Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Parasitology > Blood+Tissue Protozoa > Flashcards

Blood+Tissue Protozoa Flashcards

1
Q

List some blood and tissue protozoal diseases

A

Malaria, Toxoplasma, Trypanosoma, Leishmania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Malaria parasite

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Malaria protozoan carrier

A

Anopheles mosquito

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Malaria transmission

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define - Epidemic determinant factors

A

Environmental factors that help the parasite to survive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is drought an epidemic determinant factor for Plasmodium spp

A

Rainfall in usually dry area creates breeding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

No effective antiparasitic means more spread of Plasmodium spp.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Digenetic life cycle

A

Two host life cycle

26
Q

Trypanosoma and Leishmania have a digenetic life cycle involving insects and vertebrates (T/F)

A

True

27
Q

Hemoflagellates have up to 8 life cycle stages that differ in flagella placement (T/F)

A

True

28
Q

Two stages (hemoflagellates) in invertebrates

A

Amastigote + Trypomastigote

—in vertebrates

29
Q

Three stages

A

promastigote, paramastigote, and epimastigote

—in invertebrate hosts.

30
Q

List two stages for Leishmania and Trypanosoma

A

Leishmania (promastigote (insect->infective stage), amastigote (mammalian stage))

Trypanosoma brucei (epimastigote (insect stage), trypomastigote (mammalian stage))

31
Q

Three stage blood protozoa in Trypanosomiasis

A

Trypanosoma cruzi (epimastigote (insect stage), tripomastigote (infective stage), amastigote (mammlian stage))

32
Q

Leishmania epidemiology

A

-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
Q

American Trypanosomiasis is also called

A

Chagas Disease

34
Q

Definitive clinical sign of acute Chagas disease

A

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
Q

Palpebral

A

Related to eyelids

36
Q

Signs and symptoms - Trypanosomiasis

A

fever, general edema, adenopathy, moderate hepatosplenomegaly, myocarditis
sometimes, in children, meningoencephalitis.

37
Q

Hepatosplenomegaly

A

(HPM) is a disorder where both the liver and spleen swell beyond their normal size

38
Q

Patients can’t become lifelong carriers of Trypanomiasis (T/F)

A

False

39
Q

Leishmaniasis transmission

A

bite of infected female phlebotomine sandflies.

40
Q

Leishmaniasis life cycle

A
  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
Q

Cutaneous and subcutaneous leishmaniasis clinical features

A

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
Q

Visceral leishmaniasis clinical features

A

irregular bouts of fever, substantial weight loss, swelling of the spleen and liver, and anaemia - resembles malaria

43
Q

Leishmaniasis lab ID

A

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
Q

African sleeping sickness vs Chagas disease

A

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
Q

Trypanosoma lab ID

A

Chagas disease
Fresh blood or stained smear,
PCR, Xenodiagnosis;
Serological tests for chronic disease

African sleeping sickness
Blood smear,
PCR,
Serological tests

46
Q

Cutaneous and mucocutaneous Leishmaniasis treatment

A

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
Q

Visceral Leishmaniasis treatment

A

Drug resistance in India
- Liposomal Amphotericin B
• Sodium stibogluconate and meglumine antimoniate
• Conventional Amphotericin B deoxycholate
• Parenteral Paromomycin and Miltefosine
• Pentamidine isethionate

48
Q

Treatment for T Brucei Gambiense (early and late infection)

A

Early infection - Suramin

Late infection - Eflornithine (crosses BBB) +/- Nifurtimox

49
Q

Treatment for T Brucei Rhodesiense (early and late infection)

A

Early infection - Suramin

Late infection - Melarsoprol

50
Q

Eflornithine has no effect on T Brucei Rhodsciense so Melarsoprol is used (T/F)

A

True

Parasitology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions