**5. Clinical and laboratory diagnosis**

Leprosy is transmitted via close and prolonged contact amongst healthy individuals and a bacillus-infected patient through inhalation of the bacilli contained in nasal secretions or Flügge droplets. The main route of transmission is the nasal mucosa. Leprosy, similar to other infectious diseases is a consequence of pathogen invasion of the host organism and transposition of the immunological barrier [7].

Transmission can occur by skin erosions, blood, vertical transmission, breast milk, and insect bites.

In infected individuals, there is a transitional period of nasal release of bacilli. The presence of specific DNA sequences of M. leprae in swabs or nasal biopsies and seropositivity suggest the carrier plays a role in the transmission of leprosy.

In the individuals with the solid immune system, leprosy is presented in tuberculoid form (solitary papules and plaques). Such skin changes may form erythematous plaques with raised borders and an annular appearance.

In the case of a defected immune system, lepromatous leprosy is presented with an impaired T-cell immunity leading to anergy. Clinically, this manifestation is shown as multiple red-brown-nodular infiltrate (lepromas) in the skin and mucous membranes.

"Leonine facies" is defined as the symmetrical centrofacial presentation of the cushion-like lesions, loss of the eyelashes and eyebrows [7].

Involvement of the nasal mucosa leads to destruction of the septum and deformity of the nasal skeleton (saddle nose). Subsequently, this destructive inflammatory process may include the entire nasopharynx, clinically characterized by mucosal ulcerations of the palate and larynx.

Multiple, poorly demarcated, hypopigmented papules, nodules, and/or infiltrated plaques are the hallmark of this form.

In case of chronic cutaneous hyperalgesia, there is a local increase in NGF levels. The application of anti-NGF antibodies may be of benefit in treating hyperalgesia in patients with neuropathy and impaired nerve endings. If combined, NGF, NT-3 and glial cell-line derived neurotrophic factor may be sustainable [8].

NGF has a potential modulatory role in nociception.

NGF may restore pain sensitivity and prevent the ulcer formation caused by nociceptive loss. Anti-NGF treatment may be of benefit in patients with hyperalgesia.

Other cytokine imbalances may be described as the imbalance in the proNGF/ NGF ratio, increased TNF-α and p75 neurotrophin [9].

The main targets of M. leprae are Schwann cells. In case of the onset of Schwann cells degradation, peripheral neuropathy is the most common consequence. It has been documented that NGF may act as a protective factor for Schwann cells. Thus, low levels of NGF directly are responsible for the development of neuropathy.

NGF are involved in the reparation of neuronal cells and induction of fibroblast migration. They exhibit proliferative and antiapoptotic effects on keratinocytes and endothelial cells [10].

The incidence of nerve impairment in the individuals with paucibacillary leprosy is present in 10% of cases, whilst in multibacillary leprosy in 40%.

TGF-β is involved in the tissue reparation processes due to its anti-inflammatory attributes.

Leprosy is diagnosed mainly on the basis of a clinical picture. For bacteriological diagnosis, a nose swab, scraping or cutaneous skin changes are taken.

The diagnosis is based on the findings of acidoalcohol resistant bacteria in lepromatous leprosy and histopathological findings. Experimental animals (armadillo, mouse) are used to isolate M. leprae. Skin test with lepromine (Mitsuda test) is positive for tuberculoid leprosy. A positive lepromin test is linked to the ability to develop a granulomatous response [11].

A serological test method with good sensitivity in multibacillary forms (approximately 70%) involves the measurement of antibodies against a phenolic glycolipid (PGL-1; 35 kDa) in the bacterial cell wall.

It is recommended to perform skin biopsies taken from the margins of the lesions and should also include subcutaneous tissue.


**163**

*Leprosy in the Modern Era*

**6. Clinical presentation**

mented macules.

reaction [13].

**7. Complications**

functions with necrosis.

loss, amputations and blindness.

be present.

*DOI: http://dx.doi.org/10.5772/intechopen.91450*

In certain individuals, pseudoabscesses along nerves and nerve thickening may

Thickened nerves may be detected by palpation along the course of the supraorbital, retroauricular, ulnar, median, superficial radial, common peroneal, superficial peroneal, posterior tibial, and sural nerves. The initial functional tests implicate

Thermosensitivity is checked using a heated test tube with a lighter. The test tube is then held to the patient's skin lesion and the corresponding skin. The test is performed placing a tube with water at room temperature to the skin lesions. The

The neurological examination conducted by a specialist includes EMG, nerve ultrasound, and magnetic resonance imaging. Nerve biopsies are preferably taken from thickened superficial and thus readily accessible nerves such as the sural nerve, the superficial peroneal nerve, the ulnar nerve, and the saphenous nerve.

The initial stage of leprosy is non-specific presenting with one or more hypopig-

There have been four noted immunologic leprosy reactions. Type 1 reaction represents a hypersensitivity reaction to M. leprae antigens clinically characterized by sudden onset of urticarial swelling of the leprous skin lesions. It may also be associated with acute and very painful neuritides with loss of sensory and motor function. Pathophysiologically, type 2 reaction (Syn. erythema nodosum leprosum) is characterized by the occurrence of painful violaceous- erythematous cutaneous or

Myalgia, arthralgia, and osseous pain are symptoms associated with a type 2

The first leprosy classification by WHO was applied in 1966 based upon the histological picture – the Ridely-Jopling classification. It shows two forms of leprosy – its mild and severe defect of cell-mediated immunity: tuberculoid (paucibacillary) and lepromatous (multibacillary) leprosy with the following subgroups: borderline tuberculoid (BT), borderline lepromatous (BL) and borderline lepromatous leprosy

The most common complications are muscle weakness leading to atrophy, bone

In the case of chronic cutaneous hyperalgesia, there is a local increase in NGF levels. The application of anti-NGF antibodies may be of benefit in treating hyperalgesia in patients with neuropathy and impaired nerve endings. If combined, NGF,

In over 90% of human individuals an overall genetic resistance has been noted.

Overall, leprosy is a granulomatous inflammatory process. It causes intraneural pressure induced atrophy, palpable nerve thickening and progressive loss of neural

NT-3 and glial cell-line derived neurotrophic factor may be sustainable.

**8. Systemic involvement and special situations**

weakness (paresis) or loss (paralysis) of muscle strength [12].

patient is then asked to detect the difference between hot and cold [13].

subcutaneous nodules. Type 3 reaction (Syn. Lucio's phenomenon).

(BL) [14]. This classification is detailed earlier in the chapter.

**162**

*Pathogenic Bacteria*

endothelial cells [10].

develop a granulomatous response [11].

(PGL-1; 35 kDa) in the bacterial cell wall.

**to the bacterial count per visual field(s)**

lesions and should also include subcutaneous tissue.

a. 1–10/100 1 + b. 1–10/10 2 + c. 1–10/1 3 + d. 10–100/1 4 + e. 100–1000/1 5 + f. > 1000/1 6 +

attributes.

"Leonine facies" is defined as the symmetrical centrofacial presentation of the

Involvement of the nasal mucosa leads to destruction of the septum and deformity of the nasal skeleton (saddle nose). Subsequently, this destructive inflammatory process may include the entire nasopharynx, clinically characterized by

Multiple, poorly demarcated, hypopigmented papules, nodules, and/or infil-

In case of chronic cutaneous hyperalgesia, there is a local increase in NGF levels. The application of anti-NGF antibodies may be of benefit in treating hyperalgesia in patients with neuropathy and impaired nerve endings. If combined, NGF, NT-3 and

NGF may restore pain sensitivity and prevent the ulcer formation caused by nociceptive loss. Anti-NGF treatment may be of benefit in patients with hyperalgesia. Other cytokine imbalances may be described as the imbalance in the proNGF/

The main targets of M. leprae are Schwann cells. In case of the onset of Schwann cells degradation, peripheral neuropathy is the most common consequence. It has been documented that NGF may act as a protective factor for Schwann cells. Thus, low levels of NGF directly are responsible for the development of neuropathy.

NGF are involved in the reparation of neuronal cells and induction of fibroblast migration. They exhibit proliferative and antiapoptotic effects on keratinocytes and

TGF-β is involved in the tissue reparation processes due to its anti-inflammatory

Leprosy is diagnosed mainly on the basis of a clinical picture. For bacteriological

A serological test method with good sensitivity in multibacillary forms (approximately 70%) involves the measurement of antibodies against a phenolic glycolipid

**Bacterial index (BI): scale for assessing the number of leprosy bacteria in skin smears may be according** 

The incidence of nerve impairment in the individuals with paucibacillary leprosy is present in 10% of cases, whilst in multibacillary leprosy in 40%.

The diagnosis is based on the findings of acidoalcohol resistant bacteria in lepromatous leprosy and histopathological findings. Experimental animals (armadillo, mouse) are used to isolate M. leprae. Skin test with lepromine (Mitsuda test) is positive for tuberculoid leprosy. A positive lepromin test is linked to the ability to

It is recommended to perform skin biopsies taken from the margins of the

diagnosis, a nose swab, scraping or cutaneous skin changes are taken.

cushion-like lesions, loss of the eyelashes and eyebrows [7].

glial cell-line derived neurotrophic factor may be sustainable [8]. NGF has a potential modulatory role in nociception.

NGF ratio, increased TNF-α and p75 neurotrophin [9].

mucosal ulcerations of the palate and larynx.

trated plaques are the hallmark of this form.

**162**

In certain individuals, pseudoabscesses along nerves and nerve thickening may be present.

Thickened nerves may be detected by palpation along the course of the supraorbital, retroauricular, ulnar, median, superficial radial, common peroneal, superficial peroneal, posterior tibial, and sural nerves. The initial functional tests implicate weakness (paresis) or loss (paralysis) of muscle strength [12].

Thermosensitivity is checked using a heated test tube with a lighter. The test tube is then held to the patient's skin lesion and the corresponding skin. The test is performed placing a tube with water at room temperature to the skin lesions. The patient is then asked to detect the difference between hot and cold [13].

The neurological examination conducted by a specialist includes EMG, nerve ultrasound, and magnetic resonance imaging. Nerve biopsies are preferably taken from thickened superficial and thus readily accessible nerves such as the sural nerve, the superficial peroneal nerve, the ulnar nerve, and the saphenous nerve.
