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Clinical Parasitology > Coccidians > Flashcards

Coccidians Flashcards

1
Q

Class Sporozoea

A

Coccidia

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2
Q

Infect the intestinal tracts of animals.

A

Coccidian parasites

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3
Q

obligate, intracellular parasites, which means that they must live and reproduce within an animal cell.

A

Coccidian

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4
Q

with no definite organ of locomotion.

A

Coccidia

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5
Q

It may have body flexion, gliding or undulating of longitudinal ridges.

A

Coccidia

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6
Q

Characterized by thick-walled oocysts excreted in feces.

A

Coccidians

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7
Q

[5] Coccidian in Humans

A
  1. Cryptosporidium
  2. Isospora
  3. Cyclospora
  4. Toxoplasma
  5. Sarcocystis
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8
Q

[3] Only a single direct cycle of transmission occurs, both the asexual and sexual stages of multiplication occurs in a single host and that is to man.

A

Cryptosporidium
Isospora
Cyclospora

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9
Q

[2] The sexual stages are usually in the intestinal mucosa of a carnivorous host (the predator). The result in an oocyst or sporocyst that passes out in the feces to infect an intermediate host (the prey) in which asexual multiplication of the parasite occur.

A

Toxoplasma
Sarcocystis

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10
Q

[3] Life cycle of Coccidians

A
  1. Merogony
  2. Gametogony
  3. Sporogony
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11
Q

schizogony

[life cycle of coccidians]

A

Merogony

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12
Q

produce merozoites.

[life cycle of coccidians]

A

Merogony

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13
Q

gamogony or gametocytogenesis.

[life cycle of coccidians]

A

Gametogony

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14
Q

produce micro- and macrogametes.

[life cycle of coccidians]

A

Gametogony

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15
Q

produce sporozoites.

[life cycle of coccidians]

A

Sporogony

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16
Q

completed on host cell.

[life cycle of coccidians]

A

Sporogony

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17
Q

thin (autoinfection) or thick walled oocysts.

[life cycle of coccidians]

A

Sporogony

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18
Q

cosmopolitan distribution.

A

Toxoplasma Gondii

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19
Q

seropositive prevalence rates vary — generally 20-75%

A

Toxoplasma Gondii

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20
Q

Generally causes very benign disease in immunocompetent adults.

A

Toxoplasma Gondii

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21
Q

tissue cyst forming coccidia.

A

Toxoplasma Gondii

22
Q

It has been coined for the first, actively multiplying merozoites that develop within the intermediate host, irrespective of whether infection is from oocysts or tissue cysts.

A

Tachyzoites

23
Q

non-infectious

[metrocytes, bradyzoites]

A

Metrocytes

24
Q

infectious

[metrocytes, bradyzoites]

A

Bradyzoites

25
Q

These [2] are merozoites that develop within tissue cysts.

A

Metrocytes and Bradyzoites

26
Q

Ingestion of sporulated oocysts (cat feces + incubation)

A

Human transmission — Toxoplasma Gondii

27
Q

Ingestion of zoites (tachyzoite & bradyzoites (undercooked meat)

A

Human transmission — Toxoplasma Gondii

28
Q

Congenital infection (only during acute stage)

A

Human transmission — Toxoplasma Gondii

29
Q

Blood transfusions (only during acute stage) .

A

Human transmission — Toxoplasma Gondii

30
Q

The organisms can grow in any organs or tissues, developing in the brain, eyes and skeletal muscles.

A

Pathogenesis — Toxoplasma Gondii

31
Q

There is localized proliferation of the organisms and immunologic hypersensitivity reaction.

A

Pathogenesis — Toxoplasma Gondii

32
Q

Multiplication of the organisms within the infected cell leads to death and rupture of the cell.

A

Pathogenesis — Toxoplasma Gondii

33
Q

A clinical manifestations of Toxoplasma Gondii that is often severe and even fatal.

A

Congenital toxoplasmosis

34
Q

Sabin syndrome (tetrad of signs)

A

Clinical Manifestations — Toxoplasma Gondii

35
Q

[3] Other forms of Toxoplasmasis

A
  1. Typhus-like exanthematous form
  2. Cerebrospinal form
  3. Non-congenital retinochoroiditis infection
36
Q

May produce myocarditis, meningoencephalitis and atypical pneumonia.

[other forms of toxoplasmasis]

A

Typhus-like exanthematous form

37
Q

There is involvement of the CNS and the CSF is xanthochromic.

[other forms of toxoplasmasis]

A

Cerebrospinal form

38
Q

The ocular lesion originates in the retina and spread to the choroids.

[other forms of toxoplasmasis]

A

Non-congenital retinochroiditis infection

39
Q

likely due to both active parasite proliferation and immune hypersensitivity.

[ocular toxoplasmasis]

A

Retinochroiditis

40
Q

generally a recrudescence-rarely from primary infection.

A

Ocular toxoplasmasis

41
Q

most lesions are focal and self-limiting.

A

Ocular toxoplasmasis

42
Q

rapidly destructive in AIDS patients.

A

Ocular toxoplasmasis

43
Q

Inoculation into mice or cell culture (only acute stage).

A

Diagnosis — Ocular Toxoplasmasis

44
Q

Very sensitive and specific but requires maintenance of live organism.

A

Sabin-Feldman methylene blue dye test

45
Q

Serological test: to detect antibodies

A

Diagnosis Diagnosis — Ocular Toxoplasmasis

46
Q

[3] Treatments for Ocular Toxoplasmasis

A
  1. Pyrimethamine and Sulfadiazine
  2. Corticosteroids
  3. Trimethroprim-sulfamethoxazole
47
Q

controls Toxoplasma but do not kill it.

[treatments for ocular toxoplasmasis]

A

Pyrimethamine and Sulfadiazine

48
Q

prevent occurrence of hypersensitivity.

[treatments for ocular toxoplasmasis]

A

Corticosteroids

49
Q

prophylaxis for immunocompromised.

[treatments for ocular toxoplasmasis]

A

Treimethoprim-sulfamethaxazole

50
Q

pyrimethamine can cause lower blood counts.

A

Leucovorin

51
Q

Causes allergic reaction but can be substituted by clindamycin.

A

Sulfadiazine

Clinical Parasitology (19 decks)

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