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Buruli ulcers are indolent, necrotizing
ulcers of the skin
and the
underlying soft tissue .
It is the
third most common mycobacterial disease in immunocompetent people and
affects mainly children living in humid areas of the tropical rain
forest.
First described as a rare disease
in Australia, these ulcers are now recognized as common in Uganda and
Zaire and have been identified in other countries of West Africa, as
well as in South East Asia and central and South America.
Visit:
Atypical Mycobacterial Infection
;
Mycobacterium Leprae Inf.
;
Mycobacterium Avium Intracellulare
;
Mycobacterium ulcerans Inf.
;
Mycobacterium tuberculosis
; Mycobacterium Kansasii
; Mycobacterium Marinum
Infection.
The name is derived from Buruli Country
in Uganda, where a cluster of patients was identified in late 1950s.
The reservoir and route of infection
are unknown, but organisms are probably inoculated by minor
penetrating trauma. The major endemic areas are sparsely populated
river valleys and swampy low-lands.
Buruli ulcers(BU) are caused by
Mycobacterium ulcerans, an acid-fast bacillus that grows slowly on
routine mycobacteriological media at several degrees below body
temperature.
Most Buruli ulcers are on the limbs,
frequently over joints.
The bacilli proliferate in the skin and
subcutaneous tissues and elaborate a cytotoxin that diffuses
symmetrically and causes a contiguous necrosis of all structures in
its path - ( the epidermis, dermis, panniculus, deep fascia,
nerves, vessels, and (rarely) underlying muscle and bone).
These lesion begins as a firm,
painless, subcutaneous nodule that becomes papular and ulcerates.
The perimeter of the ulcer is typically
scalloped and often deeply undermined.
At first the ulcers spread steadily,
under the skin over large areas. After many months the perimeter
stabilizes and healing begins, a process that requires many months.
The eventual scar is broad and
depressed and resembles a healed third degree burn.
Microscopically, there is
coagulation necrosis of the deep dermis and panniculus, with
destruction of dermal collagen and all structures, including blood
vessels, appendages, and nerves.
Image1
;
Image2
Fat tissue
necrosis accompanied by minimal inflammation is considered the most
reliable histopathologic feature of BU.
Large extracellular clusters
of acid-fast bacilli are concentrated in the necrotic exudate, in the
ulcer bed, and in the necrotic adipose tissue of the undermined skin.
Smears of necrotic tissue in
the ulcer bed reveal the organisms.
Preulcerative infections may
be cured by local wide excision.
When excision is
impractical, the most effective therapy is repeated debridement and
grafting, combined with continuous heating of the area to 40 degree
centigrade, using a circulating water jacket.
Rifampin is the
chemotherapeutic agent of choice.
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