**11. Miscellaneous issues**

*Pathogenic Bacteria*

(Bell's palsy).

**9. Therapeutics**

Histologically, there is epi-, peri- and endoneural fibrosis.

in corneal anesthesia, thus facilitating bacterial corneal ulceration.

14 days, than gradually increase by 5 mg every 14 days).

(nose reconstruction, tarsorrhaphy, hand surgery, etc.) [13].

prednisolone 40 mg for 5 days [13].

**10. Prophylaxis and monitoring**

corticosteroids are the first choice (**Figure 5**).

The most commonly affected nerve structures are: n. ulnaris located in the ulnar groove, n. medianus in the vicinity of the carpal tunnel, *n. tibialis* posterior, superficial branch of the radial nerve, sural nerve posteriorly of the malleolus, great auricular nerve as well as facial nerve, frontal and cervical branches. Clinically, the resultant ocular muscle paralysis causes lagophthalmos, subsequently facilitating secondary corneal infections due to incomplete lid closure

Sensory loss of the ophthalmic branch (V1) of the trigeminal nerve, too, results

In the individuals with type 1 leprosy reactions (reversal reaction), the systemic

Type 2 reaction is treated with the administration of thalidomide (100–400 mg/

In the case of syn. Lucio's phenomenon (type 3 reaction) the use of systemic

In the patient with nerve damage, it is necessary to incorporate active and passive physical therapy, local skin care if acral mutilations are present. Certain individuals require orthopedic prosthesis as well as reconstructive procedure(s)

The early diagnosis and treatment of leprosy are preventive measures in the initial spreading of this infectious disease. Hemoprophylaxis in children exposed

administration of corticosteroids (initial dose of 40–60 mg prednisolone for

per day) plus the administration of systemic corticosteroids most commonly

**164**

**Figure 5.**

*Leprosy treatment modalities.*

Recent studies suggested that the presence of the PARK2/PACRG gene (chromosome 6q25-q27) as well as the presence of the NRAMP1 gene (chromosome 2q35) is linked to the higher leprosy susceptibility.

TAP1 and TAP2 (transporter associated with antigen processing) genes (located on chromosome 6p21), TNF-α (tumor necrosis factor alpha) (chromosome 6p21), and the VDR (vitamin D receptor) gene (chromosome 12q12) are associated with the innate and adaptive immunity [15].

In the majority of infected individuals, leprosy takes on an intermediate form, which may – to a variable degree – show clinical features of tuberculoid and lepromatous leprosy. This intermediate form is referred to as borderline leprosy.

In PB forms it has been noted higher cellular response to M.leprae due to the Th1 cytokines such as IFN-y. There are also lower antibody titers to M. leprae – specific antigens. In the individuals with MB form of leprosy there is an absence of the capacity to mount a cell mediated response due to T cell anergy. There is a high antibody titer to M. leprae antigens (PGL-1) [16].
