BIOL20202: Parasite Biology (2nd term)

MV11: Describe the use of peak shift & host immunity, including when transmission would be considered high or low...

• Compare infection between high & low transmission • Parasites induce anti-parasite immunity • Peak shift = age of maximum/peak prevalence • High transmission - more young hosts have parasite infections than older hosts • Low transmission - more old hosts have parasite infections than younger hosts

MV11: Describe the direct & indirect methods for diagnosing parasite infections....

• Direct method - involves operating on the host to extract the parasite, destructive as often harms/kills the host • Indirect method - involves identifing eggs, larvae, immune markers, or symptoms

MV13: Describe the function of antibodies including in relation to parasites trying to invade a host... (not fini) Hint:

• Directly interfere with action of an antigen e.g. so that enzyme function stopped • Stop parasite cells invading host cells • Can activate complement/cascade • Can coat parasite cell to trigger phagocytosis • Can attract killer cell that release cytotoxic molecules via antibody-depenent cell-mediated cytotoxicity (ADCC)

MV10: Describe how the movement of Wuchereria (W. bancrofti) microfilariae (larvae) during the day & night, including the cues used & why this occurs?

• During the day the microfilariae are concentrated in the lung capillaries, & only move to the peripheral circulation at night. • This reflects the insect vector biting behaviour • The cue that the microfilariae use is the oxygen gradient in the lung capillaries. • The periodicity of W. bancrofti varies geographically & by host strain. • In each case the periodicity of the parasite is matched to the biting behaviour of the insect vector.

MV14: Describe what the extent to which an immune response against one life-cycle stage has any effect against other (marial) life-cycle stages depends on...

• Effectiveness depends on the degree of antigenic cross-reactivity between different life-cycle stages • I.e. how similar the antigens are in the different life-cycles & how they react

WG4: Describe how the Tania saginata leaves the Ox stomach (duodenum), including the features involved...

• Egg contains embryo with hooks called an oncosphere • Thick wall of egg is digested in duodenum, releasing embryo/larvae • Embryo/larvae bores through gut wall by using hooks & enters circulation • It then encysts in muscle tissue (e.g. heart, masseter muscle) as cysticercus larval stage

WG6: Describe the damage that Schistosomes cause...

• Eggs cause inflammatory damage to tissues & make their way out of the body either through gut wall into faeces or through bladder wall into urine • Cercariae penetrate through intact skin & enter the bloodstream - cause "swimmer's itch" when in wrong host e.g. bird schistosomes

MV14: Describe the immune response of the host to the merozoite stage of the Erythrocytic cycle, including the molecule used by merozoites & why there is ineffective cross-immunity... Hint:

• Experimentally merozoites are vulnerable to immune responses e.g. In vitro: - antibody binds to merozoite surface which blocks its ability to invade red blood cells • Main molecule is Merozoite Surface Protein (MSP) which is antigenically highly diverse as they have different epitopes (antigens) • Ineffective cross-immunity due to strain-specific immune responses i.e. different specific anti-bodies required

WG3: Briefly describe the distribution of filariasis & onchocerciasis & how it can be treated ...

• Found across Africa & Asia • Slave trade means they have also been transported to South America • Kill adult worms using tablets (GPELF campaign) • Kill black flies by using insecticides (1980s)

MV11: Describe the research findings of Kuris et al., (2008) on the parasite biomass in ecosystems at the three Mexican estuaries....

• Found parasites account for 1% of total animal biomass (e.g. invertebrates, fish & birds) • Parasites account for 5-10% of combined biomass of free-living, multi-trophic species (such as crabs, birds, fish etc.) • Thus trematode biomass ≈ fish biomass • Trematode biomass > bird biomass

MV12: Describe the findings of Williams-Blangero et al., (1999) when looking at the effect of the environment & host genetic effects... (not fini)

• Found ~40% of worm load variation is due to host genetics (genotype) • This suggests that Ascaris is a strong selective force on the host • Also means that ~60% is due to the environment • Selective force on genes that control immune responses

WG1: Describe Naegleria fowleri - the "brain-eating amoeba"....

• Free-living amoeba • In warm freshwater • Enters brain via nose • Primary amoebic meningoencephalitis (PAM) - usually fatal

WG2: Describe the development of Nematodes...

• From 1 mm to 1 m in length • Simple development: - Start with egg which hatches in larvae as part of larval 1 (AKA L1) stage. - This leads to L2, L3, L4 & adult stage, where the cuticle is shed between larval stages

MV11: Briefly describe the global human parasite infection.... (not fini)

• Gastro intestinal nematodes = 39 million • Malaria = 36 million • 1/4 of the world's human population is infected with worms - mostly the poor & children • High prevalence of human nematodes across Africa

MV15: Describe the two immunological relevant stages, which occur once an adult schistosome infection is established....

• Once established, there are responses against subsequent invading schistosomulae; this is known as concomitant immunity. • Schistosomulae are attacked by IgE & IgG, which will stimulate the complement cascade. • These antibodies will also attract esosinophils & induce antibody dependent cell cytotoxicity.

WG4: Describe the features of the scolex (head) & strobila (body) of Cestodes AKA Tapeworms....

• Scolex has suckers, grooves, hooks, spines etc to hold on to wall of vertebrate gut • sensory organs also found on the Scolex • strobila is made of individual segments or proglottids • new segments form at neck & mature towards posterior end of worm • each segment has male & female sex organs - gravid segments full of eggs

WG7: Describe the opportunistic amoebae pathogens Acanthamoeba castellans & Naegleria fowleri...

• These amoebae normally live in soil or freshwater sediment. • Poor hygiene among contact lens wearers - contamination of storage case with Acanthamoeba castellans from tap water. • Naegleria fowleri is very rare but can cause severe brain infection contracted through water forcibly entering nasal passages when diving in freshwater - usually fatal.

MV10: Describe the similarities between the dauer larvae of free-living nematodes & the infective larvae of parasitic nematodes...

• They are both: - non-feeding - long-lived - filling the role of dispersal - developmentally arrested, & will only resume development (to the L4 stage) when: a) for free-living nematodes, environmental conditions improve e.g. more food is available b) for parasitic nematodes, when a suitable host is encountered & infected.

MV12: Describe the advantages & thus causes for the distribution of this Sickle cell trait (1 βˢ) in areas where Malaria is present....

• Those with the Sickle cell trait have reduce Malaria parasitaemia • Reduces malaria replication rate & infected red blood cells are cleared more quickly • Less severe Malaria infection, lower death rate & thus higher childhood survival rates

WG3: Describe the parasite Onchocerca volvulus, including why it is vector borne & the disease it causes...

• Transmitted by blackflies (Simulium damnosum) • Blackfly larvae live in swift-flowing streams - hence riverine distribution of disease • Disease is called river blindness (Onchocerciasis)

WG3: Describe the parasite Wuchereria, including the vector & the disease it causes...

• Transmitted by mosquitoes - similar development to that of Onchocerca in blackflies • Causes filariasis = blockage of lymph ducts by adult worms causes severe swelling known as Elphantiasis • Skin thickens due to inflammation response • Adult worms produce larvae (microfilariae) in lymph duct which enter the blood stream

MV15: Describe the research on the survival Schistosoma mansoni (trematode) by Smithers, Terry & Hockley (1969)... Hint: Don. Rec.

• Transplanted schistosome worms into blood vessels of a Monkey & Mouse donar hosts • Then surgically transplanted these schistosome worms in recipient hosts including: - Normal Monkey - 'Mouse immunised' Monkey = i.e. immunised against mouse antigens

WG5: Describe the eight stages which are part of the general Digenean life-cycle... Hint:

1. Adult in vertebrate definitive host 2. Adults lay eggs 3. These hatch to getc ciliated miracidium withe germinal cells - can give rise to multiple larval stages 4. Invades or eaten by snail intermediate host 5. Development of larvea into sporocyst, may have Redia (feeding stage), germinil cells produce cercariae 6. Release of cercariae which are motile & have two suckers 7. Cercariae encyst if un-facourable conditions into Metacercaria 8. Cercaria or Metacercaria gets into definitive host

WG6: Describe the general life-cycle of Schistosomes... Hint:

1. Adults in small veins of bladder or intestine copulate to produce eggs that pass through the bladder or gut wall 2. Eggs are eliminated with feces or urine & the eggs hatch release miracidia with cillia 3. The miracidia swim & penetrate specific snail intermediate hosts 4. In the snail production of sporocysts & production of cercariae (from germinal cells) 5. Sporocysts burst to release infective motile cercariae from the snail, which then swim & penetrate the skin (foot) of the human host

WG6: Describe the life-cycle of Leucochloridium paradoxum.... Hint:

1. Bird is definitive host, eggs are released in faeces. 2. Snail eats bird faeces & the eggs hatch 3. Sporocysts with coloured spots & bands infect the eye stalks of snail host, snails can't see properly & do not hide from predators. 4. Pulsating, brightly coloured eyestalks (look like caterpillars) cause the snail to be eaten by a bird

WG1: Name the three different types of relationship...

1. Commensalism 2. Mutualism 3. Parasitism

WG2: Describe the infection/life-cycle of Toxocara canis AKA dog roundworms...

1. Dormant L2 larvae reactivated by hormonal changes in pregnancy 2. Puppies infected in utero by L2 larvae via placenta. 3. Larvae passed to puppies in milk 4. In adult & in puppies, larvae is coughed up & swallowed resulting in L4 larvae & then adults in the gut, leading to the release of eggs 5. Eggs from bitch and puppies - both are sources of infection. 6. Eggs in feacal matter become infective at around 2-3 weeks 7. These infective eggs can be ingested

WG6: Describe the life-cycle of Dicrocoelium dendriticum... Hint:

1. Eggs (produced by adult flukes) are deposited on field in faeces 2. Miracidia hatch & swim to find snail 3. Miracidia are eaten by snail as the 1st intermediate host 4. Cercariae released from snail in a slime ball to be eaten by ant as the 2nd intermediate host 5. Metacercaria in ant ganglion causes infected ants to not be able to open jaws & get stuck on blades of grass 6. Metacercariae encyst inside ant is eaten by sheep definitive host, it then travels from gut to bile ducts of liver to develop into adult flukes

WG6: Describe the life-cycle of Fasciola hepatica AKA liver rot of sheep... Hint:

1. Eggs (produced by adult flukes) are deposited on field in faeces 2. Miracidia hatch in damp pasture & swim to find amphibious snail 3. Miracidia enter Snail (Lymnea) as the intermediate host & undergo some larval stages 4. Cercariae (from Sporocyst) released from snail & swims in damp meadow 5. Metacercariae, which is resistant to desication, encysts on grass 6. Metacercariae eaten by sheep definitive host, & migrate from gut to liver via abdominal cavity, which develop into adult flukes in bile duct of liver

WG2: Describe the direct infection/life-cycle of human hookworms...

1. Eggs in faeces are in contact with soil 2. L2 larva free-living in soil eats bacteria 3. L3 larva infective - negatively geotropic reacts to warmth and vibration, can live up to 4 weeks 4. Carried by circulation to heart & lungs - penetrates through alveoli, coughed & swallowed. 5. Adults end up in the intestine.

WG4: Describe the life-cycle of Diphyllobothrium latum.... Hint:

1. Eggs in faeces/sewage discharged into lake 2. Intermediate host 1: Copepod eats swimming larval stage called oncosphere 3. Intermediate host 2: Fish eats copepod & larvae are plerocercoid in tissues 4. Paratenic host: Predatory fish eats smaller fish - larva does not develop 5. Definitive host e.g. Human or bear catches & eats fish, adult tapeworm develops in gut

WG4: Describe the life-cycle of Taenia saginata.... Hint:

1. Eggs in sewage contaminating pasture are eaten by ox/cattle 2. Eggs hatch in ox intermediate host & larval stage cysticerci (or cysticercus (si.)) encyst in muscle 3. Cysticerci ingested by humans in undercooked meat (beef) 4. Human is the definitive host, so larvae become adults & adult tapeworms produces eggs in faeces

WG3: Describe the seven stages involved in the general life-cycle of Anisakiasis, including how humans can be infected... Hint:

1. Eggs produced by adult females are passed in the feces of marine mammals, & the first-stage (L1) larvae are formed in the eggs. 2. Larvae molt, to become L2 & after the larvae hatch from the eggs, they become free-swimming 3. Larvae released from the eggs are ingested by crustaceans & they develop into L3 larvae 4. i) Infected crustaceans is eaten by fish etc larvae migrate from the intestine to the tissues in the peritoneal cavity and grow up to 3 cm in length. ii) Upon the host's death, larvae migrate to the muscle tissues, and through predation, the larvae are transferred from fish to fish. 5. When fish or squid containing L3 larvae are ingested by marine mammals, the larvae molt twice & develop into adult worms, which produce eggs to be shed by marine mammals 6. Humans become infected by eating raw or undercooked infected marine fish containing L3 larvae 7. After ingestion, the anisakid larvae penetrate the gastric & intestinal mucosa, causing the symptoms of anisakiasis.

WG4: Describe the life-cycle of Echinococcus granulosus... Hint:

1. Embryonated eggs are passed in the feces & ingested by intermediate host e.g sheep, the egg hatches in the small bowel & releases an oncosphere 2. The oncosphere penetrates the intestinal wall & migrates through the circulatory system & develops into a Hydatid cyst that produces protoscolex etc. 3. Canine definitive host is infected by ingesting the cyst-containing organs 4. protoscolex develops into scolex that attaches to the intestine to develop into an adult in the small bowel 5. Adult E. granulosus (3-6 mm long) resides in the small intestine of the dog definitive host & release eggs

WG1: Name the four different types of parasites & provide examples of each type...

1. Endoparasite e.g. intestinal worms 2. Ectoparasite e.g. fleas, lice, ticks 3. microparasite e.g. protozoa, bacteria, viruses 4. macroparasite e.g. worms

WG8: Describe the 5 steps involved in the lifecycle of Malaria in the mosquito host... Hint:

1. Gametocytes are taken into mosquito with blood meal 2. Macrogamete develops into an 'egg' & microgamete produces 'sperm' as these gametes fuse via fertilisation in the mosquito stomach 3. The fertilised ookinate cell migrates to the linning of the mosquito stomach & penetrates the midgut wall to develop into a oocyst on the other side 4. Oocyst undergoes sporogony to produce sporozoites in the heamolymph when the oocyst bursts 5. These sporozoites infect the salivery gland of the mosquito so that they can be injected with the saliva of the mosquito

WG3: Describe the lifecycle of Dracunculus medinensis, including its Intermediate host... What type of transmission cycle does it have?

1. Humans drink water containing copepods that are carrying the larvea (L3) 2. L3 larvae released when copepods die - penetrate gut wall & enter tissues 3. Adult worms mate & female migrates into limb (e.g. leg) where they give birth to larvae in foot which creates a blister 4. L1 larvae released into water from blister 5. L1 larvae eaten by copepod 6. Larvae develop into L2 then L3 in copepod • Intermediate host = Copepods in freshwater e.g. Cyclops • Indirect transmission cycle

WG8: Describe the 6 steps involved in the lifecycle of Malaria in the human host... Hint:

1. Infected mosquito feeds on human so sporozoites are injected with saliva into the blood stream 2. Sporozoites enter the liver & use kupffer cell to penetrate liver cells & infect these cells 3. Sporozoite undergoes cellular division to result in a huge number of merozoites leavining the liver from schizont 4. Merozoites target red blood cells, which they invade - this also allows them to hide from the bodies immune system 5. Contense of red blood cell is destroyed, while the merozoites divide to produce more merozoites 6. The infected red blood cell bursts & some of these merozoites develop into macrogamete & microgamete

WG7: Describe the life-cycle of Eimeria.... Hint:

1. Ingestion of sporulated oocyst (on grass) 2. Sporozoites released from oocyst invade epithelial cells of gut in animal 3. Asexual cycle - schizogony produces merozoites 4. Sexual cycle - formation of microgametes & macrogametes from merozoites 5. Production of (resistant) oocyst which leaves the body in faeces

MV10: Describe the two hypotheses for the evolution of animal parasitism by nematodes.... (not fini)

1. Nematodes developed increasingly intimate associations with hosts: • E.g. resistant larvae stages began to live with their hosts for longer periods & were transported by the host (evolved phoretic associations) 2. Many nematodes scavenged on dead animals: • May also be a route to the evolution of obligate parasitism

WG8: Describe the three steps involved in the invasion of red blood cell by Plasmodium merozoite...

1. Parasite binds to red blood cell via apical end & reorientates 2. The parasite then enters into a parasitophorous vacuole & releases proteins from apical organelles 3. The parasite surface proteins are then shed by proteases

WG4: Describe the life-cycle of Taenia solium.... Hint:

1. Pigs ingest eggs by scavenging on human sewage 2 Eggs hatch in pig intermediate host & larval stage cysticerci (cysticercus (si.)) encyst in muscle 3. Cysticerci ingested by human in undercooked pork meat 4. Human is the definitive host, so larvae become adults & adult tapeworms produces eggs in faeces

WG8: Describe the life cycle of Toxoplasma gondii... Hint:

1. Unsporulated oocysts are shed in the cat's faeces 2. a) These oocysts sporulate & Intermediate hosts in nature (e.g rodents & birds) become infected after ingesting soil, water or plant material contaminated with oocysts b) Livestock or humans can also take in oocyst in this way 3. Oocysts transform into tachyzoites shortly after ingestion, which localize in neural & muscle tissue & develop into tissue cyst bradyzoites 4. Cats become infected after consuming intermediate hosts (e.g. rodents) harboring tissue cysts

WG4: Identify the features of a Hydatid cyst by using the diagram below.... Hydatid cyst

A = Fibrous Capsule (i = host origin, ii = parasite origin) B = germinal layer C = daughter cyst D = protoscolex

WG7: Describe the transmission/life cycle of Entamoeba....

Direct lifecycle & faeco-oral transmission: • Transmitted by cysts in faeces, cysts consumed in food or water. • Each cyst has 4 nuclei, 8 trophozoites (are feeding & dividing stage) released during encystation in intestine.

MV15: Describe Filarial nematodes (such as Onchocerca, Wuchereria and Brugia), including where they live & any similarities in their life cycles...

Filarial nematodes are parsites that are insect transmitted in tissue or blood. • Onchocerca (river blindness), Wuchereria & Brugia parasitise humans. • Onchocerca adults live under the skin • Wuchereria & Brugia adults live in lymphatic tissue • All species produce first stage larvae called microfilariae • These circulate in the blood for Wuchereria & Brugia • While microfilariae are in the skin for Onchocerca • These body areas are where microfilariae are taken-up by the insect host.

MV12: Describe normal Haemoglobin (Hb) & Sickle-cell haemoglobin (HbS)....

Haemoglobin (Hb): • four globin molecules (α & β) • four haem groups • 1 Hb molecule carries 4 oxygen molecules Sickle-cell haemoglobin (HbS): • mutation in β globin (instead have βˢ) • combines with normal α

WG9: Describe the movement of Trypanosome brucei in the tsetse fly.....

In the tsetse fly: • Differentiates & multiplies in the midgut • Migrates to the salivary glands • Differentiates & multiplies in the salivary glands • • Infective forms exuded in saliva

MV11: Describe examples of the indirect methods for diagnosing different parasite infections (including the parasites & illnesses below) & any benefits or potential issues with these methods... • Gastro-intestinal parasites (helminthes) • Schistosomes (helminthes) • Filarial nematodes e.g. Wuchereria • Onchocerciasis • Malaria

Indirect method examples: • Gastro-intestinal parasites = look for eggs in faeces • Schistosomes = look for eggs in urine or faeces - benfit as the morphology of helminth eggs can usually identify the species of parasite • Filarial nematode = look in blood for microfilariae • Onchocerciasis = Larval stages in skin so take sin samples • Malaria = take blood sample/smear • Use symptoms to identify parasite - potential issue as may identify parasite incorrectly • Look for immune markers/antiobodies via ELISA (Enzyme Linked Immunosorbant Assay) - issues as often can't distinguish between a prior & current infection.

MV11: Describe Microparasites & Macroparasites in terms of type, body, lifespan & reproduction....

Microparasites: • Protozoa • single cells • short lived • reproduce within host as number of parasites increases inside the host Macroparasites: • Helminths • metazoan / multi-cellular • long lived • no increase in parasite numbers within the host as eggs are passed out of the host

WG6: Identify the host(s) & species of helminth parasites with indirect transmission cycles which involves: a) Insect vector (intermediate host) b) Snail intermediate host

Parasites that use Insect vectors: • Black flies - Onchocerca volvulus • Mosquito - Wuchereria Parasites that use snail intermediate host: • Human - Schistosomes • Sheep - Fasciola hepatica • Sheep & ant - Dicrocoelium dendriticum • Bird - Leucochloridium paradoxum

*WG6: Identify species of helminth parasites with direct transmission cycles which involves: a) Faeco-oral transmission (not fini) b) Contaminative transmission

Parasites that use faeco-oral transmission: • Roundworms e.g. Ascaris lumbricoides (human) & Toxocara canis (dog) • Pinworms e.g. Enterobius Parasites that use contaminative transmission: • Human hookworms e.g. Necator americanus & Ancylostoma duodenale

WG5: Describe the similarities & differences between the anatomy of Monogeneans & Digeneans....

Similarities: • Both have oral suckers on anterior end • Mouth splits into two guts Differences: • Monogeneans have holdfasts which Digeneans lack • Digeneans have one oral & one ventral sucker

WG7: Describe how the coccidiosis infection from Eimeria can be controlled using different methods....

Use Eimeria with short schizogony cycle: • Infect life-stock with this to raise immunity • Not much damage as only one cycle (vs 3) Use vaccine: • Raise immunity but very expensive Other method: • Control by coccidiostats in food or vaccines - keeps it at a stable level

WG2: What is Zoonosis?

Zoonosis: disease naturally transmitted between vertebrate animals & humans

WG2: Describe the direct infection/life-cycle of Ascaris lumbricoides AKA roundworm... (check)

• 2-3 months from ingestion of egg to production of eggs by female 1. Adults in lumen of small intestine 2. Fertilized egg - takes 18 days to several weeks to develop, requires Warmth, shade & moisture 3. Embryonated egg is fully formed 4. Egg is swallowed 5. Larva hatches & invades intestinal mucosa 6. Larva carried to lungs via portal vein 7. Larva coughed up, swallowed & develops into adult in intestine

MV13: Describe the structure of immunoglobulin antibodies... Hint:

• 4 polypeptide chains of 2 long & 2 short • Has constant regions & variable regions • Variable region has a specific shape to interact with antigen • molecular shape of antigen is called an eptitope - get different shaped epitopes

WG8: Identify the 5 species of Protozoan parasites that cause Malaria in humans, including the vector used...

• 5 species in humans: Plasmodium falciparum, P.vivax, P.ovale, P.malariae & P.knowlesi • Vector: Mosquito

MV12: Describe Sickle cell trait (1 βˢ) distribution across the globe...

• 65 million sub-Saharan Africa • In tropical Africa 30% have sickle cell trait • βˢ at several different forms of frequencies (>5%) in India & Mediterranean etc. • High frequency in African & Afro-Caribbean populations • More dominant in areas where malaria is present

MV14: Briefly describe how Trypanosomes are able to evade the immune system of the host... Hint:

• Able to have variant Antigenic types - able to change their antigenic coat • Frequency dependent selection - most rare variant is advantageous • Survival by changing 'appearance' to the host immune response

WG3: Describe the lifecycle of Onchocerca volvulus...

• Adult female produces larval worms in a nodule • Larvae taken up in blood by blackfly, these enter its stomach & migrate into the thorasic muscle & then the head • Human skin is infected as larvae (L3) are released during biting by fly, larvae moult to L4 & then to adults • Blindness caused by inflamation in eye due to larvae penetrating anterior chamber & cornea

WG1: Describe the different types of transmission cycles...

• Direct - One host • Indirect - More than one host • Monogenetic - one host • Digenetic - two hosts

WG6: Describe Schistosomes, including the disease it causes, where it can be found, & how certain species (e.g. Schistosoma mansoni, Schistosoma japonicum, & Schistosoma haematobium) are transmitted...

• Adult worms live in blood vessels of bladder or gut • Intermediate host is an aquatic snail • Disease: schistosomiasis or bilharzia • >200 million people infected worldwide in 74 developing countries • Faecal transmission: S. mansoni & S. japonicum • Urinary transmission: S. haematobium • Zoonotic infection: S. japonicum

WG2: Describe the Nematode Enterobius AKA pinworm... Also, describe the autoinfection of pinworm...

• Adult ~10 mm long • Lives in colon - female migrates to peri-anal area to lay eggs. • Faeco-oral transmission. • Relatively harmless - itching, psychological damage! Pinworm autoinfection: 1. Eggs contaminate fingers after itching & eggs are ingested 2. Larvae hatch in small intestine & migrate to colon 3. Adults mature in colon & migrate to perianum 4. Adults lay eggs on perianum

WG2: Describe the nematode human hookworms e.g. Necator americanus & Ancylostoma duodenale...

• Adults are about ~10 mm long • Widespread - second most common human worm infection after ascariasis. • Important cause of iron deficiency anaemia caused by blood loss from worm attachment sites in intestine.

WG1: Identify the Advantages & Disadvantages of a parasitic lifestyle...

• Advantages: + Stable environment + Food freely available • Disadvantages: - How to find new host - How to find developmental site in host - How to avoid host defensive reactions

MV11: Describe the different distributions of parasites (e.g. helminths) in a host population...

• Aggregated - most hosts have a few parasites while most parasites are in a few of the hosts • This can be statistically modelled by the 'negative binomial distribution' • Random distribution: - When variance = mean - Use Poisson distribution • Aggregated distribution: - When variance > mean - Use negative binomial distribution

WG7: Describe Apicomplexans as a Parasitic Protozoa, including the apical complex... (not fini)

• All Apicomplexans have intracellular stages - stay inside cells in order to survive • All are animal parasites • Characterized by apical complex: 1. Recognise cell type to invade (cell to cell communication) 2. Orientation of cell 3. Organelles used for invasion of cell

MV12: Describe what parasite virulence is & what it depends on including examples to illustrate this... Hint:

• An interaction phenotype (between pathogen & host) • How ill the host is depends on it own genetics & parasite genetics too e.g. - Hosts of two qualities (more & less robust) exposed to same parasites = more harm occurs in less robust host - Hosts with equal qualities exposed to parasites of different virulence (faster & slower) = host with faster parasite becomes more ill

MV10: Describe the research & findings by Hutchings et al., (2007) on breeding genetically selected sheep to be resistant to parasites such as the nematode Haemonchus contortus.... Hint:

• Animal breeders have selected breeds of sheep that are resistant or susceptible to nematode infections. • Selected sheep for higher & lower faecal egg count. • Found differences in immune function in sheep e.g. lower faecal egg count as better immune response in those selected for lower egg count. • Can also select for sheep with different feeding behaviours (e.g. tussock grass or not) as there are more nematode parasites in the tussock grass. • When resistant sheep & those that don't feed on tussocks are selected for, then they don't get infected as they expose themselves less. • Thus host's behaviour effects the exposure of the host to parasites.

WG3: Briefly describe Anisakiasis including & how can it infect humans?

• Anisakiasis is acquired by humans eating raw fish containing larvae of anisakid nematodes (e.g. Anisakis simplex or Pseudoterranova decipiens) • Has two intermediate hosts which are crustaceans & fish • Its definitive hosts are marine mammals

MV14: Identify & briefly describe the anti-Trypanosoma responses of the immune system... (not fini)

• Antibody dependent e.g. uses IgM • Uses phagocytosis (macrophages) to kill trypanosomes in the liver • Uses complement cascades to create pores in the trypanosome cells to kill it • ~Ten million (10⁷) [arasites cleared from the blood in 20 minutes

WG9: Describe how the control of trypanosomiasis is problamatic, inckuding the different methods used & the issues with these methods...

• Antigenic variation of trypanosomes makes it very difficult to develop vaccines against African sleeping sickness or Nagana • Control relies on: • drug treatment - but drugs are few & some are extremely toxic • control of the vector - but the areas affected are vast and Africa is poor

MV12: Describe the harm to the host caused by the malarial merozoites in the erythrocytic cycle in more detail....

• At each erythrocytic cycle, red blood cells are destroyed due to the release of merozoites • This loss of iron via loss of red blood cells can lead to anemia - use iron suppliments to treat it • These red blood cells need to be replaced as energetic cost for the host • Another cost to the host is the fever that follows the red blood cells being ruptured

MV12: Describe the research by Williams-Blangero et al., (1999) on Ascaris infection & the correlations found...

• Carried out faecal egg counts (FEC) in humans & treated them with drugs • Counted worms following treatment • Repeated FEC two years later • Found strong (0.45) correlation for FEC & strong correlation (0.79) for worm burden i.e. similar number of worms bfore & after • Indicates there are wormy people

MV12: Describe Sickle cell disease including the structural components that cause it & the symptoms that result from this disease...

• Caused by having two βˢ • Causes deformed globin alignment & thus red blood cells to be sickle shaped • Cells are fragile & adhere to vasculature i.e. break & stick to blood vessels which reduces oxygen carrying capacity • Can lead to anaemia • Other symptoms are joint pain & organ failure

WG1: Describe Commensalism as a relationship...

• Commensalism - "eating at the same table" • loose association - no metabolic dependence • trophic interaction where one partner (the commensal) benefits with no cost to the other (the host) - neither benefit nor harm. • e.g. Ramora on a dolphin

MV11: Identify the different types of density dependent effects (D.D.E) on parasites (in an ecological setting)... Also, describe how density dependent effects can be important for measuring helminth infections including the graph below as an example of this... Key: Eggs per worm (Xa) = ○ ,Fecal egg count (Xb) = ●

• Competition for limited resources • Immune dependent e.g: - Density-dependent immune responses = when the immune responses generated (quantity & quality) is dependent on the number of parasites • D.D.E alter the relationship between the number of helminth worms & the number of eggs that are released in the faeces. • Problomatic to judge how many worms in gut based on number of eggs in faeces • If eggs per worm etc weren't density dependent then the line would be horizontal • This indicates that the competition between worms reduces the number of eggs produced per individual

WG8: Briefly describe the relics found in Malaria parasite Plasmodium & how one of theses may be used as a possible drug target...

• Contain mitochondria & apicoplast which is a relict chloroplast • The apicoplast is used for chloroplast-type fatty acid biosynthesis • Thus drugs could be used to target the apicoplast in many apicomplexan parasites

MV15: Describe the research findings from looking at treating the chronic infections of Heligmosomoides polygyrus in rats..... Also explain what these findings indicate.... Hint: Groups:

• Control group A had high numbers of worms - shows adults presense does have effect on 2nd (challenge) infection success • For group B a large number of worms recovered - this suggests the adults immunomodulated the immune response so it was weaker thus the larvae could survive • Control group C had a low number of worms - shows results aren't due to surgery on hosts • Found majority of worms were killed in group D & did not recover due to immune response • Success determined by presense of adult worms that carry out immunomodulation • This benefits further attempts of infection

MV13: Identify & describe the type of cells Cytotoxic T-Lymphocytes & Macrophages are, including their function & an example of this...

• Cytotoxic T-Lymphocyte: - Specialised white blood cell - Responsible for eliminating unwanted body cells e.g. cancer - Can kill cells infected with influenza virus • Macrophage - White blood cell - Engulfs/kills infected cells - Can kill opportunistic pathogenic yeast candida albicans in humans

WG3: Describe Trichinella including its main features & general life-cycle...

• Definitive & intermediate host can be same the same animal • parasites are encysted in muscle tissue of carnivores/scavengers • Zooanotic - gained by eating undercooked meat • General life-cycle: 1. Encysted larva in striated muscle is ingested in undercooked meat (e.g. pork) 2. Larva released in small intestine 3. these develop into adults which reproduce in the small intestine 4. Larva deposited in mucosa migrate into blood circulation 5. These larva then encyst in striated muscle

WG8: Describe Toxoplasma gondii, including the hosts used & the disease it causes...

• Definitive host = cat • Intermediate host = any mammal or bird • Relies on predator-prey cycle • Uses Tachyzoites (fast) & Bradyzoites (slow) • Toxoplasma is estimated to infect 25-50% of global population • Disease is called toxoplasmosis - important in pregnancy & AIDS in humans

WG1: Describe the following types of host & also describe what a vector is... • Definitive • Intermediate • Paratenic

• Definitive host = host in which parasite undergoes sexual reproduction • Intermediate host = host in which parasite develops or multiplies, but does not undergo sexual reproduction • Paratenic host = transport host, thus no development or multiplication of parasite. • Vector = micropredator that actively delivers parasite to next host e.g. malaria mosquito

WG4: Describe what the transmission of Taenia saginata AKA beef tapeworm relies on, including the types of hosts involved...

• Definitive host = human (adult tapeworm is 4-8 m in length) • Intermediate host = ox • Transmission relies on: a) human faeces contaminating pasture where cattle graze b) poor standards of meat inspection c) eating inadequately cooked rare-beef

WG4: Describe what the transmission of Taenia solium AKA pork tapeworm relies on, including the types of hosts involved...

• Definitive host = human (length 3-5 m) • Intermediate host = pig • Transmission relies on: a) contamination of pig food with human faeces b) poor standards of meat inspection - "measly pork" c) eating inadequately cooked pork - e.g. barbecued sausages

WG4: Identify the various different hosts used by Diphyllobothrium latum AKA the broad tapeworm....

• Definitive host = human or other fish-eating mammal e.g. bear etc. • Intermediate host 1 = copepod • Intermediate host 2 = fish • Sometimes there is a paratenic host = Predatory fish

WG4: Also describe how Taenia solium eggs could end up in a human, including the outcomes of this & use Ekari of New Guinea as an example... Hint:

• Definitive human host could contaminate food with eggs • Another human ingests eggs by eating contaminated food • Human develops cysticerci in tissues just like the pig, but it's a dead end for the parasite • Neurocysticercosis & epilepsy if cysticerci in brain - prevalence may be very high in some communities e.g. Ekari

MV14: Describe what happens to populations with endemic exposure to malaria.... Also, describe what is required to develop & maintain an effective immune response... Despite, this how can malaria persist?

• Develop immunity to malaria via continued exposure & exposure to antigenic diversity • Repeated exposure to develop & maintain an effective immune response against malaria • But anti-malarial immunity is short lived as poor immunological memory (due to immunomodulation) • Malaria immunomodulates - alters/reduces responses to antigens & interferes with T helper cells, thus weakening the immune response & helping malaria infections

WG1: Describe what is the features of a parasite...

• Different species to host = heterogenetic association e.g. not babies • Intimate association - inside or on body; not predator-prey relationship • Dependence - metabolic or physiological, not just living together • Recognised by host as "foreign" • Harmful - but to variable degree

MV13: Describe the function of Major Histone Complexes (MHC) including the two classes...

• Differentiates between self & non-self cells as molecules of the MHC are hypervariable MHC Class 1 : • Defines self & is never identical • Has large locus are hypervariable e.g. HLA • will reject transplant if not closely matched MHC MHC Class 2: • Plays role in regulation of the immune system

WG7: Describe the typical Apicomplexan lifecycle... Hint:

• Haploid sporozoites produced in infection stage via sporogony & these sporozoites invade the host cell • Inside host cell Schizogony occurs as sporozoites multiply by binary fission to result in mature Schizont which develop into Merozoites • Cell bursts to release Merozoites which forms microgamete & macrogamete via Gametogeny • Microgamete & macrogamete merge together in sexual reproduction to get diploid Oocyst (zygote) • Oocyst undergoes sporogony to get haploid sporozoites

MV15: Briefly describe how parasitic helminth worms such as pin worms (Ascaris Lumbricoides) & whipworms (Trichuris sus) can be used for immunotherapy....

• Helminths can be used to immunomodulate/inhibit the immune system of individuals with auto-immune diseases • Can be used to treat multiple sclerosis, Crohn's disease & asthma etc.

MV12: Describe the harm to the host caused by hookworms (such as N. americanus & A. duodenale) in more detail...

• Hookworms cuts mucosa & feeds on blood: - N. americanus takes up 50 μl blood per day - A. duodenale takes up 200 μl blood per day • Host can develop anaemia from blood (iron) loss - affects growth & cognitive development • The effect is dependent on intensity of infection

MV13: Describe host-Parasite interactions including how hosts try to prevent parasite infection & parasite establishment, include different examples for how parasite infection can be prevented.... Hint:

• Host has to prevent infection &/or to remove an infection • Use various methods to do this including innate resistance, innate immunity & acquired immunity • Innate resistance prevents infection & the two immune responses prevent establishment & remove parsites • Innate/natural resistance can occur via behaviour, physiology, or structure of host e.g. thick skin etc • Prevent chance of getting malaria by covering skin (behaviour) • Behaviour of avoiding pork so not exposed to parasites (e.g Islam & Jews) • Physiological differences between host species can mean that even though a species is exposed to a parasite species, infection won't occur due to host specificity of parasites • Acquired & innate immune response stops parasites establishing

MV11: Identify & give examples of the causes of aggregated distribution....

• Host variation e.g. - parasite exposure or susceptability - genetic, behavioural or occupational features • Parasite infection e.g. - within host reproduction (protozoa) - 'clumped' exposure

WG4: Describe Hydatid disease in humans, including in Turkana (Kenya) as an example of Echinococcus granulosus causing Hydatid disease... Hint:

• Humans become infected by ingesting eggs as they are an itermediate & dead end host • The larval tapeworm creates a hydatid cyst - called Hydatid disease • Surgical removal is the only way to remove hydatid cyst - dangerous if it bursts as it could spread to the rest of the body • Epidemic of Hydatid disease in Turkana: - dogs act as nurse maids for children thus egg ingestion occurs (cammels are another intermediate host) - Surgery is sometimes used tend to use wormers for dogs but the tapeworms come back

WG7: Describe Entamoeba e.g. Entamoeba histolytic, including the damage to the host & where the parasite lives....

• Humans host at least 6 different Entamoeba species, 50,000 to 100,000 deaths per year. • Entamoeba histolytica is major cause of disease (3rd most important parasitic disease after malaria & schistosomiasis) • Parasite lives in intestine & colon but also invades liver via bloodstream, which leads to liver abcess. • Causes amoebic dysentery as parasite colonizes epithelium of colon - diarrhoea, abdominal pain, weight loss.

MV13: Summerise the immune system responses (primary & secondary) to parasites, including the main features of the two branches...

• Humeral branch involves B cells • Cellular branch involves T helper cells & Cytotoxic T cells • Both branches occur at the same time & generate memory cells (primary response) • Results in a quicker secondary response of both branches which interact together in a controlled fashion

MV13: Identify & briefly describe the 5 types of immunoglobulin antibody...

• IgM = pentameric (5 regions) produced first • IgG = produced at the highest concentration, doninant in circulation • IgA = dimer (2 together) secreted on to mucus membranes e.g. gut & lungs • IgE = creates inflammation • IgD = unknown function?

MV13: Describe hypersensitivity in the immune system by using type 1 as an example...

• Immunoglobulin E (IgE) are used in inflammatory or allergic reactions • Type 1: - IgE antibodies bind to mast cell & antigen/allergens bind to the antibodies - This triggers the mast cells to release histamine which can cause an allergic reaction - Histamine is active against parasites & will change the body environment

MV10: Describe how the hosts physiology can determine the development of a particular larval stage of a parasitic worm by using microfilariae as an example... Hint:

• In mammalian host: - Temperature is 37˚C - The oxygen concentration/tension is high - Presence of vertebrate immune response. • In insect vector/host: - Temperature is ambient (20˚C) - Oxygen concentration is low - Different invertebrate immune response. • Microfilariae (L1) larvae has to move between these two different environments. • L1 can't grow/develop any further in mammal until it enters the new insect host, & signals in this host allow development. • L3 can't enter the next larvae stage in insect until it enters the mammalian host & signals in this host allow development. • Really tight control as biology & physiology of the worms is determined by the host via changing worm gene expression etc

MV13: Describe the hygiene hypothesis including why it is thought to occur.... Hint: Past reponsiveness: Th1 = Th2 vs. Responsiveness now: Th1 < Th2

• In the past people were exposed to equal amounts of bacteria/viruses & worm parasites • Now less exposure & thus less bacterial & viral infections results in greater Th2 responsiveness • This can lead to a greater probability of allergic reactions, & associated pathologies. • Due to evolution of vertebrate immune system in the presence of viral, bacterial, protozoan & worm infections

MV11: Define incidence....

• Incidence - number of new cases of disease or infection that appear in a population in a given period, expressed as a proportion (or a percentage) of the population size at time = 0.

MV11: Describe & discuss the evidence of the existence of 'wormy' people by using schistosomiasis & gastro intestinal parsites as an example, also include possible reasons for this aggregated distribution...

• Individuals with a high intensity of infection re-acquire high intensity infections following mass chemotherapy of the whole population. • Maybe due to genetic predisposition, age, or life style e.g. - Exposure at younger age allows children to acquire immunity - More time spent in water = exposed more to parasites so develop schistosomiasis - More time spent in field in developing world = exposed more to parasites from feaces such as gastro intestinal worms

MV10: Describe Entomopathogenic nematodes (e.g. Steinernema), including why they are not parasites & how their life-style my have resulted in the evolution of parasites...

• Infective larvae carry specialised bacteria (e.g. Xenorhabdus) • In host, the bacteria are released which grow in host body & kills the host • Worms feed on bacterial soup, multiply, & infective larvae are released from dead host • Entomopathogenic nematodes are not 'strictly parasites, because they don't live with their host, instead killing them & using them for food • This lifestyle does suggest a means by which nematode animal parasitism may have evolved.

WG8: Identify the routes of Toxoplasma gondii transmission to humans.... Also, briefly describe Toxoplasmosis in pregnancy... Hint:

• Ingestion of oocysts from soil or water contaminated with cat faeces • Ingestion of tissue cysts in undercooked or cured meat • Ingestion of infective parasites in unpasteurised milk • Transplacentally from mother to fetus Toxoplasmosis in pregnancy: • Passed to developing foetus via placenta • UK figures: babies born with congenital toxoplasmosis = 3 per 100,000 births

MV11: Define intensity & abundance, in terms of how heavy a parasite infection is....

• Intensity - how many parasites on average are there amongst the infected hosts • Abundance - average number of parasites per host in the whole population (including uninfected hosts)

WG6: Explain why Dicrocoelium dendriticum is a good example of true behavioural modification....

• Involves behavioural modification of ant host by Metacercaria parasite • When temperature drops at night, infected ant is forced to climb grass & latch onto it (abnormal behaviour)

MV15: Describe Schistosoma parasites & the main components of their lifecycle...

• Is a trematode (flat worm) • Snail is intermediate host • Humans are definitive host in which eggs end up in the liver & worms damage the gut/stomach • Found in blood of vertebrates

WG2: Describe the taxonomy of Helminths...

• Kingdom = Metazoa • Phylum = Nematoda • Phylum = Platyhelminthes: - Monogenea - mostly ectoparasites of fish & amphibia - Digenea - flukes or trematodes - Eucestoda - cestodes or tapeworms

WG6: Why is it hard to break the life-cycle of Urinary schistosomiasis in Africa in a continuous way? Also, briefly describe the damage it can cause.... Hint:

• Lack of proper toilets mean that children often deficate & urinate near lakes/rivers • These same lakes are often used by children to cool down in • Schistosomes cover themselves with human proteins to evade detection by the immune system • Liver can become calcified as white blood cells target dead eggs etc, causing more damage

MV10: Describe the three main features of parasites with free-living stages & describe some of these features in Ascaris as an example... Hint:

• Large numbers produced - e.g. ~200,000 Ascaris eggs per day - These don't have a developed embryos & thus require time externally to become infective • Environmentally resistant - e.g. Ascaris eggs are resistant to desiccation & freezing, thus they can survive for years - They are also resistant to many disinfectants • Targeted for (new) host acquisition - e.g. the strategy of Ascaris to transmit is to heavily contaminate the environment (both by large numbers & by environmental persistence), thus making it difficult for hosts to escape exposure.

MV10: Describe how Hookworms (e.g. Necator & Ancylostoma) also demonstrait the three main features of parasites with free-living stages...

• Large numbers produced - high fecundity of worms produced per day (5,000 by Necator & 15,000 by Ancylostoma) • Environmentally resistant - infective third-stage larvae maintain the cuticle of the L2 stage as a 'sheath' • Targeted for (new) host acquisition - Parasitic nematode larvae will move towards warmth i.e. vertebrate host temperature (used as a cue)

MV14: Identify three other intra-cellular protozoa...

• Leishmania spp. • Trypanosoma cruzi • Toxoplasma gondii

WG2: Describe nematodes in ruminants, include what these are similar to & give examples...

• Lifecycles of human hookworms are very similar to those of Haemonchus & Ostertagia • Haemonchus & Ostertagia are two very important veterinary pathogens of ruminants worldwide. • In this case, the infective L3 larvae are on pasture & are eaten while grazing.

MV12: Describe the α thalassaemia genotypes fond in Asia, including the reason why some are advantagous against malaria, while others are costly.... Also, identify which of the α thalassaemia genotypes shown below are normal etc... (αα, αα) (-α, -α) (--, αα) (--, --) NB: '-' indicates absence of function of the allele product

• Like the sickle cell relationship, there is a cost to the α thalassaemia as genotype (--, --) is lethal • but there is an advantage of the other normal genotypes in the presence of malaria. • It is thought that the α thalassaemia genotypes (-α, -α) & (--, αα) has an inhibitory effect on the malaria parasites.

MV13: Describe the activation of T helper cells & the function of these T helper cells, including the steps involved... Hint:

• Macrophage promotes/presents antigen from parasite using MHC class 2 molecules • The T cell receptor & cell surface marker (CD4) on the T helper cell bind the antigen • T cell receptor & cell surface marker (CD4) recognise antigen & MHC class 2, so T helper cell is activated & proliferates • The activated T helper cells promote the activity of other T cells (cytotoxic) & B cells by releasing cytokines • Activated B cells then make plasma cells etc • A small proportion of activated T cells become T memory cells (for memory of cellular arm)

WG8: Describe Malaria as selection pressure, including for Sickle cell anaemia as an example....

• Malaria has been a widespread & debilitating disease for the human population over thousands of years • Left the mark of this in our genome - particularly a range of abnormalities of haemoglobin • Sickle cell is caused by a single point mutation in haemoglobin gene - HbS • Red blood cell collapse into sickle shape in low oxygen • Lethal to the homozygote, but heterozygotes HbAS occur with high frequency in malarial regions (these people have sickle cell trait) • HbS mutation has selective advantage in malarial regions

WG2: Describe the Nematode Ascaris lumbricoides AKA roundworm....

• Male adults are ~30 cm long & female adults are ~35 cm long • Widespread & common - female can lay 200,000 eggs per day! • Extremely resistant in environment as they live in the intestine (few worms can do this) • Problems of obstruction & "wandering"

MV13: Describe the use of the immunological memory, including in vaccination... (not fini - check)

• Measure antibodies that are specific to particular antigen • Cells divide to produce more B cells & then declines • Primary response is slow while secondary response is quick due to memory B cells • Vaccination induces a primary immune response, such that when a real infection is caught by the individual a secondary immune response is generated • This secondary response is highly effective compared with a primary response.

MV10: Describe how the Metacercaria of D. dendriticum changes the behaviour of ants, as annother example of how parasites can change the behaviours of their hosts...

• Metacercaria encyst in the ant, most encyst in the haemocoel, but some migrate to the sub-oesophageal ganglia & encyst there. • The consequence of this is that the ants' behaviour changes so that they climb grass blades & then grasp on to them, thus keeping the ants in the position. • This facilitates the ants (& hence the parasites) being eaten by grazing sheep, thus completing the D. dendriticum life-cycle.

WG3: Briefly explain why antibiotics can be used to kill these microfilariae worms...

• Microfilariae worms have an endosymbiotic relationship with a bacteria (Wolbaccia) which is essential for normal function • Thus using antibiotics to kill this bacteria will aslo kill the worms

MV15: Describe the findings by Smithers, Terry & Hockley (1969) for the worms transplanted into the different recipient hosts.... Hint: Verses.

• Monkey donar host: - Worms could survive & produce eggs when transplanted in normal monkey or 'mouse immunised' monkey • Mouse donar host: - Worms transplanted in normal monkey survived, but egg-laying was interrupted for ~6 weeks - Worms transplanted in 'mouse immunised' monkey were killed in 44 hours

WG5: Describe Digenean & include examples... (not fini)

• More than one host used • Intermediate host is usually a snail • E.g. Fasciola, Dicrocoelium, Schistosoma

WG5: Describe Monogenean reproduction, including Dactylogyrus & Gyrodactylus as examples... What type of life-cycle is this?

• Most monogenean reproduction involves Adult → Egg → Free-swimming larva = oncomiracidium • E.g. Dactylogyrus • Some monogeneans are Viviparous • E.g. Gyrodactylus AKA "Russian doll parasite", can see daughter developing inside adult • Monogeneans have direct life-cycles

WG5: Describe the types of parasite Monogeneans are...

• Mostly ectoparasites of fish & amphibia • Some are also endoparasites as adults e.g. in frog bladder • Often are macroparasites (many idividuals)

WG8: Describe the vital statistics for malaria, including answering the following questions: - How many people get malaria every year? - How many people die from malaria per year & which age group is affected the most? - How many people die every day from malaria?

• Nearly half of the total world population (~3.2 billion people of 7.4 billion) are at risk from malaria • 300 million people get malaria every year • 400,000 deaths from malaria per year, mostly of children under 5 years of age • 1000 people die every day from malaria

WG2: Identify nematodes with direct transmission cycles & their common features...

• Necator & Ancylostoma - human hookworms • Ascaris lumbricoides & Toxocara canis - roundworms • Enterobius - pinworm Common features: • Direct life-cycles • Faeco-oral transmission - roundworms & pinworms • Penetration of skin - hookworms • Risk factor - poor hygiene

MV12: Describe the harm to the host caused by soil transmitted Helminthiasis & how this can be reversed/prevented....

• Negative relationship between helminth infection & cognitive performance of the host (e.g. human child) • Can use de-worming which can: - improve cognitive performance - improve school attendance

MV15: Describe the immune responses to Filarial nematodes at different levels of infection i.e. when no infection or when microfilariae is & isn't present in circulation... Also, include the immunomodulation by adult worms, the reasons why there is variation in these immune responses & how T-cell activity can be damaging... Hint: N.I:

• No infection = more active T cells respond • Infection = Adult worms immunomodulates immune sytem by secreting molecules that directly affect the control of the host immune response: - Interfere with T cell function so they are less likely to be stimulated into action - There are changes in sub-sets of active T cells • Infected hosts with low T cell reactivity: - are parasitologically positive for worms (Mf +ve) - have no pathology or disease. • Infected hosts with high T cell reactivity: - appear to control their worm infections (Mf -ve) - have pathology & disease, which is probably immuno-pathology i.e. 'collateral damage' of the host by the active immune response.

WG1: What is a Obligate parasite & a Facultative parasite...

• Obligate parasite = always parasitic for at least part of lifecycle • Facultative parasite = will be parasitic if opportunity arises e.g. accidental infection

WG4: Describe what the research by Hoberg et al (2001) indicates about the evolution of tapeworms with a human definitive host e.g. Taenia solium... (not fini)

• Occurred due to the hunting/scavenging of early humans (Homo) in Africa • suggests eggs of ancestor of T. solium passed from true carnivores to their prey, & then from those prey as larvae back to predatory hominids • suggests humans infected livestock with their own tapeworm

WG7: Describe Cryptosporidium as an example of a parasitic Apicomplexa protozoa, including how it has beeen transmitted to humans in the past...

• Outbreaks among human population associated with contamination of tap water/swimming pools with cysts from sewage & contamination of ready-to-eat salad with cysts. • Cysts are extremely resistant to chemical disinfectants e.g. water chlorination. • Causes diarrhoea & severe symptoms as host is immuno-compromised e.g. AIDS

WG9: Describe the Excavate parasite Giardia duodenal, including the type of life-cycle, transmission & risk factors...

• Parasite lives in intestine & has direct lifecycle • Uses faeco-oral transmission as it is transmitted by cysts in faeces. • Extremely common especially in institutions such as nurseries or old people's homes where hygiene is poor. • Found all over the world - also animal reservoirs e.g. beavers. • Infection may be asymptomatic, but may cause diarrhoea or a malabsorption syndrome.

MV14: Describe the immune response of the host to the liver stages (AKA Exo-erythrocytic stage), including the type of T cells used, & whether these immune reponses can be considered to be effective... Hint:

• Parasite molecules expressed with MHS class 1 molecules on hepatocyte (liver cell) surface • T cytotoxic cells kill infected hepatocytes by releasing perforin which causes lesions • Liver stages are short lived thus poorly effective immune responses

WG9: Describe the Excavate parasite Trichomonas vaginalis, including the type of life-cycle & how transmission occurs...

• Parasite of the genito-urinary tract with a direct life-cycle • Transmitted from human to human during sexual intercourse. • Extremely common & found all over the world. • Infection may be asymptomatic in males, but often causes irritation & discharge in females.

MV12: Describe how parasites induce harm on their hosts, include the harm caused by gastro-intestinal helminths, hookworms, & malaria parasites as examples...

• Parasites take nutrients & energy from hosts e.g: - gastro-intestinal helminths share host food - hookworms feed off host tissue - malaria parasites destroy red bllod cells of host • Immune responses can be energetically expensive & harmful to the host • Harm is intensity dependent for macroparasites

WG1: Describe Parasitism as a relationship...

• Parasitism - "eating at your table" • only the parasite benefits • some degree of harm to the host • intimate association - metabolic dependence • e.g. Ascaris from pig gut

WG3: Describe the periodicity of appearance of microfilarial worms in blood & possible reasons for this...

• Peak number of microfilariae in blood is about midnight • In blood capillaries of skin = more likely to be picked up by mosquito • Mosquitos are most active at night • Various theories on how they sense time e.g. body temperature or oxygen tension in blood

WG5: Describe the main features of Platyhelminthes & identify the three types...

• Platyhelminthes don't have a resistant cuticle covering their exterior surface like nematodes • Instead characterised by tegument - absorptive & secretory • Mostly hermaphrodites, but there are exceptions • 3 groups in Platyhelminthes: - Monogenea = mostly ectoparasites (fish & amphibia) - Digenea = flukes or trematodes - Eucestoda = cestodes or tapeworms

WG5: Describe the anatomical features of Monogeneans...

• Posterior "holdfast" or opisthaptor (combination of hooks & suckers) used to hold it in place on gills or body surface • Anterior end modified with mouth & oral sucker for feeding & adhesion, anterior end can move around • Don't have a proper gut - blind gut ending

MV15: Describe the primary & secondary immune response of a domesticated animal (rat) host to a single high dose infection of N. brasiliensis, including how this occurs & the molecules involved... Hint: Infection 1. Infection 2.

• Primary immune response in infected animals causes worms to be lost from rat host in under 2 weeks (spontaneous cure) • After this primary infection, a secondary infection is expelled more quickly. • In the secondary immune response T-cells (dependent), high concentrations of IgE antibodies & mast cells enter the intestine • T cell dependent processes kill infected cells • Type I (immediate) hypersensitivity response occurs as histamine-containing mast cells, release their histamine via the action of IgE • Results in the expulsion of the worms

MV15: Describe the three theories about how the production of histamine is thought to aid the secondary immune response in getting rid of N. brasiliensis...

• Production of histamine could be directly damaging & killing the worms • Or the histamine could alter the gut physiology (e.g change pH) thus making it an unsuitable environment for the worms • Or the histamine may allow the gut to become more permeable to other host effector molecules

MV11: Briefly describe what is meant by Prevalence, & what is the use of disability adjusted life years (DALYs).... (not fini)

• Proportion of host population: a) Infected with parasite b) Having parasite-induced disease • But a ≠ b • DALYs are used to compare different diseases

MV15: Briefly describe the Nippostrongylus brasiliensis & the main components of their lifecycle...

• Rat nematode • Same life-cycle as hookworms e.g. eggs pass out in faeces & larvae penetrate skin of host • Adults in the gut are long-lived & reproduce

MV13: Briefly describe T cells & identify the three types of T cells...

• Require the thymus for their development • T cells are the 'cellular arm' of the immune system. • 3 types: T helper, T cytotoxic & T memory cells

WG4: Describe the similarities & differences between the life-cycles of Tania saginata & Taenia solium, including what these transmission cycles relie on...

• Same definitive host = human • Different intermediate host = ox vs pig • Transmission cycle relies on: a) predation by humans of livestock infected with larval worms b) contamination of livestock feed with human faeces

MV14: Describe the immune response of the host to the schizont stage of the Erythrocytic cycle, including the molecules involved... Hint:

• Schizont molecules are on the red blood cell surface • However, red blood cells don't express MHC class 1 molecules so no antigen presentation • Causes T cytotoxic cells to be ineffective as they can't respond to red blood cells • Like merozoites, schizonts are antigenically diverse • Also, schizonts are relatively short-lived in red blood cells

MV13: Describe the stages & thus function of a complement/cascade including how it is triggered... Hint:

• Series of soluble proteins/molecules present in circulation that cascade & recruit each other • Binding of the immunoglobulin antibody induces the complement cascade (innate) as it brings together these molecules • Activated complement forms pore in membrane of invading cell & attract inflammatory cells • This kills the invading cell as it can't retain its internal state

MV13: Describe B cells including memory cells & what happens when B cells encounter its own specific antigen... Also describe the important products that it produces & how these products are made to be specific... Hint:

• Some are memory cells, while others produce immunoglobulin (lg) antibodies which recognise antigens (AKA epitope) • A clone of B cells that encounters its specific antigen (AKA an epitope) is stimulated to proliferate • Thus it generates more cells including memory cells, & plasma cells that release immunoglobulin of that specificity. • Memory cells are the basis of immunological memory • In genes there is somatic recombination to create unique sequences for immunoglobulin thus has unique specificity to antigen • Many types of B cells that produce different types of immunoglobulin

WG2: Describe Nematodes including their features...

• Some of the most abundant organisms on the planet • Both free-living & parasitic • Unsegmented worms • Body covered with tough cuticle - non-cellular layer secreted by dermis. • Hydrostatic skeleton, & cavity which is a pseudocoelom filled with fluid. • Both male & female worms

MV14: Describe the immune response to sporozoites, including why hosts can not become immune & thus develops malaria despite this... Hint: Also, briefly describe the type of variation used by malarial parasites... Hint:

• Sporozoites have surface Circus-sporozoite protein (CSP) which: - experimentally generate very strong immune response - allows effective immunisation with irradiated sporozoites • Antibody prevents sporozoites invading liver cells • Brief phase (45 mins); limited exposure to host immune response (poorly effective) • Inter-strain CSP variation - different strains of malarial parasites have different CSP

MV14: Identify the different life cycles/stages of plasmodium (malaria), including where they occur & thus indicate why the host's immune sytem struggles to deal with this... Hint:

• Sporozoites in blood • Enter liver to form schizonts & merozoites • Then erythrocytic cycle starts as merozites invade red blood cells (in blood) • More merozites are released, while Gametocytes can also develop from this erythrocytic cycle • Each of these stages require a different immune response

MV13: Describe the cells involved in the immune system, including where they are found in the body of different vertebrate animals...

• Stem cells in bone marrow • Two classes of B cells & T cells • Have different development requirements • B cells produced in Bursa for birds, while they are produced in bone marrow for humans • T cells produced in thymus (around heart) but production declines with age • B & T cells are preferentially concentrated in secondary lymphoid organs, e.g. lymph nodes & the spleen

MV13: Describe the T cytotoxic cells, including their features, function & the stages involved... Hint:

• T cytotoxic cells are molecularly defined by the presence of the CD8 cell surface marker • Stimulated by T helper cells • Function is to recognise & kill infected cells: 1. Infected cells with presentation of parasite antigens on the MHC Class I molecule are bound to 2. These are recognised by the T cytotoxic cell thus triggering it to release perforin 3. This causes lesions (pores) in the target cell plasma membrane, leading to the death of that cell.

MV13: Identify the two types of T helper cells, including the reponse they are part of & the specific parasites they target...

• T helper 1 cells (Th1): - Involved in cell-mediated immunity - Target micro parasites • T helper 2 cells (Th2): - Part of proinflammatory response - Target parasitic worms

MV12: Describe how malaria infection has selected for human mutations such as the Sickle cell trait & why it is considered to be a 'double-edged sword'.... Hint:

• The Sickle cell trait is advantageous for malaria exposed populations as heterozygous individuals have a greater fitness (they survive & reproduce) • Selection for Sickle cell trait is double-edged sword as individuals that are homozygous (HbSS) are unlikely to survive (costly)

MV15: Describe the vertebrate gut as a habitat, including in relation to the immune sytem.....

• The gut is connected to the immune system e.g. it has antigens on the lumen of the gut • Erythrocytes can sample & take up antigens, thus acting as Antigen Presenting Cells • IgA antibodies are secreted as part of the immune response

MV11: Describe how the host population of a parasite may vary & why knowing the prevalence is useful...

• The host is a discrete resource that can be seperated in space & time • They can vary in age & gnder etc • Can also vary by current & previous parasitism • Prevalence indicates the proportion of hosts infected & thus how common parasitism is

MV10: Describe the effect of Toxoplasma gondii on rats behaviour as found in the research results by Berdoy et al., (2000) as an example of how parasites can change the behaviours of their hosts....

• The results show that non Toxoplasma-infected rats avoid cat odours, but when infected there is a significant decrease in this avoidance. • The interpretation is that rats have a behaviour that keeps them away from cats (thereby reducing their probability of being caught by cats), • But when rats are infected with Toxoplasma, then this behaviour is lost, & the rats' behaviour will enhance the probability that they are caught by cats, thus completing the Toxoplasma life-cycle.

MV15: Describe the structural & biochemical features involved in aiding the survival of Schistosoma mansoni... Hint:

• The worm strategy is is to survive the host immune response by 'disguising' themselves as 'host'. • The tegument is a multilayered membrane that is constantly renewed, so 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.

MV15: Describe how N. brasiliensis is still successful in the wild including how the infection behaves differently & the possible reasons for this...

• Trickle infections - infections increase steadily over time to become long-lived & chronic • One possibility is that this lower rate of worm delivery, gives the worms opportunities to adapt to the host immune response. • Another possibility is that the parasites are able to modulate the host immune response, thus prolonging their survival.

WG9: Describe how Trypanosome brucei uses antigenic variation... Also, describe the following illnesses caused by Trypanosome brucei, including their alternative names: • Sleeping sickness • Nagana

• Trypanosoma brucei evades the adaptive immune response of the mammalian host by switching its surface antigens ● Sleeping sickness AKA Human African Trypanosomiasis: • In the later stages the parasite invades the central nervous system (CNS) • This causes brain inflamation which affects the CNS so that people fall asleep ● Nagana AKA African animal trypanosomiasis: • Means low spirit as animals infected loose weight etc • Affects wild & domestic animals throughout the tsetse belt

WG9: Identify the vectors that transmit the following Kinetoplastids: • Trypanosoma brucei • Trypanosoma cruzi • Leishmania spp.

• Trypanosoma brucei vector = tsetse flies • Trypanosoma cruzi vector = triatomine bugs • Leishmania spp. vector = sandflies

MV14: Describe the features & mechanisms that allow Trypanosomes to change their variant antigenic types... Also, discuss if a certain environment is required for this & how the presence of Trypanosomes seems to affect the host.... Hint: -⚪️ = VSG1 -🔵 = VSG2 -⚫️ = VSG3 -🔴 = VSG4

• Trypanosomes have Variant Specific Glycoprotein (VSG) which provide the antigenic form of the surface coat (10% dry weight is VSGs) • Each VSG is coded for by a different gene • Gene conversion allows the expression of different VSG: - The gene is 'copied' into the transcriptionally active site so its VSGs are on the surface coat - The other geens are in one site where the transcription is controlled • This process occurs both in normal & in immune-deficient hosts as well as in vitro • Hosts infected with Trypanosoma have depressed immune responses, which will enhance parasite survival.

WG9: Briefly describe the Tsetse fly as the "saviour of Africa"....

• Trypanosomiasis in vast areas of tsetse-infested land stopped agricultural exploitation • This provided the legacy of National Wildlife reserves & allowed the preservation of large wild animals

MV15: Describe the research methods when looking at treating the chronic infections of Heligmosomoides polygyrus in rats..... Hint: Groups:

• Two stages of infection given on day -7 & day 0 • 4 different treatment groups: - A: rats only infected with adults on day -7 - B: infected with adults on day -7 & with larvae on day 0 - C: control surgery on day -7 & infected with larvae on day 0 - D: rats only infected with larvae on day 0 • Day 40-42 rats are given drug to remove worms • Day 49 rats are infected again with larvae • Count number of worms 28 days after re-infection

WG7: Identify & describe what element of the Cryptosporidium life-cycle causes the immune-system of the host to be compromised....

• Two types of oocyst are produced which are thin & thick-walled. • Thick-walled oocyst exits the host in faeces • Thin-walled oocyst allows auto-infection • Triptosporidium also covers gut epithelial cells thus preventing the absorption of food

WG6: Describe Urinary schistosomiasis in Africa, including the methods used to prevent it...

• Very common in Africa • School children in Africa have their urine examined for blood & schistosome eggs • Use oral drug called Praziquantel which requires repeated treatment during childhood. • Use educational programs

WG7: Describe Eimeria as an example of a parasitic Apicomplexa protozoa...

• Very important parasites of intensive farming • Several Eimeria species specific to each host e.g. Chickens, rabbits, calves & lambs etc • Parasite multiplies inside cells of gut wall; infective cysts pass out in faeces • Diarrhoea especially in young animals & bleeding from intestinal tract (coccidiosis) • Harms animals ability to grow • Risk factors: Overcrowding, poor hygiene

MV12: Discuss the possibility of evolution for avirulence in parasites, including why virulence is always selected for & how vaccines may aid this process... Hint:

• Very virulent parasites will kill their hosts, thus losing their environment. • Advantageous to any parasite genotype to not kill its hosts. • Virulence linked to traits of growth that are competitively selected for between genotypes • Thus selection for these traits maintains/increases virulence • Vaccination that allows hosts to survive parasite episodes will lead to more virulant parasites

MV15: Explain the findings by Smithers, Terry & Hockley (1969), including what this suggests & how it occurs... Hint:

• Worms acquire host molecules/antigens on their tegument to hide themselves from the host immune sytem • Worm from monkey survives in normal monkey & 'mouse immunised' monkey as it has monkey antigens - can hide from immune system • Worm from mouse in normal monkey are un-able to produce eggs untill it aquires monkey antigens (despite primary immune system) • Worm from mouse in 'mouse immunised' monkey dies due to secondary immune response

WG1: Describe Mutualism as a relationship...

• both benefit - extreme: neither can survive without the other • intimate association - metabolic dependence • e.g. Oxpecker on rhino & Lichen = fungus & alga

WG9: Describe the anatomical features of Trichomonas vaginalis & how it survives in the genito-urinary tract...

•Three flagella at end & fourth runs along body, also has rigid rod spike • Has anaerobic metabolism - hydrogenosome, modified mitochondrion that produces ATP releasing hydrogen as a biproduct. • Lives on vaginal epithelial cells, eats cells, yeast & bacteria

WG✪: Name (common & scientific name) & briefly describe the six different parasites that use different insect vectors... Also, identify the illnesses these parasites cause.... Hint: • 2 Nematodes • 1 Apicomplexa protist • 3 Excavate (kinetoplastids) protists

✪ Nematodes: • Onchocerca volvulus - Blackfly take up microfilariae (L1) in human blood & transmits L3 larvae to humans by biting, causes river blindness • Wuchereria bancrofti - Similar life-cycle to O. volvulus but uses mosquitoes, causes Filariasis ✪ Apicomplexa protist: • Plasmodium falciparum (& P. vivax etc) - Mosquitos inject sporozoites in humans & take up gametocytes, causes malaria in humans ✪ Excavate (kinetoplastids) protists: • Trypanosoma brucei - Transmitted by Tsetse fly bitting humans, causes African Trypanosomiasis • Trypanosoma cruzi - Transmitted by triatomine bugs & causes S. American Trypanosomiasis • Leishmania spp. - Transmitted by sandflies & causes Leishmaniasis

WG✪: Name (common & scientific name)& briefly describe the seven different parasites that are transmitted via the defintive host eating uncooked/raw meat.... Hint: •2 Nematodes •4 tapeworms •1 (Apicomplexa) protist

✪ Nematodes: • Trichinella spiralis - Human ingests undercooked pork meat with encysted larvae in the meat • Anisakis simplex - Human or a marine mammal ingests raw fish that contain Anisakis larvae (L3) ✪ Tapeworms: • Taenia saginata AKA beef tapeworm - Humans eats undercooked beef containing cysticerci • Taenia solium AKA pork tapeworm - Humans eats undercooked pork containing cysticerci • Diphyllobothrium latum AKA broad tapeworm - Human or mammal eats raw fish containing larvae • Echinococcus granulosus - Dog ingests sheep meat containing hydatid cysts ✪ Protist: • Toxoplasma gondii - Cat ingests rodent containing (bradyzoite) cysts