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DTMH > Protozoa > Flashcards

Protozoa Flashcards

1
Q

Life stages of protozoa

A

Cysts
Trophozoites

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2
Q

Ciliated protozoan infecting humans

A

Balantidiasis (A pig with hairy balanitis)

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3
Q

Big signet ring shaped protozoan cyst

A

Blastocystis (Blastoise with a signet ring)

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4
Q

Intracellular gut protozoa

A

Microsporidiosis (small to fit into cell)

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5
Q

E. hystolytica (and dispar) cyst description

A

smooth outer membrane
1-4 nuclei
10-15um
chromidial bar or glycogen in immature cells

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6
Q

E.coli cyst description
(coli = cool guy = big)

A

15-25um
1-8 nuclei
irregular peripheral chromatin

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7
Q

E.nana cyct description

(na na - little kid)

A

round or oval
1-4 hole like nuclei
7.5-10 um

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8
Q

Giardia egg description

A

oval shaped
10-15um
2-4 nuclei at one end
S shaped axostyle in middle

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9
Q

Adult giardia description

A

Falling leaf motility
8 flagella
sucking disc

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10
Q

Which gut protozoa is not killed by chlorination

A

Cryptosporidium (and similar)
Giardia

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11
Q

Amoebiasis symptoms

A

Dysentery
Perianal ulceration
Tenesmus
Perianal abscess
Amoebic liver abscess - many smaller abscesses join with chocolate brown pus

(Amy has an anal ulcer and likes chocolate)

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12
Q

Diagnostics for amoebiasis

A
  • microscopy
  • PCR
  • Antigen detection test
  • Serology (only in non-endemic areas)
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13
Q

Treatment for amoebiasis and giardia

A

Metronidazole + Nitazoxanide (for cyst treatment in non-endemic areas).
Parmomycin (if pregnant) (has mom in it)

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14
Q

Giardia symptoms

A
  • eggy taste and eggy burps
  • chronic diarrhoea
  • pale greasy stools
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15
Q

Special test for giardia

A

string test

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16
Q

special test for cryptosporidia

A

Acid fast - Ziehl-Neilson stain –> bright red appearance

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17
Q

Cryptosporidia treatment

A

Nitazoxamide, Paromomycin

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18
Q

Relationship between Cryptosporidia and HIV

A
  1. HIV blocks TLR4 receptors for innate immunity, worsening Cryptosporidia infection
  2. Cryptosporidia infected cells express CXCL10 which attracts more T cells to the area, increasing the number of T cells with HIV
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19
Q

Cryptosporidia symptoms in HIV

A

Chronic (rather than self limiting)
Severe
Extra-intestinal manifestations ( cholecystitis, pancreatitis)

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20
Q

Cause of diarrhoea in Asia/Americas and its treatment

A

Cyclosporidia/Isosporidia
Can be severe and chronic in immunosuppressed
Can test with duodenal string test
Treat with Bactrim

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21
Q

Source of Toxoplasmosis infection

A

Cats
Infected meats

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22
Q

Symptoms of toxoplasmosis (in immunosuppressed only)

A

Neurological symptoms predominant - particularly basal ganglia disease
Pneumonia
EBV like illness (early)

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23
Q

Toxoplasmosis treatment

A

6 weeks of pyrimethamine, sulphadiazine, folic acid

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24
Q

Vector for Human African Trypanosoma (HAT) aka sleeping sickness

A

Tsetse fly

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25
Q

Lifecycle of T. Brucei

A

?No amastigote stage
Epimastigote in tsetse fly
Becomes trypomastigote in tsetse mouth
Trypomastigote is injected into human –> divides in lymph and blood.
Short and stumpy form –> reuptake to tsetse
long and slender form –> sexual reproduction
Can progress to meningoencephalitic stage

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26
Q

Symptoms of T.Brucei

A

(1st stage) Haemolymphatic stage:
- Chancre develops at the site of the bite -may ulcerate - is a painful lesion
- Fevers, severe pruritis, lymphadenopathy, myalgia, arthralgia, facial oedema, headaches.
- Lymphadenopathy in neck is known as Winterbottoms sign
- Organ symptoms - cardiac, liver, spleen, eyes, endocrine.
(2nd stage) Meningoencephalitic stage
- Convulsions
- Psych symptoms
- Movement disorders
- Sleep disturbance
- Coma

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27
Q

Difference between Gambiense and Rhodeiense subtypes

A

Rhodeiense = rapid (1 week), high fevers, chancre, more organ symptoms, more trypanosomes in blood. Has zoonotic reservoir.

Gambiense - gradual (weeks-months), low fevers, less chancre, lymphadenopathy, more trypanosomes in LN. NO zoonotic reservoir.

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28
Q

Cause for T.Brucei not being cleared by immune system

A
  • reservoir in skin
  • immune evasion methods with variant surface glycoproteins (VSG) which keep changing
  • mosaicism

ALSO cannot have vaccine for these reasons

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29
Q

Diagnostics for T.Brucei

A
  • thick and thin film
  • LN biopsy
  • LP + CSF
  • BMAT
  • chancre biopsy
  • centrifuge - microhaematocrit - trypanosomes in buffy layer
  • Quantitative buffy coat
  • Card agglutination test

(Buffy the trypanosome slayer)

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30
Q

Treatment for T. Brucei Gambiense

A

Non-CNS and >6yrs - Fexinidazole
CNS - NECT (combination therapy)
<6 years - Pentamidine (less than 6 is 5 (pent))

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31
Q

Treatment for T. Brucei Rhodeiense

A

Non-CNS - Suramin
CNS - Melarsoprol (Arso - Arsenic)

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32
Q

Follow up for stage 2 HAT

A

6 monthly LPs for 2 years

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33
Q

Tsetse fly description

A

hatchet cell wings
upward probiscus
striped thorax

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34
Q

Vector for Chagas disease and method of innoculation

A

Rudviig bug - Triatomine
Another host is mammals/ Sylvanian creatures
Bug defecates after biting - scratching faecal matter into wound or touching eye causes disease.

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35
Q

Distribution of Chagas

A

Central and South America (also worldwide)

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36
Q

Lifecycle of T.cruzi

A

Epimastigote within Triatomine bug
Trypomastigote enters human
Trypomastigote moves intracellularly and differentiates into amastigotes which replicate
Amastigotes maturing into trypomastigotes causes cell lysis and release if infection

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37
Q

T. cruzi appearance

A

C-shaped
darker
larger
large kinetoplast

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38
Q

Chagas symptoms

A

Acute:
- Romana sign (eye)
- Chagoma
- fever, fatigue, headache, diarrhoea

Chronic:
Silent cardiomyopathy
mega-oesophagus
mega-colon

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39
Q

Diagnostics for T.Cruzi

A

PCR
Buffy coat microscopy
Serology

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40
Q

Treatment for T.cruzi (including who and why)

A

Benznidazole or Nifurtimox
- only treat asymptomatic patients, women of child-bearing age and children
- symptomatic patients have high risk of drug side effects - derm reactions, peripheral neuropathy.

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41
Q

Vector for leishmaniasis

A

Biting sandfly (bites at night)

42
Q

Life cycle of Leishmaniasis

A

Promastigote in sandfly
Enters human - moves intracellularly (PHAGOCYTIC CELLS ONLY)
Becomes amastigote form and divides in cell
NO trypomastigote form

many animal reservoirs

43
Q

Types of leishmaniasis

A

Cutaneous (and mucocutaneous) Leishmaniasis - Baziliensis and Mexicana

Visceral Leishmaniasis - Donovani

44
Q

Symptoms of cutaneous Leishmaniasis

A

Incubation is months
Lesion with raised edges and satellite lesions
Distant lesions from lymphatic spread
10% have highly destructive mucocutaneous lesions (braziliensis)
Chiclero’s ear - mexicana type

45
Q

Which type of cutaneous leishmaniasis relapses?

A

Mexicana

46
Q

Investigations for cutaneous leishmaniasis

A

Skin scraping/biopsy
Histology
PCR - genus specific testing available

47
Q

Reservoir for Visceral Leishmaniasis

A

Zoonotic reservoir

Human skin reservoir - infection can be present in skin without visceral involvement - can later become active. May have false negative tests.

48
Q

Incubation for visceral leishmaniasis

A

Can be up to 2 years - more acute in migrants

49
Q

Symptoms of visceral leishmaniasis

A

Fever
Weight loss/ cachexia
Massive hepatosplenomegaly
lymphadenopathy
diarrhoea
cough
pigmentation changes

50
Q

Investigations for visceral leishmaniasis

A

organ biopsy
histology
culture
PCR
DAT - direct agglutination
Immunofluorescence - becomes negative 9 months post treatment

51
Q

Major complication of Visceral Leishmaniasis

A

Post Kala Azar dermal leishmaniasis
- occurs due to the dermal reservoir
- leads to large nodular lesions - usually on the face
- mainly seen in Sudan and India

52
Q

Cutaneous Leishmaniasis treatment

A

Sodium stibogluconate or Miltefosine
IM or IV for 10-20 days

53
Q

Visceral Leishmaniasis treatment

A

PO miltefosine
IV liposomal amphotericin
IV/IM pentavalent antimony

54
Q

Distribution of each type of malaria

A

Falciparum - Africa + the tropics
Vivax - South america, SE asia
Ovale - West Africa
Malariae - tropics and sub tropics
Knowlesi - SE asia

55
Q

Which cell type is infected in malaria

A

erythrocytes

56
Q

Malaria life stages

A

Sporozoite = parasite stage - passes from mosquito to human
Schizont = host cell containing mature parasites
Merozite = parasite released from liver cell
Trophozite = developing parasite in blood cell
Gametocyte = sexual stage of parasite life
Hypnozoites = dormant stage

57
Q

Malaria life cycle

A
  1. Exo-erythrocytic stage
    - sporozoites infect liver cells
    - schizonts form (some dormant hypnozoites)
    - cells burst releasing merozoites
  2. Erythrocytic stage
    - immature trophozoite
    - mature trophozoite –> then becomes:
    a) schizont - bursts RBC and merozoites release to restart the cycle
    b) gametocytes form which are taken up by mosquito blood meal
  3. Sporogonic stage
    - within mosquito
58
Q

Symptoms of malaria

A

cyclical fevers - usually every 3 days
rigors
myalgia
headaches

59
Q

Signs and symptoms of severe malaria

A

Prostration (exhaustion) / CNS symptoms
respiratory distress
Acidosis/AKI
Jaundice/hyperbilirubinemia
Bleeding / Severe anaemia <70 / splenomegaly/ splenic rupture
Hypoglycaemia
High lactate
High parasitemia

60
Q

Malaria treatment

A

Falciparum:
Non-severe: ACT = Artesunate-mefloquine
Severe: IV artesunate (Quinine is 2nd line)

Non falciparum:
Chloroquine (only in non-falciparum)
PO or IV 3 days

2nd line (in resistance areas):
artemether-lumefantrine (Coartem)
OR
dihydroartemisinin-piperaquine

Hyponozoites: Add Primaquine day 3 (avoid in G6PD and pregnancy)
1st trimester pregnancy - Quinine

May also need to consider supportive therapies, ABx

61
Q

Complications of malaria in pregnancy

A
  • pregnancy increases attractiveness to mosquito (more CO2 release)
  • more severe disease - mild pregnancy related immunosuppression.
  • anaemia
  • reduced foetal growth/ low birth weight
  • specific malaria parasites grow in the placenta - causes vascular changes and reduced O2/ nutrient transfer. Parasites in the placenta have variable surface antigens (VSG) so avoid immune detection and clearance. (1st pregnancy with malaria most severe)
  • increase risk of foetal loss (3-8%)
62
Q

WHO treatment frameworks for malaria in pregnancy

A

High incidence
1. Case management
2. ITNs
3. IPTp (intermittant preventative treatment in pregnancy)
- Sulfadoxine/pyrimethamine (SP) monthly (Bactrim if HIV+)

Low incidence
1. Case management
2. ITNs
3. Screen and treat

63
Q

How does malaria cause disease

A

Malaria parasites change the cell structure to something more rigid with outer nodules - this leads to sequestration of the RBCs and consequent cytoadherence and microvascular coagulopathy.

There may also be further involvement of cytokines - unclear.

64
Q

Malaria diagnostics

A

Thick and thin microscopy
Buffy coat
Rapid antigen tests
PCR - finger prick is best due to most parasites in the capillaries
ELISA

65
Q

Features of thin film in Falciparum

A
  • delicate structure
  • double chromatin
  • multiple infection
  • normal sized RBC
  • crescent shapes gametocytes
  • single stage
  • Maurer’s clefts
  • accole forms
66
Q

Features of thin film in vivax

A
  • schuffners dots
  • enlarged RBCs
  • amoeboid cytoplasm
  • single infections
67
Q

Features of thin film in ovale

A
  • schuffners dots
  • enlarged RBCs
  • single infections
  • fimbriae
  • 8-12 merozoites
68
Q

Features of thin film in malariae

A
  • normal sized RBC
  • single infections
  • band forms (streaky bacon form)
69
Q

Retinal changes in malaria and their importance

A

Retinal changes are important as it reflects what may be occurring in the CNS.
Malaria pathology is largely due to RBC sequestration and microhaemorrgahes.

Retinal changes
- papilloedema
- vessel whitening
- retinal cotton wool spots
- retinal haemorrhages

70
Q

When should you give a blood transfusion in malaria

A

Low transmission setting: Hb <70 or any Hb if decompensated
High transmission setting: Hb <50 or any Hb if decompensated

71
Q

Complication of malaria

A

black water fever

72
Q

Which drug(s) work on stages of malaria besides the blood stage?

A

Artesunate - works on gametocytes
Primaquine - works on hypnozoites
Anti-folates - work on liver stage

73
Q

Artesunate MOA

A

Iron binding leads to endo-peroxide bridges and free radicals

74
Q

Chloroquine side effects

A
  • arrhythmias
  • neurotoxicity
  • avoid in epilepsy
75
Q

Quinine Side effects

A
  • QT prolongation
  • deafness
  • HYPOGLYCAEMIA
76
Q

Artesunate side effects

A

post artesunate delayed haemolysis

77
Q

Whats is the ABCD of malaria prophylaxis

A

A - awareness
B - bite prevention
C - chemoprophylaxis
D - Diagnosis

78
Q

Which malaria prophylaxis can be used in pregnancy?

A

Mefloquine
Chloroquine

79
Q

Malarone pros and cons

A

Cant be used in pregnancy currently
GI upset
LFT derangement

80
Q

Mefloquine pros and cons

A

Have to take for 28 days post
Neuro psych SE
cant be used in epilepsy

81
Q

doxycycline pros and cons

A

Cant be used in children or pregnancy
photosensitivity
GI upset
take 28 days post return

82
Q

Chloroquine pros and cons

A

epilepsy
psoriasis

83
Q

Primaquine pros and cons

A
84
Q

IPT (intermittant preventative treatments) for malaria

A

Pregnancy (IPTp) - 3 doses of sulfadoxine-pyrimethamine - 4 weeks apart in 2nd and 3rd timesters
Infants (IPTi) - SP at the time of 2nd and 3rd DTP and MMR vaccines
Seasonal malaria chemoprevention (SMC) - for children <6 year - SP given monthly during season.

85
Q

Difference between stable and unstable malaria

A

Stable malaria = unaffected by natural and man-made changes
- is VERY difficult to control as moderate changes to mosquito populations do not make a difference

Unstable malaria = very sensitive to environmental changes and man-made controls.

86
Q

Retinal changes in malaria

A

Retinal whitening
cotton wool spots
retinal haemorrhage
vessel changes

87
Q

Difference in hospital admissions/severe malaria in high transmission settings and low transmission settings

A

High transmission - hospitalisation mostly in children <5
Low transmission - hospitalisation/severe malaria spread throughout the age groups.

88
Q

How is malaria controlled in the body

A

infected RBCs are taken up by dendritic cells.
Dendritic cells present infected RBC proteins in lymph node
Adaptive immunity activated.
Malaria largely controlled by antibody response

89
Q

How does malaria avoid elimination

A
  1. Sequestration prevents infected RBCs being destroyed by the spleen.
  2. Plasmodium falciparum erythrocyte membrane protein 1 (PFEMP1) has high antigenic variation - body must keep adapting its antibody strains.
  3. Merozoite antibodies only have a very small window of time.
90
Q

Current malaria vaccine mechanisms

A

Uses circumsporozoite protein (CSP) bound to Hep B antigen

91
Q

Concentration methods for trypanosomes

A

Thick film
Woo concentration - centrifuge then buffy coat
Quantitative buffy coat

92
Q

CNS Toxoplasmosis presentation

A

Retinal changes
Ring enhancing lesions on MRI

93
Q

Treatment for toxoplasmosis CNS disease

A

Pyrimethamine + Sulphadiazine or Clindamycin + Folic acid
Antiepileptics
Steroids

94
Q

when to treat iron deficiency anaemia in Malaria

A

After malaria has been treated - iron replacement can make malaria worse.

95
Q

Haemaglobinopathies protective in malaria

A

G6PD
Sickle cell

96
Q

Drugs which trigger G6PD

A

Triggering drugs - primaquine, sulfa drugs, nitrofurans.

97
Q

What are the stages in making an area malaria free?

A
  1. Control
    • A. Optimise vector control and case management
  2. Pre-elimination
    • B. Increase sensitivity and specificity of surveillance
  3. Elimination
    • Reduce transmission through population wide parasite clearance strategies
    • Investigate and clear individual cases and manage follow up
  4. Prevention of reintroduction
98
Q

What is SUFI

A

Sufi = scaling up for impact
Is a method implemented to reduce malaria by scaling up existing control measures.

99
Q

The amastigotes of which species is found in muscle tissue?

A

T. cruzi

100
Q

Periodicity in malaria

A

all are 48hrs except malariae which is 72hrs

DTMH (9 decks)

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