{"id":7744,"date":"2026-09-12T13:59:17","date_gmt":"2026-09-12T19:59:17","guid":{"rendered":"https:\/\/allphasepharma.com\/dir\/?p=7744"},"modified":"2026-09-12T14:07:31","modified_gmt":"2026-09-12T20:07:31","slug":"on-leptospirosis-weils-disease","status":"publish","type":"post","link":"https:\/\/allphasepharma.com\/dir\/2026\/09\/12\/7744\/on-leptospirosis-weils-disease\/","title":{"rendered":"On Leptospirosis (Weil’s Disease)"},"content":{"rendered":"\n

In 1886, Weil published detailed case descriptions of 4 patients with icterus, splenic enlargement and nephritis [1]<\/a>.  All four patients presented with acute onset of fever, elevated liver function tests (LFTs), hepatic enlargement, splenomegaly, and proteinuria. Two cases were recorded more than12 years earlier, but the author felt that they shared significant similarities with 2 more recent cases from 1882.  Initially, patients presented with a high fever accompanied by general malaise, headaches, somnolence and even delirium.  Many had GI symptoms.  He mentions that iridocyclitis was noticeable in one patient and a roseola-like skin rash in another.  <\/p>\n\n\n\n

The overall course of the illness was benign – there were no fatalities – and patients did not develop hepatic failure despite highly abnormal LFTs and marked jaundice.  Of note, in 3 patients, the disease was diphasic with milder symptoms reappearing after a symptom free interval  Treatment was attempted with methods typical for the era and consisted of calomel (mercury chloride), quinine, muriatic acid and such, but nothing seemed to do any good. <\/p>\n\n\n

\n
\"\"<\/a><\/figure>\n<\/div>\n\n\n

Weil had no biopsy reports, no cultures, and not even microscopic demonstration of a potential pathogen.  Nonetheless, the author felt strongly that the disease must be infectious in nature.  He goes over the differential diagnosis in great detail, yellow fever, recurrent fever, acute hepatitis, typhus including \u2018formes frustes\u2019. These are discussed and dismissed.<\/p>\n\n\n

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\"\"<\/a>
Dr. Adolf Weil<\/figcaption><\/figure>\n<\/div>\n\n\n

Weil certainly displayed extraordinary clinical acumen.  He made connections and drew conclusions based on the knowledge of only 4 cases, occurring many years apart, recognizing a pattern of signs and symptoms that he felt were due to a yet unknown infectious etiology.  While he was convinced that this was a new clinical entity, he remained cautious pointing out the lack of supporting evidence from pathology or bacteriology. <\/p>\n\n\n\n

He had an extraordinary almost prophetic sense of foresight and proved to be correct, but it took another 30 years to confirm his prescient assumptions.<\/p>\n\n\n\n

Actually, the discovery of the pathogen causing Weil\u2019s disease is yet another amazing story. The spirochete was identified during the first world war, around the year 1915.  Visualized with special stains and observed on darkfield microscopy, a new spirochete, leptospira, was identified as the cause of Weil\u2019s disease by several research groups almost simultaneously, first in Japan and a few months later in Germany.  Their efforts went on in parallel and took place independently.  In the span of only 12 months, a series of publications appeared, mutually confirming the organism’s size and shape, propagation in guinea pigs, short presence in blood but high density in the liver, asymptomatic carrier state in rodent kidneys.  With communication hampered by the war in Europe, these research groups were not aware of one another, and it was not clear in the beginning who had first identified the Weil bacillus.<\/p>\n\n\n\n

\"\"<\/a>
Uhlenhuth visualizes spirochetes in human liver. Med Klinik 47:1206,1915<\/figcaption><\/figure>\n\n\n\n

Indeed, a 1916 article in the New York Times [2]<\/a> wrongly attributed the discovery of the spirochete to Uhlenhuth who had published a detailed description of his experimental work in the March 1916 issue of the Berliner Klinische Wochenschrift.<\/p>\n\n\n\n

Uhlenhuth was already a prominent scientist in those days and contributed much to early leptospirosis research.  He was unable to infect cats, dogs, pigs, monkeys or rats; only guinea pigs and hamsters came down with the disease after inoculation with infectious blood.  The \u2018virus\u2019 could be passaged over several generations in guinea pigs.  He described spirochetes with peculiar endings in liver specimens using Levanditi staining, a treponemal silver nitrate-based method and saw spirochetal movement on darkfield microscopy.  He found organisms in large numbers in liver cells, but rarely in blood.  When immunity developed, it was transferable and partially protective.  He even tested various chemotherapeutic agents, including Atoxyl and Neo-Salvarsan, arsenicals used for the treatment of syphilis and trypanosomiasis. <\/p>\n\n\n\n

As it turned out, Uhlenhuth\u2019s publication was preceded by the work of another group of German researchers who published their findings in a series of \u2018announcements\u2019. H\u00fcbener and Reiter were in hot pursuit of a spirochete, which they saw on liver stains as mentioned in their first of 4 reports from 1915. However, their claim to have found the etiology of Weil\u2019s disease drew criticism from Dr. Weil himself who felt that the identified pathogen may not be causative of Weil\u2019s disease as he had originally described it.  H\u00fcbener\u2019s detailed response provided more data in support of the spirochetal origin and seemed to have settled the discourse.<\/p>\n\n\n\n

H\u00fcbener and his team in Berlin had indeed identified a spirochete, but – unbeknownst to them and Uhlenhuth (and the NYT) –  Japanese researchers can claim priority by a few months.  It was Inada and coworkers who first announced the discovery of a leptospiral pathogen in early 1915.  They published their findings on the spirochete which they called Leptospira icterohaemorrhagicae<\/em>. We refer you to Dr. Kobayashi\u2019s account who in 2001 chronicled the timeline of leptospirosis research ultimately leading to the discovery of the pathogen.[1]<\/a><\/p>\n\n\n\n

The race to the finish line involved at least 3 research groups, all converging on the final identification of the pathogen we now call L. interrogans<\/em>.  All contributed to our knowledge as far as epidemiology and diagnosis are concerned. <\/p>\n\n\n\n

A timeline of key events, articles and publication references is provided in the Table below (the Japanese references according to Kobayashi [1]<\/a>):<\/p>\n\n\n\n

\"\"<\/a><\/figure>\n\n\n\n

It becomes clear that keeping track of the rapid fire of publications must have been difficult for reasons of language, publication in lesser known journals, geographic distance and war-related communication issues.<\/p>\n\n\n\n

The history of leptospirosis is fascinating.  It features a clinician with an uncanny ability for recall of patient histories who reports a new disease.  He is proven right by the concerted efforts of microbiologists who – 30 years later – in quick succession were able to identify the pathogen of Weil\u2019s disease. Rightly so, Inada, Uhlenhuth and Weil are still recognized for their contributions to medicine, serology and bacteriology. <\/p>\n\n\n\n

The story does not end here. There are several cross-connections that are probably less known, like the debate about animal experimentation, defended by Uhlenhuth, the training of Japanese researchers in German labs including Inada, the role of news media sensationalizing claims that prove only partially correct, and later career and role of some key investigators during the Third Reich (Uhlenhuth, Reiter). <\/p>\n\n\n\n

There is an important zoonotic component to leptospirosis. While uncommon in humans, uveitis is fairly common in horses. Also called ERU (equine recurrent uveitis) or ‘moon blindness’, it is an immune phenomenon secondary to leptospirosis frequently leading to blindness. Antibiotics are not helpful; treatment is with steroids and NSAIDs.<\/p>\n\n\n\n

The underlying immune pathology of leptospira has been getting morre attenttion in recent years. Associations with genetic markers, interleukins like IL-6, TNF, IFN\u03b3, and pentraxins are under investigation.<\/p>\n\n\n\n

Existing diagnostic tests for leptospirosis seem antiquated. The tedious microscopic agglutination test (MAT) and other serologic assays to detect a titer increase between early and convalescent sera, ELISA and PCR tests are still mentioned in textbooks; they have significant shortcomings which result in underreporting of the disease. A recent article takes a new approach by studying virulence factors.[3]<\/a> There is clearly a need for more specific and less labor-intensive tests that could be brought to countries with limited resources. Making a diagnosis of leptospirosis by bacteriology is just as difficult today as it was for Inada, Uhlenhuth, and Huebener.<\/p>\n\n\n\n

<\/p>\n\n\n\n

\n\n\n\n

PS1.  The Weil-Felix reaction for rickettsial typhus is named after Edmund<\/span> Weil. 
No relationship to Adolf Weil of leptospirosis fame!<\/p>\n\n\n\n

PS2. Adolf Weil is sometimes listed as the discoverer of the atypical amino acid norleucine.[4]<\/a> This is incorrect: Norleucine was discovered by Arthur<\/span> Weil in 1913 together with the somewhat controversial biochemist Emil Abderhalden (who had a minor asteroid named after him).[5]<\/a>,[6]<\/a><\/p>\n\n\n\n

\n\n\n\n

REFERENCES<\/strong> (See also Table above)<\/strong>
[1]<\/a> Kobayashi Y.\u00a0 Discovery of the causative organism of Weil\u2019s disease: historical view.\u00a0 J Infect Chemother 7:10, 2001
[2]<\/a> New York Times: Find the Cause of Weil’s disease – Oct 1, 1916
[3]<\/a> Chaurasia R. Early Diagnosis of Human Leptospirosis by Detection of Antibodies to Leptospira-Secreted Virulence-Modifying Protein Exotoxins. Am. J. Trop. Med. Hyg., 114: 17, 2026
[4]<\/a> Adolf Weil (physician) – Wikipedia<\/a> (accessed 9\/12\/2026)
[5]<\/a> Abderhalden E. Spaltung von dl-Aminocaprons\u00e4ure (= Norleucin) in die optisch-aktiven Komponenten mittels der Formylverbindung. Polypeptide, an deren Aufbau Aminocaprons\u00e4ure beteiligt ist. Hoppe Seyler’s Zschrift f. Physiol. Chem. 86: 454, 1913
[6]<\/a> Emil Abderkalden u. Arthur Weil. Vergleichende Untersuchungen \u00fcber den Gehalt der verschiedenen Bestandteile des Nervensystems an Aminos\u00e4uren. 2. Mitteilung Hoppe Seyler’s Zschrift f. Physiol. Chem. 83: 425, 1913<\/p>\n\n\n\n




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That statement was later modified to mean S. pneumoniae was the underlying pathogen in 90% of bacterial\u00a0cases of CAP, i.e., those with positive cultures from sputum or\u2026","rel":"","context":"In "Recent Literature"","block_context":{"text":"Recent Literature","link":"https:\/\/allphasepharma.com\/dir\/category\/recent_literature\/"},"img":{"alt_text":"CAP slider 2","src":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2015\/08\/CAP-slider-2.jpg?resize=350%2C200","width":350,"height":200,"srcset":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2015\/08\/CAP-slider-2.jpg?resize=350%2C200 1x, https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2015\/08\/CAP-slider-2.jpg?resize=525%2C300 1.5x"},"classes":[]},{"id":7298,"url":"https:\/\/allphasepharma.com\/dir\/2026\/06\/06\/7298\/hanta-whats-next\/","url_meta":{"origin":7744,"position":2},"title":"HANTA & WHAT\u2019S NEXT","author":"Harald","date":"June 6, 2026","format":false,"excerpt":"By now, we\u2019ve had a chance to brush up on the Hanta virus, esp. the Andes variety which caused a mini-epidemic on the arctic cruise ship MV Hondius.\u00a0 Named after Hantaan, the river in South Korea where the disease first emerged, we give credit to Dr. Ho Wang Lee, the\u2026","rel":"","context":"In "Recent Literature"","block_context":{"text":"Recent Literature","link":"https:\/\/allphasepharma.com\/dir\/category\/recent_literature\/"},"img":{"alt_text":"","src":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2026\/06\/HANTA-slider-1024x169.jpg?resize=350%2C200&ssl=1","width":350,"height":200,"srcset":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2026\/06\/HANTA-slider-1024x169.jpg?resize=350%2C200&ssl=1 1x, https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2026\/06\/HANTA-slider-1024x169.jpg?resize=525%2C300&ssl=1 1.5x, https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2026\/06\/HANTA-slider-1024x169.jpg?resize=700%2C400&ssl=1 2x"},"classes":[]},{"id":2064,"url":"https:\/\/allphasepharma.com\/dir\/2015\/10\/22\/2064\/polyphor-pol7080-and-the-journey-to-the-land-of-pyocyanea-part-3\/","url_meta":{"origin":7744,"position":3},"title":"Polyphor POL7080 And The Journey to The Land of Pyocyanea (Part 3)","author":"Harald","date":"October 22, 2015","format":false,"excerpt":"VABP is clearly the main\u00a0indication to be pursued by a drug like POL7080.\u00a0 Here is the question: How to conduct a study demonstrating efficacy for a drug which only has a\u00a0single-organism spectrum? \u00a0Which is actually no spectrum at all. \u00a0Existing guidelines for the development of ID drugs are indication-driven, with\u2026","rel":"","context":"In "QIDP Antibiotics"","block_context":{"text":"QIDP Antibiotics","link":"https:\/\/allphasepharma.com\/dir\/category\/qidp_antibiotic\/"},"img":{"alt_text":"bridge Pyocyanea-P3","src":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2015\/10\/bridge-Pyocyanea-P3.jpg?resize=350%2C200","width":350,"height":200,"srcset":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2015\/10\/bridge-Pyocyanea-P3.jpg?resize=350%2C200 1x, https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2015\/10\/bridge-Pyocyanea-P3.jpg?resize=525%2C300 1.5x"},"classes":[]},{"id":885,"url":"https:\/\/allphasepharma.com\/dir\/2014\/09\/17\/885\/new-pathogens-outbreaks-epidemics-2014\/","url_meta":{"origin":7744,"position":4},"title":"Bugs and Outbreaks That Scared Us in 2014","author":"Harald","date":"September 17, 2014","format":false,"excerpt":"At the end of every year, some of us tally \u2013 in a retrospective \u2013 the most remarkable epidemics, newly recognized pathogens or resistance issues that occupied the headlines in the past 12 months.\u00a0 Here a sneak preview what you are likely to see in the coming December issue of\u2026","rel":"","context":"In "The Viewpoint"","block_context":{"text":"The Viewpoint","link":"https:\/\/allphasepharma.com\/dir\/category\/the_viewpoint\/"},"img":{"alt_text":"","src":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2014\/09\/Outbreak.gif?fit=638%2C230&ssl=1&resize=350%2C200","width":350,"height":200,"srcset":"https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2014\/09\/Outbreak.gif?fit=638%2C230&ssl=1&resize=350%2C200 1x, https:\/\/i0.wp.com\/allphasepharma.com\/dir\/wp-content\/uploads\/2014\/09\/Outbreak.gif?fit=638%2C230&ssl=1&resize=525%2C300 1.5x"},"classes":[]},{"id":4745,"url":"https:\/\/allphasepharma.com\/dir\/2025\/07\/18\/4745\/cabp-trial-enrollment-but-not-in-the-usa\/","url_meta":{"origin":7744,"position":5},"title":"CABP TRIAL ENROLLMENT \u2013 BUT NOT IN THE USA","author":"Harald","date":"July 18, 2025","format":false,"excerpt":"Today\u2019s topic is about the lackluster recruitment of US centers in recent CABP trials. 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