Wolfgang Amadeus Mozart died in Vienna on December 5, 1791, 2 months before his 36th birthday.1(p415) His 29-year-old wife, Constanze, became so distraught that she crawled into bed with her dead husband, unsuccessfully attempting to contract his illness and die with him.2(p153) A physician, legally required to examine the body to exclude foul play, found nothing amiss but performed no autopsy.1(p523) Regulations specified that interment not occur until 48 hours after death, apparently to ensure that no one was buried alive.3(p169) During that time, a service took place at St Stephen’s Cathedral, where he and Constanze had wed 9 years earlier, and probably on the night of December 7, during inclement weather, a hearse transported the corpse to a cemetery in St Marx, a village about 5 km outside Vienna. Without ceremony or a priest in attendance, Mozart was interred, probably in a coffin in a simple grave.4(p745) 5(p421) It was common practice, however, to sew the unclothed bodies of the dead in linen sacks, place several together in a communal pit,5(pp414-416) 6 and cover them with quicklime to hasten decomposition. No permanent marker commemorated his burial site, and, about 7 years later, workers dug up the grave and reused it, dispersing the remains.
These details have
fostered the view that Mozart died destitute and unappreciated, with an
ignominious funeral, but, in fact, the obsequies conformed to the edicts of the
Habsburg monarch and Holy Roman Emperor, Joseph II, whose court was in
Use of a single grave for up to 5 adults or 4 adults
and 2 children was commonplace then, because the cemeteries, surrounded by
walls, had such limited space.8(p214) Mozart’s burial was not a pauper’s, which
the parish provided without charge. Instead, his widow purchased a third-class
funeral, the least expensive and certainly the most common in
Second-class and third-class funerals, on the other hand, differed only in the church ceremony, choice of bells and music, and number of pallbearers.3(p169)
Mozart did not die in obscurity. On December 7, 1791, a Vienna newspaper printed an editorial stating: Known from his childhood as the possessor of the finest musical talent in all Europe, through the fortunate development of his exceptional natural gifts and through persistent application he climbed the pinnacle of the greatest Masters; his works, loved and admired by all . . . are the measure of the irreplaceable loss that the noble art of music has suffered by his death.1(p418)
The tribute was not just a provincial view: an account of a memorial concert in Prague on December 14, 1791, asserted that almost the entire city streamed toward the square, so that the Wälscher Platz could hardly accommodate all the carriages nor could the large church, which can house nearly 4000 persons, contain all the admirers of the transfigured [Mozart].2(p184)
At the time of his death, Mozart was not living in penury. He had had serious financial difficulties from 1788 to 1790, but the last year of his life was exceptionally remunerative. He lived well, but not extravagantly, and despite some debts, his prospects for increasing wealth were excellent.2(pp27-30) 5(pp133-141)
Mozart’s sudden death quickly engendered rumors
suggesting unnatural causes. A
This account dovetails with another story, which appeared in 1798. Friedrich Rochlitz, an editor of a music journal, wrote several anecdotes about Mozart’s life, including a tale that began in the summer of 1791:
One day . . . a carriage drew up, and a stranger was announced. . . . [A] somewhat ageing, serious, imposing man, of a very respectable appearance, unknown either to Mozart or his wife entered [and] began: “I come to you as a messenger of a very distinguished man . . . [a] man [who] does not wish to be known. . . . A person has died who is and who ever will be very dear to him; he wishes to celebrate the anniversary of her death in a quiet but worthy manner, and for that purpose asks you to compose a Requiem for him.” . . . [Mozart received a payment and] began at once to work on the commission. His interest in it seemed to grow with every bar: he wrote night and day. His body could not stand the strain: on a few occasions he fell fainting over his work.9(pp3-4)
In his biography of Mozart in 1798, Franz Niemetschek,
a
In 1829, Vincent and Mary Novello, an English music publisher and his wife, interviewed Mozart’s widow, Constanze, whose second husband, a Danish diplomat named Georg Nissen, had written a biography of Mozart, posthumously published in 1828. She told them, “Some six months before his death he was possessed with the idea of his being poisoned ‘I know I must die,’ he exclaimed, ‘someone has given me acqua toffana and has calculated the precise time of my death for which they have ordered a Requiem, it is for myself I am writing this.’”10(p125) Acqua toffana, originally formulated by a Neopolitan woman, Tofana, was a colorless and tasteless liquid containing arsenic, sold ostensibly as a cosmetic to Italian women in the 17th century, with the claim that it was a miraculous substance oozing from the tomb of St. Nicholas di Bari, a saint of healing. In truth, many used it as a poison, especially young women who wished to hasten the arrival of widowhood.11. In her interview with the Novellos, however, Constanze dismissed Mozart’s fear of poisoning as “an absurd idea,” and her husband’s biography of Mozart had attempted to refute this rumor.
An undated memorandum by Mozart’s son, Carl Thomas, who was 7 years old when his father died, however, reinforces the suspicion of an unnatural death: Particularly remarkable is . . . the fact that a few days before [Mozart’s death], his whole body became so swollen that the patient was unable to make the smallest movement, moreover there was a stench, which reflected an internal disintegration and after death increased to the extent that an autopsy was rendered impossible. Another typical circumstance is that the corpse did not become stiff and cold but, as was the case with Pope Ganganelli [Clement XIV (1705-1774)]12 and those who die from poisoning by plants, remained soft and elastic.2(p159)
A likely perpetrator, however, remained unidentified until the autumn of 1823, when reports circulated that Antonio Salieri (1750-1825), a rival composer, had become non compos mentis and unsuccessfully attempted suicide by slashing his throat.13(p228) Allegedly, he had confessed to poisoning Mozart, a rumor recorded in the “conversation books” of Ludwig van Beethoven (1770-1827) in which his interlocutors wrote their remarks to communicate with the deaf composer.14 Beethoven’s nephew Karl stated, “Salieri maintains that he poisoned Mozart,”1(p524) and Anton Schindler, Beethoven’s secretary and factotum, commented, “Salieri is very ill again. He is quite deranged. In his ravings he keeps claiming that he is guilty of Mozart’s death and made away with him by poison.”1(p524) Because Beethoven replied orally to the queries and comments that his visitors inscribed in his conversation books, his reaction to these allegations is unknown.
In October 1823, however, Ignaz Moscheles, a pupil of Beethoven’s and Salieri’s, visited the latter in the hospital where he was confined: His appearance already shocked me and he spoke only in broken sentences about his imminent death. But at the end he said, “Although this is my last illness, I can assure you on my word of honor that there is no truth in that absurd rumor; you know that I was supposed to have poisoned Mozart. But no, it’s malice, pure malice, tell the world, dear Moscheles, old Salieri, who will soon die, has told you.”2(p173)
In August 1824, Guiseppe Carpani published a vigorous defense of his friend, Salieri, in an Italian journal. In it, he included a letter solicited from Dr Eduard Guldener von Lobes, who had examined Mozart’s body and found nothing awry, and he printed the testimony of 2 nurses who had cared for Salieri continuously from the winter of 1823.
They stated that no one but they and the physicians had seen the patient, and never had he confessed to poisoning Mozart.9(pp43-44)
Furthermore, a
compelling motive remained unclear. In
You can hardly imagine
how charming they were and how much they liked not only my music, but the
libretto and everything. They both said that it was an operone [a grand opera],
worthy to be performed for the grandest festival and before the greatest
monarch, and that they would often go to see it, as they had never seen a more
beautiful or delightful show. Salieri listened and watched most attentively and
from the overture to the last chorus there was not a single number that did not
call forth from him a bravo! or
Possibly, Salieri’s reactions were disingenuous, but Mozart obviously considered them sincere, even though he, like his father, was particularly suspicious of conspiracies and cabals against him, especially among the Italian composers.16 Moreover, according to one of his students, Salieri “did not harbor a grudge against Mozart, who eclipsed him. . . .”13(p226)
In 1830, the great Russian author Aleksandr Pushkin (1799-1837) wrote a short play, Mozart and Salieri, in which he accepted the poisoning theory and supplied novel motives envy and resentment: envy because of Mozart’s palpably greater gifts and resentment because his accomplishments seemed effortless and his conduct childish.17 To Salieri, it is unjust that the sacred gift of immortal genius seems arbitrarily bestowed rather than being a reward for toil, devotion, prayer, and self-sacrifice. Part of Salieri’s motive is to benefit his fellow composers, who will welcome Mozart’s death, for the achievements of his music have established exalted standards that others can never attain. According to Niemetschek’s biography, this view had a historical correlate:
A composer . . . said to a colleague at Mozart’s death, with much truth and uprightness: “Of course it’s too bad about such a great genius, but it’s good for us that he’s dead. Because if he’d lived longer, really the world would not have given a single piece of bread for our compositions.”2(p171)
The Russian composer Nicholai Rimsky-Korsakov (1844-1908) transformed Pushkin’s work into an opera in 1898, and Peter Shaffer continued the theme of Salieri’s envy and recognition of Mozart’s superior talent in Amadeus, first as a play in 197918 and later, considerably altered, as a film in 1984, directed by Milos Forman. In Shaffer’s work, Salieri, realizing that his own achievements and gifts are mediocre, resents that God has chosen Mozart (Amadeus: “beloved of God”) to be His voice. Salieri does not poison Mozart but, pretending to be an ally, sabotages his career. Disguised as the imposing messenger commissioning the Requiem, Salieri hastens Mozart’s death by provoking him to finish this piece, even when obviously ill.
Others accepted the poisoning theory but suggested different perpetrators. In one scenario, Mozart was his own murderer: while treating himself for syphilis with mercury, he inadvertently used an excessive dose.9(p53) Some proposed that the Freemasons, whose organization Mozart joined in 178419 and for whom he wrote several works, killed him because in The Magic Flute he either challenged their doctrines or revealed their secret rituals. Erich Ludendorff, a German general in World War I, argued that the Masons and the Jews collaborated in poisoning Mozart. His wife, Mathilde, a neuropsychiatrist, proposed a conspiracy among the Jews, Masons, and Catholics.9(pp34-43) In most of the poisoning theories, the mysterious patron who commissioned the Requiem has a crucial role. His identity, however, later became apparent: he was Count Franz von Walsegg-Stuppach, a music lover and amateur composer, who regularly sponsored concerts at his castle.1(pp551-555) His motives were dishonest but not sinister. On February 14, 1791, his 20-year-old wife had died, and he wished to have a Requiem played at each anniversary of her death.
He instructed his
attorney in
The identification of Mozart’s mysterious patron substantially undermines many of the conspiracy theories, but the plausibility of poisoning or any other explanation for Mozart’s death depends mostly on analyzing the details of his illness. Certain problems, however, undermine any attempt to establish the identity of an ailment that occurred in the distant past: (1) The terminology and the concepts of disease, which partly determine what clinicians observe and the language that they use in medical discourse, have changed so extensively that understanding them now is difficult. (2) Even when earlier clinicians rendered a diagnosis that remains in use today, they may have included under the rubric of a single disease several illnesses that resemble one another but are now considered distinct entities. Accordingly, it is hazardous to assume that the label applied to a disorder in the distant past is accurate by current standards. (3)
Because of alterations in the inciting agent or the host, the manifestations of a disease may have changed substantially. (4) Until relatively recently, clinicians lacked many of the diagnostic techniques now considered fundamental. René Laennec (1781-1826) devised the stethoscope and described lung and cardiac auscultation in 1819. Ludwig Traube (1818-1876) introduced the clinical use of the thermometer in the 1850s, and Carl Wunderlich (1815-1877) in 1868 determined the normal range of body temperature. Any mention of fever in Mozart’s illness, therefore, rested on a subjective assessment, rather than an actual measurement. A practical sphygmomanometer became available only in the late 19th century. Therefore, clinicians in the late 1700s did not have the techniques to record the vital signs of temperature and blood pressure or the equipment to listen to heart and lungs sounds with ease and clarity. (5) In assessing an illness, clinicians typically used Occam’s razor, named after William of Occam (1285-1349?), an English religious philosopher. Also called the “law of parsimony,” it encourages diagnosticians to attribute all the observed phenomena to a single disorder, rather than to several concurrent diseases. Distinctive ailments may coexist, however, and treatment for an illness may produce adverse effects; accordingly, some of the clinical findings may be iatrogenic rather than manifestations of the underlying malady. Attempting to identify a single disease to explain all the features of an illness, therefore, may be misguided; the limitations and hazards of this approach are encapsulated in the title of an editorial, “Is Occam’s Razor Disposable?”20
A further problem in analyzing Mozart’s death involves the nature of the testimony. The descriptions of his disorder primarily originate from family members who had no medical background and who provided reminiscences only several decades after the event, when faltering memories or a desire to portray the composer in a certain posthumous light may have corrupted their accounts. Moreover, the absence of any of Mozart’s remains that could be examined using modern scientific techniques renders any diagnosis of his fatal illness speculative and unverifiable. All these factors make all suggested diagnoses tentative; peremptory, or even confident, conclusions are unjustified.
Mozart became ill about November 20, 1791, and died 15 days later. During his illness, his physician, Thomas Franz Closset (1754-1813), a renowned practitioner, received assistance from a younger colleague, Mathias von Sallaba (1764-1797), who had published several scientific essays and an influential medical text in 1791.8(pp221-222) Thus, 2 of Vienna’s finest clinicians cared for Mozart, but unfortunately their only direct testimony is the cause of death that Closset recorded in the register of St Stephen’s Cathedral on December 5, 1791: “hitziges Frieselfieber” [severe military fever].1(p416) This diagnosis had no more precise meaning then than it has now. Apparently, it indicated fever and a rash, although the latter may have been a nonspecific complication of high temperature, poor hygiene, or profuse sweating, 8(p168) such as miliaria (prickly heat), folliculitis, or transient acantholytic dermatosis (Grover disease).21
Obituaries mention
“dropsy of the heart”1(p428) or that Mozart was “dropsical,” 1(p432) terms
denoting edema. In 1798, Rochlitz’s anecdotes, quoted in the “Rumors of
Poisoning” section, described fainting episodes while Mozart worked on the
Requiem, and Niemetschek’s biography, published the same year, asserted,
“During his illness Mozart maintained full consciousness right up to his end,
and he died at peace, though very unwillingly. . . . The doctors were not
agreed about the cause of his death.”1(p511) While
visiting
The most distinguished doctor of the town considered Mozart’s illness to be inflammatory and ordered bloodletting. The catarrh developed into a nervous fever, which was prevalent at that time.9(p61)
In 1824, during his attempt to exonerate Salieri from the charge of poisoning Mozart, Carpani solicited a letter from Guldener, written in Italian. Although Guldener had examined the cadaver, he had not seen Mozart during life. Nevertheless, his colleague, Closset, had apprised him of the patient’s condition almost daily, and in his letter Guldener summarized his recollections:
He fell sick in the
late autumn of a rheumatic and inflammatory fever [una febbre
reumatico-inflammatoria], which being fairly general among us at that time,
attacked many people. . . . Dr. Closset . . . from the very beginning
feared a fatal conclusion, namely a deposit on the brain. One day he met Dr.
Sallaba and he said positively, “Mozart is lost, it is no longer possible to
restrain the deposit.” . . . [I]n fact, Mozart died a few days later with the
usual symptoms of a deposit on the brain. . . . [T]he very slightest suspicion
of his having been poisoned entered no one’s mind. So many persons saw him
during his illness, so many enquired after him, his family tended him with so
much care, his doctor, highly regarded by all, the industrious and experienced
Closset, treated him with all the attention of a scrupulous physician, and with
the interest of a friend of many years’ standing, in such a way that certainly
it could not have escaped their notice then if even the slightest trace of
poisoning had manifested itself. The illness took its accustomed course and had
its usual duration; Closset had observed it and recognized it with such
accuracy that he had forecast its outcome almost to the hour. This malady
attacked at this time a great many of the inhabitants of
To modern clinicians, “deposit on the brain” suggests an intracranial mass. In the 18th century, however, a humoral theory of disease still prevailed, and physicians attributed many diseases to toxic substances that provoked inflammation when present in various tissues, such as the joints, where they produced arthritis, and in the thoracic cavity, where they elicited pain and pleural effusions. In this view, such deposits commonly occurred in the brain during serious febrile illnesses, often causing death.8(pp200-201)
In 1825, while preparing his biography of Mozart, Nissen received a letter from Constanze’s sister, Sophie Haibel, who had observed Mozart’s death. She recounted some of the events:
Now, when Mozart fell ill, we both made him a night-shirt which he could put on from the front, for he could not turn over because of the swelling . . . . [When she visited him on the day of his death,] he called to me at once, “Ah, dear Sophie, it is good of you to come. You must stay here tonight, you must see me die. . . . I have the taste of death on my tongue already.” . . . [The physician] came and prescribed cold compresses on his burning head, and these gave him such a shock that he did not regain consciousness before he passed away. The last thing he did was to try and mouth the sound of the timpani in his Requiem . . . .1(pp524-525)
In the biography, Nissen mentioned Sophie’s other recollections: My sister-in-law thinks Mozart was not sufficiently well looked after in his illness, for instead of driving out the fever by other methods, they bled him and applied cold compresses to his head, whereupon his forces visibly forsook him and he lost consciousness, which he never recovered. Even in his serious illness he never became impatient, and at the end his fine ear and feeling were still sensitive to the song of his pet, a canary, which even had to be removed from the next room, because it overtaxed his emotions.1(p527)
Nissen also summarized Mozart’s quietus: His final illness, during which he was bedridden, lasted 15 days. It began with swelling in his hands and feet, and an almost complete inability to move: this illness, which later was followed by sudden vomiting, is called a heated miliary fever. He remained fully conscious until two hours before his end.9(p59)
In his notes, Nissen stated that Constanze reported, “Suddenly, he began to vomitit spat out of him in an archit was brown and he was dead.”2(p168)
In 1829, Vincent and Mary Novello interviewed Sophie and Constanze. Constanze “said his death was at last sudden, but a few moments before he had spoken so gaily, and in a few moments after he was dead. . . .”10(p97) She stated that Mozart suspected foul play:
It was about six months before he died that he was impressed with the horrid idea that someone had poisoned him with acqua toffanahe came to her one day and complained that he felt great pain in his loins and a general languour spreading over him in degrees. . . .10(p128)
Sophie added that Mozart’s “arms and limbs were much inflamed and swollen.”10(p215) Sophie recalled phlebotomies,1(p527) and von Bursy’s diary also indicated that the physician ordered bloodletting.9(p61) Because Mozart was a small man, 163 cm (5 ft 4 in) tall,22 and venesections then were often voluminous, they may have accelerated, or even caused, his demise.
These accounts constitute the major information about Mozart’s death. Notwithstanding their limitations, they suggest that any diagnosis of his fatal illness must explain several features. The “hitziges Frieselfieber” listed as the cause of death presumably indicates fever and a rash. Several people mention edema, possibly generalized, but without dyspnea. He apparently had inflammation of his extremities that affected his hands and feet. All accounts indicate a mentation preserved until death. The testimony of Guldener, the only physician’s report available and therefore deserving special attention, indicates that he died of an epidemic illness that had a substantial mortality rate. His statement that Closset forecast its outcome almost to the hour, although hyperbolic, suggests that the disease had a predictable course. A less helpful feature mentioned was an inability to move, but whether the limitation arose from pain, weakness, or the heaviness and awkwardness of swollen limbs is unclear. Vomiting and fainting also occurred, but without further information, they are nonspecific findings.
Analysis of these features (Table 1) allows an assessment of proposed diagnoses. The conspiracy theories, devoid of historical merit, also lack medical credibility. The clinical features of acute arsenic poisoning that observers should have recorded include throat burning, dysphagia, abdominal pain, nausea, vomiting, and diarrhea.23 Other prominent findings are hypotension, cyanosis, dyspnea, delirium, coma, and seizures. With chronic arsenic poisoning,23 the major manifestations are a sensorimotor polyneuropathy, an erythroderma, and respiratory complaints related to tracheitis, bronchitis, and laryngitis.
Another poisoning theory is that Mozart accidentally died from miscalculating the dose while treating himself for syphilis with mercury9(p53)the clinical course summarized by an aphorism attributed to a US physician, J. Earle Moore (1892-1957),24 “two minutes with Venus, two years with mercury.” No credible evidence supports the diagnosis of syphilis, and accounts of his demise do not mention the typical, prominent features of mercury poisoning: memory loss, excessive salivation, and erethism (from the Greek, meaning “irritation”), which denotes emotional lability, irritability, forgetfulness, timidity, and delirium.25 Inspection of his handwriting shows no evidence of intention tremor,8(p190) probably the most common manifestation of chronic mercury poisoning.
Some have argued that Mozart died of uremia.9(pp68-72) They cite an earlier illness in 1784 that
Mozart’s father, Leopold, described in a letter: My son has been very ill in
Interpretations include kidney stones and urinary tract infection, with permanent damage producing chronic renal disease. In these theories, Sophie’s report of “a great pain in his loins and a general languour spreading over him in degrees”10(p128) indicates a recurrent attack, and a progressive, fatal decline over the next several months ensued, with the “taste of death” on his tongue being a symptom of uremia.26 Mozart’s letters in his last few months of life, however, depict physical and emotional vigor, and his musical output then was prodigious: 2 operas (La Clemenza di Tito and The Magic Flute), a clarinet concerto, 2 cantatas, and the incomplete Requiem. These facts vitiate any theory of a protracted, progressive illness. Moreover, although chronic renal failure could explain edema without dyspnea and has a substantial mortality rate, it is not an epidemic disorder associated with fever, rash, limb inflammation, and preserved mentation.
Another proposed diagnosis, citing much of the same evidence, is Henoch-Schönlein purpura, named after 2 German physicians who described some of this disease’s features in the 19th century.3(p203)
Most common in children and often preceded by an upper respiratory tract infection, it is an immune complex disease with IgA deposits occurring primarily in the alimentary tract, kidneys, joints, and skin.27 Its major gastrointestinal manifestations are abdominal pain, diarrhea, and bloody stools. It causes a glomerulonephritis that results in hematuria, proteinuria, and, sometimes, renal failure. The salient rheumatologic finding is self-limited arthralgias, and the cutaneous hallmark is palpable purpura, predominantly on the lower extremities and buttocks. Studies of large numbers of patients suggest that the clinical diagnosis rests on fulfilling most of these criteria: (1) palpable purpura, (2) bowel angina, (3) gastrointestinal bleeding, (4) hematuria, and (5) age of onset younger than 21 years.28, 29 Its appearance in a 35-year-old man like Mozart would be unusual, but possible.
Series30-32 of adult patients reported in the 1980s and 1990s indicate that fever occurs in about 10% to 20%, arthralgias in 70%, renal involvement in 60% to 70%, renal insufficiency in 10%, gastrointestinal symptoms in 60%, and relapses in 35%. Acute or chronic renal failure is uncommon, and death is rare. Although Henoch-Schönlein purpura could explain certain features of Mozart’s illness, epidemics do not occur, the mortality rate of its acute stage is insubstantial, and altered mentation would have been likely if uremia caused his death.
Another suggested diagnosis is acute rheumatic fever.26, 33 When first used, the term rheumatism (which originates from the Greek rheumatismos, meaning “a flowing down”) referred to the idea of a liquid humor dripping into a joint to cause inflammation.34 In its several verbal variations, including “acute rheumatic fever,” it remained a nonspecific diagnosis for problems in diverse locations, commonly the joints, but also elsewhere, as indicated in Leopold Mozart’s letter in 1784, cited earlier in “Previously Proposed Medical Explanations,” in which he described his son as suffering from “acute rheumatic fever” when the symptoms were vomiting and colic.15(p883) Similarly, Wolfgang wrote in 1790: “my head is covered with bandages due to rheumatic pains.”15(p937) The recognition that what is now called “acute rheumatic fever” had extra-articular manifestations came slowly. Although Thomas Sydenham (1624-1689) described chorea in 1686, only in the late 18th and early 19th centuries did clinicians recognize its association with acute rheumatism.35 Similarly, widespread appreciation that heart damage could accompany rheumatic disease finally emerged in the early 1800s, partly from the reports of William Charles Wells (1757-1823),35 who also described subcutaneous nodules in 1812 and mentioned erythema, although not definitively erythema marginatum, in 1810. In the Harvey Lectures published in 1889,36 Walter Cheadle (1836-1910) provided the first comprehensive view of the clinical manifestations of acute rheumatic fever, as they are currently understood. This historical information demonstrates that Guldener’s description of Mozart’s illness as “a rheumatic and inflammatory fever”1(p523) does not necessarily correspond to what is now called “acute rheumatic fever”an immunologic reaction to a pharyngeal infection with Streptococcus pyogenes (group A streptococcus) that can affect the heart, joints, skin, and central nervous system. Those supporting this diagnosis as Mozart’s fatal illness suggest that 2 earlier episodes occurred in childhood.37 In November 1766, his father, Leopold, wrote a letter describing how his son had been sick at age 7 in January 1763: [L]ittle Wolfgang fell ill and was very sick . . . finally the trouble settled in his feet, where he complained of pains and so forth. Now he has a similar attack. He could not stand on his feet or move his toes or knees. No one could come near him and for four nights he could not sleep. . . .[T]he whole time, and especially towards evening, he was very hot and feverish. Today he is noticeably better; but it will certainly be a week before he is quite restored to health.15(p69)
Acute rheumatic fever and other diseases, such as rheumatoid arthritis and viral infections, are plausible diagnoses.38 If these illnesses were indeed attacks of acute rheumatic fever, however, they left no apparent permanent sequelae, for Mozart was physically vigorous throughout his adult life.8(p122)
The clinical diagnosis of acute rheumatic fever currently rests on criteria first proposed by T. Duckett Jones in 1944,39 subsequently revised several times.40 The latest version requires the presence of 2 major or 1 major and 2 minor criteria, conjoined with evidence of a preceding group A streptococcal infection.41 The major criteria are carditis, polyarthritis, chorea, subcutaneous nodules, and erythema marginatum. The minor criteria include a history of previous rheumatic fever or rheumatic heart disease, arthralgia, fever, and abnormal results of tests unavailable in Mozart’s time: an increased erythrocyte sedimentation rate or C-reactive protein and a prolonged PR interval on electrocardiogram. The information about Mozart’s fatal illness cannot satisfy Jones’ criteria, but does permit an analysis of whether his disease corresponds to the clinical features of acute rheumatic fever. That disorder can cause fever and a rash, erythema marginatum, which is a serpiginous macular eruption, often evanescent and typically found on the trunk and proximal extremities. It almost never occurs in adults, however.42 Acute rheumatic fever produces inflammation of the extremities. The polyarthritis generally affects the large joints in a sequential manner, as a migratory phenomenon (inflammation resolves in one joint before appearing in another) or as an “additive” one (inflammation afflicts a new joint while remaining in a previously affected one). Involvement of the joints of the hands and feet, described in Mozart, however, is uncommon.43 Acute rheumatic fever can cause edema when heart failure occurs from valvular disease, primarily mitral regurgitation but also aortic regurgitation or mitral stenosis.44 Pericarditis can develop, rarely producing cardiac tamponade44 and peripheral edema. With either cardiac disorder, however, dyspnea occurs, and no account of Mozart’s illness mentions it.
In fatal acute
rheumatic fever, mentation preserved until death is certainly expected. Acute
rheumatic fever is an epidemic disease, but without an organized reporting
system in Mozart’s time, clinicians may not have recognized outbreaks unless
they affected large numbers. Such circumstances certainly exist: in the
congested barracks during
The acute disease, however, does not have a substantial mortality rate.34 Death generally occurs from chronic valvular damage that becomes clinically apparent years to decades after the original episodes.45, 46 In acute attacks, the earliest mortality rates recorded, from the middle to late 19th century, were only 1% to 5%, even among those ill enough to require hospitalization.47 Acute rheumatic fever, therefore, fails to explain several features of Mozart’s illness. Moreover, it has always been primarily a childhood disorder, with adults uncommonly affected.48 Even in those who had attacks as children, recurrent episodes during adulthood are unusual, especially in somebody 35 years old,48, 49 and acute rheumatic fever uncommonly involves the heart in adults: arthritis is typically the preeminent manifestation.42, 50-54 Furthermore, the rheumatologic and cardiac components are usually inversely related: the disease “licks the joints and bites the heart” or “bites the joints and licks the heart.”55(p287) If acute rheumatic fever caused Mozart’s inflamed extremities, cardiac involvement would likely have been minimal or absent. In addition, attacks of acute rheumatic fever tend to be mimetic, each episode affecting the same sites as previous ones.56 Mozart’s 2 suspicious childhood illnesses consisted primarily of joint complaints, but no cardiac symptoms, such as pain from pericarditis or dyspnea from significant valvular damage, suggesting that a subsequent episode during adulthood should also have included no heart complications. Certainly, he might have had subclinical valve damage detectable only with auscultation, a technique unavailable then. Those who died of acute rheumatic fever, however, usually already had severe heart disease,45, 46 something that Mozart’s previous physical vigor discounts.
Another hypothesis is that his fatal illness was infective endocarditis,57-59 which might explain the fever and the skin lesions, which include petechiae, Osler nodes, and Janeway lesions. It would account for the inflamed extremities (arthritic and musculoskeletal complaints are common60); mentation is typically preserved until death; and it was a lethal disease. When edema occurs, however, its origin is almost always heart failure caused by valvular damage, and dyspnea is present. Conceivably, glomerulonephritis associated with bacterial endocarditis could have caused edema without dyspnea, but it uncommonly causes the nephrotic syndrome.61 Finally, infective endocarditis is not an epidemic disease.
Can a single disorder
explain Mozart’s illness? One affliction, unrecognized then, deserves
consideration. A 21-year-old, first-year medical student attending an autopsy
of a patient who died of tuberculosis at St Bartholomew’s Hospital in
The report soon ran
through the dissecting-rooms that there was another body with spiculae of bone
in the muscles. Examining some of these “spiculae” with a lens, I soon found
that they were cysts, and almost directly afterwards ascertained that nearly
every cyst contained a small worm coiled up. I was anxious to observe them with
a microscope, and, possessing none, I applied to the only man of science whom I
at that time knew in
Paget took the specimens to his teacher, Robert Owen, who promptly published a paper formally describing the new species, which he named Trichina spiralis, but giving Paget minimal credit.63 Paget had not been the first to notice these granules in cadavers. Self-trained as a botanist and already coauthor with his brother of a book about the flora and fauna near his English hometown of Great Yarmouth, however, he was the first to scrutinize them:
All the men in the dissecting-rooms, teachers included, “saw” the little specks in the muscles: but I believed that I alone ‘looked-at’ them and ‘observed’ them: no one trained in the natural history could have failed to do so.”64(pp49-50) His discovery’s clinical import remained unclear until January 1860, when a 20-year-old servant, ill since Christmas with fever, weakness, anorexia, and constipation, entered a hospital in Dresden.65-67 Her physician diagnosed typhoid fever, but she subsequently developed excruciating, diffuse muscle pain, a feature atypical for that disease. At her death 2 weeks later, the hospital pathologist, Friedrich von Zenker (1825-1898) examined a fresh specimen of her muscle and, surprisingly, detected numerous wriggling worms. He discovered that others at the inn where she worked had incurred a similar disease in January, including the butcher who had prepared the meat for the Christmas festivities. When Zenker examined ham and sausage from a pig slaughtered 4 days before the servant’s illness began, he found abundant worms and concluded that the patient had acquired her fatal disease by eating infected pork. In experiments, he fed animals infested muscles, later finding sexually mature, viviparous worms in the alimentary canal. He surmised that the newborn parasites entered the lymphatics from the intestines and then passed into the bloodstream, from which they invaded muscles.
Zenker was correct. Infection with T spiralis occurs when a mammal eats muscle contaminated with encysted larvae, which can remain viable for years.68, 69 The domestic pig is most commonly affected, but the parasite also infects bears, foxes, walruses, rats, and even herbivores, such as horses, presumably because meat from small carnivorous animals contaminates their fodder. In the late 20th century, for example, consumption of raw or lightly cooked horse meat caused large epidemics of human trichinosis in France.70 Once the infected meat reaches the stomach, the host’s gastric juices digest the cysts, liberating the larvae, which travel to the small intestine, invade the columnar epithelium, and molt 4 times before reaching maturity. The adults mate, and about 5 days later the females give birth to live larvae, which enter the lymphatic vessels and the mesenteric veins, migrating through the general circulation to invade tissues. Although larvae transiently infect many organs, including the liver and lungs, they survive only in skeletal muscle, where they induce the host cell to form a capsule around them, completing the life cycle. About 15% to 55% of infected humans experience symptoms when larvae invade the intestinal mucosa: hours to weeks after eating infected meat (but usually about 2 to 7 days later) nausea, vomiting, headache, abdominal pain and bloating, diarrhea, and low-grade fever may develop and typically resolve within a few days.68, 69, 71 About 5 to 50 days after ingesting infested meat, when circulating larvae invade tissues, patients experience symptoms of generalized infection that usually last 1 to 8 weeks. Fever, which can exceed 40°C, is common. Muscle pain, often severe, present at rest and worse with movement, sometimes becomes so pronounced that patients, refusing to move, appear paralyzed. Facial or periorbital edema occurs in about 50% of cases. Swelling in the hands, arms, and legs is frequent and results from muscle inflammation or damaged vessels leaking fluid into surrounding tissues. Rashes, present in 5% to 90% of cases, are usually diffuse and maculopapular but sometimes urticarial or pustular.72 Patients typically maintain normal mental function, but during the second to third week of illness, neurologic problems develop in 10% to 25%,73-75 primarily from occlusion or inflammation of the cerebral vessels, provoked directly by the presence of parasites in the vascular lumen or through indirect mechanisms, such as circulating toxins and eosinophils. The clinical consequences include strokes, seizures, encephalitis, meningitis, and coma. Cardiovascular manifestations may develop about this time, when larvae invade the myocardium, causing inflammation, arrhythmias, and heart failure. Deaths typically occur in the second or third week of illness, from pneumonia or from neurologic or cardiac complications.76
Fatal trichinosis is now rare, but shortly after the first clinical description in 1860, reports of German epidemics appeared, detailing varying, but sometimes substantial, mortality rates.65 In 1863, for example, 153 cases, 18% of which were lethal, occurred in Hettstädt following pork consumption at festivities celebrating the 50th anniversary of the Battle of Leipzig. In 1865, 337 people became ill in Hedersleden, with a 30% fatality rate, and a retrospective analysis of an outbreak in Wegeleben in 1849 revealed 160 cases, 19% of which were lethal. Trichinosis, then, could explain all the features of Mozart’s disease. It is an epidemic disorder characterized in the past by a substantial mortality rate and a predictable course, with deaths occurring in the second and third weeks. It causes fever, rashes, and edema without dyspnea. Limb pain and swelling from muscle inflammation and vascular damage are common, prominent findings. The plausibility of this diagnosis, however, depends on Mozart’s diet: it requires evidence that he ate meat, especially pork. In a letter to Constanze written on October 7, 1791, 44 days before his illness, Mozart asked, “What do I smell? . . . pork cutlets! Che gusto [What a delicious taste]. I eat to your health.”4(p738) If his final illness was indeed trichinosis, whose incubation period is up to 50 days, Mozart may have unwittingly disclosed the precise cause of his death: those very pork chops.