 1847–1848 and, finally, from 1889 to 1894, the so-called “Russian flu”, which spread throughout Europe and then the world. This episode was well-documented in many countries in several official reports, medical sources, and numerous press articles that covered the pandemic on a daily basis.

The first cases were reported in May 1889 in the city of Bukhara in Turkestan; curiously, a few cases were also reported in the city of Athabasca in Western Canada and in Greenland. In mid-October 1889, influenza reached the Russian Empire. It was reported in Tomks in western Siberia, Ufa (100 km from the Ural Mountains), Kazan on the Volga River in western Russia (700 km east of Moscow), Jekaterynoslav on the Dnieper River in Ukraine, and Novgorod near St. Petersburg. Kiev was stricken, as was the entire region of Lake Baikal, and then Siberia up to the island of Sakhalin. The capital of the Empire was severely hit in November 1889, with 20,000 cases. The flu afflicted all levels of society, including Tsar Alexander III himself. By the beginning of December, one third of hospital beds were occupied by flu patients. Economic activity ground to a halt, factories were closed, as were barracks and schools; 25–50% of soldiers and children had fallen ill. The peak of the epidemic occurred on December 1, 1889 in St. Petersburg. The first wave lasted five weeks with a total of 180,000 victims in a city of one million inhabitants.

From St. Petersburg, the Baltic ports were contaminated, notably Stockholm and the rest of Sweden, where the flu infected 60% of the population for eight weeks, and then Copenhagen and Oslo. The German Empire was affected in December, particularly in Poznań, Warsaw and Lodz. The epidemic resulted in 150,000 cases in Berlin for a population of 1.5 million.

What to do? Almost everywhere the unprepared authorities recommended hygienic measures such as ventilation, disinfection of public places and patients’ rooms, prohibition of public gatherings, isolation at home… Needless to say, there was no effective treatment at the time. Quinine was used to treat fever, but without success, as well as treatments such as strychnine, phenol inhalation, carbonic smoke ball that were dangerous… or fanciful (castor oil, electric current, brandy, oysters…). Commercial activity likewise collapsed, and schools, colleges, universities, public services, transportation and factories were shut down: a true disaster! Numerous eminent personalities – the President of the Republic, ministers, deputies – were stricken.

From mid-December 1889, the same scenario played out in the United Kingdom. In January 1890, there were 2258 deaths in London, including 1070 from pneumonia, far exceeding the seasonal average. The disease spread to other cities, including Edinburgh, Glasgow, Birmingham (50,000 cases) and Dublin.

The epidemic soon crossed the Atlantic, and the first cases in the United States were reported on 18 December 1889. The wave lasted five weeks, reaching a peak on 12 January 1890. The epidemic spread along the East Coast before reaching Chicago, Kansas City and San Francisco. Soon afterwards, from Mexico City to Buenos Aires, Latin America was likewise contaminated. In spring 1890, the pandemic spread widely in Africa and Asia. If Africans called it “the white man’s disease”, it was because they had apparently never previously known influenza.

Compared to the previous pandemics of the 19th century, the rapid spread of influenza was surprising. How can it be explained? In 1890, at the outset of the Pastorian era, the proponents of contagion still clashed with those of the miasma theory, which explained the rapid spread by air. In reality, the first wave did not progress steadily from east to west. It first hit successively the major European cities and capitals, which were closely connected by railroads, before disseminating to regions; this explains its predominantly urban impact. The pandemic also moved upstream, along the rivers; in addition, numerous grouped family cases were reported, indicating that influenza spreads directly through human-to-human contact. There is little doubt that influenza was borne by the European railroads, which were constantly expanding, with 202,887 km of track, and by the ever more rapid steamboats plying the waterways and seas. From May 1889 onwards, influenza was transported from Central Asia to the Russian Empire by the Transcaspian line to Samarkand in August, and then to Tomsk, 3200 km away, in October. The spread towards the East was slower because the Trans-Siberian Railway did not yet exist. St. Petersburg was afflicted in November 1889 via the Volga River trade routes.

Which agent was responsible for the pandemic? Needless to say, during the Pastorian revolution search for the germ of Russian flu became a priority, but the search began with a 50-year mistake. In the 1890s, viruses were still unknown. In November 1891, the German Richard Pfeiffer isolated a previously undescribed bacillus, which grew only on blood agar, from patients’ nasopharyngeal samples. Terming it Bacillus influenzae (now Haemophilus influenzae), on January 4, 1892 he announced that he had discovered the agent responsible for influenza. Unfortunately, he was unable to reproduce the disease experimentally in animals and did not fullfill the Koch’s postulates, which might have established a causal link. He hypothesized that the agent was a very specific human pathogen, comparable to those of leprosy or cholera. As the bacillus was repeatedly isolated during cases of flu, Pfeiffer’s observations seemed to be corroborated. In the years following the discovery, however, the bacillus was also found independently of any epidemic in otitis, mastoiditis, meningitis and pneumopathy. This is in contradiction with the existence of a specific germ at the origin of influenza. During the Spanish flu of 1918, this bacterium was once again incriminated, and many unsuccessful attempts were made to vaccinate against H. influenzae. At present, we know that it is a superinfection germ often present in nasopharyngeal samples.

While the Covid-19 pandemic resembles the other influenza pandemics, the SARS-CoV-2 coronavirus was identified by sequencing a few weeks after its onset. There are seven coronaviruses pathogenic to humans: three are highly pathogenic and epidemic: SARS-CoV-1 (9% mortality), MERS-CoV (30% mortality) and the current pandemic virus, SARS-CoV-2 (0.6%−2% mortality); four are the cause of 15–30% of common colds and have been circulating in populations for decades: HCoV-229E, HCoV-NL63, HCoV-OC43 and HCoV-HKU1. These benign viruses are of animal origin (bats or rodents) and evolve in small seasonal epidemics every three to four years during the autumn and the winter, conferring short-term immunity.

In 2005, Belgian researchers sequenced the entire genome of a laboratory strain of HCoV-OC43 (which had undergone multiple passages in culture), demonstrating its phylogenetic proximity to another beta-coronavirus of bovine origin, BCoV, which originated from rodents and yields acute diarrhea in calves. The nucleotide sequence of HCoV-OC43 is almost identical to BCov, from which it was derived in about 1890. These investigators confirmed their discovery by comparing different sequences of wild-type HCoV-OC43 strains isolated from patients with acute rhinitis. They also found these viruses to be close to PHEV, a coronavirus causing porcine hemagglutinating encephalomyelitis. In light of the Covid-19 pandemic, these phylogenic observations raise the question of the role of a coronavirus in Russian influenza and make HCoV-OC43 an unexpectedly plausible candidate.

The emergence of the SARS-CoV-2 pandemic prompts a revisiting of the cause of past influenza pandemics. It should be remembered that there exist many wild reservoirs of coronaviruses, including bats, rodents, and birds, in whom the viruses are not (or only weakly) pathogenic. As many as 5000 types of coronaviruses have been identified, including 500 in bats, which may be the cause of many animal infections and epizootics. Could the loss of virulence be due to the natural evolution of pandemic viruses, an avatar of Darwinian selection of variants well-adapted to the species and persisting in the form of benign diseases or asymptomatic carriage, as in wild reservoirs? Chiropterans that appeared 50 million years ago, most of them asymptomatic carriers of many viruses, may have survived iterative lethal epidemics since the dawn of time. A balance was conceivably found between host-adapted viruses and hosts that developed specific and original defense systems conferring “natural” resistance to viruses.

Clinical, epidemiological and phylogenetic clues point to a coronavirus that caused the Russian influenza pandemic, as occurred in Covid-19, with its flu-like symptoms. Could there exist a historical precedent of a pandemic due to a coronavirus ? Could the benign coronaviruses encountered in human populations be the relics of ancient epidemics yielding mild viruses that are perpetuated in the human species? This alternative hypothesis deserves further investigation.

Source: Science Direct

The relationship between GDP and life expectancy isn’t as simple as you might think
The relationship between GDP and life expectancy isn't as simple as you might think
January 30, 2022 - 6:23 am

By: Jeff Guo

Everyone wants economic growth, right? It’s part of every politician’s package of promises. Expanding economies make people richer, and study after study shows that the wealthier lead happier, healthier lives.

Yet in recent years, accumulating evidence suggests that rising incomes and personal well-being are linked in the opposite way. It seems that economic growth actually kills people.

Christopher Ruhm, an economics professor at the University of Virginia, was one of the first to notice this paradox. In a 2000 paper, he showed that when the American economy is on an upswing, people suffer more medical problems and die faster; when the economy falters, people tend to live longer.

“It’s very puzzling,” says Adriana Lleras-Muney, an economics professor at the University of California, Los Angeles. “We know that people in rich countries live longer than people in poor countries. There’s a strong relationship between GDP and life expectancy, suggesting that more money is better. And yet, when the economy is doing well, when it’s growing faster than average, we find that more people are dying.”

In other words, there are great benefits to being wealthy. But the process of becoming wealthy — well, that seems to be dangerous.

Lleras-Muney and her colleagues, David Cutler of Harvard and Wei Huang of the National Bureau of Economic Research, believe they can explain why. They have conducted one of the most comprehensive investigations yet of this phenomenon, analyzing over 200 years of data from 32 countries. In a draft of their research, released last week, they lay out something of a grand unified theory of life, death and economic growth.

To start, the economists confirm that when a country’s economic output — its GDP — is higher than expected, mortality rates are also higher than expected.

The relationship is clear, but the size of the effect is modest. In a year when the GDP is about 5 percent above trend — which is a respectable boom (think dot-com, not post-WWII) — adults are about 1 percent more likely to die.

Rising fortunes haven’t always been linked to increasing mortality. Data from less-developed nations showthat in places where farming is still the main economic activity, growth is associated with better, not worse health. The same is true when you look backward in history, before many countries fully industrialized. For instance, economists José Granados and Edward Ionides have shown that in the Sweden of the 1800s, economic growth was associated with longer lives — but in the 1900s, the relationship reversed, and growth became associated with death.

The turning point, Lleras-Muney and her colleagues say, comes when the wealth of societies increasingly starts to depend on factory output. They believe that pollution is a major culprit in increased mortality rates. To show this, they used data on carbon dioxide emissions, which are correlated with industrial activity and air pollution.

There’s a common misperception, Lleras-Muney says, that pollution is a problem of the past in advanced industrialized countries such as the United States. But around the world, these relationships largely hold today.

The data show that when economies are growing particularly fast, emissions and pollution are also on the rise. After controlling for changes in air quality, the economists find that economic growth doesn’t seem to impact death rates as much. “As much as two-thirds of the adverse effect of booms may be the result of increased pollution,” they write.

This helps to explain why children seem to be particularly harmed by economic expansions — or benefit from recessions. The first years of life are precarious. Studies have shown that the very young are highly sensitive to pollution. Economists Kenneth Chay and Michael Greenstone estimate that the 1981-1982 oil shock recession may have saved as many as 2,500 infant lives in the United States, just through the slight reductions in air pollution caused by the reduced economic activity.

A booming economy spurs death in other ways too. People start to spend more time at their jobs, exposing them to occupational hazards, as well as the stress of overwork. People drive more, leading to an increase in traffic-related fatalities. People also drink more, causing health problems and accidents. In particular, the economists’ data suggest that alcohol-related mortality is the second-most important explanation, after pollution, for the connection between economic growth and death rates.

This is consistent with other studies finding that people are more likely to die right after they receive their tax rebates. More income makes it easier for people to pay for health care and other basic necessities, but it also makes it easier for people to engage in risky activities and hurt themselves.

Does all this evidence mean that we should celebrate recessions and fear economic expansions? Well, no.

Cutler, Huang and Lleras-Muney find that particularly large recessions (think the Great Depression) are still bad for people’s health, and particularly large booms (think the 1950s in America) lead to longer lives. It’s best to think about economic growth as a double-edged sword. On one hand, it leads to more pollution and risky behavior; on the other hand, the additional income allows people to invest in education and health, which yields tremendous payouts, just not always right away.

In the short term, or when the economic fluctuations are small, the harmful effects of growth dominate. But in the long term, or when the economic fluctuations are big, those harms are counterbalanced by the positive effects of having more income.

“If the pollution doesn’t kill you in the short run, then in the long run the increased income will help you live longer,” Lleras-Muney says.

The lesson here is not to be wary of growth, but to manage the downsides. The economists find that countries with better social safety nets are particularly good at buffering their residents from the health consequences of booms and recessions. It may also be that these kinds of countries are stricter about managing pollution levels.

All of this research should have us thinking about inequality. If growth is not wholly good, we should pay attention to who secures its blessings and who suffers the health consequences. In the United States, the financial rewards of economic expansion have mostly accrued to those at the very top, while average Americans have faced decades of stagnant wages. The question is: Have the health consequences accrued to the bottom?

Source: World Economic Forum

https://www.weforum.org/agenda/2016/10/the-relationship-between-gdp-and-life-expectancy-isnt-as-simple-as-you-might-think

What we can learn from the 1918 Flu Pandemic as the Omicron variant spreads
What we can learn from the 1918 Flu Pandemic as the Omicron variant spreads
December 31, 2021 - 9:33 am

By: Julia Ries

Historically, most pandemics last between 2 and a half to 3 and a half years.

Over time, pandemic viruses typically mutate and evolve into an endemic disease that circulates at lower, more manageable levels.

This was the case with the influenza strain behind the 1918 flu pandemic and some virologists hope this may be happening with SARS-CoV-2, the virus that causes COVID-19.

Early reports suggest that the Omicron variant may cause milder infections, potentially due to its unique collection of mutations along with the buildup of immunity across the globe.

Still, it’s too early to know for certain how the COVID-19 pandemic will play out.

While experts generally believe viruses often mutate to become less dangerous, it’s not a 100 percent guarantee this is currently happening with the coronavirus.

Furthermore, 2021 is nothing like 1918, and the vaccines, global travel, data, and therapeutics we now have access to will significantly influence the trajectory of this pandemic.

“Since COVID-19 infections have a high number of asymptomatic transmitters, we may not fully understand how societal and environmental pressures — masks, distancing, remote working, etc. — on the virus will allow it to evolve,” said Rodney E. Rohde, PhD, a virologist and professor of clinical laboratory science at Texas State University.

What happened to the 1918 flu strain?

Within a few years, the influenza strain behind the 1918 pandemic became less life threatening.

Dr. Keith Armitage, a professor of medicine in the division of infectious diseases at Case Western Reserve University, says this is likely due to a combination of herd immunity and the virus mutating to produce a less severe illness.

The 1918 influenza strain never disappeared, rather it continued to mutate and a version of it continues to circulate to this day.

“If you think about the way viruses behave, biologically, their reason for living is to replicate and spread, and there’s really no advantage for the virus to kill the host,” said Armitage.

What a virus wants to do is infect a host and be contagious so it can infect another host and it can continue to spread.

As part of this process, respiratory viruses often mutate and become less virulent and therefore less of a serious health issue.

“The 1918 influenza virus eventually mutated to the point of not having a high number of deaths — again, eventually over 3 years or so. We may very By: Julia Ries

well be witnessing this process with ongoing variants of SARS-CoV-2,” said Rohde, noting that there is too much uncertainty to know if this is definitely the case.

Will this pandemic end similarly?

We have significantly more data about the COVID-19 pandemic than we do about the 1918 influenza pandemic.

We also have more tools to combat the coronavirus than people did back in 1918 including data about who is most at risk from COVID-19 along with vaccines and therapeutics.

But that data is ongoing and rapidly changing, said Rohde.

With new variants come new questions about where the pandemic is headed, and whether or not we will need annual boosters or modified vaccines.

“The hope is, that if the pandemic doesn’t go away, we will get new variants that are highly contagious but don’t produce much of a clinical illness,” said Armitage.

And between those mutations, less virulent strains, natural immunity, and vaccine-induced immunity, we’ll eventually get out of this.

Whether that is with Omicron or new variants we have yet to meet remains unclear.

“We’d all like it to be sooner rather than later, of course,” Armitage said.

Historically, most pandemics end within 2 to 3 years as the virus mutates into a less virulent pathogen and the population builds up immunity. This is what happened to the influenza strain behind the 1918 flu pandemic, and what many virologists hope will happen with the coronavirus — whether that happens with Omicron, a variant that appears to cause milder infections, or another future variant is unknown.

Source: Healthline

https://www.healthline.com/health-news/what-we-can-learn-from-the-1918-flu-pandemic-as-the-omicron-variant-spreads

What pandemic Christmas of 1918 looked like
What pandemic Christmas of 1918 looked like
November 25, 2021 - 2:28 pm

By: Livia Gershon

On December 21, 1918, the Ohio State Journal published a warning about the lingering flu pandemic from the state’s acting health commissioner: “Beware the mistletoe.” Not only should readers resist the temptation of a holiday kiss, but they shouldn’t even be at a social gathering where it might come up.

“You will show your love for dad and mother, brother, sister and the rest of ‘em best this year by sticking to your own home instead of paying annual Christmas visits, holding family reunions, and parties generally,” the commissioner said.

Christmas 1918 was not Christmas 2020. The pandemic had already peaked in the U.S. in the fall of 1918 as part of the disease’s second wave. Meanwhile, this week the deaths attributed to Covid-19 in the U.S. are the highest they’ve ever been, showing no signs of waning as the holiday approaches. But the flu also killed far more people (675,000) than Covid-19 has to date, in a country that was much smaller, population-wise, at the time. And it wasn’t over by any means. In some cities, a third wave was already starting as Christmas approached, says Kenneth C. Davis, author of More Deadly than War, a history of the pandemic and World War I aimed at young readers.

“There was an uptick, and it was a serious uptick in some,” he says.

A century ago, the federal government held much less authority and power than it does today; the CDC, for instance, wouldn’t get its start until 1946. Decisions about how seriously to take the disease fell to states and, especially, municipalities.

Davis says San Francisco took it quite seriously, implementing a strong mask mandate in the fall as well as measures that’d be described today as social distancing. After cases rose sharply in mid-October, the city locked down harshly; the measures worked to keep the flu at bay and, a month later, the city reopened and dropped the mask mandate. But the flu was not done with the city yet. Come Christmastime, Davis says, the cases were again on the rise, and residents, having finally escaped from the pandemic shutdown, were not eager to go back.

“San Francisco wanted to institute the mask rule again but people resisted,” he says.

Davis said some anti-maskers of the day felt their rights were infringed on. Some Christian Scientists cited religious objections. And other people simply found masks too much trouble. It didn’t help that masks at the time were generally homemade, using several layers of cheesecloth and were supposed to be boiled for ten minutes every day to keep them clean.

While it’s hard to tease out whether Christmas gatherings or shopping contributed, influenza case numbers did indeed rise again in San Francisco in early January.

Lendol Calder, a historian at Augustana College in Illinois and author of Financing the American Dream: A Cultural History of Consumer Credit, says it wasn’t just the debate over masks that seems familiar today. In some places, residents complained that officials shut down churches but left saloons open. The closing of churches was a major issue in Milwaukee, a city that took the pandemic especially seriously—and that was also home to deeply observant German and Norwegian immigrant communities.

“To have churches closed during the Advent-Christmas season was huge,” Calder says. “That was people’s social media, to go to church.”

But, Calder adds, even Milwaukee allowed churches to hold services on Christmas Day.

Of course, Christmas is also a shopping season, and that was already true in 1918. The Macy’s Thanksgiving Day Parade wouldn’t start until 1924, and Black Friday mania was decades away, but retailers were beginning to realize that the holiday shopping season could make or break their year.

“They pushed hard in November and December with advertising to get people to come shop,” Calder says. He says retailers were concerned about potential supply chain issues and urged shoppers to come in early in case items ran out. They also made sure to let potential customers know that they could deliver goods to those who were afraid to go out in public.

Davis says store-owners’ desire for a strong Christmas season also figured in anti-mask sentiment.

“They don’t want people to wear masks in the stores because they thought it was frightening,” he says.

Despite the anti-maskers, Howard Markel, director of the Center for the History of Medicine at the University of Michigan Medical School, says the question of how to guard against the flu was not politicized in the way that anti-Covid measures are today.

“Most people did comply because they had greater faith in their public officials, and they had greater faith in the science of medicine, even though it was much more rudimentary than today,” he says.

Markel notes that epidemic disease was very familiar to the early 20th century public. Families, many of which had lost a child to diphtheria or watched a loved one suffer from polio, were generally willing to comply with some limitations on their activities. Most public health departments wore badges and had police powers, and this was generally uncontroversial.

“They could forcibly quarantine you or put you on a quarantine station on an island,” Markel says.

As municipalities determined what public activities should or shouldn’t be permitted, Calder says people were puzzling through their own choices about how to celebrate the holidays.

“When you’re reading people’s diaries, they are fatigued obviously but also measured,” he says. “You don’t find people freaking out about this. They mourn the loss of traditional ways of celebrating the holidays, and they want to see relatives and are wondering whether they can or not.”

Markel, who is also editor of the Influenza Encyclopedia, a digital archive of materials from the pandemic, says one advantage people of 1918 had in terms of making holiday plans is that family gatherings were generally not the treasured once- or twice-a-year events they are for many people now.

“Extended families often lived together or right near each other, next door or upstairs,” he says. “Getting together for a holiday meal was much less of an event than it is today, when many people don’t live in their hometown.”

At the same time, Americans longed to see each other during the holiday season of 1918 for a reasons beyond the Christmas spirit: Young men were returning from the battlefields of Europe and military bases following the official end of the First World War on November 11.

“Many people had the sense that they had just lived through one of the most historic years in history,” Calder says. “[The war was a] victory for democracy over authoritarianism. Just 11 months earlier, it hadn’t looked so good. It was just a huge shock and relief to see the Armistice signed.”

For the families of more than 100,000 men lost in the war, many dying from the flu, in the course of less than a year—and for those who had lost someone to the flu at home—it must have been a somber Christmas. But, for many others, the relief of the war’s end and the apparent decline of the pandemic encouraged many Americans to come together.

“The mood was absolutely euphoric for most of the country,” Davis says. “There’s a pent-up desire to get out—that existed back then as well. The mood of the country was, ‘We’ve come through something terrible. We have something to be thankful for.’”

To whatever extent that joy encouraged people to gather in public or hold Christmas parties at home, it certainly contributed to some of the infections and deaths in the third wave of the flu. In light of the current high rate of infections, that’s something worth taking seriously today. Much like Ohio’s health commissioner in 1918, Markel says we must go against the instincts that drive us to gather together in order to protect the people we love.

“It goes against everything we love to do to not celebrate the holiday season,” he says. “And we must nevertheless not do it. It makes me sad to say it.”

Source: Smithsonian Magazine

https://www.smithsonianmag.com/history/what-pandemic-christmas-1918-looked-180976541/

This Thanksgiving, collect and share your family health history!
This Thanksgiving, collect and share your family health history!
November 20, 2021 - 8:46 am

By: Dr. Muin J Khoury, Director, Office of Genomics and Precision Public Health, Centers for Disease Control and Prevention

Happy Thanksgiving Day! It is time for our yearly message on the importance of family health history to your own health. Year after year we promote the value on family health history around Thanksgiving day and all year round. By knowing and acting on your family history, you can reduce your disease risk and actually change family health history for future generations.

Every year we emphasize a slightly different version of this message. In 2018, we announced that the My Family Health Portrait Surgeon General tool was moved to the CDC Public Health Genomics and Precision Health Knowledge Base (PHGKB). In 2017, we highlighted the simple fact that even in the age of genomics and precision medicine, family health history remains as the ultimate low tech tool (and the first genetic test) allowing people to understand their predispositions to various diseases. In 2016, we highlighted the emergence of new tools that can help consumers and providers collect and analyze family history information. In 2015, we focused on the need to “think globally and act locally” when it comes to spreading the word about the value of family health history in health care and population health. In 2014, we challenged the prevailing notion that, as a non-modifiable risk factor, family history is not worthy of public health messaging.

Since 2004, The U.S. Surgeon General has designated Thanksgiving Day as National Family History Day, a day to help families learn and collect information about their family health history. Family history can identify people at high risk for many common diseases, such as heart disease, breast, colorectal, and other cancers, diabetes, osteoporosis, glaucoma, depression and suicide, and more. In many cases, having at least one first-degree relative (parent, sibling or child) for some diseases doubles the person’s risk for the same disease. The risk is even higher if there are several affected relatives in the family, and affected relatives develop the disease at an early age. Family history is also associated with a wide range of genetic diseases such as sickle cell disease, hereditary hemochromatosis, familial hypercholesterolemia, and more.

This Thanksgiving Day, please go to the My Family Health Portrait and discover—or rediscover—how you can collect, update and act on your family health information. It could prove life-changing to your own health! If you have any comments, questions, or concerns, please submit them below.

From our family to yours, we wish you all the best for Thanksgiving and the beginning of the holiday season.

Source: Centers for Disease Control and Prevention

Happy Thanksgiving 2019: Collect and Share Your Family Health History: It Could Save Your Life!

States have mandated vaccinations since long before COVID-19
States have mandated vaccinations since long before COVID-19
October 29, 2021 - 11:42 am

By: Drew DeSilver

Many Republican governors reacted furiously after President Joe Biden said he would require employees at large businesses to either get vaccinated against COVID-19 or submit to weekly testing. But Republican- and Democratic-led states alike already require hundreds of thousands of their citizens – infants, toddlers and schoolchildren, mostly – to be vaccinated against a panoply of diseases. In fact, mandatory childhood immunizations have been a feature of American society since the 19th century.

Currently, the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices recommends routine vaccination against 16 diseases from birth through age 18. The CDC recommendations, in turn, inform individual states’ vaccine mandates: Typically, children who haven’t received the required shots for their age can’t attend school (public, private or parochial) or enroll in child care programs, though there are exemptions for religious, medical or other reasons.

Under Biden’s plan, all companies with more than 100 workers will have to either require their employees be immunized or undergo weekly testing. Biden also acted to mandate shots for federal contractors and most federal workers, and expanded a previously announced vaccine mandate for nursing-home workers to cover virtually all health care workers.

Some states already mandate certain vaccinations for specific categories of adults. New York, for example, requires that all workers in hospitals, nursing homes and other health care facilities be immunized against measles and rubella. Rhode Island requires child care workers to not only be immunized against several common childhood diseases, but to get an annual flu shot, too. Several states have specific vaccination mandates for college students.

But in the main, most vaccine mandates apply to children and teens. We studied state laws, regulations and information from state health departments to assess how widely mandated the CDC’s vaccine recommendations are.

Of the 16 immunizations the CDC recommends for children and teens, all 50 states (plus the District of Columbia) mandate diphtheria, tetanus, pertussis (whooping cough), polio, measles, rubella and chickenpox. In addition, every state except Iowa mandates immunization against mumps. (The diphtheria, tetanus and pertussis vaccines usually are given as a single combined shot, as are the measles, mumps and rubella vaccines.) Except for the chickenpox vaccine, which became available in the United States in 1995, all those vaccines have been around for 50 years or more.

Among newer childhood vaccines, though, state mandates are something of a mixed bag. Only two states (Alabama and South Dakota) don’t require vaccination against hepatitis B at some point in a child’s life, but about half (24) don’t require it for hepatitis A. Just six states – five of them in the Northeast – require annual flu vaccines for child care or preschool enrollment, and none do so for K-12 students.

Three vaccines – against rotavirus, pneumococcal disease and Haemophilus influenzae type b, or Hib – typically are recommended for children younger than 5 years old. (Hib, despite what its name might imply, doesn’t cause the flu, but it can cause a range of other ailments, from mild ear infections to potentially deadly meningitis and blood infections.) However, while all but four states mandate the Hib vaccine for day care or pre-K, 10 don’t require the pneumococcal shot, and only eight require immunization against rotavirus.

The remaining two vaccines, against human papillomavirus (HPV) and meningococcal disease, are recommended for teens and older children around age 11 or 12. A majority of states (33, as well as D.C.) require the meningococcal vaccine, although Massachusetts is phasing in its requirement and Vermont only requires it for students living on campus. But only D.C., Hawaii, Rhode Island and Virginia require the HPV shot, which protects against cervical and other cancers but has been controversial because HPV is transmitted sexually.

Vaccination mandates in the U.S. date back to the 19th century, when many cities and states started requiring children to be immunized against smallpox; the Supreme Court upheld such mandates in a landmark 1905 decision. A combination vaccine against diphtheria, tetanus and pertussis became available in 1948, and it was quickly added as a routinely recommended shot.

In 1977, the World Health Organization’s Expanded Program on Immunization set a goal of giving every child in the world access to immunization against six diseases by 1990: dipththeria, pertussis, tetanus, polio, measles and tuberculosis, or TB. (Infants and small children are commonly vaccinated against TB in countries where the disease is prevalent. In the U.S., however, only children who are specifically at risk for contracting TB – or adults in high-exposure settings, such as health care workers – are offered the shot.)

Source: Pew Research Center

How the Flu Pandemic Changed Halloween in 1918
How the Flu Pandemic Changed Halloween in 1918
October 23, 2021 - 7:32 am

How the Flu Pandemic Changed Halloween in 1918

By: Becky Little

“Witches Must Beware,” declared the Baltimore American on October 31, 1918. The Maryland city’s health commissioner had placed a ban on public Halloween events, instructing the police chief to prevent people from holding “carnivals and other forms of public celebrations.” The United States was in the midst of the second, and most deadly, wave of the 1918 influenza pandemic. And that meant Americans had to curtail their usual Halloween revelry.

In the early 20th century, revelers did not knock on doors to trick-or-treat and Halloween was in general less of a child-centered holiday than it is today. Adults dressed up and held private parties or joined celebrations in the street. Meanwhile, young people—especially boys and young men—spent the night pulling pranks and vandalizing their neighbors’ property. This might mean stealing neighbors’ gates and building a bonfire with them, or stopping a train by laying a fake stuffed “body” on the tracks.

During the pandemic, cities banned or discouraged these traditions to reduce transmission of the virus, and also to be “respectful of those who might be sick or have lost loved ones,” says Katie Foss, a professor of media studies at Middle Tennessee State University and author of Constructing the Outbreak: Epidemics in Media and Collective Memory.

Cities that had already placed bans on large gatherings might issue separate statements reminding people not to break them on Halloween, says J. Alex Navarro, assistant director of the Center for the History of Medicine at the University of Michigan and one of the editors-in-chief of The American Influenza Epidemic of 1918-1919: A Digital Encyclopedia. Even if cities didn’t ban Halloween events outright, they might encourage people to tone it down.

Officials “admonished parents to tell their kids: We know you’re going to go out and do these pranks and these tricks and be loud and rowdy,” he says; “but keep in mind there are lots of people who are convalescing at home and trying to get their rest, and who aren’t going to be able to go out the next day and fix all the damage that these rowdy kids have caused.”

In Spokane, Washington, Navarro says police were supposed to take away Halloween masks if they saw people out wearing them. While wearing cloth flu-prevention masks was encouraged or mandated in some western U.S. cities, Navarro says officials probably saw Halloween masks as dangerous because revelers commonly passed these homemade masks around, taking turns wearing them.

In many cities, it appears most people heeded officials’ bans or warnings regarding Halloween. “Hallowe’en revels lack the spirit of previous affairs: Urchins make dismal effort to revive classic forays on ash cans and fences,” reported the Buffalo Express in a headline the day after Halloween in 1918.

Still, reports of revelry differed between and even within cities. On November 3, the St. Louis Globe Democrat reported that Halloween “passed by this year without the usual gay parties and merrymaking among the youngsters, by the edict of the health commissioner.” Yet a couple of days before, the St. Louis Post-Dispatch had described a completely different Halloween night in the Missouri city.

“Influenza bans seemingly did not blight Young America’s observance of Halloween in St. Louis,” the Post-Dispatch reported. “The police report the usual number of street lights extinguished and the usual number of bread boxes overturned.” More dangerously, someone had shot a woman in a car and sent another bullet through a woman’s bedroom window.

The day after Halloween, The Birmingham News ran a headline claiming “Halloween Ghosts Are Noisiest That Ever Pestered Birmingham.” The Alabama paper speculated residents had been itching to get out after “almost a month of confinement” due to the pandemic, and may have been motivated by the news that World War I was drawing to a close.

“This night was more gloriously observed and property was more thoroughly devastated than at any time since the Magic City has sported a charter,” the article reported.

That same day in Texas, the Dallas Evening Journal ran a headline claiming “Halloween Celebration In Dallas Unusually Rough and Boisterous.” That night, a two-year-old suffered burn injuries, an eight-year-old sprained his ankle, someone struck a 14-year-old in the head with a bottle, and there were multiple injuries from drivers hitting people with their cars. There was also theft: young people stole a horse, a car, a piano and multiple tires off people’s cars.

The flu pandemic continued after Halloween, stretching past Armistice Day on November 11 and into 1919. It remains the deadliest flu pandemic ever recorded, killing roughly 675,000 people in the United States and up to 50 million people worldwide. Some experts estimate that it infected a third of the world’s population, or about 500 million people.

Source: History

https://www.history.com/news/halloween-1918-flu-pandemic

The Mahatma, an anti-vaxxer?
The Mahatma, an anti-vaxxer?
August 20, 2021 - 8:23 am

“I am & have been for years a confirmed anti-vaccinationist. Anti-vaccination has no backing from the orthodox medical opinion. A medical man who expresses himself against vaccination loses caste. Tremendous pecuniary interests too have grown around vaccination.”

A Vaccination Debate in Sabarmati Ashram, Through Mahadevbhai Desai’s Diaries

By: Nandini Oza

The conversations surrounding COVID-19 vaccines these days – including whether to take a vaccine, how effective it is, the suspension of the vaccination programmes in some countries due to fear of side effects – reminds me of an incident at Mahatma Gandhi’s Sabarmati Ashram in Ahmedabad, as recorded by Mahadevbhai Desai in his diary.

Desai was a close aide of Gandhi’s and maintained extensive diaries of events. Some of these have been published in 23 volumes in Gujarati. Of these, diary number 13 covers the period from August 31, 1929, to January 26, 1931, and includes Gandhi’s thoughts on vaccination. I reproduce some translated excerpts from the diary here about smallpox and discussions around vaccines in the Sabarmati Ashram.

“Trial and Readiness”: To the North of the (Sabarmati) Ashram is a jail and to the south is a crematorium. From the terrace of the Ashram with the Ashram flag, one can see the walls of the jail and the funeral pyres burning in the crematorium. Although we see these two places daily, and yet, so that we do not forget how close we are to death… Shitala Mata (‘deity of smallpox’) has shown its frightful appearance.

“Although people do see a crematorium, those residing at the Ashram see it daily. We are aware that people suffer from troubles and lakhs die across the country. And yet, people are so short-sighted that so long as they do not encounter a personal experience (of death), they remain carefree. As if to eliminate that carefreeness, Shitala Mata arrived in the Ashram and in spite of having taken plentiful care, (she) took oblation/ sacrifice of three tender children. One among them did not even last to avail of any care at all. This incident put several people to several types of trials.

The residents of the Ashram recite the Gita daily; they hear and recite that death is a certainty for all who are born. To them, death appeared three times within a short span of three days and this was a trial of the Gita recitals by the parents of the three children. All the three parents passed the test fully and if the death God, Yamraj could certify, he would have done so too. There is no need to mention that there was no weeping and wailing. Those who had to reach the children to the crematorium did so and the rest continued with their duties. There was no change in the daily routine of the parents of these children.

A father told patiently to his child on death bed, “Child, recite Ramnama”. The child uttered Ramnama two-four times and gestured that he was unable to speak. Another father, at the time of the evening prayers when his child was breathing his last, handed him over to his mother. The mother happily allowed the father to go to the prayer meeting. And the child passed away just when the prayer lines of ‘steadfastness of intellect’, were recited. No sooner was the prayer over that the father was informed, but the father instead of rushing home, with calm mind made everyone follow Ram Dhun (prayer lines sung repeatedly). What other sight could be better than this?

As I write this, I am aware that I do not have the capacity to remain calm in this way. I cannot welcome death like this, and so, I bow my head to the parents of the three children.

This is about the trial of the Ashram residents who undertake Gita recitals. But the trial of Gandhiji who made them fond of Gita recitals was even greater. Gandhiji’s principle of not to take vaccination has been prevailing for many years now. He has written about it several times. He has cured many children with determination from smallpox. But when three children die one after another who can remain steadfast? It is fine if I say that Gandhiji is more fond of the children in the Ashram than their own parents are of them. But it may come into his mind: ‘Am I being cruel by not recommending vaccination for the Ashram children to keep them safe from smallpox?’

Thousands of people got vaccinated in Mumbai and Ahmedabad. It is not just the critiques but even friends are saying daily: ‘Why is Gandhiji taking such unnecessary risk?’ A well-wisher too made it clear: ‘I am aware that you are not disallowing anyone from being vaccinated. But now, I wish that you insist that everyone is vaccinated.’ This gentleman is much valued by Gandhiji, and had it not been an issue of principle, he would have implemented the advice of the gentlemen. But at such time as this? He (Gandhiji) shared the letter of the well-wisher with many. He read it out at the prayer meeting but along with it he shared his inner thoughts:

“To take vaccination is a dirty act, there is extreme harm in taking it. I consider taking it equivalent to eating beef. But at a time when my own children are dying one after the other and if I change my principle and announce that there is no harm in taking vaccination, what value remains in my truth? What is the meaning of my faith in God? Even if the whole Ashram is wiped out and so long as there is no evidence of substantive mistake, it is my religion to adhere to it. Who would like to lose their own children? Those parents who feel safe in getting their children vaccinated may go ahead. I will not object at all and will also make arrangements, but how can I change my belief? How is it possible for me to provide encouragement in taking of vaccination?’”

While the above record is from Mahadevbhai’s diary, Gandhi’s views regarding vaccination have been documented in his book A Guide to Health, translated by A. Rama Iyer and published in 1921 in English. Some excerpts from the chapter ‘Contagious Diseases: Small-pox’ follow:

… We cannot, of course, assert that small-pox is never transmitted by touch, for those that are physically in a condition favourable to its transmission will catch it. This is why, in a locality where small-pox has appeared, many people are found attacked by it at the same time. And hence the attempt to mislead the people into the belief that vaccination is an effective means of preventing it. The process of vaccination consists in injecting into the skin the liquid that is obtained by applying the discharge from the body of a small-pox patient to the udder of a cow…

Vaccination is a barbarous practice, and it is one of the most fatal of all the delusions current in our time, not to be found even among the so-called savage races of the world. Its supporters are not content with its adoption by those who have no objection to it, but seek to impose it with the aid of penal laws and rigorous punishments on all people alike.

The practice of vaccination is not very old, dating as it does only from 1798 AD. But during this comparatively short period that has elapsed, millions have fallen a prey to the delusion that those who get themselves vaccinated are safe from the attack of small-pox… Moreover, vaccination is a very dirty process, for the serum which is introduced into the human body includes not only that of the cow, but also of the actual small-pox patient. An average man would even vomit at the mere sight of this stuff… And yet we do not shrink from getting ourselves vaccinated!

As has been well said, cowards die a living death, and our craze for vaccination is solely due to the fear of death or disfigurement by small-pox. I cannot also help feeling that vaccination is a violation of the dictates of religion and morality. The drinking of the blood of even dead animals is looked upon with horror even by habitual meat-eaters. Yet, what is vaccination but the taking in of the poisoned blood of an innocent living animal? Better far were it for God-fearing men that they should a thousand times become the victims of small-pox and even die a terrible death than that they should be guilty of such an act of sacrilege…

As a student of Gandhian thought, I appreciate that Gandhi has expressed himself clearly on a wide range of issues, from gram swaraj to bramchariya, from varnashrama dharma to Ram Rajya, agriculture, health, women and so on. However, many of these thoughts have not been discussed or acknowledged sufficiently. Studying these thoughts and the discussions around them can only help us understand the social, cultural, political, economic context those thoughts were located in.

As far as smallpox is concerned, India had an epidemic in 1974. Although I was just a child back then, I recall vividly that I was vaccinated in a door-to-door vaccination drive. I do not remember if our parents/guardians could refuse a vaccination back then. Smallpox was eradicated from India in the late 1970s and the World Health Organisation declared the world free from smallpox in 1980.

About the COVID-19 pandemic – only time will tell how effective or otherwise the vaccination drive will be. But reading some records around the smallpox epidemic in India has made me confident that we shall overcome the COVID-19 pandemic too.

 

Source: Science, The Wire

Of Irrationality
Of Irrationality
July 23, 2021 - 8:39 am

Irrational beliefs differentially predict adherence to guidelines and pseudoscientific practices during the COVID-19 pandemic

By: Predrag Teovanović, Petar Lukić, Zorana Zupan, Aleksandra Lazić, Milica Ninković, Iris Žeželj

With the coronavirus pandemic, societies are forced to introduce new measures to curb the infection rate. This means that ordinary people are asked to adopt enhanced protective health behaviors, such as physical distancing and frequent handwashing. However, along with these official recommendations, people are exposed to pseudoscientific information and unverified content pertaining to COVID-19, which have proliferated rapidly through social media (Depoux et al., 2020; Kouzy et al., 2020; Mian & Khan, 2020; Zarocostas, 2020). In fact, we are “not just fighting an epidemic; we’re fighting an infodemic. Fake news spreads faster and more easily than this virus, and is just as dangerous” (WHO, 2020). Pseudoscientific recommendations such as consuming garlic, drinking ginger tea or rinsing nose with saline to prevent contracting the virus, became so pervasive that the WHO (n.d.) had to officially debunk the claims about their effectiveness. Certain pseudoscientific practices (PSPs) are extremely dangerous—for example, more than 700 Iranians were reported dead of methanol poisoning falsely believing it was a miracle cure for COVID-19 (Associated Press, 2020). Another “victim” of the infodemic is the COVID-19 vaccine, which is still in development. Even amid the pandemic, the topic of vaccination has provoked an online backlash (e.g., Mooney, 2020). Given the grave consequences of vaccination refusal, such as failure to reach herd immunity, it is important to understand why some people might be reluctant to get immunized.

Both adherence to official public health recommendations and the use of PSPs might be embedded in a set of irrational beliefs. We refer to irrational beliefs as an umbrella term that covers beliefs which lack a solid evidence base or defy principles of normative rationality (Žeželj & Lazarević, 2019). It encompasses beliefs that differ in content (e.g., paranormal beliefs, conspiracy beliefs or anti-science attitudes) and form, but what they have in common is that they may inhibit reasoning processes (Rizeq et al., 2020). Irrational beliefs have also been referred to as “epistemically-suspect” (Pennycook, Cheyne, et al., 2015; Pennycook, Fugelsang, & Koehler, 2015) or “contaminated mindware” (Rizeq et al., 2020; Stanovich et al., 2016).

In this study, we explored whether people who differ in their predisposition to form irrational beliefs also differ in their tendency to follow appropriate preventive measures for COVID-19. More precisely, whether irrational beliefs such as belief in COVID-19 conspiracy theories, overestimation of one’s own COVID-19 knowledge, susceptibility to type I error cognitive biases, and cognitive intuition predict adherence to COVID-19 guidelines, use of PSPs, and intention to receive a COVID-19 vaccine if it were available. In addition to cognitive intuition and cognitive biases that are more general, knowledge overestimation (i.e., a calibration error relating to the discrepancy between actual, objectively measured and subjective, self-estimated knowledge), and belief in conspiracy theories (potential source of false knowledge about a particular subject) are measures that are content-laden and refer to a specific context, event or a class of events. Content laden beliefs, in comparison to cognitive biases and cognitive intuition, may be more or less pertinent for different health behaviors in the current pandemic.

The COVID-19 pandemic is a public health crisis and, as such, a fertile ground for conspiracy theories (Gonçalves-Sá, 2020; van Prooijen & Douglas, 2017). This aspect of the infodemic might be especially dangerous since medical conspiracy theories have been consistently associated with a range of risky health behaviors including less sunscreen use, not getting annual check-ups or vaccinations, less contraceptive use, and HIV medication nonadherence (e.g., Bogart et al., 2010; Jolley & Douglas, 2014; Oliver & Wood, 2014; Setbon & Raude, 2010; Thorburn & Bogart, 2005). However, recent studies examining the relation between belief in COVID-19 conspiracy theories and self-reported adherence to recommended behaviors have produced inconsistent results. While some found a relation with adherence to health guidelines (Imhoff & Lamberty, 2020; see also Swami & Barron, 2020), others did not (Čavojová et al., 2020; see also Plohl & Musil, 2020). Furthermore, conspiracy theories might be predictive of some, but not other types of recommended protective behaviors—for example, believing in COVID-19 conspiracy theories was related to less social-distancing but unrelated to personal-hygiene behaviors (Pummerer & Sassenberg, 2020). As for pseudoscientific practices, it was shown that people more prone to conspiratorial thinking were more likely to endorse claims related to the effectiveness of complementary and alternative medical treatments in general (Lamberty & Imhoff, 2018; Lobato et al., 2014; Pennycook, Cheyne, et al., 2015) and that they reported greater use of PSPs to prevent contracting coronavirus (Čavojová et al., 2020; Pummerer & Sassenberg, 2020; see also Imhoff & Lamberty, 2020). A possible mechanism through which conspiracy theories may influence health behaviors is by amplifying distrust toward institutions, which makes people less willing to follow official COVID-19 recommendations (Pavela Banai et al., 2020). In order to stay healthy, some people may then turn to PSPs, which are not recommended by authorities due to absence of evidence for their effectiveness. Thus, although there is converging evidence suggesting that conspiracy theories are predictive of PSPs, more studies are needed to explore their influence on adherence to COVID-19 guidelines. We expected that stronger beliefs in COVID-19 conspiracy theories would predict lesser adherence to COVID-19 guidelines (H1a), greater use of PSPs (H1b), and a weaker intention to get vaccinated (H1c).

Knowledge overestimation is typically calculated as a difference between self-assessed and objectively assessed knowledge on a certain subject (Ackerman et al., 2002; Harvey, 1997; Kleitman & Stankov, 2001; Kruger & Dunning, 1999; Stankov, 2000). Pennycook et al. (2017) showed that intuitive individuals tended to be more overconfident on the cognitive reflection test, rating themselves as relatively reflective, despite their test scores showing otherwise. Thus, it is possible that some people would overestimate their COVID-19 related knowledge because their nonreflexivity prevents them from recognizing their ignorance (see also Dunning, 2011; Kruger & Dunning, 1999), which would in turn make them less likely to engage in preventive behaviors during the pandemic. In fact, knowledge overestimation has been widely documented in the health domain (see Dunning et al., 2004). The inability to recognize one’s lack of skill or knowledge (Kruger & Dunning, 1999) can, in this context, prevent people from familiarizing themselves enough with the official guidelines. In this study, we expected that higher levels of COVID-19 related knowledge overestimation would predict lesser adherence to COVID-19 guidelines (H2a), greater use of PSPs (H2b), and weaker intention to get vaccinated (H2c).

Cognitive biases, as systematic departures from what is normatively defined rational behavior, can be viewed as a relatively broad category of irrational beliefs. Taking into account that the cognitive biases space is considerably heterogeneous (see, for example, Kahneman & Frederick, 2005; Pohl, 2004; Stanovich, 2009; Teovanović et al., 2015), we focused on a subset which concerns a general tendency to make a type I error. Such a choice was motivated by Haselton and Buss’ (2000) notion on cost asymmetry between two types of errors (type I and type II) that can occur when judgments are made under uncertainty. More precisely, as the probability of making either type of error cannot be simultaneously minimized, people tend to decrease the likelihood of making the costlier one (Haselton et al., 2009). Since the consequences of type II errors (i.e., false-negatives) refer to failures to notice actual relations between phenomena, they are usually considered as costlier. Thus, people are typically biased toward type I errors (i.e., false-positives) which refers to making incorrect conclusions about the existence of relations between unrelated phenomena. In our study, biases that are based on making a type I error were represented by the illusory correlation detection (Smedslund, 1963), base-rate neglect (Tversky & Kahneman, 1974), gambler’s fallacy (Tversky & Kahneman, 1974), and hot-hand fallacy (Gilovich et al., 1985) bias. Although cognitive biases have shown to be predictive of some paranormal (Bressan, 2002; Pennycook et al., 2012; Šrol, 2020; van Prooijen et al., 2017) and pseudoscientific beliefs (Pennycook, Cheyne, et al., 2015; Redelmeier & Tversky, 1996; Šrol, 2020), they remain underexplored in the domain of both PSPs and adherence to public health guidelines. Starting from the general hypothesis about relation between irrational beliefs and health behaviors, we expected that a higher susceptibility to such cognitive biases would predict lesser adherence to COVID-19 guidelines (H3a), greater use of PSPs (H3b), and weaker intention to get vaccinated (H3c).

Cognitive intuition is often assessed with the cognitive reflection test (CRT; Frederick, 2005), which consists of three items that lead most people to answer quickly and incorrectly. While cognitive biases are related to specific types of predictable errors on heuristics-and-biases tasks, cognitive intuition refers to an inability to “resist reporting the response that first comes to mind” (Frederick, 2005, p. 27). Previous research has shown that misleading intuitions predict paranormal beliefs (Pennycook et al., 2012; Ståhl & van Prooijen, 2018) as well as religious beliefs (Pennycook, Fugelsang, & Koehler, 2015; Shenhav et al., 2012). In the health domain, cognitive intuition was related to beliefs about the effectiveness and self-reported use of complementary and alternative treatments both before (Browne et al., 2015; McPhetres & Pennycook, 2019; see also Lindeman, 2011) and during the COVID-19 pandemic (Čavojová et al., 2020; Erceg et al., 2020; Pennycook et al., 2020). However, recent findings on the relation between CRT performance and adherence to official COVID-19 guidelines are mixed – while some found a negative relation (Stanley et al., 2020), others failed to establish any link (Čavojová et al., 2020; Erceg et al., 2020; Pennycook et al., 2020; cf. Stanley et al., 2020). We expected that higher cognitive intuition would predict lesser adherence to COVID-19 guidelines (H4a), greater use of PSPs (H4b), and weaker intention to get vaccinated against COVID-19 (H4c).

In sum, the present study builds upon emerging research on evidence and nonevidence based COVID-19 related recommendations by examining the predictiveness of different irrational beliefs for COVID-19 related health behaviors in a single design.

Source: Applied Cognitive Psychology

July Effect? Maybe not
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July 2, 2021 - 8:56 am

July Effect? Maybe not

By: Emily Hughes

In the UK they call it The Killing Season; in North America it’s called The July Effect.

It’s the time of year when newly minted physicians traditionally begin their residency training, other medical trainees advance to the next year of training, and senior residents graduate to begin their professional careers. Interest in the potential effect on patient care during this large changeover has produced a body of research. Media has been quick to pick up on some of that research indicating a possible adverse effect.

Is The July Effect something to be concerned about?

“I think it is a topic that is complex and over sensationalized,” says Dr. Salvatore Spadafora, who oversees all residency programs, fellowships and continuing professional education at the University of Toronto. “Whenever you’ve got a complex topic or problem you usually never have a simple answer … it’s probably better to take a breath, step back, and say, ‘Ok, what are the actual facts? What are the variables in the complexity?’”

The most rigorous publication on the topic to date is a systematic review published in 2011 in the Annals of Internal Medicine which found that increased mortality is associated with year-end physician changeovers. However, this finding came with the limitation that, “heterogeneity in the existing literature does not permit firm conclusions about the degree of risk posed, how changeover affects morbidity and rates of medical errors, or whether particular models are more or less problematic.”

A 2016 analysis in the Journal of Patient Safety pooled data collected between 2011 and 2015 from nearly 120 academic medical centres and more than 333 affiliated hospitals from all geographic regions in the United States. It concluded that there was no evidence to support a July effect on survival outcomes at US academic medical centres. Studies focused on specific specialties and patient populations have indicated mixed results.

Despite this lack of strong supporting evidence, a national survey of US academic leaders in internal medicine, published in 2016 in The American Journal of Medicine, revealed that most internal medicine residency program leaders believe in the potential for a July effect.

Source: Canadian Medical Association Journal (CMAJ)

Sushruta
RobertThom
June 19, 2021 - 12:28 pm

Sushruta: The father of surgery

By: Vibha Singh

The definition of an ideal surgeon according to the great surgeon Sushrutaa is “A person who possesses courage and presence of mind, a hand free from perspiration, tremor less grip of sharp and good instruments and who carries his operations to the success and advantage of his patient who has entrusted his life to the surgeon. The surgeon should respect this absolute surrender and treat his patient as his own son.”

Surgery forms a major role in general medical training. The ancient surgical science was known as Shalya Tantra. Shalya means broken arrow or a sharp part of a weapon and Tantra means maneuver. Shalya Tantra embraces all processes, aiming at the removal of factors responsible for producing pain or misery to the body or mind. Since warfare was common then, the injuries sustained led to the development of surgery as refined scientific skill.

All the four Vedas are in the form of Shlokas (hymns), verses, incantations, and rites in Sanskrit language. This treatise contains detailed descriptions of teachings and practice of the great ancient surgeon Sushruta and has considerable surgical knowledge of relevance even today.

The Rigveda – the earliest account of ancient Indian civilization – mentions that Ashwini Kumaras known as Dev Vaidya were the chief surgeons of Vedic periods, who had performed rare legendary surgical operations which included the first plastic surgery to re-join the head and trunk of saint Chyavana when Dakshya cut his head. Their other classic work included an eye operation of Reejashva, the implantation of teeth of Phushna in the toothless mouth, and the transplant of head of elephant on Ganesh whose head was cut by Lord Shiva. They transplanted an iron leg on Bispala – the wife of King Khela who lost her leg in war. Ashwini Kumaras had performed both homo- and hetro-transplantation during the very the ancient time of Rigveda which is estimated about 5000 years ago; such miraculous magical surgical skill of the Rigvedic period may seem mere legends or mystery to modern medical sciences. The surgical skill has traversed through the ages ranging from the Ashwini Kumaras, Chavana, Dhanvantari through Atereya Agnivesh and Shushruta. Craniotomy and brain surgery were also practiced in a more sophisticated way.

They do reflect some special surgical skills which laid down the foundation of Ayurveda – the fifth Indian Veda, the classical medical system of India. However, the realistic and systematic earliest compendium of medical science of India was compiled by Charak in Charak Samhita. It describes the work of ancient medical practitioners such as Acharya Atreya and Acharya Agnivesh of 800 BC and contains the Principle of Ayurveda. It remained the standard textbook of Ayurveda for almost for 2000 years. They were followed by Sushruta, a specialist in cosmetic, plastic, and dental surgery (Sandhan Karma around 600BC).

There are many Granthas and Samhitas dealing with Ayurveda; among them, Charak Samhita, Sushrutaa Samhita, and Ashtanga Sangraha are the three main pillars of Ayurveda. Charak Samhita and Ashtanga Samhita mainly deal with medicine knowledge while Sushrutaa Samhita deals mainly with surgical knowledge. Complicated surgeries such as cesarean, cataract, artificial limb, fractures, urinary stones plastic surgery, and procedures including per- and post-operative treatment along with complications written in Sushrutaa Samhita, which is considered to be a part of Atharva Veda, are surprisingly applicable even in the present time.[1]

Sushruta is an adjective which means renowned. Sushruta is reverentially held in Hindu tradition to be a descendent of Dhanvantari, the mythological god of medicine or as one who received the knowledge from a discourse from Dhanvantari in Varanasi.[2] Sushruta lived 2000 years ago in the ancient city of Kashi, now known as Varanasi or Banaras in the northern part of India. Varanasi, on the bank of Ganga, is one of the holiest places in India and is also the home of Buddhism. Ayurveda is one of the oldest medical disciplines. The Sushrutaa Samhita is among the most important ancient medical treatises and is one of the fundamental texts of the medical tradition in India along with the Charak Samhita.

Sushruta is the father of surgery. If the history of science is traced back to its origin, it probably starts from an unmarked era of ancient time. Although the science of medicine and surgery has advanced by leaps and bounds today, many techniques practiced today have still been derived from the practices of the ancient Indian scholars.

Sushruta has described surgery under eight heads: Chedya (excision), Lekhya (scarification), Vedhya (puncturing), Esya (exploration), Ahrya (extraction), Vsraya (evacuation), and Sivya (suturing).

All the basic principles of surgery such as planning precision, hemostasis, and perfection find important places in Sushruta’s writings on the subject. He has described various reconstructive procedures for different types of defects.

His works are compiled as Sushrutaa Samhita. He describes 60 types of upkarma for treatment of wound, 120 surgical instruments and 300 surgical procedures, and classification of human surgeries in eight categories.

To Sushruta, health was not only a state of physical well-being but also mental, brought about and preserved by the maintenance of balanced humors, good nutrition, proper elimination of wastes, and a pleasant contented state of body and mind.

For successful surgery, Sushruta induced anesthesia using intoxicants such as wine and henbane (Cannabis indica).

He treated numerous cases of Nasa Sandhan (rhinoplasty), Oshtha Sandhan (lobuloplasty), Karna Sandhan (otoplasty). Even today, rhinoplasty described by Shushruta in 600 BC is referred to as the Indian flap and he is known as the originator of plastic surgery.

He described six varieties of accidental injuries encompassing all parts of the body. They are described below:

Chinna – Complete severance of a part or whole of a limb

Bhinna – Deep injury to some hollow region by a long piercing object

Viddha Prana – Puncturing a structure without a hollow

Kshata – Uneven injuries with signs of both Chinna and Bhinna, i.e., laceration

Pichchita – Crushed injury due to a fall or blow

Ghrsta – Superficial abrasion of the skin.

Besides trauma involving general surgery, Sushruta gives an in-depth account and a description of the treatment of 12 varieties of fracture and six types of dislocation. This continues to spellbind orthopedic surgeons even today. He mentions the principles of traction, manipulation, apposition, stabilization, and postoperative physiotherapy.

He also prescribed measures to induce growth of lost hair and removal of unwanted hair. He implored surgeons to achieve perfect healing which is characterized by the absence of any elevation, induration, swelling mass, and the return of normal coloring.

Plastic surgery and dental surgery were practiced in India even in ancient times. Students were properly trained on models. New students were expected to study for at least 6 years before starting their training. Before beginning the training, the students were required to take a solemn oath. He taught his surgical skills to his students on various experimental models. Incision on vegetables such as watermelon and cucumber, probing on worm-eaten woods, preceding present-day workshop by more than 2000 years are some instances of his experimental teachings. He was one of the first people in human history to suggest that a student of surgery should learn about human body and its organ by dissecting a dead body.

Sushrutaa Samhita remained preserved for many centuries exclusively in the Sanskrit language. In the eight century AD, Sushrutaa Samhita was translated into Arabic as “Kitab Shah Shun al –Hindi” and “Kitab – I – Susurud.” The first European translation of Sushrutaa Samhita was published by Hessler in Latin and in German by Muller in the early 19th century; the complete English literature was done by Kaviraj Kunja Lal Bhishagratna in the three volumes in 1907 at Calcutta.

Sushruta was also known as a medical authority in Tibetan literature.

Sushruta considered surgery the first and foremost branch of medicine and stated that surgery has the superior advantage of producing instantaneous effects by means of surgical instruments and appliances and hence is the highest in value of all the medical tantras. It is the eternal source of infinite piety, imports fame, and opens the gates of heaven to its votaries. It prolongs the duration of human existence on earth and helps human in successfully completing their missions and wearing a decent competence in life.

Source: National Journal of Maxillofacial Surgery

‘Roaring 20s’ after the pandemic?
‘Roaring 20s’ after the pandemic?
May 14, 2021 - 8:29 pm

Barclays CEO Jes Staley has compared the pent up demand currently in the global economy to the end of the 1918 flu pandemic and the subsequent “Roaring 20s.”

Speaking on a panel at the World Economic Forum’s virtual Davos Agenda event, Staley laid out the British lender’s expectations for a strong second half of 2021, providing the Covid-19 pandemic can be wrestled into submission by vaccines and containment measures.

The 1918 flu infected around 500 million people in four waves between February 1918 to April 1920, resulting in tens of millions of deaths. What followed was a decade characterized by economic and cultural prosperity in the U.S. and Europe.

“What that led to when it finally got arrested was the Roaring 20s, and there was just this explosion of demand coming out of that,” Staley said Tuesday.

“When we look at the balance sheet of a JPMorgan or a Barclays, there is just enormous stored up purchasing power. Consumers are decreasing their borrowing and increasing their deposits, and small corporates are doing the same thing.”

However, Staley did also note that both the impact of the pandemic and the stabilizing effects of fiscal and monetary policy, along with hopes of an imminent rebound, were distributed unequally across both the economy and society.

He added that the greatest risk “is not an economic one but a social one” due to people being “left behind,” nodding to widespread civil unrest in the U.S. over the past year.

Source: CNBC

Dr. Stanford Emerson Chaillé
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May 8, 2021 - 10:46 am

Known as the “Father of Hygiene and Health Education” in America, Dr. Chaillé gained fame as the head of the U.S. Havana Yellow Fever Commission of 1879, organized to study the disease following the dreadful 1878 plague in New Orleans. His bacterial studies of the blood of yellow fever victims provided the links necessary for final discovery of the Aedes aegypti mosquito as the cause of the disease.

He wrote Origin and Progress of Medical Jurisprudence 1776-1876, 40 J. Crim. L. & Criminology 397 (1950).

https://scholarlycommons.law.northwestern.edu/jclc/vol40/iss4/1

A national figurehead, Dr. Chaillé was spokesman for the establishment of community sewerage and drainage systems, street paving, pure water supplies and mosquito control. He was also instrumental in the establishment of the National Board of Health, forerunner of the U.S. Department of Health, Education and Welfare.

Dr. Anandi Gopal Joshi, the first Indian physician trained in the United States
Dr. Anandi Gopal Joshi, the first Indian physician trained in the United States
May 1, 2021 - 7:33 pm

Anandibai travelled to New York from Kolkata (Calcutta) by ship, chaperoned by two female English missionary acquaintances of the Thorborns. In New York, Theodicia Carpenter received her in June 1883.

Anandibai wrote to the Woman’s Medical College of Pennsylvania in Philadelphia, asking to be admitted to their medical program, which was the second women’s medical program in the world. Rachel Bodley, the dean of the college, enrolled her.

Anandibai began her medical training at age 19. In America, her health worsened because of the cold weather and unfamiliar diet. She contracted tuberculosis. Nevertheless, she graduated with an MD in March 1886; the topic of her thesis was “Obstetrics among the Aryan Hindoos.” The thesis utilized references from both Ayurvedic texts and American medical textbooks. On her graduation, Queen Victoria sent her a congratulatory message.

Source: Wikipedia

The Development of the Immunization Schedule
The Development of the Immunization Schedule
April 24, 2021 - 1:03 pm

The United States Department of Health and Human Services and the Centers for Disease Control and Prevention offer Child and Adolescent Immunization Schedules for children aged 0-6 years and 7-18 years, as well as a “catch-up schedule” for kids four months to 18 years old who may have missed recommended vaccinations. All of these schedules are approved by the Advisory Committee on Immunization Practices (ACIP), the American Academy of Pediatrics (AAP), and the American Academy of Family Physicians (AAFP).

Some vaccinations have been recommended in the United States since the 1940s, although the official annual schedule endorsed by ACIP, AAP, and AAFP did not appear until 1995. A combined vaccine for diphtheria, tetanus, and pertussis (whooping cough) was recommended in the 1940s; a combined vaccine for those three diseases is still recommended today. The smallpox vaccine, on the other hand, was on the schedule in the 1940s but is no longer recommended, as smallpox was declared eradicated in 1980 and eliminated from the United States much earlier.

The newly developed vaccine for polio was recommended in the 1950s. The specific vaccine used has changed since then, but polio vaccine remains on the current schedule. The combined measles, mumps, and rubella vaccine was added to the list of recommendations in the 1970s, after vaccines for all three diseases were developed in the 1960s.

The resulting recommended vaccination list included vaccines for seven diseases in the 1970s:

Tetanus
Diphtheria
Pertussis (whooping cough)
Polio
Measles
Mumps
Rubella
Protection for the remaining seven diseases on the schedule, however, required only three vaccinations:

Polio vaccination
Combined vaccination for Tetanus, Diphtheria, and Pertussis (DTP vaccine)
Combined vaccination for Measles, Mumps, and Rubella (MMR vaccine).
The list of recommended vaccines continued to be updated as vaccines were developed for more diseases. The Hib (Haemophilus influenzae type b) vaccine was added to the list in the late 1980s, while a vaccine for hepatitis B was added in the mid-1990s. In 1995, the ACIP, AAP, and AAFP began issuing annual updates to the schedule. The annual updates contained detailed information about the recommended vaccines, including specific age- and dosage-related information, as well as information about new vaccines as they were added to the schedule. Since then, a number of vaccines have been added, including those for chickenpox (varicella) and hepatitis A, while others have been removed or replaced. (The first rotavirus vaccine added to the schedule was removed because of an association between the vaccine and intussusception, a type of bowel obstruction. It was later replaced with a different rotavirus vaccine that has no association with the condition.)

As of early 2014, the U.S. immunization schedule for children ages 0-6 years includes recommendations for the following vaccinations:

Hepatitis B
Rotavirus
Diphtheria, Tetanus, and Pertussis (combined DTaP vaccine)
Hib (Haemophilus influenzae type b)
Pneumococcal
Polio (inactivated vaccine)
Influenza
Measles, Mumps, and Rubella (combined MMR vaccine)
Varicella (chickenpox)
Hepatitis A
Meningococcal (certain high-risk groups only)
In addition, the 7-18 years schedule recommends human papillomavirus (HPV) vaccination and meningococcal vaccination.

These schedules are reviewed annually; new vaccines are considered for addition to the schedule after licensure, though not all licensed vaccines are added to the schedule. (The yellow fever vaccine, for example, is unlikely to be added to the schedule, as only individuals traveling to yellow fever endemic areas need to be vaccinated against it.)

Source: The History of Vaccines

The African origins of the small pox vaccine
The African origins of the small pox vaccine
April 17, 2021 - 7:06 am

The news was terrifying to colonists in Massachusetts: Smallpox had made it to Boston and was spreading rapidly. The first victims, passengers on a ship from the Caribbean, were shut up in a house identified only by a red flag that read “God have mercy on this house.” Meanwhile, hundreds of residents of the bustling colonial town had started to flee for their lives, terrified of what might happen if they exposed themselves to the frequently deadly disease.

They had reason to fear. The virus was extremely contagious, spreading like wildfire in large epidemics. Smallpox patients experienced fever, fatigue and a crusty rash that could leave disfiguring scars. In up to 30 percent of cases, it killed.

But the smallpox epidemic of 1721 was different than any that came before it. As sickness swept through the city, killing hundreds in a time before modern medical treatment or a robust understanding of infectious disease, an enslaved man known only as Onesimus suggested a potential way to keep people from getting sick. Intrigued by Onesimus’ idea, a brave doctor and an outspoken minister undertook a bold experiment to try to stop smallpox in its tracks.

Smallpox was one of the era’s deadliest afflictions. “Few diseases at this time were as universal or fatal,” notes historian Susan Pryor. The colonists saw its effects not just among their own countrymen, but among the Native Americans to whom they introduced the disease. Smallpox destroyed Native communities that, with no immunity, were unable to fight off the virus.

Smallpox also entered the colonies on slave ships, transmitted by enslaved people who, in packed and unsanitary quarters, passed the disease along to one another and, eventually, to colonists at their destinations. One of those destinations was Massachusetts, which was a center of the early slave trade. The first enslaved people had arrived in Massachusetts in 1638, and by 1700, about 1,000 enslaved people lived in the colony, most in Boston.

In 1706, an enslaved West African man was purchased for the prominent Puritan minister Cotton Mather by his congregation. Mather gave him the name Onesimus, after an enslaved man in the Bible whose name meant “useful.” Mather, who had been a powerful figure in the Salem Witch Trials, believed that owners of enslaved people had a duty to convert enslaved people to Christianity and educate them. But like other white men of his era, he also looked down on what he called the “Devilish rites” of Africans and worried that enslaved people might openly rebel.

Mather didn’t trust Onesimus: He wrote about having to watch him carefully due to what he thought was “thievish” behavior, and recorded in his diary that he was “wicked” and “useless.” But in 1716, Onesimus told him something he did believe: That he knew how to prevent smallpox.

Onesimus, who “is a pretty intelligent fellow,” Mather wrote, told him he had had smallpox—and then hadn’t. Onesimus said that he “had undergone an operation, which had given him something of the smallpox and would forever preserve him from it…and whoever had the courage to use it was forever free of the fear of contagion.”

The operation Onesimus referred to consisted of rubbing pus from an infected person into an open wound on the arm. Once the infected material was introduced into the body, the person who underwent the procedure was inoculated against smallpox. It wasn’t a vaccination, which involves exposure to a less dangerous virus to provoke immunity. But it did activate the recipient’s immune response and protected against the disease most of the time.

Mather was fascinated. He verified Onesimus’ story with that of other enslaved people, and learned that the practice had been used in Turkey and China. He became an evangelist for inoculation—also known as variolation—and spread the word throughout Massachusetts and elsewhere in the hopes it would help prevent smallpox.

But Mather hadn’t bargained on how unpopular the idea would be. The same prejudices that caused him to distrust his servant made other white colonists reluctant to undergo a medical procedure developed by or for Black people. Mather “was vilified,” historian Ted Widmer told WGBH. “A local newspaper, called The New England Courant, ridiculed him. An explosive device was thrown through his windows with an angry note. There was an ugly racial element to the anger.” Religion also contributed: Other preachers argued that it was against God’s will to expose his creatures to dangerous diseases.

But in 1721, Mather and Zabdiel Boylston, the only physician in Boston who supported the technique, got their chance to test the power of inoculation. That year, a smallpox epidemic spread from a ship to the population of Boston, sickening about half of the city’s residents. Boylston sprang into action, inoculating his son and his enslaved workers against the disease. Then, he began inoculating other Bostonians. Of the 242 people he inoculated, only six died—one in 40, as opposed to one in seven deaths among the population of Boston who didn’t undergo the procedure.

The smallpox epidemic wiped out 844 people in Boston, over 14 percent of the population. But it had yielded hope for future epidemics. It also helped set the stage for vaccination. In 1796, Edward Jenner developed an effective vaccine that used cowpox to provoke smallpox immunity. It worked. Eventually, smallpox vaccination became mandatory in Massachusetts.

Did Onesimus live to see the success of the technique he introduced to Mather? It isn’t clear. Nothing is known of his later life other than that he partially purchased his freedom. To do so, writes historian Steven J. Niven, he gave Mather money to purchase another enslaved person. What is clear is that the knowledge he passed on saved hundreds of lives—and led to the eventual eradication of smallpox.

In 1980, the World Health Organization declared smallpox entirely eradicated due to the spread of immunization worldwide. It remains the only infectious disease to have been entirely wiped out.

Source: History Channel

Neuropsychiatric Complications of the Flu Virus
Neuropsychiatric Complications of the Flu Virus
April 10, 2021 - 11:16 am

Mental and behavioral changes are a particularly disconcerting finding among flu patients. Are these manifestations an expected complication of influenza or an artifact of modern treatment options? In this context, both the virus and its treatment are potential culprits.

INFLUENZA CAN CAUSE NEUROPSYCHIATRIC MANIFESTATIONS

Historically, mental instability associated with surviving an influenza infection was well-known and accepted. For an excellent yet brief historical review, a 2013 Lancet article summarizes well the evolution of the concept of “psychosis of influenza,” from a commonly recognized psychiatric phenomenon to an oddity fueling a media craze.[1]

Reported mental health effects range from depression and other mood disturbances to insomnia and psychosis. Menninger described a series of one hundred patients with psychiatric complications after the influenza epidemic of 1918.[2] One main criticism of historical descriptions is the lack of serological confirmation of influenza infection, though viral genetic material has been recovered and tested in some cases. Mental side effects related to medical illness or treatment are not uncommon, as is exemplified by the worsening of depression with interferon treatment for hepatitis[3], but the most recent media upheaval seems to have focused mostly on the medication rather than the disease.

Effects of a flu infection on patients with pre-existing mental health issues were also found[4], and sero-positivity for influenza viruses was associated with a history of suicide attempts and mood disorders.[5]

During the H1N1 pandemic in Japan in 2009, encephalopathy and neuropsychiatric complications were commonly noted.[6,7] Examining flu patients reporting neuropsychiatric manifestations in Japan from 2006 to 2013, Nakamura et al found hundreds of cases with new severe abnormal behavior that could have culminated in harm to self or others if left unchecked.[8] About 95% of these cases were positive for the flu by the rapid diagnosis test; few were on neuraminidase inhibitors.

Modern psychiatry has turned towards assessing prenatal influence of the influenza virus on the development of mental disorders through the lifespan, rather than acute post-infectious effects. Low birth weight of infants born to mothers who suffered gestational influenza may be a mediating
factor.[9]

Gestational influenza raises the risk of bipolar disorder in young adulthood, and previous studies had indicated an increased risk of psychotic disorders, specifically schizophrenia.[10] In a strict meta-analysis of four ecological studies and three birth cohort studies, Cai et al. reported a similar finding, spanning across the various methodologies sampled.[11]

A spectrum of four syndromes of influenza-associated neuropsychiatric disorders has been advanced (Mizuguchi 2013):

1) Mild Encephalopathy with Reversible Splenial Lesions (seen on MRI, not rising to the level of Acute Encephalopathy, which would require impaired GCS for 24+ hours).

2) Febrile Delirium

3) Delirium with rushing/jumping behavior (particularly noteworthy and consequential in Japan)

4) Reproducible neuropsychiatric adverse effects of oseltamivir (believed to be rare, affecting children predominantly, and discussed later) Additionally, acute neurologic manifestations such as seizures, Reye’s Syndrome, Acute Necrotizing Encephalopathy, and aseptic meningitis have been described in the setting of influenza infection.

In summary, the influenza virus is linked to neuropsychiatric complications at various stages, from fetus to adulthood. In those winter weeks when a significant fraction of ED cases present with ILI, there’s no good way of predicting who’s particularly susceptible to these less-common manifestations. But asking about prior psychiatric comorbidities or screening for delirium may be a place to start.

TO TREAT OR NOT TO TREAT?

In terms of treatment for influenza, the options include M2 proton channel Inhibitors (amantadine and rimantadine) and the neuraminidase inhibitors (oseltamivir, laninamivir, peramivir, and zanamivir). Oseltamivir, known as Tamiflu®, remains the main treatment in the USA (though FDA had also granted approval to peramivir and zanamivir). The drug can induce neuro-psychiatric complications, sometimes delayed, by virtue of inhibiting the host native neuraminidases.[15]

Amantadine (Symmetrel®), also previously approved in the US for influenza treatment (though less commonly used, because of resistance) is associated with neuropsychiatric complications including aggression and psychosis as well.[20] The story of oseltamivir has been told in these pages over the years. Briefly – the Cochrane review (after Roche revealed more previously unpublished data) showed Tamiflu can reduce the length of symptoms from 7 days to just under 6 and a half days. Rates of hospitalization and pneumonia weren’t significantly different. The CDC continues to recommend Tamiflu for high-risk populations and those that are seriously ill, and mentions it as a “consideration” in healthy patients with ILI. Also, it’s an effective prophylactic among those at risk of exposure, but not as effective as the flu vaccine.

Tamiflu does seem to decrease viral shedding in flu-positive patients, but studies don’t show a consistent reduction in transmission to household members when a confirmed flu patient takes oseltamivir (Cochrane Database Syst Rev. 2014;4).

We’re seeing a complex interplay between public health policy, pharmaceutical companies with sales goals, and a public with ever-growing awareness and risk-aversion. (For an excellent summary, see Gupta and Okamoto).[16,17]

While exact prevalence of each kind of neuropsychiatric complications to oseltamivir is hard to determine, we know from oseltamivir prophylaxis studies that patients reported significantly more psychiatric adverse events when on treatment – Cochrane calculate a number needed to harm of 94.[18] There were other side effects noted from those on prophylaxis – headaches and nausea (NNTH 32 and 25, respectively).

The rates of headaches and nausea aren’t very different in those taking Tamiflu for active influenza infection (compared to prophylaxis), but the event rates for psychiatric adverse events seemed to be in the range of 0.5-2%. While vaccination remains the gold standard for preventing influenza, oseltamivir is recommended in select patients, and EPs will also have to weigh the CDC’s statement on “consideration” for healthy individuals and decisions about treatment of close contacts and family members when a patient is seen with flu symptoms.[19]

In summary, both the influenza virus and its treatments have been linked to neuropsychiatric complications, which can range from mood de-stabilization to frank psychosis. Suicide has not been studied specifically. The incidence isn’t exactly common, but not exceedingly rare either. With this complex challenge, what is the EP to do?

First, protect yourself: make sure you and your family members get influenza vaccine and adhere to a very strict handwashing regimen. Second, be familiar with your facility’s testing protocol and its sensitivity and specificity. In a season with multiple infections, even severe symptoms might not necessarily have seropositive results. Third, use clinical judgment and critical thinking in your decision-making. Psychiatric complications of influenza or its treatment are possible. Instruct patients about potential mental symptoms.

Mental symptoms can mask serious neurological complications such as acute disseminated encephalomyelitis.[21] Use medications judiciously. Antivirals are useful tools for the young and elderly and those with comorbidity risks.

Source:
Emergency Physicians Monthly

References (in order):

Honigsbaum M. “An inexpressible dread”: psychoses of influenza at fin-de-siecle. Lancet (London, England). 2013;381(9871):988-989.
Yudofsky SC. Contracting schizophrenia: lessons from the influenza epidemic of 1918-1919. Jama. 2009;301(3):324-326.
Schaefer M, Mauss S. Hepatitis C treatment in patients with drug addiction: clinical management of interferon-alpha-associated psychiatric side effects. Current drug abuse reviews. 2008;1(2):177-187.
Page LA, Seetharaman S, Suhail I, Wessely S, Pereira J, Rubin GJ. Using electronic patient records to assess the impact of swine flu (influenza H1N1) on mental health patients. Journal of mental health (Abingdon, England). 2011;20(1):60-69.
Okusaga O, Yolken RH, Langenberg P, et al. Association of seropositivity for influenza and coronaviruses with history of mood disorders and suicide attempts. Journal of affective disorders. 2011;130(1-2):220-225.
Okumura A, Nakagawa S, Kawashima H, et al. Severe form of encephalopathy associated with 2009 pandemic influenza A (H1N1) in Japan. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology. 2013;56(1):25-30.
Kashiwagi M, Tanabe T, Ooba C, et al. Differential diagnosis of delirious behavior in children with influenza. Brain & development. 2015;37(6):618-624.
Nakamura Y, Sugawara T, Ohkusa Y, et al. Abnormal behavior during influenza in Japan during the last seven seasons: 2006-2007 to 2012-2013. Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy. 2014;20(12):789-793.
Fineberg AM, Ellman LM, Buka S, Yolken R, Cannon TD. Decreased birth weight in psychosis: influence of prenatal exposure to serologically determined influenza and hypoxia. Schizophrenia bulletin. 2013;39(5):1037-1044.
Parboosing R, Bao Y, Shen L, Schaefer CA, Brown AS. Gestational influenza and bipolar disorder in adult offspring. JAMA psychiatry. 2013;70(7):677-685.
Cai L, Wan CL, He L, de Jong S, Chou KC. Gestational Influenza Increases the Risk of Psychosis in Adults. Medicinal chemistry (Shariqah (United Arab Emirates)). 2015;11(7):676-682.
Huang HS, Tsai CL, Chang J, Hsu TC, Lin S, Lee CC. Multiplex PCR System for the Rapid Diagnosis of Respiratory Virus Infection: A Systematic Review and Meta-analysis. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2017.
Merckx J, Wali R, Schiller I, et al. Diagnostic Accuracy of Novel and Traditional Rapid Tests for Influenza Infection Compared With Reverse Transcriptase Polymerase Chain Reaction: A Systematic Review and Meta-analysis. Annals of internal medicine. 2017;167(6):394-409.
Avril E, Lacroix S, Vrignaud B, et al. Variability in the diagnostic performance of a bedside rapid diagnostic influenza test over four epidemic seasons in a pediatric emergency department. Diagnostic microbiology and infectious disease. 2016;85(3):334-337.
Hama R. The mechanisms of delayed onset type adverse reactions to oseltamivir. Infectious diseases (London, England). 2016;48(9):651-660.
Gupta YK, Meenu M, Mohan P. The Tamiflu fiasco and lessons learnt. Indian Journal of Pharmacology. 2015;47(1):11-16.
Okamoto E. Is oseltamivir (Tamiflu) safe? Re-examining the Tamiflu ‘ado’ from Japan. Expert review of pharmacoeconomics & outcomes research. 2010;10(1):17-24.
Casscells SW, Granger E, Kress AM, Linton A. The association between oseltamivir use and adverse neuropsychiatric outcomes among TRICARE beneficiaries, ages 1 through 21 years diagnosed with influenza. International journal of adolescent medicine and health. 2009;21(1):79-89.
Esposito S, Principi N. Oseltamivir for influenza infection in children: risks and benefits. Expert review of respiratory medicine. 2016;10(1):79-87.
Xu WJ, Wei N, Xu Y, Hu SH. Does amantadine induce acute psychosis? A case report and literature review. Neuropsychiatric disease and treatment. 2016;12:781-783.
Moscovich DG, Singh MB, Eva FJ, Pari BK. Acute disseminated encephalomyelitis presenting as an acute psychotic state. The Journal of nervous and mental disease. 1995;183(2):116-117.
Beigel JH, Bao Y, Beeler J, et al. Oseltamivir, amantadine, and ribavirin combination antiviral therapy versus oseltamivir monotherapy for the treatment of influenza: a multicentre, double-blind, randomised phase 2 trial. The Lancet Infectious diseases. 2017;17(12):1255-1265.
Maruyama T, Fujisawa T, Suga S, et al. Outcomes and Prognostic Features of Patients With Influenza Requiring Hospitalization and Receiving Early Antiviral Therapy: A Prospective Multicenter Cohort Study. Chest. 2016;149(2):526-534.

Zoonoses: Animals and Major Pandemics in History
Zoonoses: Animals and Major Pandemics in History
April 3, 2021 - 11:18 am

Pandemics, antivirals, herd immunity… SARS-CoV-2 coronavirus spreading around the world has led to the repetition of several scientific concepts in news on the virus. One term that is part of this glossary is at the heart of the virus’ origin: zoonoses.

Zoonoses refers to the process by which animal diseases are naturally transmitted to human beings, either through the person’s direct exposure to the animals or by consuming food made of the animals. Although the animal from which the COVID-19 disease spread to humans has not been scientifically confirmed, the focus now seems to be on the pangolin. Even though zoonoses is all over the news today, it is a process that is very well known and which lies at the origin of many diseases, as well as major pandemics in history.

Why have human beings been, and will continue to be, exposed to these kinds of pandemics? The UN Food and Agriculture Organization’s report World Livestock 2013: Changing disease landscape provides a key fact: 70 percent of the new diseases that have emerged in human beings in recent decades are of animal original. This percentage show the extent to which human health is closely tied to livestock and animal health. The same report mentioned other factors that have contributed to the spread of these kinds of diseases in recent years, such as poverty, deficient healthcare systems and healthcare infrastructure in some places, international travel and trade, climate change and increasing pressure on ecosystems.

From the Black Death to mad cow disease, we will go over some of the most important zoonoses in the history of humankind prior to the arrival of the COVID-19 disease.

THE BLACK DEATH

In the 14th Century, the Black Death took the lives of 50 million people. This devastating epidemic, considered one of the most lethal in the history of humankind, it a bacterial form of zoonoses, as it is caused by the bacteria Yersinia pestis, which is found in small mammals and the fleas infest them. Living conditions in the Middle Age contributed to how rapidly it spread, as people had a lot of contact with fleas and other rat parasites.

The Black Death continues to exist today as an animal disease in all continents except Oceania, but most human cases are currently in Africa. The three most endemic countries are Madagascar, the Democratic Republic of the Congo and Peru.

RABIES

Rabies are a viral form of zoonotic disease caused by a virus from the Rhabdoviridae family. It can affect any wild or domestic mammal and spread to people through bites or scratches. In 99 percent of the cases, it is spread through domestic dogs. Therefore, the most effective way to combat this disease is by vaccinating dogs, which is why this vaccine is required in many regions.

Louis Pasteur developed the first vaccine for rabies in humans in the year 1885. The renowned French chemist used it to treat a nine year old boy after he had been bitten by a rabid dog, leading to his recovery and those of thousands more people in the following months.

The World Health Organization (WHO) warns that is is currently a neglected disease, as most cases are concentrated in poor and vulnerable populations. Over 95 percent of human deaths from rabies take place in Asia or Africa even though immunoglobulins and vaccinations effective in humans have existed for more than a century.

BOVINE SPONGIFORM ENCEPHALOPATHY

Better known as “mad cow disease”, the first cases of bovine spongiform encephalopathy (BSE) were detected in animals in the U.K. in 1986. In 1996, a new variant of Creutzfeldt-Jakob disease (CJD) was identified in humans, and was related to the BSE epidemic in cattle. The transmission of the disease to humans occured by consuming contaminated meat.

The appearance of BSE in cattle was related to the practice of feeding animals the remains of ruminant livestock. Abandoning this compound for cattle feed eliminated the possibility of animals getting BSE, and therefore the risk of transmitting it to humans by consuming meat.

AVIAN FLU

Avian flu is zoonoses caused by Influenza A virus subtypes. It is a type of flu that originally affects birds, but some strains can infect different mammals that are in contact with infected birds, including humans. In 1997, human infections were identified for the first time in Hong Kong. From 2004 to 2006 the virus spread from Asian fowl to Europe, and WHO warned that this could increase the possibility of avian flu becoming a pandemic. Ten years later, in 2013, it was back in the news after spreading to hundreds of people in China with the new strain, H7N9.

Even though some experts say there is a possibility of a strain of avian flu becoming the great pandemic of the 21st Century, this has not yet taken place because the virus has not yet mutated in a way that facilitates its transmission among people. In the future, if a strain is capable of overcoming this barrier, it could spark this pandemic.

Source: OpenMind BBVA

The tragic Holocaust backstory of Pfizer’s CEO
The tragic Holocaust backstory of Pfizer's CEO
March 27, 2021 - 9:13 am

Pfizer CEO Dr. Albert Bourla joined the Sephardic Heritage International on January 28th for International Holocaust Remembrance Day, where he shared his Greek Sephardic family’s story of tragedy and survival during the Holocaust.

“It’s a story that had a great impact on my life and my view of the world, and it is a story that, for the first time today, I share publicly,” said Bourla during the January 28 virtual event. “Many Holocaust survivors never spoke to their children of the horrors they endured,” he added.

Bourla’s parents were of 2,000 survivors from a community of 50,000 nearly eradicated by the Holocaust in Thessaloniki, Greece where he was born. He began by retelling the story of his father.

“My father’s family, like so many others, had been forced from their homes and taken to a crowded house within one of the Jewish ghettos,” recounted Bourla. “It was a house they had to share with several other Jewish families. They could circulate in and out of the ghetto as long as they were wearing the yellow star.”

“But one day in March 1943, the ghetto was surrounded by occupational forces and the exit was blocked. My father and his brother (my uncle) were outside when it happened. Their father (my grandfather) met them outside, told them what was happening and asked them to leave the ghetto and hide because he had to go back inside as his wife and two other children were home. So later that day, my grandfather, Abraham Bourla, his wife Rachel, his daughter Graziella and his youngest son David were taken to a camp outside the train station and from there, left for Auschwitz. My father and uncle never saw them again,” Bourla recounted.

He explained how his father and uncle were able to escape to Athens. Thanks to local police who were helping Jews escape from the Nazis, they were able to obtain fake IDs with Christian names.

“When the Germans had left, they went back to Thessalonki and found that all of their property and belongings have been stolen or sold. With nothing to their name, they started from scratch, becoming partners at a successful liquor business that they ran together until they both retired.”
Bourla then followed with his mother’s story.

According to Bourla, his mother was well known which caused her to hide at home “24 hours a day” out of fear of being recognized on the street and turned over the Germans. She left the house very rarely, but it was during one of her rare ventures outside that she was captured and taken to a local prison.

“My Christian uncle, my mother’s brother-in-law, Costas de Madis approached a Nazi official and paid him a ransom in exchange for a promise that my mother would be spared,” Bourla said.

“However, my mother’s sister, my aunt, didn’t trust the Germans. So she would go to the prison every day at noon to watch as they loaded the truck of prisoners. One day, her fear had been realized, and my mom was put on the truck. She ran home and told her husband, who then called the Nazi official and reminded him of their agreement – who said he would look into it. That night was the longest night in my aunt and uncle’s life because they knew that next morning, my mom would likely have been executed.”

“The next day, my mom was lined up with other prisoners. And moments before she would have been executed, a German soldier on a motorcycle arrived and handed some papers to the men in charge of the firing squad. They removed my mother from the line. As they rode away, my mom could hear the machine gun slaughtering those that were left behind. Two or three days later, she was released from prison after the Germans left Greece.”
Eight years later his parents met by way of matchmaking, through which they agreed to get married, according to Bourla.

“My father had two dreams – one, that I would become a scientist and two, that I would marry a nice Jewish girl. I’m happy to say he lived long enough to see both dreams come true,” Bourla said.

Source: The Jerusalem Post

Mental health during the 1918-1919 Spanish Flu
Mental health during the 1918-1919 Spanish Flu
March 20, 2021 - 10:44 pm

As we all try to acclimate ourselves to the rapidly changing circumstances brought about by the COVID-19 pandemic, comparisons are being made between this pandemic and the so-called Spanish flu pandemic of 1918-1919. (The reason it was referred to as the Spanishflu was that Spain was one of the only countries at the time to not censor reports of cases, and so it was widely publicized there by late-fall 1918.) The Spanish flu proved to be peculiar for several reasons, most noteworthy of course due to the high morbidity (as many 500 million were infected) and mortality (around 50 million deaths). It also came in waves. In the US, there were four such waves: first in spring 1918, again in August 1918 (epidemiologically the most devastating of the four), yet again in winter 1918/1919, and a final return in early 1920. Finally, the disease was unlike most flus in that it decimated even the traditionally more robust segments of the population (ages 20-40), taking the lives of many within 3 days of showing symptoms.

Exploring the pandemics

Since the pandemic of the Spanish flu, researchers dedicated themselves to identifying the origins and nature of the virus. It took decades, however, before virologists succeeded. Starting in the mid-1990s, Jeffrey Taubenberger, MD, PhD, and his team were able to carry out a sequence and phylogenetic analysis of 1918 influenza virus genes and identified it to be an H1N1 virus of avian origin.1

Until around 1970, historical research about the pandemic had been virtually non-existent. Some novels and popular histories appeared over the decades, but it was Alfred Crosby’s 1976 book Epidemic and Peace, 1918 (reissued in 1989 under the title America’s Forgotten Pandemic: The Influenza of 1918) that paved the way for international research about the subject.2 One of the book’s major achievements was to draw attention to the fact that the pandemic quickly disappeared as a topic of public conversation soon after it was over, ignored by periodicals and textbooks for decades. To many historians, this collective silence is as much a part of the pandemic’s story as the course of the disease itself.

The mental health links

In comparison to other aspects of the pandemic, little research has been done on the long-term impact of the Spanish flu on mental health. One of the few researchers to investigate the subject was historical demographer Svenn-Erik Mamelund, PhD. Looking at asylum hospitalizations in Norway from 1872 to 1929, Mamelund found that the number of first-time hospitalized patients with mental disorders attributed to influenza increased by an average annual factor of 7.2 in the 6 years following the pandemic.3 In addition, he pointed out that Spanish flu survivors reported sleep disturbances, depression, mental distraction, dizziness, and difficulties coping at work, and that influenza death rates in the United States during the years 1918-1920 significantly and positively related to suicide.4

Mamelund is among a number of scholars who have noted what many suspect to be a connection between the Spanish flu and a pronounced increase in neurological diseases. By 1919 and 1920, physicians and researchers in Great Britain were already reporting a marked rise in nervous symptoms and illnesses among some patients recovering from influenza infection; among other symptoms, depression, neuropathy, neurasthenia, meningitis, degenerative changes in nerve cells, and a decline in visual acuity were cited.5

Encephalitis lethargica: another connection or vulnerability?

Encephalitis lethargica coincided with the Spanish flu; it reached epidemic proportions alongside the Spanish flu. As Hoffman and Vilensky have recently described, the syndrome was characterized by two, often, blended phases:6

During the acute phase, patients typically experienced excessive sleepiness, disorders of ocular motility, fever, and movement disorders, although virtually any neurological sign or symptom could be exhibited, with day-to-day, and even hour-by-hour shifts in symptomatology. The chronic phase could occur months to years later and was most commonly characterized by parkinsonian-like signs.

Psychiatrists and neurologists first reported encountering encephalitis lethargica symptoms in 1916 and 1917 in Austria and France. By 1919, cases had become common throughout Europe, the United States, Canada, Central America, and India. All told, approximately 1 million people worldwide were affected by encephalitis lethargica between its outbreak in 1916 until the early 1930s. While many clinicians (both at the time and since then) have surmised an association between encephalitis lethargica and the Spanish flu,7 there is no conclusive evidence of causality.

Collateral damage

Some medical and social historians have been tracing connections between the pandemic and the other catastrophic global event of the time-World War I. In this regard, historians have flagged the ways in which the war efforts depleted medical personnel, helped disseminate the virus through the mobilization of troops, and created the conditions for the mutation of an otherwise mild flu virus.8

When it comes to mental health, the historical record shows that the pandemic, like the war, took a toll on the emotional resilience of those not (or not yet) in harm’s way. The massive and sudden loss of life plunged many into a chronic state of helplessness and anxiousness. A large portion of the population were affected by the loss of loved ones. Parents had to come to grips with losing a child (or even several children), while some children suddenly found themselves parentless. In November 1918, 31,000 children in New York City alone had lost one or both parents. For others, the experience left them feeling a mix of guilt, anger, confusion, and abandonment. Surviving health professionals were not immune to such sentiments, with many of them noting that they were haunted by a sense of frustration and grief, even years later.9

Like all mass encounters with infectious disease, the Spanish flu pandemic had its own unique features. If history teaches us anything, it is that we should always be measured in how we glean lessons from the past. That said, the example of the influenza of 1918-1920 gives us reason to expect that the present pandemic will carry in tow its own set of mental health challenges.

Source: Psychiatric Times

Did COVID-19 prove Malthusian Theory of Population correct?
Did COVID-19 prove Malthusian Theory of Population correct?
March 14, 2021 - 6:50 am

Thomas Malthus theorized that populations grew in geometric progression. A geometric progression is a sequence of numbers where each term after the first is found by multiplying the previous one by a fixed, non-zero number called the common ratio. For example, in the sequence 2, 10, 50, 250, 1250, the common ratio is 5.

Additionally, he stated that food production increases in arithmetic progression. An arithmetic progression is a sequence of numbers such that the difference between the consecutive terms is constant. For example, in series 2, 5, 8, 11, 14, 17, the common difference of 3. He derived this conclusion due to the Law of Diminishing Returns.

From this, we can conclude that populations will grow faster than the supply of food. This exponential population growth will lead to a shortage of food.

Malthus then argued that because there will be a higher population than the availability of food, many people will die from the shortage of food. He theorized that this correction would take place in the form of Positive Checks (or Natural Checks) and Preventative Checks. These checks would lead to the Malthusian catastrophe, which would bring the population level back to a ‘sustainable level.’

He believed that natural forces would correct the imbalance between food supply and population growth in the form of natural disasters such as floods and earthquakes and human-made actions such as wars and famines.

The Malthusian Trap (or “Malthusian Population Trap”) is the idea that higher levels of food production created by more advanced agricultural techniques create higher population levels, which then lead to food shortages because the higher population needs to live on land that would have previously used to grow crops.

Even as technological advancement would normally lead to per capita income gains, theorizes Malthus, these gains are not achieved because in practice the advancement also creates population growth. Once the population exceeds what food supplies can support, this supposedly creates a Malthusian crisis with widespread famine as well as rampant disease. This ends up decreasing the population to earlier levels.

The reality, however, has been that population growth has not itself created the pandemic that Malthus predicted.

Therefore, we cannot attribute the COVID-19 pandemic to the Malthusian Trap. A true Mathusian Trap occurs when the disparity between the rate of food production and the rate of population growth creates the crisis.

Source: Intelligent Economist

Demographics affect healthcare outcomes
Demographics affect healthcare outcomes
March 6, 2021 - 7:58 pm

Demographic shifts and societal changes are intensifying pressures on health systems and demanding new directions in the delivery of healthcare. We are getting older. Ageing populations in both emerging and developed nations are driving up the demand for healthcare.

According to the United Nations, the world’s population is expected to increase by one billion people by 2025. Of that billion, 300 million will be people aged 65 or older, as life expectancy around the globe continues to rise. Additional healthcare resources and service innovation is needed globally to deliver the long-term care and chronic disease management services required by a rapidly increasing senior population.

At the same time, developing countries are experiencing significant growth in their middle class. The Brookings Institute estimates 65% of the global population will be middle class by 2030. Accelerated urbanisation and access to middle-class comforts are promoting sedentary lifestyle changes that will inevitably lead to greater incidence of obesity, diabetes and other costly health conditions.

These demographic changes will not be evenly distributed across the globe, however. Growth, for example, will be more concentrated in some parts of the world. Africa’s population is anticipated to double by 2050, while Europe’s population is shrinking.

Source: PwC

How a Mongol-Genoese battle triggered the Black Plague
How a Mongol-Genoese battle triggered the Black Plague
February 26, 2021 - 11:54 am

In 1344, the Golden Horde decided to recapture the Crimean port city of Kaffa from the Genoese—Italian traders who had taken the town in the late 1200s. The Mongols under Jani Beg instituted a siege, which lasted until 1347 when reinforcements from further east brought the plague to the Mongol lines.

An Italian lawyer, Gabriele de Mussis, recorded what happened next: “The whole army was affected by a disease which overran the Tartars (Mongols) and killed thousands upon thousands every day.” He goes on to charge that the Mongol leader “ordered corpses to be placed in catapults and lobbed into the city in hopes that the intolerable stench would kill everyone inside.”

This incident is often cited as the first instance of biological warfare in history. However, other contemporary chroniclers make no mention of the putative Black Death catapults. A French churchman, Gilles li Muisis, notes that a “calamitous disease befell the Tartar army, and the mortality was so great and widespread that scarcely one in twenty of them remained alive.” However, he depicts the Mongol survivors as surprised when the Christians in Kaffa also came down with the disease.

Regardless of how it played out, the Golden Horde’s siege of Kaffa certainly did drive refugees to flee on ships bound for Genoa. These refugees likely were a primary source of the Black Death that went on to decimate Europe.

Woodrow Wilson also downplayed the Spanish flu before contracting it himself
Woodrow Wilson also downplayed the Spanish flu before contracting it himself
February 20, 2021 - 7:43 am

On the night of April 3, 1919, President Woodrow Wilson began to suffer from a violent cough. His condition quickly worsened to the point that his personal doctor, Cary Grayson, thought the president might have been poisoned. Grayson later described the long night spent at Wilson’s bedside as “one of the worst through which I have ever passed. I was able to control the spasms of coughing but his condition looked very serious.”

The culprit wasn’t poison, but the same potent strain of influenza nicknamed the “Spanish flu” that would eventually kill an estimated 20 million worldwide, including more than 600,000 in the United States. Wilson’s illness was made even worse by its timing—the president was left bedridden in the middle of the most important negotiations of his life, the Paris Peace Conference to end World War I.

The 1918 “Spanish” flu was notorious for aggressively attacking the respiratory system. The infection was worst in the young and previously healthy, whose immune systems could overreact to the virus and drown the lungs with fluid, killing patients in a matter of days. But for those who survived the initial onslaught, some also experienced neurological symptoms.

Even after their burning fevers subsided, flu victims described “post-influenza manifestations,” psychotic delusions and visions that resulted from damage to the nervous system, says John Barry, author of The Great Influenza: The Story of the Deadliest Pandemic in History.

“The most comprehensive study of the 1918 pandemic noted how common neurological disorders were,” says Barry. “They were second only to the lung. This included psychosis, which was usually temporary.”

From numerous sources, it appears that Wilson suffered from similar effects during his fight with the flu at the Paris Peace Conference.

“He became paranoid,” says Barry. “Wilson thought the French had spies all around him. He was bizarrely obsessed with his furniture and his automobiles, and pretty much everyone around him noted it.” Wilson’s chief usher, a man named Irwin Hoover, wrote later that “something queer was happening in [the president’s] mind” and that “[o]ne thing is certain: he was never the same after this little spell of sickness.”

The British prime minister, Lloyd George, came to visit Wilson during his recuperation at the Hôtel du Prince Murat and labeled Wilson’s condition a “nervous and spiritual breakdown” in the middle of the heated Paris negotiations.

Although instances of “the psychoses of influenza” had been reported by physicians as early as the Russian Flu outbreak of 1889, there was no treatment for the condition, which usually went away on its own. One hypothesis is that the neurological disorder experienced by Wilson and others was caused by brain swelling (encephalitis) associated with the flu.

Source: The Great Influenza

World Bank’s pandemic bonds failed during the pandemic
World Bank's pandemic bonds failed during the pandemic
February 13, 2021 - 7:05 pm

The World Bank has scrapped plans to launch a second sale of its Pandemic Emergency Financing Facility (PEF) bond, according to a July article in UK newspaper The Financial Times (FT).

After facing significant criticism for PEF’s delayed pay-out to developing countries during the Covid-19 pandemic, a spokesperson for the World Bank told the FT that there are “no plans for a PEF 2.0” (see Observer Spring 2020). While PEF investors had already received almost $100 million in interest payments by the end of February and some sought to quickly sell-off their bonds as the Covid-19 worsened, developing countries had to wait until mid-May for pay-outs to be issued. In a February piece in UK newspaper The Guardian, former World Bank economist Olga Jonas from the Harvard Global Health Institute argued that PEF’s design, “waits for people to die.”

PEF, launched in 2017, was designed to help developing nations facing a serious outbreak of infectious disease. But the World Bank has faced accusations that instead of preventing the escalation of infections, PEF fails to pay out until outbreaks reach a ‘trigger’, when taking preventative action is no longer possible, as illustrated by both the Covid-19 pandemic and the 2014-16 Ebola outbreak. A 2019 paper by Clare Wenham of the London School of Economics concluded that the instrument does more to serve private investor interests than contribute to global health security, an accusation often levelled at the Bank (see Observer Spring 2020).

In an October 2019 article for development news site Devex, Lawrence Summers, the World Bank’s former chief economist, was quoted as describing the PEF as, “an embarrassing mistake.” With its quiet termination of the scheme, it appears the World Bank agrees.

Source: Bretton Woods Project

The curious case of the missing Influenza
The curious case of the missing Influenza
February 6, 2021 - 4:48 pm

By mid-December, the Northern Hemisphere is usually well into the start of its annual cold and flu season — but so far this year, even as the COVID-19 pandemic surges in dozens of countries, the levels of many common seasonal infections remain extremely low.

The pandemic caused by the SARS-CoV-2 coronavirus has infected at least 67 million people and killed 1.5 million worldwide. The patchwork of responses intended to fight the pandemic — from temporary lockdowns to mask wearing, social distancing, enhanced personal hygiene and reduced travel — has had a huge impact on other common respiratory illnesses, too.

In the Southern Hemisphere — now past its winter — seasonal influenza hardly struck at all. That looks as though it might happen in the north, too. Conversely, some common-cold viruses have thrived, and tantalizing evidence suggests that they might, in some cases, protect against COVID-19.

Despite humanity’s long history with colds and flu, the viruses that cause them still hold many mysteries. Scientists hope this year’s disrupted seasons could reveal new information about the transmission and behaviour of these unwelcome annual guests: how these viruses respond to health measures, how they interact and what that might mean for long-term disease burdens. “This is a natural experiment for so many respiratory viruses,” says Sonja Olsen, an epidemiologist at the National Center for Immunization and Respiratory Diseases, part of the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia.

In May, at the tail end of the first wave of COVID-19 deaths in many nations, and when some of the strictest lockdowns were in place, health workers noted an abrupt and early halt to the 2019–20 flu season in the Northern Hemisphere.

That might partly have been an artefact caused by fewer people coming to a clinic for testing, experts say, but it was also attributable to the effectiveness of policies such as social distancing. After the pandemic started, positive tests for the flu virus plummeted by 98% in the United States, for example, whereas the number of samples submitted for testing dropped by only 61%1. In the end, the US 2019–20 flu season was rated as ‘moderate’ by the CDC, which estimates that 38 million people fell ill with influenza, and 22,000 people died. That’s fewer than in recent years, but not unprecedented.

After the flu season in the north ended early, it hardly got going at all in the Southern Hemisphere. There were astonishingly few cases of seasonal flu there from April to July 2020 — even as global COVID-19 cases continued to climb. In Australia, Chile and South Africa, a grand total of just 51 cases of flu were spotted in more than 83,000 tests1. “We know it’s less transmissible than coronavirus, so it makes sense,” says Olsen, but the decline was still “greater than expected”. Influenza’s absence has been attributed to pandemic-response measures, but they don’t tell the whole story.

“Some South American countries haven’t done such a good job controlling COVID, but even there flu is low,” says virologist Richard Webby at St Jude’s hospital in Memphis, Tennessee. “I don’t think we can put it all down to mask wearing and social distancing.” He suspects that the dearth of international travel played a part. Flu typically travels around the world from one winter to another, while maintaining a lower year-round presence in the tropics. Although the mechanisms underlying this behaviour aren’t entirely clear, the movement of people clearly contributes.

By mid-December, the Northern Hemisphere is usually well into the start of its annual cold and flu season — but so far this year, even as the COVID-19 pandemic surges in dozens of countries, the levels of many common seasonal infections remain extremely low.

The pandemic caused by the SARS-CoV-2 coronavirus has infected at least 67 million people and killed 1.5 million worldwide. The patchwork of responses intended to fight the pandemic — from temporary lockdowns to mask wearing, social distancing, enhanced personal hygiene and reduced travel — has had a huge impact on other common respiratory illnesses, too.

In the Southern Hemisphere — now past its winter — seasonal influenza hardly struck at all. That looks as though it might happen in the north, too. Conversely, some common-cold viruses have thrived, and tantalizing evidence suggests that they might, in some cases, protect against COVID-19.

Despite humanity’s long history with colds and flu, the viruses that cause them still hold many mysteries. Scientists hope this year’s disrupted seasons could reveal new information about the transmission and behaviour of these unwelcome annual guests: how these viruses respond to health measures, how they interact and what that might mean for long-term disease burdens. “This is a natural experiment for so many respiratory viruses,” says Sonja Olsen, an epidemiologist at the National Center for Immunization and Respiratory Diseases, part of the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia.

In May, at the tail end of the first wave of COVID-19 deaths in many nations, and when some of the strictest lockdowns were in place, health workers noted an abrupt and early halt to the 2019–20 flu season in the Northern Hemisphere.

That might partly have been an artefact caused by fewer people coming to a clinic for testing, experts say, but it was also attributable to the effectiveness of policies such as social distancing. After the pandemic started, positive tests for the flu virus plummeted by 98% in the United States, for example, whereas the number of samples submitted for testing dropped by only 61%1. In the end, the US 2019–20 flu season was rated as ‘moderate’ by the CDC, which estimates that 38 million people fell ill with influenza, and 22,000 people died. That’s fewer than in recent years, but not unprecedented.

After the flu season in the north ended early, it hardly got going at all in the Southern Hemisphere. There were astonishingly few cases of seasonal flu there from April to July 2020 — even as global COVID-19 cases continued to climb. In Australia, Chile and South Africa, a grand total of just 51 cases of flu were spotted in more than 83,000 tests1. “We know it’s less transmissible than coronavirus, so it makes sense,” says Olsen, but the decline was still “greater than expected”. Influenza’s absence has been attributed to pandemic-response measures, but they don’t tell the whole story.

“Some South American countries haven’t done such a good job controlling COVID, but even there flu is low,” says virologist Richard Webby at St Jude’s hospital in Memphis, Tennessee. “I don’t think we can put it all down to mask wearing and social distancing.” He suspects that the dearth of international travel played a part. Flu typically travels around the world from one winter to another, while maintaining a lower year-round presence in the tropics. Although the mechanisms underlying this behaviour aren’t entirely clear, the movement of people clearly contributes.

Increased influenza vaccination might have contributed to the disappearance, too. Australia, for example, saw more than 7.3 million flu jabs administered by 20 May 2020, compared with 4.5 million by that date in 2019, and 3.5 million in 2018. It’s unclear if that trend will hold in the north.

Vaccination rates in the United States for seasonal flu have been trending upwards for years: slightly more than half of the US population over six months of age was vaccinated in 2019–20, up 2.6 percentage points from the previous year. But it is unclear whether Americans will be more or less inclined towards flu vaccinations this year, particularly given the tumultuous backdrop of the pandemic and the change in president.

Most experts are cautiously betting on a very mild flu season for the Northern Hemisphere this year. That would be good news on many fronts — in particular, it would help to alleviate the potential burden on the health system, from hospitals to testing centres, caused by simultaneous waves of flu and COVID-19. But surprises could be in store.

No one really knows, for example, why one nation, such as Australia, can be hit hard by influenza for several years while a neighbouring country, such as New Zealand, sees very low rates, says Webby. Even influenza’s seasonality isn’t entirely understood, nor exactly how it travels around the globe. “We don’t have a real good handle on why it’s a winter disease,” he says. Untangling lessons about flu from this year’s data will be interesting but difficult, Olsen says, because pandemic policies and compliance vary on the national, state and even neighbourhood level.

And the changing trends could have consequences. If this year’s flu season does fizzle out in the Northern Hemisphere, that could make it harder to predict the right strains to put in 2021’s flu vaccine. It could also have intriguing, longer-term consequences. Webby speculates that a low-flu season might kill off less-common variants of influenza. “A lot of different flus have been circulating in recent years. Are they all going to make it out of this or not?” he asks. “It’s possible that what this season will do is actually make the virological picture a lot simpler. That may be permanent, potentially.”

At the same time, Webby adds, the lack of viral competition in human hosts could conceivably open a door for new swine-flu variants in the future. “We get a handful of those every year, in the agricultural-fair season,” Webby says. “One of the things holding those viruses back a lot is natural immunity. If flu is low for a few seasons, that might leave a gap for swine viruses to have more impact.”

“I am sure that flu will come back with a vengeance at some stage in the future,” says Robert Ware, a clinical epidemiologist at Griffith University in Queensland, Australia, “but it might take a few years.”

Source: Nature

Is the K number the new R number for COVID-19?
Is the K number the new R number for COVID-19?
January 30, 2021 - 8:09 pm

Just a few months ago, no one, aside from epidemiologists and their ilk, had heard of the R number. Now, thanks to the coronavirus, everyone has heard of it and most people can tell you that it’s the reproduction number, an indicator of whether the number of infected people is increasing or decreasing.

The R number is regularly referred to by governments around the world and by news anchors and their guests when discussing the pandemic. Yet no sooner had the public wrapped their head around one mathematical symbol than another cropped up. This time, the letter K. So what do we need to know about K and why has it suddenly become the focus of interest?

The R number represents the average number of people an infected person goes on to infect. If R is larger than one, the number of people with the disease is increasing. The target for control strategies, including lockdown, self-isolation and masks wearing, is to bring R below one and thereby reduce the number of people with the disease.

At the start of the coronavirus outbreak, R in the UK was around three. If every infected person infected exactly three people, the epidemic would have spread as in the figure below.

The R mentioned in the daily press briefings represents an average of the whole country or region, involving millions of people. But its single value hides many differences between individuals and their impact on virus transmission.

Rather than assuming that every infected person and every contact they make follows the same pattern (as with the R number), scientists working on epidemic models allow for the number of new cases caused by each infected person to vary randomly.

Some people might have high viral loads or might simply cough more and hence spread the virus more effectively.

Many people, although ill and highly infectious, don’t show any symptoms. They might make many contacts without realising they pose a danger to others. An example from history is the infamous Mary Mallon (“Typhoid Mary”), a cook in New York City in the early 1900s. Although she carried typhoid bacteria, she didn’t show any symptoms and is believed to have infected more than 50 people over seven years.

People also differ in the way they interact with others. For some, contacts might involve just the immediate family or a small group of colleagues at work or friends. The disease will then only have a chance to be transmitted to a few people. But if an infected person goes to choir practice, a football match or visits several pubs or nightclubs, the number of people who might catch the disease becomes large. Scientists call such massive and rapid outbreaks caused by one or a few infected individuals, super-spreading events, and their initiators are known as super-spreaders. In many cases, 80% of the new disease cases are caused by only 20% of such super-spreading individuals.

Different pathogens will have different ways in which they spread and statisticians use K, the so-called dispersion parameter, to describe how variable the infection can be. For some diseases, the variation will not be large, as shown below.

Simply put, a low K value suggests that a small number of infected people are responsible for large amounts of disease transmission. For the 1918 influenza, the number K is thought to be around 1, and perhaps 40% of infected people might not pass on the virus to anybody else. But for diseases like Sars, Mers and COVID-19 with K as low as 0.1, this proportion rises to 70%. In contrast, large outbreaks will be initiated by only few super-spreaders, as shown below.

There are two reasons why scientists are looking into the role of variability in controlling coronavirus transmission. First, super-spreading events are critical in the late stages of the epidemic when the virus is almost eradicated. Small values of K mean that one infected person can trigger many new cases in a very short time. If this happens, the epidemic can quickly rebound, even if locally eradicated.

Outbreaks in Seoul nightclubs in South Korea, meatpacking plants in the US, and coal mines in Poland show how damaging super-spreading events can be. So governments need to be diligent in identifying the risks associated with the reopening of industries and entertainment. A way to identify and track potential super-spreaders is fundamental to prevent future outbreaks.

But there is also a glimmer of hope. If indeed K is as low as 0.1, 70% of infected individuals fail to pass on the virus. As a result, most cases arriving from outside the country or region might recover without starting a new outbreak. It might, therefore, be easier to eradicate the disease and to maintain the disease-free status than suggested by the average reproductive number, R.

While R is not going to be replaced by K in the daily press briefing, both are needed to understand how COVID-19 spreads.

Source: World Economic Forum

Galen, the “prince of medicine”
Galen, the "prince of medicine"
January 23, 2021 - 3:22 pm

The “prince of medicine” was how Andreas Vesalius described Galen of Pergamum in the second, 1555, edition of his monumental study of human anatomy, De Humani Corporis Fabrica. By then, Vesalius knew how seriously Galen was in error because ancient Greek and Roman taboo had compelled his second-century predecessor to dissect only animals. Still, Vesalius acknowledged a deep debt.

Galen’s reputation as the leading anatomist of antiquity lives on. The most modern edition of his works, in 22 volumes, contains one-eighth of the surviving corpus of classical Greek literature.
But how many of us know about Galen’s life between AD 129 and circa 216? It was eventful and fascinating, whether in his native Pergamum, a Hellenistic city of the Roman Empire in what is now western Turkey, or in scholarly Alexandria, or in imperial Rome, as historian Susan Mattern vividly shows in The Prince of Medicine: Galen in the Roman Empire. It is “the experience of medicine in antiquity” she aims to convey to a modern reader—so utterly different from our experience, but also in some ways familiar.

Galen treated dying gladiators, for example, and thereby disproved Aristotle’s notion that the heart was the seat of reason, by remarking that a gladiator wounded in the heart remained lucid until death. He owed this particular appointment partly to his exceptional audacity in public vivisections. On one occasion, he disembowelled a live monkey and then, after challenging his dumbfounded rivals to act, replaced and secured the intestines in the hideously suffering animal.
On another occasion, he was at home, debating with his household slaves what to do with a rancid cheese, when an old man appeared at his door carried on a litter because he was arthritic with “chalkstones” (Galen’s term). Spontaneously, Galen blended in a mortar some cheese with pickled pig’s leg and applied it to the joints. This plaster apparently caused the skin to rupture and the chalkstones to ooze away through the wound, over a period of several days. The patient was probably suffering from gout. Although the cheese made no obvious contribution by modern thinking, the man procured a second rancid cheese to continue the treatment.

Having gained a stellar reputation in disease-ridden Rome and returned to Pergamum, Galen was recalled by the emperor Marcus Aurelius in order to accompany his army against “barbarian” German tribes. Galen, who apparently never bothered to learn Latin and was ambivalent about joining the Roman elite, wriggled out of what he guessed would be a protracted and gruelling war. Later, however, he learnt that the emperor had permitted dissection of one or more of the slain enemy, and regretted his evasion. “Regarding medical research his passion was intense and unambiguous”, Mattern argues. “There can be no doubt that if he had known he would be allowed to dissect a human, he would have braved the perils and discomforts of the campaign and endured the importunities of the emperor.” As for his colleagues fortunate to have dissected German corpses, Galen showed only scorn. They “did not learn more than butchers know”, he wrote.

Galen’s relationships with his medical contemporaries tended to be highly competitive, even cut-throat. With his intellect, skill, and daring—trained by 4 years as a physician to the gladiators in Pergamum—Galen usually worsted his professional rivals, while also saving his patients. Most of the competition was inevitably very public, taking place in the sickroom, surrounded by the patient’s family, friends, and other doctors. But Galen upped the ante by also offering “anatomy-as-spectacle”: demonstrations of animal vivisection while surrounded by scrolls containing the anatomical works of other physicians. He would ask his audience to name a part for dissection, then operate on the struggling creature and show how reality differed from the anatomy described in his rivals’ manuscripts.

According to Galen, he never charged a patient a fee, and regularly treated the poor for no personal advantage. The only payment he mentioned—a huge gift of 400 gold coins—came from his old friend and patron, the senator and ex-consul Flavius Boethus, for curing his wife. Mattern supports these claims, writing that: “He was a gentleman, a Greek, a leading citizen of Pergamum.

His lifestyle came to him by birthright; but his skill and reputation, by hard work, exhaustive study, experiment, experience, and proven superiority over his rivals.” However, she does criticise Galen’s “enthusiastic endorsing” of the therapeutic practice of bloodletting despite his knowing doctors who had killed their patients by taking too much blood, thereby contributing to the suffering and death of many patients in future centuries. Having read this scholarly, gripping, and often gory biography, one appreciates, exquisitely, the author’s conclusion that Galen, though “not necessarily a good man”, could still be “a good doctor”. Perhaps this has been true of many of the greatest physicians.

Source: The Lancet

Origins of the Cost Curve
Origins of the Cost Curve
January 17, 2021 - 5:56 pm

Political scientists emphasize the importance of “framing” in policy debates. The health care cost control debate in the United States has been reframed by the promotion of a metaphor, “bending the curve.” This metaphor has merits but they are decidedly mixed.

The sudden popularity of the idea of “bending the cost curve” is significant because it shows that, contrary to what policy specialists believe, politicians and interest groups do pay attention to the academic experts. Yet it is significant also because it frames cost control options in a way that favors some approaches at the expense of others, and some groups at the expense of others. In particular it reflects the dominance of the debate by budgetary perspectives, and favors the interests that benefit from high costs now by devaluing approaches that would reduce costs more quickly.

The Rapid Advent Of A Phrase

“Bending the curve” went from unfamiliar to “jargon” at warp speed. At the end of December, 2007, the Commonwealth Fund released a report on “Bending the Curve: Options for Achieving Savings and Improving Value in U.S. Health Spending.” Before that date, I can find, through journals’ own search engines, only one use of a similar phrase (e.g. “bend the cost curve” or “bending the cost curve”) in relation to U.S. health care in either of the two prominent health policy publications, Health Affairs or the New England Journal of Medicine. That was an interview with the Governor of Vermont in October of 2007. I find no use of similar terms in CQ Weekly, the closest thing to an authoritative source about Congress; and only one on the website of National Journal, the magazine and source of daily reports (such as Congress Daily and The Hotline) that is the main competition to CQ as an elite information source in Washington. I find no use in the New York Times from a search back to 1981.

By 2009, Health Affairs titled its September/October cost control issue “Bending the Cost Curve.” The term was ubiquitous in both experts’ and politicians’ commentaries. After skeptical testimony about the cost control effects of legislation by the Director of the Congressional Budget Office (CBO), Congressman Jim Cooper (D-Tennessee) blogged for National Journal that, “(i)n Washington jargon, he said the bills would bend the cost curves in the wrong direction.” (his emphasis) In an interview in February 2009, President Obama referred to the need for “bending the curve down on health care inflation,” not coincidentally in the context of “bending the [federal] deficit curve down.”

Karen Ignagni, CEO of the leading lobby for the health insurance industry, pledged in September 2009 that the industry would “do our part to bend the cost curve.” Senator Chuck Grassley (R-Iowa), senior Republican on the Finance Committee, in December blasted the bill under consideration in the Senate because it failed to “bend the cost curve the right way”. In perhaps the best indicator of a term’s use (or abuse), William Safire devoted one of his “On Language” columns in the New York Times to the “fast-blooming metaphor.”

Political Causes

Even if there were no substantive effects, the spread of this metaphor would reveal key aspects of health care politics. There could hardly be a better indication that expert discussions influence U.S. policy-makers. Moreover, it is a classic example of how health care policy and politics is often driven by budget politics.

What, a visitor from outer space or Europe might ask, is the “cost curve,” anyway? It is not the cost-benefit curve that would be familiar from discussions of “flat of the curve care.” That is a curve of diminishing returns – at some point more spending yields no benefit. The “cost curve” graphs spending over time, usually in units of constant dollars per capita, or share of GDP per capita. In any country this curve tends to slope upward; in the United States it slopes upward somewhat more steeply than in many countries, and from a higher base. It is a curve of increasing returns – to the health care sector, which gains an increasing share of the national economy.

“Bending” the curve means downward, to reduce the slope, so that spending will not be as high in the future as it would under current projections (in theory one could bend the slope negative, but that would not be “bending the curve,” it would be “cutting spending”). The message of this metaphor is about the future: that health care costs otherwise will at some point be “unsustainable,” so we must act now to prevent that from happening.

This raises a bit of a puzzle. One might expect that, with U.S. health care costs in 2008 sitting at 16 percent of GDP, and the next highest country just over 11 percent, politicians and business leaders and academics would have thought that the problem was that costs were too high at the time, rather than that they should be prevented from becoming too high in the future. Why, then, would anyone focus on the “cost curve,” rather than the costs?

One logical answer is that it’s a lot less threatening to the medical care establishment to talk about slowing cost growth in the future than about taking away some of their incomes now. One can have much more pleasant discussions, in which even the insurance companies will say they agree with the goal. Conflict is delayed or, more precisely, submerged. This pattern is reinforced by the policy choices usually associated with “bend the curve” rhetoric, as I discuss below. The Commonwealth Fund leadership surely did want to control costs, and sooner rather than later. But the term was picked up so widely, I suspect, in part because it is in many ways convenient to direct attention to the future rather than the present.

There is another reason the term was attractive: it fits with established patterns of both U.S. budgeting and crisis-mongering. Congressional budget procedures require that effects of legislation be estimated a decade into the future, and the CBO frequently reports on long-term deficit projections. The trustees of the Social Security and Medicare trust funds are also required to project balances far into the future. Therefore long-term projections of spending for health care programs, with graphs of potential trends, are an established part of the discussion.

But long-term projections have also become part of the political arsenal of the coalition of centrists and conservatives who, for different reasons, seek to raise fears about supposedly excessive federal spending. Throughout the budget battles of the 1980s and early 1990s, as the deficit did not do much immediate damage, budget hawks sought to scare others into action by extrapolating trends into a future when deficits might be enormously large, and so do economic damage. These arguments have focused on long-term projections of the costs of Social Security, Medicare and Medicaid, grouped as “entitlements,” with particular emphasis on the supposed crisis to come from an “aging society”. At present deficits actually are enormously large, but as a matter of economic necessity. So economists, as in a March 24, 2011 statement by 10 former chairs of the president’s Council of Economic Advisers, continue to emphasize the long-run: as in that group’s statement that, “repeated battles over the 2011 budget are taking attention from a more dire problem—the long-run budget deficit.”

Thus the health care “cost curve” fits easily into established thinking about long-term budget trends. President Obama’s connecting of the two topics is entirely normal in Washington, and the first use of a version of the term that I found was in the context of deficit-hawk politicians raising concern about the future in 2003: Republican Congresswoman Nancy Johnson saying that, “we have to bend the cost curve as the baby boomers retire”.

Analysts who focus on health care costs as a whole, or who believe social insurance programs are extremely important, have objected to this budgetary framing. They, including leaders of the Obama administration, have emphasized that the “budget” problem was really a “health care” problem. The problem is not the “entitlement” to care, but the system-wide increase in medical costs per capita.

From this perspective, the focus on budgetary costs of health care is particularly misguided in blaming the “entitlement” to medical care. We can see why by comparing the United States to other countries. The effects of aging on budgeted health care spending in the United States is particularly large in proportional terms not because the entitlement in the U.S. is excessive but because it is unusually limited. In the United States, for most people, on their 65th birthday, a large expense suddenly shifts to the federal government’s budget. In any other country, they remain in the same system they were in before. So the budgetary effect of aging in the United States is largely a cost shift, with corresponding savings to private budgets, rather than a cost increase. Moreover, the effect of population aging on government medical spending is particularly large in absolute terms in the United States because our baseline level of spending per person is already so much higher than in any other country.

For supporters of national health insurance and the Medicare program, the emphasis on the federal budget both overstates the societal effects of aging and diverts attention from most of the cost control challenge. Hence it seemed logical to meet the arguments about budgetary trends with arguments about system-wide medical spending trends. To do so, however, meant adopting the same frame about long-term “sustainability.”

Thus the “bending the curve” metaphor was picked up because it fits into the dominant discourse about a federal budget crisis, attracting conservatives and budget-focused elites; it is less threatening to the health care establishment than calls to “cut costs” would be; and it served as a liberal response to the overemphasis on the budget in the policy discussion about health care costs.

The difficulty is, “bending the curve” is a flawed way to think about the policy challenge. By focusing on the future, it diverts attention from cost controls that would have more immediate effects. In the middle of the worst economic crisis since the 1930s, that may be a good idea for budgeting. It is not such a good idea for health care spending.

The Metaphor’s Assumptions: A Flawed Guide To Policy

The assumption behind the metaphor is that there is a functional relationship of costs over time; presumably not caused by time but by some set of independent variables (technology, insurance, or whatever). So we can “bend the curve” at time X (say, in health care reform legislation in 2010) by changing those variables, with a predictable and desirable effect at time (X + Y).

This assumption has a major flaw: it downplays human agency. Policies do not simply play out and have predictable effects. People who object to the planned effects fight back. Health care costs at any time are the result of, among other things, efforts by people who earn their incomes from the system to extract money from it. If prices are lowered, providers may try to increase volume; if volume is constrained they may try to raise prices; if employers and insurers demand better prices the providers consolidate to increase their market power; if regulation is successful the providers claim the public is being denied quality care or campaign to create parallel markets where people can pay more for more “choice.” Whatever policy-makers do in Year One, the health care industry will seek to undo by Year Five or Year Ten. The metaphor of “bending the curve” ignores the fact that health care spending is a political/economic struggle. Either there is no function, or policy-makers are not the only ones who get to manipulate the terms of the function.

The flaw matters because the “bending the curve” metaphor directs attention to what its advocates would call “fundamental change,” and supports scorn for mere “short-term measures.” In the U.S. debate this was manifested especially in claims that reform had to reorganize delivery systems and the whole incentive structure of medical care, and in dismissal of factors that explain the differences between current spending in the United States and other countries. The major differences are prices and administrative costs, but in a typical report on “steps to address long-term spending growth,” ten of the best-known analysts in the United States started “from the conclusion that the standard short-term measures to address rising costs, like reducing prices, are not sufficient to succeed.”

This kind of perception is reinforced by an underlying belief that the dominant delivery system reform agenda – measures such as “integrated delivery systems, bundled payments, and more sophisticated comparative effectiveness analysis” are much more attractive than “crude” measures such as “across-the-board cuts in payments.” Even analysts who have long emphasized the need to adapt a system to have the same advantages as those in other countries can be caught up in the argument that much more fundamental changes are needed. Thus Tim Jost editorialized that a new Independent Payment Advisory Board created by the 2010 legislation was flawed because the “requirement that the IPAB submit annual proposals will encourage recommendations for short-term payment fixes rather than long-term changes that might in fact bend the cost curve.”

The evident problem with this focus on long-term measures is that nobody knows how to implement the various theories being proposed, such as how to create high-value “accountable care organizations.” On the one hand, the long-term focus makes it easier to advocate measures that we do not know how to do now: it is easier to advocate half-baked ideas if there is still time for some baking. On the other hand, as a taxpayer and citizen I would prefer not to rely, for cost control, on notions such as that, “these changes could spark a productivity revolution in health care that would make it much more affordable and simultaneously increase the quality of care.” The “could” is not reassuring, and the “productivity revolution” concept risks ignoring the challenge of capturing the benefits of increased productivity for the payers, rather than the providers. One of the reasons for addressing prices is to ensure that, for example, technological advances that make cataract surgery less expensive are reflected in lower prices, rather than simply higher earnings.

The de-emphasis of prices and administrative costs as “crude” concerns must be comforting to insurance company managers and medical providers. As an approach to long-term costs, however, it ignores a basic rule of mathematics: that the product of the operation of a rate of growth on a base can be altered by changing either the growth rate or the base. Hence long-term spending projections for Medicare were cut substantially by the sharp slowdown in Medicare spending in the late 1990s. A recent analysis in Health Affairs projects how shifting the level downward at any given time can have major effects on future costs; both reducing the level and reducing the growth rate are important.

Hence the “bending the curve” metaphor has two flaws as a guide to cost control. First, it suggests that there are measures that could be taken which would definitively shape future costs. This is at best questionable. Second, it directs attention away from measures that would reduce costs in the short term. This is particularly unwise since controlling costs in the short term is one of the better ways to influence future costs.

A Dangerous Metaphor, But Real Questions

The fact that we can graph costs leading up to the present does not mean that systems are on a mathematically predictable path. Future costs cannot be determined at a single point in time. They will depend on policies, responses, and unexpected events at many different times in the future: next year, in three years, in five, in eight, and so on. To a great extent, health care spending control must operate in the present tense, and controllers ought to be modest about the future.

Yet there are questions and policy choices that require judgment and evidence about results fairly far in the future. Although cost control is an endless battle, certain system features can normally favor one side or the other. For example, there are reasons to believe that systems that provide insurance to cover charges from providers tend to make it more difficult to control spending than systems that entitle people to access a government sponsored health service (Note 1). Similarly, there is strong evidence that all-payer price regulation is more effective than selective contracting if the goal is to reduce prices.

Each of these patterns has exceptions that prove the larger rule: that cost control requires continual effort. There have been times when spending grew more quickly in Sweden than in Germany, and times when it grew more quickly in Germany than in Sweden. Selective contracting controlled prices more successfully in the United States in the mid-1990s than it normally does. Still, it makes good sense to work to create institutions that provide better cost control tools in the future.

There are many reforms that might improve cost control in a given system in the future, and if we were only to focus on immediate effects we could miss useful options. Policy options such as increasing the number of primary care providers or installing better electronic medical records, could only save money, if they do so at all, in the long run. That is not a reason to reject them.

Yet it is a reason to be very cautious about such ideas, and to look for compelling evidence, preferably based on experience rather than deduction. The fact that something requires deep systemic change does not make it a good idea. Given the uncertainties about long-term approaches, it is even more important to maximize success in the short run: that is, adopt measures that somewhat restrict costs with acceptable consequences for other values.

I do not mean to suggest that excessive focus on the future is the only reason why policy-makers hesitate to address costs more quickly. The many parts of the medical industry are powerful and resist restrictions on their earnings. If the 2010 health care reform laws had included more immediate cost controls, they probably would not have passed. Yet, precisely because of such difficulties, it is important to the maximize political will for cost control and an understanding of what will work best.

From this perspective, the merits of framing the cost control problem as how to “bend the curve” are outweighed by the risks. Framing the problem this way risks believing that policy has more control over the future than it possibly can; risks ignoring the extent to which cost control is a political struggle rather than a technocratic challenge; and directs attention to situations about which we know and can do less (the future) rather than about which we know and can do more (the present). And, while this need not be the case, and I believe was not the intent of the idea’s originators, as used in the U.S. debate the focus on “bending the curve” has favored speculative ideas over measures with which there is more experience.

Source: Health Affairs

The Gospel of Wealth and the National Health
The Gospel of Wealth and the National Health
January 10, 2021 - 5:28 pm

The Rockefeller Foundation’s (RF) engagement with the British National Health Service (NHS) between 1945 and 1960 fundamentally changed the relationship between politics and health on the international stage. The foundation morally invested in the success of the NHS because, to them, it offered a world-inspiring model for how to provide medical care following the tenets of social medicine. The RF administratively and financially supported two health centers, in Edinburgh and Manchester, to help realize these ambitions.

While the development of both centers exposed conflicting understandings of social medicine, these facilities later became important examples when British health centers expanded in number after the mid-1960s. But the shift toward more communal forms of general practice provoked unease regarding privacy among patients. However, strategies used by medical professionals to offset these anxieties helped facilitate public acceptance of forms of care that aligned with the communitarian values of social democracy.

The connections between American private philanthropy and British state planning show how a routine visit to the doctor in Edinburgh or Manchester in the 1950s was implicated in the broader politics of postwar global health.

Source: Bulletin of the History of Medicine

Escape Communities of 1918 Influenza Pandemic
Escape Communities of 1918 Influenza Pandemic
January 4, 2021 - 7:12 am

Medical historians who study the 1918 Influenza pandemic have a term for communities that experienced a more severe second wave following a more mild initial wave – escape communities.

Bryn Mawr College was among the most provisional of the influenza escape communities we studied. This is because while there were zero deaths resulting from influenza during the second wave of the pandemic, there were 110 cases of influenza (a case rate of 23.6% of the campus student population, which is on par or above that seen in harder hit communities). Nevertheless, because this case study raises a number of pertinent issues related to the wide spectrum of NPI taken in 1918, we included it in our report.

The first reported case of influenza at Bryn Mawr College occurred in late September 1918 in a student staying at the College Inn. The possibility of the spread of the disease was quickly made apparent, as the patient received regular student visitors. President Thomas therefore immediately attempted to have the patient moved either to the Bryn Mawr hospital or to the campus infirmary, where she could be effectively isolated.

By October 1, campus administrators had begun to enact an “absolutely strict quarantine”—by which was meant a series of NPI designed to mitigate the spread of influenza—in an attempt to deal with the “very serious outbreak of Spanish influenza” that had erupted on campus. Thomas had a strong belief in the efficacy of influenza vaccination (which, as noted elsewhere in this report, turned out to be based on an entirely different microbe than the virus that causes influenza and, hence, not efficacious), and quickly ordered its widespread use on campus. All members of Bryn Mawr’s teaching and executive staff who commuted from Philadelphia via train, along with all managers, wardens, and housekeepers, were vaccinated at the college’s expense. Students and on-campus faculty and staff were offered the vaccine at the cost of $1.00.

A series of even more restrictive measures were then implemented. Students were advised to avoid crowds (yet they were also expected to go to chapel and association meetings) and to get plenty of both exercise and rest. Students were forbidden to enter theaters and other places of public assembly, were prohibited from crossing Montgomery Avenue (the main street separating campus from town) and were informed they could not ride public transportation. Furthermore, non-resident students were excluded from the college unless they lived near enough to campus to walk. Off-campus visitors, including mothers, were henceforth prohibited from entering residence halls; mothers were allowed to see their daughters only if the daughters were ill and being cared for at the infirmary. Students were likewise forbidden to visit private homes (even those on the campus side of Montgomery Avenue) without the express permission of the dean. All gatherings save those of an academic or religious purpose were prohibited. In late October, in response to a new regulation from the Pennsylvania Board of Health calling for an end to public gatherings and recommending the closure of schools, Thomas ordered the four-day quarantine of all students returning to campus from home.

Despite these restrictions, life at Bryn Mawr seemed to continue in a fairly regular fashion, and the various NPI to prevent the spread of influenza do not appear to have been as strict as they could have been. In the first week of October the college held its thirty-fourth annual opening ceremony in Bryn Mawr’s overflowing chapel. Liberty Loan rallies, tennis tournaments, hockey games, and chapel services continued throughout the semester. In early November, the traditional “Lantern Night” event (a ritual in which freshmen are handed colored lanterns by sophomores while singing Pallas Athena) was held before “a quarantine audience of Faculty and upperclassmen.” Some students were also allowed to sleep in residence halls other than their own, a violation of the campus health department orders. At least one student, apparently unaware of the protective sequestration and the ban on leaving campus, was discovered to be regularly wandering the aisles of Wanamaker’s department store in downtown Philadelphia.

Whether as a result of lax measures or from other causes, influenza did spread throughout the campus. On October 17 the school newspaper reported 42 cases of influenza, four of which had developed into bronchial pneumonia. By the end of the second wave of the pandemic in mid-November, the college had experienced some 110 influenza cases (not including those infected at home) out of a total population of 465 students (or 23.6% of the campus population). Several faculty members, including Dean Helen Taft (daughter of former President and Chief Justice William Howard Taft), also became ill. No deaths, however, were recorded as a result of these infections.

Source: Univeristy of Michigan Center for the History of Medicine

The Origins of COVID-19
The Origins of COVID-19
November 2, 2020 - 7:45 pm

The origins of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is part of a larger story of bat biology, animal markets, and animal to human transmission.

Researchers examining coronaviruses and bats found that almost 9% carried at least one of 91 distinct coronaviruses. The authors estimated that there are at least 3200 coronaviruses that infect bats. Moreover, there are over 1400 species of bat. Figuring out which ones are susceptible to which coronaviruses is no small task. Bats are incredibly varied and successful creatures.

A paper published in July, 2020, traced the origins of SARS-CoV-2. The researchers concluded that it came from a virus with relatively generalist properties circulating in horseshoe bats. “Everything points to a bat sarbecovirus reservoir; we are very confident about this”, said David Robertson, head of bioinformatics at the Medical Research Council–University of Glasgow Centre for Virus Research, Scotland, UK, and co-author of the paper. The evolutionary analysis suggested that the lineage from which SARS-CoV-2 emerged has been present in bats for several decades.

“The generalist property of the virus means an intermediate host is not required for any evolutionary change”, said Robertson. “As the virus has been around for decades it may have emerged in another host and this could be the missing intermediate species but we are inferring that this would only facilitate transmission.”

The fact that SARS-CoV-2 was first detected in Wuhan, China, far from where the horseshoe bat is found, hints at the presence of an intermediary.

Some have posited that the pangolin could be this missing link. Pangolins have reportedly fallen sick as a result of coronavirus infection, which would mean they are not a natural reservoir. But that leaves the possibility that the pangolin is facilitating transmission to humans. SARS-CoV-2 can jump to other animals such ferrets and cats. “The virus would not need to evolve in the pangolin, it would just need to be brought into contact with humans”, explains Robertson. And it is still too soon to rule out direct bat–human transmission.

Still, there is one theory that can be dismissed. From the earliest days of the pandemic, there has been speculation that the new virus had escaped, or even been deliberately released, from the Wuhan Institute of Virology. At a White House press conference on May 1, 2020, US President Donald Trump declined to assert that SARS-CoV-2 had occurred naturally. When asked what gave him a “high degree of confidence that this [virus] originated from the Wuhan Institute of Virology”, Trump replied “I can’t tell you that. I’m not allowed to tell you that.”

“If the virus had been human-made, that would show in its genome”, counters Robertson. “Besides, if you were going to create a coronavirus that can be transmitted by humans, you would almost certainly start with the first SARS virus. SARS-CoV-2 is like nothing we have seen before. It really is highly unlikely that someone created it; it is not put together from pieces we know about.” SARS-CoV-2 is closely related to other beta coronaviruses such as RaTG13, a bat virus that the Wuhan Institute of Virology has been working on. But it only shares 96% of its genome sequence with RaTG13, which makes them roughly as similar as human beings and chimpanzees, and points to a common ancestor rather than one springing from the other.

The plethora of bat coronaviruses, coupled with the uncertainty about the role of an intermediary animal, makes it tricky to know how to go about preventing a future spillover. Live animal markets are an obvious risk for the emergence and spread of zoonotic diseases, but they are part of the culture of south east Asia. “Certainly having a society which did not have such an interface with animals would be helpful, but I am not at all convinced that we should be telling chunks of the world that they should not be buying live animals”, said Perlman.

Learn the amazing story of how Maimonides became the Sultan’s Physician
Learn the amazing story of how Maimonides became the Sultan's Physician
October 11, 2020 - 11:54 pm

Everyone at the court of Sultan Saladin of Egypt was happy when the great Maimonides, Rabbi Moshe ben Maimon, was appointed personal physician to the sultan. Everyone, that is, except Hakim, the Muslim physician who had held the position before and was now given second place. Maimonides would now treat the sultan and his immediate family, while the Muslim physician was left to treat other members of the royal household and court.

Ever since Maimonides had come to Fostat, the old city of Cairo, his reputation as a physician had spread quickly. The Jews regarded him as the greatest scholar and Talmudist of the age, but to the non-Jews he was the greatest physician of the age. Rich and poor flocked to him for medical treatment, and he treated the poor, Jew and non-Jew alike, entirely without charge. The more Maimonides became known, the more was the Muslim physician forgotten. A deep jealousy and hatred for his Jewish rival filled the heart of Hakim, and he began to scheme and plot in order to discredit Maimonides in the eyes of the sultan and bring him to his doom.

One day Hakim came before Sultan Saladin and told him that he had discovered a plot to poison the sult anand that none other than Maimonides was at the bottom of it.

The sultan paled with fright, but could not believe such a thing of his trusted physician and friend. “If you can prove that what you say is true, I will have Maimonides beheaded; but if you cannot prove it, I shall have you beheaded instead,” the sultan said.

“I can certainly prove it,” the Muslim physician said, “and this is how: It is known in our medical profession that a deadly poison can be made harmless by a stronger poison. Now, let the king order us both to prepare the strongest possible poison, so that if the king will be given poison in his food, all he will have to do is to take the strongest poison and his life will be saved.”

“That is an excellent idea,” the sultan said, “but how am I going to know which of yours is the strongest poison, and how will you prove that Maimonides plots to kill me?”

“This is simple, Your Majesty. When we both bring our prepared poisons, I will gladly take the poison prepared by my rival, and then drink my own poison, and be none the worse for it. Let Maimonides then take my poison and afterwards his own, and he will die. You will then know that he was not truthful with you and plotted against you.”

“This means that I am going to lose one of you, but it will be worth it, for I will then know who is my real friend,” the sultan said.

The next day, the sultan ordered both physicians to appear before him.

“My dear physicians,” the sultan began. “Last night my Prophet came to me in a dream and told me that one of youhe did not say which oneis plotting to poison me. Now, do not interrupt me, I know you will both deny it, of course, and perhaps both of you would be right. However, I cannot treat the matter lightly. Can you prepare a medicine for me that would make any poison in the world harmless?”

Both physicians answered “Yes!”

“Fine, but how am I going to know which is the strongest? Well, we will have to have a little test: tomorrow both of you will bring to me your prepared medicines. Then we will carefully divide up each medicine in two parts, and each one of you will drink the others poison and then his own. . . .”

“But Your Majesty,” Maimonides said, “that would kill my good friend standing here by my side.”

“My rival is only trying to get out of it, Your Majesty. I dont mind a bit, taking the test. I will be glad to take his poison and prove to you that mine can make it harmless.”

“I am glad that both of you are sure of yourselves; that makes it a fair test,” the sultan said. “Gentlemen, the thing is settled. I will see you tomorrow at noon.”

Thoughtfully Maimonides walked out together with his rival. He did not at all like the satisfied smile on his rivals face. What was the fellow up to?

He thought about it as he rode home on his donkey, but could not understand it. Surely, Hakim must have known that he, Maimonides, could prepare a stronger poison; why should he take such a chance? Or perhaps he had thought up some trickery? Hakims happy expression betrayed some secret plan, but what might it be?

When Maimonides came home, he found the waiting-room filled with people, as usual. Some of them were patients, others were community leaders, still others, scholars who came to ask his insight into difficult passages in the Talmud. Maimonides greeted them all with a smile, and begged them to forgive him while he took some food, as he had not eaten anything that day, for he would not have anything to eat at the palace. After a hurried meal, Maimonides attended to the patients, then talked to the community leaders and scholars. By the time he had finished with all his visitors it was nearly sunset. He recited his prayers, sat down to his studies and writings, and finally retired to bed in the early hours of the morning, thoroughly exhausted.

During his busy day and evening, he had had no time to think about the important event that was to take place at the sultans palace the following day. Now, lying in bed, he could not fall asleep immediately. He had a premonition that his life was in danger and that his mortal enemy, Hakim, was at the bottom of the “life and death” contest. Suddenly light dawned on Maimonides! He knew now what the wily Hakim had thought up, and he also knew how to outwit him! Maimonides felt calm and relaxed, and soon fell asleep.

The following morning Maimonides rose early, and after reciting his prayers and taking time off for some study, he ate a light breakfast. Then he went into his laboratory and prepared a harmless solution of sweet water with red wine. He then rode off to the palace. Hakim the physician was already there, and seemed quite impatient to get on with the contest. The sultan was ready, too.

At the sultans signal, Maimonides and Hakim poured about half of their medicines into empty bottles which they had brought for this purpose, and exchanged bottles.

“Your turn first, Hakim,” the sultan said.

Hakim lost no time. He swallowed the mixture which had been prepared by Maimonides, then swallowed his own. He remained quite steady on his feet, with a broad smile on his face.

“Your turn next, Maimonides,” the Sultan said.

Slowly Maimonides swallowed the mixture which had been prepared by his adversary, and then drank his own. He, too, seemed none the worse.

For a few moments all three stood there, silently and tensely. Suddenly, Hakim cried out in an agony of pain. He dropped to the ground in painful convulsions, and soon lay dead.

“I am glad, my dear Maimonides, that you are all right,” the sultan said. “I did not doubt for a moment that you were the greater physician. As for that miserable wretch, I never liked him, and I am glad you killed him.”

“But your majesty, I did not kill him. He did it by his own hand,” Maimonides said.

“I dont understand,” the sultan said.

“Permit me to explain,” Maimonides began. “Hakim knew that I could prepare a stronger poison than he could, so he thought of a vicious plan: he would take a slow poison at home before coming here, then bring with him a harmless solution. By drinking what he thought would be a stronger poison which I would bring with me for the contest, he would be cured of the slow poison he had taken at home. He would then drink his own harmless mixture and remain well. On the other hand, I would drink his harmless solution, then drink my own strong poison, and thus, he thought, I would die by my own poison. . . .”

“The treacherous dog!” the sultan hissed. “But what really happened?”

“Well, your majesty, suspecting this trickery, I also prepared a harmless mixture. . . .”

The sultan thought for a moment, then burst out laughing, not letting Maimonides finish. It was all as clear as daylight.

“Not only are you the greatest physician, Maimonides, but you are also the wisest of men,” the sultan said. “From now on you shall be my adviser as well as my physician.”

Dr. John Snow was the first to use mapping techniques to discover how Cholera is spread
The IHME again revises its COVID-19 predictions for the remainder of 2020
August 11, 2020 - 1:04 pm

Cholera was one of the deadliest diseases to affect Britain in the nineteenth century causing a series of pandemics in London in the 19th century.

In the nineteenth century it was believed that the disease was transmitted and spread by a ‘bad air’ or ‘bad smells’ from rotting organic waste. This thinking dominated official medical and government statements. But it was not until 1854 that the physician John Snow (1813-1858) made a major contribution to fighting cholera when he was able to demonstrate a link between cholera and the contaminated drinking water through his disease maps.

John Snow was born in York on 15 March 1813. He went to Newcastle upon Tyne at the age of 14 to work as an apprentice for the surgeon William Hardcastle. He then went on to study at the Newcastle Infirmary. During the 1831 outbreak of cholera in the North East, he attended to sufferers in the Killingworth Colliery. The excellent observations he made on the disease at this time formed the basis for his later work.


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