AWARENESS DAY JANUARY 30TH
How Contagious is LeprosyJanuary 15, 2021 - Dr. Nita Sharma Nas
Nigella sativa is also known as black cumin, black seed, kalonji and haba al barakah. It is not also knows as black caraway as some sites states. There are more than 1000 peer reviews and as stated by our beloved Prophet Mohammad, PBUH, this seed should be used often as a cure for all disease,except death.
The Centers for Disease Control and Prevention (CDC) mentioned that 95% of the population in the USA develops immunity against leprosy-causing bacteria. [3] But still, the population belongs to many parts of the world to get significant health problems due to leprosy.
Leprosy primarily infects the skin tissue, peripheral nerves, bone, mucous membrane of the upper respiratory tract, eyes, testes and causes different symptoms. [4] In the past, isolation was the only measure to prevent the spreading of leprosy. [1] Therefore, we often found in history that communities, even family members, ostracized leprosy-affected patient/s. [2] In 1940, the pharmaceutical industry's discovery of sulfone gave relief from the isolation strategy as this medication had efficacy against leprosy. But in 1962, this drug was officially banned, and therefore isolation strategy again revived until mid of 1980. Leprosy patients had developed sulfone-resistance, and because of that, the World Health Organization (WHO). Therefore, since 1980, a multi-drug regimen has been introduced as a treatment strategy for leprosy. Leprosy patients are treated on an out-patient basis and cured after completion of the treatment regimen. [1] Pathophysiology of leprosy M. leprae commonly attacks different skin tissues like keratinocytes, macrophages, and histiocytes. Whereas Schwann cells present in the peripheral nerve is another favorite site of getting affected by M. leprae. However, Keratinocytes release peptide β-defensin, an antimicrobial against M. leprae antigens. But after penetrating M. leprae, the host cell interacts with lipid metabolism to adapt to the host cell. M. leprae is attached with the α-dystroglycan and ErbB2 receptors on the Schwann cell surface and interacts with α2-laminin and adhesins present in the basal lamina of the host cell. Once Schwann cells get affected with M. leprae, then the cells dedifferentiate into immature cells due to the activation of Erk1/2 pathway signaling. [1] The presence of bacilli of M. leprae in the skin leads to different dermatological changes, whereas nerve infection leads to sensory loss due to demyelination and axonal dysfunction. An aggravated condition causes disability and deformity. Inflammatory impact in the nerve cell due to leprosy is the primary contributor to degrative skin and nerve tissue changes.[4] How can a body protect Leprosy?
Leprosy alters bodily immune response. Leprosy patients often have high Th2 cytokines such as IL-4, IL-5, IL-10 levels, and low levels of Th1 cytokines, including IFNγ. The strong cellular immune response can restrict pathogenic growth and completely remove the bacilli, ultimately providing zero lesions. Interferon-γ has a natural defensive and cellular immunity mechanism as it acts as a major macrophage-activating cytokine against intracellular microbes, including M. leprae. Interferon-g increases the reactive oxygen and nitrogen intermediates production and subsequently stimulates macrophages to kill and restrict intracellular pathogens' growth. [5] |
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