Ways to Die: Snake Venom
The vast majority of snakes that one encounters in the wild (unless you live in Australia or India) are either non-venomous to humans or want nothing to do with you.
However, should you stumble upon a rattlesnake nest or coral snake hole while texting in the middle of nowhere, there will probably be a combination of different enzymes and polypeptides pumped into your body, via the modified parotid salivary glands (right below the ear in humans) that snakes have evolved over the ages, to disable their prey. Of course, you’re not prey, but you stepped on a snake while texting. It has every reason to envenomate you.
While all snakes have multiple active enzymes in their venom, all snakes dangerous to humans have either neurotoxins or cytotoxins as a significant component in their venom. For the most part, elapids (such as the cobras and mambas) create neurotoxins, while the viperids (such as vipers, adders, and rattlesnakes) create cytotoxins.
Neurotoxins
Cytotoxins
Images:
Top: Bungaris fasciatus - Banded Krait. An elapid, and the largest of the kraits. Has neurotoxic venom. [source]
Center Right: Hydrophis robusta [now Hydrophis spiralis] - Yellow Sea-Snake. The longest sea snake, at 3 m (9.8 ft). A member of the Hydrophiinae, separate from other elapids. Though they have some of the most toxic venom in the world, bites are extremely uncommon and often unnoticed. [source]
Center Left: Vipera russellii - Russell’s Viper. A particularly aggressive viperid. Necrosis and amputation following envenomation not uncommon, due to hemolysis and local cell damage. [source]
Bottom: Vipera caudisona [now Crotalus horridus] - Timber Rattlesnake. A venomous viperid endemic to the United States. Primarily hemotoxic venom, very low fatality rate, but very painful bites. [source]
Among the things to be grateful for this holiday season, you’re most likely not dying from any of these conditions…
I’ll be elaborating on all of these conditions soon, but here’s the 30,000 ft overview of some significant nutritional disorders (aside from allergies and deliberate poisoning/ordeal poisons - the latter I may cover in the future, as culturally they’re fascinating) that have plagued mankind since we took our first bite of food.
While many nutritional disorders are due to a lack of food, some are due to an excess of a toxin from some food that the body can’t process. The staple foods that end up harming people when over-consumed or not properly processed often are eaten or poorly prepared as a result of famine, and just like nutritional deficiencies, many still plague the world today.
Nutritional Disorders - Deficiencies:
- Beriberi: Thiamine (Vitamin B1) - Extreme fatigue, difficulty walking, and confusion/difficulty speaking are the primary symptoms. Also can cause heart failure, vasodilation, peripheral edema, nystagmus (involuntary eye twitching), and tingling sensation in limbs.
- Goiter: Iodine - Swelling of thyroid gland. Rarely fatal, but can cause severe deformity and hypothyroidism.
- Rickets: Vitamin D, magnesium, phosphorus - Dental problems, skeletal deformity and stunting, muscle weakness, swollen wrists, bone pain, soft skull.
- Marasmus: All nutrients, especially protein - Tissue and muscle wasting, dry folds of skin hanging from buttocks and armpits, extreme adipose loss, voracious appetite
- Pellagra:Niacin (Vitamin B3) or tryptophan - “The four D’s”: Diarrhea, dermatitis, dementia, and death. Causes extreme sunlight sensitivity, pale skin that breaks out in blisters/keratinitis upon sun exposure, insomnia, aggression, as weakness. (Basically, they’re crazy pissed-off vampires.)
- Tetany: Calcium deficiency or phosphate excess - Involuntary contraction of muscles due to increased action potential of neuronal membranes, due to low plasma calcium, which increases membrane permeability to sodium, causing progressive depolarization. It’s complicated. It’s basically involuntary and painful stiffened muscles.
- Kwashiorkor: Protein calories - Pedal edema, distended abdomen, lack of adipose tissue, anorexia (as opposed to marasmus, where the child wants to eat everything), loss of hair and teeth. More common in wetter climates, marasmus more common in dry climates.
- Scurvy: Vitamin C - Lethargy, spots on skin, paleness, spongy gums, fever, bleeding of mucous membranes. Eventually causes open and pus-oozing wounds, tooth loss, jaundice, neuropathy, and death.
- Keshan Disease: Selenium - Fosters a mutated strain of coxsackie B virus which causes pulmonary edema and heart failure, mostly in women of child-bearing age and in children. Can be cured with selenium supplementation
Nutritional Disorders - Toxicity:
- Lathyrism: Untreated grass pea - Causes an inability to move the lower limbs. Not usually fatal on its own, but when it occurs in concert with famine (as in the Spanish War of Independence), death from starvation sometimes occurs.
- Ackee Poisoning/Jamaican Vomiting Sickness: Unripe ackee fruit - Intense thirst, nausea and vomiting, tachycardia, headache, general weakness, and confusion/stupor. Death can follow in just 12 hours. Caused by hypoglycin A and B in unripe fruit and mantle of fruit (even when ripe). General symptoms of hypoglycemia, similar to diabetes.
- Konzo: Cyanide intoxication from poorly treated cassava (manioc) - “Bound legs” - extreme hypertonia in leg muscles. Causes pain and very disturbed gait, but is not progressive, so does not cause death. Does generally disable the afflicted persons, and this can be debilitating (socio-economically and physiologically) to patients.
- Lytico-Bodig: Cycad nuts and seeds - Unique to Guam, far western Papua New Guinea, and Honshu, Japan. Parkinson-dementia complex, difficulty speaking, tremor, stiffness, loss of sense of smell, lethargy, memory loss. Caused by accumulation of BMAA from cyanobacteria that grows on cycads. Incurable. Has not been seen in those born past 1961, due to elimination of both cycad products and fruit bats (which feed on cycad flowers and accumulate BMAA in their own bodies).
Thanks again to Antiquus Morbis for the inspiration; many of these terms can also be found over there, in addition to hundreds of other causes of death.
————————————————————————-
Though the Occupational Safety and Health Act as we [in the US] know it has only existed since 1970, there have been differing levels of federal oversight in the workplace since the Bureau of Labor was created as part of the Department of the Interior in 1888, and the Department of Labor was established in 1913. Though their oversight may not have been as stringent as what we have now, and laws may not have protected people as they do today, it was certainly better than nothing.
So what was working before ANY oversight like? Well, here are a few ways you could have died from your occupation, assuming you didn’t get killed by falling, getting crushed, getting impaled, or straight up getting ripped apart by the machinery (read: I’m not covering industrial disasters today; they’re coming later):
Aluminosis/Kaolinosis - Fibriod phthisis caused by the inhalation of clay dust.
Brass Founder’s Ague - A debilitating fever (often cyclical, like ague) caused by inhalation of the fumes of burned-down zinc, copper, or magnesium, in brass foundries.
Byssinosis - A lung disease caused by inhalation of cotton fiber dust or other vegetable fiber dust (flax, hemp, sissal). Leads to coughing, wheezing, progressive lung scarring and narrowing of the airways, and eventually death. Death isn’t so much due to the scarring, but more because of the highly reduced ability to fight pulmonary infections. Was particularly common in young girls and women, especially those in thread factories.
Caisson Disease - Spinal affection caused by either moving from a condensed atmosphere underground or a pressurized diving apparatus into the ground-level atmosphere again. Often occurs in conjunction with “The Bends”. Known as Diver’s Paralysis.
Cancer Scroti - …this is an awful one. A cancer noted by Percival Potts, affecting primarily chimney sweeps. Scrotal cancer, often appearing around puberty. Unfortunately was often treated as if it was a venereal disease, which wouldn’t have helped anything. Often led to the cancer spreading to the lymph nodes, leading to death before 18. Also known as Soot wart.
Danbury Shakes/Hatter’s Shakes - Symptoms of inhalation mercury poisoning exhibited by the hat-makers in Danbury, CT (the hat capital of the world in the 1800s). Often involved shaking, delirium, slurring speech, twitching, and a lurching gait. Sometimes these guys were mistaken for drunks.
Lacemaker’s Disease - Lead poisoning sometimes found in lace-makers.
Mad Hatter’s Syndrome - Differs from Danbury Shakes in that it more often leads to death, and is more often caused by unintentional ingestion of mercury (rather than inhalation). Involves severe ataxia, gastrointestinal symptoms, and emotional instability, in addition to the symptoms of Hatter’s Shakes.
Matches Disease - Oh god. Phossy jaw. Will do a full post on this and radium jaw soon. Caused by working with and inhaling the dust of white/yellow phosphorous, which was the primary ingredient in matches for a long time. Young girls and unmarried women were the primary makers of matches, and ended up the most affected by this disease. In the end, your jaw basically rots off and you go crazy and then you die. Also known as Phosphorus necrosis.
Potter’s Rot - Known as silicosis today. Caused by inhalation of silica particles often found in clay. Silica embeds itself deep in the alveolar sacs (meaning that it cant be coughed out), and the body, trying to get rid of the irritant, becomes inflamed and deposits collagen around the silica. This causes fibrotic nodules in the lungs, respiratory insufficiency, severe cough, fever, right ventricle heart disease, weight loss, and cyanosis. Silicosis leads to a significantly increased risk of tuberculosis and cancer, as well as mycobacterial infections. Also known as slate-worker’s lung/sandblaster’s asthma.
Ptilosis - Another form of fibroid phthisis, caused by inhalation of feather dust and down dust. In the ostrich feather industry of South Africa (which aside from pen quills, had a huge boom around 1880 thanks to the fashions of the time - feathers were prominent for over a decade, and came back in style frequently), this was particularly prevalent.
Rag Sorter’s/Rag-Picker’s Disease - Anthrax. Should do a post on the history of anthrax soon. Really interesting topic. Rag sorters were the women who sorted rags in the paper factories. Rag sorter’s disease often manifested itself as cutaneous anthrax, but pulmonary (inhalation) anthrax was not uncommon.
Sailor’s Fever - Yellow Fever. Almost always acquired in the tropics.
Silo-Filler’s Lung - Acute bronchiolitis fibrosa obliterans, caused by inhaling high levels of nitrogen oxides. Recently-filled silos have very high levels of nitrogen dioxide (which is one reason why you never want to be in a poorly-ventilated silo). Nitrous fume intoxication causes cough and shortness of breath, followed by high fever, chills, and a more serious shortness of breath. Death from pulmonary edema following the second phase was not uncommon.
Woolsorter’s “Pneumonia” - Inhalation anthrax. Anthrax spores are soil-borne, and when wool is sorted, it still carries the environmental dirt and grime that the sheep (who largely live outdoors) pick up. As the dirt is knocked free, soil-borne spores are also released. The sheep didn’t necessarily have to be infected itself to pick up anthrax spores as it lay on the ground. Though mortality rates from pulmonary anthrax hover around 45% these days thanks to early diagnosis, improved treatment, and (most of all) Pasteur’s anthrax vaccine for livestock, historic mortality rates were ~92%. Pretty awful thing to catch in the workplace.
Ways To Die: Amoebic Dysentery and Amoebiasis
First off, let’s get this out of the way - dysentery is not always amoebic, and the term “dysentery” refers only to the condition of having bloody diarrhea (bloody flux), caused by an infectious pathogen in the large intestine.
There are viral, protozoan, and bacillary dysenteries, in addition to the amoebic dysentery that shows up so often in tropical medicine. As a side-note, the dysentery that reared its ugly head in Oregon Trail (and on the real Oregon trail) would have been either bacillary (Shigellosis) or amoebic, depending upon the season and the location.
Amoebic dysentery and amoebiasis are caused by the amoebic pathogen Entamoeba histolytica. This single-celled organism is hardy, and able to spread easily, especially in environments where proper sanitation is not practiced.
Infection occurs by fecal-oral transmission, and begins when an encysted parasite is ingested by an individual, due to improper handling of food, water, fecal matter, or poor hand-washing practices. When the organism reaches the stomach, the acid dissolves the tough cyst surrounding the amoeba, and the now-active trophozoite (bottom) moves into the small intestine.
There are several paths that E. histolytica is known to take from here; for 90% of those infected, they’ll experience no symptoms, but will still spread encysted amoebas in their feces, possibly infecting others. Of course, acute amoebic dysentery (center left) is a possibility, and occurs in approximately 10% of infected patients. Many times, the amoebas will lie dormant in the mucosal wall of the small intestine, and not cause dysenteric symptoms until months or years later. Sometimes, chronic, long-term infection can occur (center right), especially when there is no or inadequate treatment. However, that is much more common in bacillary dysentery than amoebic dysentery. Of the 10% who become symptomatic, only 16% will experience severe ulceration and long-term damage of the intestine, and that number is much lower with proper anti-amoebic treatment.
In some people, the amoeba makes its way through the intestinal wall, and into the bloodstream. From there, it can cause amoebic liver abscesses (top), compromising liver function, and sometimes mistaken for cancers. With some Latin American strains of E. histolytica, the semi-dormant amoebae will burrow into the lining of the ascending colon or rectum, and cause a long-lasting cellular response, which eventually can end up forming a large granulomatous mass. Other strains of this amoeba can cause severe swelling and flask-shaped ulcers in the lining of the large intestine.
The most important part of treating amoebic dysentery is continuous rehydration therapy - the rapid loss of fluids severely hinders the activity of the immune system and the body at large. Amoebicides (anti-amoebic medications) are also used these days, to speed recovery. In a typical amoebic dysentery case, the patient will recover within one week, assuming a basic standard of care.
Images:
Top: Large amoebic liver abscess protruding from the epigastrum.
Center left: Intestines affected by acute amoebic dysentery.
Bottom: Entamoeba histolytica in the mucosa of the small intestine.
Center right: Intestines affected by chronic amoebic dysentery.
Source: Dysenteries; their differentiation and treatment. Leonard Rogers, 1913.
Read more:
Diseases of the Oregon Trail at APHL, by Michelle Forman
Dysentery in the Bad Bug Book, United States FDA
Humans have been out to get each other since before we were even Homo sapiens sapiens. For the strong and the brash, there was always outright physical violence; a club to the head or a knife to the throat was a simple way to destroy an unsuspecting rival.
But humanity had more than just violence at its disposal. Those inclined to plan and use their brains over their brawn found that there was an easier way to kill, one that would not risk their own body in an attack, or let others know who killed their rival, or even if the rival was killed by another person in the first place.
Enter: POISONS. Historically largely derived from plants, humans have murdered each other, and at times themselves, using various species of plants. There is an expansive list of plants that can potentially kill a human, but a few have gained reputations over the millenia as premier agents of death…
Sources:
A Modern Herbal. Mrs. M. Grieve, 1931.
Plants and Civilization. Maintained by Prof. Arthur C. Gibson, from 1985 textbook.
Ways to Die: Gangrene of the Foot
On Jan 8, 1687, Jean-Baptiste Lully was conducting a Te Deum, in honor of Louis XIV’s recovery from illness, and became so impassioned with the music that he struck his staff (a precursor to the baton used today) against the front of his foot.
An abscess developed that night, and despite treatment, Lully developed gangrene in his foot. Several court physicians strongly recommended amputation at the initial stage of gangrene, and again when it spread to his leg, but Lully would have none of it; he was much too interested in being able to conduct his own compositions, and having only one foot would not allow that.
Jean-Baptiste Lully died on March 22, 1687, due to gangrene of the foot, caused by enthusiastic conducting of his orchestra.
[image: army medical center, gangrene from war abscess, 1865.]
Pellagra (formerly “Asturian leprosy”) is one of the five pandemic deficiency diseases that have occurred in humans, and is caused by a lack of available niacin (vitamin B3) in the diet. Since niacin is a precursor to the NAD+/NADH molecules, which provide cellular energy throughout the body, many systems become disordered. Primary symptoms include weakness, insomnia, diarrhea, constant headache, sensitivity to sunlight (causing photo-dermatitis when exposed, as shown here on the face and hands), aggression, and eventually dementia. Death often follows within 4-5 years, if untreated.
One of the historical causes of pellagra was the widespread cultivation of corn, and the eventual usage of corn as a staple food, especially among the poor. While the corn plant does have niacin, it’s chemically bound and indigestible. The traditional Mesoamerican preparation of corn (now known as nixtamalization) by soaking it in limewater exposes the compound to a high pH (11+), which unbinds the niacin, and the human body is then able to absorb it. This practice is known to go back thousands of years, and is the reason that despite a maize-based diet, Native American peoples did not regularly suffer from pellagra.
Unfortunately, Europeans never really understood why the limewater was needed - indeed, we didn’t even understand what pellagra actually was until the 1930s. Up to that point, pellagra was known to be endemic to areas that were highly dependent upon corn, but it was believed to be either a germ or a maize-based toxin. It wasn’t until 1937 that Conrad Elvehjem identified the molecule in fresh meat and yeast called niacin, and its direct link to the condition was established.
Today, pellagra is very rare in the majority of the developed world, surfacing primarily in patients with chronic alcoholism or eating disorders. We now know that nuts, leafy greens, and whole-grain products also provide sufficient amounts of niacin, and the human body does not necessarily require meat or yeast as a source. However, in displaced populations requiring food aid, availability of niacin-providing nutriment is extremely limited, as many countries that provide aid still provide only oil and a basic cornmeal substance for food. Because of several outbreaks of pellagra and other deficiency diseases in refugee camps in the 1970s and 1980s, the United States and Western European food aid programmes now prepare their cornmeal with vitamin and mineral sprays to provide the necessary nutrients.
Want to know more? Read on:
The Mastery of Pellagra (1916 account of the ongoing pellagra epidemic)
Conrad Elvehjem: Further Studies on the Concentration of the Antipellagra Factor
Politics and Pellagra: The epidemic of pellagra in the U.S. in the early 20th century.
[Image Source: Tropical Diseases. Sir Patrick Manson, 1914]
From Antiquus Morbus:
A distention of the abdomen resulting from the accumulation of gas or air in the intestine or peritoneal cavity. Also called tympany.
From a 1760 English death record:

You also encounter the term “tympanum” when you look at the ear drum, so you can probably see the general etymology already. From Etymonline:
Tympanum: “drum of the ear,” 1610s, from M.L. tympanum, introduced in this sense by Italian anatomist Gabriello Fallopio (1523-1562), from L. tympanum “drum,” from Gk. tympanon “a drum, panel of a door,” from root of typtein “to beat, strike” (same root word as “type”)
Found in death records most commonly between 1700 and 1800, often referred to as “bloat” thereafter (and actually, in England at least, it was noted as “bloat” before ~1650, as well).
Who died of this?
This is the same “bloat” that you have to work to prevent in big dogs, but it’s good to note that (from what I can find), it was definitely not a common way to die. In humans, to cause the abdomen to distend to the point that it can be considered “tympanic” (drum-like and filled with air), most people would have to consume massive amounts of food or drink at one time. The full death records that I can find involving tympany or bloat all seem to come from upper-class or royal men. This is not surprising, as many of these people had massive banquets frequently (if not every night), and eating huge quantities was expected. If you’re at a banquet and already drunk off the king’s finest wines, you probably aren’t going to chew your food too well, which definitely adds to the risk of tympanites.
Why did this kill them?
When the body is presented with a massively full stomach of air or food, the pyloric sphincter can fail to respond correctly, and a clog in the pylorus (right before the pyloric sphincter) occurs. The backup of food in the stomach can cause gas distention (tympanites!), which would be the primary symptom obvious to any attending physician or anatomist. Less obviously, twisting of the stomach (volvulus) can prevent belching or vomiting to relieve gas distention, can cause lots of pressure on surrounding blood vessels, and can kill off stomach tissue due to lack of blood. The bloat and volvulus are also known to cause pressure on the portal vein, meaning that the liver cannot clean out the toxins in the blood, and the patient can die of sepsis.
So what’s the actual cause of death?
Basically, there were lots of underlying causes of death in “tympanites” or “tympany”, but they generally seem to have been caused by gluttony of the upper classes. Like I mentioned, sepsis and necrosis of the stomach tissue (which would have led to sepsis in the end, too) would not have been uncommon root causes. Hypotension (due to the blood unable to flow back to the heart from the stomach), general shock, and peritonitis also could have also been the true cause of death.
The similarity is that they either showed themselves in the form of a massively distended gut, or actually caused the drum-like abdomen itself, and generally under the same circumstances. I guess you could call it an “occupational hazard” of the royalty and their diplomatic “duties” of hosting giant feasts! Or you could just say they were gluttonous pigs who should have learned to chew their food.
Toxemia of Pregnancy [this liver damage caused by HELLP Syndrome - “hemolysis, elevated liver enzyme, low platelets”]
You can see the breakdown of the liver where incoming toxins and dead tissues are taken up to be processed (around the central vein, which is in the center of that deeper red area at the bottom). When the liver is overwhelmed by all the incoming toxins and dead cells, the liver cells themselves start to die, as they’re destroyed by what they’d normally be able to neutralize. This liver lobule still had normal liver cells on the surface, but would have had little to no processing ability to eliminate toxins in the blood. When the liver fails, death is often not far behind.
The Practice of Obstetrics, Designed for the Use of Students and Practitioners of Medicine. J. Clifton Edgar, 1907.
Nutritional Disorders: Rickets
One of the characteristic symptoms of rickets in infants and younger children is the “beading” of the costochondral joints. This is caused due to a deficiency of available calcium (either because of a lack of vitamin D to process the calcium, or a primary deficiency of calcium), leading to a lack of joint mineralization. This causes the costochondral joint cartilage to become overgrown to make up for it.
Diseases of Infancy and Childhood: Their Dietetic, Hygienic, and Medical Treatment. Louis Fischer, 1917.
I’ll be elaborating on all of these conditions soon, but here’s the 30,000 ft overview of some significant nutritional disorders (aside from allergies and deliberate poisoning/ordeal poisons - the latter I may cover in the future, as culturally they’re fascinating) that have plagued mankind since we took our first bite of food.
While many nutritional disorders are due to a lack of food, some are due to an excess of a toxin from some food that the body can’t process. The staple foods that end up harming people when over-consumed or not properly processed often are eaten or poorly prepared as a result of famine, and just like nutritional deficiencies, many still plague the world today.
Nutritional Disorders - Deficiencies:
Nutritional Disorders - Toxicity:
Thanks again to Antiquus Morbis for the inspiration; many of these terms can also be found over there, in addition to hundreds of other causes of death.
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Though the Occupational Safety and Health Act as we [in the US] know it has only existed since 1970, there have been differing levels of federal oversight in the workplace since the Bureau of Labor was created as part of the Department of the Interior in 1888, and the Department of Labor was established in 1913. Though their oversight may not have been as stringent as what we have now, and laws may not have protected people as they do today, it was certainly better than nothing.
So what was working before ANY oversight like? Well, here are a few ways you could have died from your occupation, assuming you didn’t get killed by falling, getting crushed, getting impaled, or straight up getting ripped apart by the machinery (read: I’m not covering industrial disasters today; they’re coming later):
Aluminosis/Kaolinosis - Fibriod phthisis caused by the inhalation of clay dust.
Brass Founder’s Ague - A debilitating fever (often cyclical, like ague) caused by inhalation of the fumes of burned-down zinc, copper, or magnesium, in brass foundries.
Byssinosis - A lung disease caused by inhalation of cotton fiber dust or other vegetable fiber dust (flax, hemp, sissal). Leads to coughing, wheezing, progressive lung scarring and narrowing of the airways, and eventually death. Death isn’t so much due to the scarring, but more because of the highly reduced ability to fight pulmonary infections. Was particularly common in young girls and women, especially those in thread factories.
Caisson Disease - Spinal affection caused by either moving from a condensed atmosphere underground or a pressurized diving apparatus into the ground-level atmosphere again. Often occurs in conjunction with “The Bends”. Known as Diver’s Paralysis.
Cancer Scroti - …this is an awful one. A cancer noted by Percival Potts, affecting primarily chimney sweeps. Scrotal cancer, often appearing around puberty. Unfortunately was often treated as if it was a venereal disease, which wouldn’t have helped anything. Often led to the cancer spreading to the lymph nodes, leading to death before 18. Also known as Soot wart.
Danbury Shakes/Hatter’s Shakes - Symptoms of inhalation mercury poisoning exhibited by the hat-makers in Danbury, CT (the hat capital of the world in the 1800s). Often involved shaking, delirium, slurring speech, twitching, and a lurching gait. Sometimes these guys were mistaken for drunks.
Lacemaker’s Disease - Lead poisoning sometimes found in lace-makers.
Mad Hatter’s Syndrome - Differs from Danbury Shakes in that it more often leads to death, and is more often caused by unintentional ingestion of mercury (rather than inhalation). Involves severe ataxia, gastrointestinal symptoms, and emotional instability, in addition to the symptoms of Hatter’s Shakes.
Matches Disease - Oh god. Phossy jaw. Will do a full post on this and radium jaw soon. Caused by working with and inhaling the dust of white/yellow phosphorous, which was the primary ingredient in matches for a long time. Young girls and unmarried women were the primary makers of matches, and ended up the most affected by this disease. In the end, your jaw basically rots off and you go crazy and then you die. Also known as Phosphorus necrosis.
Potter’s Rot - Known as silicosis today. Caused by inhalation of silica particles often found in clay. Silica embeds itself deep in the alveolar sacs (meaning that it cant be coughed out), and the body, trying to get rid of the irritant, becomes inflamed and deposits collagen around the silica. This causes fibrotic nodules in the lungs, respiratory insufficiency, severe cough, fever, right ventricle heart disease, weight loss, and cyanosis. Silicosis leads to a significantly increased risk of tuberculosis and cancer, as well as mycobacterial infections. Also known as slate-worker’s lung/sandblaster’s asthma.
Ptilosis - Another form of fibroid phthisis, caused by inhalation of feather dust and down dust. In the ostrich feather industry of South Africa (which aside from pen quills, had a huge boom around 1880 thanks to the fashions of the time - feathers were prominent for over a decade, and came back in style frequently), this was particularly prevalent.
Rag Sorter’s/Rag-Picker’s Disease - Anthrax. Should do a post on the history of anthrax soon. Really interesting topic. Rag sorters were the women who sorted rags in the paper factories. Rag sorter’s disease often manifested itself as cutaneous anthrax, but pulmonary (inhalation) anthrax was not uncommon.
Sailor’s Fever - Yellow Fever. Almost always acquired in the tropics.
Silo-Filler’s Lung - Acute bronchiolitis fibrosa obliterans, caused by inhaling high levels of nitrogen oxides. Recently-filled silos have very high levels of nitrogen dioxide (which is one reason why you never want to be in a poorly-ventilated silo). Nitrous fume intoxication causes cough and shortness of breath, followed by high fever, chills, and a more serious shortness of breath. Death from pulmonary edema following the second phase was not uncommon.
Woolsorter’s “Pneumonia” - Inhalation anthrax. Anthrax spores are soil-borne, and when wool is sorted, it still carries the environmental dirt and grime that the sheep (who largely live outdoors) pick up. As the dirt is knocked free, soil-borne spores are also released. The sheep didn’t necessarily have to be infected itself to pick up anthrax spores as it lay on the ground. Though mortality rates from pulmonary anthrax hover around 45% these days thanks to early diagnosis, improved treatment, and (most of all) Pasteur’s anthrax vaccine for livestock, historic mortality rates were ~92%. Pretty awful thing to catch in the workplace.
Erysipelas:
A skin infection, typically caused by an acute streptococcal infection (typically Streptococcus pyogenes), characterized by hot skin, fever, infected dermis and lymphatics, and when the infection reaches deeper tissues, can lead to serious complications. Erysipelas can often lead to dissection of the dermis from the epidermis. Basically the skin gets removed from its base and forms a bubble. Erysipelas can also be present at the onset of gangrene.

The skin also takes on a peau-de-orange appearance where the infection has spread - it looks like the skin of an orange peel in texture.
[Illustration from A Manual of Pathology. Joseph Coats & Lewis K. Sutherland, 1900.]
In our age of antibiotics and prophylactics and cleanliness, it’s very rare that erysipelas leads to severe complications, but it was a very dangerous condition to acquire in centuries past.