Buruli Ulcer Flashcards

1
Q

What causes Buruli Ulcer ?

A

Mycobacterium ulcerans

Occurs in :

  • people living close to lakes, rivers, or marshy areas
  • mining, deforestation or flooding
  • Trauma- most likely means by which Mycobacterium ulcerans is introduced
  • Hypothesis: Inoculation of Mycobacterium ulcerans into the skin -by aquatic insects or -by mosquitoes (Australian scientists) So basically nobody fucking knows.
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2
Q

Disease geographical distribuion?

A

SSA West > east and Australia (just a few coastal locations

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3
Q

Disease epidemiology?

A

In Africa overwhelmingly affects children. In Australia, adults

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4
Q

Pathogenesis

A

The ulcer is caused by M Ulcerans secreting a toxin called MYCOLACTONE

It causes:

  • Cell cycle arrest
  • Apoptosis
  • At low concentration it suppresses – Dendritic cells – Macrophage – T-cell function abrogating cytokine and chemokine secretion in response to mitogens • Down regulation of: – Inflammatory mediators – Lipid metabolism – Coagulation – Tissue remodeling
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5
Q

Clinical presentation

A

Active disease is divided into: • non-ulcerative (papule, nodule, plaque, oedema) • ulcerative forms and osteomyelitis

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6
Q

Differential for non ulcerative buruli

A
  • Abscess—————————Painful
  • Lipoma———————– Mobile
  • Ganglion————————-Close to joints
  • Tuberculous lymphadenitis—-Constitutional symptoms
  • Onchocerciasis nodule———-Painless, longhistory
  • Subcutaneous infections such as fungal infection
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7
Q

Differential Diagnosis for ulcer

A
  • Tropical phagedenic ulcers
  • Arterial and venous insufficiency • Diabetic ulcers
  • Sickle cell ulcer
  • Cutaneous leishmaniasis
  • Extensive ulcerative yaws
  • Haemophilus ducreyi ulcers
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8
Q

Diagnosis of Buruli

A
  • Swabs for ulcerative lesions
  • Fine needle aspiration (FNA) for mainly

non-ulcerative lesions

– nodules,
– papules
– oedema
– some ulcerative lesions

Goal is PCR. Highly sensitive and specific.

• Biopsy in case of surgery

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9
Q

Management

A

Principles of current BU management

• Antibiotic appropriate to kill organisms • Enhance wound healing

Nutrition Wound care Skin grafting

• Disability prevention (simple exercises) • Rehabilitation

RIFAMPICIN + CLARITHROMYCIN

Or Streptomycin (never in pregnant women) or Moxifloxacin

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10
Q

Antibiotic side effects

A

Antibiotic side effects

In less than 2% of patients

skin rash (streptomycin & rifampicin)

deafness, dizziness, vomiting, decreased urine output (streptomycin),

anorexia, nausea, abdominal pain, jaundice and renal failure (rifampicin)

Nausea, altered taste, jaundice, hepatitis (clarithromycin)

Tendonitis, rash (moxifloxacin)

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11
Q

Describe Paradoxical reactions and their management

A

Paradoxical reactions

Occurred in 8.4% of patients

Lesion enlargement, pus filled, same/new site

May be culture positive during antibiotic treatment

Associated with high bacterial load

Heal without antibiotic treatment beyond 8 weeks and with & without corticosteroids

Unpredictable

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12
Q

Describe the WHO Buruli ulcer Control Strategy

A

Early case detection (education at village level)

Improved care (labs, treatment, wound care etc)

Supporting activities (Supervision advocacy and research)

all leading to: health system improvement

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