Protozoa Flashcards

(100 cards)

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
Lifecycle of T. Brucei
?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
26
Symptoms of T.Brucei
(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
27
Difference between Gambiense and Rhodeiense subtypes
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.
28
Cause for T.Brucei not being cleared by immune system
- reservoir in skin - immune evasion methods with variant surface glycoproteins (VSG) which keep changing - mosaicism ALSO cannot have vaccine for these reasons
29
Diagnostics for T.Brucei
- 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)
30
Treatment for T. Brucei Gambiense
Non-CNS and >6yrs - Fexinidazole CNS - NECT (combination therapy) <6 years - Pentamidine (less than 6 is 5 (pent))
31
Treatment for T. Brucei Rhodeiense
Non-CNS - Suramin CNS - Melarsoprol (Arso - Arsenic)
32
Follow up for stage 2 HAT
6 monthly LPs for 2 years
33
Tsetse fly description
hatchet cell wings upward probiscus striped thorax
34
Vector for Chagas disease and method of innoculation
Rudviig bug - Triatomine Another host is mammals/ Sylvanian creatures Bug defecates after biting - scratching faecal matter into wound or touching eye causes disease.
35
Distribution of Chagas
Central and South America (also worldwide)
36
Lifecycle of T.cruzi
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
37
T. cruzi appearance
C-shaped darker larger large kinetoplast
38
Chagas symptoms
Acute: - Romana sign (eye) - Chagoma - fever, fatigue, headache, diarrhoea Chronic: Silent cardiomyopathy mega-oesophagus mega-colon
39
Diagnostics for T.Cruzi
PCR Buffy coat microscopy Serology
40
Treatment for T.cruzi (including who and why)
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.
41
Vector for leishmaniasis
Biting sandfly (bites at night)
42
Life cycle of Leishmaniasis
Promastigote in sandfly Enters human - moves intracellularly (PHAGOCYTIC CELLS ONLY) Becomes amastigote form and divides in cell NO trypomastigote form many animal reservoirs
43
Types of leishmaniasis
Cutaneous (and mucocutaneous) Leishmaniasis - Baziliensis and Mexicana Visceral Leishmaniasis - Donovani
44
Symptoms of cutaneous Leishmaniasis
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
Which type of cutaneous leishmaniasis relapses?
Mexicana
46
Investigations for cutaneous leishmaniasis
Skin scraping/biopsy Histology PCR - genus specific testing available
47
Reservoir for Visceral Leishmaniasis
Zoonotic reservoir Human skin reservoir - infection can be present in skin without visceral involvement - can later become active. May have false negative tests.
48
Incubation for visceral leishmaniasis
Can be up to 2 years - more acute in migrants
49
Symptoms of visceral leishmaniasis
Fever Weight loss/ cachexia Massive hepatosplenomegaly lymphadenopathy diarrhoea cough pigmentation changes
50
Investigations for visceral leishmaniasis
organ biopsy histology culture PCR DAT - direct agglutination Immunofluorescence - becomes negative 9 months post treatment
51
Major complication of Visceral Leishmaniasis
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
Cutaneous Leishmaniasis treatment
Sodium stibogluconate or Miltefosine IM or IV for 10-20 days
53
Visceral Leishmaniasis treatment
PO miltefosine IV liposomal amphotericin IV/IM pentavalent antimony
54
Distribution of each type of malaria
Falciparum - Africa + the tropics Vivax - South america, SE asia Ovale - West Africa Malariae - tropics and sub tropics Knowlesi - SE asia
55
Which cell type is infected in malaria
erythrocytes
56
Malaria life stages
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
Malaria life cycle
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
Symptoms of malaria
cyclical fevers - usually every 3 days rigors myalgia headaches
59
Signs and symptoms of severe malaria
Prostration (exhaustion) / CNS symptoms respiratory distress Acidosis/AKI Jaundice/hyperbilirubinemia Bleeding / Severe anaemia <70 / splenomegaly/ splenic rupture Hypoglycaemia High lactate High parasitemia
60
Malaria treatment
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
Complications of malaria in pregnancy
- 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
WHO treatment frameworks for malaria in pregnancy
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
How does malaria cause disease
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
Malaria diagnostics
Thick and thin microscopy Buffy coat Rapid antigen tests PCR - finger prick is best due to most parasites in the capillaries ELISA
65
Features of thin film in Falciparum
- delicate structure - double chromatin - multiple infection - normal sized RBC - crescent shapes gametocytes - single stage - Maurer's clefts - accole forms
66
Features of thin film in vivax
- schuffners dots - enlarged RBCs - amoeboid cytoplasm - single infections
67
Features of thin film in ovale
- schuffners dots - enlarged RBCs - single infections - fimbriae - 8-12 merozoites
68
Features of thin film in malariae
- normal sized RBC - single infections - band forms (streaky bacon form)
69
Retinal changes in malaria and their importance
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
When should you give a blood transfusion in malaria
Low transmission setting: Hb <70 or any Hb if decompensated High transmission setting: Hb <50 or any Hb if decompensated
71
Complication of malaria
black water fever
72
Which drug(s) work on stages of malaria besides the blood stage?
Artesunate - works on gametocytes Primaquine - works on hypnozoites Anti-folates - work on liver stage
73
Artesunate MOA
Iron binding leads to endo-peroxide bridges and free radicals
74
Chloroquine side effects
- arrhythmias - neurotoxicity - avoid in epilepsy
75
Quinine Side effects
- QT prolongation - deafness - HYPOGLYCAEMIA
76
Artesunate side effects
post artesunate delayed haemolysis
77
Whats is the ABCD of malaria prophylaxis
A - awareness B - bite prevention C - chemoprophylaxis D - Diagnosis
78
Which malaria prophylaxis can be used in pregnancy?
Mefloquine Chloroquine
79
Malarone pros and cons
Cant be used in pregnancy currently GI upset LFT derangement
80
Mefloquine pros and cons
Have to take for 28 days post Neuro psych SE cant be used in epilepsy
81
doxycycline pros and cons
Cant be used in children or pregnancy photosensitivity GI upset take 28 days post return
82
Chloroquine pros and cons
epilepsy psoriasis
83
Primaquine pros and cons
84
IPT (intermittant preventative treatments) for malaria
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
Difference between stable and unstable malaria
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
Retinal changes in malaria
Retinal whitening cotton wool spots retinal haemorrhage vessel changes
87
Difference in hospital admissions/severe malaria in high transmission settings and low transmission settings
High transmission - hospitalisation mostly in children <5 Low transmission - hospitalisation/severe malaria spread throughout the age groups.
88
How is malaria controlled in the body
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
How does malaria avoid elimination
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
Current malaria vaccine mechanisms
Uses circumsporozoite protein (CSP) bound to Hep B antigen
91
Concentration methods for trypanosomes
Thick film Woo concentration - centrifuge then buffy coat Quantitative buffy coat
92
CNS Toxoplasmosis presentation
Retinal changes Ring enhancing lesions on MRI
93
Treatment for toxoplasmosis CNS disease
Pyrimethamine + Sulphadiazine or Clindamycin + Folic acid Antiepileptics Steroids
94
when to treat iron deficiency anaemia in Malaria
After malaria has been treated - iron replacement can make malaria worse.
95
Haemaglobinopathies protective in malaria
G6PD Sickle cell
96
Drugs which trigger G6PD
Triggering drugs - primaquine, sulfa drugs, nitrofurans.
97
What are the stages in making an area malaria free?
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
What is SUFI
Sufi = scaling up for impact Is a method implemented to reduce malaria by scaling up existing control measures.
99
The amastigotes of which species is found in muscle tissue?
T. cruzi
100
Periodicity in malaria
all are 48hrs except malariae which is 72hrs