Yellow fever stops at the Miami airport.

Initially, new infectious diseases could spread only as fast and far as people could walk. Then as fast and far as horses could gallop and ships could sail. With the advent of truly global travel, the last five centuries have seen more new diseases than ever before become potential pandemics. The current reach, volume and speed of travel are unprecedented, so that human mobility has increased in high-income countries by over 1000-fold since 1800. Aviation, in particular, has expanded rapidly as the world economy has grown, though worries about its potential for spreading disease began with the advent of commercial aviation. [1]

Podcasts are great. But in the world of science podcasts, many are simply boring because there is only one person talking, or one person interviewing another person. Unless it’s slickly produced and edited (the Nature or Science Times podcasts), I’ll quickly lose interest.

It’s better when the podcast is three or four people who know each other, having a conversation. This is is the format of the TWi[X] series, particularly the flagship This Week in Virology. TWiV co-host Dickson Despommier, though not a virologist, contributes a big-picture point of view when the show leaves its territory of basic lab science and moves into epidemiology and patterns of disease outbreaks. Here’s his lecture on how West Nile arrived in North America and spread from state to state, energized by a very hot summer at the Bronx Zoo.

More than once I recall Dr. Despommier pointing out that though it’s all well and good to model how a epidemic might spread by looking at the day-to-day movements of people and mosquitoes, the most powerful and mobile disease vector is… the airplane.

That fact has become ever more clear with the SARS and West Nile outbreaks, as we used genetic analysis to track them across the continents in real time. But you might be surprised at how long ago people recognized the airplane as a challenge to disease control.

* * *

80 years ago, yellow fever was the archetypal mosquito-transmitted disease. Particularly as the disease was endemic in some parts of the world (e.g. South America), but not in others (e.g. North America), despite both places being home to the vector, Aedes genus mosquitoes. A 1934 article [2] coauthored by Henry Hanson, veteran of battles against yellow fever on three continents, points out that dengue fever (also transmitted by Aedes) had reappeared in Florida after an eleven-year absence, and yellow fever could do the same at any time.

Hanson and coauthor T. H. D. Griffitts go on to chide the cities of Florida and Georgia for their complacency in providing countless unsupervised water vessels in which the mosquitoes can reproduce.

Practically every urban community in the South has its array of artificial containers, from flower vases to catch basins, cuspidors and discarded automobile tires, producing Aedes aegypti. For example, the city of Tampa in eight weeks reported finding 1,091,823 containers (potential mosquito “hatcheries”). Of these, larvae were found in 20,864, or approximately 2 per cent. This was an unusually dry season (average rainfall of 1 1/2 inches a month for this period). It is interesting to note that in Miami for a like period only 56,598 potential breeding containers were reported, with 38,401, or 68 per cent, of the total actually breeding.

So I made an error above. The vessels aren’t quite “countless”. There are 1,091,823 of them in Tampa, give or take a dozen.

Though concerned that yellow fever could reach North America (again), Hanson and Griffitts are more concerned about India. The disease is only known in jungle areas of Brazil, Colombia and Bolivia (they claim); by comparison, Africa is its ancestral “home” and India, fairly nearby by plane, is virgin territory for yellow fever epidemics.

Today there is a feeling of concern … that Old World territory, where the vectors abound and where yellow fever has never before stalked, may experience widespread and devastating epidemics. One infective mosquito traveling in an airplane from the home of yellow fever (Africa) to India could be the spark to start the conflagration.

Thus there was considerable surveillance for mosquitoes and infected passengers at airports worldwide.

The earliest article I can find specifically discussing airplanes as disease vectors is from 1930, the first [3] of two identically titled 1930s editorials in the American Journal of Public Health. I don’t know if the international rules discussed here were enacted, but they show awareness that quarantine and disinsectization measures developed for ocean travel need to be multiplied and intensified to cope with passenger aircraft. Click for a bigger view.

* * *

For the purpose of determining whether or not mosquitoes are carried in airplanes, and, if so, to what extent, the distance of such transportation, the species of mosquitoes, and the type of planes on which they are carried, the United States Public Health Service began, on July 23, 1931, the inspection of all airplanes from tropical ports arriving at the airports of the Pan American Airways System at Miami. [4]

An anecdote from less than a year later illustrates how the search for mosquitoes had become a normal part of a plane’s arrival in the U.S. from South America.

A very Normal Rockwell scene of mosquito inspection. From LIFE Magazine, 5/27/40.

The story of “the first international aerial hitchhiker” is as follows.

Paul Kaiser, 25, tried to immigrate from Czechoslovakia to America via a circuitous route. First, he got to the German port of Bremen, from which he sailed to Colón, Panama on an ocean liner. Sneaking into the nearby Canal Zone airport, he climbed into the baggage compartment of a “big 22-passenger Commodore plane”. The plane first landed in Barranquilla, Colombia, where he was not detected. It then landed in Kingston, Jamaica, where he was not detected. Finally, after Kaiser had spent 2 days without food, he landed in Miami. However, in Miami “a very thorough inspection is given every plane for mosquitoes, for there is always danger of the deadly yellow fever mosquito surviving the short trip and landing in the United States, a most undesirable immigrant”. Check out the April 1933 issue of Flying magazine for more details.

A few months earlier, T.H.D. Griffitts (coauthor of the aforementioned Henry Hanson article) performed the first experiments on mosquito transport by aeroplane. These were published in late 1931, in an enjoyably conversational article in Public Health Reports [4].

Dr. Griffitts, you don’t really have to describe the experiments you WANTED to do but then decided were unnecessary.

T.H.D. Griffitts (and J.J. Griffitts — his son?) start out by describing all the mosquitoes observed on normal commercial flights between July and September of 1931. Most were Culex quinquefasciatus, but several other species were observed including Aedes aegypti. In fact, a later Griffitts paper [5] indicates that the historic first mosquito discovered on a Miami-bound plane was Aedes aegypti. (It’s somewhat confusing that the insect apparently arrived on a “ship from San Salvador, El Salvador”, but I think that at this time the word “ship” could be used for aircraft. And San Salvador is definitely not a port city.)

Griffitts also put mosquitoes on three planes departing from San Juan, Puerto Rico, and looked for them upon arrival in Miami. Today it takes 2.5 hours to fly from SJU to MIA, but in 1931 they stopped at three other airports along the way and the average travel time was over 10 hours. A total of 100 mosquitoes were labeled with eosin dye (to distinguish them from non-experimental and Miami-resident mosquitoes). 22 were observed upon arrival in Miami, after 1,250 miles of flying, opening of doors and hatches, loading and unloading of luggage, etc. It seems obvious that the insects can be imported… but these experiments prove it.

* * *

Eight years after 1930’s “The Airplane and Yellow Fever” editorial, the American Journal of Public Health published another one [5], describing the policies for infectious mosquito control in Khartoum, Miami, and “the French Colonies and Mandates”.

As the 1930s progressed and India remained devoid of yellow fever, public health doctors kept amplifying their alarms about how devastating such an epidemic would be. From the 1938 editorial:

75 years after that was published, yellow fever still hasn’t swept through India.

In 1938, the number of people who’d been vaccinated against yellow fever was less than a hundred thousand, mostly in Brazil. It had taken a long time to make a vaccine strain of YFV that was weak enough that it could be given as a live vaccine, but the 1938 trial (run by the Rockefeller Foundation) was successful, and in 1942 the number of people vaccinated was over 10 million. For his two decades of work on the vaccine, which along the way required multiple basic science breakthroughs for it to be manufactured in large quantities, Max Theiler of Rockefeller University received the 1951 Nobel Prize in Physiology or Medicine. Read more here [6] about Theiler’s story; read more here [7] about the many problems and hurdles that were overcome to end up with a safe vaccine. (I think the second one is open-access and the first one isn’t.)

Within a decade, though complications from the vaccine were common and the virus stayed endemic in the tropics, Theiler’s YFV vaccine had eliminated yellow fever as a source of large-scale epidemics.

* * *

Coda: As early as the airplane was recognized as a vector for disease… it was harnessed as a weapon against disease.

From a 1932 report in Science (8), Joseph Ginsburg of the New Jersey Agricultural Experiment Station explains how large regions of standing water that previously were inaccessible to mosquito control workers can now be reached by plane, so that the surface can be coated with larvicidal pyrethrum or oil.

 

* * *

1. Tatem AJ, Rogers DJ, Hay SI (2006). Global transport networks and infectious disease spread. Adv Parasitol 62:293-343.

2. Griffitts THD, Hanson H (1934). Significance of an epidemic of dengue. JAMA 107(14):1107-1110.

3. Editorial (1930): The airplane and yellow fever. Am J Public Health 20(11):1221-1222.

4. Griffitts THD, Griffitts JJ (1931). Mosquitoes transported by airplanes: Staining method used in determining their importation. Public Health Rep0rts 46(47):2775-2782.

5. Editorial (1938): The airplane and yellow fever. Am J Public Health 28(9):1116-1118.

6. Norrby E (2007). Yellow fever and Max Theiler: The only Nobel Prize for a virus vaccine. J Exp Med 204(12):2779-2784.

7. Frierson JG (2010). The yellow fever vaccine: A history. Yale J Biol Med 83(2): 77-85.

8. Ginsberg JM (1932). Airplane oiling to control mosquitoes. Science 75(1951):542.

 

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.

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)

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.

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.

“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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We have no fear of the coffee

If you’ve taken a microbiology class you probably learned how the bacterial pathogen known as “plague” still exists in the United States. It’s still virulent, but has degraded so far from its status as a civilization-toppling “black death” that it’s mostly associated with the undignified creatures known as prairie dogs.

Here’s something I didn’t know. Before the San Francisco Plague of 1900-04, plague was believed to be unknown in the Western Hemisphere. This was reviewed clearly and concisely by Elizabeth T. Anderson in an article called “Plague in the Continental United States, 1900-76”. (available here for free download (1))

From Anderson (1978), Plague in the Continental United States, 1900-76

The “Third Plague Pandemic” was largely an Asian phenomenon, killing millions in the Far East. In the 1890s the disease was ravaging Hong Kong, it reached India in 1896, and there was great concern in North and South America that it would arrive aboard a steamship. Anderson quotes the Surgeon General as saying at the time:

The appearance of the plague in Santos, Brazil, in October 1899 marks an important epoch in plague literature as furnishing the very first recorded instances of the occurrence of the disease in the Western Hemisphere.

In 1899 the inevitable happened. Ships with infected passengers arrived in Honolulu, New York City, and also Port Townsend, Washington. The latter two threats were eliminated via quarantine, but bubonic plague victims started to be seen in the Chinatown region of Honolulu. Authorities tried to control the illness by burning the houses of victims, which led to out-of-control fires that destroyed most of Chinatown.

So it was through San Francisco that the disease came to the mainland. The San Francisco plague was comprehensively mishandled in an effort to downplay the risks, including claims that it had been “eradicated” in 1904 which ignored the possibility that it had not been eradicated in rodents.

But it surely would have become endemic here at some point. Ever since then, there have been incidents of plague in North America, mostly in rural, dry areas. Like so many unfortunate things, it is now most common in Africa. See this review by Thomas Butler (2) for the present state of affairs.

The “plague-ship” that menaced New York was the J. W. Taylor, bringing a cargo of coffee from the previously-menaced Brazilian port of Santos. Here’s a Public Health Reports report (3) on how the threat was dealt with, written at the height of the crisis.

Immediately after the arrival of the ship in quarantine, and after the removal of the patients, the living apartments, cabin, and forecastle of the ship were most thoroughly disinfected by sulphur and corrosive sublimate solution, and all bedding, clothing, and textile fabrics, without exception, were subjected to the action of steam at a temperature of 230°F. for fifteen minutes, a perfectly safe and efficient process of disinfection.
…

The sacks have been so stowed upon the lighters as to admit abundant circulation of air and exposure to wind and sunlight during the day, and in addition have, during every night, been subjected to a temperature very near the freezing point, as there has been a heavy frost every night since the unloading was commenced. In addition to this thorough aëration, disinfection, and low temperature, it is the determination of Dr. Doty to keep these lighters in quarantine for a period of at least eight days before discharging them.

…The stevedores engaged in the unloading are kept in quarantine and are every night sent to Hoffman Island and brought back to their work in the morning. A careful watch has also been kept for rats, especially those dead; but 1 dead rat has been found and bacteriological examination so far would seem to indicate that he was a victim to the sulphur fumigation and not to plague. I should mention here that the hawsers securing the lighters to the ship are also guarded by large funnels of galvanized iron to prevent the passage of rats from the ship to the lighters.

From these passages, it becomes clear that the authorities had no desire to destroy the ship’s cargo. In fact, it was an insult to the brave people of New York to suggest that they were petrified of these sacks of coffee. Here’s an editorial from the New York Medical Journal, that concludes with an inspirational call to arms.

Let the cargo come to town!

* * *

1. Anderson ET (1978), Plague in the continental United States, 1900-76. Public Health Reports 93(3):297-301.

2. Butler T (2009), Plague into the 21st century. Clinical Infectious Diseases 49(5):736-742.

3. Geddings HD (1899). Plague on the steamship J. W. Taylor at New York quarantine. Public Health Reports XIV(49):2165-2167.

Data Update: Typhoid ice cream

To this day, the safety of the ice cream supply is a field of inquiry among microbiologists, as can be seen in recent findings from Croatia (1), Zimbabwe (2),  Argentina (3), and other places (4,5). Here in the U.S. there’s not as much concern; as far as I can tell the last outbreak of food poisoning caused by mass-produced ice cream in a rich Western country was in 1994 (6), when beloved Minnesota company Schwan’s Ice Cream was transporting ingredients in unsterilized egg tankers. Since then there have been outbreaks on farms, such as two big ones in Belgium and Wales. Most are like the Belgian case (7), which was blamed on ice cream produced right there on the farm, rather than industrially. The Welsh case (8) was blamed not so much on the ice cream itself, but on ice cream’s notorious ability to make children’s hands sticky, turning them into repositories for farm filth. A comparison between desserts in Houston and Guadalajara (9) suggests that the US is fortunate not to have this problem. But back in the 1910s and 1920s it was a different story.

Looking at old tables of contents from the Journal of Bacteriology, it’s striking how many articles are about milk. Even more than other food products, there was a need for science to improve the safety of milk, cream, cheese, etc. Pasteurization was established as useful in the late 19th century, but it would not become widespread until a 1913 typhoid epidemic in New York. This convinced local authorities that the improvement in public health outweighed people’s concerns about what boiling milk did to its taste and possibly its nutritional content (for more on this see Neatorama, “The Fight for Safe Milk”). But still, outside major urban centers where access to fresh milk was limited, people figured that raw milk was fine because the farms were nearby.

And ice cream was contaminated, too. By tuberculosis, typhoid, Bacillus coli, and others. But how big a problem was it, really? The bacteria wouldn’t multiply if they were frozen. But would they actually be killed?

The results on this were basically in by 1926, when Michigan State professor Frederick Fabian collected them in a great review in the American Journal of Public Health (10). Some excerpts:

The rapid rise of the ice cream industry and the general use of ice cream as a food in the past few years has added another item to the public health official’s responsibilities. If an epidemiologist had been tracing an epidemic a few years back, he could have practically left ice cream out of consideration. However, today it has become such a common article of diet that it should be taken into account in any work of this nature.

…Although there has been a vast amount of work done to show that pathogenic bacteria are not readily killed by freezing, yet, due to the nature of the product ice cream has not always been considered a serious source of bacterial infection. This view is held especially among laymen and those not familiar with the facts.

…To test out the extreme temperature which pathogenic bacteria could withstand Macfayden and Rowland (11) subjected the same organisms to the temperature of liquid hydrogen (-252° C.) for 10 hours without any appreciable effect on them. A great deal of work has been done also to show that pathogenic bacteria live for a considerable length of time in ice and a great many epidemics have been traced to this source.

…In practically every city of any size today pasteurization of the milk supply is required by ordinance. The time and temperature are also pretty well established. There are not many such ordinances or laws pertaining to ice cream in most cities or states. …Many of the old experienced producers from their experience with milk have the good judgment to pasteurize the ice cream mix. However, the unscrupulous and the ignorant are allowed to do as they please.

In short, by 1926 public health authorities have got a handle on milk contamination, but for the very reason that ice cream seems safer (nothing can grow in it! most of the time), it has not been regulated and may now be more of a risk than milk.

Along the way, Fabian lists all known ice cream-associated outbreaks, and describes the experimental evidence for bacterial survival in frozen ice- and cream-like substances. Let’s clarify those results, now that we have the ability to make graphs.

* * *

Four experimental papers are mentioned. Mitchell 1915 (12), Bolten 1918 (13), and Prucha and Bannon 1926 (14) use Salmonella Typhi (or “Bacillus typhosus“, or “Bacterium typhosum“). Davis 1914 (15) uses hemolytic Streptococcus. I found two later papers in the Journal of Dairy Science by G. I. Wallace of the University of Illinois, but as he himself seems to think his results are unimportant, we won’t bother with them.

G. I. Wallace (1938) is not trying very hard to inflate the importance of his results.

O. W. H. Mitchell (1915) doesn’t even have a table in his paper. He describes six experiments which involved similar ice cream preparation and storage, but with different ingredients. For each experiment, he introduced some typhoid bacilli to the ice cream mixture, checked after 24 hours of freezing to see how much bacteria there was, and continued measuring until “the last positive examination” for typhoid bacilli. This seems like a badly-controlled series of experiments, since the amount of bacteria introduced into the cultures varies widely between experiments, and I can’t tell the difference between Experiment 1 and Experiment 2. Apparently in Experiment 2, “Ice cream made with 1 pint of thin cream, one-half cup of sugar and 1 tablespoonful of vanilla was treated similarly to the ice cream in Experiment 1.” But… all three of those ingredients are also in Experiment 1. Because of the order things are listed in, my guess is that Experiment 2 has an extra 1/2 cup of sugar.

Also the description of “Flake” powder does not enable colleagues to easily replicate the experiment.

Flake is a powder prepared by the Murray Company, 224 State Street, Boston. According to a circular accompanying the powder, the preparation “is a pure, wholesome powder, which can always be relied on, and is essential in making an exquisitely smooth ice cream.”

That doesn’t help. Anyway, the jumble of descriptive paragraphs can be entirely summed up in this table.

O. W. H. Mitchell’s 1915 data, presented in no particular order

Guess what! That tells us nothing. Pasteurization didn’t help; adding gelatin made things worse somehow; and extra sugar led to less bacteria at the late timepoint. Also, there’s no more bacteria after a couple weeks than there was at 24 hours, even though “After a few days [the samples] began to lose their sweetness of odor, and at the time of the last examinations they gave off mildly unpleasant odors.”

Yes, this was while frozen. They were only slightly below freezing (-3° to -4° Centigrade). Sample size is 1. Total waste of time, I say with 98 years of hindsight.

* * *

Let’s move on to Bolten (1918). He looks at both typhoid and diphtheria bacilli. He shows even less data than Mitchell, but at least the experiments make sense. Basically, small containers of frozen cream (not ice cream, I guess there was no sugar or vanilla) had been inoculated with a growing culture of typhoid, at a 10:1 ratio of cream to bacterial broth, and “immediately placed in a brine tank”. They were “partly melted” daily, and a sample was taken to see how many typhoid bacteria were growing. You’d think that one of the advantages of ice cream as an experimental system is that you don’t have to thaw it in order to take a sample. But that was their procedure.

According to more than one article in the Jan-June 1904 issue of Ice and Refrigeration Illustrated (mental note: look for blog topics in Ice and Refrigeration Illustrated), a “brine tank” typically froze things to between 8 and 16 degrees Fahrenheit (-13° to -9°C). So, quite a bit colder than the ice cream in Mitchell’s study. This type of freezing is pretty good at killing bacteria, given that they started with a substance that was fully 10% bacterial broth. After 2 weeks they had a 50% reduction in colonies; after 4 weeks they had a 95% reduction; and after 10 weeks two of the four containers had no detectable germs at all. Maybe it’s not so much the low temperature as the daily freeze-thaw cycle killing the bacteria.

Skipping gracefully over the diphtheria portion of the paper (which is more confusing), our last entry on ice cream typhoid is the most data-intensive, by Prucha and Brannon of the University of Illinois in the relatively rigorous Journal of Bacteriology. (The other two are in medical journals… who cares about lab experiments in those?) They standardize their experiments by mixing bacteria with ice cream mix, incubating, and freezing it when it gets to 25 million bacteria per cubic centimeter. They keep it in a “hardening room” which fluctuates between -8° and 8°F (-22° to -13°C) – the coldest freezing conditions we’ve seen so far. They take samples not every day, but at increasingly sparse intervals – and they actually show us their data in a table. Which can easily be turned into a graph.

I should use the word “germs” more often in writing about these things. I forget about the word “germs”.

A summary:

Here we see something much closer to Bolten’s “bacteria are mostly killed by freezing”, rather than Mitchell’s “bacteria keep growing in the cold”. And this wasn’t with constant refreezing and rethawing, either. Just low temperatures.

You may notice that the number increases 3-fold between day 134 and 165. Well, they explain that too.

It will be observed in table 1 that the samples taken when the ice cream had been in storage for 165 days gave higher counts than the previous samples. To check this point, another set of samples was taken five days later which again gave similar counts. An inquiry brought out the fact that one of the attendants had removed the experimental ice-cream a few days before to an adjoining room for an hour and one-half. This room had a temperature of 40°F. The ice cream did not melt. Whether there was any multiplication of the germs at this time could be determined.

The conversation that led to that passage:

Prucha: What happened here?

Brannon: I looked into that. You won’t believe it. One of the fellows in the dairy husbandry program, who we told to keep an eye on the freezer…

Prucha: Yes?

Brannon: Well, some of his fraternity brothers let him know it would be a great joke to take the experimental ice-cream into the common room and start eating it.

Prucha: Oh, goodness. Doesn’t he know we put typhoid in it?

Brannon: I think we were a little too excited when we found out freezing had reduced the germs by 99%.

Prucha: So did it melt? Is that why the numbers are high?

Brannon: Luther says he told the boob to put it back in the freezer before it got soft. It was out for maybe 90 minutes.

Prucha: Undergraduates! Damned impudent wastrels!

Brannon: Do we really need “attendants” for this experiment at all?

* * *

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2. Igumbor EO et al (2000). Bacteriological examination of milk and milk products sold in Harare. Afr J Health Sci 7:126-131.

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