**4. Classification**

In addition, a study showing that bimodal distribution of risk for age has been shown that the

Although there are a number of studies showing no significant difference between men and

Compared to the general population, sharing the same house with a leprosy patient increases the risk. Contact with MB leprosy patients is more risky when compared to contact with patients with PB single lesion leprosy, while the risk of contact with MB patients is similar to contact with PB leprosy patients with 2–5 lesions [34, 36, 38]. If there are two or more patients

For individuals in contact with the general population and leprosy patients, BCG vaccination administration at repeated doses provides protection against the leprosy [39–41]. Those who live in the same household and do not vaccinated with BCG vaccine are at greater risk [42].

Studies have been carried out for years to clarify whether there is a relationship between leprosy and genetics. Although not fully adequate, there are conclusions that support this idea. Moet et al. reported that genetic association is a risk factor predisposing to leprosy, regardless of physical distance [34]. Mire et al. found that the chromosome 6q25 locus was associated with leprosy susceptibility; Siddiqui et al. showed that the 10p13 locus was associated with PB leprosy [43]. There are also studies showing that HLA DR2 and non-HLA (SLC11A1, formerly NRAMP1 and TNF alpha) genes are also associated with leprosy [44, 45]. Genomic studies are important in combating leprosy in terms of having potential for improvement in treatment and vaccination. On the other hand, the presence of IL-17F (7488 t > C) single nucleotide polymorphism and the presence of IL-4 gene 4-590 T/C polymorphism are associated with

*M. leprae* is a compulsory intracellular organism, which is a fast-staining, very slow-growing (doubling time 14 days), which can reproduce at lower temperatures than body temperature [48]. Unlike other bacteria, it is thought that the reproduction pattern is not algorithmic. While the regions where it can reproduce in human body are at 25–33**°**C, whereas no *M. leprae*

women, there is also a study reported that men are at greater risk [34–36].

risk increase ages 5–15 years and over 30 years.

40 Hansen's Disease - The Forgotten and Neglected Disease

*2.4.4. Leprosy type and physical distance to the patient*

decreased predisposition to leprosy [46, 47].

involvement is observed at 35–36**°**C regions [49].

**3. Microbiology and genetic**

in the same house, the risk of contamination doubles [11].

*2.4.3. Gender*

*2.4.5. BCG vaccine*

*2.4.6. Genetic distance*

Leprosy exhibits a broad spectrum of clinical and histopathological findings based on the cellular immune response of the host. In 1966, Ridley and Jopling classified leprosy according to clinical and histopathologic features [54, 55]. According to this classification system there is a tuberculous form (TT) consisting of a strong immune response and a small number of microorganisms at one end and a weak immunologic response and a lepromatous form (LL) overloading of microorganisms at the other end and three types of borderline leprosy; borderline tuberculoid leprosy (BT), mid-borderline (BB), borderline lepromatous leprosy (BL) between these two end. Conceptually, tuberculoid leprosy (TT) and lepromatous leprosy (LL) are clinically stable, while borderline forms may shift to stronger or weaker immunity.

In 1997, the WHO created a classification to provide leprosy treatment based on the number of lesions present, regardless of the size, localization, and histopathological features of the lesions, without laboratory support in endemic areas [56]. According to these, leprosy is divided to 3 subgroup: single lesion leprosy, PB, 2–5 lesions and MB, more than 5 lesions. According to the WHO classification, BT may be considered in the PB, BB and BL may be considered in the MB spectrum.
