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Lecture 3
Tissue Protozoa I (Malaria, Babesiosis, Toxoplasmosis)
| Question | Answer |
|---|---|
| What disease must be ruled out for a fever in a returning traveler? | Malaria |
| Four species of Plasmodium that cause Malaria in humans | (1) Plasmodium falciparum (2) Plasmodium vivax (3) Plasmodium ovale (4) Plasmodium malariae |
| Schizogony | Asexual propagation of Plasmodium in the human host |
| Sporogony | Sexual cycle of Plasmodium in the female mosquito vector |
| (T or F) Both male and female mosquitos are responsible for the transmission of sporozoites to humans | False. Sporozoites fromt he salivary gland of female Anopheles mosquitos are injected into the host as the mosquito takes the blood meal needed for egg maturation. The male mosquito does not feed on blood. |
| Plasmodium species with hypnozoite stages | Plasmodium vivax and Plasmodium ovale |
| Hypnozoites | Are time-released form of merozoites produced by Plasmodium vivax and Plasmodium ovale. Activation of P. vivax and P. ovale may take several months to 2 years after infection, which results in the delayed onset of symptoms. |
| Describe the exo-erythrocytic cycle of Plasmodium in humans | The sporozoites of all Plasmodium species target and invade hepatocytes, developing into merozoites in about one week. P. vivax and P. ovale produce hypnozoites in hepatocytes. |
| Describe the intra-erythrocytic cycle of Plasmodium in humans | Merozoites are released from the liver and enter into erythrocytes.Merozoites then develop into trophozoites which mature into schizonts.Schizonts produce many merozoites.The erythrocytes ruptures, the merozoites are released and invade other erythrocytes |
| Pathophysiologic characterisitcs of Plasmodium falciparum malaria | (1) Hemolytic anemia (2) Metabolism of hemoblogin by intraeyrthocytic parasites (3) Hypoglycemia (4) Cytokine production by host (5) Microvascular obstruction by parasitized erythrocytes (6) Immune complex glomerulonephritis (7) Splenomegaly |
| Population most commonly affected with severe Malarial disease | (1) Children less than 18 months (2) Pregnant women (3) Non-immune visitors to endemic areas. |
| Genetic polymorphisms that provide increased resistance and/or diminished severity of Malarial disease | (1) Duffy negative blood group (2) Glycophorin A-deficiency (3) Ovalocytosis or elliptocytosis (4) G-6-PD deficiency (5) Sickle cell anemia and Thallassemia |
| Duffy negative individuals are resistant to which Plasmodium species? | Plasmodium vivax. The Duffy blood group antigen is the erythrocyte receptor for P.vivax merozoites. |
| Glycophorin A-deficient individuals are protected from which Plasmodium species? | Plasmodium falciparum. Glycophorins are receptors are receptors for P. falciparum. |
| (T or F) Sterile immunity develops in infected individuals. | False. Sterile immunity does not develop in infected indivduals. After repeated infections, patients have attenuated symtpoms, but a low level of parasitemia can remain. |
| What organ is necessary for control of Malarial parasitemia? | Spleen |
| Typical clinical symptoms of malaria in a non-immune individual | Symptoms are similar to severe influenza: fever, headache, backache, myalgias, abdominal pain, nausea, vomitting, and/or diarrhea. |
| Complicaton of Plasmodium falciparum malaria which is considered a medical emergency | Cerebral malaria is the most serious complication which is characterized by the rapid progression from stupor to coma to death within 24 hours. |
| Complications of Plasmodium falciparum malaria | (1) Cerebral malaria (2) Acute renal failure (3) Disseminated intravascular coagulation (4) ARDS (5) Severe anemia (6) Hypoglycemia (7) Hypotensive shock |
| Compication of Plasmodium malariae | Nephrotic syndrome. This is likely caused by antigen-antibody complex deposition. |
| Diagnostic workup of Malaria | (1) Thin and thick blood smears or (2) PCR |
| Advantages of thin blood smears for Malaria diagnosis | (1) Show parasites in greater detail (2) Useful for speciation |
| Advantages of thick blood smear for Malaria diagnosis | (1) More sensitive than thin blood smears (2) Identify the level of parasitemia |
| Characteristics of Plasmodium falciparum in blood smear | (1) Parasitized erythrocytes are noraml size and shape; no dots (2) High parasite density (3) Delicate ring forms (4) Banana-shaped gametocytes |
| Characteristics of Plasmodium vivax in blood smear | (1) Parasitized eyrthrocytes are often large (2) Schuffner's dots (3) All stages of growth are seen |
| Characteristics of Plasmodium ovale in blood smear | (1) Parasitized erythrocytes are large and deformed (oval and fimbriated) (2) Schuffner's dots |
| Characteristics of Plasmodium malariae in blood smear | (1) Parasitized erythrocytes are normal size and shape; no dots (2) "Band" form (trophozoite) |
| Species that cause human babesosis | (1) Babesia microti (2) Babesia bovis (3) Babesia divergens |
| Vector for Babesia | Ixodes scapularis is a small, hard shell tick |
| US distribution of cases of Babesia | Northeastern costal areas: Nantucket, Martha's Vineyard, Shelter Island, and New Jersey. |
| What population of patients would be most likely have symptomatic and severe Babesiosis? | 1)asplenic 2)elderly 3)immunocompromised individuals by HIV/AIDS |
| Clinical manifestations of Babesiosis | 1)Fever/Chills 2)Myalgias 3)Fatigue/Weakness 4)Hepatosplenomegaly 5)Hemolytic anemia 6)Low WBC count |
| What organ is critical in the host defense aganist Babesiosis? | Spleen |
| What are the blood film findings of Babesiosis? | Presence of intra-erythrocytic parasites. Babesia tetrads are characteristic, but not common. |
| Treatment for severe symptoms of Babesiosis | Atovquone+Azithromycin or Clindamycin+Quinine. Exchange transfusions have been beneficial in person with severe disease. |
| Where does the sexual cycle of Toxoplasmosis occur? | In the intestinal epithelial cells of cats and other felines. The oocysts are produced and shed in feces, sporulate in several days, and persist in soil for years. |
| Is there vertical transmission of Toxoplasmosis in cats? | No, cats do not pass the infection vertically; therfore, kittens reared indoors with commerical food are typically free of toxoplasmosis. |
| Clinical manifestations of Acquired Toxoplasmosis | Majority of infections are asymptomatic. Some will present with lymphadenopathy and mononucleosis-like syndrome with lymphadenopathy and malaise. Generalized disesase: myocarditis, polymyositis, pneumonitis, and encephalitis. Can have Chorioretinitis. |
| Clinical manifestation of early congential Toxoplasmosis infection | May cause abortion in early gestation or cerebral damage (calcifications, seizures, microcephaly, mental retardation) |
| Clinical manifestation of late congential Toxoplasmosis infection | Late gestational infecgtions may be initially silent. But later manifestations may include ocular disease, seizures, or mental retardation in childhood or adolescence. |
| What is the characterisitc radiographic finding of Toxoplasmosis in immunocompromised hosts? | Brain lesions - ring enhancing brain abscess. |
| What are the serologic studies for Toxoplasmosis? | ELISA, IFA and agglutination assays. IgG antitoxoplasma Ab are present in infected persons. IgM antitoxoplasma Ab distinguish acute from chronic infection. |
| How is Toxoplasmosis infection prevented? | 1)Avoid litter boxes and contamination of food with cat feces 2)Cook pork, mutton, and other meats thoroughly |
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