"Leprosy and the Modern Plague" by Annie Albright
The urban streets of Madurai, a temple city in central Tamil Nadu, India, are overflowing; auto-rickshaws, stands overladen with mangoes and pomegranates, businessmen burden with briefcases and papers, women garlanded with strands of sweet, pungent jasmine flowers, and intermittent herds of cows, goats, and chickens all spill from the various side streets into the dried up Vaigai river that bisects the town, in a scene of commotion incarnate
Just 30 miles south-east of the city, however, stands a compound- a colorless splotch in the center of an otherwise vibrant tapestry- where the chaos gives way to quiet and sterility. Coating the compound walls is a curious, tin-scented yellow dust; turmeric powder, a natural antiseptic. This is the Mission Leprosy Hospital, Manamadurai.
Leprosy is a disease of dichotomies. It is simultaneously ancient and contemporary, disfiguring and inconspicuous, and infamous for its communicability, though the contagion, Mycobacterium Leprae, is really quite reserved in its spread.
Stereotypical leprosy presents with the appearance of pigmentless spots, or lesions, on the skin. It was these lesions that denoted “lepers” in the biblical era, though this characterization was unfortunate, because the lesions, like so much associated with the disease, have no uniform identity; they may be sunken or raised, splotchy or defined; they may not be pigmentless at all, but red or copper-colored. This variability adds to the difficulty of diagnosing leprosy. Further complicating the issue, are the two subsets of leprosy, tuberculoid and lepromatous, which have differing pathologies and prognoses, with the latter posing a far more lethal threat.
Leprosy is associated with the invasion of Mycobacterium Leprae into human macrophages and Schwann cells. Whether the disease will develop, and which subset path it will take, is dependent on the bacteria’s ability to trigger a specific immune response in its host. Infected macrophages in a host are immediately tagged with an antigen that is then recognized by an undifferentiated CD4 helper T cell. The differentiation of this helper T cell into either T-helper1 (tuberculoid) or T-helper2 (lepromatous) determines the path of the disease, and this immune response produces the peripheral neuropathy and nerve degeneration characteristic of the malady. For this reason, leprosy susceptibility has a significant but poorly understood genetic component likely related to the Human Leukocyte Antigen (HLA) genes, including the DRB1, DQA1, DQB1, and DQ promoters. Both successful infection and the disease progression are fostered by malnutrition and a compromised immune system; in fact, such environmental factors might be essential to the development of leprotic symptoms.
Far from being the wildly contagious blight as it has historically been cast, our modern understanding of immunobiology reveals leprosy to be a relatively incommunicable disease, which poses little to no threat from simple skin-to-skin contact or brief exposure. This has presumably always been the case- and yet, for the past two-thousand years, it has been viewed as necessary to separate, isolate, and ostracize lepers from greater society. Even today, though patients at the Mission Leprosy Hospital in Manamadurai aren’t explicitly forced to reside within the compound, the stigma they face outside of its walls, and rejection from their families and community hold many of the inmates within the hospital as effectively as bars.
Few diseases conjure up as strong an intrinsic sense of repulsion as leprosy. In light of the recent Ebola epidemic, and the anxiety it has stirred up in the United States population, it is interesting to consider what turns an infectious disease- something which can be remediated and cured- into a “plague,”- something virulent and lethal- in the eyes of the public. While the term “plague,” originally referred only to the deadly, infectious disease caused by the bacteria Yersinia Pestis, in the twenty first century it has taken on a new meaning. There are several contributing factors that together constitute the parameters of a modern plague.
One such aspect is the ability of a disease to disfigure or disable. Smallpox, for instance, is infamous for the pitted, granular scars it left on its survivors, frequently on highly visible areas such as the hands and feet. Leprosy’s potential to disfigure, usually through amputation of extremities or limbs has long been a hallmark of the disease. The mechanism of peripheral neuropathy that leads to ulceration and ultimately amputation in leprosy patients is not unique to the leprotic condition it functions in the exact same way as that in diabetes patients. There are 62 million diabetics in India; there are also 134,000 new leprosy patients a year.[4,5]
In considering the implications of the infamous and storied medical history of leprosy we readily see that lepers have long been ostracized and isolated from their communities, in most cases cruelly and unnecessarily. The legacy of this stigma is difficult to escape. “Hansen's disease is still called kusht in most Indian languages, as it was in the sixth century during Sushrutha the Indian Hippocrate’s time. Even Mohandas “Mahatma” Gandhi's efforts to destigmatize the disease fell short”. Mental disorders face an equal stigma to that leveled against lepers. Some, such as schizophrenia, bipolar disorder, and depression, inspire prejudice. Others engender intense fear; according to Alzheimers.org, a recent poll conducted by Home Instead of Senior Care found that Americans across all age groups are more afraid of developing Alzheimer’s than heart disease, stroke, or cancer.
Intimately tied to the stigma surrounding both leprosy and mental illness is the fear of the unknown; while leprosy is the oldest recorded human disease, and the discovery of its pathology and causal agent Mycobacterium Leprae was made in 1873, M. Leprae is one of the only human disease-causing bacterium that has never been cultured in the lab.[1,3] As discussed above, very little is known about its method of infection, beyond the fact it is minimally communicable. Ebola poses a similar enigma; its animal vector is unknown and its mutagenic potential is theoretically boundless. Similarly the brain and its pathophysiology continue to be counted among science’s greatest mysteries.
“Fear is a contagious disease, spreading from its first victim to others in the vicinity until it is powerful enough to take charge of a group, in which event it becomes panic.” - Ernest Gann
The fear of disease has its own symptoms and pathology. For all our fear of the unknown it is the specter we recognize we seem to fear most. The term “plague” engenders fear far greater than does “Yersinia pestis”. Similarly leprosy is much less intrinsically frightening than Hansen’s disease (the name given to the condition in the 19th century in an attempt to change public perception). The recent incidence of the Ebola virus in the United States and the media coverage that turned it into a household name that in addition to the very real threat posed by the virus, has spurred the onset of an even more resistant pathogen: panic.
 Jacob, Jesse T. and Carlos Franco-Paredes. 2008. “The Stigmatization of Leprosy in India and Its Impact on Future Approaches to Elimination and Control.” PLoS Negl Trop Dis 2(1): e113. Accessed November 2th, 2014. doi:10.1371/journal.pntd.0000113
 Fitness, J, and K Tosh and AVS Hill. 2002. “Genetics of susceptibility to leprosy.” Nature 3:441-453. Accessed November 25th, 2014. doi:10.1038/sj.gene. 363926
 Luka, Edward E. 2010. “Understanding the Stigma of Leprosy” South Sudan Medical Journal. Accessed November 25th, 2014.
 Kaveeshwar, Seema Abhijeet and Jon Cornwall. 2014. “The current state of diabetes mellitus in India.” Australas Med 7(1): 45-48. Accessed November 25th, 2014. doi: 10.4066/AMJ.2013.1979
 “Global leprosy: update on the 2012 situation.” World Health Organization Weekly epidemiological records 35:365-380. Accessed November 25th, 2014.
 Sartoris, Norman. 2007. “Stigmatized Illnesses and Health Care” Croat Med J 48(3): 396-397. Accessed November 25th, 2014