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Flashcards in Parasite biology Deck (139):

What is the intermediate host of a digenean?

usually a snail


How do we know that parasites have specialised mechanisms to avoid immune responses of hosts?

That helminth infections are typically long-lived (i.e. chronic) infections, tells us that hosts typically are unable to remove parasites


What is the definitive / intermediate host of toxoplasma gondii?

intermediate: bird, rodent, human


what is the lifecycle of Leucochloridium paradoxum?

1. Bird definitive host - eggs in faeces.
2. Snail eats bird faeces.
3. Sporocysts have coloured spots and bands - they infect the eye stalks of snail host and pulsate.
4. Snails can't see properly í can't hide from predators (can't sense daylight so doesn't hide under leaves + sometimes actually crawl into the view of the birds (which they never do w/out)
5. The pulsating, brightly coloured eyestalks are conspicuous and resemble caterpillars so attract bird predators.
No release of cercaria: the snail is just predated with it inside it.


Evolution of nematode parasitism?

It is hypothesised that in the evolution of animal parasitism by nematodes, that nematodes developed increasingly intimate associations with hosts (evolved at least 5 times, more likely 12 times)


Heritability of infection traits (Ascaris infection): How much of that variation is due to genetic effects and what does that imply?

c. 40% of worm load variation is host genetics

Given that there is a significant effects of host genotype on Ascaris infection, this implies that Ascaris is a strong selective force on the host population.


what is an apicoplast? what does it do?

relict chloroplast(not fully functioning as in plants), present in plasmodium
o Enzyme reactions: Chloroplast-type fatty acid biosynthesis
o Possible drug target - could attack it using weedkillers?


How is anisakis acquired?

by eating raw fish containing larvae of anisakid nematodes such as anisakis complex or pseudoterranova decipiens.


Why are schistosomes an exception to typical digenean?

- Exception to being hermaphrodite: M+ F worms, copulating all their lives: F lives within a groove in the M body.


What is the differences between endo + ectoparasites?

end live in internal organs / tissues of host / ecto parasite: out of the body


Why is toxoplasma dangerous for pregnant women?

: can pass through the placenta to the developing embryo - you will be tested to see if you have antibodies for toxoplasma to see if already infected or not: if you get infected in pregnancy, you are mildly ill but developing foetus has severe abnormalities.


what type of lifecycle and transmission does Entamoeba have?

o Direct lifecycle: faeco-oral transmission - transmitted by cysts (thick wall, environmentally resistant)


Some facts about free living stages (in the environment, outside of host) and example

o Large numbers
o Environment resistant
o Targeted for (new) host acquisition


o Large round worm
o Nematode
o 1 host lifecycle with free living larval stage
o Gastro-intestinal

Eggs require time external to the host before becoming infective. This process is temperature dependent such that, for example, with Ascaris infection of pigs, there is a peak of infective eggs present in the spring and summer, coinciding with the availability of Ascaris-naive piglets.

Ascaris eggs are resistant to desiccation and freezing and most disinfectants.


How does Dicrocoelium dendriticum modify the behaviour of its host?

host = sheep; Metacercariae encyst preferentially in ant neural ganglion so when temperature drops at night, walks up blades of grass + latches onto them with jaws ( infected ants cannot open jaws + get stuck on blades of grass)
- Normally ants go back to their nest at night.
- Parasite is in the NS controlling it's BHV.


2 way of prasite-induced harm

o Parasites take nutrients / energy from hots in some way (competing for food with host/feeding off the host; Energetic cost of the immune response; Immunopathology)
o Intensity dependent (for marcoparasites especially, such as nematodes)


how does Plasmodium merozoite invade the red blood cell?

o Parasite binds & reorientates
o Enters into a parasitophorous vacuole, eeleasing proteins from apical organelles
o Parasite surface proteins are shed by proteases. Takes 30 seconds.


What is an example of a viviparous monogean?

Gyrodactylus "Russian doll parasite" - in any individual worm (hermaphrodite), you can see developing daughter.


What is the role of apical complex?

" Recognition. - of cell type to invade (RBC/ intestinal / nucleated cell) - cell to cell communication
" Orientation. - the infective cell has to orient with apical complex forward to it can invade
" Invasion - secreting proteases +structural proteins.


what is Apicomplexa? what is characteristic about them?

Parasitic Protozoa , all animal parasites
intracellular stages - get inside cells to survive (Characteristic of apicomplexan)
have apical complex.


Nematodes with direct transmission cycles

o Necator, Ancylostoma - human hookworms
o Ascaris lumbricoides, Toxocara canis - roundworms
o Enterobius - pinworm


What parasites can you get from eating undercooked food?

From eating raw/ undercooked meat or Fish - trichinella, Taenia (Solium + saginata), Anisakis, Diphyllobotrhium (fish tapeworm)


what are the routes by which toxoplasma gondii can be transmitted to humans?

o Ingestion of oocysts from soil or water contaminated with cat faeces
o Ingestion of tissue cysts in undercooked or cured meat
o Ingestion of infective parasites in unpasteurised milk


Body (strobila) and scolex (head) of cestodes (tapeworms)

o Made of individual segments = proglottids
o Each segment has male and female sex organs
o Skin allows absorption
o No mouth but suckers, grooves, hooks, spines to hold on to wall of vertebrate gut


what can schistosomes cause?

schistosomiasis or bilharzia
and "swimmer's itch" when in wrong host e.g. bird schistosomes


What is the vector of Onchocerca volvulus

Blackflies Simulium damnosum. live in fast-flowing well oxygenated streams


what are obligate + facultative parasites?

obligate: always parasitic for at least part of lifecycle
Faculative: will be parasitic if opportunity arises (accidental infection)


How do schistosomes avoid the host immune response?

acquisition of host molecules: a dynamic process - the parasites are continuously renewing their surface (called the tegument). Overall, the worm strategy is to survive the host immune response by 'disguising' themselves as 'host'. The tegument is a multi-layered membrane that is constantly renewed. Therefore, any immunological damage that occurs can be repaired by this tegmental renewal. Schistosomes also have glutathione peroxidase on their surface, which protects from free-radical damage.


what is the definitive intermediate host Nematodes Trichinella - causes trichinosis?

in the same animal (pigs / humans)


what is spontaneous cure.

a phenomenon in Nippostrongylus brasiliensis ( rat, like hookworms), In under two weeks from infection, the worms are lost from the host. In fact, the hosts have cured themselves from this infection.
This is a primary infection + primary response + kills and / or expels the worms.
If you give them a second infection, the infection is even more short-lived.


Differences between Protozoa and helmints?

o Single cells
o Often within host cells
o Short-lived, infection stages short but infection might be long-lived (e.g. malaria)
o Multiply within host

Helminths (trematodes, platyhelminths and cestodes)
o Physically large & multi-cellular
o Extracellular (too large)
o Long-lived
o Do not multiply within host


What is a definitive host?

a host in which the parasite undergoes sexual reproduction (meiosis for haploid gametes)


what are outbreaks of human Cryptosporidium associated with?

o Contamination of tap water/swimming pools with cysts from sewage. (outbreak in Lancashire in 2016)
o Contamination of ready-to-eat salad with cysts. (outbreak in Humberside , all adults + more women than men)


How does Giardia move?

o Creeps along the epithelial surface of the intestine + moves its flagella to hold its self in place, which create a current so they body becomes a suction cup, so it is stuck down by virtue of the suction power created by the movement of the fluid caused by the flagella.
o Feeds on the surface of the intestine.


what is the mechanism for worm killing / expulsion in Nippostrongylus brasiliensis

is immune mediated, T-cell dependent accompanied by high concentrations of IgE and an influx of mast cells to the intestine. Together, this suggests that there is an inflammatory response; more precisely a type I (immediate) hypersensitivity response. In this, histamine-containing mast cells, release their histamine via the action of IgE. Hay fever is a typical type I hypersensitivity response. In the N. brasiliensis infections, it looks like this type of response in the gut is responsible for the expulsion of the worms. This effect on the worms could come about directly (for example, by directly damaging and killing the worms); or, the histamine could alter the gut physiology, thereby making it an unsuitable environment for the worms; or, the histamine may allow the gut to become more permeable to other host effector molecules.


What is parasitism?

eating at your table, only the parasite benefits, intimate association, e.g. ascaris


Why was it difficult to eliminate Dracunculus medinensis completely? (once levels were ~26)

Because there was a reservoir host: some dogs can be infected which we didn't know before the numbers of cases came to this level - this is a reason why it didn't go to 0: animal reservoir kept the transmission cycle going.


what is Eimeria

A Coccidians important parasites of intensive farming
o Chickens, rabbits, calves, lambs , goats- several Eimeria species specific to each host
Parasite multiplies inside cells of gut wall; infective cysts pass out in faeces
direct lifecycle, feaco-oral transmission.


life cycle of Cryptosporidium?

1 thick walled- oocyst ingested, multiplication in the gut
Oocusts released in faeces
Oocysts contaminate water (used to wash salads / irrigate fields / swimming pools) and are then ingested.


Symptoms of helimthiasis?

o Negative relationship of helminth infection + cognitive performance (the more worms the less cognitive performance í Direct cost of parasitism)
o Deworming can: improve cognitive performance + school attendance.


What is Lymphatic filariasis?

Lymphatic filariasis, also known as elephantiasis, is a human disease caused by parasitic worms known as filarial worms. Most cases of the disease have no symptoms. Some people, however, develop a syndrome called elephantiasis, which is marked by severe swelling in the arms, legs, breasts, or genitals.


why do we know that spontaneous cure doesn't happen in all hosts?

it did, these parasites would be extinct (and most worm infections are long-lasting, chronic infections).


why is malaria more dangerous than eimeria?

b. The cycle of schizogony is uncontrolled (unlike in eimeria where there is ¾ cycles then gametocytes); this can just continue dangerously í once you're infected the cycle just continues in the RBC.
c. Single infected liver cell can give 1000s of parasites


What are the diffs/ similarities in the structures of monogeneans and digeneans?

both have uterus, ovavries + testies, a mouth and a pharynx that leads to two blind ending guts.

Digenea: 2 suckers in ventral + oral region (instead of posterior haptor)
Monogenean have haptor on posteria,


Why is the teste fly both bad. + good for Africa?

Vector of Trypanosoma brucei. Distributions of tsetse and cattle in Africa are mutually exclusive: stopped development of agriculture
saviour: Trypanosomiasis in vast areas of tsetse-infested land stopped agricultural exploitation - legacy of National Wildlife reserves and preservation of large wild animal


Why is the 3rd larval stage in nematode importnant?

For animal parasitic nematodes whose host infective stage is larval, it is always a third larval stage, either ensheathed or not.
The other similarities between dauer larvae of free-living nematodes and the infective larvae of parasitic nematodes is that they are both non-feeding, they are long-lived, and they are developmentally arrested, and will only resume development (to the L4 stage) when:

(a) for free-living nematodes, environmental conditions improve, such as more food is available or
(b) for parasitic nematodes, when a suitable host is encountered and infected. Biologically dauer larvae and infective larva are fulfilling the same role of dispersal.


why is Cryptosporidium bad for people who are immune-compromised people?

o In lifecycle: Autoinfection is possible. Two types of oocyst are produced: thin (allows autoinfection) and thick-walled (goes into environment) (this is all you need to see from the more complicated lifecycle)
o í if you are immunocompromised with a Cryptosporidium infection you will reinfect yourself (autoinfection)
o Trophozoites take place at surface of epithelial cell: bubbles on epithelial cell are the Schizonts of Cryptosporidium
o This means the gut won't be able to absorb food í become v. thin


what are the defintive+ intermediate hosts of schistosomes?

definitive: humans
intermediate: aquatic snail


What are 2 theories for why parasite infection 'tickles' into the host?

1) One possibility is that this lower rate of worm delivery, gives the worms opportunities to adapt to the host immune response.
2) An additional possibility is that the parasites are able to (immuno)modulate the host immune response, thereby prolonging their survival.


3 types of platyhelminthes

Monogenea - mostly ectoparasites of fish and amphibia
Digenea - flukes or trematodes
Eucestoda - cestodes or tapeworms


How do filarial worms interfere with the immune response?

Parasites immunomodulate the host immune response. Adult worms interfere with T cell function, such that T cells are less likely to be stimulated into action.
There are changes in the sub-sets of T cells that are activated.
Very recent evidence suggests that worms are secreting molecules that directly affect the control of the host immune response.


What are microfilariae worms?

an early stage in the life cycle of certain parasitic nematodes in the family Onchocercidae.[2] In these species, the adults live in a tissue or the circulatory system of vertebrates (the "definitive hosts"). They release microfilariae into the bloodstream of the vertebrate host. The microfilariae are taken up by blood-feeding arthropod vectors (the "intermediate hosts"). In the intermediate host the microfilariae develop into infective larvae that can be transmitted to a new vertebrate host.


How can humans become infected with trichinella?

if ingest undercooked pork (larval worms encysted in the muscle will be released + most to become adults + release eggs in intestinal mucosa)


What kind of 'immunity' can be developped against Schistosoma mansoni infection?

o Concomitant immunity (worms in blood vessels but resistant to new infections, IgG and IgE: complement cascade).

Schistosomulae are attacked by IgE and IgG, which will stimulate the complement cascade. These antibodies will also attract esosinophils and induce ADCC.


what Taenia solium - pork tapeworm cause?

Infection with larvae in the human brain which can cause epilepsy (neurocysticercosis)


what are the species of malaria vectors in humans?

plasmodium (parasitic protozoans)
o 5 species in humans: Plasmodium falciparum, P.vivax, P.ovale, P. malariae, P. knowlesi


What is a vector?

a micropredator that actively delivers parasite to next host


how does trickling an infection change parasite / immune system behaviour?

If you trickle an infection, it behaves differently.
Measured in two ways: egg out put in faeces / no. of worms in gut. í nuber of worms / eggs in faeces increases.
not completely understood. One possibility is that this lower rate of worm delivery, gives the worms opportunities to adapt to the host immune response. An additional possibility is that the parasites are able to modulate the host immune response (manipulating the IR of the host), thereby prolonging their survival. - this takes time so doesn't happen immediately


What is an oncosphere

the larval form of a tapeworm once it has been ingested by an intermediate host animal.


What is the lifecycle of anisakiasis?

1. Marine mammals like dolphins excrete umebryonated eggs
2. Eggs become embryonated in water + L2 form from eggs
a. After L2 larvae hatch they become free swimming
3. Free swimming larvae are ingested by crustaceans + they mature into L3 larvae
4. Infected crustaceans are eaten by fish + squid + when host dies, the larvae migrate to muscle tissues + through predation, the larvae are transferred from fish to fish
5. Fish + squid maintain L3 larvae that are infective to humans + marine mammals
6. When fish or squid containing l3 larvae are ingested by marine mammals, the larvae molt twice + develop into adult worms
7. Adult worms produce eggs that are shed by marine mammals
8. Humans become incidental hosts through eating infected raw or undercooked seafood


what is the role of bacteria in microfilarial worms?

Endosymbiotic bacteria essential for worm to survive so can use antibiotics effective for people with LF. (instead of using an anti-helmintic).


what are filarial nematodes?

Filarial nematodes are insect-transmitted tissue or blood parasites.
Those that parasitise humans are Onchocerca (causative agent of river blindness), Wuchereria and Brugia. Onchocerca adults live under the skin; Wuchereria and Brugia adults live in lymphatic tissue. All species produce first stage larvae (microfilariae) which circulate in the blood (Wuchereria and Brugia) or are in the skin (Onchocerca), from where they are taken-up by the host.
Microfilariae in the blood → vector í moult into l2 í released by feeding í moult in adult.


How do the larvae of trichinella survive in a human?

after being deposited into the mucosa, they enter circulation + encyst in striated muscle - Nurse cells.


How to excavates move?

by one or more flagella


Sickle Cell trait - why?

o SCT < malaria parasitaemia
o SCT < death rate from severe malaria
o SCT > childhood survival rates
o SCT < malaria parasite replication
o Because infected RBC cleared more quickly


What is o Concomitant immunity in schistosomes?

(worms in blood vessels but resistant to new infections) - once an adult infection is established there are responses against subsequent invading schistosomulae


what is the Basic Digenean lifecycle.

1. Adult in vertebrate definitive host
2. Produce eggs. - hermaphrodite adults
3. Eggs hatch out into ciliated miracidium which can swim, and in the middle have germinal cells (counter to what we know about macroparasites, these germinal cells can generate more organisms í one ciliated miracidium can give rise to multiple larvae
4. Eaten by snail / bores into snail
5. Inside the snail, the worm develops into a Sporocyst (still has germinal cells inside)
a. Sometimes there is a redia (feeding stage)
b. Or multiplication of the sporocysts
c. Diff things happen in diff dignean lifecycle
6. Either the redia or sporocyst release cercaria which are released from snail, which start to look like a worm: have two suckers as seen is adult worms. These are motile as they have a long tail that propels them through water
a. It is the germinal cells that gives rise to the many cercaria
7. Encyst into metacercaria (thick walled cyst with cercaria inside) so it can survive in the environment
8. Cercaria or metacercaria gets into vertebrate definitive host + produces eggs etc.


How does Onchocerca volvulus cause river blindness?

6. Some of the microfilariae: get into eye + cause inflammation í blindness.


what are Oncomiracidium

the free swimming larval stage of a monogean


Different qualities of host with equal intensity of infection

more susceptible: symptoms (virlent
resistant: no symptoms (avirlent)


what is the life cycle of Fasciola hepatica

1. Adult flukes (flattened, leaf shaped, hermaphrodite worms - classic Digenean) live in bile ducts of liver of sheep
2. eggs released into gut with the bile + then into the faeces + into the pasture
3. reliant on damp pasture: miracidia hatch in damp pasture + swimp to find amphibious snail (= INTERMEDIATE HOST + LYMNEA) + forms sporocysts in snail
4. cercariae released from snail which are swimming, drops tail + builds strong body to resist dessication in the enrionment
5. METACERCARIAE encyst on blades of graph + so when sheep eats the grass the lifecycle is completed as the adults develop in the liver.


What is Helminthiasis ?

infection of helminths


What is the definitive + intermediate host of Dicrocoelium dendriticum?

definitive: sheep
intermediate: Snail
intermediate 2: ant


what is commensalism?

"eating at the same table" loose association (no metabolic dependence), trophic interaction)


How are the kinetoplastids species transmitted + where do they live in the host?

o The parasite is in RBC + eats the glucose dissolved in the serum
o Human and animal diseases.
o All vector borne.
o Trypanosoma brucei transmitted by tsetse flies
o T. cruzi transmitted by triatomine bugs
o Leishmania spp. transmitted by sandflies


What diseases are caused by trypanosomes?

Human African Trypanosomiasis (sleeping sickness)
o In later stages of disease, parasite invades CNS + causes coma: brain inflation which affects CNS so fall asleep during the day.
o 2. Nagana ("low spirits" Zulu) - African animal trypanosomiasis
o Lose weight, weak, malnourished, lame, eventually die
o Wild & domestic animals throughout the tsetse belt


What is the first place in the human body where plasmodium sporozoites develop?

the liver


How does trypanosoma Brucei evade the adaptive immune system of the mammalian host?

by switching its surface antigen =trypanosomes have a surface coat of a single protein (antigen) & they multiply up until IS recognises it + kills off, but then switch to a different antigen (coat), so ↑ in numbers until antibody response catches up, switches again etc.
í each of the peaks is actually different antigens appearing.


How do pathology and disease depend on the immune response of the host (infected by filarial nematodes)?

For infected individuals, those hosts with comparatively low reactivity of T cells are still parasitologically positive for worms (Mf +ve), but they have no pathology or disease.
In contrast, individuals that have more reactive T cells appear to control their worm infections (as shown by the absence of Mf in the circulation), but the consequence is that there is pathology and disease.
--> This pathology is therefore probably immuno-pathology - 'collateral damage' of the active immune response. --> IR is induced by the parasite and will act against the parasite, which causes damage in the host tissue.


What are parasites with Indirect transmission cycles?

- Intermediate hosts - Dracunculus (guinea worm, copeopod)), Fasciola, Schistosoma, Dicrocoelium, Leucochloridium, + Tapeworms: Taenia, Diphyllobothrium (copepod), Echinococcus +
- Insect vector (= intermediate host) - Onchocerca , Wuchereria
- Trichinella - definitive and intermediate hosts are the same


What are the symptoms of hookworm anaemia?

Hookworms: Ancylostoma + Necator
o Anaemia (in heavy infections)
o Affects growth + cognitive development (in children with long-term infection)
--> School attendance less
--> Less success at school
o Effect dependent on intensity of infection (number of worms, the more worms the more harm is caused)


What role do mast cells and histamine play in the spontaneous cure of N. brasiliensis infections?

1) effect on the worms could come about directly
2)histamine could alter the gut physiology, thereby making it an unsuitable environment for the worms
3) histamine may allow the gut to become more permeable to other host effector molecules.


what can wuchereria, brugia cause?

o Causes Filariasis = blockage of lymph ducts by adult worms causes severe swelling
o Blood supply delivers fluid to tissues, then is carried from tissues back to blood by lymphatic system
o If blocked: fluid collects + leads to swelling of legs (Due to gravity), skin is thickened (inflammatory response)
o í can't wash properly, cracked leathery skin


Echinococcus granulosus - dog tapeworm

o Small tapeworm 3-6 mm with only 3 proglottids


Where does T.vaginalis live? how. is it transmitted?

o Parasite of the genito-urinary tract (lives in epithelial surface) - Feeds on yeast / bacteria that are there.
o transmitted from human to human during sexual intercourse.
o Doesn't need cyst stage / intermediate stage : DIRECT lifecycle - one host to another during copulation


What are kinetoplastids?

o Name derives from kinetoplast, a unique organelle that contains the mitochondrial DNA.


what is the tegument?

- Platyhelminthes do not have a resistant cuticle covering their exterior surface like nematodes
- Instead characterised by tegument - absorptive and secretory


how does adult worms being put into the gut of a mouse effect immnuisation against worms?

infective larvae of H. polygyrus are capable of stimulating an immune response that is effective against worms, but the presence of adult worms in a host alters the host immune response to remove this effect.
Furthermore, if one tests H. polygyrus-infected animals for their ability to make immune responses to other antigens, this too is impaired. This is conceptually analogous to malaria and schistosomes infections.


what is the lifecycle of toxoplasma?

1. Definitive host is the cat: inside you have a lifecycle like Eimeria: parasite inside gut cells, producing oocysts.
2. Cat sheds the oocysts in the faeces (this is why pregnant women shouldn't handle litter boxes / dig in the garden
3. Oocyst can be taken up by rodent /bird í tachyzoites í bradyzoites í preyed on by a cat
4. OR oocyst can go into livestock by ingestion OR into humans like vegetables + water (ingestion), or by contamination of hands with soil
5. In all the animals: same development: Tachyzoites + bradyzoites forming.


How can trypanosomiasis be consoled? why is it difficult?

Antigenic variation of trypanosomes makes it very difficult to develop vaccines against African sleeping sickness or Nagana

Control relies on
o Drug treatment - but drugs are few and some are extremely toxic
o Control of the vector - but the areas affected are vast and Africa is poor


What are defining features of a parasite?

Hterogenetic association, intimate association, dependence, recognised by host as foreign, + harmful


What is the definitive host and intermediate of Fasciola hepatica?

definitive: Sheep, lives in bile ducts
intermediate: amphibious snail.


What is the difference between micro parasite + macroparasite?

micro: microscopic size, if one infects can cause death as divide by binary fission)
Macro: can be seen with the naked eye: number of parasites a host takes in is the number that remain in your body


What is Onchocerciasis ?

Onchocerciasis (river blindness): Onchocerciasis, also known as river blindness, is a disease caused by infection with the parasitic worm Onchocerca volvulus. Symptoms include severe itching, bumps under the skin, and blindness. It is the second-most common cause of blindness due to infection, after trachoma.



1. Ingestion of oocyst (sheep on pasture; poultry in the litter in poultry house etc)
2. Sporozoites released (Proteases break down wall of oocyst so sporozoites released + infect cells. )+ each invade an intestinal cell (asexual cycle of schizogony), then the sexual cycle which produces gametes + oocysts.
3. Oocysts released in faeces + develop on pasture:
a. Invidivudal orgs develop in the oocyst: undergo meiosis + maybe mitotic division depending on how many sprozoites are inside there.
4. Proteases inside the intestine
Diff sp of Eimeria have diff numbers of sporozoites.


What are parasites with direct transmission cycles?

Direct transmission cycles
- Faeco-oral transmission - roundworms e.g Ascaris
- Contaminative transmission - hookworms e.g. Necator - bores into skin.
- Monogeneans - ectoparasites of fish e.g. Gyrodactylus


What does the transmission of Taenia saginata - beef tapeworm & Taenia solium - pork tapeworm rely on?
what are the definitive and intermediate hosts?

Definitive host = human; Intermediate host = ox, pig
Transmission cycle relies on:
a) predation by humans of livestock infected with larval worms
b) contamination of livestock feed with human faeces


Common features between nematodes with direct life cycles

o Faeco-oral transmission - roundworms, pinworms
o Penetration of skin - hookworms
o Risk factor - poor hygiene


how does a mosquito transmit malaria to a human?

when it takes a blood meal, injects it's saliva to prevent the blood clotting. The salvia contains sporozoites of plasmodium.


What are the definitive and intermediate hosts of Diphyllobothrium latum - the broad tapeworm?

- Definitive host = human or other fish-eating mammal (bear etc.)
- Intermediate hosts = copepod, fish


what are the two forms of toxpoplasma gondii?what are they?

Tachyzoites (="tachy = speed) + Bradyzoites (brady=slow)
Bradyzoites are in cysts, lodged somewhere in tissues / brains.
Tachyzoites are infective + can infect any nucleated cell, multiply up inside í destroy cell í release more etc.


What can Onchocerca volvulus cause?

Onchocerciasis = river blindness
- large lumps under skin + itchy skin


Define Filariasis

Filariasis is a parasitic disease caused by an infection with roundworms of the Filarioidea type.


What type of metabolism does Trichomonas vaginalis have?

o Anaerobic metabolism - hydrogenosome, modified mitochondrion that produces ATP releasing hydrogen as a biproduct.
o Hydrogenosome - hydrogen producing body


How are the different species of schistosomes transmitted?

- Schistosoma mansoni, S. japonicum - faecal transmission
- Schistosoma haematobium - urinary transmission: blood in wee is symptom.


what is the vector of Wuchereria, brugia?

transmitted by mosquitoes


Spontaneous cure of N. brasiliensis infections?

Worm expulsion is immune mediated, T-cell dependent accompanied by high concentrations of IgE and an influx of mast cells to the intestine. Together, this suggests that there is an inflammatory response; more precisely a type I (immediate) hypersensitivity response. In this, histamine-containing mast cells, release their histamine via the action of IgE .


main features of Taenia saginata - beef tapeworm

o Larval stage = cysticercus (plural cysticerci) in muscle in beef
o Tapeworm and larvae thought as different species: larvae known as Cysticercus bovis!


how do amoeba, and flagellates move?

amoeba: psuedopodia
flagellates: locomotion by one or more flagella


What is the definitive host of malaria?

a. Technically it is the mosquito where the actual sexual repro occurs of the gametes: fusion of the M+F gametocytes is inside the stomach of the mosquito (the mosquito is technically the definitive host and humans are the intermediate)


How do Apicomplexa move>

no moving parts but do move: move by the Gliding motion
o Circular or helical gliding of sporozoites on a surface - crescent-shaped.
o Temporary attachment of cell membrane to surface - internal linkage to actin cytoskeleton via a myosin motor


What are the differences between protozoa and helminths?

o Single cells
o Often within host cells
o Short-lived, individual stages short but infection might be long lived (e.g. malaria moves quite quickly through stages but infection logn)
o Multiply within host
Helminths - nematodes (round worms), trematodes (flatworm, playhelminth) + anatha - spiny headed worms.
o Large & multi-cellular
o Extracellular - too big to be inside a cell
o Long-lived -can live up to a year, Ascaris 3/4/5 years.
o Do not multiply within host


What is special about filarial nematodes?

During the day the MF are concentrated in the lung capillaries, and only move to the peripheral circulation at night (which is when the vector is most likely to bite the host). The cue that the MF use is the oxygen gradient in the lung capillaries.
The periodicity of W. bancrofti varies geographically and by host strain. In each case the periodicity of the parasite is matched to the biting behaviour of the insect vector.


what is the periodicity of appearance of microfilarial worms in blood?

- If take a blood sample from an infected person: rise in microfilarial worms in the blood at around midnight.
- Produced in deeper tissues in day + come into peripheral (skin cappileries) at night, this in turn coincides with when mosquitoes tend to bite.
- í thought the microfilarial time their emergence to tie up with biting habitats of the transmission vector.


What is a intermediate host?

host in which parasite develops or multiples but does not undergo sexual reproduction


Heligomosomoides polygyrus experiment on secondary infection and vaccination, what did they find?

o D shows that irradiated larvae are immunogenic and will immunise a host.
o B shows that this immunisation (D) fails if there are already adults in the gut.
o A and C are controls for surgery and worm presence?)

In summary, infective larvae of H. polygyrus are capable of stimulating an immune response that is effective against worms, but the presence of adult worms in a host alters the host immune response to remove this effect.
This is conceptually analogous to malaria and schistosomes infections.


Life cycle of D. latum?

1. Human host has worm in gut + eggs released on faeces.
2. Transmission depends on eggs going into water bodies (e.g. sewage discharge into lake
3. Copepod (intermediate host 1) eats swimming larval stage, the oncosphere
4. Fish (intermediate host 2) eats the copepods. Larval stage becomes pleroceroid in tissues.
5. Predatory fish (PARATENIC HOST) eats smaller fish - larvae doesn't develop.
6. Human or bears eat raw or undercooked infected fish + become infected etc.


What is special about the entomopathogenic nematodes: Steinernema and Heterorhabditis

o Infective larvae carry specialised bacteria (e.g. Xenorhabdus)
o In host, the bacteria are released which grow in the host body, killing the host
o Worms feed on the bacterial soup, multiplying as they do
o Infective larvae are released from dead 'exhausted' hosts

Also: Entomopathogenic nematodes are not 'strictly' parasites, because they don't live with their host. Rather entomopathogenic nematodes kill their hosts and use them as a food factory.


which nematodes have indirect lifecycles with intermediate hosts?

Dracunculus + Anisakiasis


what is a Paratenic host?

a transport host: no development or multiplication of parasite


why has malaria put a selection pressure on humans?

has been a widespread and debilitating disease for the human population over thousands of years
o Left the mark of this in our genome - particularly a range of abnormalities of haemoglobin : acted as a big selective pressure on us as humans.
o We have developed mutations that protect us from severe consequences of malaria.


Is the gut external to the body/separated from host immune system?

Is connected, because gut cells act as antigen-presenting cells (enterocytes). Lumen is an external service but still immune responses:
o Enterocytes take-up antigen and act as APCs
o Antibody responses
o IgA
o Dimer


which nematodes have indirect lifecycles with vectors?

Onchocerca, Wuchereria


Mf/L3 developmentally blocked: can't go to the net stage until they get the signal. What does the signal induce?

o Re-commence development
o Changed gene expression
o Morphology
o Physiology
o Biochemistry


What did the experiment by Smithers, Terry & Hockley (1969) on Schistosoma mansoni survival in monkey show?

1) effect is antibody dependent.
2) acquisition of host molecules is a dynamic process
3) immunological damage that occurs can be repaired by this tegmental renewal. Schistosomes also have glutathione peroxidase (enzyme) on their surface, which protects from free-radical damage.

--> Test the idea that parasite survive the immune response and disguise themselves: Use the host's specificity.


How are parasitic protozoans limited?

Limited number of cycles of schizogony: destruction of epithelial cells + production of sporozoites limited: only ¾: intensity of pathogenicity depends on how many oocysts were ingested initially.
After these cycles: get the sexual cycle: formation of micro + macrogametes. - these form within the intestinal cells.


What are the definitive and intermediate hosts of Echinococcus granulosus (tapeworm)?

Definitive host Dog or other canid; Intermediate host Herbivore e.g. sheep, human


What is mutualism?

both benefit, in extreme: can't survive without either, intimate association + metabolic dependence)


Facts about Host-host transmission?

o Host directly acquires parasites from another host
o Adaptations to facilitate (new) host acquisitions (- behaviour)
o Survival in hosts of different physiology etc.


What is the intermediate host of Dracunculus medinensis? how is it involved in the lifecycle?

Copepods in freshwater.
Humans drink water with copepods that have the larvae in them which from the stomach penetrate the gut wall + netter tissues + migrate to arm pit or groin + mate. then migrate down leg or arm + release larvae. Ulcer where they are released, and then L1 larvae released when ulcer bursts when placed in water


Give some examples of Gastro-intestinal nematodes

In humans there is Ascaris, Trichuris, Necator and Ancylostoma (hookworms), Enterobius (pinworms). In domesticated animals there are genera such as Haemonchus and Ostertagia/Teladorsagia. Laboratory work is often done with laboratory rodents, such as Nippostrongylus brasiliensis.


Nematode characteristics

o Some of the most abundant organisms on the planet
o Both free-living and parasitic
o Unsegmented worms
o Body covered with tough cuticle - non-cellular layer secreted by dermis.
o Hydrostatic skeleton. Cavity = pseudocoelom filled with fluid.
o Both male and female worms
o From 1 mm to 1 m in length
o Simple development:


What type of lifecycles do monogeans have?



what are monogenea?

- mostly ectoparasites of fish and amphibia, but also aquatic chelonians and hippo eye
- some are also endoparasites as adults e.g. in frog bladder (take up residence inside the body e.g. inside the body to be protected from desiccation in the environment)
- AQUATIC environment (FW + marine)


what is the lifecycle of apicomplexa?

1. Infectious stage: "Sprorozoites
2. Sprorozoites hatch from oocyst --> sporogony
3. These penetrate a cell in the body + undergo a further stage: schizogony (splitting
a. Division stages: 1 sporozoite invades a cell, multiples up by mitosis (binary fission); fills the cell as a mature SCHIZONT
b. The cell bursts releasing lots of invasive merozoites which will then infect other cells + cycle continues

4. In sexual repro microgamete (M) + macrogamete (F) are formed.
a. Microgamete forms motile sperm that search for macrogamete + penetrate it (haploid)
c. When they have fused: diploid zygote (oocyst)
d. This zygote (oocyst) then undergoes meiosis - This is gametogony
5. Once oocyst undergoes meiosis it is a sprozoite again (HAPLOID)


What are the advantages and disadvantages of a parasitic lifestyle?

+ve: Stable environment (no dehydration / temp changes)
o Food freely available
o How to find new host (host will die eventually so always need to find a new host - if very specific to host you need to make sure you end up in appropriate host)
Disadvantagees: How to find developmental site in host (humans are large so parasites need to navigate)
o How to avoid host defensive reactions (innate + adaptive immunity)


Where do adult Schistosomes live, how big are they?

-small blood vessels of bladder or gut / intestine
Quite small: m 15mm, F 20mm.
female lives inside a groove on males' body


Which type of mosquito bites blood? why?

pregnant female, needs the nutrition for developing eggs.


what is characteristics about Giardia duodenalis?

Has 2 nuclei, 8 flagella.


why haven't parasites evolved to be avirulent?

Group selection argument (selection working for the benefit of the group í WRONG, it's working for the benefit of an individual)
o Parasite traits ~virulence, often traits of growth etc. (malaria erythrocytic growth rates)
o Selection for these traits maintains virulence
o Vaccination that allow hosts to survive parasite episodes, will lead to still more virulent parasites í allows parasite to evolve to be more virulent because the vaccine protects the host (argument of anti-bacterial resistance)