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116 Cards in this Set
- Front
- Back
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What, if any, taxonomic significance is attached to the term “amoebae?”
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No taxonomic significance
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What is the key morphological feature that distinguishes amoebae?
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No form retaining pellicle, uses pseudopods for locomotion and feeding. 4 kinds of pseudopods: filipodia, axopodia, rhizopodia and lobopods
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What is the function of the cyst stage in parasitic amoebae?
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transmission
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Is Entamoeba histolytica of minor or major health significance worldwide, and why? In what 2 morphological forms does it occur?
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Major health significance
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Where do you find the trophozoite of E. histolytica in humans? In what kind of stools is it seen?
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In the colon; loose/watery stools - not in formed stools
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What stimulates the trophozoite to encyst? What are the 3 stages of encystations and what are the morphological features of each stage? Which stage is most common in stools?
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Dehydration of feces in the colon. precyst, cyst, and metacyst. Cysts found in formed stools.
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What type of cell emerges from the metacyst when it is ingested and reaches the duodenum? How many daughter cells are produced by this cell?
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Quadrinucleate . 8 daughter cells
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How frequently is disease associated with infection in the case of E. histolytica? What specific event is associated with disease? What are some of the factors that could result in disease?
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90% show no symptoms of the disease. Lysis of epithelial cells and flask shaped ulcer resulting in long-lasting diarrhea / ulcerative colitis; amoebic dysentery; tissue consumed by amoeboma formation; may lead to perforated colon / peritonitis; OR extraintestinal amebiasis which infects liver via blood (fatal if it reaches the brain). Sx easily confused with non-pathogens; requires six consecutive stool samples
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What is the mechanism by which E. histolytica is able to invade tissues and avoid being killed by white blood cells? What is the histological appearance of an area of tissue invasion by E. histolytica?
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Secretion of hydrolytic enzymes; secretion of pore-forming protein (amebapore); inhibition of inflammation (immune response) results in lysis of epithelial cells and bleeding in the gut. Flask shaped ulcer
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What are the ranges of symptoms that occur in amoebiasis? With respect to ulcerative colitis, what factor determines whether mild or severe symptoms occur? What are some of the complications that can occur in the colon? What are some of the complications that can occur if amoebae enter the bloodstream?
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Difficult to diagnose because it is easily confused with non-pathogens; negative diagnosis requires six consecutive stool samples - 50% of patients with liver abcess have no history of colitis and the stool is negative, may require liver biopsy, xray, ELISA. ______. Peritonitis. May get to the liver via blood, if it reaches the brain it is 100% fatal
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Why is it difficult to rule out E. histolytica as a cause of gastrointestinal disease? What is the crystal that is often present in the stool of patients with colon infections, and what is the source of this crystal? Why is extraintestinal amoebiasis even more difficult to diagnose?
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Easily confused with non-pathogen; require extensitve diagnostic measures (6 stool samples; liver biopsy, x-rays, ELISA. _____. 50% of patients with liver abcess have no history of colitis and stool sample is negative.
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What are the fairly obvious steps that can be taken to prevent outbreaks of infection?
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Eliminate fecal contaminiation of food and water; address poor sanitation; nightsoil; phoresis; screen food handlers
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Why is it necessary to know about and be able to recognize nonpathogenic amoebae in humans?
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symptoms
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How is E. gingivalis transmitted? What is the association between infection with E. gingivalis and gum disease?
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No cyst form. Requires direct transmission. Non-pathogenic but found in 95% of people with gum disease and in 50% of people with gum disease
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How does E. hartmanni differ morphologically from E. histolytica?
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Smaller in size (half the size); non-pathogenic
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Why is Entamoeba coli often found in stools of patients being treated for E. histolytica? How does it differ morphologically from E. histolytica in the trophozoite and cyst stages?
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Co-infects with E. histolytica. Trophozoite form ingests bacteria, has a dirtier cytoplasm; appears more granular; no RBC's; larger eccentric endosome, chromatin less defined; In the cyst form it has 8 nuclei, and jagged ends of the chromatoidal bars
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What is the usual host for E. polecki, and how does its cyst differ from that of E. histolytica?
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Infects pigs and rarely humans; uninucleate cyst
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What are some of the features of Endolimax nana and Iodamoeba butschlii that allow you to distinguish them from E. histolytica at the trophozoite and cyst stages? Where is Naegleri fowleri normally found in nature? Why is N. fowleri considered a facultative parasite? What additional stage is found in the life cycle of N. fowleri that doesn’t occur in that of E. histolytica? What is the infective stage? What environmental factor causes numbers of the infective stage to increase? How do humans commonly become infected? What is the name of this disease that invariably results, and what is the outcome
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In soil and fresh water. Lives outside the host and takes advantage of the opportunity to infect when it is pushed up swimmers nose; It has a biflagellated form reduce food and increased temperatures. Humans infected swimming/diving. PAM (Primary Amebic Meniogeoencephalitis); fatal within 2 weeks
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Where are Acanthamoeba spp. normally found in nature? What stages occur in its life cycle? Which is the infective stage? In histological sections of infected tissue, what difference would immediately distinguish Acanthamoeba from Naegleria or E. histolytica? Where do infections occur in immunocompetent persons, how are they typically acquired, what are the pathological effects, and are they easy to treat? Where do infections occur in immunodeficient persons, how are they typically acquired, what are the pathological effects, and are they easy to treat? What is the name of the disease that results when Acanthamoeba reaches the brain, and what is the outcome?
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Found in dry soil. Trophozoite and cyst states. Cyst is the infective stage. Cyst formation in tissue. Pathological effects include contaminate across injured conjunctiva (eye); corneal infection (acanthamebic keratitis); Infection comes from contaminated contact lens solution; difficult to treat.
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What are the 2 main cellular features that characterize ciliates? What is the function of each of the 2 types of nuclei? How do ciliates obtain their food, get rid of excess water, and eliminate indigestible wastes?
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Cilia and two kinds of nuclei; appear to have fuzzy edges. Macroneucleus - polyploidy regulates daily activities (sausage shaped) - micronucleus - diploid and handles conjugation. Ciliates obtain food phagotropically, cytosome with oral ciliature and cytophage; water balance is handled by contractile vacuole in the kidney of the cilia
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In what part of the body is Balantidium coli usually found? What 2 stages occur in the life cycle of B. coli? In what type of stool is each stage found? Which is the infective stage?
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Found in cecum or colon. Stages: trophozoite and cysts. Trophozoite found in loose stools; cyst found in solid stools. Cyst is infective stage.
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Under what circumstances do B. coli cause disease? Where is infection with this parasite most common? How is infection treated?
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Encystations stimulated by fecal dehydration. Occurs worldwide but very rare, 1%. Treated with tetracycline.
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In what type of host does infection with Ichthyopthirius multifiliis occur, what are the pathological effects, and of what economic importance is this parasite?
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Host is fish; impacts the aquaculture industry.
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What are the life cycle stages and types of hosts?
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Pustules on fish skin contain trophozoites which escape and fall to bottom (secretes cyst wall); multiples by binary fission and mature into theront; theronts are ciliated and find a fish to infect; cycle repeats.
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What is the infective stage (for vertebrates) in the apicomplexan life cycle? What is the defining feature of the phylum Apicomplexa? How do apicomplexans obtain their food?
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Sporozoite is infective stage. Has a apical complex. _____.
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What are the 3 stages in the life cycle of a “typical” apicomplexan? Which stage would you expect to cause the most tissue destruction?
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3 phases: schizogonic (merogony), sexual reproduction phase, sporogonic phase. Schizogonic (merogony most destructive)
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Define schizogony (merogony). How does this process differ from typical mitotic cell division? What is the intracellular stage that gives rise to the schizont? What are the daughter cells called?
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Sporozoite invates cell, becomes trophozoite, undergoes schizogony (multiple mitosis followed by simultaneous cytokenosis = merozoites (1N), merozoites escape and reinvade. Sporogonic phase produces schizont (2N) undergoes meiosis
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What 2 stages are involved in sexual reproduction in Apicomplexa (or for that matter, any sexually-reproducing organism)? What is the intracellular stage that gives rise to the gametes? What 2 types of gametes are formed, and how do they differ in terms of size and number?
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Gametogenesis (gamete formation) and Fertilization (zygote formation). Produce microgametes (many) and macrogametes (single)
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Once the zygote is formed, what type of cell division does it then undergo? What daughter cells are initially formed, and what do these in turn produce?
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zygote undergoes meiosis. Produces 4 sporoblasts. Sporoblasts undergo mitosis to form sporozoites
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In the apicomplexan life cycle, which stages are haploid, and which are diploid?
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____
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In which class are all of the medically important apicomplexans found? What 3 general life cycle strategies are employed by these pathogens?
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Class Coccides. 3 life cycles: sporogony, schizogony, and sexual reproductive fertilization
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In what structure are sporozoites of Eimeria tenella enclosed, and what are the various components of this structure? How do chickens become infected? Where does the life cycle take place in the animal? Do chickens remain infected for life, and why? What is the pathological effect?
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Oocyst with two layered wall, micropyle. Homoxenous tissue parasite - schizogony in intestinal epithelium of host = diarrhea. _____. Pathological effect: Destroys cecal mucosa. Remain infected.
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How does the mature oocyst of Isospora belli differ from that of Eimeria tenella? At what stage of development is the oocyst when passed in the feces? In what part of the world are infections with I. belli most likely to be found? What is the pathological effect in immunocompetent and immunodeficient persons?
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Has similar life cycle. Has 1 or 2 sporoblasts when freshly passed and is autoflourescent. Found in the tropics. Pathological effect: causes self-limiting diarrhea except in AIDS patients
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What is the structure of the freshly passed and mature oocyst of Cyclospora cayetanensis? What special microscopical technique can be used to identify oocysts of I. belli and C. cayetanensis in stool specimens?
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Oocysts with globular contents when freshly passed. Microscopically autofluorescent at 340-380 nm
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How does the oocyst of Cryptosporidium parvum differ from that of the above coccidian? What rather unusual part of the intestinal epithelial cell does this parasite infect?
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Oocyst is small, contains 4 sporozoites (no sporocysts). Infects brush border of intestinal epithelium
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During schizogony of C. parvum, what 2 types of merozoites are formed, and what is the fate of each? What is the pathological effect in immunocompetent and immunodeficient persons? What is the main difference in the life cycle of the above coccidians and that of Toxoplasma gondii? Which of the above species has an oocyst that most closely resembles that of T. gondii?
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merzoite I becomes sporozoite; merozoite II becomes microgamete. Pathological effect: severe but self-limited diarrhea in immunocompetent; lethal in AIDS patients. ____. Resembles T. gondii life cycle: merogony, gamogony, sporogony
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In what type of host(s) does the enteroepithelial cycle of T. gondii occur, and in which tissues? Which parts of the 3-part coccidian cycle occur? What are the pathological effects?
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Cat is definitive host and intestinal epithelium. Sporozoites excyst in duodenum, penetrate epithelial cells, invate connective tissue cells; sporozoite undergoes schizogony in parasitophorous vacuole, prducing merozoites; merozoites burst the cell, invade new cells and proliferate rapidly producing tachyzoites which spread through blood and lymph infecting many tissues. Pathological effects: cell lysis and inflammation
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In what type of host(s) does the extraintestinal cycle occur, and in which tissues? Which parts of the 3-part coccidian cycle occur?
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extraintestinal cycle occurs in mannals and birds. Sporozoites excyst in duodenum, penetrate epithelial cells, invate connective tissue cells; sporozoite undergoes schizogony in parasitophorous vacuole, prducing merozoites; merozoites burst the cell, invade new cells and proliferate rapidly producing tachyzoites which spread through blood and lymph infecting many tissues.
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What is the difference between a tachyzoite and a bradyzoite, and what triggers the switch from one to the other? Which causes the most damage? What intracellular structures do bradyzoites eventually form, and in what tissues are these structures most common?
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bradyzoites accumulate in large intracellular cysts and are ingested in uncooked meat; tachyzoites spread through blood and lymph. Triggered by slowing schizogony in slowly proliferating merozoites (bradyzoites). Damages placenta to infect fectus and kill brain cells. Bradyzoites form in zoitocysts. In enteroepithelial cycle of cat and extraintestinal cycle in intermediate host.
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Which of the above stages are infective for new hosts? How are human infections typically acquired? Why aren’t parasites killed when ingested by a macrophage?
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Human infections acquired by uncooked meat, oocysts on food (from insects and contamination with cat feces). parasites are located intracellularly in a priviledged site; phagosome eysosome in macrophases blocked.
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Why is it safe to say that acquired (i.e., after birth) infection with T. gondii usually causes no serious problems? What are the symptoms associated with acute, subacute, and chronic forms of infection? Which is most dangerous? Which groups of individuals are at greatest risk?
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Usually asymptomatic (after birth). Acute infection: usually asymptomatic or mimics mononeucleosis. Subacute: causes severe disease in immunodeficient persons including myocarditis, encephalitis, blindness. Chronic: if immunity develops, zoitocysts form.
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How does congenital toxoplasmosis occur? What are the pathological effects in the fetus? What proportion of infected fetuses develop severe disease or die? What type of damage sometimes shows up later in life?
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Occurs when pregnant female is infected for the first time. Pathological effects: birth defects. 9% fatal. Later in life adult reinochoroiditis
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What steps should a pregnant woman take to avoid infecting her fetus?
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Don't clean litter box, control fly and cockroach populations, and eat only cooked foods
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How is toxoplasmosis diagnosed immunologically, and how could you distinguish an acute infection from a chronic one?
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Diagnosed by looking for specific antibody IgM (acute) or IgG (chronic)
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How are subacute cases treated?
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treated with pyrimethamine and sulfonamides
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How does the life cycle of Sarcocystis spp. differ from that of T. gondii? What stage occurs in the feces of the definitive host?
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Lifecycle is always heteroxenous (unlike T. gondii)
Sporocyst in feces |
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What 3 characteristics do members of the Plasmodiidae have in common, relative to their sporozoite, type of life cycle, and location of each phase of the cycle? Of the 4 species of Plasmodium that infect humans, which shows the greatest and which shows the lowest prevalence?
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Have naked sporozoites in the infective stage; have heteroxenous life cycle; and have schizogony in vertebrate, sporogony in insects, and gamogony in both. P. falciparum (50%) most prevalent and P. ovale (<1%) least prevalent
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What is the prevalence, incidence, and annual mortality of malaria?
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Prevalence: 489M. Incidence: 100M per year. Mortality: 3M per year.
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What is the malaria vector? How does the vector introduce the parasite into the body?
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Malaria vector: anaopholes mosquito. Introduces the parasite into the body by transfer of saliva in mosquito bite.
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Once sporozoites enter the bloodstream, which cells do they infect first? What stage of the vertebrate life cycle is this called?
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Sporozoites infect liver first and become trophozoite. Starts the exoerythrocytic cycle.
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Of the 4 human-infecting species, which produces the most merozoites in the shortest period of time?
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P. falciparum produces 40,000 in 5-7 days
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What is a hypnozoite, in which species does it occur, and what is its clinical significance?
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Occurs only in P. vivax and P. ovale. Causes relapse when schizogony occurs.
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What are the events during invasion of a red blood cell by a merozoite? What stage of the vertebrate life cycle does this begin? Are all stages of red blood cells equally susceptible to invasion by all species? Which species prefers which stage? How does this preference explain the observed levels of parasitemia that develop in the different species?
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RBC invaded by merozoites in erythrocytic cycle. Starts when Merozoite contacts RBC. Different species invade at different ages of RBC. Random selection of RBC. P. vivax and P. ovale occur in reticulocite. P. falciparum in mature RBC. P.malariae in senescent RBC.
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What are the stages of development that the parasite undergoes in the red blood cell, and what are the morphological features associated with each stage? What are some of the key morphological features that allow you to distinguish one species from another, e.g., appearance of trophozoite, presence or absence of Schuffner’s dots, appearance of infected red blood cell? What is hemozoin? Why does P. falciparum “disappear” from the peripheral blood at a particular stage?
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Stages in RBC: Merozoite contacts RBC, attachment, and endocytosis. Morphological features: P. vivax has ameboid trophozoite and enlarged decolorized RBC. P. ovale troph is not amoeboid, RBC is slightly enlarged, orvally distorted, has Schuffer's dots, and prominent nucleus. P. malariae has band form troph, prominent hemozoin, and RBC's are not enlarged or decolorized. Hemazoin: ___.
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What is the infective stage (for vertebrates) in the apicomplexan life cycle? What is the defining feature of the phylum Apicomplexa? How do apicomplexans obtain their food?
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Sporozoite is infective stage. Has a apical complex. _____.
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What are the 3 stages in the life cycle of a “typical” apicomplexan? Which stage would you expect to cause the most tissue destruction?
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3 phases: schizogonic (merogony), sexual reproduction phase, sporogonic phase. Schizogonic (merogony most destructive)
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Define schizogony (merogony). How does this process differ from typical mitotic cell division? What is the intracellular stage that gives rise to the schizont? What are the daughter cells called?
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Sporozoite invates cell, becomes trophozoite, undergoes schizogony (multiple mitosis followed by simultaneous cytokenosis = merozoites (1N), merozoites escape and reinvade. Sporogonic phase produces schizont (2N) undergoes meiosis
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What 2 stages are involved in sexual reproduction in Apicomplexa (or for that matter, any sexually-reproducing organism)? What is the intracellular stage that gives rise to the gametes? What 2 types of gametes are formed, and how do they differ in terms of size and number?
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Gametogenesis (gamete formation) and Fertilization (zygote formation). Produce microgametes (many) and macrogametes (single)
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Once the zygote is formed, what type of cell division does it then undergo? What daughter cells are initially formed, and what do these in turn produce?
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zygote undergoes meiosis. Produces 4 sporoblasts. Sporoblasts undergo mitosis to form sporozoites
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In the apicomplexan life cycle, which stages are haploid, and which are diploid?
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____
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In which class are all of the medically important apicomplexans found? What 3 general life cycle strategies are employed by these pathogens?
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Class Coccides. 3 life cycles: sporogony, schizogony, and sexual reproductive fertilization
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In what structure are sporozoites of Eimeria tenella enclosed, and what are the various components of this structure? How do chickens become infected? Where does the life cycle take place in the animal? Do chickens remain infected for life, and why? What is the pathological effect?
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Oocyst with two layered wall, micropyle. Homoxenous tissue parasite - schizogony in intestinal epithelium of host = diarrhea. _____. Pathological effect: Destroys cecal mucosa. Remain infected.
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How does the mature oocyst of Isospora belli differ from that of Eimeria tenella? At what stage of development is the oocyst when passed in the feces? In what part of the world are infections with I. belli most likely to be found? What is the pathological effect in immunocompetent and immunodeficient persons?
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Has similar life cycle. Has 1 or 2 sporoblasts when freshly passed and is autoflourescent. Found in the tropics. Pathological effect: causes self-limiting diarrhea except in AIDS patients
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What is the structure of the freshly passed and mature oocyst of Cyclospora cayetanensis? What special microscopical technique can be used to identify oocysts of I. belli and C. cayetanensis in stool specimens?
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Oocysts with globular contents when freshly passed. Microscopically autofluorescent at 340-380 nm
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How does the oocyst of Cryptosporidium parvum differ from that of the above coccidian? What rather unusual part of the intestinal epithelial cell does this parasite infect?
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Oocyst is small. Infects when passed from the host
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During schizogony of C. parvum, what 2 types of merozoites are formed, and what is the fate of each? What is the pathological effect in immunocompetent and immunodeficient persons? What is the main difference in the life cycle of the above coccidians and that of Toxoplasma gondii? Which of the above species has an oocyst that most closely resembles that of T. gondii?
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Merozoite I becomes sporozoit and Merozoite II becomes macrogamete. Pathological effect: severe but self-limiting diarrhea - can be lethal in AIDS patients. Unsporolated when passed out in cat feces; sporulation takes 2-4 days. Similar to isospora.
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In what type of host(s) does the enteroepithelial cycle of T. gondii occur, and in which tissues? Which parts of the 3-part coccidian cycle occur? What are the pathological effects?
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Occurs in Cat. Sporozoites or merozoites invade intestinal epithelium. Undergoes merogony, gamogony, sporogony. Pathological effects: low except in kittens.
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In what type of host(s) does the extraintestinal cycle occur, and in which tissues? Which parts of the 3-part coccidian cycle occur?
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Ocurs in mammals and birds and affect duodenum, epithelial cells, and connective tissue cells. Schizogony
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What is the difference between a tachyzoite and a bradyzoite, and what triggers the switch from one to the other? Which causes the most damage? What intracellular structures do bradyzoites eventually form, and in what tissues are these structures most common?
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Merozoites burst cell, invade new cells and proliferate rapdily - called tachyzoites. After a few weeks, host immunity slows schizogony, resulting in slowly proliferating merozoites called bradyzoites. Tachyzoites do most damage. Bradyzoites accumulate in large intracellular cysts (zoitocysts). Affect enteroepithelial and intraintestinal cycles.
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Which of the above stages are infective for new hosts? How are human infections typically acquired? Why aren’t parasites killed when ingested by a macrophage?
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Bradyzoites are infective for cat. Human infections acquired by ingesting uncooked meat, or oocysts on food transferred by insects or contamination with cat feces. Evades immune response by intracellular location (privileged site) and blocks phagosome - eysosome in macrophages.
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Why is it safe to say that acquired (i.e., after birth) infection with T. gondii usually causes no serious problems? What are the symptoms associated with acute, subacute, and chronic forms of infection? Which is most dangerous? Which groups of individuals are at greatest risk?
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usually asymptomatic. Acute infection: usually asymptomatic or mimics mono. Subactute infection: causes severe disease in immunodeficient persons, myocarditis, encephalitis, blindness. Chronic infection: if immunithy develops, zoitocysts form. Greatest risk to immunodeficient persons.
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How does congenital toxoplasmosis occur? What are the pathological effects in the fetus? What proportion of infected fetuses develop severe disease or die? What type of damage sometimes shows up later in life?
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Pregnant female infected. Pathological effects: kills brain cells. 9% die, 30% with severe damage. Later in life can cause adult retinochoroiditis..
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What steps should a pregnant woman take to avoid infecting her fetus?
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Don't clean litter box; control fly and cockroach populations; eat only cooked meat
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How is toxoplasmosis diagnosed immunologically, and how could you distinguish an acute infection from a chronic one?
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Diagnosed by looking for specific antibody: IgM for acute infection and IgG for chronic infection.
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How are subacute cases treated?
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Treated with pyrimethamine and sulfonamides
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How does the life cycle of Sarcocystis spp. differ from that of T. gondii? What stage occurs in the feces of the definitive host?
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Sarcocystis life cycle always heteroxenous. Sexual reproduction and sporogony phases occur in feces of definitive host.
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What 3 characteristics do members of the Plasmodiidae have in common, relative to their sporozoite, type of life cycle, and location of each phase of the cycle? Of the 4 species of Plasmodium that infect humans, which shows the greatest and which shows the lowest prevalence?
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3 characteristics: naked sporozoites, heteroxenous life cycle, schizogony in vertegrate, sporogony in insect and gamogony in both. Greatest prevalence: P. falciparum. Lowest prevalence: P. ovale.
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What is the prevalence, incidence, and annual mortality of malaria?
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Prevalence: 489 M
Incidence: 100M/year new cases Mortality: 3M/yr |
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What is the malaria vector? How does the vector introduce the parasite into the body?
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Vector: anopheles mosquito
Introduced by bite (saliva) |
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How does the oocyst of Cryptosporidium parvum differ from that of the above coccidian? What rather unusual part of the intestinal epithelial cell does this parasite infect?
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Oocyst is small. Infects when passed from the host
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During schizogony of C. parvum, what 2 types of merozoites are formed, and what is the fate of each? What is the pathological effect in immunocompetent and immunodeficient persons? What is the main difference in the life cycle of the above coccidians and that of Toxoplasma gondii? Which of the above species has an oocyst that most closely resembles that of T. gondii?
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Merozoite I becomes sporozoit and Merozoite II becomes macrogamete. Pathological effect: severe but self-limiting diarrhea - can be lethal in AIDS patients. Unsporolated when passed out in cat feces; sporulation takes 2-4 days. Similar to isospora.
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In what type of host(s) does the enteroepithelial cycle of T. gondii occur, and in which tissues? Which parts of the 3-part coccidian cycle occur? What are the pathological effects?
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Occurs in Cat. Sporozoites or merozoites invade intestinal epithelium. Undergoes merogony, gamogony, sporogony. Pathological effects: low except in kittens.
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In what type of host(s) does the extraintestinal cycle occur, and in which tissues? Which parts of the 3-part coccidian cycle occur?
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Ocurs in mammals and birds and affect duodenum, epithelial cells, and connective tissue cells. Schizogony
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What is the difference between a tachyzoite and a bradyzoite, and what triggers the switch from one to the other? Which causes the most damage? What intracellular structures do bradyzoites eventually form, and in what tissues are these structures most common?
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Merozoites burst cell, invade new cells and proliferate rapdily - called tachyzoites. After a few weeks, host immunity slows schizogony, resulting in slowly proliferating merozoites called bradyzoites. Tachyzoites do most damage. Bradyzoites accumulate in large intracellular cysts (zoitocysts). Affect enteroepithelial and intraintestinal cycles.
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Which of the above stages are infective for new hosts? How are human infections typically acquired? Why aren’t parasites killed when ingested by a macrophage?
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Bradyzoites infective for Cat (enteroepithelial cycle) and intermediate host (extraintestinal cycle). Human infections acquired by ingestion of bradyzoites in uncooked meet, oocysts on food, inhaled or swallowed oocysts from litter box. Evades immune response by its intracellular location (privileged site) and blockage of phagosome - lysosome in macrophages
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Why is it safe to say that acquired (i.e., after birth) infection with T. gondii usually causes no serious problems? What are the symptoms associated with acute, subacute, and chronic forms of infection? Which is most dangerous? Which groups of individuals are at greatest risk?
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only affects unborn. Acute infection: asymptomatic or mimics mono. Subacute infection: causes severe disease from immuno deficient persons - myocarditis, encephalitis, blindness. Chronic infection: if immunity develops zoitocytsts form. Most dangerous is subacute infection. Immuno deficient are most at risk.
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How does congenital toxoplasmosis occur? What are the pathological effects in the fetus? What proportion of infected fetuses develop severe disease or die? What type of damage sometimes shows up later in life?
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Pregnant female infected. Pathological effects: kill brain cells. 9% of fetuses die, 30% have severe damage. Can cause adult retinochoroiditis later in life.
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What steps should a pregnant woman take to avoid infecting her fetus?
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Don't clean litter box, control fly and cockroach populations, and eat only cooked meat
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How is toxoplasmosis diagnosed immunologically, and how could you distinguish an acute infection from a chronic one?
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Diagnosed by identifying specific antibody IgM (acute) and IgG (chronic)
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How are subacute cases treated?
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Treated with pyrimethamine and sulfonamides
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How does the life cycle of Sarcocystis spp. differ from that of T. gondii? What stage occurs in the feces of the definitive host?
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Life cycle always heteroxenous (unlike T. gondii). Stages in definitive host: sexual reproduction and sporogony
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What 3 characteristics do members of the Plasmodiidae have in common, relative to their sporozoite, type of life cycle, and location of each phase of the cycle? Of the 4 species of Plasmodium that infect humans, which shows the greatest and which shows the lowest prevalence?
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characteristics of Plasmodiidae: naked sporozoites, heteroxenous life cycle, schizogony in vertebrate, sporogony in insect and gamogony in both. Most prevalent: P. falciparium. Least prevalent: P. ovale.
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What is the prevalence, incidence, and annual mortality of malaria?
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Malaria prevalence: 489M
Incidence: 100M/yr new cases Mortality: 3M/yr |
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What is the malaria vector? How does the vector introduce the parasite into the body?
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Anopheles mosquito is vector. introduces parasite through saliva in bite.
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Once sporozoites enter the bloodstream, which cells do they infect first? What stage of the vertebrate life cycle is this called?
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Infect hepatocyte (liver) cells; Called the exoerythrocytic cycle
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Of the 4 human-infecting species, which produces the most merozoites in the shortest period of time?
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P. falciparum produces 40,000 merozoites in 5-7 days
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What is a hypnozoite, in which species does it occur, and what is its clinical significance?
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Hypnozoites are dormant trophozoites. Can cause relapse when schizogony occurs (only in P. vivax and P. ovale)
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What are the events during invasion of a red blood cell by a merozoite? What stage of the vertebrate life cycle does this begin? Are all stages of red blood cells equally susceptible to invasion by all species? Which species prefers which stage? How does this preference explain the observed levels of parasitemia that develop in the different species?
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3 stages: merozoite contacts RBC, attachment, endocytosis.
Starts the erythrocytic cycle. Different species invade different ages of RBC. P.. vivax, P.ovale invide reticulocyte RBC. P. falciparum invades mature RBC. P. maleriae invade senescent RBC. P. vivax, ovale, & malariae parasitemia is usually low. In P. falciparum parsitemia can reach 50% (fatal over 25%) |
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8. What are the stages of development that the parasite undergoes in the red blood cell, and what are the morphological features associated with each stage? What are some of the key morphological features that allow you to distinguish one species from another, e.g., appearance of trophozoite, presence or absence of Schuffner’s dots, appearance of infected red blood cell? What is hemozoin? Why does P. falciparum “disappear” from the peripheral blood at a particular stage?
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Hemozoin - undigested RBC remains. Disappears because it adheres to endothelial cells in tissue to avoid clearance in the spleen.
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Which species produces the most merozoites from red blood cells in the shortest time? What two paths of development can the merozoite undergo?
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P. vivax and P. falciparum produce 16 merozoites/RBC in 48 hrs. Bursting of RBCs causes release of hemozoin and causes chlls and fever. 48 hr (tertian malaria): P. vivax, ovale and falciparum. 72 hr (quartan malaria) P. malaraie
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What is the explanation for the periodic chills and fever associated with malaria? What is the timing of the periods for each of the 4 human-infecting species?
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Bursting of RBCs causes release of hemozoin and causes chlls and fever. 48 hr (tertian malaria): P. vivax, ovale and falciparum. 72 hr (quartan malaria) P. malaraie
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What is recrudescence, which species demonstrate it, and how does it differ from relapse?
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recrudescence: parasites persist at undetectable levels, without symptoms, years after "cure". If parasitemia is high, get reappearance - recrudescense (not a relapse). All species have this. Relapse in a recurrence of the disease, where recrudescense is when disease has been there all along but only occasionally exhibits Sx.
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What stage indicates the beginning of gamogony (gametongony)? Where are gametes finally formed? Why is microgametogenesis referred to as “exflagellation?”
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Merozoites develop into gametocytes. Formed in mosquito midgut. Exflagellate makes macrogamete.
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Where does sexual reproduction occur?
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Occurs in midgut epithelium
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Where does sporogony occur, what developmental stages are involved, and what is the final product?
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Occurs in midgut epithelium, stages: meiosis, mitosis, cytokinesis produce oocyst with sporozoites that goes to salivary glands.
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What are the main symptoms of malaria? What causes the high fever? Why do malaria patients show marked anemia? What are the complications of malaria caused by P. malariae?
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Sx: chills, fever, heptaosplenomegaly. Fever caused by release of toxins to microphage to TNF to hypothalamus affecting "normal" body temp. Many have anemia bedause of lysis of infected RBC due to parasitemia; lysis of uninfected RBC (B cell antibodies attack healthy RBC); bone marrow suppression. P. malariae causes kidney damage and tropical splenomegaly symdrome (enlargement of the spleen).
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What are the complications specifically associated with malaria caused by P. falciparum? Which is the most dangerous complication? What is a possible consequence of the severe immunosuppression caused by P. falciparum?
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Blackwater fever, pulmonary edema, cerebral malaria, immunosupression. Most dangerous is Blackwater fever and cerebral malaria. consequence P. falciparum is exhaustion of B cell memory causing Burkitt's lymphoma from Epstein-Barr virus in any organ and most common in malarial area.
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What genetic traits are found in people living in certain P. falciparum transmission areas? In certain P. vivax transmission areas?
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Sickle cell trait. Duffy antigen receptor on RBC for P. vivax merozoites.
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How do the malaria parasites avoid the immune response, and what special technique is used by P. falciparum?
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intracellular location, immuno suppression, antigenic variation in P. falciparum. Antigenic variation varies endothelium binding ligand, prevents clearance in the spleen
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What is the evidence that protective immunity actually occurs against malaria? What type of immunity is this (e.g., compared to immunity induced by the polio vaccine) ?
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Premunition
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What are the harmful effects of the immune response on the host?
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Immune complex formation, autoimmunity, TNF effects.
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How is malaria diagnosed, and why is P. falciparum at times particularly difficult to diagnose?
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Diagnosis important for P. falciparum - symptoms unreliable, requires b lood film, "disappears' from blood
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What are the strategies for preventing disease if a person is going to travel to a malarious area?
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High doeses of chlorquine
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Why was it believed after WWII that malaria was on the verge of being eradicated? What happened to dash this hope?
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Chloroquine to prevent and treat disease; DDT to kill mosquitos. Setbacks result from multi-drug resistance by P. falciparium and insectacide resistance by mosquitos
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How does the parasitology of Babesia differ from that of Plasmodium? Of what veterinary significance is babesiosis? What species cause infections in humans, where are these infections most prevalent in the US, and what are the health consequences? Are there any patients at high risk for fatal babesiosis?
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No EE cycle in vertebrate; tick is the vector (not mosquito); transvarial tranmission in tick; no homozoin pigment. Causes Texas cattle fever - 50-90% mortality in adult cattle. caused by several species of cattle and rodents, most common on NE coast of US. Spontaneous recovery. Can be fatal in patients with splenectomy
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Taking everything (e.g., prevalence, biotic potential, pathological effects, immune interaction, diagnosis, treatment, prevention) into consideration, why is Plasmodium falciparum one of humanity’s greatest scourges?
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Blocks blood flow in brain causing death in one week without Sx to children and non immune adults.
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