Blood+Tissue Protozoa Flashcards

1
Q

List some blood and tissue protozoal diseases

A

Malaria, Toxoplasma, Trypanosoma, Leishmania

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2
Q

Malaria parasite

A

Plasmodium spp:
P. falciparum, P. vivax, P. ovale, P. malariae, P.
Knowlesii
(similar life cycles)

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3
Q

Malaria protozoan carrier

A

Anopheles mosquito

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4
Q

Malaria transmission

A

Person to person via mosquito
Shared needles by drug users
Blood transfusion
Organ transplant

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5
Q

Define - Epidemic determinant factors

A

Environmental factors that help the parasite to survive

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6
Q

Epidemic determinant factors for Plasmodium spp

A

(a) Drought
(b) Elevated drug resistance
(c) Abnormal temperature
(d) Land pattern changes
(e) High malnutrition rates

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7
Q

How is drought an epidemic determinant factor for Plasmodium spp

A

Rainfall in usually dry area creates breeding sites

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8
Q

How is elevated drug resistance an epidemic determinant factor for Plasmodium spp

A

No effective antiparasitic means more spread of Plasmodium spp.

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9
Q

How is abnormal temp an epidemic determinant factor for Plasmodium spp

A

hot temp -climate change allows for optimal survival of mosquito species

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10
Q

How is land pattern changes an epidemic determinant factor for Plasmodium spp

A

People moving from country-town, less trees due to buildings, carbon emissions

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11
Q

How is high malnutrition rates an epidemic determinant factor for Plasmodium spp

A

anorexic + obese =malnourished b/c abnormal nutrition, easier for parasite to proliferate in malnourished host

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12
Q

Does each type of pathogen have virulence factors?

What makes it difficult for pathogens to invade?

A

Each pathogen has virulence factors - fungi, parasite, bacteria, virus
-If the host factors (normal flora etc) are intact it is difficult for pathogens to invade and overwhelm

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13
Q

Virulence factors of Plasmodium spp

A

-Antigenic variations (antigens on spp can change; fool host cell into thinking it isn’t a foreign pathogen)

  • Cytoadherence of infected rbc (site adherence factor, allows pathogen infect rbc
  • > RBC well protected but spp overcome this
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14
Q

Malaria life cycle

A
  1. Sporogenic cycle -> mosquito ingests gametocytes (male+female) via human
  2. Gametocytes form macro and microgametes.
  3. Develop ookinetes then oocysts,
  4. They get to cavity of mosquito, burst open and releases sporozoites
  5. Sporozoites in saliva which passes to human via bite (infective stage)
  6. Sporozoites move to liver then form another cycle called exo-erythrocytic cycle.
  7. Takes place outside rbcs.
  8. Schizont (mature sporozoite) ruptures then goes to rbcs.
  9. Now Erythrocitic cycle. (rbc stage)
  10. It will enter rbcs, rbc will rupture and schizonts go to liver or blood.

P vivax and P ovale can remain dormant as hypnozoites in liver.

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15
Q

Lab ID - Malaria

A

Microscopy: Thick & Thin Blood film staining
Stained with Giemsa
-looking for the small trophozoites (ring) in the cells or the banana shaped gametocytes.
Gold std. id method
(purple capped tube - malaria)

Serological methods: to detect Abs is only used
for screening in blood donors. Ab may not be
present in acute infection.

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16
Q

Fluorescent dye technique - Malaria ID

A

Fluorescent dyes that stain nucleic acids have been used in the detection of blood parasites.

  • Kawamoto technique - blood smears on a slide are stained with acridine orange and examined with either a fluorescence microscope or a light microscope adapted with an interference filter system.
  • Differential staining of nuclear DNA in green and of cytoplasmic RNA in red, which allows recognition of the parasites.
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17
Q

Additional Diagnostic Tests - Malaria

A

Ag detection (rapid test):

(a) Plasmodium lactate dehydrogenase-pLDH,
(b) Histidine rich parasite-HRP2,
(c) Pan-Plasmodium LDH,
(d) Quantitative buffy coat-QBC

Molecular tests: PCR

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18
Q

Does Quantitative Buffy Coat Method have good sensitivity in detecting malarial parasites?

A

The QBC method is reported to have a good sensitivity for detection of malaria parasites.

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19
Q

Treatment for blood and tissue protozoa

A

Tissue Schizonticides: - Primaquine

• Blood Schizonticides: - Chloroquine-susceptible -
Chloroquine phosphate; Chloroquine-resistant -
Mefloquine, Quinine sulfate, Pyremethamine-
Sulfadoxine; Doxycycline, Halofantrine, Artemisinin
(Quinghaosu), Atovaquone-proguanil

•Gametocytocidal: - Quinidine gluconate, Artesunate,
Quinine dihydrochloride, Artemether

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20
Q

Malaria species - range in severity of anemia and list symptoms

A

Anaemia usually results mildly in P. ovale, moderately in P. vivax and P. malariae and very severe in P. falciparum.

Symptoms:
- Quotidian/recurring fever, nausea, vomiting,

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21
Q

Malaria - complications

A
  • CNS involvement (cerebral malaria) - may or may not be in P. vivax, P. ovale or P. malariae type but in P. falciparum, there is and usually very severe.
  • Nephrotic syndrome does not occur in P. ovale, may occur in P. vivax, mildly in P. falciparum but usually always in P. malariae

• Hypoglycaemia; Pulmonary oedema & Respiratory distress;
Metabolic (Lactic) Acidosis; Malaria of Pregnancy

22
Q

Malaria prevention

A

Chemoprophylaxis (killing effect against parasite, either within the erythrocytes/ hepatocytes)
Chloroquine phosphate, Mefloquine,
Doxycycline, Atovaquone-proguanil

• PPE & Avoidance: Protective clothing, eradication of
mosquitoes and their breeding sites, use of mesh in
houses, use of insect repellants; health education

• Vaccines – still being developed

23
Q

Parasitic flagellate protozan diseases from family Trypanosomatidae

A

Trypanosoma and Leishmania

24
Q

Why is Trypanosoma and Leishmania called hemoflagellates?

A

• Because these protozoans require hematin obtained

from blood hemoglobin for aerobic respiration

25
Digenetic life cycle
Two host life cycle
26
Trypanosoma and Leishmania have a digenetic life cycle involving insects and vertebrates (T/F)
True
27
Hemoflagellates have up to 8 life cycle stages that differ in flagella placement (T/F)
True
28
Two stages (hemoflagellates) in invertebrates
Amastigote + Trypomastigote | ---in vertebrates
29
Three stages
promastigote, paramastigote, and epimastigote | —in invertebrate hosts.
30
List two stages for Leishmania and Trypanosoma
Leishmania (promastigote (insect->infective stage), amastigote (mammalian stage)) Trypanosoma brucei (epimastigote (insect stage), trypomastigote (mammalian stage))
31
Three stage blood protozoa in Trypanosomiasis
Trypanosoma cruzi (epimastigote (insect stage), tripomastigote (infective stage), amastigote (mammlian stage))
32
Leishmania epidemiology
-Range from rain forests to deserts -More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil.
33
American Trypanosomiasis is also called
Chagas Disease
34
Definitive clinical sign of acute Chagas disease
Romaña’s sign - eyelid swelling/ unilateral bipalpebral edema (due to either bug feces rubbed into eye/bite wound on same side of face as swelling)
35
Palpebral
Related to eyelids
36
Signs and symptoms - Trypanosomiasis
fever, general edema, adenopathy, moderate hepatosplenomegaly, myocarditis sometimes, in children, meningoencephalitis.
37
Hepatosplenomegaly
(HPM) is a disorder where both the liver and spleen swell beyond their normal size
38
Patients can't become lifelong carriers of Trypanomiasis (T/F)
False
39
Leishmaniasis transmission
bite of infected female phlebotomine sandflies.
40
Leishmaniasis life cycle
1. Sandflies inject the infective stage (i.e., promastigotes) from their proboscis 2. Promastigotes that reach the puncture wound are phagocytized by macrophages etc. 3. Promastigotes transform in these cells into the tissue stage of the parasite (i.e., amastigotes), which multiply by simple division, then burst to release parasites and proceed to infect other mononuclear phagocytic cells .
41
Cutaneous and subcutaneous leishmaniasis clinical features
Cutaneous + subcutaenous causes skin lesions, mainly ulcers, on exposed parts of the body Cutaneous Secondary bacterial infections - from ulcerated wounds Subcuteanous Diff is in the destruction of mucus membranes + tissues. Lesions dont heal spontaneously like cutaneous lesions.
42
Visceral leishmaniasis clinical features
irregular bouts of fever, substantial weight loss, swelling of the spleen and liver, and anaemia - resembles malaria
43
Leishmaniasis lab ID
Cutaneous and muco-cutaneous: - PCR - Antigen detection - Biopsy - Touch preparation - Culture (Promastigotes) - Serological tests Visceral: - PCR - Antigen detection, - Bone marrow or splenic aspiration - Touch preparation - Culture - Serological tests (not useful) - Lymph node biopsy
44
African sleeping sickness vs Chagas disease
African sleeping sickness Vector: Tsetse fly Protozoa: Trypanosoma brucei gambiense & T. b. rhodesiense Symptoms: Chancres, seizures, insomnia Treatment: Suramin, melarosprol, pentamidine, eflornithine ``` Chagas disease Vector: Triatomine bugs/ kissing bugs Protozoa: Trypanosoma cruzi. Symptoms: Chagomas (lesions), heart, gastrointestinal Treatment: Benznidazole, nifurtimox, ```
45
Trypanosoma lab ID
Chagas disease Fresh blood or stained smear, PCR, Xenodiagnosis; Serological tests for chronic disease African sleeping sickness Blood smear, PCR, Serological tests
46
Cutaneous and mucocutaneous Leishmaniasis treatment
Cutaneous • The pentavalent antimonial drugs, sodium stibogluconate and meglumine antimoniate, (most widely used) Pentostam (sodium stibogluconate) - safer - (reduces progression to mucosal disease) •Oral antifungal drugs (fluconazole, ketoconazole, itraconazole) Mucocutaneous - Stibogluconate, Amp B, Miltefosine
47
Visceral Leishmaniasis treatment
Drug resistance in India - Liposomal Amphotericin B • Sodium stibogluconate and meglumine antimoniate • Conventional Amphotericin B deoxycholate • Parenteral Paromomycin and Miltefosine • Pentamidine isethionate
48
Treatment for T Brucei Gambiense (early and late infection)
Early infection - Suramin | Late infection - Eflornithine (crosses BBB) +/- Nifurtimox
49
Treatment for T Brucei Rhodesiense (early and late infection)
Early infection - Suramin | Late infection - Melarsoprol
50
Eflornithine has no effect on T Brucei Rhodsciense so Melarsoprol is used (T/F)
True