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History of Medicine |

The Death of Wolfgang Amadeus Mozart: An Epidemiologic Perspective

Richard H.C. Zegers, MD, PhD; Andreas Weigl, PhD; and Andrew Steptoe, DSc
[+] Article and Author Information

From the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Municipal and Provincial Archives of Vienna, University of Vienna, Vienna, Austria; and University College London, London, United Kingdom.


Note: An earlier version of these analyses was included in Dr. Zegers's Academisch Proefschrift at the University of Amsterdam in 2008.

Acknowledgment: The authors thank Mag. Martha El Hadidi, Wienbibliothek im Rathaus, Vienna, Austria, for providing several missing pages of Verzeichnis der Verstorbenen and Anton Neumayr, MD, PhD, professor of gastroenterology, Vienna, for assistance with the translation and interpretation of the original names of diseases. They also thank Johan W.G. Tielen, MD, gastroenterologist, Gouda, the Netherlands; Jos G.U. Ridderbeks MD, general practioner, Ulestraten, the Netherlands; Peter Speelman, MD, PhD, professor of infectious disease, and Ray T. Krediet, MD, PhD, professor of nephrology, Amsterdam, the Netherlands; L.P. (Berto) Roegholt, MD, PhD, internist, Middelburg, the Netherlands; and Martin Hohenegger, MD, PhD, professor of pharmacology, Vienna, for fruitful discussions of Mozart's possible cause of death. Finally, they thank Josephine M.E. Tusveld, MD, Utrecht, the Netherlands, for her support in preparing this manuscript.

Potential Financial Conflicts of Interest: None disclosed.

Requests for Single Reprints: Richard H.C. Zegers, MD, PhD, Department of Ophthalmology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands; e-mail, r.h.zegers@amc.uva.nl.

Current Author Addresses: Dr. Zegers: Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands.

Dr. Weigl: Municipal and Provincial Archives of Vienna, MA 8, Rathaus, 1082 Vienna, Austria.

Dr. Steptoe: Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, United Kingdom.


Ann Intern Med. 2009;151(4):274-278. doi:10.7326/0003-4819-151-4-200908180-00010
Text Size: A A A

The early death of the composer Wolfgang Amadeus Mozart on 5 December 1791 has fascinated the world for more than 2 centuries. It has been suggested that his final illness was caused by poisoning, renal failure, Henoch–Schönlein purpura, trichinosis, and many other conditions. The official daily register of deaths in Mozart's Vienna was evaluated to provide an epidemiologic framework into which the observations of contemporary witnesses of his death can be integrated. All recorded deaths in Vienna during November and December 1791 and January 1792 were analyzed, together with the corresponding periods in 1790 to 1791 and 1792 to 1793. The deaths of 5011 adults (3442 men, 1569 women) were recorded over these periods. The mean ages of death were 45.5 years (SD, 18.5) for men and 54.5 years (SD, 19.9) for women. Tuberculosis and related conditions accounted for the highest number of deaths; cachexia and malnutrition ranked second, and edema was the third most common cause. According to eyewitness accounts, the hallmark of Mozart's final disease was severe edema. Deaths from edema were markedly increased among younger men in the weeks surrounding Mozart's death compared with the previous and following years. This minor epidemic may have originated in the military hospital. Our analysis is consistent with Mozart's last illness and death being due to a streptococcal infection leading to an acute nephritic syndrome caused by poststreptococcal glomerulonephritis. Scarlet fever, which represents the same underlying disease from an etiologic perspective, is a less likely possibility.

Figures

Grahic Jump Location
Figure.
Deaths from edema and related conditions in Vienna during November, December, and January, 1790–1793.

Top. Deaths among men and women in the fall and winter of 1790–1791, 1791–1792, and 1792–1793. Error bars represent SEs. Bottom. Deaths among civilians and soldiers in the fall and winter of 1790–1791, 1791–1792, and 1792–1793. Error bars represent SEs.

Grahic Jump Location
Grahic Jump Location
Appendix Figure.
Deaths among men and women in the 3 periods studied.

A. Total deaths. B. Deaths from tuberculosis and related diseases. C. Deaths from gastrointestinal inflammatory diseases. D. Deaths from fever and inflammatory conditions.

Grahic Jump Location

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Beyond Tourette's syndrome: other possible Mozart's neurological disorders
Posted on August 18, 2009
Tomislav Breitenfeld
Sestre milosrdnice University hospital, Neurology dpt., Vinogradska 29, 10000 Zagreb, Croatia
Conflict of Interest: None Declared

Only few composers in history have earned any fame from their medical history investigated by several experts. Besides Georg Friedrich Handel and Maurice Ravel it is for rare composers to have numerous pathographies but Mozart, with about 100 articles on Medline, is one of them. However no autopsy was performed and there is no medical documentation preserved that would be acceptable by current scientific standards, so it is almost impossible to perform a proper pathography. Although most commonly noted in medical literature, Tourette's syndrome in not only neurological disorder Mozart suffered from during his life (1). Davies and Bett reported on lapses of consciousness but also convulsions. Mozart did probably faint occasionally, but probably out of his sloppy lifestyle, overworking, alcohol consumption or occasional malnutrition, however there is no evidence he suffered from epilepsy. Mozart's immobility as sign of muscular paralysis assuming postinfectious polyradiculoneuritis was discussed by Davies (2). Complete immobility, severe weakness and preserved consciousness during his final illness may support that theory but pain, absence of paresthesiae and generalized excessive swelling of limbs and body suggest other conditions.

Many authors have supported the kidney disease theory for Mozart's final and fatal illness - taking in account his fatigue, depressive tendencies, headaches, syncopes, anorexia, insomnia, increasing weakness, nausea, vomiting and peculiar metallic taste in his mouth, all as signs of uraemia and renal failure, thereby Karhausen suggested diagnosis of uraemic and hypertensive encephalopathy (3). It was described that Mozart's sudden deterioration 2 hours before death included possible convulsions, delirium, coma, face turned to wall, cheek puffed out so Davies reads those symptoms (consciousness impairment, paralysis, conjugate gaze and facial nerve palsy) suggesting massive brain hemorrhage as a consequence of vasculitis in Schoenlein Henoch syndrome (4). Nevertheless there is no evidence that Mozart showed any signs of focal neurological deficit during his final illness. In such manner Baroni unconvincingly suggested stroke as terminal cause of Mozart's death (5). Theory about Mozart's multiple congenital malformation syndrome including his famous left ear malformation, polycystic kidney as onset of subsequent renal failure and intracranial arterial aneurysm (malformation) that caused fatal subarachnoidal hemorrhage is inconsequent since the clinical course of his final illness rule out that possibility. Puech explained that the linear fracture in the temporoparietal region oriented anteriorly and downwards, without displacement, was found on the skull owned by the Mozarteum in Salzburg and attributed to Mozart and he reasoned chronic extradural hematoma with headaches, fainting, vomiting, chronic weakness and exhaustion (6). Further on Drake suggested chronic subdural hematoma which could be consistent with described skull fracture, several falls in 1789 and 1790 and weakness, headache and fainting Mozart experienced in 1790 and 1791 (7). Both authors failed to work out the substantial question: is the Mozarteum skull Mozart's skull at all? Even DNA analysis performed 2006, on 250th anniversary of Mozart's birth, did not solve that mystery.

References:

1. Ashoori A, Jankovic J. Mozart's movements and behaviour: a case of Tourette's syndrome? J Neurol Neurosurg Psychiatry. 2007 Nov;78(11):1171- 5.

2. Davies PJ. Mozart's death: a rebuttal of Karhausen. Further evidence for Schönlein-Henoch syndrome. J R Soc Med. 1991 Dec;84(12):737-40.

3. Karhausen LR. Contra Davies: Mozart's terminal illness. J R Soc Med. 1991 Dec;84(12):734-6.

4. Davies JP. Mozart's illnesses and death. J R Soc Med. 1983 Sep;76(9):776-85.

5. Baroni CD. The pathobiography and death of Wolfgang Amadeus Mozart: from legend to reality. Hum Pathol. 1997 May;28(5):519-21.

6. Puech B, Puech PF, Dhellemmes P, Pellerin P, Lepoutre F, Tichy G. Did Mozart have a chronic extradural haematoma? Injury. 1989 Nov;20(6):327-30.

7. Drake ME Jr. Mozart's chronic subdural hematoma. Neurology. 1993 Nov;43(11):2400-3.

Conflict of Interest:

None declared

Forensic comment on Mozart's Death
Posted on August 20, 2009
Pierre Francois Puech
Lab. anatomy Medicine Univ.
Conflict of Interest: None Declared

The BBC

http://www.bbc.co.uk/dna/h2g2/A1304957

have the following comment on Mozart's Death - Murder, Accident or Disease?

A couple of investigators have surprisingly broken from the norm of attributing Mozart's death to murder and strange ailments by announcing that Mozart died from complications arising from accidents. The first to push this story was French anthropologist Pierre-Francoise Puech, who claimed to have positively identified a skull at Salzburg's Mozarteum to be that of Mozart. Puech drew attention to a fracture in the skull, claiming that it had been sustained from one of Mozart's many falls in 1791, and that it had caused a chronic bruising that had eventually put Mozart in a coma and killed him. The skull was supposed to have been rescued by a gravedigger named Joseph Rothmayer during the reorganisation of the composer's grave, who later gave it to the Salzburg Mozarteum.

Three years later, the American physician Niles E. Drake concurred with Puech's theory in an article that was published in the journal BioScience. This theory would indeed help explain why Mozart was depressed and dizzy not long before his death. The obvious problem with this theory is that there is still no consensus as to whether the skull actually belonged to Mozart. Rothmayer had allegedly wrapped wire around the neck of Mozart's corpse before burying it, and had retrieved the skull ten years later when it was exhumed. Research had concluded that the skull belonged to a 20-40 year old South German male who suffered a developmental abnormality called premature synopsis of the metopic suture (PSMS). This abnormality is characterised by the bone of the forehead developing in two halves, and the failure of the metopic suture to close after birth, resulting in a broad midface and a small, abnormally-shaped skull.

As Mozart's portraits depicted a straight, vertical forehead, bulbous nose, prominent cheekbones and upper lip, and prominent brow arches, it was supposed that the skull did indeed belong to him. Further research involving the superimposition of a photograph of the cranium of the skull on portraits of Mozart painted between 1778 and 1788 indicated conformity with all side proportions of the head. However, Nova Scotian neurologist Professor TJ Murray, who founded the Dalhousie Society for the History of Medicine, denied that the skull was that of Mozart as seen in portraits. Walter Brauneis, archivist of the Office for the Preservation of Historical Monuments in Austria, undertook to carry out his own research by locating official medical records concerning Mozart's death. Surprisingly he found a doctor's description of the body, which noted that Mozart (the dentist's worst nightmare!) had only seven teeth remaining in his mouth (the rest having rotted or fallen out)!

When the Mozarteum skull was re-examined, it was found to have four more teeth than had been recorded by the doctor. Puech supporters countered that the doctor probably counted only the healthy teeth. Puech Pierre Francois (pfpuech@yahoo.fr)add: The only way to be sure just whose skull was to perform DNA analysis on the skull; unfortunately, all of Mozart's children died childless, and his parents' grave has been disturbed and was not able to give an answer. DNA analysis of the "Mozart" skull confirmed that it was masculine, or it was on the simple assetion that the skull dimention where feminine that the Mozarteum rejected the forensic anthropological studies that gives a positive identification. There is no more objections to the identification of the skull. PS for the supposed wrong number of teeth, a simple photo give evidence that the 4 incicives crowns are broken off and there presence can or can't be counted.

Conflict of Interest:

None declared

Mozart's Death, a diagnostic Dilemma.
Posted on August 21, 2009
Munir E. Nassar, M.D.
N/A
Conflict of Interest: None Declared

I would like to point out that having treated or examined over 200 cases of Rheumatic Heart Disease with collegues at the American University of Beirut Medical Center, it is difficult to conceive that beta hemolytic Streptococci infection causing post stretococcal glomerulonephritis would from an epidemiologic point of view affect only Mozart, without other members of the household, his spouse Constanza,or his children, as was shown by our studies. Beta Hemlytic Streptococcus infects more than one member of a household. The majority of our patients studied after the fact, developed Acute Rheumatic fever and later Rheumatic Heart Disease as a consequence of acute Beta Hemolytic, Streptococcal Tonsillitis infection. Minority of patients came down with Acute Glonerulonephritis. Although certainly Mozart's fatal symptoms do suggest genralized edema secondary to renal failure and its complications as noted by Drs Richard H.C.Zegers and colleagues (1).

References

1. Richard H.C. Zegers, Andreas Weigl, and Andrew Steptoe The Death of Wolfgang Amadeus Mozart: An Epidemiologic Perspective Ann Intern Med 2009; 151: 274-278

Conflict of Interest:

None declared

Re: Forensic comment on Mozart's Death
Posted on August 22, 2009
Pierre Francois Puech
Lab. Anat. Medicine Univ.
Conflict of Interest: None Declared

Precisions: The mandible was lost and the skull has 15 teeth. If Mozart's maxillary had 11 teeth, as counted after the time of death (per a medical certificate discovered by Walter Brauneis), it is because the crowns of the four upper incisors are broken off. Two children of Mozart survived and 4 died in infancy. The younger son surviving, Franz X. Wolfgang, died on 29 July 1844 in Karlsbad where he was buried. His tomb, the only one known for the children, was moved ten years later to a different cemetery of the town. It has been reported that the body is now missing (1,2).

References

1. Puech PF, Puech B, Tichy G. Identification of the cranium of W.A. Mozart. Forensic Sci Int. 1989 April-May;41(1-2):101-102.

2. Dr. Walther Parson, 2006. Army helps DNA scientists unravel Mozart mystery. Accessed at http://www.scienceblog.com/cms/army_helps_dna_scientists_unravel_mozart_mystery_9713

Conflict of Interest:

None declared

Mozart's Death: Other Possibilities
Posted on August 23, 2009
Denis L. Keleher
University of Colorado
Conflict of Interest: None Declared

In 1988 H.C. Robbins Landon in Mozart's Last Year:1791, discussed all the evidence and subsequent discussions by scholars about Mozart's fatal illness which included pretty much the same conclusions as Zegers et al. Volkmar Braunbehrens in 1986, Mozart in Vienna, (translation 1989), covered the same ground extensively. I've never seen anyone consider one of the acute leukemias as a likely cause for his illness. We all know another half century would pass before this was recognized as a pathological entity, but it seems a possible, even likely, candidate. Comment would be welcomed.

Conflict of Interest:

None declared

Mozart's Death
Posted on August 27, 2009
George E Ehrlich
No Affiliation
Conflict of Interest: None Declared

To the Editor:

The work undertaken to discover the reason Mozart died so young was truly prodigious, but I wish to draw your attention to an article entitled "New Thouts on Mozart's Terminal Illness" in the Dalhousie Review in 1993. I came to the same conclusion, that Mozart's anasarca was a result of renal failure, but there was no evidence of acute illness or fever preceding his demise. A survey of causes of death at the time could not have produced evidence that led to Mozart, but renal failure is a sure possibility, as the earlier paper also claimed.

Reference

1. Ehrlich, George E.: New Thoughts on Mozart's Terminal Illness, in: Dalhousie Review 73 (1993), No. 2, Halifax, Summer 1993, S. 241-245

Conflict of Interest:

None declared

The cause of Mozart's death
Posted on August 28, 2009
Jan V Hirschmann
Puget Sound VA Medical Center, University of Washington
Conflict of Interest: None Declared

The proposal that Mozart died from acute post-streptococcal glomerulonephritis (APSG) (1) following streptococcal pharyngitis fails to explain several features of his disease. It does not account for the two components, pyrexia and skin rash, inherent in the diagnosis of "miliary fever" that Mozart's highly respected physician, Thomas Closset, listed as the cause of death(2). Fever is rare in adult APSG (0-10%) (3-5), and skin rash is not a feature of the disease, except for residual pyoderma when the preceding streptococcal infection is cutaneous, not pharyngeal. The authors assert that the omission of a skin rash in the family's accounts of Mozart's illness suggests that it was a late manifestation noted only by those attending his death. Yet, Sophie Haibel, his sister- in-law, saw him on his last day of life and mentioned no dermatologic problems in her account (2). More plausible explanations about the absence of a rash in the family's recollections are: 1) they had forgotten about this finding in the three decades that had elapsed between Mozart's death and their testimony; 2) the eruption was subtle or transient and seen only by his doctors; or 3) not realizing its diagnostic import, they simply omitted mentioning what seemed inconsequential in an illness dominated by massive edema and pain.

The authors' explanation for that pain is unsatisfactory. Attempting to support their diagnosis of APSG, the authors assert, without any documentary justification, that Mozart had back pain. The accounts indicate a different type and location of the discomfort. Dr. Guldener, who examined the body after death and was knowledgeable about Mozart's clinical course said that he had a "rheumatic and inflammatory fever." Sophie Haibel stated that his "arms and limbs were much inflamed and swollen (2)." The terms "rheumatic" and "inflamed" suggest musculoskeletal pain accompanied by such features as erythema, tenderness, and warmth. APSG cannot explain rheumatic inflammation of the arms and legs.

Another problem with APSG is that Dr. Guldener asserted that the disease causing Mozart's death had a considerable mortality rate (2). APSG is nearly always self-limited, and, even if untreated, is rarely lethal. The rate of death or uremia requiring dialysis in epidemics exclusively or primarily affecting adults is <10%. (3,4) The only disease that satisfactorily explains all the features Mozart's illness is trichinosis (2). Once clinicians recognized this infection in the 19th Century, they recorded mortality rates as high as 19% and 30% in epidemics.

References

1.Zegers RHC, Weigl A, Steptoe A: The death of Wolfgang Amadeus Mozart: an epidemiologic perspective. Ann Intern Med 2009;151:274-8.

2. Hirschmann JV. What killed Mozart? Arch Intern Med 2001;161:1381-9.

3. Stetson CA, Rammelkamp CH, Krause RM, Kohen RJ, Perry WD: Epidemic acute nephritis: studies on etiology, natural history and prevention. Medicine (Baltimore). 1955 Dec;34:431-50.

4. Balter S, Benin A, Pinto SWL, et al: Epidemic nephritis in Nova Serrana, Brazil. Lancet 2000;355:1776-80.

5. Lien JWK, Mathew TH, Meadows R: Acute poststreptococcal glomerulonephritis in adults: a long term study. Q J Med. 1979 Jan;48(189):99-111.

Conflict of Interest:

None declared

Re: The cause of Mozart's death
Posted on August 31, 2009
Richard HC Zegers
Academic Medical Center/University of Amsterdam
Conflict of Interest: None Declared

I appreciate the comments of Dr Hirschmann, but have to notice that he brings up some incorrect issues that are presented as accomplished facts. First he states that the official diagnosis of Mozart's death was listed by Mozart's physician Closset and uses his own article as a reference (1). Unfortunately there is no documentary justification for this assumption. In fact, the diagnosis of "miliary fever" might has not been given by a physician at all, as Maximilian Stoll "“ of whom Closset was a faithful scholar "“ already had demonstrated that fever and a rash were not a disease entity, but represented symptoms (2). We simply do not know who introduced the official diagnosis and hence cannot estimate the significance of this piece of information.

The same applies to the localisation of the pain. Naturally, being present day physicians, we think of musculoskeletal pain when the term "rheumatic" and "inflamed" are involved, but Sophie Haibel could have thought of something completely different, like Mozart for example did when he described a "rheumatic pain of the head" in one of his letters (3). Also for physicians, the term "rheumatic" was not specified in those days, since this term can be found in many diseases like "rheumatic pain of the head", "rheuma of the breast", "rheumatic biliary fever", and "rheumatic stroke" (2). Guldener's diagnosis is an unspecified one, just like miliary fever. Dr Hirschmann states even himself that "inflammation" and "rheumatism" are somewhat non-specific terms (4).

What should be considered in reading our article on Mozart's death is that we studied the causes of death and this is exactly what our finding of a minor epidemic of edema represents: the number of people that died from edema, might as a consequence of an acute poststreptococcal glomerulonephritis (APSG). This can imply that many more suffered from APSG, but only the people that died as result from this cause were registered and hence included in our study. As a consequence, the self- limiting cases were not reported; and percentages of fever, death, or uremia requiring dialysis in epidemics do not make sense in this discussion as we know nothing about the total number of people affected by APSG around Mozart's time of death. Furthermore, since we are talking about Europe in the 18th century, it would seem more reasonable to compare this case to the present day situation in developing countries rather than compare it to the epidemiology and "˜natural' course of APSG nowadays in Europe and the United States. Studies from developing countries question whether the outcome is always benign; and APSG remains a cause of morbidity and mortality in developing countries and among impoverished populations (5).

I feel our hypothesis provides a fine epidemiological reconstruction of what might could have happened to this great composer.

References

1. Hirschmann JV. What killed Mozart? Arch Intern Med. 2001; 161: 1381-9.

2. Bär C. Mozart. Krankheit "“ Tod "“ Begräbnis. Schriftenreihe der Internationalen Stiftung Mozarteum Salzburg. Kassel: Bärenreiter; 1972.

3. Bauer WA, Deutsch OE. Mozart. Briefe und Aufzeichnungen. Gesamtausgabe. Band V: 1787-1857. Kassel: Bärenreiter; 1971.

4. Hirschmann JV. In reply. Trichinellosis is unlikely to be responsible for Mozart's death. Arch Intern Med. 2002; 162: 946-7.

5. Ahn SY, Ingulli E. Acute poststreptococcal glomerulonephritis: an update. Curr Opin Pediatr. 2008; 20: 157-62.

Conflict of Interest:

None declared

Mozart's Glomerulonephritis
Posted on August 28, 2009
Philip A. Mackowiak
Maryland VA Health Care System
Conflict of Interest: None Declared

TO THE EDITOR: Zegers and colleagues are to be congratulated for adding an important piece to the puzzle concerning the etiology of Mozart's final illness (1). Their contribution is to have corroborated a statement made by Dr. Eduard Vincent Guldener von Lobe at the time of the composer's death that: "A great number of the inhabitants of Vienna were at this time laboring under the same complaint, and the number of cases which terminated fatally, like that of Mozart's, was considerable." (2) In effect, their findings confirm that Mozart died of an epidemic disorder. Unfortunately, they do not identify the specific disorder responsible for the epidemic . Nevertheless, given the clinical characteristics of Mozart's illness, an acute glomerulonephritis is, by far, the most likely diagnosis for the reasons enumerated by Zegers et al in their paper.

In considering possible etiologies of both Mozart's death and the epidemic of which it was a part, Zegers et al conclude that post- streptococcal glomerulonephritis is the best diagnosis. Although not specifically stated, the variety of post-streptococcal glomerulonephritis they appear to favor is the classical one caused by Lancefield group A, Streptococcus pyogenes . It produces generalized edema as one of its most striking and consistent features . Fever, which Mozart also seems to have had, is less common, developing only in approximately half of the cases. Muscle and joint pains, which Mozart might or might not have had, are not prominent in cases of classical post-streptococcal glomerulonephritis. The disorder occasionally occurs in epidemics, but is a disease primarily of children between the ages of 2 and 10 years. Fewer than 10 percent of cases are older than 30 years of age. Moreover, classical post- streptococcal glomerulonephritis is typically an acute, but reversible disorder from which patients normally recover fully within 2 to 4 weeks (3). Thus, classical post-streptococcal glomerulonephritis leaves much to be desired as the cause of the epidemic that took Mozart's life. There is, however, another form of post-streptococcal glomerulonephritis - - one that affects adults, sometimes with fatal consequences "“ that is a better fit. This variety of acute glomerulonephritis is caused by streptococci belonging to a different Lancefield group -- group C. The particular species of streptococcus responsible for such epidemics is Streptococcus equi. It primarily attacks horses, causing strangles, a highly contagious infection characterized by fever, lymphadenitis and abscesses of the head and neck (4). It also infects cows. In the rare instances in which human outbreaks occur, generally as a result of the consumption of milk or milk products contaminated with S. equi, fever, headache and muscle aches are initial manifestations of the illness, followed in a week or so, by bloody urine, kidney failure and anasarca. Rash is uncommon. In outbreaks of the disorder, over ninety percent of the victims have been adults. One in fifty has died. One in twenty patients has required renal dialysis and, presumably, would have died in Mozart's time because of the lack of such treatment (4). Thus, epidemic, acute post-streptococcal glomerulonephritis caused by S.equi "“ contaminated milk or cheese is, in many respects, the best explanation for Mozart's terminal illness (5). It would explain Mozart's edema, his fever, his pain and also the epidemic nature of his illness, so cleverly documented in the recent investigation by Zegers and colleagues.

References

1. Zegers RHC, Weigl A, Steptoe A. The death of Wolfgang Amadeus Mozart: An epidemiologic Perspective. Ann Intern Med 2009, 151: 274-8.

2. Robbins Landon HC. 1791: Mozart's Last Year. New York: Thames and Hudson, 1999; p. 175.

3. Hricik DE, Chung-Park M, Sedor JR. Glomerulonephritis. N Engl J Med 1998; 339: 888-99.

4. Balter S, Bennin A, Pinto SWL, et al. Epidemic nephritis in Nova Serrana, Brazil. Lancet 2000; 355: 1776-80.

5. Mackowiak PA. Post Mortem. Solving History's Great Medical Mysteries. Philadelphia: ACP Press, 2007:p. 173-202.

Conflict of Interest:

None declared

The Death of Wolfgang Amadeus Mozart: An Epidemiologic Perspective
Posted on September 2, 2009
Kenrad E. Nelson
Johns Hopkins School of Public Health
Conflict of Interest: None Declared

To the Editor: The article by Zegers and colleagues speculating on the cause of death of Wolfang Amadeus Mozart on 5 December, 1791 is of considerable historical interest (1). After reviewing the death records in the 2 months proximate to Mozart's death compared to those from the preceding and following years together with eyewitness accounts of his symptoms, the authors concluded he died of an acute nephritic syndrome due to post-streptococcal glomerulonephritis. It appears there was an epidemic of mortality among younger men during the period surrounding Mozart's death compared with the years before and after his death. This suggested that an infectious agent may have been transmitted in December 1791. Also, Mozart's most prominent symptom prior to his death was edema.

In light of the credible epidemiologic and clinical evidence that his death may have been caused by acute post-streptococcal glomerulonephritis (AGN), it is curious that the authors dismissed the skin lesions, which were described as a "white eruption." These skin lesions could have been impetigo caused by infection with a nephritogenic strain of Group A streptococcus. It would be of interest to know how many of the other excess deaths in the young men during November 1791-January, 1792 were listed as "Hitziges Frieselfieber" and also were accompanied by a white eruption? Post-streptococcal acute glomerulonephritis (AGN) can result from infections of either the skin or throat with nephritigenic Group A streptococci (2, 3). However, epidemics of AGN following skin infections with Group A streptococci are generally much more common in summer than in winter in countries with temperate climates (4-6). Nevertheless, the post -hoc diagnosis of glomerulonephritis from Group A streptococcal infection postulated by the authors certainly seems reasonable.

References:

1. Zegers RHC, Weigl A, Steptoe A. The death of Wolfang Amadeus Mozart: An epidemiologic perspective. Ann Intern Med 2009; 151:224-228.

2. Stollerman GH. Rheumatogenic and nephritogenic streptococci. Circulation 1971; 43:915-921

3. Dillon HC Jr. Post-streptococcal glomerulonephritis following pyoderma. Rev Infect Dis 1979; 1: 935-945.

4. Bisno AL, Pearce IA, Well HP et al. Contrasting epidemiology of acute rheumatic fever and acute glomerulonephritis. Nature of the antecedent streptococcal infection. N Engl J Med 1970; 283:561-565.

5. Nelson KE, Bisno AI, Waytz P, Brunt J, Moses VK, Haque R. Epidemiology and natural history of streptococcal pyoderma: an endemic disease of the rural southern United States. Am J Epidemiol 1976; 103:270 -283.

6. Meekin GE, Martin DR. Autumn- the season for post-streptococcal acute glomerulonephritis in New Zealand. NZ Med J 1984; 97:226-9.

Conflict of Interest:

None declared

Alternative Explaination
Posted on September 8, 2009
Petros Kopterides
Attiko University Hospital
Conflict of Interest: None Declared

Dear Editor, In their article, Zegers et al. (1) examine the circumstances of Mozart's death from an epidemiological perspective and come to the interesting conclusion that the great composer died of post-streptococcal glomerulonephritis (PSGN).

Even though PSGN can appear in epidemics, the sporadic form is more frequent. PSGN is usually a childhood disease with an incidence peak between the ages of 2 and 14 years. Outbreaks might affect family members in a significantly greater percentage compared with the general population. Subclinical disease is four to five times as common as clinically evident nephritis. Overall, the prognosis is good, with permanent renal failure being very uncommon (1-3%).

To our view, PSGN seems less likely in the case of the Mozart's death, taking into account the following facts: (i) an acute disease led him to be confined in bed for 2 weeks until the very end, whereas in PSGN there is an asymptomatic interval of 10 days between acute pharyngitis and the manifestations of nephritis (2), (ii) there was no testimony of hematuria or tea-colored urine, the worrisome tell-tale symptom of PSGN that would probably have been documented by Mozart's attending physician, and (iii) the illness had an unrelenting clinical course with a fatal outcome.

We agree that an acute illness with the cardinal features of fever and generalized edema clearly raises suspicion of acute glomerulonephritis. However, we think a more plausible alternative explanation needs to be considered: a Hantavirus-associated infection caused Mozart's illness.

The group of Hanta viruses is endemic in Europe and can lead to epidemic outbreaks. The human hemorrhagic fever with renal syndrome epidemiology follows the local rodent cycle (which is the host), meaning that human cases occur in the same rhythm as the rodent cycles. Austria, the home country of Mozart, experiences the co-circulation of two or three hantavirus serotypes, Puumala (PUUV), Dobrava (DOBV) and Saaremaa (SAAV) (3). The clinical presentation is characterized by the acute onset of fever accompanied by backache, abdominal pain, chills, myalgia, malaise, and bradycardia. Photophobia, pharynx enanthema, and a diffuse reddening of the face are also observed. The clinical manifestation can be differentiated into five chronological phases: the febrile phase lasting 3 -7 days, ending up with the appearance of severe proteinuria, the hypotonic phase with the appearance of hemorrhages and a possible petechial rash, associated with shock in most severe cases, the oliguric phase associated with acute renal failure and often combined with hypertension due to simultaneous hypervolemia, the diuretic phase, indicating a good case prognosis and the convalescence phase with complete recovery of renal function in most cases.

Renal involvement is characterized by acute renal failure as a result of interstitial hemorrhage and interstitial infiltrates (4). Severe cases show a case fatality rate which may exceed 10% (5).

Notwithstanding the gaps in the description of Mozart's illness, we conclude that a Hantavirus infection can explain most of the already discussed symptoms and signs of his illness, including the contemporary minor epidemic in deaths of young adults highlighted by Zegers et al.

References

1. Zegers RH, Weigl A, Steptoe A. The death of Wolfgang Amadeus Mozart: an epidemiologic perspective. Ann Intern Med. 2009;151(4):274-8. [PMID: 19687494]

2. Tejani A, Ingulli E. Poststreptococcal glomerulonephritis. Current clinical and pathologic concepts. Nephron. 1990;55(1):1-5. PMID: [2191230]

3. Heyman P, Vaheri A; ENIVD Members. Situation of hantavirus infections and haemorrhagic fever with renal syndrome in European countries as of December 2006.Euro Surveill. 2008;13(28). pii: 18925. [PMID: 18761927]

4. Muranyi W, Bahr U, Zeier M, van der Woude FJ. Hantavirus infection. J Am Soc Nephrol 2005;16:3669"“3679. [PMID: 16267154]

5. Faulde M, Sobe D, Kimmig P, Scharninghausen J. Renal failure and hantavirus infection in Europe. Nephrol Dial Transplant. 2000;15(6):751-3. [PMID: 10831620]

Conflict of Interest:

None declared

Did Mozart die of TTP?
Posted on September 13, 2009
P Dileep Kumar
Port Huron Hospital
Conflict of Interest: None Declared

Zegers and others present interesting information about the death of Mozart. Could Thrombotic thrombocytopenic purpura (TTP) be the cause of his death? Out of the five diagnostic features of TTP (pentad), Mozart had at least 3; fluctuating neurologic symptoms, fever and possible renal failure. The other two criteria for the diagnosis of TTP are thrombocytopenia and microangiopathic hemolytic anemia, discernable only by a laboratory examination. The etiology of TTP could be idiopathic or secondary to infections such as E. coli. The fact that there were several deaths associated with edema also supports this speculation. Infections such as E. coli might have been common in this pre-antibiotic era, leading to several clusters of cases. An unknown viral illness capable of triggering TTP is also a possibility as suggested by Zegers' data.

Conflict of Interest:

None declared

Questionable Conclusion
Posted on October 13, 2009
Lucien R. Karhausen
No Affiliation
Conflict of Interest: None Declared

To the Editor:

Zegers and colleagues (1) recently presented an "epidemiologic perspective" on the death of Wolfgang Amadeus Mozart. This paper calls for some comments. 1. The authors' basic assumption that "according to the eywitness accounts, the hallmark of Mozart's final disease was severe edema" is unwarranted and wide off the mark (2). What did the eywitnesses actually state? None of them mentions the prsence of sever edema (3). Sophie Haibel, Mozart's sister in law, who attended his last illness, merely reported that "his arms and limbs were much inflamed and swollen (4)." Moreover, neither "severe edema" nor even "edema" were mentioned by Guldener von Lobes, even though he saw Mozart's body after his death and wrote that "he made a careful inspection of the cadaver and saw nothing unusual (5)." To be sure, Sophie Haibel attricuted Mozart's "almost complete inability to move" to his swelling (6). But Benedikt Schack (1758 -1826), a tenor and close friend of Mozart, who attended his last illness said that his "weakness was such, that he was obliged to be drawn forward whenever he required to sit up in bed (4)." This suggests that weakness besides swelling of the extremities may have explained Mozart's inability to move.

Further more, according to the four death notifications (7), Mozart died of Hitziges Frieselfieber (heated miliary fever), a diagnosis made by Dr. Closset. Incidentally, there were two brothers, Thomas and Nikolaus Closset: both were physicians and the original sources never mention Dr. Closset's first name, so that we do not know which was which. Be that as it may, Thomas Closset in his 1783 treatise on Faulfieber (putrid fevers) (8) described a condition which helps us to figure out a picture of what Mozart's illness was like. Edema was not part of its manifestations. Actually Hitziges Frieselfieber implied a diagnosis of hitziges Fieber (heated fever) and an additional sign: the Friesel (rash). Death assigned to miliary fever (Friesel, hitziges and galliges Fieber) corresponded to 14% of all causes of death, and, between 21 and 40 years of age, it referred to every third death, i. e. "a common clinical condition comparable to influenza or pnuemonia (9,10)." Guldener von Lobes in two written documents went beyond this merely descriptive label, and proposed a diagnosis of Rheumatische Entzungsfieber (Inflammatory rheumatic fever). On this score, Mathias Edler von Sallaba (1764-1797), who visited Mozart during his last illness and wrote an Historia Morborum published in 1791, described what he called rheuma inflammatorium, a blanket diagnosis that conflated musculoarticular conditions with a mixed bag of disorders which attacked the brain, lung (pluerisy) and instestine (enteritis) (11). There was no necessary connotation implying arthritis. Lord byron, Emperor Leopold II and King Gustave XII of Sweden, supposedly died from rheumatic inflammatory fever. But again, neither was edema nor severe edema listed in the manifestatations of this condition.

2. In light of this, what is the epidemiological evidence? Mortality tables set up by Ignaz von Lucca (1746-1799) have been reprinted in fac simile for the International Mozarteum Foundation by Car Bar (4). According to the death statistics, there were 858 adult deathls in Viennna in November and 874 in December 1791, i.e. a death rate which was 17% higher than the death rate observed in the two previous months. There was a corresponding 14% increase during the same period of the previous year in 1790. If one makes a seasonal adjustment, there is not much of an epidemic. But what were then the death rates for specific diseases? These rates are available for Vienna in 1791. Car Bar writes that if one looks at the registers of death in the months of November and December 1791, Mozart was the only case of Hitziges Frieselfieber. In a span of six months, there was only one other recorded instance of this same cause of death besides that of Mozart: two cases in six months comparred with six from gangrene in one month alone cannot be described as an epidemic! According to von Lucca, during the months of Novemeber nad December 1791, the death certificates showed 636 cases of stroke (Schlag), 440 of putrid fever (Faulfieber), 149 of smallpox (Pocken) and 64 miscellaneious diseases (zufallig). Yet one has to assume that the death certificates were not entered in a very consistent way: thus, the deaths attributable to the alleged epidemic which killed Mozart must have been spread over different diagnostic categories instead of being assigned to a single disease entity. In view of the available clinical evidence, Carl Bar identified a list of death certificates among the months of Nov and Dec 1791, which would be compatible with the diagnosis attributed to Mozart, inasmuch as the put forward different clinical aspects of a similar condition. Again, not much for an epidemic of a sever emematous condition!

3. Then beyond this, Zegers and colleagues underplay the importance of venesections. The brothers Closset, both physicians, were pupils of professort Stoll, the medical head of Vienna's general hospital. It is now generally admitted following Car Bar, that Mozart may have bled two or three times during his last two weeks, thereby losing roughly two liters of blood. Moreover, the documents pertaining to Mozart's estate include a document listing Mozart's unpaid bills. This includes a bill amounting to 9 silver florins for bloodlettings made a home, though the fee could be larger when the practitiioner was called at night or on emergency. In addition the outstanding debt owed to the pharmacist amounted to 139 florins and 30 Kronen. This could have included various prescriptions made by Closset such as sudorifics, saline beverages and emetics in addition to time-honored procedures such as enemas.

4. What's more, Zegers and colleagues rule out the hypothesis that Mozart could have been poisoned. However, during the last months of his life and his final illness, Mozart was treated by Closset and Sallaba: potential iatrogenic poisoning (12)included mercury chloride, used for its diuretic properties, calomel (mercurous choloride) used as a purgative, arsenic, as well as anitmony salts used for the treatment of febrile conditions. Finally, during the summer and fall of 1791, when Constanze spent much time taking a cure in Baden, Mozart stayed in Vinenna and often put up at an inn: wine was then quite often adulterated with various forms of lead compounds such as lead oxide, ceruse, or metallic lead (13). Even though such iatrogenic or accidental poisonings cannot by themselves explain Mozart's death, they were probably contributing causes.

5. Besides sever edema, Zegers and Colleages mention several other undocumented signs and symptoms such as pain of unknown localisation and back pain. Nether was pain, nor backache mentioned by the eyewitnesses such as Sophie Haibel or Constance Mozart; neither were they brought up by Nissen, in his biography of Mozart. To be sure, Rochlitz claims that Mozart last illness was painful but he was not an eyewitness and his writings are considered to be a very unreliable source and are now excluded from use as authentic sources.

To sum it up then, Mozart died from an acute, feverish, unspecified, infectious condition, compounded by heavily aggressive medical treatment. It was not characterised by severe edema, but rather by a mere sweling of the extremities, severe weakness, vomiting, fever, hyperacousia, dysgeusia, stench and a skin rash evolving into a brief coma preceding death. One hundred eighteen causes of death have been attributed to Mozart up to this publication by Zegers and colleagues, and it does not seem that this paper is shoring up any additional line of diagnosis.

References

1. Zegers, RHC, Weigh, A., Steptoe, A. The death of Wolfgang Amadeus Mozart; an epiedmioligic perspective. Ann Intern Med 2009; 151: 274-278.

2. Karhausen, L. Mozart's terminal illness: unravelling the clinical evidence. J. Med Biography. 2001; 9:34-48.

3. Karl Thomas Mozart, Wolfgang's son, wrote in 1824 that his father's body showed "a generalised edema (una gonfiezza generale) a few days before his death" but cannot rely on this statement since he was only seven years of age when his father died!

4. Medici, N & Hughes, R. A Mozart Pilgrimage, London, 1951, p. 214-215.

5. Deutsch, OE. Mozart: die Dokumente seines Leben. Barenreiter Kassel. 1961, p. 450.

6. B. Schak in Holmes, E. The Llife of Mozart. 1845, London. Chapman and Hill, p. 347.

7. Carpani, G. Lettera del sig. Carpani in defesa del M. Salieri calumniato dell' avvelanamento del M. Mozzard. Bibliotheca italiana s sia giornale di letteratura, science ed arti. 1825; 35: 262-276.

8. This includes the death certificate, the notification in the register of deaths record office of Sankt Stephan Cathedral, the notification of Sankt Stephan Parish book of accounts, and the death certificate signed by Dr. Franz Bierner, physician in charge of infectious diseases.

9. Kisskalt, K. Die Sterblichkeit im 18. Jahrhundert. Zeitschrift fur Hygiene und Infektionskrankheiten. 1921; 93: 438-511.

10. Peller, S. Zum Kentnnis des stadlichen Mortalitat im 18. Jarhrhundert mit besonderer Berkucksichtigung des Sauglings -und Tuberkulosesterblichkeit (Wien zur Zeit des ersten Volkszahlung) Zeitschrift fut Hygiene und Infektionskrankheiten. 1920; 90: 227-262.

11. Fuhrmann, R. Frieselfiber und aderlass. Mitteilungen der Internationale Stifttung Mozarteum. 1989; 37: 83-136.

Conflict of Interest:

None declared

An Epidemic Nephritis in Vienna in 1791
Posted on October 13, 2009
C.J. Kooiker
Retired Senior Lecturer, State University of Utrecht, Netherlands
Conflict of Interest: None Declared

To the Editor:

Zegers, Wiegl, and Steptoe discovered a significant increase in the number of young soldiers dying in Vienna from edema and related illnesses during the months surrounding Mozart's dealth (1). This increase occurred in the midst of a Russian-Turkish war, in which the Austrians had joined the Russians. The Austrian armies occupied Moldavia and Walachia, where the Austrian emperor contracted a deadly illness amidst his troops. His successor ended the war with the Peac of Sistowa in August 1791, whereupon the Austrian army withdrew. The soldiers in Vienna presumably came from those battlefields. Their renal disease seems identical with the 'trench nephritis' or Feldnephritis' of "Flanders Fields.'

In World War II thousands of patients on the German Eastern front suffered from Feldnephritis, which could clearly be differentiated from postsreptococcal glomerulonephritis (2). There was no preceding infectin, a causative agent was never found, and after 1947 the illness was gone. From epidemic transmissions an incubation period of 3-4 weeks was calculated. Acute massive edema was the first and dominant symptom, in contrast with little or no urine abnormalities. A diet of hunger and thirst reduced the acute mortality to less than 1%. The outcome was better than that of poststreptococcal glomerulonephritis: 82% as against 30% cured with little or no rest symptoms (2). The kidneys showed a diffuse exsudative and proliferative glomerulonephritis (3,4), as in poststreptococcal glomerulonephritis, but this is an aspecific reaction on immune complexes.

Zegers, Weigl and Steptoe seem to have detected the first documented outbreak of Feldnephritis. It is sad to learn that Mozart may have died of this epidemic, whereas a simple diet could have saved his life.

References

1. Zegers RHC, Weigl A, Steptoe A. The death of Wolfgang Amadeus Mozart: An edpidemiologic perspective. Ann Intern Med. 2009; 151: 274-278, W 96-97.

2. Sarre H. Nierenkrankheiten. 2er Auflage. Stuttgart: Thieme; 1959: 291-323.

3. Allen A. The Kidney. New York: Grune and Stratton; 1951: 116-118.

4. Staemler M. Die Kriegs -oder Feldnephritis. In: Kaufmann E, Staemler M, eds. Lehrbuch der speziellen pathologischen Anatomie. II. Bd, 1. Tiel. Berlin: Walter de Gruyter & Co; 1957: 623-624.

Conflict of Interest:

None declared

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