Ulcer Buruli: Causes, Symptoms, Diagnosis, Treatment

, medical expert
Last reviewed: 18.10.2021

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The nosological independence of the Buruli ulcer is recognized by most authors due to the fairly typical clinical and epidemiological features. Buruli ulcer was named in the 60s of the last century, when for the first time a large number of its observations in the form of a local epidemic in Uganda in the province of Buruli was described. At present, numerous cases of Buruli ulcer are observed mainly in West Africa (Benin, Cote d'Ivoire, Ghana, Guinea, Liberia, Togo), French Guiana, Papua New Guinea and Australia.

Significantly, the disease is described in the countries of South-East Asia, isolated cases are noted in China. Buruli ulcer is registered in 27 countries of the world, mainly in wet marshy places with standing water. According to the national health of Ghana, the incidence of Buruli ulcer in this country is 3.2 cases per 1000 population, and in some rural areas of Cote d'Ivoire, 16% of residents suffer from this disease. According to WHO experts, the Buruli ulcer is the third most frequent occurrence of mycobacteriosis after leprosy and tuberculosis.

Causes of Ulcer Buruli

The etiological factor of ulcerative skin lesions in the Buruli ulcer is recognized as Mycobacterium ulcerans. Mycobacterium ulcerans is an acid-fast mycobacterium that grows on the Levenstein-Jensen medium at a temperature of 30-32 ° C, with a reduced partial pressure of oxygen - for 6-8 weeks.

Unlike other mycobacteria, Mycobacterium ulcerans produces a toxin that by chemical structure represents a macrolide derivative called mycolactone. The toxin has an affinity for fat cells, has a cytotoxic effect, contributes to the development of necrotic processes, and an immunosuppressive effect, since the sensitivity of skin tests falls in the necrotic phase of the disease. Unlike other mycobacteria, which are facultative intracellular parasites and located inside phagocytes, Mycobacterium ulcerans forms extracellular colonies.

As with other mycobacteriosis in humans, the mechanisms of the pathogenesis of this disease are closely related to the characteristics of the immune response of a particular organism, the duration of contact with the source of infection, and numerous endogenous and exogenous factors. A distinctive feature of M. Ulcerans is the ability to produce toxin mikolactone, which explains the profound nature of ulcerative lesions. The entrance gates for the pathogen are usually banal skin lesions (scratches, abrasions, schools, insect bites, crushing tissues, etc.), i.e. What is commonly called microtrauma. Apparently, such aggravating diseases as malaria, helminthiases, hypovitaminosis, drug addiction, etc. Seem to be important. Children and adolescents up to 15 years old, and more rarely adults and older, are most prone to the emergence and severe course of Buruli ulcer.

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Symptoms of Ulcer Buruli

Symptoms of Buruli ulcer most often begin with the appearance on the ground, as a rule, of the previous skin injury of the dense subacute-inflammatory painless infiltrate (tubercle, papule), most often in the legs, thighs, forearms and less often in other parts of the body. As it ripens through the central softening stage, the tubercle transforms into a painless ulcer, which, without treatment, occurs in the vast majority of cases. Much less frequently (10%), the decomposition of the tubercle without opening occurs in the direction of the underlying tissues, up to the destruction of the bones and the development of osteomyelitis. Very typical symptoms of the Buruli ulcer are more pronounced hyperpigmentation of the skin in the palpable infiltrate region, which is due not so much to the local disturbance of the melanogenesis function as to the stagnant-cyanotic color and partly the development of hemosiderosis. In the stage of infiltrate formation, general phenomena are usually absent, patients can feel only a feeling of tension in the area of the lesion.

In a week or two (less often before), as a result of central softening, decay and opening of the focus, one, sometimes several ulcers, typical features of which are noticeable depth, up to the subcutaneous fat, unevenly covered with fetid purulent-necrotic masses, seal in the base of the ulcer. The reaction of the regional lymph nodes and the more so the phenomena of periadenitis and lymphangitis are extremely rare and occur only in cases of stratification of the secondary pyococcal flora.

The dynamics of the development of the Buruli ulcer is characterized by peripheral growth and at times a migrating character. As the tendency to scarring on one side of the ulcerative defect, it continues to develop in a different direction. Sometimes, as a result of inoculation near the main, "maternal" ulcers, small, "daughter" foci may form, while their course becomes more torpid, often they are connected along the surface or in the depth, forming fistulous movements and bridges.

The process in many cases lasts from 2 months to 6 months or more and sometimes, even without treatment, is completed by complete scarring of ulcerative defects and deep tissue damage by coarse tightening and deforming scars, which subsequently limit the amount of movement in the affected limb.

Diagnosis of ulcer Buruli

Diagnosis of Buruli ulcer is based in most cases on a typical clinical picture.

Laboratory diagnosis of Buruli ulcer is carried out by a microscopic method (coloring according to Tsil-Nielsen), bacteriologically and PCR. The material for the study is necrotized tissue. The isolation of the pure culture is carried out by directly sowing the test material on the Levenstein-Jensen medium or pre-infecting the mice in the paw pads or subcutaneously into the tail, followed by the transfer of the inflamed tissues to the Levenstein-Jensen medium. The grown up colonies are identified from other species of mycobacteria due to the inability to grow at 37 ° C, the absence of catalase and urease, the inability to reduce nitrate, isoniazid resistance, PASC and ethambutol. Identification should take into account the differences observed between Mycobacterium ulcerans, isolated from different geographical sources. Identification of PCR can be carried out either directly from clinical material or grown culture

Differential diagnosis of Buruli ulcer in tropical conditions is necessary with tropical ulcers, leishmaniasis, skin tuberculosis, nome and other ulcerative processes.

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Treatment of Buruli ulcer

Treatment of Buruli ulcer in the stage of infiltration before ulceration is the administration of antibiotics, primarily rifampicin, as the most effective for all mycobacteriosis. With a formed ulcer, the surgical excision of defects with subsequent possible plastic surgery becomes the method of choice. Outwardly, various disinfectants and cleansing agents in the form of bandages are applied to ulcerative defects. Necrotic lesions are excised, in advanced cases, amputation of the affected limb may be required. The earlier the treatment of Buruli ulcer is started, the faster the scarring and with less disabling effects.

How is Buruli ulcer prevented?

There is no specific prophylaxis of Buruli ulcer. However, it is believed that repeated BCG can provide a protective effect by 30-40%. In the main endemic countries, under the auspices of WHO, special educational programs are carried out among the population aimed at eliminating environmental factors that increase the risk of acquiring Buruli ulcers.

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