PANDEMICS IN HISTORY

Historical accounts of epidemics are often vague or contradictory in describing how victims were affected. A rash accompanied by a fever might be smallpox, measles, scarlet fever, or varicella, and it is possible that epidemics overlapped, with multiple infections striking the same population at once. It is often impossible to know the exact causes of mortality, although ancient DNA studies can sometimes detect residues of certain pathogens.

It is assumed that, prior to the Neolithic Revolution around 10,000 BC, disease outbreaks were limited to a single family or clan, and did not spread widely before dying out. The domestication of animals increased human-animal contact, increasing the possibility of zoonotic infections. The advent of agriculture, and trade between settled groups, made it possible for pathogens to spread widely. As population increased, contact between groups became more frequent. A history of epidemics maintained by the Chinese Empire from 243 B.C. to 1911 A.C. shows an approximate correlation between the frequency of epidemics and the growth of the population.

The incomplete list of known epidemics which spread widely enough to merit the title "pandemic".

Plague of Athens (430 to 426 BC): During the Peloponnesian War, an epidemic killed a quarter of the Athenian troops and a quarter of the population. This disease fatally weakened the dominance of Athens, but the sheer virulence of the disease prevented its wider spread. The exact cause of the plague was unknown for many years. In January 2006, researchers from the University of Athens analyzed teeth recovered from a mass grave underneath the city and confirmed the presence of bacteria responsible for typhoid fever.

Antonine Plague (165 to 180 AD): Possibly measles or smallpox brought to the Italian peninsula by soldiers returning from the Near East, it killed a quarter of those infected, up to five million in total.

Plague of Cyprian (251–266 AD): A second outbreak of what may have been the same disease as the Antonine Plague killed (it was said) 5,000 people a day in Rome.

Plague of Justinian (541 to 549 AD): Also known as the First Plague Pandemic. This epidemic started in Egypt and reached Constantinople the following spring, killing (according to the Byzantine chronicler Procopius) 10,000 a day at its height, and perhaps 40% of the city's inhabitants. The plague went on to eliminate a quarter to half the human population of the known world and was identified in 2013 as being caused by bubonic plague.

Black Death (1331 to 1353): Also known as the Second Plague Pandemic. The total number of deaths worldwide is estimated at 75 to 200 million. Starting in Asia, the disease reached the Mediterranean and western Europe in 1348 (possibly from Italian merchants fleeing fighting in Crimea) and killed an estimated 20 to 30 million Europeans in six years; a third of the total population, and up to a half in the worst-affected urban areas. It was the first of a cycle of European plague epidemics that continued until the 18th century; there were more than 100 plague epidemics in Europe during this period, including the Great Plague of London of 1665–66 which killed approximately 100,000 people, 20% of London's population.

1817–1824 cholera pandemic. Previously endemic in the Indian subcontinent, the pandemic began in Bengal, then spread across India by 1820. The deaths of 10,000 British troops were documented - it is assumed that tens of thousands of Indians must have died. The disease spread as far as China, Indonesia (where more than 100,000 people succumbed on the island of Java alone) and the Caspian Sea before receding. Subsequent cholera pandemics during the 19th century are estimated to have caused many millions of deaths globally.

Great Plague of Marseille in 1720 killed a total of 100,000 people

Third plague pandemic (1855–1960): Starting in China, it is estimated to have caused over 12 million deaths in total, the majority of them in India. During this pandemic, the United States saw its first outbreak: the San Francisco plague of 1900–1904. The causative bacterium, Yersinia pestis, was identified in 1894. The association with fleas, and in particular rat fleas in urban environments, led to effective control measures. The pandemic was considered to be over in 1959 when annual deaths due to plague dropped below 200. The disease is nevertheless present in the rat population worldwide and isolated human cases still occur.

The 1918–1920 Spanish flu infected half a billion people around the world, including on remote Pacific islands and in the Arctic—killing 20 to 100 million. Most influenza outbreaks disproportionately kill the very young and the very old, but the 1918 pandemic had an unusually high mortality rate for young adults. Mass troop movements and close quarters during World War I caused it to spread and mutate faster, and the susceptibility of soldiers to the flu may have been increased by stress, malnourishment and chemical attacks. Improved transportation systems made it easier for soldiers, sailors and civilian travelers to spread the disease.

Pandemics in indigenous populations

Beginning from the Middle Ages, encounters between European settlers and native populations in the rest of the world often introduced epidemics of extraordinary virulence. Settlers introduced novel diseases which were endemic in Europe, such as smallpox, measles, pertussis and influenza, to which the indigenous peoples had no immunity. The Europeans infected with such diseases typically carried them in a dormant state, were actively infected but asymptomatic, or had only mild symptoms.

Smallpox was the most destructive disease that was brought by Europeans to the Native Americans, both in terms of morbidity and mortality. The first well-documented smallpox epidemic in the Americas began in Hispaniola in late 1518 and soon spread to Mexico. Estimates of mortality range from one-quarter to one-half of the population of central Mexico. It is estimated that over the 100 years after European arrival in 1492, the indigenous population of the Americas dropped from 60 million to only 6 million, due to a combination of disease, war, and famine. The majority these deaths are attributed to successive waves of introduced diseases such as smallpox, measles, and typhoid fever.

In Australia, smallpox was introduced by European settlers in 1789 devastating the Australian Aboriginal population, killing an estimated 50% of those infected with the disease during the first decades of colonization. In the early 1800s, measles, smallpox and intertribal warfare killed an estimated 20,000 New Zealand Maori.

In 1848–49, as many as 40,000 out of 150,000 Hawaiians are estimated to have died of measles, whooping cough and influenza. Measles killed more than 40,000 Fijians, approximately one-third of the population, in 1875, and in the early 19th century devastated the Great Andamanese population.[110] In Hokkaido, an epidemic of smallpox introduced by Japanese settlers is estimated to have killed 34% of the native Ainu population in 1845.

SOURCE: https://en.wikipedia.org/wiki/Pandemic

DIABETES HISTORY

The condition known today as diabetes (diabetes mellitus) is thought to have been described in the Ebers Papyrus (c. 1550 BC) Ayurvedic physicians (5th/6th century BC) first noted the sweet taste of diabetic urine, and called the condition madhumeha ("honey urine"). The term diabetes traces back to Demetrius of Apamea (1st century BC). For a long time, the condition was described and treated in traditional Chinese medicine as xiāo kě (wasting-thirst). Physicians of the medieval Islamic world, including Avicenna, have also written on diabetes. Early accounts often referred to diabetes as a disease of the kidneys. In 1674, Thomas Willis suggested that diabetes may be a disease of the blood. Johann Peter Frank is credited with distinguishing diabetes mellitus and diabetes insipidus in 1794.

 

In regard to diabetes mellitus, Joseph von Mering and Oskar Minkowski are commonly credited with the formal discovery (1889) of a role for the pancreas in causing the condition. In 1893, Édouard Laguesse suggested that the islet cells of the pancreas, described as "little heaps of cells" by Paul Langerhans in 1869, might play a regulatory role in digestion. These cells were named islets of Langerhans after the original discoverer. In the beginning of the 20th century, physicians hypothesized that the islets secrete a substance (named "insulin") that metabolises carbohydrates. The first to isolate the extract used, called insulin, was Nicolae Paulescu. In 1916, he succeeded in developing an aqueous pancreatic extract which, when injected into a diabetic dog, proved to have a normalizing effect on blood sugar levels. Then, while Paulescu served in army, during World War I, the discovery and purification of insulin for clinical use in 1921–1922 was achieved by a group of researchers in Toronto—Frederick Banting, John Macleod, Charles Best, and James Collip—paved the way for treatment. The patent for insulin was assigned to the University of Toronto in 1923 for a symbolic dollar to keep treatment accessible.

 

In regard to diabetes insipidus, treatment became available before the causes of the disease were clarified. The discovery of an antidiuretic substance extracted from the pituitary gland by researchers in Italy (A. Farini and B. Ceccaroni) and Germany (R. Von den Velden) in 1913 paved the way for treatment. By the 1920s, accumulated findings defined diabetes insipidus as a disorder of the pituitary. The main question now became whether the cause of diabetes insipidus lay in the pituitary gland or the hypothalamus, given their intimate connection. In 1954, Berta and Ernst Scharrer concluded that the hormones were produced by the nuclei of cells in the hypothalamus.

SOURCE: https://en.wikipedia.org/wiki/History_of_diabetes

HYPERTENSION HISTORY

The modern history of hypertension begins with the understanding of the cardiovascular system based on the work of physician William Harvey (1578–1657), who described the circulation of blood in his book De motu cordis. The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733. Descriptions of what would come to be called hypertension came from, among others, Thomas Young in 1808 and especially Richard Bright in 1836. Bright noted a link between cardiac hypertrophy and kidney disease, and subsequently kidney disease was often termed Bright's disease in this period. In 1850 George Johnson suggested that the thickened blood vessels seen in the kidney in Bright's disease might be an adaptation to elevated blood pressure. William Senhouse Kirkes in 1855 and Ludwig Traube in 1856 also proposed, based on pathological observations, that elevated pressure could account for the association between left ventricular hypertrophy to kidney damage in Bright's disease. Samuel Wilks observed that left ventricular hypertrophy and diseased arteries were not necessarily associated with diseased kidneys, implying that high blood pressure might occur in people with healthy kidneys; however, the first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed in 1874 using a sphygmograph. The concept of hypertensive disease as a generalized circulatory disease was taken up by Sir Clifford Allbutt, who termed the condition "hyperpiesia". However, hypertension as a medical entity really came into being in 1896 with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896, which allowed blood pressure to be measured in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is ausculted with a stethoscope while the sphygmomanometer cuff is deflated. Tracking serial blood pressure measurements was further enhanced when Donal Nunn invented an accurate fully automated oscillometric sphygmomanometer device in 1981.

 

The term essential hypertension ('Essentielle Hypertonie') was coined by Eberhard Frank in 1911 to describe elevated blood pressure for which no cause could be found. In 1928, the term malignant hypertension was coined by physicians from the Mayo Clinic to describe a syndrome of very high blood pressure, severe retinopathy and inadequate kidney function which usually resulted in death within a year from strokes, heart failure or kidney failure. A prominent individual with severe hypertension was Franklin D. Roosevelt. However, while the menace of severe or malignant hypertension was well recognised, the risks of more moderate elevations of blood pressure were uncertain and the benefits of treatment doubtful. Consequently, hypertension was often classified into "malignant" and "benign". In 1931, John Hay, Professor of Medicine at Liverpool University, wrote that "there is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery, because then some fool is certain to try and reduce it". This view was echoed in 1937 by US cardiologist Paul Dudley White, who suggested that "hypertension may be an important compensatory mechanism which should not be tampered with, even if we were certain that we could control it". Charles Friedberg's 1949 classic textbook "Diseases of the Heart", stated that "people with 'mild benign' hypertension ... [defined as blood pressures up to levels of 210/100 mm Hg] ... need not be treated". However, the tide of medical opinion was turning: it was increasingly recognised in the 1950s that "benign" hypertension was not harmless. Over the next decade increasing evidence accumulated from actuarial reports and longitudinal studies, such as the Framingham Heart Study, that "benign" hypertension increased death and cardiovascular disease, and that these risks increased in a graded manner with increasing blood pressure across the whole spectrum of population blood pressures. Subsequently, the National Institutes of Health also sponsored other population studies, which additionally showed that African Americans had a higher burden of hypertension and its complications.

SOURCE: https://en.wikipedia.org/wiki/History_of_hypertension