Parasitology lab Flashcards

1
Q

Malaria RBC enlarged

A

Pv Po

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2
Q

Malaria Multiple trophozoites

A

Pf

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3
Q

Malaria Maurers clefts Pf

A

few, unevenly distributed

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4
Q

Malaria Schuffner’s dots Pv

A

many, evenly distributed

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5
Q

Malaria Fimbriation

A

Po

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6
Q

Malaria Lifecycle (exoerythrocytic human)

A

Malaria-infected female Anopheles mosquito inoculates sporozoites into human host during blood meal, sporozoites infect liver cells, mature into schizonts which rupture and release merozoites, Pv & Po have hypnozoites that can persist and cause relapse

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7
Q

Malaria Life cycle (erythrocytic human)

A

Merozoites infect RBC, ring stage troph mature into schizonts which rupture releasing merozoites, most infect RBC continuing the cycle, some differentiate into sexual stage (gametocytes) esp as the human host becomes unwell

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8
Q

Malaria Life cycle (mosquito)

A

Female Anopheles takes blood meal and ingests male and female gametocytes, these fertilise creating zygotes, become motile ookinetes which invade the midgut wall, develop into oocyst, grow, rupture and release sporozoites which migrate to mosquito’s saliva glands ready to infect human

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9
Q

Leishmania Life cycle human

A

Phlebotamine blood meal transmits promastigote to human, phagocytosed by macrophage, replicates as amastagote intracellularly

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10
Q

Leishmania Life cycle phlebotamine

A

Phlebotamine blood meal ingests parasitised cell, amastigotes transform into promastigote in midgut, divide in midgut and migrate to proboscis

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11
Q

Leishmania Amastigote

A

In human only

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12
Q

Leishmania Promastigote

A

In phlebotamine sandfly only, not human

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13
Q

Malaria Life cycle (mosquito)

A

Female Anopheles takes blood meal from human ingesting female and male gametes, change in temperature inside mosquito -> fertilisation, ookinete burrows stomach wall forms oocyst, sporozoites develop in oocyst, mature oocyst ruptures, sporozoites migrate to salivary glands

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14
Q

Malaria Life cycle (human)

A

Female Anopheles takes blood meal and injects sporozoites within saliva

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15
Q

Microfilariae Life cycle

A

No multiplication of parasite in mosquito, sex and reproduction occurs in vertebrate host

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16
Q

Arbovirus Definition

A

Arthropod borne virus

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17
Q

Leishmania VL symptoms

A

Fever >2 weeks, splenomegaly or wasting - rule out malaria

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18
Q

Leishmania VL diagnostic algorithm

A

RDT rK39 serum/plasma if pos =confirmed; neg>DAT if >1:3200 =confirmed, if 1:400-1600 borderline - tissue aspirate/microscopy

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19
Q

Leishmania VL relapse algorithm

A

Previous VL - tissue aspirate/microscopy essential

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20
Q

Leishmania PKDL features

A

Papules and nodules with macular hypopigmentation AND lived in or traveled to endemic areas AND/OR PMHx VL treatment

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21
Q

Leishmania PKDL diagnostic algorithm

A

rK39 (South Asia only) - if positive = probable case, treat

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22
Q

Leishmania VL diagnostics

A

RDT rK39 - performs well South Asia, reduced sensitivity in East Africa; DAT direct antigen test more sensitive

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23
Q

Leishmania Feature

A

Intracellular amastigote, reticuloendothelial system, e.g. macrophages of the liver, spleen, bone marrow and skin

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24
Q

Cystoisospora belli Oocyst

A

Oval, large 25-30um, may contain two sporocysts (often not visible), ZN stain

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25
Q

Cystoisospora belli Clinical

A

Self-limited watery diarrhoea, more prolonged in immunocompromised

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26
Q

Cystoisospora belli Treatment

A

SXT

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27
Q

Cyclospora catetanensis Life cycle (human)

A

Human ingest sporulated oocyst, small bowel excyst and relase of sporocyst, sporozoite invasion of epithelium, asexual reproduction merozoite, then sexual reproduction gametocytes to zygote to faeces release of unsporulated oocyst

28
Q

Cyclospora catetanensis Life cycle (environment)

A

Unsporulated oocyst, sporulates in the environment, ready for human ingestion in contaminated food/water

29
Q

Cyclospora catetanensis Oocyst

A

Round 8-10um, variable stain with ZN, classic ‘refractile’ wall with iodine

30
Q

Cyclospora catetanensis Clinical

A

Acute self-limiting diarrhoea or asymptomatic, can be more prolonged in immunosuppressed

31
Q

Cyclospora catetanensis Treatment

A

SXT

32
Q

Pneumocystis jirovecii Pathogenesis

A

Adheres to type 1 pneumocytes, inflammatory response is responsible for significant part of pathology

33
Q

Pneumocystis jirovecii Life cycle (human)

A

Inhalation, asexual replication, sexual conjugation, diploid precyst, maturation, excystment

34
Q

Pneumocystis jirovecii Cysts

A

Black on green Grocott silver stain

35
Q

Pneumocystis jirovecii Diagnosis

A

B-d glucan sens but not spec

36
Q

Pneumocystis jirovecii Treatment

A

SXT, second line = pentamidine, dapsone-trim, clinda-primaquine, atovaquone

37
Q

Microsporidia Names

A

Enterocytozoon bieneusi, Encephalitozoon intestinalis

38
Q

Microsporidia Pathogenesis

A

Hatched spores with extruded polar filaments, eject and impale target cell and pass into cytoplasm

39
Q

Microsporidia Life cycle (human)

A

Human ingest spore (very hardy) germinate, proliferate within cytosol or parasitophorous vacuole, replicate until host cell ruptures, mature spores released and can infect new cells continuing the cycle

40
Q

Microsporidia Clinical

A

Majority asymptomatic, may cause chronic diarrhoea

41
Q

Microsporidia Treatment

A

Albendazole for Encephalitozoon (Enterocytozoon - Fumagillin)

42
Q

Free-living amoeba N fowleri reservoir

A

Warm stagnant water - exists as trophozoite, flagellate, double-walled cyst, including swimming pools

43
Q

Free-living amoeba Acanthamoeba reservoir

A

Water salt or fresh, including chrlorinated, in addition to soil and air (droplet particles)

44
Q

Free-living amoeba Balamuthia mandrillaris reservoir

A

Soil

45
Q

Free-living amoeba PAM Pathogenesis

A

N fowleri enter nasal sinuses, migrates along olfactory nerve, incubation 2-5d severe headache, meningism -> coma

46
Q

Free-living amoeba PAM Diagnosis

A

Direct exam of CSF (Naegleria, Balamuthia not Acanthamoeba), PCR

47
Q

Free-living amoeba PAM Treatment

A

Amphotericin B, Miltefosine, Nitroxoline (none work well, 97% mortality)

48
Q

Free-living amoeba GAE Pathogenesis

A

Acanthamoeba more commonly than Balamuthia mandrillaris - intranasal or break in skin followed by spread to CNS over 3-6 months

49
Q

Free-living amoeba GAE Diagnosis

A

Amoeba rarely present in CSF, H&E stained specimens cysts and trophozoites are found in tissue (may be mistaken for macrophage)

50
Q

Free-living amoeba GAE Treatment

A

Uncertain, Miltefosine, Nitroxoline tried, most patients diagnosed at post mortem

51
Q

Free-living amoeba Amoebic keratitis

A

Acanthamoeba infect cornea - trauma then contamination, both trophozoites and cysts can infect, 93% cases occurred in contact lens wearers

52
Q

Free-living amoeba Amoebic keratitis diagnosis

A

Corneal scrape, troph and cysts, culture, PCR

53
Q

Free-living amoeba Amoebic keratitis treatment

A

PHMB polyhexamethylene biguanide hourly drops, chlorhexidine gluconate, minimum 4-6 weeks

54
Q

Cryptosporidium Oocyst

A

5um (exactly) ZN bright cherry red, auramine, iodine

55
Q

Cryptosporidium Lifecycle (human)

A

Human ingest thick-walled oocyst, small bowel oocyst releases sporozoite infects lumen, matures to trophozoite, asexual to meront or sexual to merozoite to gametes to zygote to oocyst if thin-walled (20%)- autoinfection cycle and thick-walled (80%) exits host ready to infect another human

56
Q

Cryptosporidium Clinical

A

Watery diarrhoea, can vary from asymptomatic to life-threatening, 2-4w in immunocompetent, chronic in immunosuppressed, infection does not provide immunity to further infection. Contributes to childhood malnutrition, growth impairment and cognitive deficit

57
Q

Cryptosporidium Transmission

A

Faecal oral contaminated foods, aerosolised droplets, note infected children shed oocysts for up to a month after diarrhoea resolved, waterborne outbreaks, chlorine has little effect, water needs to be filtered, small infectious dose (100 oocysts), animal reservoirs

58
Q

Cryptosporidium Epidemiology

A

Globally caused 133,000 deaths and loss of 820,000 DALYs

59
Q

Cryptosporidium Treatment

A

Mostly self-limited. Paromomycin, nitazoxanide in immunocompetent effective, but not in immunosuppressed - healthy host immune system is essential to effectiveness of nitazoxanide

60
Q

Toxoplasma gondii Lifecycle (human)

A

Ingestion of free oocysts (cat faeces) or tissue cysts (undercooked meat) - transform into tachyzoites shortly after ingestion, invade leukocytes (promote dissemination) tachyzoites replicate rapidly, cell ruptures, tachyzoites released, tissue cysts (esp brain, muscle) are bradycysts containing bradyzoites, tachyzoites can cross the placenta (bradyzoites do not)

61
Q

Toxoplasma gondii Pathogenesis

A

Toxoplasma is forever - none of the drugs that affect tachyzoites will affect bradyzoites

62
Q

Toxoplasma gondii Congenital

A

T1 less likely to infect but more severe, T3 more likely to infect, less severe - cerebral calcification, retinal lesions

63
Q

Toxoplasma gondii Clinical

A

Toxo encephalitis - can be reactivation or new acquisition

64
Q

Toxoplasma gondii Diagnosis

A

IgG lifelong, rising titre or avidity useful, IgM useful in neonate, PCR on placenta, cord blood, or immunosuppressed patient

65
Q

Toxoplasma gondii Treatment

A

Acute not required, Pregnant spiramycin or pyrimethamine/sulfonamide (controversial) - bradyzoites resistant to drug therapy

66
Q

Toxoplasma gondii Prevention

A

Avoid undercooked meat and contact with cat faeces (esp kittens <1y) any cause for cat to have diarrhoea can start shedding of oocysts again briefly