Leprosy

Organism Mycobacterium leprae.

Clinical features Leprosy illustrates the conflict between the infecting organism and the host more dramatically than any other disease. M. leprae is widespread in the environment, yet only a small proportion of people ever show clinical symptoms of the disease and those few who do get the disease respond in different ways to the challenge.

The generation time from inoculation to multiplication of a stable number of M. leprae is only 18-24 days, but the development of the disease will take anything from 7 months to in excess of 7 years (mean 3-6 years). The first lesion is described as indeterminate (Fig. 12.3) because at this early stage, it is impossible to decide to which place in the spectrum of disease it will develop. There is either a single ill-defined, slightly hypopigmented macule, commonly seen on the face, trunk or exterior surfaces, or there may be a small anaesthetic patch. The lesion will then develop into a leproma-tous or tuberculoid type or oscillate in the transitional state of borderline leprosy between these two extremes.

Lepromatous leprosy (LL) reflects the complete breakdown of the host's immune responses and the maximum infection with M. leprae. In the early stages, the signs

Leprosy Beginning Stages

Fig. 12.3. The spectrum of leprosy illustrating the proportion of bacilli, the cell-mediated immune response and the level of instability, in the different forms of the disease.

of the disease may be very few, but a skin smear will reveal large numbers of mycobac-teria (multi-bacillary). Early signs that have been described, but rarely observed, are oedema of the legs and nasal symptoms of stuffiness, crust formation and bloodstained discharge. These are unlikely to be recognized as leprosy and it is generally not until the more obvious skin lesions become apparent that the diagnosis is made.

Leprosy lesions favour the cooler parts of the body, so the buttocks, trunk, exposed limbs and face are the more likely sites. Lesions may be macules, papules or nodules, with or without a colour change and often show lack of sweating when the patient becomes hot. The signs of nerve damage do not appear until much later in LL, with a concurrent thickening of the skin of the forehead, loss of eyebrows and damage to the cartilage of the nose. The eyes are also attacked with an infiltrative kera-titis, iritis and eventually leads to blindness.

Tuberculoid leprosy (TT) is at the opposite end of the spectrum, showing the full response of cell-mediated immunity to the attacking organism (Fig. 12.3). M. leprae has a predilection for nervous tissue and it is within this nervous tissue that the cellmediated response takes place, causing early damage to the nerves. The tuberculoid patient, therefore, tends to present early with signs of weakness or loss of sensation. Palpation of the nerves will often demonstrate a thickening with loss of sensation or motor power in the distribution of the affected nerve. The ulna nerve, as it bends over the medial epicondyle at the elbow, or the lateral popliteal nerve, where it curves round the neck of the fibula, are good places to palpate nerves for thickening. Dermal lesions are not raised, often appearing as apparently normal areas of the skin, lacking sensation or sweating when the patient exercises. Occasionally though, they are well-defined and scaly with raised edges, but quite different from the succulent macules and papules of LL. Loss of sensation should be elicited with a pin as well as light touch. A skin smear in TT is nearly always free of bacilli (pauci-bacillary), so the diagnosis depends upon the detection of nerve damage.

Borderline leprosy, as its name suggests, is on the border between the two extremes of LL and TT. True borderline (BB) is uncommon, with the disease tending to progress to either the lepromatous (BL) or tuber-culoid (BT) part of the spectrum. Signs, therefore, vary between the two extremes with features of each, but predominating in one or the other. Borderline leprosy is common, but its instability leads to reaction and nerve damage, which can often be severe.

Where the host response is adequate and cell-mediated immunity high, the disease tends towards the tuberculoid end of the spectrum, where it is low to LL. Simultaneous HIV infection will shift the host response from the tuberculoid towards the lepromatous. Otherwise the host response can vary over the course of the illness producing reactions, which can either be upgrading (towards TT) or downgrading (towards LL). These are type 1 reactions. The nearer the case is to the centre of the spectrum, the more severe is the reaction. Type 1 reactions may affect all tissues, skin and nerves only or produce a generalized systemic reaction.

A different type of reaction (type 2) is found in lepromatous and borderline lepro-matous cases and is associated with massive destruction of bacilli. Immune complexes are formed in the tissues and these lead to an increased reaction in existing lesions. The characteristic finding is erythema nodo-sum leprosum, which appears on the skin as painful red nodules commonly on the face and exterior surfaces.

Diagnosis A skin smear is made from every suspected case of leprosy, collecting dermal tissue without drawing blood. A negative smear does not mean that a case is not leprosy as tuberculoid cases rarely have mycobacteria. Smears are stained with Ziehl-Neelsen stain and the number of mycobacteria counted, giving the bacterial index:

6+ Over 1000 bacilli in an average field

5+ 100-1000 bacilli in an average field

4+ 10-100 bacilli in an average field

3+ 1-10 bacilli in an average field

2+ 1-10 bacilli in 10 fields

1+ 1-10 bacilli in 100 fields

Mycobacteria can also be obtained from nasal scrapings of the inferior turbinate. A skin biopsy is taken from tuberculoid and borderline patients or a nerve biopsy where there is no skin lesion.

Transmission The method of transmission has not been conclusively demonstrated, but several factors, such as prolonged close contact, the finding of large numbers of bacilli in the nasal discharges of lepromatous cases and in the skin, suggest that both airborne and direct skin contact are important. M. leprae have been found to survive from 2 to 7 days outside the body in nasal secretions. Individuals vary in their susceptibility and it is possible that repeated doses of bacilli or a large infective dose are required to produce the disease.

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