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23 Cards in this Set
- Front
- Back
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How has a parasitic life-style arisen?
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Free-living amoebae may become endoparasites
Enter brain via nasal mucosa Feed on host tissues in brain and nasopharyngeal regions and multiply Brain a dead end, can't get out to reach another host |
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Facultative
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Can complete lifecycle without depending on a host
Acanthamoeba cyst |
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Obligate parasite
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Require a host to complete cycle
Trophozoites of E.histolytica live and multiply in crypts of large intestine, feed on starch and mucous secretions, Amoebae form cysts, exit in faeces, ingested in contaminated substances, ingest RBC and attach and digest host cells when they invade the gut wall Cause ulcers in gut wall |
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Direct life cycle
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Zoite always in host
Transmission via intimate contact, sexual Trichomonas flagellate causing trichomoniasis in humans |
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Faecal-oral cycle
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Resistant cysts stages passes in faeces of one host and ingested with food/water by another
Balatidium coli |
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Vector-borne cycle
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Trophozoites taken up by blood-sucking arthropods (insects/arachnids) and passed to new hosts when they next feed
Plasmodium |
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Predator-prey cycle
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Intermediate host, zoites in tissue of prey animal which is eaten by a predator that sheds spores into the environment to be ingested by new prey animals
Toxoplasma gondii |
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4 groups of protozoa
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Flagellates: 1 host, Giardia lamblia
Amoeboids: 1 host, Entamoeba histolytics Cilliates: 1 host, Balantidium coli Sporozoans: 1 or 2 hosts, Plasmodium |
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Trophozoite
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Active, feeding, motile stage of a sporozoan parasite
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Flagellates: Giardia lamblia
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Cosmopolitan, most common in warm climates
Transmission due to poor hygiene and contaminated water Trophozoites multiply in gut lumen, transform to cysts, pass into environment and ingested Oval shape: 2 nuclei, 2 suckers, 4 pairs flagella, feed on mucus Children most susceptible, large populations interfere with absorption of lactose Beavers can be source of infection to humans in USA Associated with HIV-infections/AIDS |
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Flagellates: Giardia duodenalis
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Ingest dormant cyst, excystation, trophozoite emerges to an active state of feeding and motility, asexual reproduction
1/3 exhibit symptoms, cysts and trophozoites in faeces Only cysts survive outside the host, weeks to months in cold water |
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Amoeboids: Entamoeba histolytica
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Most common in tropics, cysts survive longer in high temp
Temperate: poor hygiene Carriers: asymptomatic with cysts in faeces, amoebic dysentery and amoebae not cysts in faeces Transmission: contaminated foor and water Abscesses in liver, centre necrotic, damaged liver tissue, attach to healthy areas, ulcers in gut wall Travel to liver in veins of hepatic portal system |
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Entamoeba life cycle
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Ingestion in food/water, cyst matures
Excystation, 1 trophozoite with 4 nuclei, divides 3 times, each nucleus divides to produce 8 trophozoites Migrate to large intestine, binary fission Intestinal mucosa, infection through blood, liver, brain, lungs Ecystation, immature cyst, non-invasive infection, exit in faeces |
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Cilliates: Balantidum coli
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Cosmopolitan, common in young pigs, humans in close contact with pigs or faeces in water
Faecal-oral, trophozoites in pig colon lumen Cyst ingested, some invade colon wall, binary fission to form cyst, excreted in faeces |
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Factors affecting one host parasite transmission
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Levels of environmental contamination
Cyst numbers, environment temp/humidity, number infected hosts, integrity of water sources, poor hygiene and sanitation, presence of flies, occupational hazards Behaviour of infected and uninfected hosts Personal hygiene, ingestion of possible contamination Host susceptibility Impaired young mammal immune system, immuno-suppressed people |
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Sporozoans: Emeria
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Grazing mammals, ground feeding birds, poultry
Host specificity, usually gut, site in organ, location in wall, particular cell type, position in cell Reduced competition, extent of damage depends on locality, size and rate of multiplication Self-limiting infections inducing protective immunity Some species damage host, others dont Host physiological processes may protect from damage |
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Emeria life cycle
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Infected bird, sheds non-infective oocytes with faeces
Sporulate within 48 hours and become infective Susceptible birds ingest with feeding/drinking Schizonts form 5 days after infection, develop into merozoites in subepithelial tissues in intestinal tissue |
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Host protection against Emeria
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Breakout of cell and fail to enter others, lost in faeces
Cells shed during normal turnover of gut epithelium Acquires immunity to re-infection Self-limiting infection, once oocytes produced the infection is over, Plasmodium continue until host dies/cured |
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Emeria tenella
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Damages caecum, large second generation schizonts growing and multiplying, not repaired, lumen filled with clotted blood, dead tissue and parasites
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Emeria acervulina
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Forms oocysts fast, infective stages increase rapidly
Older birds ingest large number of parasites, affects absorption of nutrients in small intestine Affects condition and egg laying |
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Coccidian life cycle adapted for predator-prey
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Sarcocystis cruzi: Dogs/cattle/cat and humans/pigs/horses
Host specific for both predator and prey Carnivore: definitive host, may be asexual, sexual cycle, oocysts, more likely to ingest dormant cysts in prey than pick up from ground/water Intermediate host: behaviour predisposes oocyst ingestion leading to asexual reproduction in tissues Dormant tissue cysts favourable for parasites to increase and wait for next host |
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Plasmodium
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Rbc and others parasites, produce characteristic pigment
Vectors: mosquitoes, sand flies Infect vertebrates: reptiles, birds, mammals 4 species cause human malaria Appearance of gametocyte in blood may be synchronised to coincide with biting times of vectors |
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Plasmodium falciparum
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Fatal malaria in humans, mosquitoes
Sporozoites infect liver cells, schizogony, merozoites Only first ring stage and gametocyte circulate in blood RBCs with schizonts stick to capillaries of organs Pigment in brain capillaries indicate infected cells Blocking leads to impaired oxygen flow, coma |
