Parasites Flashcards
Trichuris Tricuria (whipworm)
Ingestion of embryolated eggs
Colonises LI epithelium
Mature females lay fertilised eggs that pass out into faeces and take 2 weeks to embryolate
Cause of whipworm disease
Severe pathology includes rectal prolapse
Enterobius vermicularis (pinworm)
Very common
Cause of enterobiasis (pinworm)
Adults female worms migrate out to perianal region to lay eggs; infective within hours
Ascaris lumbricoides
Mechanically block gut
Live 1-2 years and shed 200,000 eggs per day
Eggs take weeks to develop in environment
Often asymptomatic and
Toxocara canis
Definitive host dogs
Incidental host humans; ingest embryolated eggs that stay in larval form; cause human toxocariasis (migrate to eye and brain)
- Epilepsy and ocular inflammation
Necator Americans (hookworm)
Filarial larvae develop in environment and penetrate skin
Develop into adults in SI and shed eggs in faeces + larvae coughed up
Lose 200ml blood per day
Onchocerca volvulus
Cause of African river blindness
Infective form is L3 which migrates to head/probiscus of blackfly
Humans = definitive host
Blackfly = intermediate host
Adults develop in subset nodule and produce unsheathed microfilarae (L1 form)
Wucheria bancrofti
Filarial; cause of elephantiasis (neglected tropical disease)
Adult worms reside in subcutaneous nodules
Transmitted by night feeding mosquitos
Taenia solium pathology
Pork tapeworm
Humans are definitive host
Pigs are intermediate host
Human cysticerosis caused when humans become intermediate host via ingestion of embryolated eggs; oncospheres hatch and penetrate intestine to circulation
Cysticerci develop in submit tissue, brain and eyes
Get neurocystercosis
Taenia sodium normal cycle
Pig eats embryolated egg
Oncopheres hatch and larvae penetrate intestine wall
Develop into cysticerci in muscles where larval development is arrested
Humans eat cysticerci in meat
Develop into mature adult using scolex to maintain position in SI
Enter sexual cycle; hermaphrodites; shed gravid proglottid (contains male and female reproductive apparatus and eggs)
Echinococcus
Definitive host dogs
Intermediate host sheep (can get embryonate egg being consumed by humans and oncospheres release in gut
- Hydatid cyst in brain causes epilepsy
- Alveolar disease (of liver) causes jaundice
Fasciola hepatica
Liver fluke
Definitive host = sheep/cows
Intermediate host is snail
Eggs embryolate in water and miracidia hatch out, penetrate snail and develop into cercariae
Metacercariae leave intermediate host and are eaten by definitive host; immature flukes can harm and penetrate GI wall to reach liver
Immature eggs discharged in biliary system
Schistosoma haematobium
Urogenital infection
Schistosome japonicum
Intestinal infection
Schistosoma mansoni
intestinal infection
Schitosome lifecycle
Eggs release miracidia in the water which penetrate snail and develop into sporocyst
Cercariae (free living and infectious) attracted to human secretion and penetrate skin; form schistosomulae
Migrate to portal blood in liver to develop into adults which go to mesenteric veins of GI tract or bladder venous plexus
Adults live in pairs; female resides in gynocophoral canal of the male
I’ve 5-10 years and deposit 3000 eggs per day
Intestinal schistosomiasis morbidity
Eggs can reflux to liver where they can’t develop but secrete antigens that cause granuloma formation, liver fibrosis (Sumer clay pipestem fibrosis) and calcification + hepatosplenic megaly in children and abdominal varsities in adults
Urogenital schistosomiasis morbidity
Bladder fibrosis and calcification
Cervical sandy patches
Katayama fever (can cause bladder cancer)
Blood in urine
Leishmania sandfly lifecycle
Amastigotes taken up in blood meal
Start to form flagella in peritrophic matrix
Attach to villi on wall of midgut using LPG on surface to interact with galactin
Develop into promastrigotes and increasing complexity of LPG allows release; re-enters foregut and injected with blood meal
Leishmania human lifecycle
Promastigotes injected by sandfly in blood meal
Presented by dendritic cell to Th1 at lymph node so macrophages recruited (via IFNgamma)
Macrophages take up promastigote; develops into replicative amastigote
Released into blood or may be taken up inside macrophages (by sandfly)
Old world Leishmania
Major (cutaneous)
Aethiopica (cutaneous)
Infantum (cutaneous)
New world Leishmania
Brasiliensis (mucocutaneous)
Chagasi (visceral); closely related to L infantum having been brought from Portugal to Brazil by explorer’s dogs
Plasmodium Papatasi
Distribution: South Asia, Middle East, Egypt
Low lying regions
Restrictive vector: only supports L major as midgut parasite (lectins not suitable for L infantum)
Plasmodium Arabica
Distribution: Egypt, Saudi Arabia
Mountaneous regions
Permissive vector: can carry L major and infantum but get competition
Toxoplasma gondii
Definitive host = cat
Intermediate host = everything warm blooded
Resting form = bradyzoites (eaten by cat from within mouse)
Enters gut and infects gut cells; transforms to Tachzoites (rapidly dividing)
-> May become gametocytes and form oocytes shed in faeces (develop into sporozoites in oocyst)
-> OR can travel to immunopriviledged sites and cause acute infection/chronic resting form
Apicomplexa secretory organs
Micronemes: for motility via interaction with the actin myosin motor of the inner membrane
Rhoptres: for invasion and formation of parasitophorus vacuole
Dense granules: for PV housekeeping and protection
P falciparum lifecycle in human (intermediate host)
Sporozoites injected Ito blood and move to liver
Invade hepatocytes and replicate (merogeny stage)
Merozoites form, re-enter circulation and infect RBCs
Ring form = trophozoite which is feeding and making proteins
Parasites then reform as merozoites so RBC now called schizont
- Some merozoites transform to micro and macrogametocytes which are taken up by the mosquito
Cyclical fever in malaria
Synchronised release of merozoites via RBC rupture which triggers cytokine production so get fever
P vivax dormant stage
also P oval has this
Has dormant stage in liver called hypnozoite to allow survival during winter months without many mosquitos
P falciparum lifecycle in mosquito
Micro and macro gametocytes taken up
Exflaggelation to gametocytes that use and form ookinete
Ookinete will penetrate gut wall and make oocyst on outside of gut
Meiosis and replication to give sporozoites (to salivary gland)
Malaria symptoms in different ages
Newborns: mild as have maternal antibodies
Infants: high death rate
Teens: more mild as have some immunity
Adult: clinically immune
P vivax binding to RBCs
Duffy binding protein in apical complex binds irreversibly with Duffy antigen receptor on RBCs
Since lots of sub-saharan Africa is Duffy -ve, don’t get this here
P falciparum binding RBCs
can still infect Duffy -ve as use lots of receptors
so greater distribution esp in SS Africa with no competition
Rosetting
infected RBCs have PfEMP surface protein; can stick to uninfected RBCs via CR1?
Sequestration
infected RBCs interact with vascular endothelium (has unregulated adhesion molecules e.g ICAM1, E selection)
PfEMP variation
encoded by 60 var genes but only one on at a time
get somatic recombination and antigenic variation
Malaria natural resistance
Sickle cell anaemia: sicks cells RBCs become distorted when infected and are taken up by spleen and cleared
G6PD deficiency: less to use to make GSH which allows oxidative stress and more free radicals which is hostile to parasite
- X linked
DARC -ve alleles
Ivermectin/avermectin
Macrocyclic lactones
neurotransmitter inhibitor that targets glutamate gated Cl- channels
Roundworms
NB: when treating oncocercis volvularis doesn’t kill adults so need continuous treatment
Albendazole
Inhibits tubular
Roundworms + tapeworm (echinococcus for hydatid disease and cysticercosis from toxocara Canis)
Praziquantel
Membrane permeability to Ca2
Flatworms
Quinine/chloroquinine
Target harm detoxification process in mature trophozoites so organelles can’t replicate properly and get faulty merozoites
Artemisinin combination therapy
check past papers
DDT
highly active insecticide used to eradicate malaria in USA BUT killed other insects so banned
- Can be used for indoor residual spraying
Biological vector control
Wolbachia colonises gut of insects to make it a hostile environment for plasmodium
- Infected female lays infected eggs
- Infected male’s eggs won’t hatch
CRISPR/Cas9 gene drive
Individuals tend towards being male/intersex therefore decreases population
