Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Parasitology
Parasites, life cycles, hosts
| Term | Definition |
|---|---|
| How do protozoa move? | Amoeboid mvmt via cytoplasmic protrusions, ciliary mvmt via hair-like projections, flagellar mvmt via beating flagella, gliding motility via parasite actin-myosin motor interactions w/ host PM |
| Which protozoa species are apicomplexans? | Plasmodium, Toxoplasma |
| What is the structure of apicomplexans? | Apicoblast and apical complex |
| What is the apicoblast? | Apicomplexans -> vestigial photosynthesis organelle (evolved from plants) -> FA/iipid synthesis/storage |
| What is the apical complex made of? | Apicomplexans -> dense granules, rhoptry, microneme, conoid structure |
| What are dense granules? | Apicomplexans -> housekeeping of parasitic vacuole (immune defence) -> regulate entry/exit of parasite nutrients |
| What is the rhoptry? | Apicomplexans -> injected into host PM -> form tight junctions -> form PV -> decorated w/ host proteins (against host immunity) -> aids intracellular invasion |
| What are micronemes? | Apicomplexans -> adhesins binding to host PM to pull parasite along via actin-myosin motor gliding motility |
| What is the conoid structure? | Apicomplexans -> secrete proteins for active parasitic invasion -> forms PV -> protect parasite inside host cells from acidification/lysosomal fusion/destruction |
| What are the hosts of Toxoplasma gondii? | Definitive host -> feline, IM host -> rodent/bird |
| What is the lifecycle of Toxoplasma gondii in its definitive host? | Infected animal tissue ingested by cat -> latent bradyzoites reactivated as tachyzoites -> fe/male gametocytes fuse in intestine -> oocytes expelled in faeces -> sporulate (infective/highly persistent) |
| What is the lifecycle of Toxoplasma gondii in its IM host? | Spores ingested by rodent/bird -> parasites penetrate GI wall -> infect macrophages/nucleated cells -> reside as tachyzoites in PV -> proliferate via asexual reproduction -> lyse/reinfect cells -> convert into bradyzoites -> latent in brain tissue cysts |
| What is the pathology of Toxoplasma gondii? | Latent bradyzoite cyst formation -> mild flu-like symptoms, immunocompromised patient -> acute toxoplasmosis (encephalitis, chorioretinitis, death), hemiplegia in HIV patients -> neurologically reduced fear of failure |
| How is Toxoplasma gondii transmitted? | Ingestion of uncooked meat w/ cysts, transplacental -> still birth, congenital blindness, CNS damage -> chorioretinitis, hydrocephalus, intracranial calcifications, wastewater runoff -> coastal areas w/ rising sea temperatures (oocyte survival) |
| What are the hosts of Trypanosome brucei? | Definitive host -> mammal, IM host -> Tsetse fly |
| What is the lifecycle of Trypanosome brucei in its definitive host? | Tsetse fly takes blood meal from mammal -> injects metacyclic trypomastigote -> transform into bloodstream trypomastigote -> multiply by binary fission |
| What is the lifecycle of Trypanosome brucei in its IM host? | Tsetse fly takes blood meal -> ingests bloodstream trypomastigote -> midgut -> procyclic trypomastigote -> multiply by binary fission -> leave midgut -> epimastigote -> multiply in salivary gland -> transform into metacyclic trypomastigote |
| What is the pathology of Trypanosome brucei? | ENlarged lymph nodes, recurring fever from Ag variation, somnolence (African sleeping sickenss), coma |
| What are the hosts of Plasmodium? | Definitive host -> Anopheles mosquito, IM host -> mammal |
| What is the lifecycle of Plasmodium in its definitive host? | Mosquito takes blood meal -> ingested macrogametocyte and exflagellated microgametocyte fuse -> foorm ookinete -> oocyst -> rupture oocyst releases sporozoites |
| What is the lifecycle of Plasmodium in its IM host? | Mosquito takes blood meal from mammal -> injects sporozoites -> infects liver cells -> transform into schizont -> enter RBCs -> transform into immature trophozoite (ring) -> mature -> schizont -> rupture releases merozoite -> gametocytes form in RBCs |
| What forms of natural resistance are there to Plasmodium? | HbS -> sickle cell anaemia, alpha-thalassemia, beta-thalassemia |
| How does HbS confer natural resistance to Plasmodium? | Beta Glu -> Val -> low O2 tension (impair RBC invasion/growth), different RBC morphology (enhanced parasite-infected HbS RBC removal), reduced PfEMP expression (lower Ag variation) |
| How does alpha-thalassemia confer natural resistance to Plasmodium? | Absent (alpha 0) or reduced (alpha +) HbA globin chain -> ineffective haemopoiesis -> reduced RBC rosetting/sequestration -> reduce pathogenicity |
| How does beta-thalassemia confer natural resistance to Plasmodium? | Mutation -> absent (beta 0) or reduced (beta +) HbB globin chain -> ineffective haemopoiesis -> reduced RBC invasion/growth |
| Where is Plasmodium falciparum located? | 50% cases -> all continents xcp Europe -> concentrated in Africa, Caribbean, SE Asia |
| What are the symptoms of Plasmodium falciparum? | Quotidian fever (everyday), respiratory distress, cerebral malaria (parasitised RBCs occlude brain capillaries), 10 day delay in symptomatic infection (asymptomatic liver development) |
| What are the virulence factors of Plasmodium falciparum? | CR1 receptor -> export PfEMP1 protein on RBC PM -> multisubunit protein from 60 var genes -> highly Ag recombinant -> evade immune system, endothelial receptors -> sequester parasitised RBCs in vessels -> continue replicating/avoid spleen clearance |
| What are the RBCs and histology of Plasmodium falciparum? | Infects all RBCs -> unenlarged, distorted, no stippling -> banana-shaped gametocyte, no mature trophozoites/schizonts visible (sequestered in small blood vessels) |
| What is the treatment for Plasmodium falciparum? | Artemisinin -> target RBC stage (trophozoites, schizonts, merozoites) -> inhibit Ca2+ ATPases -> accumulate intracellular Ca2+ (cell death), RTS,S vaccine -> target pre-RBC stage (sporozoites) -> block hepatocyte invasion (merozoite formation) |
| What is the RTS,S vaccine made of? | Plasmodium falciparum -> virus-like particle -> HBsAg fused w/ Plasmodium circumsporozoite protein |
| Where is Plasmodium vivax located? | 15% cases -> outside Africa -> requires Duffy binding protein (minor RBC Ag) that is not present in African RBCs |
| What are the symptoms of Plasmodium vivax? | Tertian fever (every other day) |
| What are the RBCs and histology of Plasmodium vivax? | Infects young RBCs -> enlarged, fimbriated edges, stippling -> latent hyponzoites in liver |
| What is the treatment for Plasmodium vivax? | Quinolines -> accumulate inside food vacuole -> inhibit Hb detoxification of haem into hemozoin (haem accumulation is toxic to plasmodia) |
| Where is Plasmodium ovale located? | <5% cases -> sub-Saharan Africa, western Pacific |
| What are the symptoms of Plasmodium ovale? | Tertian fever (every other day) |
| What are the RBCs and histology of Plasmodium ovale? | Infects young RBCs -> enlarged, fimbriated edges, stippling -> latent hyponzoites in liver |
| What is the treatment for Plasmodium ovale? | Primaquine -> eliminates latent hypnozoites by doing oxidative damage to hepatocytis |
| Where is Plasmodium malariae located? | <5% cases -> Sub-Saharan Africa, SE Asia |
| What are the symptoms of Plasmodium malariae? | Quartan fever (1st and 4th day), relatively asymptomatic |
| What are the RBCs and histology of Plasmodium malariae? | Infects aged RBCs -> unenlarged, no stippling -> no hyponozoite stage (prlonged asymptomatic RBC infection becomes symptomatic years after leaving endemic area), schizont (loose merozoite cluster w/ thickened ring), trophozoite (band formation) |
| Where is Plasmodium knowlesi located? | <5% cases -> SE Asia, zoonosis from primates |
| What are the symptoms of Plasmodium knowlesi? | Quotidian fever (everyday) |
| What are the RBCs and histology of Plasmodium knowlesi? | RBCs unenlarged, no stippling -> schizont/trophozoites (banded w/ loose cluster of merozoites) |
| What are the hosts of Trypanosome cruzi? | Definitive host -> mammal, IM host -> triatomine bugs |
| What is the lifecycle of Trypanosome cruzi in its definitive host? | Triatomine bug takes blood meal from mammal -> faecal deposits transfer metacyclic trypomastigotes -> enter bite wound/mucosal membranes -> transform into amastigotes (binary fission), transform into trypomastigotes -> lyse cell entering bloodstream |
| What is the pathophysiology of Trypanosome cruzi? | Heart failure, oesophageal dilation, Chagas' disease -> Romana's sign -> conjunctiva acute unilateral swelling |
| What is the lifecycle of Trypanosome cruzi in its IM host? | Triatomine bug takes blood meal -> ingests trypomastigotes -> transform into epimastigotes in midgut -> multiply by binary fission -> transform into metacyclic trypomastigotes in hindgut |
| How is Trypanosome cruzi transmitted? | Improperly processed acai berries -> triatomine faeces contaminate fruit |
| What are the hosts of Leishmania? | Definitive host -> sandfly, IM host -> humans |
| Where are Leishmania located? | Restricted by permissive sandfly vectors -> P. patasi binds L. major LPG only (not L. infantum) -> restricted to Mediterranean basin/Middle-East, P. arabica binds L. major and L. nfantum LPG) -> found in Egypt, Saudi Arabia |
| What is the lifecycle of Leishmania in its definitive host? | Sandfly takes blood meal -> ingests macrophages w/ amastigoties -> transforms into promastigotes in gut -> multiply by binary fission -> migrate to proboscis |
| What is the lifecycle of Leishmania in its IM host? | Sandfly takes blood meal from mammal -> injects flagellated promastigotes into bloodstream -> phagocytosed by macrophages/neutrophils -> transform into non-motile amastigotes -> multiply in cells -> burst into bloodstream |
| What is the pathophysiology of Leishmania? | Cutaneous -> facial ulcers, granulomas 12-16 months, diffuse cutaneous -> non-ulcerated facial pustules, anti-inflammatory, mucocutaneous -> nasal/vaginal mucus membranes, pro-inflammatory, visceral -> spiking fever, hepatosplenomegaly, pancytopenia |
| What is LPG? | Leishmania surface CHO-> binds to sandfly midgut galectin -> prevent defaecation loss -> amastigote to promastigote -> LPG changes length/chains -> detaches/migrates to proboscis, promastigote to amastigote -> LPG lengthens -> resist macrophage O2 bursts |
| What is GP63 protease? | Leishmania -> binds/inactivates C3b -> evades MAC -> preserves opsonisation for macrophage uptake |
| What are the virulence factors of Leishmania? | LPG, GP63 protease |
| How do we categorise helminths? | Roundworms (nematodes) -> pin/round/hook/whipworm, flatworms -> cestodes (tapeworms), trematodes (flukes) |
| What are the treatments for helminths? | Albendazole (nematodes) -> inhibit helminth beta-tubulin polymerisation, praziquantel (cestodes/trematodes) -> increases permeability of cell membranes -> increased ion flux throughVGCaC -> contract parasite muscle |
| What and where are pinworms found? | Enterobius vermicularis -> UK |
| What is the lifecycle of pinworms? | Larvae hatch in intestine -> penetrate and develop in mucosa -> mature in lower GI tract -> female worms migrate to rectum -> lay itch eggs in perianal region -> infectious w/in hours -> survive for weeks -> spread by scratching -> ingest embryonated egg |
| What are the symptoms and transmission of pinworms? | Anal pruritus (itching), orofaecal |
| What are roundworms and their transmission? | Ascaris lumbricoides, orofaecal/transQ |
| What is the lifecycle of roundworms? | Fertilised egg matures in small intestine -> defaecated into soil -> embryonated egg hatches -> release 2nd state larvae -> transQ transmission penetrates skin -> hatched larvae enter circulation -> migrate to lungs -> coughed/swallowed -> GI tract |
| What are the symptoms of roundworms? | Transmission -> asthma symptoms (Th2) -> bronchospasm when entering lungs, obstruction -> ileocaecal valve, biliary tree, intestinal perforation |
| What are the GI signs of roundworms? | Mucosal lining remains intact -> feeds on liquid intestine contents rather than bloodstream, malnutrition -> worm secretes anti-trypsin factor |
| What and which species are hookworms found? | Ancyclostoma duodenale, necator americanus (human), ancyclostoma caninum (zoonotic stray dog -> humans) |
| What is the lifecycle of hookworms? | Fertilised egg matures in small intestine -> defaecated into soil -> embyronated eggs hatch -> release 2nd state larvae -> transQ transmission penetrates skin -> enter bloodstream -> mgirate to lungs -> cough/swallow -> teeth latch onto GI tract lining |
| What are the symptoms of hookworms? | Microcytic anaemia -> suck blood from intestinal wall, malnutrition -> interrupted nutrient absorption, distended belly -> obstructed air |
| What is the transmission of hookworms? | Orofaecal, transQ |
| What are whipworms and how are they transmitted? | Trichuris trichiura, orofaecal |
| What is the lifecycle of whipworms? | Embryonated eggs ingested -> 3 month development in small intestine -> tail burrows into GI tract -> larvae hatch into small intestine -> adults mate in caecum -> unembryonated eggs defaecated |
| What are the symptoms of whipworms? | Anaemia w/out bleeding, malabsorption (diarrhoea), bone marrow failure (pore-forming toxin), rectal swelling (false urge to strain), rectal prolapse (fatal w/out surgical intervention) |
| What are tapeworms, their hosts and their transmission? | Taenia, definitive host -> human, IM host -> pig, orofaecal transmission |
| What is the lifecycle of tapeworms in their definitive host? | Human ingests undercooked meat -> larva develops into adult worm in intestine -> feeds on host ingested material -> each proglottid develops into male/female (cross-fertilisation) -> most mature segment detaches laying embryolated eggs -> faeces |
| What is the lifecycle of tapeworms in their IM host? | Pig ingests eggs/proglottids -> develop porcine cysticercosis -> larvae form cysts in animal muscle |
| What is the difference between cysticercosis and taeniasis? | Cysticercosis -> pig/human ingests eggs -> tissue infection w/ larvae stage -> dangerous, taeniasis -> human ingests undercooked meat -> GI infection w/ adult stage -> less problematic |
| What cells modulate the nematode response? | Tuft cells of intestinal epithelium -> upregulation when infected by worms -> ILC2 releases type II cytokines -> IL-4/5/13 -> basophil/eosinophil recruitment, upregulate goblet cell (mucus), skew immunity to Th2 |
| What and where are trematodes? | Flukes -> Schistosoma, sub-Saharan Africa |
| What are the species of trematodes? | Schistosoma mansoni/japonicum/mekongi/intercalatum -> GI disease, haematobium -> urogenital disease |
| What are the morphology of trematodes? | Mansoni -> oval shape, off-centre spike, found in stool, japonicum -> circular shape, rudimentary spike, haematobium -> central spike |
| What are the hosts of trematodes? | Definitive host -> human, IM host -> snail |
| What is the lifecycle of trematodes in their definitive host? | Cerceriae burrow into human skin (lose tail) -> larval schistosomula develop into adult blood fluke -> adult fe/male migrate -> attach to hepatic mesenteric venules/bladder venous plexus -> 10 yr deposition of 300 daily eggs -> faeces |
| What is the lifecycle of trematodes in their IM host? | Eggs hatch and release miracidia -> burrow into snail -> develop and leave snail as cerceriae w/ tail for motility |
| What is the pathology of trematodes? | Fluke surface w/ host proteins -> immune evasion, glucose consumption -> large egg release, chronic phase -> GI bleeding, diarrhoea, portal hypertension (liver fibrosis), schistosomiasis |
| What are the symptoms of schistosomiasis? | Intestinal -> ankle red dots, hepatosplenomegaly, varices, fibroses, liver calcification, bladder -> haematuria, cancer, sandy cervix, fibrosis, calcification, morbidity -> egg secrete proteases (bleeding) |
| What is the immune response to schistosomiasis? | Retrograde blood flow into liver/bladder -> granuloma w/ M2 macrophages, Th1 response to cerceriae penetration/larval worm migration, Th2 response to egg deposition |
| What is the transmission of schistosomiasis? | Water contamination |
Created by:
vykleung
Popular Pathology sets