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University of Toronto Scarborough
Health Studies
Caroline Barakat

PLAGUES AND PEOPLE LEC 3 – Hansen’s disease – Leprosy arose in far east about 1400 BC earliest account of leprosy occur in Indian text written between 600 and 400 BC Nei Chang (textbook of medicines) describes: patient has stiff joints, the eyebrows and beard fall off, flesh becomes nodular and ulcerates, numbness results, and bridge of the nose changes colour and rots claimed that leprosy was brought from India to Greece in fourth century by soldiers but also possible that leprosy spread from the far east to the west along the trade routes arriving in Mediterranean about the time of Christ th th leprosy spread from Spain and Africa to the Americas in 16 and 17 centuries in the middle ages, the disease was considered sinfulness stigmatized the leper. Medieval medical authors refer to lepers as being crafty irascible and suspicious, above all having a desire for lustful sex - was known as satyriasis – an insatiable sexual appetite the disfigurement of the face and hands contributed to the alienation of the leper, and the sores on the body led to the belief that leprosy was contagious. -lepers were not considered nice people, and they were cast out of society th pandemic leprosy reached epidemic proportions in the 12 century and has its peak in Europe in the 13 and 14 centuries -19,000 lazarets document this increase in leprosy in Europe -by 18 century, they all had disappeared has been hypothesized that the increased supplies of wool clothing have reduced the chain of skin-to- skin contact needed for the spread of the disease and contributed to typhus The Disease of Leprosy first leprosy came in 1873 with the discovery of the leprosy bacillus, Mycobacterium leprae, by Gerhard Amauer Hansen (1841-1912) in Norway an acid-fast bacillus -but it cannot be grown in tissue culture and it grows very slowly and only in humans, mice, and nine- banded armadillos, taking about 2 weeks to divide (in the mouse, bacteria grows best in the footpad, at temperatures 30 degrees Celsius and as few as 1- 10 bacilli can initiate infection, but to get a million bacilli takes 5 to 6 months) (in the armadillo, the disease becomes disseminated, and one can get a billion bacilli in 15 months) no known vectors or reservoir hosts leprosy is a disease of low infectivity, and is also a spectral disease, meaning, showing different manifestations: -tuberculoid lepros, localized in skin nodules where bacteria may be abundant, and disseminated or lepromatous leprosy, with bacteria in macrophages and the skin most patients show the tubercloid type, which develops 1-2 years after exposure lepromatous leprosy requires longer periods manifestation depend on the immune status of host Tuberculoid leprosy is associated with severe nerve damage -the disease involves cell-mediated immunity with T-helper cells and interleukin-2 secretion in tuberculoid leprosy, but since the bacteria multiple within the Schwann cells that insulate the nerve, there is damage to the nerves, and anesthesia results. In lepromatous leprosy, the T-helper cells do not respond to the bacilli-gamma interferon is not produced, macrophages are not activated, as a consequence, the bacteria multiply within the macrophages and the disease spreads with multiple organ involvement, leading to facial deformity and blindness -there is osteoporosis and shortening of the digits death results most commonly from renal failure, pneumonia, and tuberculosis *Natural resistance to leprosy is highest in African blacks and lowest among Caucasians it is believed that after the bacteria enter the body via the nose or open wounds, they somehow find their way to the Schwann cells that surround the nerve cells - the affinity for Schwann cells by M.Leprae is due to the high affinity of the bacterium for a specific region of the molecule laminin found on the outer surface of these cells; once they adhere to the laminin using a bacterial surface protein called H1p, they invade -once in Schwann cell, they are protected from host’s immune system -overtime, however, the immune system attacks the infected Schwann cells, destroying nerves in the process Where Leprosy is found mostly in tropics fear of contagion, coupled with the possibility of disfigurement, has contributed to an acceptance of terrible cruelty towards lepers the higher of standard of living, the less the incidence of leprosy usually acquired in childhood, but infection can occur even at age 70 Leprosy Today because leprosy bacilli cannot be cultured in the laboratory, it is difficult to assess the onset of the disease diagnosis of leprosy relies on microscopic examination and evaluation of the response of the patient to a pinprick or heat newer methods, such as polymerase chain reaction, are being tested to detect the presence of M. Leprae nucleic acids Dapsone, made in 1940, controls the growth of the bacilli -interferes with the synthesis of bacterial nucleic acids by blocking the conversion of p-aminobenzoic acid to folic acid -Mycobacterium bovis BCG vaccination reduce leprosy incidences by 20% to 80% -1998, India approved leprosy vaccine, Leprovac, containing heat-killed, fast-growing, non-pathogenic mycobacterium called Mycobacterium w (mw) -Leprovac stimulates the immune system of patients by disrupti
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