Amboceptor

Microbiological, virological, bacteriological, immunological, medical, epidemiological, historical, anecdotal

Category: Epidemiological

Taiwau Bozu: The bald geisha plague of 1901

The strange disease which has produced so much hilarity came, it is said, from Formosa; and a person may conclude that he has been attacked by it when he gets up in the morning and finds a hitherto hairy poll as bare as a billiard ball. No other symptoms make their appearance. It is bad enough for the Japanese gentlemen, but the ladies are quite terrified at the prospect of losing those coiled masses of glistening, jet-black hair which are often veritable works of art.hairless-japan

In this light-hearted style, English-language newspapers noted of an “epidemic of baldness” which afflicted the rapidly-modernizing nation of Japan in 1900 and 1901. The Sydney Daily Telegraph‘s unnamed Tokyo correspondent, writing in March 1901, goes on to rhapsodize about the “long raven locks”, the “shiny coils and bride-cake intricacies”, which rested on the heads of “singing girls of the well-known type of Rudyard Kipling’s ‘O-Toyo, ebon-haired, rosy-cheeked, and made throughout of delicate porcelain’,” before revealing that “in at least three or four cases” prominent Japanese ladies have had their heads rendered egg-like and their status in society thereby ruined.

The article gives the impression that a lot more men than women have been afflicted, but “[t]he strong point of a Japanese [man] does not by any means lie in his hair, which generally sticks up on his head as bristly and as stiff as the hairs on a blacking brush.” Thus our sympathy should be directed at the “singing girls” or “dancing girls” who so prize their raven tresses. And the Japanese, led by their one famous bacteriologist (probably Shibasaburo Kitasato, though Hideyo Noguchi would soon achieve similar fame) can surely deal with this problem.

The study of medicine is pursued with great ardor and success in Japan, which claims the honour of having produced at least one bacteriologist of international fame; and it is not surprising, therefore, that the doctors are studying the new disease with the liveliest interest. It should be no difficult matter to get hold of the pestilent little microbe that is the cause of all the trouble.

* * *

The mysterious plague apparently originated on the island of Formosa (now called Taiwan), which was under Japanese military occupation, following the island’s relinquishment by China under the Treaty of Shimonoseki. Formosa was a poor place at the time, compared to Japan, and a plausible source for a tropical disease.

Also in 1901, the London Spectator gave a more clinical report of the outbreak, courtesy of Berlin correspondent Louis Elkind, probably summarizing German press reports. Evidently “there was an epidemic of baldness at Chiba last year, and there has been an even more serious one quite recently at Osaka, the same province where, as it will be remembered, an extensive epidemic of plague … prevailed in the last months of 1899 and at the very beginning of 1900.”

The effects of the disease exhibit several interesting peculiarities. The bald patches are irregularly spread over the head, but the first large one generally appears on the crown and extends down the back of the head instead of forwards towards the forehead; thus it may be that the back of the head is quite bald and the front covered with hair — the opposite of the course of baldness as we know it in Europe. Then, also, men’s beards are ravaged in a peculiar manner. The left cheek, say, may be completely bereft of hair while the rest of the beard is as usual, as also is the moustache, which, fortunately, is but slightly affected by the disease.

* * *

Elkind’s report sounds more plausible than the Sydney correspondent’s chatter about ladies “shedding their ebony tresses — and shedding at the same time tears large as eggs”.

Utamaro (1753-1806), Kami-yui (Hairdressing)

Utamaro (1753-1806), Kami-yui (Hairdressing)

But did this really happen?

No, according to Dr. Stuart Eldridge, friend of Ulysses Grant and longtime contributor of short dispatches from Japan to the ASPH journal Public Health Reports. Eldridge’s obituary suggests an interesting career, including at age 28 being part of “the scientific mission to Japan under General Horace Capron,” and staying in Japan until his death 30 years later.

After updating Public Health Reports on Japan’s plague outbreak of 1899-1900, Eldridge sent in two brief reports about the bald geisha plague (Report #1, Report #2). Here’s the first.

eldridge-japan-1

No source is cited, but Eldridge thinks the disease is spread quickly, is spread by barbers, originated in Osaka (though the Spectator claims it was in Chiba first), and there is evidence for all these assertions though we don’t know yet whether the baldness is permanent.

However… one week later, Eldridge has consulted with the leader of Japan’s bacteriological efforts, and now doubts that the outbreak ever happened.

I have communicated with Professor Kitasato, thinking that, if it was of the importance and malignity ascribed to it by the newspapers and common fame, the institution under his charge would have already begun the investigation of the matter. Professor Kitasato informs me that so far he has been unable to obtain proper material for study, and that the cause of the malady has not been, as yet, ascertained. I am now somewhat inclined to believe that both the number affected and the severity of the disease have been greatly exaggerated, and that it may eventually prove that the ordinary cases of alopecia, always rather prevalent in Japan, and neither contagious nor particularly severe, have been magnified by newspaper sensationalism into something new and alarming.

At the same time Kitasato published an article in the newspaper Jiji Shinpo. Given his stature in Japanese medicine, I’m guessing this was a decisive blow against the local baldness hysteria. Kitasato’s thoughts were summarized by Albert Ashmead in American Medicine — after first giving a sample of that hysteria.

albert-ashmead-taiwau-bozu

“In some villages the hair of all the women in the place has fallen out. The people call the hair plague ‘Taiwau Bozu.’ The disease has robbed several dancing girls of their beauty. It is said to have been imported from Formosa, and the health authorities have gangs of men at work disinfecting the poor quarters of the towns. The hair plague seems to be spreading over a large area.”

Allow me to observe that Taiwau Bozu is not a new disease. The words mean Formosan Priest. All Buddhist priests in Japan have the head shaved, and thus one who is completely bald is said to look like a priest, in fact is called “priest.” … Dr. Kitasao says that “it is not the first time the disease has been epidemic in Japan. It does not come from Formosa, although the people think so. It is not very contagious. It is the same disease which occurs all over Europe, etc.” Inasmuch as the syphilis of Formosa is fiercer than the syphilis of Japan, and the syphilis of Europe is fiercer than that of Formosa, so Taiwau Bozu’s ravages differ in different countries.

… The disease is simply epidemic Tokuhatz-fizo (bald disease); Alopecia areata of specific origin (syphilitic), and it is contagious.

So according to the experts, we have a minor urban flare-up of secondary syphilis. (“The classic alopecia of secondary syphilis is patchy with a “moth-eaten appearance” and has been reported in up to 7% of patients.”) Possibly associated with the return of military forces from Taiwan (or Taiwau), as outbreaks of venereal disease sometimes are. Albert Ashmead’s interest in Japanese history lets him put the whole thing into perspective.

I add that in 1967, when the licensing of prostitution went into effect in Japan, the professions for women of “Geisha” dancing, tea-house and archery-gallery keeping, became crowded with prostitutes (more or less syphilitic) to evade the payment of the government tax. Then the hospitals of Tokio had to do with a great number of cases of syphilitic alopecia in no way different from the present outbreak

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So you want to be an industrial glassblower

So, you’re interested in a job as a glassblower. That’s no surprise. For 50 years glassblowing has been a good way for a skilled industrial laborer to earn a comfortable living, and today as we enter the 1920s, demand for these workmen shows no signs of lessening. But what are the risks?

Since there are so many glassblowers around, it’s important for society to properly assess what diseases they are likely to suffer. Frederick L. Hoffman writes, in the 231st Bulletin of the United States Bureau of Labor Statistics (“Mortality from Respiratory Diseases in Dusty Trades”, 17th in the Industrial Accidents and Hygiene Series):

The hygiene of glass blowers with special reference to pulmonary tuberculosis is of exceptional interest as a labor problem in the glass industry. The number of blowers employed proportionate to the total number of wage earners is relatively large, and, from a wage point of view, the employment is of the first order of importance.

From this US government document we can see some statistics on the prevalence of tuberculosis in this population. It’s not so much that they are exposed to the bacteria to a high degree. But continual low-level lung damage by inhaling high-temperature air containing various dusts means that once the bacteria are inevitably inhaled, they have a place to roost. The lung equivalent of abrasions, you might say.

glassblowers-table-118

So they have higher mortality rates than men in general of the same age. With regard to tuberculosis in particular, here’s a table compiled by Prudential Insurance researchers.

glassblowers-table-119

Carboy blowing? Carboys are huge! It’s hard to contemplate the human lungs being the engines of inflation for one of these. Or thisHand Blown Monumental Demijohn.

Some other recent statistics, from the Chicago Tuberculosis Institute. This table is on page 153 of the July 1915 – June 1916 annual report of the Illinois Chief State Factory Inspector.

glassblowers-chicago-tuberculosis-institute

So as a glassblower you’re not as likely to fall prey to the dread tubercular bacillus as you would be as a marbleworker or upholsterer, but it’s a concern.

* * *

What about other lung conditions?

This turns out to be controversial. As a person with no medical training, I’d imagine that the risk factors for tuberculosis and emphysema are pretty similar. Inhaling poisons or microscopic things that damage the alveoli (alveoli are tiny air sacs which combine to make up a massive surface area for oxygen to enter the blood). However, the evidence regarding glassblowers suggests that the two diseases are uncorrelated.

In 1904 Prettin and Leibkind of the Stadtkrankenhaus Dresden-Friedrichstadt analyzed 230 glassblowers for an article entitled “Kann durch Glasblasen ein Lungenemphysem erzeugt werden?” JAMA (the Journal of the American Medical Association) deemed this an important finding, a perfect example of the sort of science-based result that supersedes old-fashioned beliefs that were based only on common sense.

emphysema-in-glass-blowers-1904

* * *

We already know that the southeastern regions of New Jersey are great for making wines and wine-related medicinal concoctions. Meanwhile southwestern New Jersey was a hotbed of glass production, as seen in the history of the large town of Glassboro in Gloucester County. To the northeast are two townships called Waterford and Winslow, both of which are named for large glassworks that existed in the 1860s.

In 2006 Erik Schwartz of the Cherry Hill Courier-Post wrote about the long-gone legacy of glass in areas including Waterford and Winslow townships. And in 1869 Dr. John Snowden sent in some observations about the health of workers at the Waterford and Winslow glassworks, included in the Camden County report (p. 134-136) in the Transactions of the Medical Society of New Jersey. “Phthisis” means tuberculosis.

trans-med-soc-nj-1868

A very interesting communication on the subject of Phthisis has been received from Dr. John W. Snowden, who had practiced for more than twenty-three years at the seat of two of the largest manufactories of glass in this State — at the Waterford and Winslow glass manufactories, where several hundred hands are employed in the manufacture of glass. Dr. Snowden says that among the glass-blowers themselves Phthisis is not at all frequent; but that many of these operatives suffer from emphysema of the lungs. But that among the batch-makers (those who prepare and mix the materials of which the glass is composed), and also among the pot-makers, who make the pots in which the glass is melted in the furnaces, Phthisis is very common indeed, and that few can follow this branch of the business for many years without being liable to Phthisis.

Dr. Snowden says that many of those men, months after they have been compelled by the progress of the disease to leave off work, expectorate with tuberculous matter small masses of German clay, one of the materials of which the pots are made. This undoubtedly being drawn into the lungs by inspiration, in a state of fine powder, and being insoluble, is deposited in the tissue of the lung, where it serves as a point of irritation around which the tubercle is first deposited.

So now glass-blowers don’t get tuberculosis, but they do get emphysema? I guess it depends on the facility.

There is a lot of clay powder involved in glass-making, that’s for sure. Here are the ads at the top of three straight pages of the August 25, 1917 National Glass Budget.

pittsburg-clay-pot-co highlands-fire-clay-co-st-louis laclede-christy-clay-products

* * *

Really, a lot of risks that apply to other glassworkers do not apply to glassblowers. In terms of health hazards, one of the longest assessments was written in this series of articles for insurance men, highlighting how to avoid physical accidents and the subsequent payouts for broken bones, burns, deafness, that sort of thing. I don’t know exactly what it means by “Live Articles”. Maybe it means “This is the current standard of what we expect”.

weekly-underwriter-1917-18

Here’s a typical illustration.

carrying-sheet-of-glass-wrong-way

The Travelers Insurance agent who wrote “Glass Manufacturing Hazards” for this series agrees that emphysema is not a major problem for glassblowers, despite what one might expect. The men who work with the raw glass ingredients, and the “bottle-breakers” who smash undesirable glass so it can be re-melted, are more at risk for this — as they are for skin irritation, painful abrasions, burns from molten glass, and foot lacerations.

Glass-blowers do sometimes break their teeth when the iron blow-pipe strikes some hard object. They slip on the smooth, worn wooden foot-benches that are often without railings. They drink too much water, causing cramps. They get blisters, which should, but usually aren’t, dealt with by puncturing the blister with a needle threaded with white sewing silk, to provide drainage before the blister bursts. And they get infectious diseases from the shared water cup used to cool down between blows, and more importantly, from the shared mouthpiece on the blow-pipe. This has been the subject of several studies. Studies of syphilis.

* * *

The first link between glass-blowers’ pipes and syphilis I can find is from 1862, when the British Medical Journal relayed a report from France. Apparently in “Giers and Vernasion” (which probably means Rive-de-Gier and Vernaison), transmitting diseases is virtually inevitable because the normal procedure is for three men to collaborate (taking turns in quick succession) on blowing a single piece of glass. Is this the normal method? Anyway, this leads to the men giving each other “the three syphilitic disease of the mouth”.

1862-syphilis-bmj

In a 1904 issue of the Indianapolis Medical and Surgical Monitor, Dr. Nelson D. Brayton of the Indiana Medical College collects a large number of reports under the title “Syphilis, a Non-Venereal Disease”. Along with dozens of other anecdotes of people acquiring the dreaded disease through innocent means, he mentions a 162-person outbreak of syphilis among glass-blowers, along with other professions where people risk disease by putting common instruments in their mouths (assayers, weavers, goldsmiths, train conductors, music teachers).

In his 1906 dissertation at the University of Würzburg, Joseph Kaesbohrer described 290 cases of syphilis in which the first observed chancre (hard sore) was seen in the tonsillar region. These frequently occurred from kissing and from nursing, as well as from medical instruments, shared eating utensils, and tobacco pipes. In a summary in the Medical Review of Reviews, the only occupation listed as a risk factor is glass-blowing. So be cautious. But should you acquire this or other so-called venereal disease from your blow-pipe, don’t fear rumors and innuendo, as Kaesbohrer found that “sexual perversion, which many have assumed to be a frequent cause, is, as a matter of fact, an infrequent cause of tonsillar chancre.”

* * *

Depending on what sort of glass works you find yourself in, the risk factors can be different. Most glass doesn’t have lead in it, but some does, and that’ll be bad if it ends up in your lungs, as seen in this 1920 case from Italy.

Unshielded eyes are at risk for “glass-blowers’ cataract”. One reason why we can’t see long-wavelength “infrared” light is that the lens of the eye absorbs this light instead of letting it through to the retina where we could perceive it. Long-term exposure to this light, which we can sense only as heat radiation, can lead to a forty-year-old having the cataracts of a man of eighty. According to the Illinois Medical Journal, the eminent Dr. de Schweinitz can look at the clouding of a furnace-worker’s eyes and tell if he is right- or left-handed.

Finally, a health consequence of glassblowing that may be the most obvious of all if you know someone who’s spent a couple decades in the job. From The Sanitarian, March 1892:

According to Le Progres Medicale, the Societe de Biologie, of which M. Brown-Sequard is president, received from M. Regnault, of Marseilles, at its session on November 7th, 1891, a communication on a disease which is met with in about one third of the workmen. This condition does not attain complete development until the men have been from ten to fifteen years in the business. They are taken into the glass factories, usually, about fifteen years of age; and at first the young workmen complain of great fatigue and a painful feeling in the cheeks which extends to the ears; later, the cheek becomes gradually weakened, is easily puffed out, and the deformity, of which the cases presented were in an advanced stage, progresses steadily. This deformity is caused principally by the weakness of the buccinator muscle, whereby the cheek becomes swollen and permanently enlarged.

The swelling is limited by the masseter muscle. There is also a special dilation of the duct of Steno, the calibre of which is increased and the orifice enlarged. This duct is filled with air, which may be forced out by pressure on the external surface, when a distinct gassy sound is heard.

In short, after years of glass-blowing, your face may be altered. The buccinator muscle is weakened, the cheeks expand into jowls, and the inner mucous lining “is thrown up into vertical and circular folds, giving it an appearance which has been likened to that of a tobacco-pouch.”

Neither M. Regnault of Marseilles nor Dr. Liaras of Bordeaux, summarized in “The Mouths of Glass-Blowers” in the June 1898 Medical Bulletin, see these altered facial features as a serious problem. But in severe cases, the primary salivary duct (the parotid duct, a.k.a. duct of Stensen, a.k.a. duct of Steno) is forced open by the intense pressure in the mouth, and it becomes dilated, forcing air into the salivary gland. I can’t imagine what that feels like. Maybe not painful, but certainly weird. It sounds like a fun party trick to be able to puff up your salivary glands on command… but when it happens unbidden at work, it’s a problem. The final citation on this subject comes from JAMA of November 23, 1912.

jama-glass-blowers-tumor

So, the word “Tumor”. This is not “tumor” as in cancer, it’s the form that simply means “swelling”. As in the four elements of inflammation, rubor/calor/dolor/tumor, defined by Celsus in the first century A.D. Air goes into the parotid gland, and then you have “tumor” in the parotid gland. As described here by the surgeon Narath, you may have to quit your job if the “chronically stretched duct and gland” get too bad. But you’ll always have the party trick.

* * *

And one more thing. Yet another German article paraphrased by a English-language journal, in this case the March 1899 Canada Lancet.

luxation-of-eye-from-blowing-the-nose

“Luxation of the eye”? “Proptosis”? Does that mean… yes, just search for some images. So with your newly enhanced lung power as a glass-blower, just make sure that when you sneeze, really let that sneeze escape. Don’t keep it bottled up, if you value your eyeballs’ position behind their eyelids. And good luck!

Pit pony work dust factor

It has long been known that coal dust is one of the least harmful of all the dusts inhaled industrially. Since the practice of laying down stone dust in coal mines was adopted, however, a certain degree of uneasiness has been felt as to the possible effect of the stone dust on the collier’s lung.

With a somewhat dubious reassurance of the safety of coal dust (“least harmful dust inhaled industrially” is kind of like “least fattening cheesecake eaten voraciously”), F. Haynes of the University of Oxford begins an investigation(*) of the real menace to coal miners’ lungs: stone dust. To combat explosions, ground-up stone is applied inside mine shafts, diluting the highly combustible coal dust.

  1. How much dust ends up in a miner’s lungs?
  2. Does it get worse and worse over, say, a 20-year career?
  3. How much lung damage does this produce?

To answer these questions, Haynes got mines to send him lung samples from various workers who either died on the job or were euthanized when they became unable to work. Not human miners — pit ponies, who were employed in large numbers before the advent of mechanized rail cars.

Coal miners and pit pony, 1913. Source: ancestry.com, which inserts this photo into random entries for people who happened to be coal miners.

Coal miners and pit pony, 1913. Source: ancestry.com, which inserts this photo into random entries for people who happened to be coal miners.

To cut a long story short, the answers are:

  1. Lots of dust.
  2. No, it gets worse for about 2 years and then stays about the same.
  3. Not much damage.
  4. This does not apply to extremely dusty dusts, like those from fireclay or Bute clod(**).

And how did he measure dust, to answer 1 and 2?

Dust was quantified as “dust value”, graded from 0 (horse that did not live in a mine shaft) to 10.

To look for a relationship between quantity of dust and time spent in the mine, Haynes created the “work-dust factor”. This is simply a ratio of “dust value” to the number of years spent mining. If you have a dust value of 6 and have been working for 11 years, your work-dust factor is (6 / 11) or 0.545. If the dust keeps accumulating year after year, everyone’s work-dust factor should be similar. But as you can see from this table, as ponies keep working, their work-dust factor decreases.

work-dust-factor

Which means… as ponies keep working, their dust levels stay about the same. This becomes clear if we multiply the number of years by the “work-dust factor”. Which just gives us the original dust value that we started with. Which is about the same for all groups.

For combining two simple numbers into a confusing metric that was never used again by anyone, F. Haynes receives a special posthumous commendation in the fields of toxicology and biostatistics.

Samples of Haynes's pony pathology reports

Samples of Haynes’s pony pathology reports

* * *

Data Update: Look at the polio fly

In our last Data Update, the table that I turned into figures was not a bad table. It was pretty clear. It just contained some unnecessary information, and was spread across two pages, which is always bad. Today, the table in question is really hard to interpret. I could not make heads or tails of it without going over the text, piece by piece. It’s from a 1943 paper (1) in the Journal of Infectious Diseases.

* * *

Like the pictures of cockroach feeding contraptions, this data comes from a laboratory that was using what could be called “experimental epidemiology” techniques, to figure out how much of a public health hazard these bugs really are. To see if bugs could actually ingest, preserve, and spread germs.

This time the bug is the common house fly. Thomas Francis Jr. had just joined the faculty of the University of Michigan from NYU, and with technician Robert Rondtorff he conducted this study in the interest of public health. Soon Francis would be supervising graduate student Jonas Salk, with whom he worked a lot in the 1940s and 1950s, as you might be able to guess from the fact that Dr. Francis now has a Wikipedia page.

By 1943 we knew that polio was spread by filth and tainted water (the fecal-oral route, as we call it). But flies feed on that stuff, and fly around. Does the virus replicate inside the flies, like malaria? This paper established that when flies ingest poliovirus, the virus disappears from the digestive system within 2 days. And therefore, flies probably aren’t making the poliomyelitis epidemic worse. The significance of these findings is indicated by the introduction to a 1950 paper (2) by children’s television character “Herbert Hurlbut”.

Poliomyelitis virus has been isolated from filth-frequenting flies caught in nature during several epidemics in recent years.(3-5) When the Lansing strain of the virus was fed to house flies under experimental conditions, virus was not recovered after 48 hours.(1,6) Recently Melnick and Penner (7) fed virus in human stools to the blowfly Phormia regina and were able to recover it from the flies after about two weeks[.]

* * *

First of all, their experimental system. Feed the flies on polio-infected material. To make sure there was a lot of polio in the flies’ diet, they did not use excrement from polio-infected animals. They used “a 10% suspension of infected [mouse] spinal cords in boiled milk”. In the not-entirely-robotic prose of scientific papers of the era, they say they “offered” this to the flies. Earlier they had just diluted the mashed spinal cords in saline solution, and the flies “did not feed readily”, so they switched to a solution in milk, which the flies found far more appealing.

For this experiment, the flies enjoyed their neuronal polio-milk for 1 hour, after which it was removed and they were allowed to feed on regular milk if they wanted to. The scientists then waited either 0, 2, 7, 13, 25, 49, 120, 240, or 480 hours. After each of these periods, a certain number of flies were killed, and their abdomens were cut away from the rest of the body. Earlier in the paper it had been established that poliovirus does not leave the abdomen (gut) of an infected fly and reach the rest of the body (thorax and head). Now they are looking to see how much polio virus is in the infected flies.

To get an extract containing poliovirus, they took the fly parts and ground them in saline solution using a mortar and pestle. For best results, they ground the samples with alundum (an abrasive preparation of aluminum oxide). They added some ether (diethyl ether, I assume) to the solution, and let it sit in the refrigerator until it was “bacteriologically sterile”. I’m not familiar with the use of ether to remove bacteria, but it looks very suitable to this procedure.

Experimentally and clinically, ether, whether in its vaporous or liquid state, has been proved to have a bactericidal action. Spore bearing organisms, however, are strongly resistant to it. (7)

Not only did ether treatment remove bacteria from the extract, but it also removed most other viruses. Poliovirus, as a non-enveloped virus, is resistant to ether, a substance which destroys the membranes of enveloped viruses. Here’s a table that summarizes, as of 1949 (8), which viruses are ether-resistant.

andrewes-horstmann-ether

from Andrewes and Horstmann (1949)

Note that most viruses are ether-sensitive and should be removed by this sort of treatment, meaning you’re left with polio, papilloma, bacteriophages, and a few other viruses. Including some, but not all poxviruses, for reasons that are unclear to me. Parapoxviruses (myxoma, BPS virus) are ether-sensitive, and orthopoxviruses (smallpox, vaccinia) are ether-resistant, which is still the dogma (see Chapter 21 of Medical Virology). And chordipoxviruses are maybe one or maybe the other. The above table puts sheep-pox and goat-pox (chordipoxviruses) in the resistant group, whereas Plowright and Ferris (9) say that sheep-pox (SP) and lumpy skin disease (LSD) viruses are ether-sensitive.

from Plowright and Ferris (1959)

from Plowright and Ferris (1959)

Anyway, poliovirus is definitely ether-resistant. So this extraction method is useful for studying this particular virus [here’s another example (10)].

It wasn’t possible in 1943 to measure the amount of virus by using a plaque assay, as we do now (applying a solution of virus to a plate of cells and seeing how many plaques [empty spots] form in the cells by being killed by virus). What the authors do instead is infect mice with the fly extract and see if they become paralyzed and/or dead. In Table 1 they established that the virus survives in the flies, but only in the abdomens. Here’s Table 2.

rondtorff-table-2

So one half of the table is data from the flies, and one half is data from the mice, right? That’s what I thought. But no. This table is made up of almost entirely unnecessary information, and only makes one point. I’ve taken the liberty of highlighting the important parts.

rondtorff-table-2-2

In the text, Rendtorff and Francis go into great detail about how they prepared the ground fly mixtures so they could be compared fairly. They weighed the samples before grinding, and added more or less saline depending on how many fly abdomens were in the sample, and what their weight was. In deciding how much saline to add to dilute the sample, they also factored in what the average unfed weight of an abdomen should be, which should be the same for all the flies. This process was to normalize the data, which could be thrown off by the flies’ unequal eating and excreting habits. I feel like pooling together somewhere between 44 and 66 fly abdomens would already take care of the issue of some flies eating more than others, but they did this statistical technique to account for possible variation.

Most of this table is the raw data they used to do the normalization. But… I don’t need to know what the weight of the fly abdomens were. Or how much saline was added. And I definitely don’t need the “Calculated Unfed Weight of Abdomens” column, which is nothing but the “No. of Flies Sampled” column multiplied by the average weight of an unfed abdomen. It’s good to present raw data, I guess. But this data is not important. Maybe it should be separated from the important data.

The least important data of all is the dates on which the experiments were performed. This is something that absolutely never shows up in research articles anymore. In fact, we may have gone too far in the opposite direction, pretending that we did experiments in a certain order because it makes for a better narrative.

All that matters here is two independent variables and one dependent variable. The independent variables are:

  • Temperature of the incubators in which the flies were living, eating and loving life. (25, 30, or 35 °C)
  • Number of hours the flies were allowed to live, between eating the polio-infected meal and being killed. (0, 2, 7, 13, 19, 25, or 49 hours)

The dependent variable is:

  • Time of death (or paralysis) for a mouse injected with fly extract

So all we really need is a bunch of survival curves.

polio-survival

Figure 2: Poliomyelitis virus is destroyed by the fly digestive tract within 2 days, irrespective of temperature. Flies were fed on a suspension of infected spinal cord in milk for 1 hour. Flies were then incubated in a chamber at 25, 30, or 35 degrees Celsius, for 0 (positive control), 2, 7, 13, 19, 25, or 49 hours. At each timepoint, between 45 and 65 flies in each chamber were killed, and abdomen tissue was extracted using ether. After dilution in saline and evaporation of the ether, each sample was used for intracerebral infection of 9 or 10 mice. Twice a day, mice were monitored for death or paralysis.

* * *

1. Rendtorff RC, Francis T Jr (1943). Survival of the Lansing strain of poliomyelitis virus in the Common house fly, Musca domestica L. J Infect Dis 73(3):198-205.

2. Hurlbut HS (1950). The recovery of poliomyelitis virus after parenteral introduction into cockroaches and houseflies. J Infect Dis 86(1):103-104.

3. Trask JD, Paul JR (1943). The detection of poliomyelitis virus in flies collected during the epidemics of poliomyelitis. J Exp Med 77:531-544.

4. Sabin AB, Ward R (1941). Flies as carriers of poliomyelitis in urban epidemics. Science 94:590-591.

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