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

Tag: Journal of Bacteriology

Gnezda, Pittaluga, Zipfel, Goré, and Berschaffelt back me up on this

Sometimes you see an old scientific paper that does a lot of name-dropping. Instead of saying something like “we used an isothermal calorimeter incorporating a constant-flux modification”, it’ll say “we used a Stanpfer device incorporating a Billigs modification, as demonstrated by Reemis”. I guess this sort of thing is still common in chemistry where every reaction is named after some long-dead German or Japanese person, but to me it seems to hearken back to the days when science was a pursuit for punctilious aristocrats and eccentric showmen.


W. L. Holman and F. L. Gonzales are classic name-droppers.

Some excerpts from A Test For Indol Based on the Oxalic Acid Reaction of Gnezda (found in the November 1923 Journal of Bacteriology, 8(6):577-583):

Gnezda described a pink or purple color reaction formed by the union of oxalic acid and indol in 1899. It is not clear whether Morelli or Pittaluga first applied this reaction to bacteriologic studies.

Morelli does not refer to Gnezda’s work and Zipfel thought that this was simply a return to the principle of the Crisafulli pine splinter hydrochloric acid procedure.

Verschaffelt used the method to demonstrate indol from jasmine and orange blossoms.

Konrich is reported to have found it unsatisfactory. Zipfel, Baudet and Freund obtained results which compared favorably with other standard methods.

The results given with the Salkowski and Ehrlich tests frequently fail to agree. It would appear from the studies of Frieber and many previous workers that the Salkowski test is not reliable as a test for indol, since it gives a reaction quite similar when indol acetic acid is formed from the tryptophane molecule. The Ehrlich-Böhme test has been found to react with other compounds than indol.

Of course, this paper is under no obligation to explain what the “Salkowski test”, the “Ehrlich test”, or the “Ehrlich-Böhme test” are. The audience was probably familiar with these things. The concept of an indol test, or indole test as we call it now, is not that complicated, and in fact is still performed today, with continued improvements and modifications.

And most of the names dropped here are found in the bibliography. In fact, here’s the bibliography.


That’s actually a very long bibliography for a 1923 paper. It would take some effort to find all those papers to see what the authors are talking about, if you’re not actively keeping up with the various permutations of the indole test.

Just as important… most of those papers are not in English. We can’t be sure because there’s no paper titles listed, only the names of the journals. But I count 5 references to English-language journals (J Biol Chem, J Bacteriol, Indian J Med Res); 4 French; 2 Italian; 1 Spanish; 2 Dutch (Folia Microbiol Delft?), and 14 German. There were some synopses of the foreign literature in American journals — unnecessary nowadays when almost everything is in English. But it seems like you had to at least read both English and German (and French?) to follow the scientific literature.

* * *

Personally, I want to know more about “the Crisafulli pine splinter hydrochloric acid procedure”. That sounds great. So evocative of austere old-world elegance. If anyone has a copy of the 1895 Rivista d’Igiene e Sanità Pubblica, containing Gugliermo Crisafulli’s influential article “La reazione rossa del legno di pino per la ricerca dell’indolo nelle culture in brodo dei microrganismi”, please send it in. Or send in a translation.

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 exactly making a big effort to inflate the importance of his results here, is he?

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?

* * *

1. Mulić R et al (2004). Some epidemiological characteristics of foodborne intoxications in Croatia during the 1992-2001 period. Acta Med Croatica 58:421-427.

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

3. Di Pietro S et al (2004). Surveillance of foodborne diseases in the province of Rio Negro, Argentina, 1993-2001. Medicina [B Aires] 64:120-124.

4. Gücükoğlu A et al (2012). Detection of enterotoxigenic Staphylococcus aureus in raw milk and dairy products by multiplex PCR.
J Food Sci 77:M620-623.

5. el-Sherbini M et al (1999). Isolation of Yersinia enterocolitica from cases of acute appendicitis and ice-cream. East Mediterr Health J 5:130-135.

6. Hennessy TW et al (1996). A national outbreak of Salmonella enteritidis infections from ice cream. N Engl J Med 334:1281-1286.

7. De Schrijver K et al (2008). Outbreak of verocytotoxin-producing E. coli O145 and O26 infections associated with the consumption of ice cream produced at a farm, Belgium, 2007. Euro Surveill 13:8041.

8. Payne CJ et al (2003). Vero cytotoxin-producing Escherichia coli O157 gastroenteritis in farm visitors, North Wales. Emerg Infect Dis 9:526-530.

9. Virgil KJ et al (2009). Coliform and Escherichia coli contamination of desserts served in public restaurants from Guadalajara, Mexico, and Houston, Texas. Am J Trop Med Hyg 80:606-608.

10. Fabian FW (1926). Ice cream as a cause of epidemics. Am J Public Health (N Y) 16:873-879.

11. Macfayden A & Rowland S (1900). A further note on the influence of the temperature of liquid hydrogen on bacteria. Lancet 156:254-255.

12. Mitchell OWH (1915). Viability of Bacillus typhosus in ice cream. JAMA LXV:1795-1797.

13. Bolton J (1918). Effect of freezing on the organisms of typhoid fever and diphtheria. Pub Health Rep 33:163-166.

14. Prucha MJ, Brannon JM (1926). Viability of Bacterium typhosum in ice cream. J Bacteriol 11:27-29.

15. Davis DJ (1914). The growth and viability of streptococci of bovine and human origin in milk and milk products. J Inf Dis 15:378-388.

Data update: Bacterial growth on tellurite

If you’ve read Ruth Gilbert and E.M. Humphreys (1926), The use of potassium tellurite in differential media (J. Bacteriol. 11(2):141-151) recently, you’ve probably noticed that the bacterial nomenclature is out of date and it’s hard to tell which species they’re talking about. The descriptions of colony morphology don’t help much, as they only tell us what the colonies look like on beef infusion agar with 5% horse serum and 1/34,000 tellurium content. So here we present the first in what may be a series, of ancient data updated for the modern reader.

Table 2

This table is clear and concise. I would not have made the text in the headers smaller than the text in the columns, and the spacing/justification is inconsistent, but it tells us a lot. Fungi (ActinomycesAspergillusSaccharomyces) had no trouble growing on tellurified plates, but both bacilli and cocci showed the full range between being unaffected and being totally wiped out.

However, the viewer used to modern bacterial nomenclature is perplexed. Some amendments to the names of these organisms have been made over the years. I was able to figure out what all of them are called nowadays, except “Bacillus pestis caviae” (probably some sort of Salmonella) and the Mt. Desert thing (probably a strain of Shigella). And I can’t get to square one of figuring out what “Type I, Type II and Type III” Pneumococcus correspond to today. That way lies madness.

The table has been amended using the modern graphical presentation package MS Paint, which was not available until almost sixty years after this paper was published (1985).

Table 2.0.1

To summarize:

  • 3 out of 3 fungal species are unchanged.
  • 3 out of 53 bacterial species/subspecies are unchanged. Only Bacillus anthracis, Bacillus subtilis, and Staphylococcus aureus. Bacillus proteus vulgaris is almost the same, with Bacillus removed and the remaining, oddly medieval name intact. Pneumococcus is still pneumococcus.
  • Every bacillus really used to be called Bacillus, didn’t it?
  • The only instance of “lumping” rather than “splitting” genera I see is moving Sarcina in with Micrococcus.
  • Meanwhile, most of the Micrococcus species were split into different genera, and what was once called Micrococcus tetragenus based on its  tetrad morphology is now close to being synonymous with the genus Micrococcus as a whole.
  • “Pestis caviae” means “plague of guinea pigs”. I’ve seen one reference to Bacillus pestis-caviae being the same as Bacillus typhimurium, and one reference to it being the same as Bacillus aertrycke, which seems to in turn be the same thing as Bacillus suipestifer. I can’t quite tell what the difference is between Bacillus suipestifer and Bacillus choleraesuis is either, as both are described (etymologically as well) as the agent that causes hog cholera. All of these were at one point designated as part of the “Paratyphoid B” group of bacilli, which were then renamed Salmonella. And then a bunch of others were moved into Salmonella, and then it was determined that basically all Salmonella were in the same species and subspecies, and could only be classified as “serovars” of S. enterica enterica. So who knows.
  • As it was then, this remains a list of the most significant human pathogens. Plus some that affect farm animals, and two that look cool (P. fluorescens and C. violaceum).
  • The veil of history is drawn back, and patterns emerge. We can now tell that Corynebacterium species are not inhibited by tellurium, and Clostridium are very inhibited. And Klebsiella and Salmonella are in the middle.
  • In fact… how about a new table?

Table 2.1

Journal of Bacteriology, issue 11 (February 1926), is available here.

The Clinical Research Laboratory: where ophthalmology meets urine

That last article had another odd element that warrants further study. No, not Table 1, which lists the counts of Clostridum welchii per gram of dry feces for 30 donors of varying degrees of anonymization (“H.”, “J. J.”, “L. W. R.”, “Mr. L.”, “Mrs. C. H.”, “Irwin H.”, “Gladys H.”). I’m referring to the author’s affiliation.


Clinical Research Laboratory? What’s that?

Probably a branch of the city health department. But wouldn’t “clinical” be more likely part of a hospital?

I had to find out. Now, searching for “Clinical Research Laboratory” “New York” is useless. That is the ultimate generic name. Maybe if it was the Clinical Research Laboratory, Manitowoc, Wisconsin I could find details on this now-defunct facility.

But looking for other papers by George H. Chapman gives the answer.

* * *

Over the 25 years following the 1928 paper which documents him burning his hands on a jar, Chapman shows up again and again in the Journal of Bacteriology, mostly as a single author, mostly suggesting small improvements in how to culture and differentiate common bacteria. If we ignore the ones by a George H. Chapman, M.Sc. who worked at the Massachusetts Agricultural Experiment Station, and the other bacteriological George Chapman at Princeton University, there are still about 40.


There are also a couple in journals other than J. Bacteriol.


Without exception, George H. Chapman is affiliated with the Clinical Research Laboratory. Occasionally co-authors appear, most often from the Lighthouse Eye Clinic of the New York Association for the Blind.

The New York Association for the Blind is an organization that started out as “The Lighthouse” and is now “Lighthouse International”. According to their website, “In 1952, the Lighthouse forged an affiliation with the Ophthalmological Foundation, which became the research arm of the Lighthouse at that time. The Foundation was the first to devote its resources to the research of blindness.”

About half of the Chapman papers have a footnote reading “Aided by grants from the Ophthalmological Foundation, Inc.” Does this mean the “Clinical Research Laboratory” was the laboratory of the Ophthalmological Foundation, which ceased to exist after 1952 when it was folded into the Lighthouse? Is that what happened? And why do I care?

More likely, the Ophthalmological Foundation was what it sounds like, a charitable organization that funded all kinds of research. Searching for “Ophthalmological Foundation Inc” did bring up a bunch of articles that don’t mention George H. Chapman. But for most or all of them, if they don’t include him as an author, they do include Conrad Berens, M.D.

The beginning of Berens's 5-page obituary in the Transactions of the American Ophthalmological Society

The beginning of Berens’s 5-page obituary in the Transactions of the American Ophthalmological Society

Noted ocular surgeon Berens was apparently quite the fundraiser and organizer. The obituary goes on to credit him with founding or leading a dozen societies, receiving the Chevalier de l’Ordre de la Santé Publique and the Orden al Mérito de Duarte, Sánchez y Mella, and being a consulting ophthalmologist at eleven hospitals including his primary appointment at the New York Eye and Ear Infirmary. He was also Managing Director of The Ophthalmological Foundation, Inc.

The various affiliations on Berens’s papers include:

Department of Research, New York Eye and Ear Infirmary
Department of Motor Anomalies, New York Eye and Ear Infirmary
Orthoptic Training Department, New York Eye and Ear Infirmary
Department of Ophthalmology, New York University Post-Graduate School of Medicine
Department of Research, New York Association for the Blind

So was this the clinical lab of the New York Eye and Ear Infirmary? If so, why not say that?

More from Berens’s obituary:

At the height of his career, Dr. Berens enjoyed one of the most varied practices of ophthalmology in the United States. His patients came from all walks of life and received the same courteous treatment whether rich or poor. At one time, he employed five medical associates and nine ancillary aids to help him with his private work and he usually had one or two visiting ophthalmologists learning his office technique. His assistants were always known as associates and learned early never to discuss diagnosis and treatment in front of the patients.

The Berens Clinic of the New York Eye and Ear Infirmary early became one of the most progressive in the New York area and popularized a general medical survey before operation or treatment was started. He required orthoptic analysis and treatment before surgery for squint and established the first course in orthoptic training at the Infirmary. Through the aid of the Ophthalmic Foundation, Inc. he established the original Department of Research in Ophthalmology at the hospital. His clinic was the first to make use of preoperative bacteriologic tests and sterile gloves in the operating room.

So he had a private practice with a dozen or so staff, and also founded a “Berens Clinic” at the hospital where he did his published research and tried out new devices. This “Berens Clinic” pioneered doing general physicals and bacteriological tests on all patients, on a larger scale than ophthalmologists had done before. Most likely George H. Chapman was essentially an employee of Dr. Conrad Berens, in charge of whatever bacterial tests were needed for all kinds of patients (certainly most of the samples he handled were from regions of the body distant from the eye) from the New York Eye and Ear Infirmary. And in the process of improving his lab’s techniques, he kept careful track of everything and came up with some stuff that could be published.

* * *

Wait. Isn’t there an address after the words “Clinical Research Laboratory” up there? Can’t we look up which hospital or clinic was at that address?

604 Fifth Avenue is actually a well-known building. A well-known, tiny building in Midtown Manhattan, right near Rockefeller Center. It was built in 1925 to house a Childs restaurant. Childs Restaurants was a pioneer in the concept of fast food, and just like today’s fast food chains, they hired top architects to create novel architectural treasures which would house distinctive flagship restaurants. Here’s a 2010 New York Times article by Christopher Gray, spotlighting this exact building and its current status wedged between two much taller and more important architectural treasures.

604 Fifth Avenue, by the way, is far from the New York Eye and Ear Infirmary, which is and was in Lower Manhattan between 14th and 13th Streets. I can’t find a reference to 604 Fifth Avenue containing anything other than a Childs restaurant, a T.G.I. Friday’s, a series of jewelry stores, or the apartment of Mrs. Russell Sage, widow of one of Jay Gould’s plutocratic pals. We could investigate what hospitals were nearby, but that would take forever. So let’s just say the Clinical Research Laboratory, despite its considerable interest in the bacteria of the GI tract, was run by a ophthalmologist and loosely affiliated with the New York Eye and Ear Infirmary.

* * *

As for George H. Chapman, the flood of bacteriological articles stopped in 1952, the same year the Lighthouse and the Ophthalmological Foundation merged. Years later, he reappeared with a 34-page treatise that was presented at the October 1962 meeting of the New York Academy of Sciences’ Division of Microbiology, and published that November in Trans. N.Y. Acad. Sci.

The title is “Microbial origin of the gummy substance of Fujita and Ging”. It’s a weird article, but not weird in the way that the title sounds weird. Basically he takes the established idea that there are probably distinct toxic chemicals in the bodily fluids of people with schizophrenia, and explains that they are signs of bacterial infection.

The substance of Fujita and Ging had been described less than a year earlier, in “Presence of toxic factors in urine from schizophrenic subjects” (Fujita S, Ging NS [1961] Science 134(3491): 1687-1688). The table of contents for that issue of Science is in JSTOR here. At the time Science was mostly editorials, book reviews, and extremely short research “Reports”, plus a couple longer articles. This was one of the Reports, and as such documented a single experiment, in which a series of mice were injected intracranially with extracts of urine from schizophrenic or non-schizophrenic men “who had been kept for at least 4 weeks under controlled conditions” at the Ypsilanti State Hospital. Looking for signs of schizophrenia in bodily fluids was a frequent topic of study, though urine was not looked at as often as blood; Fujita and Ging explain that they are extending into mice the studies of Wada and Gibson, who did a lot of experiments of this sort on monkeys and cats in a 1959 paper that appeared in the very last issue of AMA Archives of Neurology & Psychiatry.

Fujita and Ging were part of the research team of the University of Michigan’s legendary neuroscientist Ralph W. Gerard. Fujita was visiting from the University of Sapporo, and did eventually publish a follow-up paper on what the chemicals might be in the schizophrenic urine. But for me the trail ends there, since it’s in Japanese.


Fujita and Ging describe the toxicity of schizophrenic urine

Fujita and Ging were only cited five times, once by Chapman. And the Chapman article was cited once, by an book called “Brain Allergies: The Psycho-Nutrient Connection”. The search for signs of schizophrenia in the blood and urine seems to have yielded diminishing results over the years, whereas Chapman’s idea that these things were bacterial metabolites is still plausible, as there are still many studies hoping to link schizophrenia to infections. The infection in question is most often Chlamydia, the bacterium that causes urinary tract infections, or more recently Toxoplasma, the brain parasite popular with cat lovers (reviewed in Yolken et al [2009], Parasite Immunol 31(11): 706-715).

So the idea behind Chapman’s paper makes sense. And it contains a lot of data. However, the text shows worrying signs of crackpotism.

  • Grandiosity: “My primary object throughout this research was to seek the cause of the obscure toxic states that accompany most chronic diseases.”
  • Overambition: “…although time and space will not permit presentation of all the significant data, the statements which I shall make are based on careful and extensive experimentation, although this still does not preclude the possibility of error. Much of the detailed experimental data and its statistical analysis will be submitted to appropriate journals.” (this did not happen)
  • Confusion: I think that when Fujita and Ging used the phrase “gummy substance”, they were referring to the entirety of the dried acetone extract of a urine sample, which was temporarily gummy because it had been processed in a certain way. They did not find a “gummy substance” in the urine. What they did find were unknown compounds that made spots on a Whatman chromatography paper.
    Whereas Chapman talks about a “gummy substance” that makes up a particular alcohol fraction of the urine sample, that he observed in samples specifically from streptococcal UTI patients.
  • Trying to reduce things to simple physical laws: in this case, the redox potential of bodily fluids. Some of this looks logical and I don’t remember enough chemistry to judge. But I don’t know about statements like “A third example is the aggravation of colds following sexual indulgence. Loss of highly oxidized fluids causes a drop in the O/R potential of the body.”
  • Auto-experimentation: “Therefore, I studied the effect of desiccated thyroid on the reducing power of the urine. I took 4 grain doses at frequent intervals and found that they improved, not only the oxidation of the urine, but the quat titer, rate of excretion, urates on refrigeration, and H-ion concentration. …Simultaneously with improvement in these findings there was dramatic improvement in general health.”
  • Hobo legends: The low O/R potential, particularly in severe cases, may provide an explanation for some unsolved phenomena. For example, “Bowery bums” are able to drink “smoke,” which is a water extract of shellac and consists mostly of crude methanol, and yet show no defect of vision.”

* * *

A full fourteen years after “Microbial origin of the gummy substance of Fujita and Ging”, and 48 years after the initial Chapman paper on Clostridium welchii, two other publications appeared. Both are in the 1976 issue of PDM: Physicians’ Drug Manual, which seems to be a book series published once each in 1973, 1974, and 1976. PubMed also lists 13 PDM articles from between 1958 and 1963. I don’t know what that means. And I don’t know how long the papers were either, since PubMed incomprehensibly cites them as PDM 1976 Jan-Dec;7(9-12)8(1-8):90-1 and PDM 1976 Jan-Dec;7(9-12)8(1-8):80-2. Probably short.

These papers (Acid-base and oxidation-reduction relationships and pH and eH relationships in the body) certainly seem to be by the same George H. Chapman. Based on the abstracts, there is a continuing fascination with redox potential and using urine as a readout for various health problems. In the second one, he also coins something called “Chapman’s Law”, another sign of crackpotism. Who knows what he was up to after the end of the Clinical Research Laboratory, but I’m sure he helped a lot of people with bacterial infections.