Sweating sickness | |
---|---|
Other names | English sweating sickness, English sweat, (Latin) sudor anglicus |
Illustration by the Virgil Master depicting the sweating sickness | |
Specialty | Infectious diseases |
Symptoms | chills, body pains, weakness [1] |
Causes | Unknown |
Sweating sickness, also known as the sweats, English sweating sickness, English sweat or sudor anglicus in Latin, was a mysterious and contagious disease that struck England and later continental Europe in a series of epidemics beginning in 1485. Other major outbreaks of the English sweating sickness occurred in 1508, 1517, and 1528, with the last outbreak in 1551, after which the disease apparently vanished. [1] The onset of symptoms was sudden and death often occurred within hours. Sweating sickness epidemics were unique compared with other disease outbreaks of the time: whereas other epidemics were typically urban and long-lasting, cases of sweating sickness spiked and receded very quickly, and heavily affected rural populations. [2] Its cause remains unknown, although it has been suggested that an unknown species of hantavirus was responsible.
John Caius was a physician in Shrewsbury in 1551, when an outbreak occurred, and he described the symptoms and signs of the disease in A Boke or Counseill Against the Disease Commonly Called the Sweate, or Sweatyng Sicknesse (1552), which is the main historical source of knowledge of the disease. It began very suddenly with a sense of apprehension, followed by cold shivers (sometimes very violent), dizziness, headache, and severe pains in the neck, shoulders, and limbs, with great exhaustion. The cold stage lasted from half an hour to three hours, after which the hot and sweating stage began. The characteristic sweat broke out suddenly without any obvious cause. A sense of heat, headache, delirium, rapid pulse, and intense thirst accompanied the sweat. Palpitations and pain in the heart were frequent symptoms. No skin eruptions were noted by observers. In the final stages there was either general exhaustion and collapse, or an irresistible urge to sleep, which Caius thought was fatal if the patient were permitted to give way to it. One attack of the disease did not result in immunity to subsequent occurrences, and some people suffered several bouts before dying. [1] The disease typically lasted through one full day before recovery or death took place. [3] The disease tended to occur in summer and early autumn.
Thomas Forestier, a physician during the first outbreak, provided a written account of his own experiences with the sweating sickness in 1485. [4] Forestier put great emphasis on the sudden breathlessness commonly associated with the final hours of sufferers. [4] Forestier claimed in an account written for other physicians that "loathsome vapors" had congregated around the heart and lungs. [4] His observations point towards a pulmonary component of the disease. [4]
Transmission mostly remains a mystery, with only a few pieces of evidence in writing. [3] Despite greatly affecting the rural and working classes of the time, the sweating sickness did not discriminate, as it was no less likely to affect young, seemingly fit men, including those of the elite or privileged classes. Based upon recorded accounts, the mortality rate among victims was highest in males aged 30–40 years. [4] The fact that it infected all levels of society, from rich to poor, earned the sweating sickness various nicknames, such as "Stoop Gallant" or "Stoop Knave"—referencing how the 'proud' castes were forced to 'stoop' and face their own humanity, thus relinquishing their higher status. [5] [3]
The large number of people present in London to witness the coronation of Henry VII may have accelerated the spread of the disease, and indeed many other airborne pathogens. [3]
The cause is unknown. Commentators then and now have blamed the sewage, poor sanitation, and contaminated water supplies. The first confirmed outbreak was in August 1485 at the end of the Wars of the Roses, leading to speculation that it may have been brought from France by French mercenaries. [6] However, an earlier outbreak may have affected the city of York in June 1485, before Henry Tudor's army landed, although records of that disease's symptoms are not adequate enough to be certain. [7] Regardless, the Croyland Chronicle mentions that Thomas Stanley, 1st Earl of Derby cited the sweating sickness as reason not to join Richard III's army prior to the Battle of Bosworth. [1]
Relapsing fever, a disease spread by ticks and lice, has been proposed as a possible cause. It occurs most often during the summer months, as did the original sweating sickness. However, relapsing fever is marked by a prominent black scab at the site of the tick bite and a subsequent skin rash, neither of which are described as the symptoms of sweating sickness.
The suggestion of ergotism was ruled out due to England growing much less rye (which ergots typically grow on) than the rest of Europe. [3]
Researchers have noted symptoms overlap with hantavirus pulmonary syndrome and have proposed an unknown hantavirus as the cause. [1] [4] [8] Hantavirus species are zoonotic diseases carried by bats, rodents, and several insectivores. [9] Sharing of similar trends (including seasonal occurrences, fluctuations multiple times a year, and occasional occurrences between major outbreaks) suggest the English sweating sickness may have been rodent-borne. [9] The epidemiology of hantavirus correlates with the trends of the English sweating sickness. Hantavirus infections generally do not strike infants, children, or the elderly, and mostly affect middle-aged adults. In contrast to most epidemics of the medieval ages, the English sweating sickness also predominantly affected the middle-aged. A criticism of this hypothesis is that modern-day hantaviruses, unlike the sweating sickness, do not randomly disappear and can be seen affecting isolated people. [3] Another is that sweating sickness was thought to have been transmitted from human to human, whereas hantaviruses are rarely spread that way. [10] However, infection via human contact has been suggested in hantavirus outbreaks in Argentina. [11]
In 2004, microbiologist Edward McSweegan suggested the disease may have been an outbreak of anthrax poisoning. He hypothesized that the victims could have been infected with anthrax spores present in raw wool or infected animal carcasses, and suggested exhuming victims for testing. [12]
Numerous attempts have been made to define the disease origin by molecular biology methods, but have so far failed due to a lack of available DNA or RNA. [13]
Sweating sickness first came to the attention of physicians at the beginning of the reign of Henry VII, in 1485. It was frequently fatal; half the population perished in some areas. The Ricardian scholar John Ashdown-Hill conjectures that Richard III fell victim the night before the Battle of Bosworth Field and that this accounted for his sleepless night and excessive thirst in the early part of the battle. [14] There is no definitive statement that the sickness was present in Henry Tudor's troops landing at Milford Haven. The battle's victor, Henry VII, arrived in London on 28 August, and the disease broke out there on 19 September 1485; [15] it had killed several thousand people by its conclusion in late October that year. [16] Among those killed were two lord mayors, six aldermen, and three sheriffs. [17]
Mass superstition and paranoia followed the new plague. The Battle of Bosworth Field ended the Wars of the Roses, between the houses of Lancaster and York. Richard III, the final York king, was killed there and Henry VII was crowned. As chaos, grief, and anger spread, people searched for a culprit for the plague. English people started to believe it was sent by God to punish supporters of Henry VII. [18]
The sickness was regarded as being quite distinct from the Black Death, the pestilential fever or other epidemics previously known because of its extremely rapid and fatal course, and the sweating which gave it its name. It reached Ireland in 1492 when the Annals of Ulster record the death of James Fleming, 7th Baron Slane from the pláigh allais ["perspiring plague"], newly come to Ireland. [19] The Annals of Connacht also record this obituary, [20] and the Annals of the Four Masters record "an unusual plague in Meath" of 24 hours' duration; [21] people recovered if they survived it beyond that 24-hour period. The sickness didn't affect infants or young children. English chronicler Richard Grafton mentioned the sweating sickness of 1485 in his work Grafton's Chronicle: or History of England. He noted the common treatment of the disease was to go immediately to bed at the first sign of symptoms; there, the affected person was to remain still for the entire 24-hour period of the illness, abstaining from any solid food and limiting water intake. [22]
The ailment was not recorded from 1492 to 1502. It may have been the condition which afflicted Henry VII's son Arthur, Prince of Wales, and Arthur's wife, Catherine of Aragon, in March 1502; their illness was described as "a malign vapour which proceeded from the air". [23] [24] Researchers who opened Arthur's tomb in 2002 could not determine the exact cause of death. Catherine recovered, but Arthur died on 2 April 1502 in his home at Ludlow Castle, six months short of his sixteenth birthday. [25]
A second, less widespread outbreak occurred in 1507, followed by a third and much more severe epidemic in 1517, a few cases of which may have also spread to Calais. [15] In the 1517 epidemic, the disease showed a particular affinity for the English; the ambassador from Venice at the time commented on the peculiarly low number of cases in foreign visitors. A similar effect was noted in 1528 when Calais (then an English territory) experienced an outbreak that did not spread into France. [5] The 1528 outbreak, the fourth, reached epidemic proportions. The earliest written reference to it was on 5 June 1528, in a letter to Bishop Tunstall of London from Brian Tuke, who said that he had fled to Stepney to avoid infection from a servant at his house who was ill with "the sweat.", [26] suggesting that it broke out in London at the end of May. The sweats spread over the whole of England, save the far north. It did not spread to Scotland, though it did reach Ireland where Lord Chancellor Hugh Inge, who died on 3 August 1528, was the most prominent victim. [27] Mortality was very high in London; Henry VIII broke up the court and left London, frequently changing his residence. In 1529 Thomas Cromwell lost his wife and two daughters to the disease. It is believed several of the closest people to Henry VIII contracted the sickness. His love letters to his mistress, Anne Boleyn, reveal that physicians believed Anne had contracted the illness. Henry sent his second-most trusted physician to her aid, his first being unavailable, and she survived. [28] Cardinal Wolsey contracted the illness and survived. [29]
The disease was brought to Hamburg by a ship from England in July 1529. [30] It spread along the Baltic coast, north to Denmark, Sweden, and Norway as well as south to Strasbourg, Frankfurt, Cologne, Marburg, and Göttingen in September of that year. [31] Cases were unknown in Italy or France, except in the English-controlled Pale of Calais. It emerged in Flanders and the Netherlands, [15] possibly transmitted directly from England by travellers; it appeared simultaneously in the cities of Antwerp and Amsterdam on the morning of 27 September. In each place, it prevailed for a short time, generally not more than two weeks. By the end of 1529, it had entirely disappeared except in the eastern part of the Swiss Confederacy, where it lingered into the next year. The disease did not recur in mainland Europe.
The last major outbreak of the disease occurred in England in 1551. [32] Although burial patterns in smaller towns in Europe suggest that the disease may have been present elsewhere first, [4] the outbreak is recorded to have begun in Shrewsbury in April. [5] It killed around 1,000 there, spreading quickly throughout the rest of England [2] and all but disappearing by October. [2] It was more prevalent among younger men than other groups, possibly due to their greater social exposure. [2] John Caius wrote his eyewitness account A Boke or Counseill Against the Disease Commonly Called the Sweate, or Sweatyng Sicknesse. Henry Machin also recorded it in his diary:
the vii day of July begane a nuw swet in London…the x day of July [1551] the Kynges grace removyd from Westmynster unto Hamtun courte, for ther [died] serten besyd the court, and caused the Kynges grase to be gone so sune, for ther ded in London mony marchants and grett ryche men and women, and yonge men and old, of the new swett…the xvi day of July ded of the swet the ii yonge dukes of Suffoke of the swet, both in one bed in Chambrydge-shyre…and ther ded from the vii day of July unto the xix ded of the swett in London of all dyssesus… [872] and no more in alle
The Annals of Halifax Parish of 1551 records 44 deaths in an outbreak there. [34] An outbreak called 'sweating sickness' occurred in Tiverton, Devon in 1644, recorded in Martin Dunsford's History, killing 443 people, 105 of them buried in October. [35] However, no medical particulars were recorded, and the date falls well after the generally accepted disappearance of the 'sweating sickness' in 1551. [36]
Between 1718 and 1918 an illness with some similarities occurred in France, known as the Picardy sweat. [37] It was significantly less lethal than the English Sweat but with a strikingly high frequency of outbreaks; some 200 were recorded during the period. [3] Llywelyn Roberts noted "a great similarity between the two diseases." [15] There was intense sweating and fever, and Henry Tidy found "no substantial reason to doubt the identity of sudor anglicus and Picardy sweat." [1] [38] There were also notable differences between the Picardy sweat and the English sweating sickness. It was accompanied by a rash, which was not described as a feature of the English disease. Henry Tidy argued that John Caius's report applies to fulminant cases fatal within a few hours, in which case no eruption may develop. The Picardy sweat appears to have had a different epidemiology than the English sweat in that individuals who slept close to the ground and/or lived on farms appeared more susceptible, supporting the theory that the disease could be rodent-borne, common in hantaviruses. [3] In a 1906 outbreak of Picardy sweat which struck 6,000 people, a commission led by bacteriologist André Chantemesse attributed infection to the fleas of field mice.
A 'plage of pestilence' was known in York as early as June 1485, but no symptoms were described, and we cannot tell what gave [Sir Thomas] Stanley the idea to cite the sweating sickness.
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: CS1 maint: multiple names: authors list (link)1551 44 persons died of the 'sweating Sickness' in the Halifax Parish.
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: CS1 maint: location missing publisher (link)Orthohantavirus is a genus of viruses that includes all hantaviruses that cause disease in humans. Orthohantaviruses, hereafter referred to as hantaviruses, are naturally found primarily in rodents. In general, each hantavirus is carried by one rodent species and each rodent that carries a hantavirus carries one hantavirus species. Hantaviruses in their natural reservoirs usually cause an asymptomatic, persistent infection. In humans, however, hantaviruses cause two diseases: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). HFRS is mainly caused by hantaviruses in Africa, Asia, and Europe, called Old World hantaviruses, and HPS is usually caused by hantaviruses in the Americas, called New World hantaviruses.
Sin Nombre virus (SNV) is the most common cause of hantavirus pulmonary syndrome (HPS) in North America. Sin Nombre virus is transmitted mainly by the eastern deer mouse. In its natural reservoir, SNV causes an asymptomatic, persistent infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection leads to HPS, an illness characterized by an early phase of mild and moderate symptoms such as fever, headache, and fatigue, followed by sudden respiratory failure. The case fatality rate from infection is high, at 30–50%.
Seoul virus (SEOV) is one of the main causes of hemorrhagic fever with renal syndrome (HFRS). Seoul virus is transmitted by the brown rat and the black rat. In its natural reservoirs, SEOV causes an asymptomatic, persistent infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection leads to HFRS, an illness characterized by general symptoms such as fever and headache, as well as the appearance of spots on the skin and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. The case fatality rate from infection is 1–2%.
Andes virus (ANDV) is the most common cause of hantavirus pulmonary syndrome (HPS) in South America. Andes virus is transmitted mainly by the long-tailed pygmy rice rat. In its natural reservoir, ANDV causes an asymptomatic, persistent infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection leads to HPS, an illness characterized by an early phase of mild and moderate symptoms such as fever, headache, and fatigue, followed by sudden respiratory failure. The case fatality rate from infection is high, at about 40%.
Puumala virus (PUUV) is the main cause of hemorrhagic fever with renal syndrome (HFRS) in Europe and Russia. Puumala virus is transmitted by the bank vole. In its natural reservoir, PUUV causes a persistent infection with few symptoms and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection is usually asymptomatic but can lead to a mild form of HFRS often called nephropathia epidemica (NE). Symptoms include fever and headache, impaired vision, as well as the appearance of spots on the skin and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. The case fatality rate from infection is less than 1%.
The Picardy sweat was an infectious disease of unknown cause and one of the only diseases that bears resemblance to the English sweating sickness. The Picardy sweat is also known as the miliary fever, suette des Picards in French, and picard'scher Schweiß,picard'sches Schweissfieber, or Frieselfieber in German. It appeared in the northern French province of Picardy in 1718. The Picardy sweat was mainly confined to the northwest part of France, particularly in the provinces of Seine-et-Oise, Bas Rhin, and Oise. Although the Picardy sweat began in Northern France, outbreaks also occurred in Germany, Belgium, Switzerland, Austria, and Italy. Between 1718 and 1874, 194 epidemics of the Picardy sweat were recorded. The last extensive outbreak was in 1906, which a French commission attributed to fleas from field mice. A subsequent case was diagnosed in 1918 in a soldier in Picardy.
Bayou virus (BAYV) is a species of Orthohantavirus comprising enveloped and spherical viruses. It was first identified in 1993 in Louisiana and later confirmed by other investigators. BAYV was recognized as a distinct form of hantavirus disease, now known as hantavirus pulmonary syndrome (HPS). It now represents the second most common hantavirus in the United States behind the Sin Nombre virus. In 1996, the marsh rice rat, which is seen in marshes in the southeast and mountain streams in the northeast, was identified as the natural reservoir of the virus. Due to the virus being first identified in Louisiana, this indicated the virus to be widespread throughout the Southeastern United States. This hantavirus disease is known as a severe and sometimes fatal respiratory disease, and HPS has a case-rate fatality of almost 50%.
The 1993 Four Corners hantavirus outbreak was an outbreak of hantavirus disease that occurred in the Four Corners region of the US states in Arizona, Colorado, and New Mexico. The outbreak marked the discovery of hantaviruses in the Western Hemisphere that could cause disease and revealed the existence of a novel type of disease caused by hantaviruses: hantavirus pulmonary syndrome (HPS). Hantaviruses that cause disease in humans are native to rodents and, prior to the outbreak, were known to exist in Asia and Europe, but previously were only associated with a different disease called hemorrhagic fever with renal syndrome (HFRS).
Hantavirus hemorrhagic fever with renal syndrome (HFRS) is a hemorrhagic fever caused by hantaviruses. Symptoms occur usually occur 12–16 days after exposure to the virus and come in five distinct phases: febrile, hypotensive, low urine production (oliguric), high urine production (diuretic), and recovery. Early symptoms include headache, lower back pain, nausea, vomiting, diarrhea, bloody stool, the appearance of spots on the skin, bleeding in the respiratory tract, and renal symptoms such as kidney swelling, excess protein in urine, and blood in urine. During the hypotensive phase, blood pressure lowers due to microvascular leakage. Renal failure then causes the diuretic phase, before recovering and increasing urine production as disease progression improves. The severity of symptoms varies depending on which virus causes HFRS and ranges from a mild illness to severe. The case fatality rate likewise varies by virus, at less than 1% up to 15%.
Hantavirus pulmonary syndrome (HPS), also called hantavirus cardiopulmonary syndrome (HCPS), is a severe respiratory disease caused by hantaviruses. The main features of illness are microvascular leakage and acute respiratory distress syndrome. Symptoms occur anywhere from 1 to 8 weeks after exposure to the virus and come in three distinct phases. First, there is prodromal phase with flu-like symptoms such as fever, headache, muscle, shortness of breath, as well as low platelet count. Second, there is cardiopulmonary phase during which people experience elevated or irregular heart rate, cardiogenic shock, and pulmonary capillary leakage, which can lead to respiratory failure, low blood pressure, and buildup of fluid in the lungs and chest cavity. The final phase is recovery, which typically takes months, but difficulties with breathing can persist for up to two years. The disease has a case fatality rate of 30–60%.
Dobrava-Belgrade virus (DOBV) is the main cause of hemorrhagic fever with renal syndrome (HFRS) in southern Europe. In its natural reservoirs, DOBV causes a persistent, asymptomatic infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection causes such as fever and headache, as well as the appearance of spots on the skin and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. Acute respiratory distress syndrome occurs in about 10% of cases.
Soochong virus (SOOV) is a zoonotic negative sense single-stranded RNA virus. It may be a member of the genus Orthohantavirus, but it has not be definitively classified as a species and may only be a strain. It is one of four rodent-borne Hantaviruses found in the Republic of Korea. It is the etiologic agent for Hantavirus hemorrhagic fever with renal syndrome (HFRS). The other species responsible for HFRS in Korea are Seoul virus, Haantan virus, and Muju virus.
Hantaan virus (HTNV) is the main cause of hemorrhagic fever with renal syndrome (HFRS) in East Asia. Hantaan virus is transmitted by the striped field mouse In its natural reservoir, HTNV causes a persistent, asymptomatic infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection causes such as fever and headache, as well as the appearance of spots on the skin, hepatitis, and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. Rarely, HTNV infection affects the pituitary gland and can cause empty sella syndrome. The case fatality rate from infection is up to 6.3%.
Imjin thottimvirus(MJNV) is a single-stranded, enveloped, negative-sense RNA virus of the orthohantavirus genus in the Bunyavirales order. It is a newly identified hantavirus isolated from the lung tissues of Ussuri white-toothed shrews of the species Crocidura lasiura (order Soricomorpha, family Soricidae, subfamily Crocidurinae) captured near the demilitarized zone in the Republic of Korea during 2004 and 2005.
Choclo virus (CHOV) is a single-stranded, negative-sense RNA zoonotic New World hantavirus. It was first isolated in 1999 in western Panama. The finding marked the first time Hantavirus pulmonary syndrome (HPS) was found in Central America.
In 1557, a pandemic strain of influenza emerged in Asia, then spread to Africa, Europe, and eventually the Americas. This flu was highly infectious and presented with intense, occasionally lethal symptoms. Medical historians like Thomas Short, Lazare Rivière and Charles Creighton gathered descriptions of catarrhal fevers recognized as influenza by modern physicians attacking populations with the greatest intensity between 1557 and 1559. The 1557 flu saw governments, for possibly the first time, inviting physicians to instill bureaucratic organization into epidemic responses. It is also the first pandemic where influenza is pathologically linked to miscarriages, given its first English names, and is reliably recorded as having spread globally. Influenza caused higher burial rates, near-universal infection, and economic turmoil as it returned in repeated waves.
Trench nephritis, also known as war nephritis, is a kidney infection, first recognised by medical officers as a new disease during the early part of the First World War and distinguished from the then-understood acute nephritis by also having bronchitis and frequent relapses. Trench nephritis was the major kidney problem of the war. The cause was not established at the time, treatments were ineffective, and the condition led to 35,000 British and 2,000 American casualties.
Guy Edward Thwaites is a British professor of infectious diseases at the University of Oxford, and director of the Oxford University Clinical Research Unit (OUCRU) in Ho Chi Minh City in Vietnam. His focus is on severe bacterial infections, including meningitis and Staphylococcus aureus bloodstream infection, and tuberculosis. He is a former first-class cricketer.
Hantavirus, especially hantavirus pulmonary syndrome (HPS), is a zoonotic disease primarily transmitted through contact with infected rodents, posing significant public health risks in Latin America and the Caribbean (LAC) where biodiversity is high. Notably, rodent species like those in the Cricetidae family serve as reservoirs for various hantavirus strains, including the Andes virus (ANDV), which uniquely transmits between humans. Climate change, with its effects on rainfall, temperature, and extreme weather patterns, is increasingly altering environmental conditions in these regions, amplifying rodent population dynamics and thus the potential for hantavirus outbreaks.