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The Second History of Man
The Second History of Man
The Second History of Man
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The Second History of Man

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In the spirit of medieval writer Chaucer, all human activity lies within the artist’s scope, the History of Man Series uses medicine as a jumping off point to explore precisely that, all history, all science, all human activity since the beginning of time. The jumping off style of writing takes the reader, the listener into worlds unknown, always returning to base, only to jump off again. History of Man are stories and tales of nearly everything.


 


The Second History of Man focuses mostly on bacteria and bacterial infections as the foundation, jumping off into Darwin and evolution, gin & tonics and the discovery of the first antibiotic to treat infection (and it wasn’t penicillin), visiting with those clever chaps who cook up drugs in the lab. We’ll call upon poets & poetry, celebrities like Frank Sinatra, the Rat Pack, and Bobby Darin, the classical music of Haydn, Mozart and Beethoven, the tragic story of World War II, Anne Frank and the Holocaust, tuberculosis, and a few of the rich & famous who suffered from TB, travelling back in time to the Black Death which wiped out 25 percent of humans on Earth, exploring the origins of a salon and a saloon, Columbus and the Age of Discovery, the lost generations of childhood, ending with the invention of the Internet.

LanguageEnglish
PublisherPublishdrive
Release dateMay 16, 2024
ISBN9798711953517

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    The Second History of Man - John Bershof, MD

    1

    GIN & TONICS

    There I was with wife and daughters, New Year’s Eve 1995 in Tampa visiting with my mother-in-law, having done the Disney World thing in Orlando. My sister-in-law Deborah quite ill in California with a lower respiratory illness, and me doing my best impersonation of trying to stay out of it. You can’t dial a patient into better health who is not your patient, you can’t dial a patient into better health who is on the other side of the country. Attempts to pull me into that California whirlwind were met with all the resistance I could muster in Florida. That’s what was unfolding before me when I was vacationing in Florida and Deborah was laid out ill in her Los Angeles home, me the reluctant physician trying desperately to not get involved in a situation I had no control over. It’s sort of like Michael Corleone’s lament in The Godfather Part III 1990: Just when I thought I was out, they pull me back in! Yes it is true, men quote The Godfather movies with much abandon: Clemenza: That Sonny's runnin' wild. He's thinking of going to the mattresses already, in which going to the mattresses means going to war with rivals using ruthless, brutal tactics. Although I suspect the brutal part is not exactly what Joe Fox played by the ever-skilled Tom Hanks meant when he said to Kathleen Kelly brought to life by delightfully beautiful Meg Ryan in the wonderful 1998 romcom You’ve Got Mail: Go to the mattresses. You’re at war. It’s not personal, it’s business. As for medicine and not getting involved, there are actually laws within the medical practice act for most states that censures physicians taking medical care of family members. Why? One word: duress. Duress leads to poor decisions and poorer outcomes. Which is why through my intermediary, my mother-in-law Barbie, I refused to take the phone call, refused to get involved in a situation I had not control over, and in the strongest terms possible, made it clear a visit to the emergency room for Deborah was the only course of action.

    But then that phone rang.

    Earlier that evening, Alan had asked that I phone in, from Tampa to a Los Angeles pharmacy, antibiotics for Deborah, a request coming to me through my intermediary, my mother-in-law Barbie—a request I refused. At that point, I knew that Deborah had crossed over to the dark side of human infection, had zipped past Hippocrates’s crisis point—sometimes called the tipping point—where a person either gets better or does not get better. I knew prescribing a course of oral antibiotics would just further delay a foregone conclusion, one that had likely become inevitable hours or a day or two earlier. Oral antibiotics at that point in her disease progression would be like bringing harsh words to a gun fight.

    And speaking of guns, I knew Deborah needed big-gun IV antibiotics—the equivalent of an Avada Kedavra spell for pathogens—probably two or three Avada Kedavra–level antibiotics that would be able to hammer a broad range of bacteria, antibiotics delivered not by snail-mail oral but rocket-speed IV infusion. (Avada Kedavra, if you didn’t know, is the ultimate Killing Curse from J. K. Rowling’s always enthralling Harry Potter series.) Oral antibiotics take a day or two to reach therapeutic levels. IV antibiotics, on the other hand, are therapeutic practically by the time the nurse hangs the IV bag and walks out of the room. IV infusion bypasses the time delay caused by the intestinal absorption of oral antibiotics (that first require a transit through the liver, which is where all blood leaving the gut goes, a sort of filter system, before being allowed into the rest of the body), such that IV antibiotics deliver a devastating blow to bacteria more quickly, more lethally. Further, some spectacularly lethal antibiotics can only be delivered by IV, lacking any intestinal-absorption capabilities.

    But Avada Kedavra–style IV antibiotics were only part of what Deborah needed by that point. She had more—much more—than an infection going on. She was beyond your garden-variety infection, even beyond a more advanced local infection. Confusion means a lot of things to a lot of people, but in the context of an infection, it’s a screaming sign that organ systems are being targeted and are falling off the grid, not just the brain, but the heart, lungs, kidneys, and liver too. I suspected as much when Alan asked me to call in oral antibiotics. Not only would they have been useless, they would have delayed emergency treatment, delayed the inevitable, and I would have been party to that delay— In delay there lies no plenty. By refusing to call in antibiotics I had drawn my next line in the sand. I assumed it would encourage Alan to abandon half measures and embrace the emergency path.

    After Barbie told Alan over and over again to take Deborah to the ER, to call 911, and then hung up the phone, I took the opportunity to explain to my wife and my mother-in-law why I refused to call in antibiotics. I was walking a tightrope explaining this to them—a high-wire act with no net. I still kept my cards close to my vest, so I could illustrate that Deborah was really ill without being unnecessarily graphic, without scaring them half to death. It was a tactical game I was drawn into, and they sort of understood my chess move, I think, not wanting to delay necessary treatment even if they did not quite grasp the gravity of the situation. Moves and counter moves.

    When it comes to infection, there is nothing good about confusion—Toto, I have a feeling we’re not in Kansas anymore. Confusion means, is screaming out at the top of its lungs, that the body has been dealt a massive blow, that organs are being targeted, cells are dying in droves, things are dysfunctional, we are not in Kansas. And in Deborah’s situation, her confusion was spelling out two specific words: septic shock.

    Shock can mean a lot of things that have nothing to do with medicine, such as a sudden upsetting or unexpected event or experience, like the hit America took on 9/11, the day JFK was shot, or the Janet Jackson wardrobe malfunction 2004 Super Bowl halftime show with Justin Timberlake. Or coming home and finding your wife in bed with another woman, with the wife of your best friend. Which would probably be better than finding her in bed with your best friend.

    In medicine, shock means something a little bit different than emotional shock: the partial, evolving, or complete collapse of blood pressure. The causes of medical shock include about four pathophysiologies to be covered momentarily. Regardless of cause, the sequence encompasses blood pressure drop, blood flow drop—or worse, blood flow stops—and things down the line, organ things, cell things needing blood flow, needing oxygen, begin to drop off. Drop is an important verb here. A drop in pressure equals a drop in blood flow, equals cells dropping off, that is, dying on the vine.

    Shock is divided into four types of pathophysiological drops: volume, cardiogenic, obstructive, and distributive. The concept of volume loss is easier to grasp, but the other three are medicine-specific terms, and rather scary ones at that.

    The easier to grasp classic shock is volume loss shock or low volume shock. If the volume loss is from blood loss, it is termed hemorrhagic shock. The most obvious example is blood loss such as from a person visibly bleeding to death due to the obvious, an externally bleeding wound. Internal bleeding is where you can’t see the bleeding—ruptured abdominal aortic aneurysm, esophageal varices bleed—but just because it is out of sight doesn’t mean it is out of mind, the patient can easily exsanguinate to death internally. Less obvious volume loss shock occurs with massive vomiting or diarrhea coupled with a failure to replenish this fluid loss. The 1854 Broad Street cholera outbreak in Soho, London, falls into this category, where people were dying, not from fulminant infection but due to losing so much fluid (and electrolytes) that they weren’t able to replenish it.

    Cardiogenic shock is the result of the heart being unable to do its job, revealed by the prefix of the Latin cardio, from the Greek kardio for heart, and the second part of the word, genic, is from the Latin for produce. Put together, cardiogenic shock means the shock is generated from the heart itself. It occurs when the heart can’t pump effectively, as seen during a heart attack, where heart muscle cells are dropping off, or from a troublesome arrhythmia, where inefficient arrhythmic pumping action is from a misfiring heart, or from long-standing congestive heart failure, where the heart is just plumb tuckered out. Heart muscle injury from infection is possible, seen in viral myocarditis, as are other things that can render the heart unable to pump. A broken heart when your girlfriend dumps you for another guy certainly feels like cardiogenic shock, but it is emotional shock.

    Obstructive shock, not terribly common, is when the heart is being compressed or the blood flow is blocked from leaving the heart. It is perhaps the least well-known type of shock. Some process adjacent to or downstream from the heart is impeding the ability of that heart to do its thing, to pump. Examples include a fluid collection around the heart, termed pericardial effusion, or a dropped lung with a tension pneumothorax, resulting in air pressure buildup inside the chest, pushing against the heart. A clot in the lung, called a pulmonary embolus, which often originates in the lower leg, can push back against the heart. These are only a few types of obstructions that can impede the heart’s ability to pump. Just go stand on a hose when someone is trying to water the flowers and the idea of obstructive shock will be apparent.

    The fourth type of shock, distributive shock, at first might sound complicated to understand, but it’s actually familiar to most of us. It means all is well with the heart, but the distribution of blood after it has left the heart is all messed up. That is, the heart is doing its part and rather the flow downstream is the problem. Anaphylactic shock is the poster child for distributive shock, such as from a bee sting or an allergic reaction, releasing immune vasoactive components into the blood, which then overly dilate blood vessels to the point where there is little or no blood flow. This is your classic distributive shock—allergic shock. The dilated arteries and veins just can’t distribute blood, because the channels are too wide open, they lack muscle tone.

    The interesting thing about the flow of a fluid through a cylindrical pipe—no, I’m not about to discuss the Poiseuille law of fluid dynamics and certainly not write the equation—is two-fold, if the pipe is too narrow flow is impeded; alternatively, if the pipe is too wide open flow is also impeded. This is especially true when you take into consideration the pump, the force of the source. If blood vessels are too narrow, such as in longstanding hypertension with peripheral vascular disease, the heart can’t pump blood easily through those narrowings. Alternatively, if the vessels are too wide open, not enough appropriate arterial resistance, absent arterial tone, blood flow just peters out, this latter of which is allergic distributive shock.

    Think of a straw that you might use to slurp up a cold, refreshing beverage, such as a nice tart lemonade at the malt shop with your best gal. That straw has a certain diameter because it works. If the straw were too narrow, the normal negative pressure produced by sucking wouldn’t be able to overcome the tight channel. Conversely, if the straw were the size of a plumber’s pipe, the negative pressure needed to make use of such a wide pipe also wouldn’t be possible to achieve. A drinking straw is the size it is because it works. Blood vessel lumens with their increasing and decreasing muscle tone are the size they are because they work, and they work with the heart that is doing the pumping. Vessel lumen size normally fluctuates within narrowly defined parameters, most of which is maintained by muscle tone—all of which is adversely impacted in distributive shock.

    Which leads back to another type of distributive shock: the shocking story of Deborah appearing to be descending into septic shock. Septic shock is a type of distributive shock, the result of a fulminant bacterial infection within the bloodstream. Although all the components of septic shock are not known, we do understand that it shares an eerily similar cascade to allergic shock. In septic shock, the bacteria often release endotoxins that trigger an immune response. Without getting too technical, that response ends up dilating the arteries and veins, which decreases the vasculature resistance, which then diminishes the blood flow downstream, which then ends up with things dropping off. This specific process is termed warm septic shock.

    For reasons that are unclear, in warm septic shock the body reflexively bypasses the normal capillary exchange network in end organs, which is how tissues receive their oxygen and goodies. Between decreased flow and bypassed capillary exchange, oxygen depletes in tissues as waste products build-up—lactic acid, carbon dioxide, nitrites, sulfides and things like that. Tissues begin to die off. Then things start clotting off. As a physician treating someone in septic shock, it is a nightmare. So many variables are going off all at once, like herding cats.

    Cold shock, as you might have guessed, onsets due to experiencing sudden extreme cold, like falling through an icy pond, or being Leonardo DiCaprio holding onto Kate Winslet’s floating board in the 1997 film Titanic (wasn’t there room for him on that floating board?). The pathophysiology of cold shock, or cold water shock, is different than septic or warm shock and need not overly concern us here. Cold decreases muscle function, including muscles of the heart and breathing. The body instinctively attempts to preserve blood flow to vital organs, the brain first, but also internal organs including the heart itself, all at the expense of extremities. Especially in freezing water, which induces an increase in breathing despite chilled muscles of breathing, coupled with an inability to swim due to those chilled, poorly perfused extremities—well, a single gasping gulp of water can be easily inhaled, which then sparks the drowning cascade. Drowning, along with being buried alive, are two events I don’t care to contemplate too much, so this concludes our discussion on cold shock and DiCaprio’s character Jack dipping under the icy Atlantic waters rather than share the board with Rose.

    Whatever the cause of the shock, it involves two fundamental processes: blood is not flowing, and end organs are dying. That is the long and short of it. Kidneys are usually affected first, as they’re very sensitive to a drop in blood flow. Then the liver begins to die, although it’s a bit tougher than the kidneys. The lungs take the hit next, then the brain, and eventually even the heart takes a hit—trying nobly, desperately, to keep blood flowing to all those organs under its charge.

    The heart is especially vulnerable because, unlike the rest of the body, which receives its blood from the systolic beat of the heart, called systole, the heart itself receives its blood from the backwash diastolic moment, where residual blood in the aorta washes backward toward the heart when it is in between beats, called diastole. Backwashing blood against the closed aortic heart valve is when blood flows into the heart coronary arteries. Right next to that closed aortic valve—it has to be closed for this to work—are three aortic sinuses—no valves—through which backwashing aortic blood enters the coronary arteries, which then feed the heart. In short, the heart gets fed during diastole (heart relaxation), after everyone else gets fed during systole (heart contraction).

    This feeding of the heart during diastole makes further sense when you consider this fact: because a contracting heart muscle during systole necessarily squeezes shut its own coronary arteries, those coronaries then unable to accept blood flow. It is precisely when the heart is in between beats, when the coronary arteries are not being squeezed that those coronary arteries are open and can accept blood flow. Clever design.

    In most instances, a normal bacterial infection—a basic strep throat or urinary tract infection—treated in a timely fashion with an oral antibiotic will usually be eradicated. Rarely, a switch in the antibiotic regimen and a smidge more time might be needed. But, in the end, the bacteria are ended. Between the immune system and the prescribed antibiotics and the normal course of most infections, the pathogen is given a deadly Avada Kedavra blow. A more severe infection treated in a timely fashion with the more powerful IV antibiotics can usually eradicate a more resilient pathogen, or a pathogen that has dug itself some serious trenches to hide out in. Such infections include routine bacterial pneumonia, kidney infection, and any number of bacterial infections that grow severe enough to demand IV antibiotics over oral ones. But, in the end, the bacteria are ended. Antibiotics coupled with the immune system usually do the trick, do it gloriously in an anticipated fashion. That is to say, usually patients recover within a defined convalescence. Usually. It is when a person falls out of that anticipated recovery, falls off the curve, that eyebrows begin to raise.

    In the year 1900, the four most common causes of death for children under age five were pneumonia, flu, tuberculosis, and viral gastroenteritis with diarrhea. All infections. When diarrhea is really bad and you don’t have IV hydration, which was not available in 1900, children will die from volume loss shock. Along with children, the elderly and the infirm cannot tolerate that type of severe dehydration.

    Which brings us to the topic of childhood death 100 years ago versus today. It is an eye-opener. I dare say an eye-popper.

    On one of my running paths—when I actually get my weary bones out to exercise—takes me through a nearby cemetery, the one where my parents are buried. Cemeteries are basically parks, and although many people might find strolling or jogging through a cemetery morbid or macabre, it isn’t really. That particular cemetery, like many cemeteries, has a section for children, with some headstones over 100 years old, often adorned with a little stone lamb carved into or placed on top of the stone marker. When I see a headstone from that era—or even in modern times—of an infant who died within a few days of birth, I know it was likely from a birth defect incompatible with life, such as a severe congenital heart malformation. But that’s newborn deaths—usually caused by something incompatible with life. What about a child who dies at a year or two or so of age?

    When I see a 100-year-old headstone of a child who died as a toddler, more likely than not it was from infection. Before the age of antibiotics, toddlers and children regularly left this world from infections that are so easily treatable today.

    Fast-forward to modern times, and the landscape has changed drastically. In today’s world, children don’t die as frequently as they did a century past—overall mortality has dropped—but when they do pass on, it’s not often from infection. The top killers of children today, excluding congenital issues incompatible with life, are, in order: accidental trauma especially motor vehicle accidents, followed by (horrifically) firearm-related injury, cancers like leukemia, and most disturbingly and alarming of all, homicide. That’s right, the fourth leading cause of death for children under age five in the United States is a child being killed by traumatic intentional means. There’s no way to get one’s mind around that statistic.

    Actually, these days, homicide—meaning murder and manslaughter—makes the top-ten causes of death for nearly all age groups, except the very, very young (less than one year old) and the very old. For deaths between the ages of ten and about fifty-five in America, getting killed, usually by a gun, is on the top-ten list.

    Suicide, you ask. It’s there, too. It’s a common killer. Suicide is the second most common cause of death for ages ten through thirty-four, and it’s still in the top ten for ages thirty-five through sixty-four. Alarmingly, for teenagers and young adults, not only is suicide the second most common cause of death, but accidental trauma takes the top spot. For ages ten through thirty-four, the top five are trauma, suicide, then homicide, drug and alcohol overdose, and cancer.

    For nearly all eras but our own, infection as a cause of death reigned terrifyingly supreme. But with better sanitation, better nutrition, healthier lifestyles, the discovery of antibiotics, and modern medical resuscitation, infection has been forced to relinquish its top position. Having said that, no matter what station on the actuary table one looks at, from infancy to old age, death from infection still makes its presence known.

    One of the tenets of medicine is to never mask a symptom with a drug. For instance, if someone bangs their head on a wall while reading this book and gets a concussion and an accompanying headache, you don’t prescribe narcotics for the headache. In prescribing narcotics in the presence of head trauma, you might mask a brain bleed, the quick recognition of which can save a life, the delay of which can end one.

    As for Deborah, she initially had something akin to a cold and apparently might have stocked up on cold remedies, including cough suppressants. Whether Deborah used a lot of cough suppressants was never made clear. Not to beat a dead horse (and certainly never a live horse), but the cough is the watchdog of the lungs. Coughing protects the lungs from bacterial secretions that seep and creep and crawl and slide and ooze down from the upper respiratory reaches into the lower respiratory nooks and crannies and cracks and fissures. In the face of a throat or upper airway infection, coughing is good and should only be suppressed if the need for a few hours of sleep outweighs the need to keep the cough’s sentry function in play.

    It is thought Deborah was possibly self-medicating—we all, or at least most of us, do it. We reach into the medicine cabinet for all sorts of cold and flu remedies. But the reality is that making liberal use of cough suppressants is a circumstance that can facilitate the evolution of a primary viral cold into a secondary bacterial defilement of the lungs, a bacterial pneumonia. Certainly, the flu can evolve into a viral pneumonia on its own without suppressing the cough reflex, which then lays the groundwork for a secondary bacterial pneumonia to take hold. Conversely however, suppressing a cough might allow that evolution into a bacterial pneumonia to proceed unhindered without the need for a viral pneumonia first. The comatose alcoholic is at risk for bacterial pneumonia by inhaling secretions.

    If prevention hasn’t kept an infection at bay, and if the immune system is struggling and sometimes even if it’s not, many infections are treated with anti-infective drugs classified into the four subtypes briefly previewed: antibacterials, antiparasites, antifungals, and antivirals. Although the antivirals tend to be in a class of their own, the other three—antibacterials, antiparasites, antifungals—sometimes overlap on the anti-infective spectrum. The most common word used for the anti-infectives is antibiotic, but often folks think of antibiotics as only antibacterials, when technically is can be applied to antiparasites and antifungals. As for antivirals, I do not believe anyone calls them antibiotics. There is nothing biotic about a virus.

    Remember those Venn diagrams from high school, those overlapping circles used to describe relations between different sets of objects or numbers? The teacher would go on and on talking about overlapping sets, and all you could think was, Venn is she going to stop talking about this? Venn is the school bell going to ring?

    John Venn was born in 1834 in Yorkshire, England, into a family of evangelicals, a Protestant denomination whose fundamental principle is salvation by grace through faith in Jesus—salvation through saving the soul from sin and damnation, and grace implying the love and mercy of God. After attending secondary school in London, Venn went on to study mathematics at Caius College at the University of Cambridge and became an Anglican priest, a religious tradition within the Church of England. Anglican, a word specifically signifying the Church of England and sometimes the country of England in general, makes crystal clear its separation from the Catholic Church in Rome.

    As time went on, for reasons that aren’t quite clear, Venn distanced himself from the Anglican Church, which he found incompatible with his emerging beliefs. In 1880, he published his landmark paper dealing with diagrams and sets in formal logic theory, which became the basis of the Venn diagram. Many years after Venn died, his alma mater Caius College erected a stained-glass window in its dining hall featuring three overlapping circles to commemorate him.

    Venn’s highly useful overlapping circles can be used to show the overlapping efficacies of the antibacterials, antiparasites, and antifungals. Take penicillin, for instance, the first antibiotic discovered. It is really only effective against bacteria. By contrast, the anti-infective metronidazole, commonly sold under the name Flagyl, is effective against the STD parasite Trichomonas, the upset-stomach parasite Giardia, and the amoebic-dysentery parasite Entamoeba histolytica, and it’s also used to treat several bacterial infections, notably those caused by Bacteroides—an evil bacterium if there ever was one. Therefore, Flagyl sits in two overlapping circles on the anti-infective Venn diagram: antibacterial and antiparasite.

    The azole derivatives are a class of anti-infectives used against parasitic worms. Albendazole, for example, can hammer tapeworms, hookworms, pinworms, and blood flukes. Other derivatives of the basic azole structure can kill many varieties of fungus. Ketoconazole is one of the prime antifungal weapons against histoplasmosis, blastomycosis, and valley fever. Recently azoles have shown promise in treating some forms of tuberculosis, a bacterial infection, which would mean that some azole derivatives sit where the three Venn circles overlap—antiparasite, antifungal, antibacterial—smack dab in the middle of the Venn world.

    The take-home lesson is that most anti-infectives belong in their own area of effectiveness, of expertise, yet some anti-infectives can cross taxonomic kingdoms and lay waste to a variety of pathogens. Sort of like Rome at the end of the Punic Wars that began in 264 BC and ended 118 years later in 146 BC when Rome sacked Carthage. Just to make sure Carthage did not rise again, at least anytime soon, the Romans salted the earth to make sure nothing grew. Anti-infectives are supposed to salt the infection site so no microbes grow.

    The Punic Wars pitting Rome against Carthage (modern day Tunisia along the Maghreb) started when Rome attempted to check Carthage expanding into the Sicily and other Mediterranean islands. Things really got going around 220 BC when the great Carthaginian general Hannibal having already crossed Gibraltar into the Iberian Peninsula with his elephants, crossed the Pyrenees into Gaul in 219 BC along with all his elephants, then crossed the Alps into northern Italy in 218 BC. Most of his elephants were dead (I guess they didn’t like the cold weather) or were starving after crossing the Alps, but his army was still intact. Despite the losses of his elephants, Hannibal marched from northern Italy into southern Italy. Eventually, to make a long war short, by 206 BC the celebrated Roman General Scipio Africanus who was only about twenty years old had chased Hannibal’s Carthaginians out of Italy, out of Gaul, out of the Iberian peninsula and back into northern Africa. Payback is a biatch. By 204 BC Scipio invaded Carthage, and by 201 BC the Carthaginians sued for peace.

    As Rome had become mighty powerful, and for reasons that are unclear, despite defeating Carthage fifty years earlier in 201 BC, in 149 BC the Third Punic War was fought. Although Carthage was weak militarily, they had recovered economically and that did not sit well with Rome. Rome under a different Scipio (adopted grandson of Scipio Africanus) laid siege to Carthage, fighting the Third Punic War 149-146 BC entirely within the Maghreb. In a not very pleasant ending, Scipio Aemilianus and his Roman soldiers sacked Carthage, killed everyone, destroyed every structure and salted the earth. At least that is what some accounts claim. The ancient city of Carthage, what’s left of it is about ten miles from Tunis.

    Punic as in Punic Wars is derived from the Greek Phoinix for Phoenician which were the original peoples who settled in Carthage. Phoenicians were an ancient Semitic-speaking people that originated along the Levant in what would be modern-day Lebanon. They left the Levant traveled across the Maghreb eventually creating the once fabled majestic city of Carthage.

    Is there anything that routinely kills pathogens from all three groups besides the azoles? Yes, there are. Lots of them. We just don’t ever want to ingest or inject them. Agents that kill topically include isopropyl alcohol, which can annihilate bacteria, parasites, fungus, denature many viruses, and even kill insects like fleas and ticks. Of course, isopropyl alcohol can also kill humans—it is a poison. The alcohol we drink to get a buzz is ethyl alcohol or ethanol, which also can kill humans, but in the form of drunk driving and alcohol-related liver disease.

    Other anti-infectives not swallowed or injected, even at the suggestion of a president or two, but applied topically are the solutions we surgeons use to sterilize our hands and the patient’s skin before an operation begins. These include, in addition to isopropyl alcohol, chlorhexidine and povidone-iodine, also known as Betadine—that orange-brown stuff—and many more, all of which share a similar kill range. How do such solutions kill things? Usually by messing with the cell wall or cell membrane of the pathogen, which is either dissolved or denatured or dealt a fatal blow by the antimicrobial solution. In the case of viruses, the denaturing involves rendering ineffective their fatty capsid coverings or even rupturing their genetic material, their RNA or DNA sequences.

    Some people might have the idea that penicillin was the first anti-infective drug ever discovered, but that’s not the case. Penicillin was the first antibacterial discovered, but not the first anti-infective. The antiparasites, and specifically the quinine used to treat malaria, were discovered long before the antibacterials. Which is the direction our story is headed in now: first the discovery of quinine, and then the discovery of penicillin. To find the origins of quinine, we must travel back in time to the 1600s and trek to the mountains of Peru.

    The Andes, which is the longest mountain range on Earth, is part of the American Cordillera, a series of mountainous ranges that begins deep in the icy waters of the Antarctic Ocean near the South Pole, emerging in Chile and Peru as the Andes, continuing on as the Sierra Madres in Central America, splitting in the United States into the Rocky Mountains, Sierra Nevada and the Cascades, continuing into Canada as the Rockies and Columbia ranges, ending in Alaska as the Alaska and Brooks ranges. This entire cordillera formed together beginning 200 million years ago when the supercontinent of Pangaea broke up, thanks to plate tectonics, and what would become the Americas—the North American and the South American tectonic plates—pushed westward crashing into the Pacific Ocean tectonic plate, the leading edge of that crash pushing up the American Cordillera from pole-to-pole.

    Seventeenth-century Jesuit priests slogging their way through the Peruvian rain forests and trudging up the Andes were the first Europeans to learn the antimalarial secrets hidden in that New World country. The Indigenous Peoples of Peru would grind up a concoction from the bark of the cinchona tree, and whatever was in that bark provided protection from the fever, as malaria was called. How or why the Quechua peoples of Peru figured out hundreds and hundreds of years ago that the bark of a specific tree fought malaria is unknown.

    The Jesuits passed this information along to British apothecaries through detailed notes that accompanied ships destined for England, ships whose hulls contained ample supplies of cinchona tree bark. The British apothecaries would then grind up their own concoction out of the bark—a terribly, abhorrently bitter brew—to produce a remedy for malaria. The horribly disgusting mixture was then dispatched to British soldiers in India and sub-Saharan Africa, as well as workers for the British East India trading company, all of whom were not terribly enthralled about drinking such a bitter concoction daily. It was believed the elixir would make its imbibers immune to the fever, and thus give Britain and the British East India Company a step up on their competition, even though no one knew what the magical, malaria-killing chemical was exactly.

    Gin is flavored with the juniper berry, which has a rather strong taste, and in today’s world, when you belly up to the bar and order a gin and tonic, the tonic is little more than carbonated water with a tincture of quinine added for its faint bitter taste that goes very well with gin. When it comes to quinine, a little tincture goes a long way. But back in the early 1800s, gin and tonics did not exist. Whatever folks diluted their gin with at the time, we can be sure it was not quinine tonic.

    Early apothecaries made medicinal quinine from pulverized cinchona tree bark, which was not drinkable—at least not according to anyone other than the Quechua people of Peru. The cinchona blend was unknowingly concentrated with quinine, as well as other not very tasty tree debris, and it really was a bitter potion to swallow. Even adding gobs of sugar to the mixture did little to alleviate the awful taste. Mary Poppins’s spoonful of sugar to help the medicine go down provided little relief for the British soldiers and merchants in India and Kenya.

    As British imperialism advanced in India and sub-Saharan Africa, with the ever clear and present danger of malaria just a mosquito bite away (although at the time no one knew how malaria was transmitted), the British high command had a bright idea: gin. Especially because of the juniper flavorant added to gin, it was correctly believed it would mask anything distasteful. In a unique mixological twist, the British military ordered their soldiers, who were understandably refusing to drink cinchona straight up, to water down the concoction with gin, in the belief that the strong but tolerable taste of juniper berry would do more to mask the bitterness of quinine than sugar. The soldiers, needless to say, more than complied; they were after all being encouraged to drink alcohol by the high command. What soldier would say no to that, especially if the gin was being offered for free. The incidence of new malaria cases among British soldiers and merchants dropped, and those burdened with malaria began to recover, all by drinking a pulverized tree bark mixed with gin. And just so we’re clear here, it wasn’t the gin decimating the malaria.

    While the British in Africa and India turned quinine tonic with gin into a nightly medicinal ritual, the custom was apparently not shared by other European colonialists. Subsequently, the British flourished in those regions while their competitors more or less withered from malaria. To be fair, the Brits did not keep their medicinal advantage secret—doctors don’t do that. The recipe for quinine tonic from the cinchona tree to treat malaria was published in a series of eighteenth-century British pharmacopeia books.

    In today’s world of internet connectivity, a new therapy in medicine can become known worldwide overnight. A century or two ago, it might take decades for a therapeutic modality to make it into daily medical practice. For the British, what began as a medical therapy in the 1700s and 1800s to treat malaria—cinchona quinine watered down with gin—ended up being reversed and taken up for general consumption: gin watered down with quinine tonic. Your average nightly gin and tonic, to be enjoyed on warm summer nights in such places at the Ye Olde Mitre Pub, located at 1 Ely Place in Holborn, London.

    Eventually, in the 1800s, the magical compound in cinchona tree bark was isolated. The French scientists who discovered it, the chemist Pierre-Joseph Pelletier and pharmacist Joseph-Bienaimé Caventou, dubbed it quinine, from the Spanish quina in turn from cinchona. Some years later, they were also able to reliably synthesize quinine in the laboratory. The days of gulping disgusting pulverized cinchona tree bark watered down with gin to combat malaria had at last come to its bitter end. What began as traditional Quechua knowledge, conveyed by very observant Jesuit priests from Peru to Britain in the 1600s, ended up being the world’s very first isolated and purified antimalarial drug in the 1800s. And technically the world’s first isolated anti-infective drug. Isolated quinine beat penicillin to the anti-infective punch by at least 100 years. Which is where our story now turns: the discovery of penicillin.

    Mold spores floating in the air and alighting upon things is how Alexander Fleming accidently—or more accurately, serendipitously—discovered the great antibiotic known as penicillin in 1928. Spores floating in the air also helped Louis Pasteur prove his life from life theory around 1860, sixty-eight years before penicillin’s discovery, with his swan-neck beaker experiment, and helped solidify his germ theory. We’ll loop back to that again later on. Mold is a member of the fungus kingdom and comes in two types: the kind that has adopted a single or unicellular lifestyle—the loner we call yeast spores—and the kind that grows as a multicellular filament called hyphae.

    Fleming was born in 1881 at Lochfield Farm in Ayrshire, Scotland, and received his medical training at St. Mary’s Hospital in Paddington, London. He apparently became interested in treating infections after witnessing the horrendous afflictions that came off the battlefields during World War I. His discovery of penicillin is the quintessential serendipity story and always deserves a retelling.

    One day Fleming was growing bacteria on Petri dishes—for what purpose is not clear to history—when his lab assistant forgot to close a window at day’s end. Apparently that second-story window at St. Mary’s Hospital, off Praed Street, London, was open all night long, and we can only imagine what wafted in through it that warm September evening in 1928. Glass Petri dishes in those days did not have accompanying glass covers, or if they did, Fleming’s didn’t. When Fleming returned to his laboratory a day or so later, upon inspecting his Petri dishes he observed that, much to his dismay, they were contaminated with mold. Spotting the open window, Fleming assumed correctly that something from outside had floated in and landed on those Petri dishes, contaminating them.

    After Fleming finished scolding his lab assistant for ruining his Petri dish experiment—the young scientist now weeping and cowering in the corner—Fleming took a moment of pause and noticed that there was more to those Petri dishes than unwanted mold growth. He gazed contemplatively and noticed that, beneath it all, beneath the mold, was an incredible sight. Wherever the mold had landed, the bacteria he had been trying to cultivate had died, almost as if—exactly as if—the mold was killing the bacteria. A zone of death. Fleming’s serendipitous moment of pause would change medicine forever.

    While it was quite apparent the mold was killing the bacteria, how it was doing so took some time for Fleming to work out. Let me make a long story short: in competing for food sources several billion years ago, in another example of Darwinian evolution where survival favored the fittest, molds accidentally but fortuitously developed the ability to secrete a chemical that killed nearby bacteria, thus beating out the competition as they both wiggled toward the same food source. All cells have waste products, but that particular species of mold had a waste product that killed bacteria, while other less clever molds did not. Those species of mold that could annihilate bacteria with a chemical survived—winning the race to food sources—and those species of mold that could not apparently starved into extinction. Or found something else to eat.

    It seems bacteria and molds have been waging microscopic battles with each other for eons, as there are several other examples of such chemical warfare on the microbe level. A gazillion years ago, bacteria and fungi started, by chance, producing chemicals that killed each other. They didn’t plan it, it just happened. Like with the molds, as time passed, those bacteria and those fungi whose DNA produced a favorable killing chemical went on to the next stage of evolution, and the rest likely did not.

    As for Fleming and his Petri dishes, in a classic unfolding of scientific discovery, Fleming’s seemingly accidental observation was in fact the quintessential example of how chance favors the prepared mind—a phrase attributed to Louis Pasteur. Fleming, through serendipity accompanied by astuteness—a prepared mind—knew that he had by chance stumbled upon the world’s first antibiotic.

    According to legend, Fleming supposedly remarked to his tearful lab assistant sniffling in the corner: That’s funny. Seriously. According to history, that is precisely what Fleming muttered: That’s funny. What Fleming was really saying was: that’s curious or that’s odd or wait a minute or what have we got here?

    Science has had many similar that’s funny moments, and that’s not even including all the science jokes, like: Light travels faster than sound, which is why some people appear smart until they speak. Or: There are three kinds of people in this world—those who are good at math and those who are not. I once tried to tell a chemistry joke, but there was no reaction. Or maybe: Dear algebra, quit asking us to find your X, she’s not coming back.

    But seriously—people utter some strange things when they discover something.

    A classic example of a that’s funny moment—perhaps the classic example—is that of the Greek mathematician Archimedes, who despite being Greek was born in Syracuse, Sicily, in 287 BC. Sicily is that island part of Italy, where the country’s boot kicks the soccer ball island if Sicily. How was the Greek Archimedes born in far-flung Sicily? Before Rome conquered everything, Greece, through Alexander the Great, had conquered everything. So, it is really no surprise that ethnic Greeks were living in Sicily in 300 BC. Conquerors do that. As we just visited, the Carthaginians attempted to capture Sicily and then some, from the Romans who had taken control from the Greeks, and which launched the Punic Wars.

    Archimedes was related to the king of Sicily, Hiero II. At some point during his formative years, the brilliant Archimedes traveled to Alexandria, Egypt, to continue his studies—Alexandria being home to the greatest library in the world at that time, the Library of Alexandria. If you wanted to be a well-learned man, reading the scrolls in Alexandria was just the ticket.

    There were Seven Wonders of the Ancient World—to be distinguished from the Seven Wonders of the Modern World—only one of those ancient wonders survived into modern times, the Pyramids of Giza. The other six ancient wonders were lost to history: Hanging Gardens of Babylon, Statue of Zeus at Olympia, Mausoleum at Halicarnassus, Temple of Artemis, Colossus of Rhodes and the Lighthouse of Alexandria. For completeness, the Seven Wonders of the Modern World (debatable list): Great Wall of China, Christ the Redeemer, Chichen Itza, Machu Picchu, Taj Mahal, Roman Colosseum, and Petra in Jordon.

    After his studies in Alexandria, Archimedes returned to Sicily. One day, King Hiero II commissioned a Sicilian goldsmith to create a votive crown for his temple—a crown made of pure gold. A votive is an offering or consecration as payment or fulfillment of a vow. The precious gold for the votive was supplied to the goldsmith by the king himself. Votive crowns can be quite ornate, with intricate design, which is important to this story.

    When the votive crown was completed and given back to King Hiero II, the king suspected the goldsmith had cheated him by not using all of that precious gold he had supplied. Even worse, the king suspected the goldsmith might have mixed silver into the gold to further the deception, silver being less expensive not affecting gold’s luster if just a little bit is added. Why exactly Hiero II suspected all the gold had not been used cannot be answered with certainty over such a distance of time, but likely the crown just didn’t seem right. Whatever the exact reason, the king tasked his brilliant cousin Archimedes—recently returned from Alexandria—to determine if the goldsmith had bamboozled the king. You don’t bamboozle kings, especially Sicilian kings.

    Geometry in the third century BC was pretty advanced when it came to things like squares and circles, and even cubes and spheres, thanks to the geometry system of Euclid, another brilliant Greek living in Alexandria. And thanks to Euclid, to this day many a young boy and girl walk into fourth-period geometry class, where the fun of the previous third-period drawing and painting class, goes to die. Archimedes likely knew Euclid. Their paths possibly crossed somewhere among all the scrolls of the Library at Alexandria, with Archimedes at the beginning of his life and Euclid nearing the end of his.

    Yet nothing in Euclidian geometry could have prepared the young Archimedes for the task at hand. There was no known Euclidian equation to help determine the weight of an intricate, ornate crown. Without the option of melting the crown back down to uniform shape, the task of proving whether his uncle, the king, had been swindled was definitely a challenging one. Especially since the votive crown was a consecrated gift created to fulfill a vow, Archimedes could not in any way harm the crown. It was a religious relic.

    Archimedes retired to his home, perhaps grabbed a little vino, and went to soak in a bathtub to ponder the solution. What better way to ruminate on a problem than by sipping some wine and soaking one’s weary bones in a bathtub? The Romans also loved their baths, or thermae, as they were known. Roman baths weren’t just large swimming pools—in fact, they weren’t swimming pools at all. They were major social venues, a place to relax, clean, and conduct business. There were hot thermae, warm thermae, cold thermae, all surrounded by a structure with changing rooms and rooms for … whatever: use your imagination. Many thermae baths were public, some were private. More often than not, men bathed together with women, rich men bathed with poor men, and even servants bathed alongside masters. Just as the water in a thermae levels out from gravity, apparently the social classes or caste system leveled out, too, when everyone bathed together. This leveling of water figures into the story, as we shall soon see.

    As the story goes, Archimedes must have had his own private bath, and it must have been a small bath of sorts—what you and I would call a bathtub. Bathtubs were not common then, only for the well-to-do. It had to have been a bathtub for the story to have unfolded as it did. Upon entering his bathtub or maybe upon leaving his bathtub—history is not clear on that—Archimedes noticed that the water level had changed. At that precise moment, he realized that a submerged solid object, like a person or perhaps a gold votive crown dunked into a bathtub full of water, would displace a volume of water equal to its mass, which loosely translates into its weight, which loosely translates to its volume. The goldsmith had been given a volume of gold, and Archimedes needed to determine if that volume had been used.

    According to legend, Archimedes dashed out of the bathtub, without remembering to put on so much as a stitch of clothing, and ran through the streets of Syracuse, butt naked, yelling Eureka! Eureka! Eureka! From the Greek, eureka means I have found it. That is what a scientist is supposed to scream when they make a discovery— Eureka!—but what someone mutters really matters not. That’s funny, that’s curious, that’s odd, wait a minute, eureka, or even the onomatopoeic word hmm?—all serve the same purpose: discovery.

    After determining the volume of pure, solid gold in an easy to calculate configuration such as a cube, one could then precisely measure how much water that cube displaced when fully submerged in water, and, eureka, you’ve created a standard against which to measure the mass of any bit of gold, no matter its shape, no matter if it was an intricate votive crown, because its mass is its mass. Displacement equals mass or volume. Archimedes submerged the crown in question to see how much water it displaced and was able to work backward to determine if all the gold had been used. And, all the gold had not been used. It’s worth mentioning that when you mix gold with a little silver, its density changes, even though it still appears as pure gold—and as its density changes, so does the amount of water it displaces.

    Dutifully, Archimedes calculated for his cousin King Hiero, that all the gold had not been used, and further, that the goldsmith had alloyed the gold with silver to further dupe the king. No one knows for certain what happened to that goldsmith. My guess is that he too was submerged in water, along the beautiful coastline of Sicily. In the classic Sicilian way, he swam with the fishes.

    In addition to defining displacement of mass in water, Archimedes is also famous for this line credited to him: Give me a lever long enough and a fulcrum on which to place it, and I shall move the world. Although ancients predating Archimedes used the fulcrum—the stationary point—upon which the lever—which rests, moves and pivots on the fulcrum—to move objects, like large stones, Archimedes was the first to put the math to it. Examples of fulcrums and levers other than the obvious include a seesaw kids play on and the scale Lady Justice holds. The latter, Lady Justice is an allegorical blindfolded (impartial) woman holding a scale of justice in her right hand and a sword in her left, the sword signifying that depending upon how the scales of truth were weighed, the sword offered swift and final justice. Of course, even with statues of liberty and statues of lady justice, even presidents can crack their foundations.

    What is the difference between mass and weight? According to Isaac Newton—and we don’t argue with Newton—weight is calculated as mass times gravity, or W = mg. Mass is the actual amount of material in a defined body or object. It doesn’t change. Weight is the force of gravity exerted on that mass. For argument’s sake, take Neil Armstrong, the first man to step on the moon. On Earth Armstrong perhaps weighed about 180 pounds (but truly I have no idea how much the great celestial explorer weighed). A weight of 180 pounds converts to a mass of 80 kilograms on Earth. The pound is a unit of weight; the kilogram is a unit of mass—although most times here on Earth we consider both pounds and kilograms to be units of weight. It is not an easy imperial-to-metric conversion, like yards to meters, which are both units of length. But for everyday purposes, we ignore the fact that grams and kilograms are units of mass, not weight.

    Anyways—Armstrong flies to the moon aboard Apollo 11 along with Michael Collins and Edwin Buzz Aldrin. On July 21, 1969, Armstrong steps onto the moon. Ignoring his fancy NASA spacesuit, his mass is still 80 kilograms. That is to say, if you were to completely dunk a nude Armstrong into a bathtub of water on the moon, besides yelling several expletive deletives, he would displace a volume equal to 80 kilograms—and if you had performed the same experiment on earth prior to going to the moon, he’d similarly displace 80 kilograms. If you were to pull him out of the moon tub, dry him off, and have him stand on a scale that doesn’t lie (my scale at home I’m sure lies), he would weigh a svelte 30 pounds—not the 180 pounds he weighed on Earth. Weight on the moon is roughly 17 percent of what it is on Earth, but mass—or kilogram volume displacement—on the moon is the same as it is on Earth.

    But now let’s leave the moon and get back to that eureka!, or rather that’s funny, moment we were originally talking about.

    After Alexander Fleming repeated his experiment a few more times, placing mold on Petri dishes growing staph bacteria, he deduced that the mold was making some type of chemical that was not at all friendly to bacteria. The particular mold that had alighted upon Fleming’s agar turned out to be Penicillium chrysogenum, and the chemical discovered was in turn named penicillin—the first true antibiotic and was the reason Fleming received the Nobel Prize in 1945. In reflecting on his discovery years later, the microbiologist supposedly mused: When I woke up just after dawn on September 28, 1928, I certainly didn’t plan to revolutionize all medicine by discovering the world’s first antibiotic, or bacteria killer. … But I suppose that was exactly what I did.

    It was a good thing Fleming’s lab assistant left that window open. It was also a good thing Archimedes took that bath.

    In figuring out that mold was creating an antibacterial chemical, which soon led to his discovery of penicillin, Fleming offers a classic example of deductive reasoning, moving from several generalized findings to a specific conclusion. When Archimedes realized that a submerged votive crown displaced its mass, displaced its volume, he was using inductive reasoning: he moved from that single example to the generalized statement that all objects when submerged in water displace their mass. Which is where our story now turns: displacing—or more specifically, blowing up—mass, as it is the story of the Nobel Prize being established.

    Nitroglycerin, a rather explosive liquid, was first synthesized by the Italian chemist Ascanio Sobrero in 1847, made by mixing glycerol with nitric acid and sulfuric acid. The finished concoction has three nitro groups attached to the glycerin, which gives it its name, or at least one of its names: trinitroglycerin, or TNG. Due to its unmanageable explosive nature, Sobrero felt TNG was too volatile and unstable to be much use for anything at all, let alone as a controlled explosive. A person was just as likely to blow up themselves as the mountainside they had meant to in their search for gold or that vital bridge in a move of ingenious warcraft. So, Sobrero did nothing much with the substance he had created, referring to it as black powder, probably because it was literally a black powdery compound. There was one problem with that, though: the name black powder was already taken.

    There are indeed two types of black powder and because of that, it ignites some confusion. The black powdery substance of TNG is to be distinguished from the real black powder of gunpowder. Nitroglycerin is a single compound that has nitrogen, hydrogen, and oxygen, and when that oxygen is liberated, the nitrogen bonds break, releasing a boom! Gunpowder, on the other hand, is not a single compound but a mixture, a transmutation of three substances: sulfur, charcoal (which is carbon), and potassium nitrate, also called saltpeter, which has the chemical structure KNO 3. When the three compounds are mixed together and ignited, the oxygen in the saltpeter reacts mostly with the carbon, some with the sulfur, and also goes boom! The saltpeter gunpowder, which was invented in China in the ninth century, is the original black powder.

    Alfred Nobel, a Swede and also a chemist, had a different view of nitroglycerin than Sobrero did. Unlike its inventor, Nobel thought TNG could have some practical application. To achieve this, he took the nitroglycerin compound and combined it with diatomaceous earth, which is a silicon-type sedimentary rock, to formulate a more stable mixture. Nobel then patented his concoction in 1867 as dynamite, a name derived from the Greek dynamis, meaning power, and the suffix -ite, meaning belonging to—as in, this stuff is connected to, belongs to something really powerful, really explosive. Alfred Nobel made a huge fortune off his dynamite. Huge. It should be noted that, in working with the unstable nitroglycerin to arrive at the stable dynamite, several workers in his factory got blown to bits, including his brother, Emil Oskar Nobel. Family—what can you do?

    Nobel died in 1896, age sixty-three, from a stroke, leaving an estate that established the Nobel Prize in five areas: chemistry, physics, physiology & medicine, literature, and peace. The Nobel Prizes are awarded every year in Stockholm, Sweden, except the Peace Prize, which is awarded in Oslo, Norway. As we know, the Nobel is not given posthumously. Other than brother Emil getting blown up, two other Nobel brothers, Ludvig and Robert were endeavoring to be successful in their own right, were well on their way to making a fortune in the oil exploration business in Baku along the Caspian Sea. But when the Bolshevik Revolution came down in 1917, all their Russian businesses were confiscated by the state. Communism does that.

    Beyond the black powder confusion between black powder gunpowder and black powder nitroglycerin, further bewilderment reigns with the assorted names for nitroglycerin. It is variously called trinitroglycerin or TNG or trinitropropane or TNP, all of which refer to the same compound. Whatever you call it, it has three nitro groups attached to the main chain propane molecule, and when those nitro groups release, it goes boom! If you mix that TNG or TNP with diatomaceous earth you call it dynamite. Later in this journey, much later, we’ll discuss nitroglycerin as a treatment for chest pain versus the kind used to blow things up, hopefully not patients.

    We all know what propane is: a highly volatile hydrocarbon gas at standard temperature that we place into tanks—under pressure, propane is a liquid in tanks—and use to fuel our barbecues on warm summer nights, grilling hamburgers and guzzling a cold one, or several cold ones. Adding trinitro to propane converts the base structure from a gas at normal temperatures to a liquid at normal temperatures, and, unsurprisingly, makes for a rather explosive situation. You would have thought that turning a volatile gas into a liquid theoretically would allow a liquid to be more carefully stored than a gas, more carefully moved, and then when desired, used to blow things up. But, as Sobrero discovered, even as a liquid TNG is too explosive—merely looking at nitroglycerin suspiciously can make it go kaboom! If you’re clever like Nobel and add the diatomaceous earth, it, finally, makes it more stable. Then you call it dynamite, a great name, and you make a bucketload of Swedish Krona.

    We’ve parsed the difference between three explosives: black powder gunpowder (from China), black powder trinitroglycerin (Sobrero), and trinitroglycerin plus a slightly off-white diatomaceous earth, otherwise known as dynamite (Nobel). Now we need to add to the embarrassment of confusion and parse the difference between trinitroglycerin (dynamite) and trinitrotoluene (TNT)—since they also are often confused as being one and the same, partly because they both have the prefix trinitro- in their chemical names: TNG is trinitroglycerin and TNT is trinitrotoluene.

    But the real reason, at least for my generation, that dynamite trinitroglycerin TNG is confused with trinitrotoluene TNT is not as much the

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