The Great Influenza

by John M. Barry

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Part 6: The Pestilence Summary

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Last Updated on June 8, 2022, by eNotes Editorial. Word Count: 1089

Chapter Twenty

The influenza virus is “transmitted so effectively that it exhausts its supply of susceptible hosts.” In 1918, the influenza virus spread “rapidly and widely.” In the majority of cases, people endured and recovered. In a minority of cases, however, the virus exhibited such unusual and severe symptoms that scientists wondered if it was a new disease.

In the West, the virus “demonstrated extreme virulence or led to pneumonia” in ten to twenty percent of cases. In parts of the world less exposed to other influenza viruses, the rate was even higher.

Common symptoms of the disease followed typical influenza signs: headache, achiness, fever, chills, congestion, nausea, and coughing. In the minority of cases—the ones that became violent attacks—the disease often caused intense pain. People suffered numbness, clumsiness, shaking, high fever, and “ghastly symptoms of intestinal poisoning.” Victims of the influenza pandemic “came with an extraordinary array of symptoms,” causing the disease to be “routinely misdiagnosed.”

Some symptoms, such as subcutaneous emphysema—“pockets of air accumulating just beneath skin”—had not been seen before. Doctors noted “extreme earaches,” intense headaches, paralysis, and loss of vision and smell.

Cyanosis was a particularly chilling symptom: sometimes victims’ entire bodies “partook of a dusky, leaden hue,” and medical staff treated such patients as “the walking dead.” The occasional symptom of “blood pouring from the body”—trickling and even spurting from the “nose, mouth, even from the ears or around the eyes”—was also terrifying.

The influenza virus of 1918 killed many, but it was also unusual in its selection of victims. During the pandemic, “young adults, the healthiest and strongest part of the population, were the most likely to die.” Among young adults, pregnant women were the “most likely of the likely to die.”

The virus posed many puzzles for scientists, some of which were not understood for decades. In the meantime, it spread across the world and, in its victims, “left almost no internal organ untouched.” Some of the damage done in the body, particularly in the lungs, had only been seen in cases of pneumonic plague or death from toxic gas.

Chapter Twenty-One 

The 1918, influenza virus “struck so suddenly that many victims could remember the precise instant they knew they were sick.” Across the world, there were reports of people who simply collapsed and died.

For pathologists and physicians, the lungs of the dead were a source of mystery. The later a victim died after the initial symptoms of the disease, the more likely it was that their lungs would resemble the lungs of “normal pneumonia, bacterial pneumonia” during autopsy. Those who died quickly, however, had lungs that “bore no resemblance to normal pneumonias at all.” These lungs caused pathologists to wonder if they were faced with an entirely new disease.

The purpose of the respiratory tract is to “transfer oxygen from the air into red blood cells.” The entire system, Barry writes, can be imagined as “an inverted oak tree.” The tree trunk is the trachea, or windpipe, which carries air into the lungs. This trunk divides into the “primary bronchus,” the path for oxygen to get to both the right and left lung. Within each lung, the branches become smaller and smaller. Emerging from these branches, called bronchi and bronchioles, are “clusters of tiny sacs called alveoli.” These are like “tiny but porous balloons,” and it is in the alveoli that “the actual transfer of oxygen into the blood takes place.”

A healthy lung is “light, spongy, and porous.” A healthy lung sounds different from a congested lung; in a congested lung, “crackling or wheezing sounds” can be heard. In bronchopneumonia, bacteria infects alveoli, causing the alveoli to become dense and “consolidated.” In lobar pneumonia, an entire section of a lung—called a lobe—“becomes consolidated and transformed into a liver-like mass.”

During the 1918 pandemic, pathologists did see the typical damage done by bronchopneumonia and lobar pneumonia. In victims who died quickly, however, “those lungs were different.” It appeared that “toxic damage” had been done to the alveolar walls, and “very little evidence of bacterial infection could be found.” Instead of the inside of the alveoli being the site of infection, the area between the alveoli were filled with “debris of destroyed cells,” blood, and “every element of the immune system.”

These strange lungs were evidence that it was the immune system itself that was “[ripping] apart” victims’ lungs. Because of its importance, the respiratory tract is typically well defended. Specific types of white blood cells “that seek and destroy all foreign invaders… patrol the entire respiratory tract and lungs.”

The immune system is “at its core a killing machine.” Sometimes, the balance between “kill and overkill” is thrown off. In 1918, young adults were not dying from the virus. Instead, “the killer was the massive immune response itself.”

The influenza virus begins an attack on the body by attaching itself to epithelial cells, cells that “line the entire respiratory tract.” After invading a cell, the virus reproduces at a phenomenal rate and begins weakening the immune system. The immune response of inflammation is caused by white blood cells releasing proteins called “cytokines.” Cytokines have “toxic effects,” and any influenza symptoms outside of the respiratory tract are actually caused by cytokines.

The virus of 1918, unlike many other influenza viruses, successfully went beyond the upper respiratory tract and invaded the inner lungs. The immune system “followed the virus into the lungs and there waged war.”

Young adults have the strongest immune systems, a fact that “normally makes them the healthiest element of the population.” In 1918, it was the strong immune systems of young adults that “filled the lungs with fluid and debris, making it impossible for the exchange of oxygen to take place.” Ironically, “the immune response killed.”

Over fifty years later, scientists began to officially recognize a phenomenon called ARDS: acute respiratory distress syndrome. Many of the unusual lungs noted in 1918 would today be diagnosed as ARDS. Even modern medicine cannot stop ARDS; it can only “[keep] the victim alive until he or she can recover.”

Only a diagnosis of ARDS explains the deaths of those who died within a few days during the 1918 pandemic. Most non-ARDS deaths were caused by bacterial pneumonia. The virus’s destruction of epithelial cells and, possibly, its ability to make it easier for specific bacteria to attach to lung tissue, made victims of the virus susceptible to bacterial infections. Various types of bacteria—these “second invaders” following influenza—have become resistant to antibiotics, making them more lethal today than they were in 1918.

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