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Plasmodium, Toxoplasma, Cryptosporidium.docx

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Boston College
BIOL 2000

Parasite Plasmodium Toxoplasma Cryptosporidium Type Apicomplexa Apicomplexa Apicomplexa Transmission FEMALE MOSQUITOES -Broad host range (CAT), Broad Tissue Range -oocyst viable for many months - persons heterozygous for sickle cell abnormal hemoglobin -Water or food contaminated with cat feces (oocysts), -MAINLY – fecal-oral (drinking water, pool S are resistant – cannot fit in abnormal C shaped cells, changing cat litter box, undercooked meat (bradyzoites), water, recreational water) HemoglobinB cannot be digested by para mother to fetus, organ transplant, blood transfusion -zoonotic transmission – lack of host -negative for Duffy blood group have RBC resistance -Horizontal transmission with tissue cysts = unique for specificity - women who are immune, lose immunity of P.falciparum toxo, because rest need a sexual cycle -contaminated food – unpasteurized milk, when pregnant sausages, or foods grown in soil fertilized with waste -person to person Movement Conveyor Belt Model (Twirling, Circular Gliding, Helical Gliding) -attaches to host cell -motility depends on parasite actin/myosin -microvilli of host elongate along both sides of -myosin anchored into inner membrane complex through protein complex parasite, dense band under host cell -short actin filaments form and grow through polymerization bound to myosin membrane, (induction of host cell actin -a second protein complex which include parasite surface ligands bound to actin and moved against IMC through this polymerization) polymerization -completely enclosed by membrane from -parasite glides over substrate microvilli (PV – parasitophorous vacuole) Invasion: Sequentional secretion from 3 Different organelles parasite stays on periphery (pedestal actin -micronemes secreted when detects right cell, bind to host cell, and insert into plasma membrane of parasite push – ACTIN FROM HOST) -stay attached to host cell and allow movement into cell as actin polymerized -dedifferentation of host and parasite, dense -Rhoptries (contain RON4, which localize to moving junction during invasion) – formation of the vacuole and host cell band forms electron dense border modification -host nutrients go to feeder organelle -Dense granules - modification of vacuole Extra or Intra Extracellular for short time, then mostly Intracellular Intracellular Intracellular Life Stage 1) Female mosquito injects sporozoites (invade mosquito Tachyzoite – rapidly growing meront or zoite in early Opportunistic Infections – infections in patients salivary glands and liver cells), which invade liver cells stage of infection (acute disease) with weakened immune systems by recognizing surface proteoglycans on Kupffer cells in Bradyzoite – (highly infective) slow-growing zoite in (immunosuppressant therapy, chemotherapy, liver sinoid tissue cysts, mark begin chronic phase of infection, AIDS) 2) in liver parasite changes to trophozoite followed by resistant to low pH/digestive enzymes, protective cyst -all stages within one host (human = definite schizont (contain merozoits thousands) wall dissolves and infect tissue and become tachyzoites host) 3) Merozoites (invade erythrocytes) are released into Tissue Cyst – found in tissues, contain bradyzoite 1) oocyst ingested blood (recognize surface molecules on RBC) Oocyst – zygote form; highly environmental resistant; 2) sporozoites released during excystation, 4) Erythrocytic cycle: Merozoites transform into ring stage, contains sporozoites attaches to host epithelial cell, forms trophozoite, schizont (late trophozoite to schizont eats Sporozoites – emerge from ingested oocysts and invade trophozoite hemoglobin) Parasite ingests hemoglobin through gut epithelium 3)becomes Type 1 meront and Type 1 cytosome to food vacuoule and get toxic heme product Invasive Stages: tachyzoite, bradyzoite, sporozoite have merozoites released and become Type 2 meront ferriprotoporphyrin (FP), polymerized to hemozoin apical complex which release Type 2 merozoites that attach to (chlorquine, quinine, and mefloquine disrupt) IN CAT (intestional): epithelial cell 5)After a number of asexual generations, some merozoites -cats ingest tissues with bradyzoites (mouse) 4) form microgamont and macrogamont, become gametocytes (in RBC) -asexual reproduction within cell (lytic) microgametes released and penetrate 6) mosquito ingests gametocytes (macro from RBC, micro -merozoites become gametes to form oocyst (sexual) macrogamete to form zygote forms 8 gametes [exflagellation]) which combine to form -oocyst sporulates when in oxygen (feces) 5) thick walled oocyst leaves, thin walled self zygote = ookinate (invades mosquito gut epithelial cells) injects to epithelial cell (SEXUAL) 7) forms into oocyst on outside of gut which bursts releasing sporozoites that go to the salivary gland of mosquito invasive: sporozoite, merozoite, ookinate (have apical complex) Diseases Malaria Encephalitis Symptoms -9-14 day incubation period -most infections pass with no or mild flu like symptoms -incubation period 2-14 days -fever, chills, back and joint pain, gastrointestinal -congenital disease – acute infection of expectant -watery and profuse diarrhea, abdominal symptoms (nausea/vomiting) mother (severity depends on stage of pregnancy – early cramps, vomiting -cold, hot, sweating stage low transmission but server, late is opposite), -self limited in immunocompetent individuals -irregular high fever spontanteous abortions, blindness, mental retardation, -prolong duration in immunocompromised -anxiety, delirium, mental prlbems neurological disoders can result (degree of immunodeficiency correlates with -sweating, increased pulse rate -ocular toxoplasmosis – congenital can become this, disease) -enlarged spleen and liver, worsening GI symptoms leading to infection and scarring of retina, blindness -malabsorption wasting away inAIDS -Cerebral Malaria – irritability, loss of reflexes, coma -opportunisitic infections in immunocompromised -Bile duct infection = jaundice -Severe anemia – severe drop of hematocrit, poor oxygen individuals – reactivation of latent infection, recently supply for organs and tissues, acquired infection, causes lesions in brain (encephalitis), -Renal Failure – dwindling urine, high urea level in serum, organs like heart and liver can be fatal outcomes of hyperventilation, coma, acute or reactiveated in both immunocom and non.
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