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Parasitology Exam 1 – Review.docx

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Boston College
BIOL 2000

Exam 1 – Review Human Parasitology • Who is a Parasite? o Parasite usually smaller than host o Parasite does not kill host before eating o Live in intimate relationships with hosts depending on more than food o Many parasites show strict specificity • Concepts in Parasitology o Parasite and Parasitism are terms that define a way of life rather than a coherent and evolutionary related group of organisms o Symbiosis: “any two organisms living in close association, commonly one living in or on the body of the other, are symbiotic, as contrasted with free living” o Commensalism: Sharing the table. One partner benefits, but the other is not hurt o Mutualism: both partners benefit o Parasitism: one partner (the parasite) harms or lives on the expense of the other (host) • Parasites: A very divers group of Eukaryotes o Protozoa: unicellular eukaryotes o Platyhelminths: flatworms including flukes and tape worms o Nematodes: elongated worms with rigid cuticula o Arthropodes: insects and ticks and mites which either are parasitic or transmit parasites as vectors • Ecto- & Endo- Parasitism o Ectoparasites live on, but not in their hosts (they can nevertheless cause severe illness). Ich, a protozoan ectoparasite of the skin of fish o Endoparasites live within the body and tissues of their hosts. Trypanosomes, which cause sleeping sickness, within the blood of an infected animal • Infection and Infestation o Infection usually implies replication of the agent resulting in growing number of pathogens o Infestation is characterized by a constant number of pathogens o Severity of disease often depends on infection dose • Obligate/facultative and permanent/intermittent parasites o Most parasites are obligate parasites and cannot live free o Sometimes only some life cycle stages, e.g. the larvae are parasitic, in others parasitic and free living generations can alternate depending on environmental conditions • Host and Life Cycles o Definitive host is by definition the host in which the parasite reproduces sexually o Additional hosts are then designated intermediate hosts o Hosts which actively transmit parasites to humans are called vectors o In paratenic or transport hosts no parasite development occurs o Reservoir hosts are alternate animal hosts from which the parasite can be transmitted to humans (zoonosis) or domestic animals o Accidental or dead end host: not suitable for parasite development but can cause disease • Disease Terminology o Prepatency: infected but parasite presence cannot be detected yet o Patency: established infection, parasite stages can be detected (malaria parasites in blood smears; worm eggs in feces etc.) o Incubation period: time between infection and the development of symptoms o Acute disease: can lead to crisis, which can resolve in spontaneous healing, chronic infection or death o Convalescence: period after healing, absence of infectious agents, no symptoms, in certain cases immunity to reinfection o DALY: DisabilityAdjusted Life-Years o Morbidity:  the ratio of deaths in an area to the population of that area expressed per 1000 per year  the relative incidence of a particular disease  the quality of being unhealthful and generally bad for you • Medical Parasitology o Overall there is a much stronger association with the level of sanitation and general public health than climate. Parasitic diseases are in their majority the diseases of the poor around the globe Global and Public Health Initiatives Parasite-Host Interactions: Immunology Amoeba Flagellates: Giardia, Trichomonas Kinetoplasts: Leishmania • Move using a single flagellum • VECTOR = SANDFLY • Confusing distribution, because of the amount of places you can get it from and amount of sandflies • 3 different disease syndromes o visceral Leishmaniasis targets liver and spleen, fatal infections  Leishmania donovani o cutaneous Leishmaniasis - not usually lethal, creates sores  Leishmania major o mucocutaneous Leishmaniasis – targets soft tissue on face, not usually lethal  Leishmania braziliensis • Life Cycle of Leishmania o sandfly bites and injects (metacyclic) promastigotes o macrophages eat the promastigotes and started developing in macrophages o loose flagellum and begin replicating in macrophages as amastigotes o sandfly bites and takes it up, amastigotes (no flagellum) and transform into promastigote and begin to replicate (procyclic) o divide in mid gut, and cluster at mouth (proboscis) clogging digestive track • Procyclic and Metacyclic o Procyclic promastigotes attach to midgut of sandlfy and divide o Metacyclic stop dividing and go into pharynx • 3 different complex disease migrate to different regions • Leishmania infect and thrives in macrophages o Replicates as an intracellular amastigote in mammals o Macrophages are phagocytic cells part of innate immune system than can activate adaptive response o Parasites invades passively by phagocytosis o Binds elements of compliment system to surface to be taken up, but prevents formation of fully functional membrane attack complex (pores) o Phagosomes enter cell to bind with primary lysosome to become secondary lysosome and destroy inside o The dense surface coat covering Leishmania seems to protect the parasite from the action of the lytic enzymes o However, with help from T cells macrophages can be stimulated to kill the parasite • ATh1 response is required for parasite control and healing, Th2 will only help because only dead parasites present o Leishmania manipulate in favor of Th2 • Disease varies with sandfly • urvan Kinetoplasts: Trypanosoma brucei (Sleeping Sickness) • Move using a single flagellum • VECTOR = TSETSE FLY • Life Cycle of T.brucei (ALWAYS EXTRACELLULAR) (2 duplications in vector and 1 in humans) o Tsetse fly injects metacyclic trypomastigotes o Transform into bloodstream trypomastigotes o Multiply by binary fission (slender at first injection/ stumpy once densely populated) o Tsetse fly ingests trypomastigotes o Blood stream trypomastigotes become procyclic trypomastigotes and multiply o Leave mid gut and transform into Epimastigotes and multiply o And transform into metacyclic tyropmastigotes • Several species of T.brucei o T. brucei brucei – Nagana (cattle) o T. brucei rhodesiense – Sleeping Sickness (eastAfrica) o T. brucei gambiense - Sleeping Sickness (westAfrica) • Nagana o Fever, diarrhea, rapid loss of conditions o Prevents farming of cattle in areas where tsetse fly endemic o Trypano-tolerant cattle • Gambiense and Rhodesiense o Rhodesience progesses to fast to have asymptomatic individuals, found in both animals and humans (animal reservoir) o Gambiense has human reservoir • Trypanosome transmission o Rhodesiense: ungulate-fly-human o Gambiense: human-fly-human o Brucei: game animals-fly-livestock • Only fraction of total population under surveillance, spreads with socio-economic problems • Brought under control by mass campaigns but increase after control lifted, now trying again • Eliminating public health problem: less than 1 new case per 10,000 inhabitants at least 90% of endemic foci reporting less than 2000 cases annually • Disease Course and Symptoms o First Stage  Trypanosomes multiply in the tissue around the initial bite site  This often results in a characteristic local inflammation the trypanosomal “chancre”. Usually not painful  From there they enter the blood and lymphatic system  Enlargement of the lymphatic glands (especially in the posterior triangle of the neck) can be an early sign of the disease (Winterbottom sign, not as common in rhodesiense infection)  Aspiration of swollen gland often reveals parasites o Second Stage  After 1-2 week period of asymptomatic incubation, parasites invade blood leading to fever and headache 
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