Cutaneous leishmaniasis of the New World (American cutaneous leishmaniasis) Medical Assignment Help

Chiclero’s ulcer

This is caused by L. mexicana and is found in Mexico, Guatemala, Brazil, Venezuela and Panama. It occurs on the exposed parts of the body, and runs a benign course with spontaneous healing within 6 months. However, infection of the pinna (chiclero’s ear) results in gross destruction of the external ear. A lesion at this site may persist for over 20 years.

Espundia (mucocutaneous leishmaniasis)

This is caused by L. braziliensis and is found in Brazil, Ecuador, Bolivia, Uruguay and northern Argentina. Initially painful, itchy nodules appear on the lower limbs, and then ulcerate. Lymphangitis is usual. Healing occurs spontaneously in 6 months. Several years later, secondary lesions develop at mucocutaneous junctions such as the nasopharynx. There is evidence of nasal obstruction, ulceration, septal perforation and destruction of the nasal cartilages. Death usually occurs from secondary bacterial infection or aspiration.

Diffuse cutaneous leishmaniasis

This is caused by L. amazonensis and is characterized by diffuse infiltration of the skin by Leishman-Donovan bodies. Visceral lesions are absent. Clinically this chronic condition resembles lepromatous leprosy, although it does not involve the nasal septum. Uta ‘Uta is a similar disease to diffuse cutaneous leishmaniasis and is caused by L. peruviana. It occurs in cooler climates in the Andes. It produces single or multiple ulcers, which usually heal spontaneously.

DIAGNOSIS

The diagnosis is established by demonstrating Leishman- Donovan bodies in spleen or bone marrow smears or histological sections of tissues. Parasites are scanty and hence a positive leishmanin skin test is useful.

TREATMENT

Chiclero’s ulcer has been treated effectively with a single intramuscular injection of cycloguanil pamoate. Sodium stibogluconate in a dose similar to that used for kalaazar is effective for most other forms of cutaneous and mucocutaneous leishmaniasis. Amphotericin is usually required for severe infections. Reconstructive surgery of any deformity is an important part of therapy. Cutaneous leishmaniasis of the Old World L major and L. tropica are found in the former USSR, the Middle East, around the Mediterranean and sub- Sahara and west Africa. The reservoir for L. major is infected desert rodents whilst L. tropica has an urban distribution with dogs and humans as reservoirs. L. aethiopica is found in the highlands of Ethiopia and Kenya and the animal reservoir is often the hyrax. The vectors are usually the phlebotomus sandfly.

CLINICAL FEATURES

ingle or multiple papules occur on exposed areas within _ weeks to 3 months of infection. These enlarge and ulcerate, often with an overlying crust. The lesions heal spontaneously with scarring but may take years. Leishmaniasis recidivans, which is characterized by features resembling lupus vulgaris, describes the lesions seen many years after the healing of the primary lesions.

TREATMENT

Cutaneous lesions respond to application of direct heat .w°C). Pentavalent antimony compounds provide the mainstay of therapy. In patients with indolent lesions, levamisole has been used with some success.

TRYPANOSOMIASIS

African trypanosomiasis
African trypanosomiasis (sleeping sickness) follows the bite of the tsetse fly and is caused by Trypanosoma brucei.T. brucei is found in West and Central Africa between latitudes 200N and 200S. Two clinical forms are recognized.

rypanosomiasis-geographical distribution.

rypanosomiasis-geographical distribution.

GAMBIAN SLEEPING SICKNESS is found mainly in West Africa, but also in southern Sudan and Uganda. Gambian sleeping sickness is caused by T. b. gambiense and transmitted to humans by the tsetse fly species Glossina palpalis and G. tachinoides. Humans are the only important reservoirs although domestic and wild animals may carry the infection. Transmission occursmost frequently at river banks where the flies lie  under trees.
RHODESIAN SLEEPING SICKNESS is found from Ethiopia in the north to Botswana in the south. T. b. rhodesiense, the causative agent of Rhodesian sleeping sickness, is a zoonosis and is transmitted by G. morsitans, G. swynnertoni, G. pallidipes, and G. palpalis. Antelopes and other wild animals as well as domestic animals are reservoirs. Tsetse flies are daylight biting and both male and female flies can be infected. Following the bite, metacyclic forms (the infective forms of trypomastigotes) are deposited into the subcutaneous tissue, where a marked perivascular reaction occurs. Lymphatics are then invaded, followed by spread to the lymph nodes. Invasion of the bloodstream occurs in 2 or 3 weeks, at which time the organisms reach all parts of the body, especially the CNS. In the CNS they elicit a marked perivascular mononuclear infiltration that results in leptomeningitis or encephalomyelitis.

Comparison between Gambian and Rhodesian sleeping sickness

Comparison between Gambian and Rhodesian sleeping sickness

CLINICAL FEATURES

A tender nodule appears at the site of the bite. This is referred to as a trypanosoma chancre and is seen more commonly in Rhodesian sleeping sickness and in Caucasians. Tachycardia and persistent headache are common. Spontaneous healing of the chancre occurs at about 3 weeks and this is followed by haematogenous dissemination. The lymph glands are discrete, non-tender and have a peculiar rubbery consistency. Splenomegaly and hepatomegaly may also occur. After a variable period of time, there is evidence of CNS involvement and features of a chronic meningo-encephalomyelitis with behaviouralchanges. The patient loses interest in the surroundings, becomes apathetic, has a mask-like facies, and a tendency to fall asleep during the day and inability to sleep at night. The eyelids tend to droop, there is facial puffiness, the lower lips are swollen and hang loosely and the patient’s attention span decreases. Later, tremor of the hands, areas of hyperaesthesia, especially over the ulnar nerve (Kerandel’s sign), choreiform movements, seizures and finally coma develop. Myocarditis, hepatitis, petechiae and pleural effusions may occur, particularly in Rhodesian sleeping sickness. Gambian sleeping sickness is a chronic illness with symptom-free periods, while Rhodesian sleeping sickness is an acute, more severe form, and death usually occurs within 1 year, often due to myocarditis. Features of CNS involvement are therefore less prominent than in the Rhodesian form Unusual manifestations An erythematous, patchy, annular rash that fades in a week may be seen in the early stages of infection in Caucasians. Facial oedema, paraesthesiae, periosteitis, especially of the tibia resulting in hyperaesthesia, iridocyclitis and choroiditis may occur. Endocrine dysfunction may develop, manifesting as amenorrhoea or impotence.

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