All posts by Gordon Short, MD

Dr. Gordon Short is a trained pathologist and the founder, chief designer and inspirator of Brevis Corporation since 1977.

Syphilis, the Great Imitator

I wouldn’t put any money on the accuracy of my memory as to the attitude of Alexander Langmuir about Tuskegee. What I think I remember distinctly is that the Tuskegee Syphilis Study was briefly mentioned and discussed in the Epidemic Intelligence Service course I audited in the summer of 1957at the CDC. It was discussed as if it were an ordinary investigation to discover more about the natural course of syphilis.

Syphilis, the Great Imitator, has 4 phases: Primary (chancre), Secondary (rash– the Great Pox), Latent, and Tertiary. Each has its own unique characteristics that help to make syphilis “The Great Imitator.” Treponema pallidum, the causative agent is a sneaky devil that can go underground for decades clinically while eating away at vital organs. In 1932, when the Tuskegee Study began, there was considerable uncertainty about many aspects of the natural history of this disease. For example, when syphilis enters its latent stage, is it inevitably going to end in tertiary syphilis with aortic aneurysms or general paresis of the insane or tabes dorsalis or gummas? Or might there be a spontaneous cure? And what is a “cure”? A negative Wassermann test (which was known to be unreliable at that time)? Since the latent phase could last for several decades, there would be a good chance that the patient would die of some unrelated condition such as stroke or heart attack. So what effect would syphilis have on life expectancy?

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In 1930 there was considerable speculation about these questions and so it seemed desirable to study the disease prospectively over an extended period of time. And so the Tuskegee Syphilis Study was begun in 1932. But why Tuskegee and who were the subjects?

It had been observed that in Macon county, home of the famous Tuskegee Institute founded by Booker T. Washington, about 35% of the male, Negro population had a positive Wassermann test for syphilis. (About 80% of the Macon County population was black.) These men were mostly sharecroppers, many illiterate. They were poor and unlikely to be able to afford antisyphilitic therapy. Therefore this population represented a group that could be observed for an extended period without ethical concerns about “doing no harm” since they weren’t going to be able to afford treatment anyway.

Incidentally, the study was later heavily criticized because the subjects were treated as “guinea pigs” and not as humans. But may I remind any gentle readers that Negro slaves were defined in the US Constitution (Article 1, Section 2) as 3/5 of a white person. Negro slaves were further defined as “property” and could not become citizens (See Dred Scott decision and Roger Taney , Chief Justice of the US Supreme Court). Thank you, Founding Fathers (who were mostly slave-owning southerners). Not guinea pigs but maybe like upright beasts of burden. This attitude did not disappear immediately after the Emancipation Proclamation.

The plan was to recruit about 400 men with a positive Wassermann who were in the latent, asymptomatic phase. Those who were in the early stage, roughly five years after the primary chancre, would be referred for treatment and were not eligible for the study. About 200 men with negative Wassermanns would be recruited as controls. But what does it mean to “observe”? The patients had to be given physical exams periodically and also have repeat Wassermanns and spinal fluid exams to look for neurological changes. That’s heavy-handed “observation.”

The study has been criticized because the subjects were not treated with a full course of the prevailing antisyphilitic drugs. (They were treated with a suboptimal course of several months.) But before the late forties when penicillin became the accepted treatment, the standard treatment was the arsenicals, arsphenamine or neoarsphenamine. These treatments consisted of painful intramuscular injections administered monthly for at least a year. All aside from the possibility of a Jarisch-Herxheimer reaction, an asymptomatic patient had a right to to question this procedure. Furthermore, from a medical perspective it was unclear as to the effectiveness of treatment at this stage of the disease and what benefit might ensue. The youngest subjects recruited in 1932 were age 25. By 1948 the subjects were then at least 41 and most were older. At this point the ethical situation begins to become murky. Would treatment be beneficial? But there was much uncertainty and that is why the study was being done. There was considerable incentive to continue as before.

In studies such as this, the investigators have been criticized for treating the subjects as guinea pigs and not as human beings. How could this be so if the study was utilizing some black doctors and the Tuskegee Institute and the indomitable black nurse, Nurse Rivers?

I got some insight into this by my experience living in the South, first from February 1942 to June 1943 on Parris Island, the Marine boot training camp. The top medical officers for the Parris Island base hospital consisted of a Commanding Officer, a Chief of Surgery, an Executive Officer, and a Chief of Medicine (my father). The separate houses were lined up in a row and behind each pair was a maid’s quarters. One weekend when our maid, Lucy, was at her home on the mainland, I looked into these quarters. These consisted of two plain bare rooms each containing a bed and a dresser and bare wooden floor. Between the rooms was a “bathroom” with a sink and toilet. If there was a tub or shower, I didn’t notice it. To the eyes of this 11-year-old kid, raised in an upper middle class suburb of New York, this was a shock, to use a mild expression. But Lucy was always cheerful with nary a complaint. I guess she “knew her place.”

It took me a bit longer to learn mine. One time I had occasion to ride by myself on a public bus some where off the island. At age 11 I wasn’t very tall and when I got on the bus, it looked like every seat was taken. Except that straight down the aisle there was a vacant seat in the middle of the back row. To which I headed.
After I sat down and started looking around, I noticed that all the people sitting around me were highly pigmented and all the palefaces were in the front half. What to do? Nothing that seemed reasonable. So I sat there. The black people around me were too polite to say anything and I was too bashful. But I couldn’t help wondering what they were thinking.

Fifteen years later with a wife and baby son, I returned to the deep South to begin my service as a medical officer with the USPHS in Savannah from August 1957 to August 1959. We attended a small Adventist church, membership about 100, that was on a side street that wasn’t paved. The church itself was clean but definitely showing its age. Not antebellum but certainly not modern. However, we soon fell in love with the members there, all delightful, kind souls. In Savannah at that time there was a new, black Adventist church with a membership of around 400. Sometime in 1958 or 59, Little Richard came to town during his sojourn in the Adventist church and was the featured guest at the black church. My wife and I decided to go hear him. For some reason we were a minute or two late and the place was packed. But immediately a smartly dressed usher wearing immaculate white gloves approached us and ushered us down to seats in the front of the church. Why? What was so special about us? I wasn’t wearing a uniform. We were just a young couple with no VIP markers. Except white skin. It made me distinctly uncomfortable. Especially since the black choir, when guests of the white church, was required to enter via the back stairs into the church rather than the front entry.

In those presegregation days, restrooms were always “Men,” “Women,” and “Colored.” And, of course, the “Colored” were always consigned to the back of the bus.

My job was as a “toxicologist” at CDC’s Technical Development Laboratory on Oatland Island. The building was originally constructed as a retirement home for railway workers. Later it was acquired by the government to be used as a rapid treatment center for syphilis. After the arrival of penicillin, it was turned into TDL. As if the swampy southern east coast didn’t raise enough mosquitoes in the great outdoors, TDL raised millions more in its own mosquito vivarium. The purpose was to study the biology of different species. This was undoubtedly an improvement of my observation that whenever I patted one on the back it left a red splotch as a reminder of why I observed that mosquitoes suck.

So, after all this rambling, let’s get back to is my bottom-line assessment of the Tuskegee Syphilis Study. This is how this one observer sees it:

In 1932 the study was reasonable and justifiable given the current state of knowledge about syphilis.
The study was flawed from the beginning because the participants were treated with arsenicals although in a suboptimal dosage.
When penicillin became widely available and accepted circa 1950, the youngest subjects were at least in their forties and it was unclear whether treatment would significantly alter their health status.
In 1957 (when I was at CDC), it was deemed advisable to continue the study because there was much more to be discovered. But by then it was a bit like holding a tiger by the tail.
The participants were generally well treated, if Nurse Rivers story is to be believed. And I believe her.
But it is true that the participants were treated as guinea pigs in the sense that they did not give “informed consent.” But how does one “inform” uneducated sharecroppers?
The study helped result in more stringent ethical guidelines – as it should have – but it is unfair to retroactively apply those guidelines.
Others may disagree (and have) but these are my tentative conclusions. What think you?

P.S.: The best definitive study is “Bad Blood. The Tuskegee Syphilis Experiment” by James H. Jones. (1993)

Gordon Short, MD
Brevis Corporation

The Deadly Plum

If history is correct, there was a day when there were plum trees on Plum Island. But the history of Plum Island is so convoluted that it is hard to say. Anyway, it got its name and who really cares how.

Some years ago a good friend, Jay Dirksen, PhD, (pharmacology and bionucleonics) said that I might enjoy Nelson DeMille’s book “Plum Island.” Although I love good fiction, I’m always frustrated by not knowing how much is based on fact and how much is made up. Although I grew up in Queens, Long Island, I had never heard of Plum Island and had trouble believing much of what DeMille described.

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An internet search led me to a book by Michael Christopher Carroll called “Lab 257, The Disturbing Story of the Government’s Secret Plum Island Germ Laboratory” (2004). In this factual account I learned that essentially everything that DeMille said about Plum Island was true and that the story of Plum Island is frightening in the extreme. Or at least should be.

Plum Island is an 840 acre island that is only a mile away from the north fork at the eastern end of Long Island. It has a long and unremarkable history going back to when it was owned by native Americans. Whites took over before the Spanish American War and the military built the large Fort Terry there and also a lighthouse.

With the military still in charge after World War II, the story becomes more interesting. The military imported a Nazi scientist, Dr Erich Traub, through Operation Paperclip, to be a founding father of a biological warfare laboratory on Plum Island. Traub had worked for the Nazis (reporting to Heinrich Himmler) in the arena of biological warfare. When the USDA took over management of Plum in 1954, it was ostensibly to do research on diseases that could be a threat to domestic animals – cattle, horses, sheep, chickens, etc. Such diseases as foot and mouth disease and many others. But the dividing line between research to protect domestic livestock and to disable the same (of an enemy) is blurry.

While Carroll’s book well describes all that has been wrong with the operation of the Plum Island Animal Disease Center, the more encyclopedic history of the island from its earliest days called “A World Unto Itself, The
Remarkable History of Plum Island, New York” by Bramson, Fleming and Folk (2014) takes a less histrionic viewpoint and describes some of the scientific discoveries that were developed by PIADC scientists under the direction of Drs. Maurice Shahan, Jerry Callis, Roger Breeze and others.

Nevertheless, the history of Plum Island has enough mystery associated with it to have generated a plethora of fantastic fables, urban legends, conspiracy theories or whatever. Such as the Montauk Monster or that Lyme Disease was actually invented on Plum Island and released on an unsuspecting public.

Plum Island operates at a BS-3 level, some would say at an enhanced BS-3 level that approaches BS-4, the highest level. There are BS-4 labs at Fort Detrick, MD and at CDC in the Atlanta area. BS-4 means that the disease being studied is very serious in its potential to harm humans – usually deadly – and there is no vaccine or reliable treatment. It requires the researcher to wear a fully enclosed space suit connected to a hose that keeps positive pressure inside the suit. Strict protocols are observed with decontamination before exit from the suit and return to outside clothing. It was hoped by the Plum Island scientists that such a lab could be built on the Island but this did not happen.

Which reminds me of an experience I had many years ago here in Salt Lake City. At the time I was chairman of the Environmental Health Committee of the Utah State Medical Association. I was no longer in the practice of pathology, but I continued to pay my dues so that I could be on this committee. (My interest at the time was in trying to influence legislation to restrict smoking in public places.) One of the other members of the committee (Dr. Buchi?) said that he had heard that there were plans to build a BS-4 lab at the Dugway Proving Ground southwest of Salt Lake City. With the previous history of the Skull Valley sheep kill of 1968 (where several thousand sheep were killed, apparently from VX nerve gas that drifted east from Dugway during a test, it seemed to our committee that building a BS-4 lab upwind from Salt Lake City was undesirable. We strenuously opposed the plan and the lab was never built. But I’m not sure there was a cause and effect relationship to our opposition.

Dugway is to Utah what Area 51 is to Nevada. Secrecy prevails. However, I had a tenuous connection to Dugway when I was at CDC’s lab in Savannah. When I was engaged in the malathion study in the Federal Correctional Institution in Tallahassee, Florida, I used a micro method for determining serum cholinesterase activity that was developed by a scientist at Dugway. (I get a kick out of watching the expressions on people’s faces when I mention that I was in a Federal Prison in Florida.)

Well, I have wandered a ways away from Plum Island Animal Disease Center in New York to Utah and Nevada and then down to Georgia and Florida. But that is the prerogative of old men so perhaps I can be forgiven. (Are you familiar with “The Story of the Old Ram” by Mark Twain? You should be. )

Happy Meanderings! (But I don’t recommend going to Plum Island in search of plums. Unless you want the deadly variety.)

Gordon Short, MD
Brevis Corporation

Image by WikiMedia

How I Came Not To Be (Almost)

My father was raised on a farm in western New York near Canandaigua in the Finger Lakes region. On the farm he had a dog (I think his name was Shep). One day a neighbor said that he thought Shep had rabies. Dad begged to differ and to prove that Shep was OK, he put his hand up to Shep’s mouth. When Shep did not not bite him, he said, “See. He is normal. Nothing wrong with him.” However, the next day Shep disappeared and a neighbor related seeing him running wildly away (“furious rabies”). If Shep had bitten Dad, the Short genealogy would have been even shorter and I would not be writing this story.

Some 20 years ago or so, my wife and I went up to Sandpoint, ID to visit my wife’s folks, who had retired there. Their house was a bit out in the country and one day I took a walk down a country road past widely scattered homes. Just as I was walking past one house, a medium size mutt of indeterminate breed, ran out and before I knew what was happening, it bit me on the back of my right thigh. It was not a serious bite – I hoped – but it did break the skin. I called the sheriff so that we could go to the house to determine if the dog had received the normal shots including, of course, rabies. The lady of the house was quite hostile to think that I would call the sheriff. But we got her calmed down enough to tell us that she was just caring for the dog who actually belonged to her offspring who was away on vacation. She assured us that she was sure the dog had received all its immunizations, but the dog had no collar and there was no confirmation.

That left me to decide what my next step should be. What were the considerations? The bite had just barely gone through the fabric of my heavy pant’s leg, but it had been enough to draw a little blood. I seemed to recall from medical school that the virus was in the saliva, but if the cloth absorbed the saliva, it might not get into the bite wound. A slightly encouraging thought (if true), but that still left considerable doubt. I should have insisted that the dog be quarantined for observation for a couple of weeks, but I guess I was too distraught to think of that and anyway Sandpoint was a small town where they may not have had the appropriate facilities.

Incidentally, the sheriff told me that in Idaho a dog that bites you is considered “vicious” by law and you are entitled to shoot the critter. Not knowing, and not having a weapon on me (I never carry), I didn’t exercise that option. Which, of course, is not a good option anyway if rabies is suspected.

Well, I opted not to do anything, beside cross my fingers and hope. And I never became rabid (although some who know me well might dispute that). Anyhow, just remember, don’t let the bed bugs bite. Or rabid canines for that matter.


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Parris Island

I was born in lower Manhattan (just a few blocks from where the World Trade Center would later be built) in October of 1931. My earliest memories are of growing up in Forest Hills, an upper middle class, pleasant neighborhood on Long Island. Life was simple, enjoyable, worry-free.

My father was an internist with an office on Park Avenue. He had deep patriotic instincts and was inspired to join the Naval Medical Reserve about the time I was born and was commissioned a Lieutenant Commander. Life took a dramatic change on December 7, 1941. In what seemed like a matter of minutes, Dad received orders to report for active duty early January in the Marine boot training camp on Parris Island, SC. Within days he had to get his new uniform from Brooks Brothers, arrange for another doctor to take over his practice, get ready for Christmas for my sibs and me, and get himself out the door and down Highway 17 to South Carolina. Meanwhile Mother had to pack all her dishes, etc. in barrels in the basement, rent the house and get ready to move my sister and brother and me to follow at the semester break the end of January.

What I remember most that a friend drove us to Pennsylvania Station on a miserable evening with freezing rain to give us a cold send-off. My mother and sister slept on the lower bed of a pullman car while my younger brother and I slept on the upper bunk. But in the morning when I looked out the window, we were in Virginia and the sun was shining. Wow! That afternoon the train arrived at the whistle-stop town of Yemassee, SC where Dad was there to meet us in his trusty 1941 black Dodge sedan. He drove us to our new home on the island. It was a single story affair with a screened porch on two sides where I slept in the warmer weather and listened to the buglers around the island play a nameless tune at 9:00 PM and taps at 10:00.

Although I was only 10, I remember how impressed Dad was when he came home and reported that there was a case of spinal meningitis in a recruit. At that time it was not only highly contagious but essentially untreatable and with a very high mortality rate. No antibiotics then. But there was sulfadiazine and this was given prophylactically to everyone(?). Anyway, Dad was mightily impressed with that seeming miracle of stopping a threatened epidemic in its tracks. I’m sure he well remembered the influenza pandemic beginning in September, 1918 that exploded in a similar military camp in Camp Funston, KS, since he graduated from medical school about the same time.

My mother, who was raised in New York City, used to tell about meeting a friend who would say something like, “Did you hear that Bill died last Tuesday.” And Mother would say, “How could that be? I just saw him a week ago and he looked fine.” It is hard for me to imagine what it was like to live when the possibility of a random strike of lightning could hit you with a rapidly fatal illness like influenza. We can be happy that we live in an age where that does not happen in this country while continuing to remind ourselves that the possibility of a new pandemic hangs over our heads like the Sword of Damocles. Carpe diem! Make every day count.

Cheers!


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Image by USMC Archives, Platoon 903, Parris Island, 1942

Dead Mosquitoes and Live Lice, Part 2

Continued from “Dead Mosquitoes and Live Lice, Part 1

So what about the live lice? When I went into the US Public Health Service in 1957, it was to fulfill my draft obligation after student deferments. Recall that the Korean War was from 1950 to 1953. Also that during WW II, DDT dusting powder was widely used to kill lice, especially in conquered civilian populations, to prevent the spread of typhus. But by the Korean War some lice had sneer at DDT and so something else was needed. Enter Dr. Wayland J Hayes and yours truly. Dr Hayes arranged for prisoner volunteers at the Federal Correctional Institution in Tallahassee, FL to be recruited to test the toxicity of malathion formulated as a dusting powder substitute for DDT. Malathion is an organophosphorus compound unrelated to DDT and was thought to have similar effectiveness and human toxicity.

Dr Hayes was the lead researcher and I was the lackey who did the cholinesterase analyses, etc. in the prison. (I have always enjoyed watching the expressions on people’s faces when I say I was in prison once.) The prisoners were told the possible adverse effects of the program and were given “good time” (reduced sentences) for participation. (After this one prisoner opted out but was later found to be consuming his own brew made with a smuggled, homemade still. Was that less toxic?)

The results were published in the Bulletin of the World Health Organization, (1960, vol 22, page 503-514) and on review I was impressed by one observation: “Although one of us (J.G.S.) had received, without injury, a 30-hour application of 10% malathion powder in preparation for the study of volunteers, . . . .” My small contribution to the advancement of science. Well, in retrospect I have to say that it was safer than dodging bullets in the Vietnam War, which was waging at that time.

Human infestation with lice is uncommon in this country and typhus is really rare. We have a lot to be thankful for in this country in spite of the vicissitudes of politics and the stock market. But there are still enough problems with antibiotic resistance and the lack of proper hand hygiene, etc. Maybe our watchwords should be Thankfulness, Vigilance, and Diligence. “May the Force be with you!”


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Dead Mosquitoes and Live Lice, Part 1

Having recently talked about pigs from Jersey and trichinosis, I decided to see what other stories Berton Roueche had that might be of interest. Looking at the table of contents in his compendium called “The Medical Detectives” (1980), my eye was caught by “The Dead Mosquitoes.” Why did “dead mosquitoes” catch my eye? Therein lies a tale.

In August, 1957, having finished the course for the Epidemic Intelligence Service at the CDC in Atlanta, I headed down the road to Savannah and the Technical Development Laboratories, a branch of the CDC, on Oatland Island. (The drive, without air conditioning in those days, when the temp and humidity both hover around 90 is another story.)

TDL, as the lab was called, was set on a marshy island that bred mosquitoes in impressive battalions that found my blood especially delicious and inviting. I therefore found it ironic that inside the lab mosquitoes of several species were being raised by the millions. Why? To study their habits. Such as, how far do they range. Radioactively tagged mosquitoes of different species were released from a central spot and collection traps were spaced at a variety of distances. Turns out some species do not fly more than several feet high and have small ranges while others fly much higher and get caught by wind currents and travel much farther. (Thought you would like to know that.)

Mosquito larvae are so sensitive to insecticides that they were used for bioassays. Except when they weren’t. Also indigenous to the lab were great hordes of American cockroaches. (American cockroaches are up to 2 inches long vs the puny German variety at 1/2 inch). TDL was in a 240 foot long building. Someone at one end of the building decided to attack the roaches with a pyrethrum spray. The spray traveled 200 feet down the hall and wiped out the mosquito larvae in the bioassay lab. After that all insecticides were strictly verboten in the building which must have made the cockroaches deliriously delighted.

Anyway back to the Medical Detectives. It’s a complex story of poisoning by an organophophorus insecticide that was accidentally spilled on some blue jeans that were subsequently sold at discount in Fresno, CA. A pair of these were worn by a boy who then rapidly became violently ill. Another boy wore another pair of the blue jeans with the same result. (He was diagnosed by a classmate of mine, Merritt Warren, MD, who had heard about the first case.) Pinpoint pupils, low cholinesterase levels in blood and rapid response to atropine cemented the diagnosis. But which insecticide? While waiting for a chemical analysis in a research lab, the pants were left overnight in a room with some mosquito-laden cages. In the morning the mosquitoes were all stone cold dead, killed by insecticide vapors.

The insecticide was determined to be Phosdrin and it was later shown to have come from a leaking container being transported on the same truck as the package of blue jeans. One lesson to be drawn from this episode is that if the jeans had been laundered before being worn (they were not), the Phosdrin would have been washed out.


Continue reading (Part 2)

A Pig from Jersey

The last Saturday of June, 1957, having finished my internship, I left Lansing, MI, about midnight in my little VW with orders to report to CDC in Atlanta at 8:00 AM Monday to begin my two years of service in the US Public Health Service. I was to audit the course for the Epidemic Intelligence Service before reporting to the Technical Development Laboratory in Savannah, GA. The EIS course was founded and taught by Alexander Langmuir. Langmuir was a bigger than life, charismatic story teller who quickly made me feel that epidemiology was the most fascinating subject available to mere humans. There were maybe 40 or 50 of us taking the course and in front of our assigned seats there was a stack of reading material that looked generally pretty serious. But on the top of the stack there was a small paperback book with the title “Eleven Blue Men” by Berton Roueche. It looked strangely out of place and unserious and I put it aside for later.

I don’t remember when “later” arrived, but when it did, I was treated to a series of fascinating articles of which the Jersey pig was the first. It concerned a schlachtfest being held at the New York Labor Temple, a German-American meeting-and-banquet hall. A schlachtfest, for those of you uninitiated, is a pork feast. The pig in question was purchased by a butcher in Staten Island and the carcass was taken to the Labor Temple in Manhattan where it was converted into sausage among other things. One of the men involved in this escapade had eaten some of the raw sausage to check on the seasoning, and the rest is history. The man became very ill with fever (he later died) and the physician, a Dr Levy, came to the diagnosis when he discovered an elevated eosinophil count in his blood smear. It was then confirmed by a muscle biopsy which showed numerous Trichinella spiralis parasites.

Trichinosis is one of the many parasites one studies about in Microbiology, but I had never seen a case until some years ago when I was assisting in an outpatient laboratory here in Salt Lake City. I didn’t see the patient myself but I heard her story second-hand. This young lady had been on vacation in Hawaii and had been invited to a luau. The luau was the genuine thing apparently with a whole roast pig on a rotisserie above a fire. Everybody enjoyed the fresh roast pork. Except that the young lady in question arrived somewhat late to the proceedings and her portion of pork was from a more interior portion of the carcass that had not been adequately heated to kill the larvae.

Here the details are sketchy but she apparently had the usual GI symptoms followed by severe muscle pain. By this time she was back home in Salt Lake City and her doctor ordered the usual lab tests including a CBC. Thus the blood smear that showed more eosinophils than I had ever seen before. This was some time in the 1970s and I don’t remember the percentage of eosinophils
but I think it may have been around 30%, about 10 times normal. The smear was lit up with red lights like a Christmas tree. That number of eosinophils doesn’t define trichinosis but it certainly is highly suggestive.

Today trichinosis is very rare, but it is just the rare diseases we don’t think of that can rear their ugly heads and bite us in the rear. Tricky trichinosis. Maybe the ancient Hebrews knew something important. Whatever. May Trichinella spiralis rest in peace and bother us no more.

Gordon Short, MD
Brevis Corporation


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Flu Education – Another Anniversary?

2018 – Another Anniversary?

Anniversaries. To celebrate or just to observe?

2018 is the fortieth anniversary of the incorporation of Brevis. Yeah!

2018 is the anniversary of the end of World War One.

Great Influenza Pandemic

But 2018 is also the one-hundredth anniversary of the Great Influenza Pandemic. And a dramatic start of a hundred years war that has no end in sight. World-wide this pandemic claimed somewhere between 20 and 100 million victims in 1918-1919. Pick your source to pick your number.

In previous essays we have shown how the flu predisposed us to World War II by disabling Woodrow Wilson during the writing of the Treaty of Versailles. We have also talked about the search by intrepid scientists for the original virus which took them to frozen corpses in Brevig Mission, Alaska. The virus may have been identified but that does not explain how the original epidemic starting in Fort Funston, Kansas was quite mild and then became much more virulent in subsequent outbreaks. One thing is clear: Army forts were crowded with new recruits who were destined for Europe. Crowding was ideal for spread of this virus.

The highly mutable virus appears to have a natural host in ducks and ducks seem happy to share with chickens and pigs. Of which multitudes reside in China. So we go to China to discover each year which strains are on the current hit parade so that we can develop effective flu vaccines. Maybe this is how China is demonstrating the importance of their trade with the US. Or is it just a free gift as a way of saying Thank You for all the other goodies we import from them?

Wash Your Hands

Regardless of all the ins and outs of influenza – and all other infectious diseases – the best we can come up with for prevention are proper hand hygiene and vaccination. As the decades roll by replete with outbreaks of new often more virulent strains of nasties the most effective strategy remains the same. Wash your hands. Wash them often. Wash them well.

Happy Anniversaries!

Gordon Short, MD
Brevis Corporation
13 November 2018


New Flu Posters

 

Ah, the Staph of Life! Ether Frolics & Gas Gangrene…

Gangrene and Glory Book Cover

I have found very few good books on Civil War medicine. One of the better ones is “Gangrene and Glory” by Frank Freemon (1998). With an MD and a doctorate in American History, Freemon fills in many of the blanks. In the last post I mentioned that battlefield amputations were often done with only a shot of whiskey for anesthesia. While whiskey was ubiquitous and available, both armies supposedly had access to ether and/or chloroform.

“Ether frolics” were popular entertainments during the 1830s. Traveling lecturers dispensed diethyl ether to any audience member who wanted to test its mind-altering effects, which were similar to those of nitrous oxide.

William Edward Clarke (1819-1898) participated in these events. When he became a medical student, he administered ether to a Miss Hobbie to assist in a dental extraction, thereby establishing himself as the first to use an inhaled anesthetic for a surgical procedure.

In 1842 Crawford Long (1815-1878) used ether before removing a neck tumor from a James Venable. Later he used ether for limb amputations. A hospital in Atlanta is named after him and is now a part of Emory University.

In 1846 William T. G. Morton (1819-1868), a New England dentist, used ether as a general anesthetic at Massachusetts General Hospital.

In 1847 Scottish obstetrician James Young Simpson (1811-1870) used chloroform for general anesthesia. Chloroform became very popular thereafter at least partly because it was non-flammable, but its popularity waned after its toxicity to heart and liver was discovered.

During the Civil War (now there’s an oxymoron!) those dripping ether or chloroform had little, if any, training. But they did have one advantage I supposeif the patient died on the table they always had the excuse that it was because of their battle injuries and not their incompetent anesthetist. Under those primitive conditions it is a miracle that any patient survived. Yet thousands did.

With luck, the patient developed “laudable pus” instead of gas gangrene. Infection was expected, and if it was just staph the patient was considered well on the road to recovery (of course, in those days they didn’t know staph from staff). So that was the staph of life? How times have changed!

Civil War Medicine: Surgeons With Saws & A Stiff Shot of Whiskey

Civil War Polaroid Transfer_s

On April 29, I had a right half-knee arthroplasty. The procedure was done with epidural anesthesia and some additional propofol. I requested a minimal dose of the latter so that I could be more or less awake during the procedure — which happened — and I remember hearing the electric saw doing its thing and also apparently a mallet and chisel. The procedure went smoothly and with dozens of people taking care of me in the hospital, and several more from home health care, I am making a good recovery ahead of schedule.

What a contrast from Civil War medicine! If you have ever been to a Civil War battlefield, you may have seen what passed for a hospital then. At the Battle of Bull Run I believe it was a little one-room schoolhouse that was pressed into service by the Union army. The “service” consisted mainly of a surgeon with a saw who knew how to separate limbs from injured soldiers. Anesthesia was a stiff shot of whiskey and some helpers to hold the screaming patient immobile.

How the patient was sewed up didn’t attract much attention in the few books on the subject, but the suturing and dressing had to have been pretty primitive. If the patient was lucky, he was transferred to an “ambulance” for a very bumpy trip back to Washington or wherever and a “respectable” hospital. Pictures show some of these hospitals to have been large tents with hundreds of bunks lined up cheek by jowl.

How anyone could have survived this level of care boggles the bean, but thousands did from all accounts. The alternative to surgery they learned early, was likely to be gas gangrene with certain death. Why this nasty bacterial infection? Those noxious Clostridium spore formers lived largely in the guts of horses. And horses — the engines of the Civil War — were ubiquitous. They contaminated the soil and the soil contaminated soldiers.

I once did an autopsy on a case of gas gangrene. The man had been kicked on the shin by a horse with an injury that just barely broke the skin. When crepitation was first detected around the knee, a hindquarter amputation was performed immediately. The patient still showed up in the morgue a couple of days later. Makes one a believer in the power of Clostridium.

So, how did those survivors survive? They must have been some tough dudes!

There’s an interesting audio quiz and history lesson on the Public Radio International website about first responders and the Civil War. Have a listen here.