Parasitology lab Flashcards
Malaria RBC enlarged
Pv Po
Malaria Multiple trophozoites
Pf
Malaria Maurers clefts Pf
few, unevenly distributed
Malaria Schuffner’s dots Pv
many, evenly distributed
Malaria Fimbriation
Po
Malaria Lifecycle (exoerythrocytic human)
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
Malaria Life cycle (erythrocytic human)
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
Malaria Life cycle (mosquito)
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
Leishmania Life cycle human
Phlebotamine blood meal transmits promastigote to human, phagocytosed by macrophage, replicates as amastagote intracellularly
Leishmania Life cycle phlebotamine
Phlebotamine blood meal ingests parasitised cell, amastigotes transform into promastigote in midgut, divide in midgut and migrate to proboscis
Leishmania Amastigote
In human only
Leishmania Promastigote
In phlebotamine sandfly only, not human
Malaria Life cycle (mosquito)
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
Malaria Life cycle (human)
Female Anopheles takes blood meal and injects sporozoites within saliva
Microfilariae Life cycle
No multiplication of parasite in mosquito, sex and reproduction occurs in vertebrate host
Arbovirus Definition
Arthropod borne virus
Leishmania VL symptoms
Fever >2 weeks, splenomegaly or wasting - rule out malaria
Leishmania VL diagnostic algorithm
RDT rK39 serum/plasma if pos =confirmed; neg>DAT if >1:3200 =confirmed, if 1:400-1600 borderline - tissue aspirate/microscopy
Leishmania VL relapse algorithm
Previous VL - tissue aspirate/microscopy essential
Leishmania PKDL features
Papules and nodules with macular hypopigmentation AND lived in or traveled to endemic areas AND/OR PMHx VL treatment
Leishmania PKDL diagnostic algorithm
rK39 (South Asia only) - if positive = probable case, treat
Leishmania VL diagnostics
RDT rK39 - performs well South Asia, reduced sensitivity in East Africa; DAT direct antigen test more sensitive
Leishmania Feature
Intracellular amastigote, reticuloendothelial system, e.g. macrophages of the liver, spleen, bone marrow and skin
Cystoisospora belli Oocyst
Oval, large 25-30um, may contain two sporocysts (often not visible), ZN stain
Cystoisospora belli Clinical
Self-limited watery diarrhoea, more prolonged in immunocompromised
Cystoisospora belli Treatment
SXT
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
Cyclospora catetanensis Life cycle (environment)
Unsporulated oocyst, sporulates in the environment, ready for human ingestion in contaminated food/water
Cyclospora catetanensis Oocyst
Round 8-10um, variable stain with ZN, classic ‘refractile’ wall with iodine
Cyclospora catetanensis Clinical
Acute self-limiting diarrhoea or asymptomatic, can be more prolonged in immunosuppressed
Cyclospora catetanensis Treatment
SXT
Pneumocystis jirovecii Pathogenesis
Adheres to type 1 pneumocytes, inflammatory response is responsible for significant part of pathology
Pneumocystis jirovecii Life cycle (human)
Inhalation, asexual replication, sexual conjugation, diploid precyst, maturation, excystment
Pneumocystis jirovecii Cysts
Black on green Grocott silver stain
Pneumocystis jirovecii Diagnosis
B-d glucan sens but not spec
Pneumocystis jirovecii Treatment
SXT, second line = pentamidine, dapsone-trim, clinda-primaquine, atovaquone
Microsporidia Names
Enterocytozoon bieneusi, Encephalitozoon intestinalis
Microsporidia Pathogenesis
Hatched spores with extruded polar filaments, eject and impale target cell and pass into cytoplasm
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
Microsporidia Clinical
Majority asymptomatic, may cause chronic diarrhoea
Microsporidia Treatment
Albendazole for Encephalitozoon (Enterocytozoon - Fumagillin)
Free-living amoeba N fowleri reservoir
Warm stagnant water - exists as trophozoite, flagellate, double-walled cyst, including swimming pools
Free-living amoeba Acanthamoeba reservoir
Water salt or fresh, including chrlorinated, in addition to soil and air (droplet particles)
Free-living amoeba Balamuthia mandrillaris reservoir
Soil
Free-living amoeba PAM Pathogenesis
N fowleri enter nasal sinuses, migrates along olfactory nerve, incubation 2-5d severe headache, meningism -> coma
Free-living amoeba PAM Diagnosis
Direct exam of CSF (Naegleria, Balamuthia not Acanthamoeba), PCR
Free-living amoeba PAM Treatment
Amphotericin B, Miltefosine, Nitroxoline (none work well, 97% mortality)
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
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)
Free-living amoeba GAE Treatment
Uncertain, Miltefosine, Nitroxoline tried, most patients diagnosed at post mortem
Free-living amoeba Amoebic keratitis
Acanthamoeba infect cornea - trauma then contamination, both trophozoites and cysts can infect, 93% cases occurred in contact lens wearers
Free-living amoeba Amoebic keratitis diagnosis
Corneal scrape, troph and cysts, culture, PCR
Free-living amoeba Amoebic keratitis treatment
PHMB polyhexamethylene biguanide hourly drops, chlorhexidine gluconate, minimum 4-6 weeks
Cryptosporidium Oocyst
5um (exactly) ZN bright cherry red, auramine, iodine
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
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
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
Cryptosporidium Epidemiology
Globally caused 133,000 deaths and loss of 820,000 DALYs
Cryptosporidium Treatment
Mostly self-limited. Paromomycin, nitazoxanide in immunocompetent effective, but not in immunosuppressed - healthy host immune system is essential to effectiveness of nitazoxanide
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)
Toxoplasma gondii Pathogenesis
Toxoplasma is forever - none of the drugs that affect tachyzoites will affect bradyzoites
Toxoplasma gondii Congenital
T1 less likely to infect but more severe, T3 more likely to infect, less severe - cerebral calcification, retinal lesions
Toxoplasma gondii Clinical
Toxo encephalitis - can be reactivation or new acquisition
Toxoplasma gondii Diagnosis
IgG lifelong, rising titre or avidity useful, IgM useful in neonate, PCR on placenta, cord blood, or immunosuppressed patient
Toxoplasma gondii Treatment
Acute not required, Pregnant spiramycin or pyrimethamine/sulfonamide (controversial) - bradyzoites resistant to drug therapy
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
