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Leprosy is literally an ancient disease, one that has been around several millennia beginning with the Ancient Greek and Egyptian civilization. To garner a better idea of what the current status of the leprosy is in this day and age, it is necessary to investigate the evolutionary background of this disease to gain a better understanding from where it came from, and how it evolved into the disease it is today. Gordon Grice (2000), author of "Where Leprosy Lurks", an article in the November 2000 issue of Discover Magazine, believed that the oldest evidence of Leprosy dated back to the skulls of four Egyptians that were discovered in second century B.C. This finding is shared by Dr. Grimm (2005), who as the author of "The Global Spread of Leprosy Tied to Human Migration, used a comparative study on different strains of leprosy worldwide to show that the origin of Leprosy was centered around East Africa near Mesopotamia and present-day Egypt. With the advent of paleopathological technology, more and more of these findings are being excavated as DNA bone analysis can search for the detection of leprosy in past civilizations, such as the recently excavated site in the Hinnom Valley of Jerusalem that is over two thousand years old. This finding, which is one of the first complete skeletal body's of a Leprosy-stricken individual, is only possible because the disease produces visible changes to the skeleton (Weizmann, 2003). Even the Bible's Old Testament makes references to a sinful, hereditary disease translated as leprosy, although there is still much disagreement to whether these references are specific to leprosy or other skin diseases such as smallpox (White, 2009; 9).
According to Grice (2000), the spread of the disease to other parts of the world was heavily aided by the major conquests of empires such as that of Alexander the Great, who conquered East Africa and the Middle East and brought the disease back to Greece along with various spices and silks. From Greece, the disease spread around the Mediterranean basin as Romans introduced it into Western Europe (Grice, 2000). Over time, this process was further carried out as war, trade, and colonialism established a complex route of transmission for leprosy that involved the migration and influx of many people in many different parts of the world. Throughout Africa, Europe, and parts of Asia, where much of the leprosy was still centered around, much stigma developed around people affected with disease, who were often persecuted and isolated from the rest of the community based on their condition, giving rise to the term "lepers" (White, 2009; 10). For example, during the Middle Ages, many Leprosy-stricken individuals were forced to inhabit isolated leper colonies that were established on remote islands far away from densely populated communities (White, 2009; 10). Furthermore, during the colonial era, many European missionaries believed that a degree of shame should be put on the disease because it was considered unholy (Vaughan, 1991).
While there is no credible evidence that to show that these leper communities passed on the disease through genetic clustering, the disease was labeled as hereditary during this time as it was believed that relatives of lepers were more likely than to catch the disease than anyone else (Grice, 2000). This theory was abandoned when in 1870, Christian missionary Father Damien, caught the disease while working with Lepers on the Hawaii Island of Molokai, despite having a family background that contain history of leprosy (Grice, 2000). This lead to a severe scare among European societies as many people though the disease was so contagious that that one could contract leprosy from just standing next to some one else. Although, this far-fetched assumption was put to rest in 1873, when Norwegian doctor Armauer Hanson, discovered that the disease was caused by a source of bacteria known as Mycobacterium leprae (Grice, 2000). No cure for leprosy was known until the 1940 when Dr. Guy Faget, a physician at Carville Treatment Center, a specialized institution designed for leprosy patients in the U.S., discovered that sulfone drugs were successful in killing the bacillus (White, 2009; 10). This treatment was used solely until M. leprae began to grow resistant to dapsone, a sulfone derivative. This prompted the usage of multidrug therapy, which began in 1981 when it was administered by the WHO using a combination of dapsone, clofazimine, and rifampcin (White, 2009; 10). After the real source of the disease was identified, the real question that has been consistently asked about leprosy is why the disease continued to spread in particular areas over time. Take for instance the United States, which for the past ten years, has maintained its Leprosy count at around 6,500 cases, and has only had approximately 35-50 new cases a year, most newly admitted immigrants, while India and Brazil, the two countries with the highest leprosy rates respectively, contain approximately 150,000 cases between the two of them, out of a total of 211,903 worldwide cases (World Health Organization, 2010).
Etiology/ Symptoms of Leprosy
Before constructing an evolutionary framework to why humans are vulnerable to leprosy, it is necessary to fully understand the causes of the disease that give rise to the overall biomedical characteristics of leprosy. According to Cassandra White (2009), the author of An Uncertain Cure: Living with Leprosy in Brazil, leprosy is caused by an infection of the rod-shaped bacteria Mycobacterium leprae. The most familiar symptoms of leprosy, that has publicized its classification for hundreds of years, are the appearance of one or more lesions on the skin. Marcia Gaudet (2009), the author of the groundbreaking book Carville: Remembering Leprosy in America, concludes that one of the major misconceptions of leprosy is that there is a immediate loss of limbs, but this is not true as untreated leprosy initially starts out by the bacilli causing nerve damage in the body ultimately results in loss of muscle control, and above all else, skin lesions. Most of these skin patches are not painful, and disease can be dormant for months and years as it grows very slowly compared to other bacteria (doubles every 14 days), which is why it is very common for physicians and patients themselves to overlook the initial symptoms. Gaudet (2004) explains that it is possible for an individual under drug therapy to show no signs of the disease for as long as 10 years.
While the cause of the disease is known throughout the medical community, there is still quite some debate on how the transmission of the leprosy occurs, and more importantly how an individuals immunological activity plays a part in his or her response to the disease (White, 2009; 7). The current biomedical of leprosy transmission states that it is primarily based in the respiratory, and is passed from person to person through the emission of nasal droplets when one sneezes or coughs (White, 2009; 7). Once it enters the body, the bacilli attack the peripheral nervous system, consequently damaging nerve endings, which leads to reduced sensitivity and numbness the body's extremities (White, 2009; 7). As a result, a person afflicted with leprosy could further complicate his or her condition by walking around barefoot and exposing himself or herself to infections through open wounds. Unfortunately, once leprosy is left untreated early in its conception, it can result in more severe complications, primarily the deformity of limbs that include the "claw hand", where the fingers become paralyzed in a claw-like position, "penciling", which give the hands and feet a shrunken and swollen appearance, and eventually the deterioration of limbs and outward body parts (White, 2009; 7). In many parts of Africa, leprosy is referred to as "leonine", which translates to "lion face" because the bacilli can localize in the forehead and give the outward appearance of lion's facial appearance (White, 2009; 8). Leprosy can also cause destruction of nasal bones, cartilage, particularly the eyes and the areas surrounding. Dr. Brand and Dr. Yancey (1993), authors of Pain: The Gift Nobody Wants, concluded that until a decade ago, leprosy was the leading cause of blindness worldwide as the disease's bacilli accumulate in the cornea and cause major damage in the cataracts. Leprosy patients in advance stages may also lose their eyebrows/eyelashes and commonly suffer from anesthesia in the eyes causing serious damage and infections from constant rubbing (White, 2009; 8).
Proximate Explanation: Immunological Response of Leprosy
There has been quite some debates as to what is the exact source of a immune response to leprosy as it may occur before, during, or after treatment of the disease (White, 2009; 9). Dr. Paul Saunderson (2002), a key WHO consultant on leprosy, estimated that 25-30% of leprosy patients experience an immunological reaction that is characterized by fever, pain, and the inflammation of preexisting skin patches. These responses are known as type 1 reactions because they result from an spontaneous increase in cell-mediated immunity, which becomes activated when the invading bacilli and their antigens stimulate specific defense cells, which then attack the antigens, producing a inflammatory response (White, 2009; 9). In the case of leprosy, these special cells are lymphocytes that accumulate around the peripheral nerves, particularly in the nerve's Schwann cell (White, 2009; 9). The lymphocytes main function is to secrete certain chemicals that attract larger macrophages to the antigen build-up site, and assist the macrophages in digesting the bacilli since they cannot actually perform phagocytosis themselves. The bacilli have significant affinity to cooler areas of the body such as the peripheral nerves, which is why deformities in the extremities are the most distinct symptom among leprosy-stricken individuals.
Type 2 reactions of leprosy are inflammatory responses that are more comprehensive in their mechanisms and interactions within the body. It mediates a humoral immunity, which is also known as antibody mediated immunity, because it involves generating certain antibodies that aim to destroy foreign antigens that invade the immune system. While humoral immunity is particularly effective in fighting various forms of pathogens, it uncharacteristically has little effect against M. leprae as it has shown to cause erythema nodosum leprosum (ENL), which cause painful papules that gave rise to conditions such as neuritis, lymphadenitis, orchitis, arthritis, and glomerulonephritis. These are all severe conditions that affect the joints of the body.
Both the type 1 and type 2 inflammatory immune system reactions form the basis of the two main forms of leprosy: multibaccillary and paucibaccillary, which are based on the number skin lesion they contain (White, 2009; 11). Paucibaccillary, which is classified under tuberculoid leprosy, contains less than five skin lesions, while multibaccillary, which is categorized as lepromatous leprosy, has more than six skin lesions (World Health Organization, 2010). Lepromatous leprosy is the most contagious form of the disease because individuals who have it contain a weaker immune response, and as a result, their bodies are unable to stop the proliferation of bacilli, which results in them exhaling it in the environment (Scollard, 2004). Tuberculoid leprosy, on the other hand, is characterized by a stronger cell-mediated response that allows individuals with it to fight the bacilli so that they don't persist in the body. This form is much less milder, less contagious, and unfortunately less common because of its passivity (Scollard, 2004).
Ultimate Explanation: Why We Are Vulnerable to Leprosy
Based on what has been discussed about history, epidemiology, etiology, and immunology of leprosy, the question still remains as to why we are still vulnerable to leprosy in a world filled with new medical innovations and treatments. While there are many different avenues that lead into this question, the most important is why leprosy rates have increased and become endemic in the developing countries of Asia, Africa, and Latin America, while rates have declined in the U.S. and Europe? What evolutionary pathways give rise to this phenomenon? Why are there are more new cases discovered in countries such as India, Brazil, Indonesia, Tanzania, and South Africa than in the America, the U.K., and other parts of Western Europe?
To uncover this mystery, many scientists have tried to manipulate M. Leprae in the laboratory, but the bacilli cannot be kept alive inside a dish since it starts to die when it is extracted out of human tissue. Dr. Han et al, a leprosy researcher at the National Allergy and Infectious Disease Institute, proposed that the reason that these mycobacteria cannot be cultured in the lab is because they lost the genes necessary to survive outside their host, a process he refers to as reductive evolution (Han et al, 2008). As a result, much of the leprosy research conducted in the past was difficult to investigate in the lab. Although, these studies became possible after it was found that armadillos could be easily infected by the disease, and were able to propagate large amounts of it (Grice, 2000). Dr. Han et al also concluded that one of the reasons why leprosy has been so puzzling to study is because the various strains that have collected worldwide are almost nearly identical, yet in the lab, the disease varies greatly from person to person in different geographic locations (Han et al, 2008). This suggests that individual's host immune factors play a significant role in how the disease progresses within the human body (Han et al, 2008).
Groundbreaking research findings such as Han's et al refocuses the discussion of leprosy's pathogenicity on cell-mediated leprosy immunity, which as noted earlier, is a vital defense needed to protect individuals against leprosy. Fortunately, approximately 90% of the human race has cell-mediated immunity in varying degrees, which has led researchers and evolutionary biologists to believe that people who develop leprosy have a certain genetic predisposition to the leprosy because they do not have the innate immunological defenses that provides them the ability to fight off the disease and prevent it from worsening (Comeu, 2003). This genetic predisposition has been synonymous with researchers around the world, particularly McGill University's leading genetic scientists Erwin Scharr and Tom Hudson. Scharr and Hudson, with the help of a team of researchers, who were successfully able to isolate a section in human chromosome 6 that has shown to make people more vulnerable to leprosy (Comeu, 2003). Schurr (2003) lead the team to a number of countries such as India, Brazil, and Ethiopia to collect DNA samples from members of affected families and individuals. While the actual gene has not been identified yet, Schurr and Hudson found that a specific area on chromosome 6 contains genetic information that houses M. leprae and provides it a friendly environment, essentially providing a selection for the pathogen comparison to other bacteria (Comeu, 2003). The research team used gene mapping techniques to look for common similarities in genetic makeup between families affected with leprosy. They noticed that brothers and sisters who were both afflicted with leprosy has shown to inherit the same pieces of chromosome 6, and since siblings share 50% of the same genes, the correlation heredity and leprosy became very plausible (Comeu, 2003).
More importantly, Hudson (2003), who is also the director of McGill's Genomic Innovation center, believes that the gene is a mutant version of a healthy gene carried by humans, "People at the McGill Center for Host Resistance have been working for two decades to show that we get infectious diseases not just because of bugs, but also because of genes that make us susceptible (Comeu, 2003)." So if there is a gene that is responsible for increasing an individual's likelihood to get leprosy, then why does it continue to persist? While the answer is still unknown, Dr. Randolph Nesse and Dr. George Williams, authors of Why We Get Sick and sculptors of various evolutionary theories on the vulnerability of disease, providing an ultimate explanation on the evolutionary significance of mutant genes such as the ones identified in Scharr and Hudson's comparative leprosy study. Nesse and Williams argue that because natural selection selects for reproductive success, and not health, a faulty gene may remain common if it does not decrease the average number of offspring, even if it may cause debilitating effects (Nesse & Williams, 1994). Such is the case of leprosy, because it exists in multiple forms and is only considered fatal if it progresses into the later stages of its disease cycle, which can go unnoticeable for many years as leprosy has a long incubation period. As a result, an individual could pass his or her mutant gene to the offspring before they even know they are diagnosed with the disease. Thus, if a gene still manages to increase the rate of reproduction, it will spread by the forces of balancing selection. While it is still uncertain why leprosy continues to increase every year in developing countries such as India and Brazil, and not in developed areas such as North America and Europe, the gene pathway proposed by Nesse and Williams gives an evolutionary insight as to why leprosy still continues to pervade throughout the developing world.