Leprosy in the middle ages – Elizabeth Ashworth – author The de Lacy Family Leprosy in the middle ages Leprosy, or Hansen’s disease (so named because it was G.H. Armauer Hansen who discovered, in Norway in 1873, that the bacterium Mycobacterium leprae was the cause) has been known to man for over 4000 years. The word leprosy comes from ancient Greek meaning ‘scaly skin’ or ‘scaly back’. Most people are naturally immune to the disease and nowadays it mostly affects people in developing countries where resources are scarce. It is not highly infectious and is probably transmitted through airborn droplets. After infection symptoms can take up to 20 years to develop and begin by affecting the nerves that control feeling in the skin. If left untreated, further nerve damage occurs and ulcers may develop. Because of the loss of sensation, wounds and cuts go unnoticed and the consequent damage leads to the visible signs commonly associated with leprosy. Leprosy appeared in Europe in the early 11th century and by the 15th century it had all but disappeared.

It is thought that the disease may have been brought to Europe from Middle Eastern countries by those who had been on Crusade and it was regarded as being an upper-class disease rather than a disease of the poor. In fact early sufferers were pitied and treated well, but as the prevalence of the disease grew those with leprosy were reviled and seen as unclean and sinful. They were forced to carry a clapper, and later a bell, to warn of their coming so that people could avoid them and not come into close contact with them. A person with leprosy from a 14th century manuscript. The bell may have been to attract charitable donations as well as warning that a diseased person was in the vicinity. In the Middle Ages, many skin conditions were labelled as ‘leprosy’. These may have included such conditions as eczema, psoriasis and skin cancers and by the 12th century those with leprosy became regarded as unclean. Around this time many leper houses were built to keep sufferers separate from society as it was believed that the disease was very contagious.

The Benedictine monk and chronicler, Matthew Paris, who lived from around 1200 to 1259, estimated that there were 19,000 leper houses in Europe, with 2000 being in France and over a hundred in England. These houses were run along similar lines to monasteries and convents and were for care as well as quarantine. In fact those with leprosy were sometimes viewed as experiencing purgatory whilst still on earth and their suffering was viewed as holy. The residents spent much time in prayer and, as it was also popularly thought to have been a sexually transmitted disease, the leper houses made the sufferers take a vow of chastity. Those who did not enter leper houses took the vows that are listed in the Mass of Separation including vowing not to enter any church or marketplace and not to touch the rim or rope of a well except with gloved hands. They were also excluded from inheriting. Famous sufferers include Baldwin IV, king of Jerusalem, who continued to rule despite his illness and Alice the Leper, a Cistercian nun who became a leprous martyr.

There is also, of course, Richard FitzEustace, in my novel The de Lacy Inheritance, who is based on a real person. Many wealthy people in the middle ages gave donations to the leper houses and Roger de Lacy (who was Richard’s brother) gave land for a leper hospital on the banks of the river Ribble near Clitheroe. The site is now the Edisford Hotel near the bridge that spans the river. The hospital was named St Nicholas’s. Nowadays leprosy is curable with treatment by a multidrug therapy that combines dapsone, clofazimine and rifampicin. However the disease remains in parts of Africa, Asia and South America and there are still occasional cases of leprosy treated in the UK. I have also been told by Sian Arulanantham, Head of Programmes at The Leprosy Mission, that legislation still exists that discriminates against people affected by leprosy. This is just one of the issues that The Leprosy Mission is trying to address.

You can find out more about their work at: Like this: Leprosy Leprosy background Leprosy, also called Hansen's disease, is an infectious disease that is characterized by disfiguring skin sores and progressive nerve damage. Armauer Hansen discovered the disease-causing bacteria in 1873. There are two types of leprosy: tuberculoid and lepromatous. Both forms cause skin sores and peripheral nerve damage, but lepromatous is more severe. It causes large, disfiguring lumps and bumps (nodules) on the skin. Only the lepromatous form is considered contagious. Researchers estimate that more than one million people worldwide have leprosy. It is most common in Asia (especially Nepal and India), Latin America, and Africa. An estimated 4,000-6,000 Americans have leprosy. Nearly all cases of leprosy in the United States occur in patients who emigrated from developing countries. Leprosy is more common in developing countries because these areas are more likely to be unsanitary and highly populated.

According to the World Health Organization (WHO), access to information, diagnostic procedures, and treatment have helped decrease the prevalence of leprosy worldwide. Since 1985, 113 countries out of the 122 countries where leprosy was a public health concern have eliminated the disease. Since 2001, the number of new leprosy cases has decreased by 20% each year. Individuals can develop leprosy at any age. However, it is most common among patients who are in their 20s and 30s. The severity of leprosy does not vary with age. Individuals can become infected with either form of leprosy after coming into contact with Mycobacterium leprae when they are exposed to contaminated soil or armadillos that carry the bacteria. However, researchers have not discovered exactly how the disease spreads from person to person. It was initially believed that the disease was transmitted after physical contact with an infected individual. However, experts currently believe that the lepromatous form of leprosy is passed from person to person through expelled droplets from the mouth and nose of an infected person.

Experts believe that most cases are spread after close, long-term contact with an infected individual. According to this new theory, individuals who inhale these droplets may become infected. Leprosy is not considered a highly contagious illness. About 95% of people who are exposed to the bacteria that causes leprosy do not develop the disease. Healthcare workers often treat people with leprosy for many years without contracting the disease. A combination of medications, called antibiotics, is used to kill the bacterium that causes leprosy. These medications cure the disease and prevent it from progressing, but they do not reverse nerve damage or physical disfiguration. Therefore, it is important to visit a healthcare provider as soon as symptoms develop. Related Terms Antibiotics, bacteria, bacterial infection, bacterium, clofazimine, dapsone, Hansen's disease, immune response, leper, lepromatous, lepromatous leprosy, lepromin skin test, MDT, multidrug therapy, Mycobacterium leprae, nerve damage, nodules, peripheral nerve damage, peripheral nerves, tuberculoid, tuberculoid leprosy, reconstructive surgery, rifampin.

Popular Leprosy, Hansen's Disease LEPROSY, HANSEN'S DISEASE Leprosy is caused by bacteria or germs called Mycobacterium leprae. It is an infection that affects the skin and the nerves of the hands and feet and can also cause problems in the eyes and nose. A BRIEF HISTORY Dr. Armauer Hansen of Norway was the first to see the leprosy germ under a microscope. This was 1873, and Hansen's discovery was revolutionary. The evidence was clear for all the world: leprosy is caused by a germ (Mycobacterium leprae). It was not hereditary, a curse, or from sin. Because of Dr. Hansen's work, leprosy is also called Hansen's Disease. Gerhard Armauer Hansen (1841-1914) Leprosy has tormented humans throughout recorded history. The earliest possible account of a disease that many scholars believe is leprosy appears in an Egyptian Papyrus document written around 1550 B.C. Around 600 B.C. Indian writings describe a disease that resembles leprosy.

In Europe, leprosy first appeared in the records of ancient Greece after the army of Alexander the Great came back from India and then in Rome in 62 B.C. coinciding with the return of Pompeii's troops from Asia Minor. Throughout its history, leprosy has been feared and misunderstood. For a long time leprosy was thought to be a hereditary disease, a curse, or a punishment from God. Before and even after the discovery of its biological cause, leprosy patients were stigmatized and shunned. For example, in Europe during the Middle Ages, leprosy sufferers had to wear special clothing, ring bells to warn others that they were close, and even walk on a particular side of the road, depending on the direction of the wind. Even in modern times, leprosy treatment has often occured in seperate hospitals and live-in colonies called leprosariums because of the stigma of the disease. Leprosy has been so prevalent in various areas as certain times throughout history that is has inspired art work and influenced other cultural practices. TRANSMISSION of LEPROSY Leprosy is a chronic disease caused by a bacillus, Mycobacterium leprae, M.

leprae multiplies very slowly and the incubation period of the disease is about five years. Symptoms can take as long as 20 years to appear. Leprosy is not highly infectious. It is transmitted via droplets, from the nose and mouth, during close and frequent contacts with untreated cases. At least until recently, the most widely held beliefs was that the disease was transmitted by contact between cases of leprosy and healthy persons. More recently the possibility of transmission by the respiratory route is gainning ground. SYMPTOMS Leprosy mainly affects the skin and nerves. If untreated, there can be progressive and permanent damage to the skin, nerves, limbs and eyes. Whonamedit - dictionary of medical eponyms Whonamedit? - A dictionary of medical eponyms Gerhard Henrik Armauer Hansen Norwegian physician, Born July 29, 1841, Bergen; died February 12, 1912, Florø. Biography of Gerhard Henrik Armauer Hansen Gerhard Henrik Armauer Hansen's discovery of the Mycobacterium leprae was historic for reasons beyond its significance to the fight against leprosy.

As the first identification of a bacteria as the causative agent of a human disease, his study was a precursor to Robert Koch's conclusive demonstration of the bacterial cause of anthrax three years later. Although Hansen was unable to cultivate the leprosy bacillus in vitro as an experimental confirmation of his hypothesis. It has still not been done, and this is the reason why it has not been possible to develop a vaccine. His research helped to establish fundamental principles in immunology, bacteriological medicine and public health policy. Gerhard Henrik Armauer Hansen was the eight of fifteen children. His mother was Elizabeth Concordia Schram, who was a member of a family of master joiners long established in Bergen. His father, Claus Hansen, was a wholesale merchant until the severe contraction of credit in 1848-1851 drove him into bankruptcy. He then worked as a cashier in a bank. In 1859 Hansen worked his way through the gymnasium and medical school. He began his medical studies at the University of Christiania (now Oslo). It was necessary for him to earn his own living while he was as student. He first taught at a girl’s school and later spent a year as substitute for the prosector in anatomy.

He then began his own tuition courses in anatomy. In later years he said that during this period he had known neither physical nor mental fatigue and had found that he did his best work between six and eight in the morning. He passed his degree with honours in 1866, having already proved himself an exceptional research talent. He completed his internship at the National Hospital in Christiania (Rikshospitalet). He then served as doctor to a fishing community of some 6.000 inhabitants at Lofoten, a string of Islands off northern Norway. In 1868 Hansen returned to his native town of Bergen, the centre for Norwegian leprosy research. At this time the disease was still a social problem in Norway, with some 3,000 patients for whom 800 nursing places were reserved. In Bergen alone there were no less than three lepra hospitals. Here Hansen entered service at the Pleiestiftelsen for spedalske nr 1. He soon moved on to the position of assistant physician at the Lungegaardshospitalet under Dr. Daniel Cornelius Danielssen. With C. W.

Boeck Danielssen in 1847 had published the major work Om Spedalskhed (On Leprosy). His efforts in organizing Bergen's leprosy care program had helped to establish Bergen as the European centre for leprosy research. Danielssen was a foremost authority on the clinical and pathological aspects of the disease but, like other investigators of the time, regarded the affliction as hereditary, a belief he continued to hold even after Hansen's discovery. Many physicians believed the disease to be caused by miasma. Hansen later wrote that he had never before seen so much misery in one place. Because the lepers were so disfigured and stunted, they were outcasts. Both Danielssen and Hansen travelled around to attended to the sick, which were often isolated in remote farms where nobody helped, and collect material. The disease was not uncommon in western parts of Norway in the nineteenth century. Hansen quickly concluded on the basis of epidemiological studies that leprosy was a specific disease that must have a specific cause, not an inheritable plague holding man hostage.

He was convinced that a bacterium carried the disease from person to person; a daring speculation at a time when the concept of contagion was still poorly understood, and no one had shown that bacteria could cause human diseases. Challenging Danielssen's authority, Hansen in one of their first meetings declared his views, and thus ran into a professional, but in no way personal conflict with his superior. The fact that the number of new leprosy cases was diminishing, Hansen saw as a support for his theory and the efficacy of measures taken against contagion. However, his relationship to Danielssen improved, and Hansen was able to commence his research, comprising both experimental and epidemiological efforts. In his first work, of 1869, published in Norwegian only in 1871, Hansen among other things described the appearance of leprous changes in lymphoid tissue. Here Hansen applies the term ”infectionsstoff” (“infectious substance”) for the changes he saw in association with lymph nodes. He was, however, very uncertain about what these findings really meant. His poor equipment complicated his work, and he was unsuccessful in his attempts to cultivate and stain the changes.

In 1870 a grant allowed Hansen to travel to Bonn and later to Vienna for advanced training in histopathology. Returning to Norway, using primitive staining methods and working with biopsy specimens from patients with leprosy, Hansen continued his intensive microscopy work. On his return to Bergen in 1871 Hansen launched his search for the causative agent of leprosy, using biopsy specimens drawn from patients. A physically strong and unflagging young man, Hansen decided to look for bacteria in patients, first in blood, and on finding none, in skin nodules. He wrote: At that time . . . I could sit tirelessly for hours on end, focusing through the microscope with great enlargement . . . One day I was positive I had discovered the bacteria, the next day magnificent certainty had collapsed, and I would be back where I started . . . Finally, though, I wrote the first record of my research. In every nodule he saw rod-like bodies inside cells that looked like bacteria; they were not present in all cells, but in most of them. At first he was unable to see rods in patients with tuberculoid leprosy, but after prolonged studies he found them there also.

He could not see any difference between these bodies and true bacteria, but hedged on claiming they were actually identical. In 1873, aged 32 years, he discovered the rod-shaped bodies - Mycobacterium leprae, sometimes called Hansen’s bacillus, in leprous nodules. This epoch-making discovery was published in his major work of 88 pages that year. Most of his colleagues and physicians elsewhere laughed. Hansen, they said, may have seen these bodies in tissues, but it did not mean they caused disease. It did. His findings were also published in English in an abridged edition. His description of the findings is rather careful: “Though unable to discover any difference between these bodies and true bacteria, I will not venture to declare them to be identical” This carefulness on Hansen’s side certainly contributed to the priority conflict which was soon to blossom. By 1879 he was able, through the use of improved staining methods, to show great numbers of the rod-shaped bodies typically aggregated in parallel cells. He believed the bacillus to be the causative agent of leprosy and thereby became the first investigator to suggest that microorganisms might cause a human disease.

The tuberculosis bacillus, for example, was not discovered until 1882. The Neisser-Hansen conflict of priority. In the beginning of 1879 Hansen was visited by the German bacteriologist Albert Neisser, then 24 years old, who was on a research trip to Norway to study leprosy. Neisser was able to examine more than 100 patients with leprosy in Trondheim, Molde, and Bergen. From Hansen he received preparations made from lepra node in which unstained rode were just recognizable. Back home in Germany Neisser in a very convincing way was able to stain the bacteria, and found, in almost all cases, "bacilli as small, thin rods, whose length amounts to about half the diameter of a human red blood-corpuscle and whose width I estimate at one-fourth the length." Neisser did not hesitate to publish his results, without first contacting Hansen, in the paper Über die Aetiologie des Aussatzes (1880). In a paper Neisser writes: Having quickly returned home with this wealth of material, I immediately began to study it, and to my intense surprise found bacilli in large numbers . . .

These rods appeared to be something previously unknown . . . The singularity of their appearance awakened the hope that further investigations might bring light to an obscure question. At the same time, In Bergen, Hansen, with the help of new methods, also succeeded in staining his preparations. In the following year, 1881, Neisser published the article Weitere Beiträge zur Aetiologie der Lepra in Virchows Archiv in which he claimed the honour of discovering a microbe that caused disease, and sought to discredit Hansen. There is no doubt that Neisser intended to steal Hansen's discovery, and might well have succeeded. The priority conflict is to some extent a parallel to that between the French discoverer of the HIV virus, Luc Montagnier at Pasteur Institute, and the American Robert C. Gallo, who falsely claimed credit for the discovery. However, Norwegian reaction to Neisser’s behaviour was indignation, particularly because the term Neisser’s bacteria was soon in use. Encouraged by his colleagues, Hansen defended his position, though without entering into a direct polemic. Instead, he summarized his findings from the beginning of the 1870s and published them in Norwegian, German, English, and French.

He described Neisser's visit to Bergen, and stated firmly that he was making the report to maintain his priority, and bring his work up to date. The conflict proved to be long lasting, and it was not until a lepra congress in Berlin that Hansen in an international context was officially recognized as the true discoverer of the lepra bacillus. It is clear, however, that while Hansen first discovered the leprosy bacillus, Neisser was the first to identify it as the etiological agent of the disease. The aetiology, diagnosis, and prophylaxis of leprosy occupied Neisser for much of his subsequent career. In 1955, George L. Fite and Herbert W. Wade reviewed the Hansen-Neisser controversy in depth. They commented that: When one looks back at Neisser's first article and begins to realize the situation, one can understand how Hansen must have felt about it. He could scarcely have failed to be infuriated. Neisser started by discrediting Hansen, who had willingly shown him everything he could and had surely, been instrumental in providing Neisser's material. Far from genuinely giving Hansen any credit, Neisser spent much effort to assert the importance of his organisms as against Hansen's.

In his memoirs, written 30 years later, Hansen claims he took Neisser's move to pre-empt his discovery without excitement. He wrote that his chief, Danielssen was furious, and dressed him down severely for not responding more aggressively to this deliberate attempt to steal his idea. Fite and Wade did not believe that Hansen understood the full import of his discovery, since the paper he published in 1879 did not contain much more information than the one published in 1874. They thought Hansen had done little additional work, and that inadequately. Ethics The fault was not Hansen's. Unlike most bacteria causing human diseases, scientists have been unable to culture Mycobacterium leprae on artificial culture media. This was true in 1879 and is still true today. Hansen was also unable to infect rabbits. It would be almost 100 years before Polly's armadillos would supply the animal host and bountiful supply of bacilli that Hansen needed. His failure to grow the bacillus or infect rabbits had bitter consequences.

In a less well-advised effort, Hansen inoculated the eye of a woman suffering from a neural form of the disease with material drawn from a leprous nodule of a patient suffering from the cutaneous form. There were no clinical consequences of the inoculation, but the woman claimed it was painful and impaired here sight. She took her case to court. According to the records of the city of Bergen Law Courts, May 31, 1880: He did not succeed in inoculating the material into the eye, as she did not keep the eye still. One of the other doctors . . . calmed down the despondent and placed her in a chair. It was then possible to carry out the operation, placing the material from the cataract knife under the conjunctiva of the eye . . . The defendant . . . admitted that he had neither obtained her permission in advance, nor told her of his aim in doing it. The defendant then explained his motives for this unjustified operation . . . He said he had failed in his attempts to infect animals. Thus he could not prove that his rod shaped bacilli caused leprosy; so he could not quarantine patients to protect the people of Bergen.

The court found him guilty. Hansen had to pay costs, and was removed from his post as resident physician of the Bergen Leprosy Hospitals in May 1880. After the trial he made no major contributions to research. Hansen’s sentence was less severe than it might seem, however, since he was allowed to retain his position as leprosy medical officer for the entire country of Norway - an appointment conferred on him in 1875 and one that held until his death. He was thus able to implement changes in the methods of control of leprosy in Norway - changes that had been in part made necessary by his own hypothesis concerning the aetiology of the disease. The Norwegian leprosy act of 1877 and the amended act of 1885 were the fruits of his untiring work. Under these laws health authorities could order lepers to live in precautionary isolation away from their families (subsequent studies have shown leprosy to be a familial affliction); enforcement of the law led to a quick and steady decline of the disease in Norway.

There were 1.752 known cases of leprosy in Norway in 1875; by the beginning of the twentieth century there were 577. The last outbreak in Norway was in the 1950's. During the last five years of the twentieth century four cases were reported in immigrants from other parts of the world, and there are now 1-2 such cases each year. This, however, is the tuberceloid form, which is generally a skin disease and not contagious. All cases having been treated, there are presently nobody with the chronic form of lepra in Norway. The word «hansenarium was suggested to replace the still more standard «leprosarium». Twice married Hansen married Danielssen’s daughter, Stephanie Marie, "Fanny", on January 7, 1873. Only a few months after the wedding it was discovered that she was infected with pulmonary tuberculosis. Like all her three sisters, who also died from the disease, she had been infected by her father. The disease had a fast course and she died on October 25 of the same year.

On August 27 1875 he married Johanne Margrethe Tidemand, a widow related to almost the entire Bergen Commercial patriarcate. She brought two children into their marriage. Their only child, a son, was named Daniel Cornelius Armauer Hansen for Hansen’s superior and previous father-in-law. The son became a physician specializing in tuberculosis and in 1929 was appointed chief of the tuberculosis hospital in Bergen. The first period after the birth of their son, Hansen's second marriage was happy. However, his wife soon started complaining that her husband neglected her for his scientific work. Still, the couple had a large social circle among the intellectuals of the city, counting the composer Edvard Grieg and his wife Nina among their closest friends. It was said that the marriage successively became one only in the name, and that his wife wanted to divorce him in order to marry a musician named Iver Holter. Hansen had an open mind for the themes of his times and, among other things, contributed money from his own pocket to pay for a visiting lecture by the Danish author Georg Brandes on the Romantic period in France.

He also enjoyed theatre, often attending performances in the metropoles of Europe when on his numerous travels abroad. Over the years Hansen developed a distance to his native country, which he came to consider “lay outside the world." His autobiography indicates a resignation over the mental condition and cultural views of his countrymen. Armauer Hansen suffered from syphilis For the better part of a century after his death, only his family knew of the fact that Armauer Hansen suffered from syphilis, contracted from a consenting seamstress in Christiania during his student years in the 1860s. At the age of 36, in 1877, he suffered a brain stroke, which may have been provoked by this disease. Hansen suffered the first symptoms of heart disease as early as 1900. In the following years he had several severe heart attacks that confined him to bed for long periods of time. In the intervals of his illness, however, he continued to travel around the country on official inspection tours. In February 1912 he made such a trip to the fishing areas north of Bergen.

In Florø, a little town on the western coast, he was invited to stay in the home of a friend, and it was there that he died. He was given a funeral at state expense; he had been president of the Bergen Museum and the ceremony took place from its hall. A Darwinian blasphemer in Bergen While Hansen was chiefly known for his work on leprosy, he also played a role in the dissemination of Darwin’s ideas. Early in his career, during his stay in Vienna Hansen was introduced to the teachings of Charles Darwin, and then set about to study Darwin’s books. In Darwinian doctrine he discovered a scientific ideal, particularly in its methodology of dispassionate observation. In 1886 he published a book on Darwinism in Norwegian. In his apostolic zeal for Darwin’s work, Hansen also gave numerous lectures and published articles in the popular press. These evoked a great sensation, especially from the clergy and religious organizations - who reacted violently against the «blasphemer» in their midst. Hansen was, however, devoid of philosophical speculations and had no aptitude for martyrdom. He did not acknowledge the attacks made against him; he continued to sit at his microscope, smoking his pipe, and do his work.

The uncomfortable radical Armauer Hansen was a radical in his time, an atheist with a hostile attitude to the church. Among other things he was indignant of the preaching of guilt by the clergy, which he considered to hamper the development of society. All through his life he was an oppositional. Whilst a medical student he stopped attending the lectures because he thought he understood things better than his teachers. Hansen sometimes was considered rigid in his views and was not known to be a flexible debater. However, people in his closest circle described Hansen described as an amiable, warm-hearted and entertaining person void of superior manners and personal ambitions. In the final chapter of his autobiography Hansen presents strings of thoughts that certainly mirror his personality. He questions whether religion will prevail among men and predicts that the puzzle of the origin of life will be solved in the twentieth century. He supports workers demands for a larger share of production value and expects socialism to be carried out in some modified form. At the same time, however, he was extremely critical of women’s emancipations, considering the role of men founded in his superior physical and mental capacity, thus doubting whether women were fit to become doctors.

Hansen considered the two most important scientific events in his lifetime to be Pasteur’s discovery of the importance of microbes and Darwin's theory of evolution. Power to the people Hansen saw the need for bringing scientific results to a broader public. Over many years he wrote numerous papers of popularised science and was a prolific lecturer. As an organization man he was active in various bodies, like the board of the Bergen Museum, Selskabet for de norske Fiskeriers fremme (Society for the Advancement of Norwegian Fisheries), and Det medicinske selskab i Bergen (Bergen Medical Society). Hansen was one of the founders of the journal Medicinsk Revue, later to be ranamed Nordisk Medicin, of which he was one of the editors for many years. Honours and awards Hansen received many international assignments and honours for his leprosy studies. He was president of honour of the section for dermatology and syphilis at the international medical congress in Copenhagen in 1884.

He served as chairman of the International Leprosy Committee, and in 1897 was elected honorary chairman of the first Conférence Internationale de la Lèpre, held in Berlin, and was president of the second such conference, held in Bergen in 1909. The meeting was something of a peak in Hansen’s scientific career. Here he was acclaimed as the discoverer of the lepra bacillus and one of the foremost figures in suggesting measures to prevent the spread of the disease. He was honorary chairman of the International Leprosy Committee, corresponding or honorary member of numerous scientific societies, and was decorated several times. In 1900 contributions toward a portrait bust of Hansen were solicited internationally; the bust, made by Jon Visdal, was unveiled with great ceremony the following year in the museum garden, now the university garden, in Bergen. In 1892 he received the St. Olavs Orden (Order of Saint Olav) for scientific contributions and two years was conferred doctor of honour at the University of Copenhagen.

In recognition of scientific and administrative contributions, Hansen in 1901 was given a rise of wages corresponding to that of a professor of the highest degree, by Stortinget – the Norwegian parliament. Dear armadillo Hansen never achieved Koch’s fame, since he could not grow his bacillus in the test tube or infect animals. His attempt to inoculate a woman demonstrates his desperation. Since then some five generations of scientists have striven in vain to grow Hansen's bacilli. Without them, it was impossible to develop vaccines and diagnostic reagents, or find out how disease is transmitted. Thus, leprosy lingered in the shadow of medieval medicine for another century. A major advance in experimental leprosy occurred when Eleanor Storrs reported a leprosy infection in the nine-banded armadillo. During the course of obtaining normal tissues from captured armadillos, some animals were found to be infected with acid-fast bacilli similar to Mycobacterium leprae. These findings caused considerable public and scientific controversy in America. The possibilities of an infected animal escaping from the experimental farm, insect vectors or healthy animals scavenging on dead animals were all proposed to explain the transmission of leprosy disease to armadillos.

Unfortunately, some sceptics questioned the validity of experimental infection of armadillos with M. leprae and suggested that the Louisiana workers were detecting the indigenous disease. This view has not prevailed. USPHS banished Storrs from leprosy research before this controversy was resolved. Yet, her discovery revolutionized research on all aspects of the disease. A few armadillos can supply enough of the once scarce reagent, lepromin, to meet the world’s needs. NIH has funded a program top map the genome of the leprosy bacillus. Trials are in progress on 470,000 people in India, Malawi, and Venezuela on armadillo-derived vaccines. A recent WHO report describes a broad spectrum of programs in immunology and biochemistry made possible by her vision. Storrs also dispelled an ancient stigma. Her finding of leprosy in wild armadillos, stilled those who claimed leprosy was a curse of God, visited only on sinners. Hansen’s name is attached to the Armauer Hansen Reasearch Institute in Addis Ababa in Ethiopia, which was established by the Norwegian and Swedish Save the Children foundation.

Today the University of Bergen is the main financial supporter of the institute, which does basic research on lepra, particularly its immunology. Attached to the Institute is a village of cured lepers, whose stigma makes it impossible for them to return to their own villages. During a visit to the institute in 1980, the editor of this dictionary experienced a moment of happiness for two elderly men. After they hade been through their cure, which included operations, the doctor had ordered them to retrain the muscles of their face. This they did by making faces at each other in a mirror. Unfortunately, the opportunity knox agent was not there. And: next time you are in Baton Rouge, Louisiana, USA, visit The National Hansen’s Disease museum. We thank Patrick Jucker-Kupper, Switzerland, for information submitted. Dr Gerhard Armauer Hansen | International Leprosy Association - History of Leprosy International Leprosy Association - Norway Notes Gerhard Armauer Hansen (29 July 1841 – 12 February 1912) was a Norwegian physician known for his discovery of Mycobacterium leprae, the bacterium that causes leprosy (sometimes called Hansen’s bacillus).

Hansen was born in Bergen, Norway, and studied medicine at the University of Christiana (now University of Oslo), graduating with honours in 1866. He completed his internship at the National Hospital in Christiania (Rikshospitalet), and afterwards briefly served as a doctor to the fishermen who worked in the Lofoten archipelago. In 1868 Hansen returned to his native town of Bergen, which was centre of European leprosy research. At this time, Norway had around 3000 leprosy patients, more than any other European country, and the disease was most concentrated in Bergen, which had three leprosy hospitals. Hansen initially worked in Pleiestiftelsen for spedalske nr 1 , but soon moved on to the position of assistant physician at the Lungegaardshospitalet , where he worked under Dr Daniel Cornelius Danielssen, a foremost authority on the clinical and pathological aspects of the disease. With C W Boeck, Danielssen in 1847 had published the major work Om Spedalskhed (On Leprosy); he had also helped to organise Bergen's leprosy care program.

While Danielssen regarded leprosy as hereditary, Hansen was convinced that a bacterium carried the disease from person to person; a daring speculation at a time when the concept of contagion was still poorly understood, and no one had shown that bacteria could cause human diseases. In his first work of 1869, published in Norwegian only in 1871, Hansen among other things described the appearance of leprous changes in lymphoid tissue. Here Hansen applies the term ‘infectionsstoff” (‘infectious substance’) for the changes he saw in association with lymph nodes. He was, however, uncertain about what these findings really meant. His poor equipment complicated his work, and he was unsuccessful in his attempts to cultivate and stain the changes. In 1870 a grant allowed Hansen to travel to Bonn and later to Vienna for advanced training in histopathology. Returning to Norway, using primitive staining methods and working with biopsy specimens from patients with leprosy, Hansen continued his intensive microscopy work. On his return to Bergen in 1871, Hansen launched his search for the causative agent of leprosy, using biopsy specimens drawn from patients.

Hansen decided to look for bacteria in patients, first in blood and, on finding none, in skin nodules. He wrote: ‘At that time ... I could sit tirelessly for hours on end, focusing through the microscope with great enlargement ... One day I was positive I had discovered the bacteria, the next day magnificent certainty had collapsed, and I would be back where I started ... Finally, though, I wrote the first record of my research.’ In 1873, aged 32 years, Hansen re-examined leprous skin nodules and discovered the rod-like bodies inside cells that looked like bacteria; they were not present in all cells, but in most of them. He believed these bodies to be the causative agent of leprosy and thereby became the first to suggest that microorganisms might cause a human disease.

He published his findings in an 88-page monograph in 1874, but remained cautious: he wrote, ‘Though unable to discover any difference between these bodies and true bacteria, I will not venture to declare them to be identical.’ Hansen’s hesitance to claim that the rod-shaped bodies were actually bacteria would later cause problems: in 1879, Albert Neisser attempted to claim discovery of the leprosy bacillus, using material he obtained from Hansen during a visit to Bergen. Hansen was outraged, and updated his original report to publish new articles simultaneously in English, German, and Norwegian journals in 1880, establishing his priority in the discovery. In recognition of his discovery, Hansen was appointed Chief Medical Officer for Leprosy in Norway in 1875. He believed that the isolation of leprosy patients was crucial to stop the spread of the disease, and he developed a series of laws to put such a system into effect in Norway. An 1877 law required impoverished people with leprosy to be isolated in special homes instead of travelling from place to place in search of aid.

A second law, passed in 1885, was much more widespread, requiring all people with leprosy to be isolated from their communities and families (except for spouses). Many in the medical community were not firmly convinced that leprosy was contagious, and protested the laws as inhumane. However, opposition decreased as leprosy began to decline in Norway. Many other countries soon adopted similar laws. Because the hypothesis that leprosy was contagious, as opposed to hereditary, was still unproven, Hansen conducted a study among emigrants to the United States who had leprosy. He observed that none of the subjects’ descendants developed leprosy; in combination with his discovery of the leprosy bacillus, this allowed him to establish that leprosy is a contagious disease. He presented these findings at the first International Leprosy Conference in Berlin in 1897. Hansen's discovery of Mycobacterium leprae was historic for reasons beyond its significance to the fight against leprosy.

As the first identification of a bacteria as the causative agent of a human disease, his study was a precursor to Robert Koch's conclusive demonstration of the bacterial cause of anthrax in 1875, and the tuberculosis bacillus in 1882. Although Hansen was never able to cultivate the leprosy bacillus in vitro as an experimental confirmation of his hypothesis, it has still not been done. His research helped to establish fundamental principles in immunology, bacteriological medicine and public health policy. Hansen married Stephanie Marie, the daughter of his mentor, Daniel Danielssen, in 1873, but she died of tuberculosis the same year. He remarried in 1875. Hansen died of a heart attack in 1912. In his honour, leprosy is sometimes referred to as Hansen’s disease. Sources: Grzybowski, Andrzej, Guido Kluxen, and Klaudia Półtorak. "Gerhard Henrik Armauer Hansen (1841–1912) – 100 years Anniversary Tribute." Acta Ophthalmologica 92.3 (2014): 296-300.

Web. Jay, Venita. "The Legacy of Armauer Hansen." Archives of pathology & laboratory medicine 124.4 (2000): 496-7. Web. Marmor, Michael F. "The Ophthalmic Trials of G. H. A. Hansen." Survey of Ophthalmology 47.3 (2002): 275-87. Web. Schmidt, Mathias. "The 100th Anniversary of Armauer Hansen's (1841-1912) Death." Leprosy review 83.4 (2012): 408. Web. Publications Causes Of Leprosy Disease - Doctor answers on HealthTap Dr. Heidi Fowler Dr. Fowler 2 doctors agreed: Leprosy: Per WHO- Leprosy in endemic in 91 countries. Over 50% of Leprosy in the world is centered in India. There are areas of high prevalence within Nepal, Burma, Brazil, Tanzania, Madagascar & Mozambique. There are about 6,500 people w Leprosy in the US.

In 2009 there were 213 new US cases. Most new cases are in: California, Florida, Hawaii, Louisiana, Massachusetts, New York & Texas. Leprosy may be > ...Read more What is the Cause of Leprosy What is the Cause of Leprosy 05 Mar, 2012 Health 0 Leprosy, also known as Hansen’s disease after the physician who identified the cause, is a disease that is best known for causing skin lesions that often appear as deformations or growths. If it is untreated the disease commonly progresses and leads to permanent disfiguration and damage to the eyes, skin, nerves and limbs. Evidence for this disease dates back to at least 4000 years ago and it has affected many people and civilizations through the years. Leprosy drugs are now available to cure this disease, but in the past those suffering leprosy were quarantined or segregated in leper colonies and some of these still exist today. What causes leprosy? Although the disease is ancient the cause of leprosy wasn’t discovered until 1873 when Norwegian physician G. H.

Armauer Hansen discovered a bacteria called Mycobacterium leprae (also known as Hansen’s coccus spirilly). This was the first time a bacteria was shown to cause disease in humans. In 2008 a new species of bacteria, called Mycobacterium lepromatosis, that also causes leprosy was discovered. It is a separate, but closely related species to the previously discovered bacteria. It is known to cause a type of leprosy called diffuse Lepromatous leprosy, which is most commonly found in the Caribbean and Mexico. The transmission of the disease is still not very well known, but most experts think that it is passed through respiratory droplets. The disease has a varied incubation period, from a few weeks through to 30 years. Did you know? It has been shown that leprosy can be passed onto humans by armadillos! It is estimated that 95% of the population is naturally immune to the disease. Related Articles Leprosy - Rising Star Outreach - Medical Care India MY DONATIONS About Leprosy In India, there are an estimated one million cases of Leprosy.

While many of these cases include patients who no longer have active Leprosy, the stigma and complications from the disease continue to consign them to a life of deplorable conditions. While the prevalence rate in Tamilnadu is lower than the national average, it still merits attention in light of the dreadful nature of the disease. Studies have indicated that the mortality rate among lepromatous patients can be four times higher than the general population, although Leprosy itself is rarely the direct cause of death. Unlike many other widespread diseases, Leprosy also comes attached to a social stigma. The term leprosy originates from the Latin word lepros, meaning defilement. Due to the deforming effects of the disease, its victims are readily identifiable by society. And even in today's world of science and information, lepromatous patients are commonly believed to be incurable, resulting in severe social discrimination. The lasting physical and social effects of the disease result in double suffering by its unfortunate victims. Leprosy has existed for thousands of years, dating back to the earliest civilizations of China, Egypt and India. From as early as 600 B.C.

there is evidence of Chaulmoogra Oil (a tree found in Eastern India) being used to ameliorate symptoms of the disease. Written accounts are common in ancient literature such as the Bible, and even earlier in Susrutha, regarded as the first Indian book on surgery, dating back to 400 B.C. The cause of Leprosy was not discovered until 1873 by a Norwegian scientist named G.H Armauer Hansen. Until that time, most experts on the subject considered leprosy to be a hereditary disease. However, Hansen suspected its cause to be a specific, contagious agent and, with this in mind, set out to study individual leprosy patients. He decided to first look for variations in the blood of his patients. Finding nothing, he moved on to examine his patients skin cells. Here, he discovered a foreign bacterium not found in uninfected skin cells. After prolonged studies, these were found to be the cause of Leprosy, now known as Hansen's Disease. After Hansen's discovery, it took science over 70 years for medicine to develop a cure in a drug known as Diamino Diphenyl Sulphone (Dapsone DDS).

In 1946 Dr. Robert Cochrane successfully treated an Indian patient with the drug by an intramuscular injection. Though the use of Dapsone was effective in fighting Leprosy, further study showed that it had two disadvantages: 1) prolonged use can cause anemia, and 2) it does not actually kill the bacterium, but only stops its multiplication. Finally, the discovery of Dapsone-resistant bacteria heightened the need for a new drug. In the early 1960s two doctors experimenting in Nigeria found a drug named Clofazamine to be useful in treating lepromatous patients. While the drug has none of the disadvantages of Dapsone, it is classified as a dye and can lead to skin discoloration as well as ocular pigmentation. While the advancement of science yielded the discovery of more effective medicines, it also revealed various forms of the disease. It was obvious that no one drug was totally effective against each variation. So in the 1970s medical facilities began employing a multi-drug therapy for many of the patients.

Depending on the type of Leprosy and the progression of the disease within the patient, treatment is currently prescribed with a combination of several possible drugs. Some of these, such as Dapsone, Clofazamine and Thalidomide, may also be effective by themselves. Other drugs, like Rifampicin, Ofloxacin, Minocycline and Tetracycline, must be used in combination. After receiving treatment for three months, a Leprosy patient is normally considered non-infective to others. The danger of that person spreading the disease becomes null, regardless of the stage of progression at which the disease was diagnosed and treatment was started. If the patient has developed deformities before treatment was started, those deformities can be corrected only by surgery. If the treatment is begun before deformities develop, the condition can be completed cured without leaving any visible evidence on the body. The cause of Leprosy is a biological agent called Mycobacterium leprae. As indicated by the name, this bacterium resides in masses within the bodys lepra cells (in the lungs, the liver and the nervous system) during leprous inflammatory reactions.

Leprosy manifests itself in two immunological stages: Multibacillary or Lepromatous Leprosy, which affects the skin and organs, is at the infectious end of the scale; and Paucibacilliary or Tuberculoid Leprosy, primarily affecting the nerves, is non-infectious. Within these two classifications, there are also several sub-classes, which facilitate diagnosis and treatment. Generally, one or more of the following symptoms may characterize the disease : •Hypo-pigmented patches The discovery of Mycobacterium leprae. A medical achievement in the light of evolving scientific methods. - PubMed - NCBI The discovery of Mycobacterium leprae. A medical achievement in the light of evolving scientific methods. Irgens LM . Abstract The discovery of M. leprae by G. H. Armauer Hansen (1841-1912) in 1873 represents a link in a chain of development in international medicine that was influenced by two main concepts, namely, that germs may be causes of disease and that social conditions may be related to disease, either as causes or consequences or both.

Hansen's work is also a link in a chain of research on leprosy in Norway. Hansen met with serious challenges in addition to those that were purely scientific. To prove the causative effect of the microorganism according to principles that later came to be known as Koch's postulates, Hansen felt compelled to conduct experiments that were deemed illegal by the authorities. At the same time, he was fighting to establish priority for his discovery. Later, Hansen was honored as the discoverer of the bacillus of leprosy and was privileged to see benefits in the public health as a consequence of the discovery. Hansen's epoch-making achievements may serve as an inspiration to all who aspire to combat disease by seeking answers to questions about causes of disease, modes of prevention, and social consequences of disease. PMID:

Question: G. H. Armauer Hansen discovered the cause of what disease in 1873?
Answer: Leprosy