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17 Cards in this Set
- Front
- Back
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Protozoa cell structure |
Eukaryotic No cell wall Single cell Major organelles besides chloroplasts Ecto/Endoplasm Shape can be constant or change 2 stages |
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Ectoplasm |
Clear outer layer involved in locomotion, feeding, and protection |
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Endoplasm |
Granular inner region housing the nucleus, mitochondria, food and contractile vacuoles |
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Trophozoite |
Active feeding form Replicating Various species Different intermediate stages (Sporozoites, etc) Can be infectious |
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Cysts |
Stage 2 Encystment (trophozoite to cysts) (like endospores) Can be infectious Excystment- cyst changes back to trophozoite |
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Pseudopodia (Sarcodina) |
Amoeboid motion Feed by phagocytosis *Naegleria fowleri |
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Flagella (Mastigophora) |
One or many flagella May be over the whole cell Complex life cycles *Giardia lamblia |
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Cilia (Ciliophora) |
Over the entire cell Most are free living (paramecium) *Balantidium coli |
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Apicomplexa (Sporozoa) |
Non-motile Obligate parasites No movement *Plasmodium spp. |
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Amoeba -Acanthamoeba spp. -Balamuthia mandrillaris |
Route: via broken skin, conjunctiva Granulomatous amoebic meningoencephalitis (GAM): Blood flow allows to reach the brain and form granulomas in the brain Can be treated |
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Amoeba Entamoeba histolytica |
Gastro amoebiasis Route: contaminated food or drink, poor sanitation, cecum, appendix, colon, rectum (fecal-oral) Enzymes destroy tissues-> erosive mucosal ulcers (in large intestine) Dysentery, abd pain, fever, diarrhea, wt loss, hemorrhage, perforation, appendicitis, amoebomas Extraintestinal: liver (amoebic hepatitis), lungs (pulmonary amoebiasis) (amoebomas looks like lung cancer) Prevention: sanitation, boiling, iodine water tx Treatment: metronidazole, chloroquine, relieving symptoms |
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Malaria Plasmodium falciparum, P. Vivax, P. Ovale, P. Malariae |
Apicomplexan Protozoa Obligate parasite Cause malaria Effects RBC’s leading to cerebral malaria if untreated Biological vector: Anopheles mosquitoes Incubation: 10-16 days Ssx: malaise, fatigue, vague aches, nausea with or without diarrhea Bouts of chills, fever, and sweating @2-3 day intervals *the intervals vary by type Treatment: chloroquine, quinidine, mefloquine, quinine (+ doxycycline or clindamycin) Side effects: vivid dreams, hallucinations Prevention: vector control (bed nets, repellent) Different geographical areas Children highest risk No vaccine |
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Malaria Lifecycle (varies in length depending of species) |
1. Mosquito takes a blood meal and injects PLASMODIUM 2. Gets into liver. Infects liver cells.(causes hepatomegaly) 3. Plasmodium replicates in liver cells 4. Plasmodium enters the blood and infects RBC’s 5. a. When plasmodium leaves the RBC pt has fever, sweating every 2-3 days b. Some plasmodium goes through meiosis and produce gametes 6. Gametocytes ingested by mosquito. 7. Microgamete fertilizes macrogamete 8. Gametes to zygote(haploid)(in the mosquito) 9. Mitosis..ruptured oocysts 10. Parasite differentiates and enters saliva |
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Definitive Host |
Host in which the sexual stage of reproduction happens Where gametes fuse and form zygote Or host in which eggs are produced ex.*mosquito in malaria |
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Intermediate Host |
A link in the change. Human is food source for mosquito in malaria. Ex. *human in malaria |
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Toxoplasmosis |
Apicomplexa Obligate parasite Most successful parasite on Earth Route: cysts in cat feces, contaminated or undercooked food from cattle or pigs Can cross placenta Can cause CNS symptoms No risk for healthy people Problem for AIDS pts, encephalitis in immunocompromised Alters host behavior Affected rodents no longer fear cats |
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Leishmania |
Flagellated mastigophora T. Sand fly bite, zoonotic (dogs) 3 forms: Cutaneous-(chiclero ulcer) skin lesions; parasite can be isolated from the edges of wound bed of bite ulcer Mucocutaneous-(espundia) mouth & nasal cavity. Disfiguring lesions on cutaneous membranes. May lead to soft palate destruction Visceral-(kala-azar) most severe, systemic, liver, spleen, and bone marrow infection. Lethal without Tx. No vaccine Remain positive for life |
