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NTD Flashcards

1
Q

Schistosomiasis - definition/organisms

A

Water-borne parasitic infection with an intermediate host of freshwater snails. Two primary syndromes including intestinal (S.mansoni, S. japonicum) and urogenital (S.haematobium)

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2
Q

Schistosomiasis - geographical distribution

A

Mansoni - Sub-Saharan Africa and Brazil

Japonicum - China, Philippines, Indonesia

Haematobium - Sub Saharan Africa

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3
Q

Intestinal schistosomiasis clinical features

A

Diarrhoea, abdominal pain, blood in stool
Chronic inflammation can lead to intestinal strictures and obstruction, as well as liver fibrosis and portal hypertension

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4
Q

Urogenital schistosomiasis clinical features

A

Haematuria, dysuria. Chronic inflammation leading to contractures, hydronephrosis and squamous cell carcinoma of the bladder

Male/female genital schistosomiasis can cause STI symptoms like vaginal/bloody discharge and itch, pain during sex, infertility, increased risk of HIV

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5
Q

Acute (Katayama fever)

A

4-6 weeks later fever, urticaria, cough, abdominal pain

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6
Q

Schistosomiasis non-specific clinical features

A

Anaemia, growth faltering, reduced educational performance, cecariae dermatitis

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7
Q

Ectopic presentations of schistosomiasis

A

Transverse myelitis, pulmonary HTN and cerebral schistosomiasis

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8
Q

Schistosomiasis diagnostics - parasitological methods

A
  1. Stool microscopy - Kato-Katz (thick faecal smear)
  2. Urine microscopy - egg count, urine filtration and centrifugation
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9
Q

Intestinal schistosomiasis - diagnostics

A
  1. Stool microscopy
  2. Faecal occult blood/calprotectin
  3. Eosinophils + Hb
  4. Colonoscopy
  5. US liver
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10
Q

Urogenital schistosomiasis - diagnostics

A
  1. Urine microscopy
  2. Urine dip (haematuria)
  3. Urine antigen detection CAA (cannot speciate)
  4. Ultrasound and cystocopy
  5. Eosinophilia
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11
Q

Schistosomiasis - returning traveller approach to diagnostics

A
  1. Asymptomatic – wait for 3 months after last freshwater contact.
    - Serology for schisto antibodies
    - Blood count (Hb, eosinophilia)
    - 3 x MSU for RBCs/ova
    - 3 x stool for ova
  2. Febrile presentation
    - Exclude other life threatening illnesses
    - Will need repeat PZQ if diagnosis confirmed
    - Unclear whether steroids might be worth giving
  3. Symptoms e.g. haematuria/change in ejaculate
    Same as 1. and refer to Urology/Gastro/Gynae depending on symptom
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12
Q

Schistosomiasis - returning from an endemic area - approach to diagnostics

A
  1. Asymptomatic
    - Blood count (eosinophilia)
    - 3 x MSU RBCs/ova
    - 3 x stool for ova
    - Urine antigen detection CAA (most sensitive and can be used for all types, CCA for S mansoni)
  2. Symptoms or signs (e.g. haematuria, splenomegaly)
    Same as 1 and include onward referral to Urology/Gastro/Gynae
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13
Q

Schistosomiasis treatment

A

Praziquantel
Needs repeat as not effective against non-adult forms

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14
Q

Praziquantel in schistosomiasis - pros and cons

A

Pros:
- Safe
- Effective against all species

Cons:
- Only effective against adults
- Global shortage
- Requires second dose a month later
- Taste is horrible

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15
Q

Prevention measures in schistosomiasis

A
  1. MDA annually in endemic regions
  2. Improved sanitation (open defecation and urination)
  3. Snail control - mulluscicides, habitat modification
  4. Safe water provisions
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16
Q

Onchocerciasis - organism

A

Onchocerca volvulus parasite

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17
Q

Onchocerciasis - transmission

A

Transmitted by blackflies (Simulium damnosum and Simulium ochraceum). Females bite outdoors in the daytime

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18
Q

Onchocerciasis - life cycle

A
  1. Blackflybites host and delivers 3rd stage larvae into the skin
  2. Larvae mature into adult worms in the subcutaneous tissue (itching)
  3. Adult worms produce microfilariae which migrate through the skin and eyes. They die, leading to inflammation and pathology
  4. When a blackfly bites a human it ingests the microfilariae which move into the midgut then to flight muscles before moving on to the mouthparts
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19
Q

Onchocerciasis - clinical features

A
  1. Skin - itching and firm/painless subcutaneous nodules in the acute stage followed by skin atrophy and patchy depigmentation (leopard skin) chronically
  2. Eye symptoms including keratitis, anterior uveitis, secondary cataracts, optic atrophy and chorioretinitis.
  3. Neurological - epilepsy, nodding phenomenen
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20
Q

Ochocerciasis - diagnostics

A
  1. Skin snips with microscopy to see the microfilariae
  2. Ov16 ELISA test
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21
Q

Onchocerciasis - treatment

A
  1. Ivermectin - does not kill adult worms so often needs prolonged/recurrent treatment
  2. Doxycycline - kills the Wolbachia bacteria which is needed for worm fertility. Give a 4 week course for definitive treatment.
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22
Q

Prevention strategies in onchocerciasis (5)

A
  1. Community directed treatment with ivermectin (MDA)
  2. Vector control - insecticide and environmental management
  3. Health education
  4. Surveillance and mapping
  5. Cross-border collaboration
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23
Q

Challenges in eliminating onchocerciasis (7)

A
  1. Cross border re-invasion
  2. Treatment limitations (ivermectin does not kill adult worms)
  3. Co-infection with Loa Loa endemicity as ivermectin can be life-threatening
  4. Sustaining public interest and funding in the longterm
  5. Conflict zones
  6. Competing public health concerns
  7. Capacity building of expertise - public health, entomologists, laboratories
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24
Q

Baylisascaris procynosis - definition

A

A racoon round worm infection from old poo (not fresh).
Found in Europe, N.America, Japan

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25
Q

Baylisascaris - clinical features

A

Human infections often asymptomatic but can cause visceral larva migrans, neural larva migrans and ocular larva migrans

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26
Q

Baylisascaris - treatment

A

Zap the eye with laser
Albendazole
Steroids in neurological diseases

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27
Q

Diffuse unilateral subacute neuroretinitis - definition and causes (5)

A

DUSN is caused by a live, motile nematode infecting the retina
It primarily affects one eye and leads to inflammation, vision loss, and retinal damage if untreated

  • Gnathatoma - Thailand - eating raw fish/frog (drill head)
  • Angiostrongylus - America, Vietnam, Thailand, Hawaii
  • Toxocara canis, ancylostoma caninum (dog poo)
  • Strongyloides
  • Baylisascaris
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28
Q

Ciguatera poisoning - symptoms

A

Diarrhoea and vomiting within hours of ingestion
Neurological symptoms 3-72 hours after ingestion (paraesthesia, metallic taste, hot/cold allodynia, reversible cerebellar dysfunction)
Cardiovascular: Bradycardia, heart block, hypotension

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29
Q

Ciguatera poisoning - definition

A

Non-bacterial fish poisoning which can occur worldwide - especially Asia and Caribbean

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30
Q

Ciguatera poisoning - differentials

A

GBS, MS, organophosphate poisoning, botulism, scombroid, shellfish and pufferfish poisoning

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31
Q

Scombroid - symptoms

A

ALLERGY - Rash, palpitations, tachycardia

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32
Q

Shellfish poisoning - symptoms

A

GI upset, rapid onset pararesthesia and paralysis

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33
Q

Pufferfish poisoning - symptoms

A

Weakness (Na channel blockage)

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34
Q

Botulism - symptoms

A

GI upset, CN dysfunction, descending paralysis

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35
Q

Sea urchin injury - definition and treatment

A

Painful, visible puncture wounds
Causes granulomatous inflammation
1. Hot water soak
2. Remove visible spines where possible
3. Cover with antibiotics (staph, strep, mycobacterium marinarum, aeromonas hydrophilia) and topical steroids

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36
Q

Phytophotodermatosis - definition

A

Contact dermatitis on the skin when certain compounds are exposed to sunlight. This reaction results in skin inflammation and can cause blistering, redness, and hyperpigmentation.

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37
Q

Cutaneous leishmaniasis (diagnostics)

A

Slit skin smear (Giemsa stain) and biopsy

38
Q

Cutaneous leishmaniasis (types)

A

American (more aggressive) - L.brasiliensis/viannia, L.Mexicana
Non-American - L.tropica, L.major, L.aethiopica

39
Q

Leishmaniasis - treatment

A

Local
1. Intra-lesional antimony
2. Heating/freezing

Systemic:
1. PO/IV miltefosine
2. IV liposomal amphotericin B

40
Q

Migratory rashes differentials

A

Gnathastoma spinigerum
Sparganosis
Cutaenous larva migrans
Strongyloides sterocoralis
Loa loa

Eczema
Phytophotodermatosis
Trichinosis (raw pig)

41
Q

Gnathostomiasis - organism, geographical distribution and exposure risk

A

Gnathastoma spinigerum
SE Asia, increasingly in Mexico
Eating undercooked/raw freshwater fish which is the intermediate host

42
Q

Gnathostomiasis - symptoms

A

Acute
Fever, urticaria, GI symptoms

Chronic
Migratory swelling, visceral (lung, GI, meningitis)

43
Q

Gnathostomiasis - Treatment

A

Albendazole 3 weeks

44
Q

Gnathostomiasis - Diagnosis

A

Clinical
Eosinophilia
Serology

45
Q

Leptospirosis

A
46
Q

GBS infectious causes

A

Campylobacter, shigella, influenza, mycoplasma, HIV, covid

47
Q

Visceral leishmaniasis case definition

A

Fever (>2 weeks) + splenomegaly + positive RDT

48
Q

Visceral leishmaniasis - geographical distribution

A

South Asia, East Africa, Latin America

49
Q

Visceral leishmaniasis - transmission

A

Vector: Sandfly - night biting females, can feel the bite.
Reservoirs: Humans, dogs

50
Q

Visceral leishmaniasis - clinical features and labs

A

Fever, splenomegaly, hepatomegaly, anaemia
Weight loss, anorexia, cough, diarrhoea

Labs:
Hypergammaglobulinaemia, anaemia, leucopenia, thrombocytopenia, proteinuria and haematuria

51
Q

What is PKDL?

A

Post Kala Dermal Leishmaniasis
Non-fatal skin considition post visceral leishmaniasis

52
Q

Diagnostics in visceral leishmaniasis

A
  1. Gold standard: Microscopy of LD bodies in Giemsa-stained smears from spleen, lymphoid tissue and bone marrow
  2. Slit skin smear in PKLD
  3. HIV screen
  4. PCR (more often used in research setting, can speciate)
  5. Serology (rk39 antigen test)
53
Q

What is rk39 antigen test used for?

A

Serology for visceral leishmaniasis in Asia

54
Q

How do you diagnose PKDL?

A

Slit skin smear

55
Q

Treatment in visceral leishmaniasis

A
  1. Liposomal amphotericin B
  2. Miltefosine
  3. Paromomycin

HIV: Combination L-AMB + miltefosine

56
Q

Cutaneous leishmaniasis - epidemiology

A

Old world (Non-American) - Phlebotomus sandfly

New world (Americas) - Lutzomyia sandfly (also think viannia)

57
Q

Cutaenous leishmaniasis clinical features

A

Localised:
Wide range of skin lesions including ulcers, nodules, keratotic plaques on exposed areas

Systemic (more common in HIV/immunsuppression)
Mucosal involvement (nose, throat and mouth)
Disseminated, nodular lymphangitis

58
Q

Cutaneous leishmaniasis - diagnostics

A
  1. Microscopy and histology - visualisation of amastigotes in smears or tissue sections
  2. Culture
  3. PCR

NO ROLE FOR SEROLOGY

59
Q

Treatment cutaenous leishmaniasis

A

Key concept: localised vs diffuse infection, is there a risk of mucosal spread (i.e. Americas, viannia, immunosuppressed)

  1. Conservative
  2. Local
    - Intralesional antimonials
    -Cryotherapy
    -Surgery
  3. Systemic
    - Pentavalent antimonials e.g. meglumine
    - Miltefosine (PO) 28 days, teratogenic + nausea
    - Amphotericin B
60
Q

Meglumine

A

Pentavalent antimonial used in the treatment of leishmaniasis

61
Q

Miltefosine

A

Used in treatment of leishmaniasis, teratogenic and associated with nausea

62
Q

Viperidae snake features

A

Vipers, adders, rattlesnakes
Short thick body
Slow moving, ambush
AKI
severe local swelling and bruising

63
Q

Elapidae snake features

A

Cobra, kraits, coral snakes, all Australian venemous snakes
Long thin body
Fast moving
Descending flaccid paralysis. Ptosis –> bulbar/resp paralysis –> necrosis

64
Q

Classic features of a scorpion bite

A

Autonomic storm - massive release of acetylcholine and catecholamines
Cardiorespiratory effects - HTN, shock, pulm odoema
Neurotoxic effects - fasiculation, muscle spasm

65
Q

How to manage a snake bite?

A

Remove from danger
Reassure
Remove tight clothing from the leg
Immbolisation
Pressure pad

66
Q

Trachoma - organism and pathophysiology

A

Chlamydia trachomatis
Recurrent infections leads to inflammation, leading to scarring of the eyelid and entropion. This continued trauma leads to corneal scarring.

67
Q

Trachoma - transmission

A

The 3 F’s

Fingers, flies and formites (surfaces)

68
Q

Trachoma - clinical features

A

Stage 1 - Trachomatous inflammation (follicular) TF
Stage 2 - Trachomatous inflammation intense (TI)
Stage 3 - Trachomatous scarring (TS)
Stage 4 - Trachomatous trichiasis (TT)
Stage 5 - Corneal opacity (CO)

69
Q

Trachoma Stage 1 - Trachomatous inflammation (follicular) TF

A

5 or more follicles on the conjunctiva

Treat with antibiotics - single dose of azithromycin

70
Q

Trachoma Stage 2 - Trachomatous inflammation intense (TI)

A

Tarsal conjunctiva appears red, rough and thickened

Treat with antibiotics - single dose azithromycin

71
Q

Trachoma Stage 3 - Trachomatous scarring (TS)

A

C trachomatis not often found, just evidence of the scarring
Therefore no treatment suggested

72
Q

Trachoma Stage 4 - Trachomatous trichiasis (TT)

A

C trachomatis not often found
Evidence of at least one eyelash rubbing on the eye
Needs surgical management - posterior lamellar tarsal rotation surgery

73
Q

Trachoma Stage 5 - Corneal opacity (CO)

A

Pupil margins blurred due to opacity
Past the point of treatment as the damage has already been done

74
Q

Which stages of trachoma do not warrant treatment?

A

Stage 3 - trachomatous scarring
Stage 5 - corneal opacity

75
Q

Which stages of trachoma warrant antibiotics?

A

Stage 1 - trachomatous inflammation (follicular) TT
Stage 2 - trachomatous inflammation (intense) TI

76
Q

What is the treatment strategy for trachoma?

A

S - surgery
A - antibiotics, including MDA
F - facial cleanliness
E - environmental (better access to water and sanitation)

77
Q

What makes an NTD suitable for elimination? (4)

A
  1. No animal reservoir
  2. Effective intervention
  3. Amenable to surveillance
  4. Public health importance
78
Q

What is the difference between elimination and eradication?

A

Elimination is reducing the incidence of a disease to zero in a defined geographical area. Continued interventions are required to prevent re-introduction

Eradication is permanently reducing the incidence of a disease to zero worldwide

79
Q

Yaws - organism

A

Treponema pertenue
Gram negative spirochaete

80
Q

Clinical stages of Yaws

A

Primary: Initial skin lesion at infection site
Secondary: Spread to other parts of the body, characterised by more extensive lesions
Tertiary: Severe tissue and bone destruction to the face and lower limbs
Latent: Can become formant and asymptomatic

81
Q

Yaws - treatment

A

Azithromycin

82
Q

Noma - definition

A

Rapidly acting orofacial gangrene most commonly affecting children aged 2-5 years

83
Q

Noma - treatment

A

Antibiotics
Antiseptic mouthwash (e.g. chlorhexidine)
Nutritional support
Surgical debridement

84
Q

Buruli ulcer - organism

A

Mycobacterium ulcerans

85
Q

Buruli ulcer - geographical distribution

A

Africa + Australia

86
Q

Buruli ulcer - diagnosis

A

PCR is the gold standard
Takes months to culture
Histopathology can be helpful

87
Q

Buruli ulcer - clinical features

A

Papules, nodules, plaques and odoema

88
Q

Buruli ulcer - treatment

A

Rifampicin + clarithromycin for 8 weeks

89
Q

Guinea worm - organism

A

Dracunculus medinensis

90
Q

Guinea worm - life cycle

A

Drink unfiltered water with L3 larvae
Spend 14 months in the intestine
Females migrate to the skin and release larvae into the water which take 14 days to mature

91
Q

Risk factors for crusted scabies

A

Older age
Immunosuppression
HIV/HTLV1
Malnutrition

ID study (22 decks)

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