Geographic latitude and socio-economic situations appeared to be the main causes of leprosy, and the healthcare condition was an important factor associated with leprosy incidence.
Only about 5 percent of all people are susceptible to the disease. More than one-half of new cases give no history of any known contact with a leprosy patient.
Paucibacillary: Fewer skin lesions. Single-lesion paucibacillary: Single skin lesion.
leprae, is characterized by nerve damage, disfiguring skin sores and progressive debilitation that affects various parts of the body. M. leprae is an intracellular bacterial pathogen that invades the Schwann cells of the PNS.
Mycobacterium leprae infects Schwann cells by binding to α-dystroglycan, causing sensory mononeuritis multiplex, a major complication of leprosy.
Leprosy can develop at any age but appears to develop most often in people aged 5 to 15 years or over 30. It is estimated that more than 95% of people who are infected with Mycobacterium leprae do not develop leprosy because their immune system fights off the infection.
The nose and skin are considered the main routes of M. leprae infection and transmission (3–5). Nasal mucosa involvement is observed in early leprosy even before lesions become apparent in the skin, nerves, and other parts of the body (6), suggesting that the airways are the primary infection sites.
Enlarged nerves below the skin and dark reddish skin patch overlying the nerves affected by the bacteria on the chest of a patient with Hansen's disease. This skin patch was numb when touched. Symptoms caused by the disease in the mucous membranes are: A stuffy nose.
It can affect the skin and the nerves of the hands and feet as well as the eyes and the lining of the nose. In some cases, leprosy can also affect other organs, such as the kidneys and testicles in men. If left untreated, leprosy can cause deformities of the hands and feet, blindness, and kidney failure.
mycolic acidsThe complex and unique cell wall that makes members of the genus Mycobacterium difficult to destroy is apparently also the reason for the extremely slow replication rate. Virulence factors include a waxy exterior coating, formed by the production of mycolic acids unique to Mycobacterium.
leprae to rely on the host cell to survive. The bacteria needs an extremely specific environment to thrive in. It is extremely difficult to culture Mycobacterium leprae. All attempts to create a medium that the bacteria are able to grow in has failed.
M. leprae primarily invades Schwann cells (SCs) in the peripheral nerves leading to nerve damage and the development of disabilities [2]. As described by Ridley and Jopling, disease classification is defined within two poles with transition between the clinical forms [3].
Infection of humans with Mycobacterium tuberculosis (Mtb) results in diverse outcomes that range from acute disease to establishment of persistence and to even clearance of the pathogen.
Tuberculosis, caused by the pathogen Mycobacterium tuberculosis (Mtb), is responsible for more than two million deaths worldwide every year ( W.H.O, 2014, Knechel, 2009 ). Rapid emergence of drug resistance has further compounded the problem ( Rowland, 2012 ).
The balance between lipid mediators during mycobacterial infection is of crucial importance in defining the outcome and severity of infection.
In an attempt to define the role of every single parameter on the overall system׳s dynamics an exploration of the parameter hyperspace was attempted locally, by varying each parameter over a ± 10 fold range.
In humans, sensitivity to M. tuberculosis (Mtb) infection can range from heightened susceptibility on the one hand, to marked resistance on the other. In between these two extremes is the condition of persistence where bacteria maintain at low levels in the host for extended periods of time ( Antia et al., 1996 ).
The relationship between host and pathogen during infection depends on a combination of host phenotype heterogeneity and pathogen׳s variable virulence. By varying the parameter values we could simulate how these interacting factors define the possible outcome of infection.
Globally, nearly 10 million new cases of tuberculosis (TB) resulting in 1.3 million deaths, are reported annually despite intensive global strategies to fight the TB epidemic ( 1, 2 ).
Participants aged 18–70 years diagnosed with pulmonary TB (PTB), extrapulmonary TB (EPTB) or latent TB infection (LTBI) were recruited from the Dep. of Infectious Diseases and Dep. of Pulmonary Medicine at the Oslo University Hospital into a prospective observational cohort study ( Prognostic Immunological markers in Tuberculosis ).
Thirty patients with TB disease (14 patients with EPTB and 16 patients with PTB) and 17 patients with LTBI, were included. Demographic and clinical variables of Mtb infected patients are listed in Table 1.
Several studies have emphasized the role of eicosanoids and lipid mediators in TB pathogenesis ( 30 – 32 ). We hypothesized that the AA-derived metabolites PGE2, LXA4, and LTB4 reflects the ongoing inflammation and resolution processes orchestrated by eicosanoids in TB.
The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.
The studies involving human participants were reviewed and approved by the Regional Committees for Ethics in Medical Research (REK-Sør-Øst 2016/2123). Biobank samples were collected and stored in the “Research Biobank Infectious Diseases” (“Forskningsbiobank Infeksjonssykdommer” (REK 1.2006.181-S-0885, SHDNR.
Conceived and designed the experiments: KN, MJ, KT, SJ, and AD-R. Recruited patients and collected clinical data: SJ, AD-R, and KT. Data acquisition: KN and MJ. Analyzed the data: KN, MJ, SJ, AD-R, and KT. Drafted and reviewed the manuscript: KN, MJ, SJ, AD-R, and KT. All authors contributed to the article and approved the submitted version.