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Chapter: Clinical Dermatology: Infections

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Mycobacterial infections

Tuberculosis: Most infections in the UK are caused by Mycobac-terium tuberculosis.

Mycobacterial infections

Tuberculosis

Most infections in the UK are caused by Mycobac-terium tuberculosis. Mycobacterium bovis infection,endemic in cattle, can be spread to humans by milk, but human infection with this organism is now rare in countries where cattle have been vaccinated against tuberculosis and the milk is pasteurized. The steady decline of tuberculosis in developed countries has been reversed in some areas where AIDS is especially prevalent. Dormant tuberculosis of the skin can also be reactivated by systemic corticosteroids, immuno-suppresants and new anti TNF biological agents.

Inoculation tuberculosis

Lupus vulgaris (Fig. 14.8) can follow the inoculation of tubercle bacilli into the skin of a person with high immunity, the direct spread of the organism from an underlying infected lymph node, or blood-borne spread from a pulmonary lesion. Lesions occur most often around the head and neck. A reddish-brown scaly plaque slowly enlarges, and can damage deeper tissues such as cartilage, leading to ugly mutilation. Scarring and contractures may follow.


Diascopy  shows up the characteristic brownish ‘apple jelly’ nodules and the clinical dia-gnosis should be confirmed by a biopsy. A warty variant exists.

Scrofuloderma

The skin overlying a tuberculous lymph node or joint may become involved in the process. The subsequent mixture of lesions (irregular puckered scars, fistulae and abscesses) is most commonly seen in the neck.

Tuberculides

A number of skin eruptions have, in the past, been attributed to a reaction to internal foci of tuberculosis. Of these, the best authenticatedaby finding mycobac-terial DNA by polymerase chain reaction (PCR)a are the ‘papulonecrotic tuberculides’arecurring crops of firm dusky papules, which may ulcerate, favouring the points of the knees and elbows.

Erythema induratum (Bazin’s disease)

In erythema induratum, deep purplish ulcerating nodules occur on the backs of the lower legs, usually in women with a poor ‘chilblain’ type of circulation. Sometimes this is associated with a tuberculous focus elsewhere. Erythema nodosum  may also be the result of tuberculosis elsewhere.

Investigations

Biopsy for:

   microscopy (tuberculoid granulomas);

 

   bacteriological culture; and

 

   detection of mycobacterial DNA by PCR. Mantoux test.

Treatment

The treatment of all types of cutaneous tuberculosis should be with a full course of a standard multidrug antituberculosis regimen. There is no longer any excuse for the use of one drug alone.

Prevention

Outbreaks of pulmonary tuberculosis are reminders that this disease has not yet been conquered and that vigilance is important. Bacillus Calmette–Guérin (BCG) vaccination of schoolchildren, immunization of cattle and pasteurization of milk remain the most effective protective measures.

Leprosy

Cause

Mycobacterium leprae was discovered by Hansen in1874, but has still not been cultured in vitro, although it can be made to grow in some animals (armadillos, mouse foot-pads, etc.). In humans the main route of infection is through nasal droplets from cases of lepro-matous leprosy although, interestingly, some cases have occurred in Louisiana from eating infected armadillos.

Epidemiology

Some 15 million people suffer from leprosy. Most live in the tropics and subtropics, but the ease of modern travel means that some cases are seen in northern Europe and the USA.

Presentation

The range of clinical manifestations and complications depends upon the immune response of the patient (Fig. 14.9). Those with a high resistance develop a paucibacillary tuberculoid type (Fig. 14.10) and those with low resistance a multibacillary lepromatous type. Nerve thickening is earlier and more marked in the tuberculoid than lepromatous type (Fig. 14.11). Between the extremes lies a spectrum of reactions classified as ‘borderline’.





Those most like the tuberculoid type are known as borderline tuberculoid (BT) and those nearest to the lepromatous type as borderline lepromatous (BL). The clinical differences between the two polar types are given in Fig. 14.12.


Differential diagnosis

Tuberculoid leprosy. Consider the followingain noneof which is there any loss of sensation.

  Vitiligo aloss of pigment is usually complete.

   Pityriasis versicolor ascrapings show mycelia and spores.

   Pityriasis albaaa common cause of scaly hypopig-mented areas on the cheeks of children.

   Postinflammatory depigmentation of any cause.

 

Lepromatous leprosy. Widespread leishmaniasis canclosely simulate lepromatous leprosy. The nodules seen in neurofibromatosis and mycosis fungoides, and multiple sebaceous cysts, can cause confusion, as can the acral deformities seen in yaws and systemic sclerosis. Leprosy is a great imitator.

Investigations

   Biopsy of skin or sensory nerve.

   Skin or nasal smears, with Ziehl–Nielsen or Fité stains, will show up the large number of organisms seen in the lepromatous type.

   Lepromin test. This is of no use in the diagnosis of leprosy but, once the diagnosis has been made, it will help to decide which type of disease is present (positive in tuberculoid type).

Treatment

The emergence of resistant strains of M. leprae means that it is no longer wise to treat leprosy with dapsone alone. It should now be used in combination, usu-ally with rifampicin, and also with clofazimine for lepromatous leprosy. A brief period of isolation is needed only for patients with infectious lepromatous leprosy; with treatment they quickly become non-infectious and can return to the community. How-ever, their management should remain in the hands of physicians with a special interest in the disease. Tuberculoid forms are usually treated for 6–12 months; multibacillary leprosy needs treatment for at least 2 years.

Special care is needed with the two types of lepra reaction that can occur during treatment:

   Type 1 (reversal) reactions are seen mainly in border-line tuberculoid disease (Fig. 14.13). Lesions become red and angry, and pain and paralysis follow neural inflammation. Treatment is with salicylates, chloro-quine, non-steroidal and steroidal anti-inflammatory drugs. 


   Type 2 reactions are common in lepromatous leprosy and include erythema nodosum, nerve palsies, lymphadenopathy, arthritis, iridocyclitis, epididymo-orchitis and proteinuria. They are treated with the drugs used for type 1 reactions, and also with thalidomide.

The household contacts of lepromatous patients are at risk of developing leprosy and should be followed up. Child contacts may benefit from prophylactic therapy and BCG inoculation.

 

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