Introduction to Neglected Tropical Diseases Flashcards

1
Q

What are NTDs?

A

» Ancient diseases of poverty
» Affect the world’s poorest populations
“bottom billion”
» Impact educational and economic stability
» Many are preventable and treatable

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2
Q

Global burden of NTDs?

A

» Affect >1 billion people worldwide
» Often cause chronic disease
» >200 000 people die annually from snakebite evenoming, dengue & rabies
alone

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3
Q

Why do NTD’s promote poverty?

A
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4
Q

What are the UN sustainable development goals?

A
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5
Q

What are the main Neglected ZOONOTIC diseases

A
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6
Q

What are some Vector Borne NTDs?

A
  • Dengue
  • Chagas
  • Lymphatic filariasis
  • Onchocerciasis
  • Leishmaniasis
  • Trypanosomiasis
  • Dracunculiasis
  • schistosomiasis
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7
Q

What is the echinococcus transmission cycle

A
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8
Q

What are some other transmission routes?

A

» Faecal oral-transmission (soil-transmitted helminthiasis)
» Direct skin penetration (hookworm disease)
» Close contact (scabies) & contact of minor injuries (yaws)
» Droplets from nose & mouth (leprosy)
» Bite of infected animal (rabies)
» Transmission route unclear (Buruli ulcer)

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9
Q

What happens with mycetoma, chromoblastomycosis and other deep mycoses?

A

» Chronic, progressively destructive inflammatory disease, usually of foot
» Thought to be caused by traumatic inoculation of fungi or bacteria into subcutaneous
tissue

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10
Q

Nomea?

A

» Severe gangrenous disease of the mouth and face linked to non-specific polymicrobial
organisms
» Associated with poverty and malnutrition, poor access to sanitation and oral hygiene,
recent/ concurrent infection

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11
Q

What causes Buruli ulcer?

A

» Skin infection caused by Mycobacterium
ulcerans

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12
Q

Describe prevalence of Buruli ulcers?

A

» Globally, third most common mycobacterial
disease after TB and leprosy
» Infection is chronic and without treatment can cause permanent disfigurement and disability

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13
Q

Buruli ulcer dx progression?

A

» First sign of infection is a small painless nodule
» Nodule may develop into a plaque, sometimes with oedema
» Over a period of months an open lesion with characteristic undermined edges develops

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14
Q

Buruli ulcer pathogenesis?

A

» Buruli ulcer pathology attributable
to production of a polyketide
lactone
» Mycolactone inhibits sec61
dependent translocation of
proteins into the ER, blocking
immune responses and triggering
cell death pathways

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15
Q

Diagnosis of Buruli ulcer?

A

» Case definition: undermined edges, cotton wool appearance, thickening of skin,
characteristic smell
» Microscopy: Ziehl-Neelsen staining for acid fast bacteria and histopathology
» Culture of M. ulcerans, PCR

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16
Q

Tx of Buruli ulcer?

A

» 8-week course of rifampicin and streptomycin or a combination of rifampicin and clarithromycin (early stages)
» Surgical debridement, skin grafts and antibiotic therapy (late stages)
Wound healing may up to a year

17
Q

Buruli ulcer increasing prevalence & signs?

A

» Buruli ulcer spreading and
showing increasing virulence
» Infection acquired from the
environment
» Most lesions on limbs (55% on
lower and 35% on upper limbs)
» Infections seasonal, most
common in warmer months
» Lesions predominantly on
exposed areas, suggestive of
biting

18
Q

Transmission in australia?

A

» Infected wild possums are a potential
reservoir
» Appearance of possums with visible lesions precedes human cases
» M. ulcerans DNA found in possum faeces
» Infection also found in other domestic and
wild animals
» Direct or indirect mechanical transmission
by mosquitos is thought to lead to human
infection

19
Q

Buruli ulcer transmission in west africa?

A

» Most lesions on limbs and exposed areas
» Seasonal infection, risk highest in rainy
season
» No animal reservoir has been identified
» No insect vector has been found
» No evidence for transmission by mosquitos

20
Q

What is buruli ulcer associated with in west africa?

A

» Infection is associated with water
contact
» Environmental disturbance by
flooding, mining, deforestation and
farming has been linked to
transmission
» Water bugs found to carry M.
ulcerans, not known to bite humans
» No human-to-human transmission

21
Q

Buruli ulcer contorl?

A
  • No vaccine
  • Prophylaxis impractical
  • Contorl relies on education & early detection

-> Local & national infrastructure
-> Standardised reporting and case management
-> Integrated approaches

22
Q

What causes Chagas disease? & what does it cause

A

» Caused by the protozoan parasite Trypanosoma cruzi
» Acute infection is systemic
» Chronic infection can damage heart, oesophagus or colon

23
Q

Transmission of Chagas?

A

» Chagas disease is transmitted by bloodsucking
triatomine bugs or “Kissing bugs”
» Parasite found in bug faeces and urine
» After a bloodmeal, bug defecates and parasite
introduced into the wound by scratching

24
Q

Lifecycle of chagas?

25
Q

What are some other transmission mechanisms of chagas?

A

» Oral infection: ingestion of contaminated food or drink
» Blood transfusion
» Transplantation
» Congenital (mother to child during pregnancy)
» Laboratory infection
» Sexual transmission

26
Q

Diagnosis of Chagas?

A

» Acute stage: blood smear, Romaña sign, epidemiology
» Chronic stage: clinical symptoms, epidemiology, serology (ELISA,
indirect immunofluorescence and indirect hemagglutination, positive in
at least two tests)

27
Q

Tx for chagas?

A

» Nifurtimox or benznidazole
» Highly effective in acute stage, limited efficacy in chronic stage
» Multiple adverse effects, contraindicated in pregnancy

28
Q

Control of chagas?

A

» Vector control: house spraying, housing improvement, bednets, community education
» Blood screening: serological testing of blood for
transfusion
» Patient care
» International co-operation