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DTM&H 2024 > Parasitology lab > Flashcards

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
Cystoisospora belli Clinical
Self-limited watery diarrhoea, more prolonged in immunocompromised
26
Cystoisospora belli Treatment
SXT
27
Cyclospora catetanensis Life cycle (human)
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
Cyclospora catetanensis Life cycle (environment)
Unsporulated oocyst, sporulates in the environment, ready for human ingestion in contaminated food/water
29
Cyclospora catetanensis Oocyst
Round 8-10um, variable stain with ZN, classic 'refractile' wall with iodine
30
Cyclospora catetanensis Clinical
Acute self-limiting diarrhoea or asymptomatic, can be more prolonged in immunosuppressed
31
Cyclospora catetanensis Treatment
SXT
32
Pneumocystis jirovecii Pathogenesis
Adheres to type 1 pneumocytes, inflammatory response is responsible for significant part of pathology
33
Pneumocystis jirovecii Life cycle (human)
Inhalation, asexual replication, sexual conjugation, diploid precyst, maturation, excystment
34
Pneumocystis jirovecii Cysts
Black on green Grocott silver stain
35
Pneumocystis jirovecii Diagnosis
B-d glucan sens but not spec
36
Pneumocystis jirovecii Treatment
SXT, second line = pentamidine, dapsone-trim, clinda-primaquine, atovaquone
37
Microsporidia Names
Enterocytozoon bieneusi, Encephalitozoon intestinalis
38
Microsporidia Pathogenesis
Hatched spores with extruded polar filaments, eject and impale target cell and pass into cytoplasm
39
Microsporidia Life cycle (human)
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
Microsporidia Clinical
Majority asymptomatic, may cause chronic diarrhoea
41
Microsporidia Treatment
Albendazole for Encephalitozoon (Enterocytozoon - Fumagillin)
42
Free-living amoeba N fowleri reservoir
Warm stagnant water - exists as trophozoite, flagellate, double-walled cyst, including swimming pools
43
Free-living amoeba Acanthamoeba reservoir
Water salt or fresh, including chrlorinated, in addition to soil and air (droplet particles)
44
Free-living amoeba Balamuthia mandrillaris reservoir
Soil
45
Free-living amoeba PAM Pathogenesis
N fowleri enter nasal sinuses, migrates along olfactory nerve, incubation 2-5d severe headache, meningism -> coma
46
Free-living amoeba PAM Diagnosis
Direct exam of CSF (Naegleria, Balamuthia not Acanthamoeba), PCR
47
Free-living amoeba PAM Treatment
Amphotericin B, Miltefosine, Nitroxoline (none work well, 97% mortality)
48
Free-living amoeba GAE Pathogenesis
Acanthamoeba more commonly than Balamuthia mandrillaris - intranasal or break in skin followed by spread to CNS over 3-6 months
49
Free-living amoeba GAE Diagnosis
Amoeba rarely present in CSF, H&E stained specimens cysts and trophozoites are found in tissue (may be mistaken for macrophage)
50
Free-living amoeba GAE Treatment
Uncertain, Miltefosine, Nitroxoline tried, most patients diagnosed at post mortem
51
Free-living amoeba Amoebic keratitis
Acanthamoeba infect cornea - trauma then contamination, both trophozoites and cysts can infect, 93% cases occurred in contact lens wearers
52
Free-living amoeba Amoebic keratitis diagnosis
Corneal scrape, troph and cysts, culture, PCR
53
Free-living amoeba Amoebic keratitis treatment
PHMB polyhexamethylene biguanide hourly drops, chlorhexidine gluconate, minimum 4-6 weeks
54
Cryptosporidium Oocyst
5um (exactly) ZN bright cherry red, auramine, iodine
55
Cryptosporidium Lifecycle (human)
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
Cryptosporidium Clinical
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
Cryptosporidium Transmission
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
Cryptosporidium Epidemiology
Globally caused 133,000 deaths and loss of 820,000 DALYs
59
Cryptosporidium Treatment
Mostly self-limited. Paromomycin, nitazoxanide in immunocompetent effective, but not in immunosuppressed - healthy host immune system is essential to effectiveness of nitazoxanide
60
Toxoplasma gondii Lifecycle (human)
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
Toxoplasma gondii Pathogenesis
Toxoplasma is forever - none of the drugs that affect tachyzoites will affect bradyzoites
62
Toxoplasma gondii Congenital
T1 less likely to infect but more severe, T3 more likely to infect, less severe - cerebral calcification, retinal lesions
63
Toxoplasma gondii Clinical
Toxo encephalitis - can be reactivation or new acquisition
64
Toxoplasma gondii Diagnosis
IgG lifelong, rising titre or avidity useful, IgM useful in neonate, PCR on placenta, cord blood, or immunosuppressed patient
65
Toxoplasma gondii Treatment
Acute not required, Pregnant spiramycin or pyrimethamine/sulfonamide (controversial) - bradyzoites resistant to drug therapy
66
Toxoplasma gondii Prevention
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

DTM&H 2024 (32 decks)

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