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The clinical description of the chronic bacterial disease leprosy

Bacterial load In lepromatous leprosy, bacilli spread haematogenously to cool superficial sites including eyes, upper respiratory mucosa, testes, small muscles, and bones of the hands, feet, and face as well as to peripheral nerves and skin. The heavy bacterial load causes structural damage at all these sites.

In tuberculoid leprosy, bacilli are not readily found. Nerve damage Neural inflammation is pathognomonic of leprosy. Nerve damage occurs in small nerve fibres, both sensory and autonomic, in the skin and in peripheral nerve trunks. Nerve damage occurs before diagnosis, during treatment, and after treatment. In lepromatous infection, almost all the cutaneous nerves and peripheral nerve trunks are involved.

Bacilli are found in Schwann, perineural, and endothelial cells. Extensive demyelination occurs and later wallerian degeneration. Despite large numbers of organisms in the nerve there is only a small inflammatory response, but ultimately the nerve becomes fibrotic and is hyalinized. At the tuberculoid end of the spectrum nerve damage is secondary to a granulomatous response to M.

Perineural inflammation and epithelioid granulomas destroy the Schwann cells and axons. In borderline leprosy the combination of M.

  1. In these circumstances, suspect cases should be referred to health facilities with more capacities for diagnosing leprosy.
  2. Suspecting and then diagnosing someone with leprosy is called case finding. MDT has resulted in the elimination of leprosy in many countries.
  3. Where possible, compare your findings with those shown on any earlier records — look for differences over time.
  4. Diagnosis of leprosy is most usually based on the clinical features. On it, you can record all the important details that relate to the patient, such as the skin lesions you can see, the results of palpation and the outcomes of the voluntary muscle tests you will perform.

The persistence of M. Leprosy reactions Leprosy reactions are events superimposed on the Ridley—Jopling spectrum. Type 1 reversal reactions occur in borderline patients BT, BB, BL and are delayed hypersensitivity reactions caused by increased recognition of M. They are characterized by an increase in lymphocytes CD4 and ILproducing cells within lesions, severe oedema with disruption of the granuloma, and giant cell formation.

Clinical features of leprosy Patients commonly present with skin lesions, weakness or numbness due to a peripheral nerve lesion, or a burn or ulcer on an anaesthetic hand or foot. Borderline patients may present in reaction with nerve pain, sudden palsy, multiple new skin lesions, pain in the eye, or a systemic febrile illness. The cardinal signs are: The classic early skin lesion is indeterminate leprosy, which is commonly found on the face, extensor surface of the limbs, buttocks, or trunk.

Indeterminate lesions consist of one or more slightly hypopigmented or erythematous macules, a few centimetres in diameter, with poorly defined margins. Hair growth and nerve function are unimpaired. A biopsy may show the perineurovascular infiltrate and only scanty acid-fast bacilli. The indeterminate phase may last for months or years before resolving or developing into one of the determinate types of leprosy. Skin The commonest skin lesions are macules or plaques; papules and nodules are more rare.

Lesions may be found anywhere although rarely in the axillae, perineum, or hairy scalp. Skin lesions should be assessed for inflammation, colour, and sensation. Tuberculoid patients have few granulomatous hypopigmented lesions while lepromatous patients have numerous, sometimes confluent lesions. The few tuberculoid lesions are usually asymmetrical; more numerous lesions are likely to be distributed symmetrically. Anaesthesia Anaesthesia may occur in skin lesions when dermal nerves are involved or in the distribution of a large peripheral nerve.

In skin lesions the small dermal sensory and autonomic nerve fibres supplying dermal and subcutaneous structures are damaged causing local sensory loss and loss of sweating within that area.

Peripheral neuropathy Peripheral nerve trunks are vulnerable at sites where they are superficial or are in fibro-osseous tunnels. At these points a small increase in nerve diameter raises intraneural pressure causing neural compression and ischaemia.

  1. Charcot—Marie—Tooth disease is an inherited neuropathy that causes distal atrophy and weakness. Avoid repetitive testing at any one test point.
  2. Ask the patient to stare at you during the test, while you try to push his thumb out and across, away from his little finger.
  3. On the first visit there should be a careful assessment of skin and mucosal involvement and accurate evaluation of nerve and eye function. The peak time for reactions in the first 2 months after starting treatment and in the puerperium.

Damage to peripheral nerve trunks produces characteristic signs with dermatomal sensory loss and dysfunction of muscles supplied by that peripheral nerve.

The predilection sites for peripheral nerve involvement are ulnar nerve at the elbowmedian nerve at the wristradial nerve, radial cutaneous nerve at the wristcommon peroneal nerve at the kneeposterior tibial and sural nerves at the ankle, facial nerve as it crosses the zygomatic arch, and great auricular nerve in the posterior triangle of the neck. All these nerves should be examined for enlargement and tenderness. Peripheral nerve function should be assessed by testing the motor function of the small muscles of the hands and feet using the Medical Research Council MRC grading scale.

Sensory function is best assessed using graded nylon monofilaments Semmes—Weinstein as in diabetic screening. Patients should be asked about symptoms of neuropathy. Tuberculoid leprosy TT Infection is localized and asymmetrical. A typical tuberculoid skin lesion is a macule or plaque, single, erythematous, or purple, with raised and clear-cut edges sloping towards a flattened hypopigmented centre.

The surface is anaesthetized, dry, and hairless. Sensory impairment may be difficult to demonstrate on the face where there are abundant nerve endings.

  • The consequent loss of testosterone leads to azoospermia and gynaecomastia;
  • Diagnosis The diagnosis is made on the clinical findings of one or more of the cardinal signs of leprosy and supported by the finding of acid-fast bacilli on slit skin smears;
  • There was general agreement that leprosy, a chronic infectious disease caused of the bacterial clinical description of the first t1r;
  • Damage to peripheral nerve trunks produces characteristic signs with dermatomal sensory loss and dysfunction of muscles supplied by that peripheral nerve.

If peripheral nerve trunk involvement is present, only one nerve trunk is enlarged. True tuberculoid leprosy has a good prognosis, many infections resolve without treatment, and peripheral nerve trunk damage the clinical description of the chronic bacterial disease leprosy limited. Borderline tuberculoid leprosy BT The skin lesions are similar to tuberculoid leprosy and there may be few or many lesions.

The margins are less well defined and there may be satellite lesions. Damage to peripheral nerves is widespread and severe, usually with several thickened nerve trunks. It is important to recognize borderline tuberculoid leprosy because these patients are at risk of reversal reactions leading to rapid deterioration in nerve function with consequent deformities. Borderline leprosy BB Borderline disease is the most unstable part of the spectrum and patients usually downgrade towards lepromatous leprosy if they are not treated or upgrade towards tuberculoid leprosy as part of a reversal reaction.

There are numerous skin lesions which may be macules, papules, or plaques and they vary in size, shape, and distribution. The edges of the lesions may have streaming, irregular borders. Annular lesions with a broad irregular edge and a sharply defined punched-out centre are characteristic of borderline disease. Nerve damage is variable. Borderline lepromatous leprosy BL This is characterized by widespread variable asymmetrical skin lesions.

There may be erythematous or hyperpigmented papules, succulent nodules or plaques, and sensation in the lesions may be normal. Peripheral nerve involvement is widespread. While patients with borderline lepromatous leprosy do not have the extreme consequences of bacillary multiplication that are seen in lepromatous disease, they may experience either or both reversal and ENL reactions.

Lepromatous leprosy LL The patient with untreated polar lepromatous leprosy may be carrying leprosy bacilli. The onset of disease is frequently insidious, the earliest lesions being ill-defined, shiny, hypopigmented, or erythematous macules. Gradually the skin becomes infiltrated and thickened and nodules develop; facial skin thickening causes the characteristic leonine facies.

Hair is lost, especially the lateral third of the eyebrows madarosis. Dermal nerves are destroyed leading to a progressive glove and stocking anaesthesia. Position sense is preserved. Sweating is lost, which is uncomfortable in the tropics as compensatory sweating occurs in the remaining intact areas. Damage to peripheral nerves is symmetrical and occurs late in the disease.

Infiltration of the corneal nerves causes anaesthesia of the cornea, which predisposes to injury, secondary infection, and blindness.

Nasal symptoms can often be elicited early in the disease. Septal perforation may occur. There may be papules on the lips and nodules on the palate, uvula, tongue, and gums. Bone involvement is common, with absorption of the terminal phalanges and pencilling of the heads and shafts of the metatarsals. Testicular atrophy results from diffuse infiltration compounded by acute orchitis that may occur during ENL reactions.

The consequent loss of testosterone leads to azoospermia and gynaecomastia. The extremities become oedematous. The skin of the legs becomes ichthyotic and ulcerates easily. Other forms of leprosy There are several variant forms of leprosy. There is asymmetrical involvement of peripheral nerve trunks and no visible skin lesions. On nerve biopsy all types of leprosy have been found.

Communicable Diseases Module: 18. Leprosy Diagnosis

Histoid lesions are distinctive nodules occurring in lepromatous patients who have relapsed due to dapsone resistance or noncompliance with chemotherapy. Eye disease in leprosy Blindness due to leprosy, which occurs in at least 2. Eye damage results from both nerve damage and bacillary invasion.

Lagophthalmos results from paresis of the orbicularis oculi due to involvement of the zygomatic and temporal branches of the facial VIIth nerve. These superficial branches are frequently involved in borderline tuberculoid cases, particularly if there are facial skin lesions.

Leprosy (Hansen’s disease)

In lepromatous disease, lagophthalmos occurs later and is usually bilateral. Damage to the ophthalmic branch of the trigeminal Vth nerve causes anaesthesia of the cornea and conjunctiva resulting in drying of the cornea and making the cornea susceptible to trauma and ulceration. Lepromatous infiltration in corneal nerves produces punctate keratitis and corneal lepromas. Invasion of the iris and ciliary body makes them extremely susceptible to reactions.

Nerves become tender with new loss of sensation or motor weakness. Existing skin lesions become erythematous or oedematous; new lesions may appear. Occasionally oedema of the hands, face, or feet is the presenting symptom, but constitutional symptoms are unusual. Patients often present with a skin lesion in reaction since a previously quiescent lesion has become active and visible. The peak time for reactions in the first 2 months after starting treatment and in the puerperium.

Late reactions may occur years after finishing multidrug treatment.

The clinical description of the chronic bacterial disease leprosy

Some patient experience repeated reactions. Type 2 ENL reactions These occur in lepromatous and borderline lepromatous patients.

Attacks are acute and may recur over several years. ENL manifests most commonly as painful red nodules on the face and extensor surfaces of limbs. The lesions may be superficial or deep, with suppuration or brawny induration when chronic.