Presentation On Buruli Ulcer

1. BURULI ULCER DISEASE

2. WHAT IS BURULI ULCER ?
 Buruli ulcer, is a devastating skin disease caused by
Mycobacterium ulcerans.
 It is named after a region called Buruli, near the Nile
river in Uganda, where in 1961 the first large number
of cases were reported. But the first case of BU was
reported in Australia in 1948.
 It is one of the most neglected but treatable tropical
diseases.
 The causative organism is from the family of bacteria
which causes tuberculosis and leprosy but Buruli
ulcer has received less attention than these diseases.
 Infection leads to extensive destruction of skin and
soft tissue with the formation of large ulcers usually
on the legs or arms.
 Patients who are not treated early often suffer long-
term functional disability such as restriction of joint
movement.
 Early diagnosis and treatment are vital in preventing
such disabilities.

3. EPIDEMIOLOGY
 Buruli ulcer occurs most frequently among people who
live or work close to rivers and slow- moving bodies of
water.
 Activities that take place near water bodies, such as
farming, are risk factors, and wearing protective clothing
appears to reduce the risk of the disease.
 The reasons for the growing spread of BU remain unclear.
 All ages and sexes are affected, but most patients are
among children under 15 years.
 The disease can affect any part of the body, about 90% of
the cases are on the limbs, with nearly 60% of all lesions
on the lower limbs.
 Unlike tuberculosis (TB), there is no evidence to suggest
that infection with the human immunodeficiency virus
(HIV) predisposes individuals to BU infection.
 There is also no evidence that the disease can be
transmitted from person to person.

4. THE ORGANISM
 M. ulcerans is an environmental
mycobacterium.
 The organism does not live freely in the
environment
 The organism occupies a specific place
within aquatic environments (e.g. small
aquatic animals, biofilms) from where it
is transmitted to humans by an unknown
mechanism.
 M. ulcerans produces a destructive toxin,
mycolactone, which causes tissue damage
and inhibits the immune response.

5. TRANSMISSION
 The exact mode of transmission is still under
investigation.
 More recent data from Australia suggest that
salt marsh mosquitoes test positive for M.
ulcerans DNA,
 Transmission by this type of mosquito has not
been established.
 Further research is in progress to establish the
exact role of insects and other factors in the
transmission of the disease to humans.
 If confirmed, BU will be the only known
mycobacterial disease to be transmitted by
insects

6. DISTRIBUTION OF THE DISEASE
 About 33 countries worldwide report the disease. Eg.
Benin,Cameron,Togo, Australia, Côte d'Ivoire, Papua New Guinea
etc
 In Ghana, Ashanti, Brong Ahafo, Central, Eastern,
Greater Accra and Western regions routinely report
on the disease.
 Some endemic districts in Ghana are
Amansie West,
Amansie Central,
Ahafo Ano North
Asante Akim North
Atwima Nwabiagya
Sekyere Afram
Plains
Upper Denkyira
Ga West
Akwapim South
Asutifi North & South
Suhum Kraboa Coaltar
Dormaa East / West
Gomoa
Bia
Ahanta West
Asunafo North&South
Ahanta West

7. COUNTRIES WHERE BURULI IS
REPORTED
•Buruli ulcer is still considered a “mystery” disease that many people do not know about.(Health Workers, Teachers, Pastors,
Herbalists, Jounalists, Lawmakers, Law enforcers , General Society)
•As a result, it is under-reported (or poorly documented).
•Today, Buruli ulcer is reported in 33 countries worldwide.
•Within countries, Buruli ulcer occurs in some localized places
.

8. CONTROL STRATEGIES
 In the absence of effective tools to control
BU,current control strategies are aimed at
reducing the prolonged suffering disabilities and
socioeconomic burden associated with the disease
.
Community level activities
 Early case detectionat the community level using
CBSVs
 Information,education and co,,unication (IEC)
campaigns in communities and schools
 Training of CBSVs and strenghtening of
comminity based surveillance system

9. Strenghtening of health system
 Infracstucture,equipment and logistics
(decentralized health centers)
 training of health workers.
 Standardised recording and reporting using
BUO1, BUO2 and BUO4.
 Standardised case management
 Specific antibiotics
 Wound care
 Surgery
 POD
 laboratory confirmation of cases

10. CLINICAL FORMS.
 NODULE
 PLAQUE
 OEDEMA
 ULCER
 OSTEOMYELITIS

11. NODULE STAGE
THIS IS USUALLY PAINLESS,PALPABLE,FIRM LESION 1-2 CM
IN DIAMETER,SITUATED IN THE SUBCUTANEOUS TISSUE
AND TYPICALLY ATTACHED TO THE SKIN.

12. PLAQUE STAGE
IS USUALLY PAINLESS,WELL-DEMARCATED,ELEVATED,INDURATED
LESION,MORE THAN 2CM IN DIAMETER.

13. OEDEMA STAGE
Diffuse, extensive, usually non-pitting
swelling. The affected area has ill-defined
margins, is firm and painless and involves
part or all of a limb or other part of the
body. There may be colour changes over
the affected area and the disease may be
accompanied by fever.

14. OSTEOMYELITIS

15. A TYPICAL BU IS DEFINED AS A SKIN ULCER CHARACTERIZED BY
NECROTIC SLOUGH AND UNDERMINED EDGES. IN THE ABSENCE
OF SECONDARY BACTERIAL INFECTION, THE ULCER IS USUALLY
PAINLESS.

16. CATEGORIES

17. CATEGORY L
A SINGLE LESION < 5CM IN DIAMETER. MOST
CATEGORY 1 LESIONS MAY COMPLETELY HEAL WITH
ANTIBIOTIC TREATMENT.

23. CATEGORY II
A SINGLE LESION BETWEEN 5 AND 15 CM IN
DIAMETER. SOME CATEGORY II LESIONS MAY
COMPLETELY HEAL WITH ANTIBIOTIC TREATMENT

26. CAT III
A SINGLE LESION > 15 CM IN DIAMETER, MULTIPLE
LESIONS, LESIONS AT CRITICAL SITES
(EYE,BREAST,GENITALIA) AND OSTEOMYELITIS.IN
ADDITION TO ANTIBIOTICS, MOST OF CATEGORY III
LESIONS REQUIRE SURGERY(EXCISION,SKIN GRAFTING OR
AMPUTATION IN SEVERE CASES).

34. BURULI ULCER AT THE CRITICAL SITES

37. TREATMENT
 WHO RECOMMENDATION
 All patients with BU lesions should be
treated with streptomycin 15mg/
Body kg + Rifampicin 10mg/ Body kg
for 8 weeks.
 Surgery reserved as adjuvant therapy.
 Wound care
 Prevention of disability

38. BEFORE AND AFTER ANTIBIOTIC
TREATMENT

39. BEFORE AND AFTER ANTIBIOTIC
TREATMENT

40. BEFORE AND AFTER SURGERY

41. BEFORE AND AFTER
SURGERY

42. BURULI ULCER ACTIVITIES .
 Surveillance for early case detection.

43. PUBLIC EDUCATION IN COMMUNITIES AND
VIDEO SHOW ON WHO BURULI ULCER
DOCUMENTARY.

44. WEEKLY FOLLOW UPS TO HEALTH
CENTRES TO ENSURE PATIENTS
COMPLY WITH CHEMOTHERAPY
REGIMEN.

45. SURGICAL MANAGEMENT OF
CASES (DEBRIDEMENT AND SKIN
GRAFTING)

46. CONTINUED
 Weekly Wednesday BU clinic in consulting
room 3
 Photograph of lesions (documentation)
 Dispensing of Antibiotics & other logistics.

47. LABORATORY CONFIRMATION
-FINE NEEDLE ASPIRATION (FNA)

48. PUNCH BIOPSY

49. SWAB

50. DRESSING OF WOUNDS

51. PREVENTION OF DISABILITY
(POD)
THE TEN TASKS
 Early diagnosis and treatment for Buruli
ulcer
 Hygiene
 Nutrition
 Wound and skin care
 Movement and Exercise
 Positioning
 Reduce swelling
 Scar care
 Participation
 Extra help or Referral

52. LEGACY OF BURULI
ULCER
 Buruli ulcer disease often leaves victims with
harrowing scars and severe contractures,
resulting in social stigma and functional
limitations such as :
 Eye complications
 Contractures
 Amputations

53. EYE COMPLICATIONS.

55. CONTRACTURE

56. CONTRACTURE

58. AMPUTATION

60. SOME CHALLENGES
 Insufficient knowledge of the disease
among both health workers and the
general public, leading to significant
underreporting.
 Late reporting of cases .
 Lack of Funds to do active case search.
 Difficulty for the patients to comply
with chemotherapy treatment.
(injections)

61. THANKTHANK
YOU.YOU.