BLOOD PROTOZOA
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| 🇬🇧 | 🇬🇧 |
| SPECIES of plasmodium that are human pathogens | PLAsmodium ( falciparum,vivax,ovale,malariae, kowlesii, cynomolgi) |
| Mode of transmission of malaria | From person to person by the ANOPHELINE mosquito, by contaminated needles, blood transfusion and organ transplant. |
| Distribution of malaria | Tropical regions of sub saharan africa, asia, oceania and latin america |
| Epidemic determinants factors of malaria | 1)drought 2) elevated drug resistance 3) abnormal temperature 4) land pattern changes 5) high malnutrition rates |
| Species virulence factor of plasmodium sp. | 1)antigenic variation 2) drug resistance, 3)cytoadherence of infected rbc, 4)intracellular multiplication 5) life cycle |
| 4 stages of malaria parasite | 1) exo-erythrocytic stage 2) erythrocytic stage 3)sexal/asexual stage 4) sporogenic stage |
| Where does the sporogenic stage of the malaria paraiste life cycle takes place | In the malaria: after injection of gametocytes from the transport host, they mature into : microgametocyte- microgametocyte with exflagellate- macrogametocyte- ookinen- oocyct- sporozoites. |
| Describe the human stage of the malaria parasite life cycle: | Infection occurs when malaria takes a meal an injects the sporozoites into the human. human liver stage is the exo-erythrocytic stage: where sporozoites develop into schizont in the liver cells. schizonts rupture and enter into the Erythrocytic stage in the human rbc; where trophozoites develop into gametocytes. |
| What is the infective stage of the malaria parasite | Sporozoites injected into the blood stream when mosquito takes a meal |
| What is the diagnostic stage of the malaria parasite | When the parasite enters the erthrocytic stage in the rbc. schizont develops into gametocytes. |
| What is the gold standard laboratory diagnosis of malaria parasite | Thick or thin BF with Giemsa/hematoxillin stain and whole blood and look for trophozoites and gametocytes in the : cytoplasm, nucleus for schuffners dot and pigments which indicate the presence of the parasite |
| OTHER lab and serological methods for screening for malaria parasite | 1)used to detect antibodies: limited because antibodies may be absent in acute infection. 2)antigen detection is a rapid test that may tell the presence of the parastate but not the species 3)PCR 4) detection using fluorescent dyes: using the kwamato technique to stained with acridine orange or BCT(benzo. DNA stain green and cytoplasmic RNA stain red. viewing in done with a florescent microscope or light microscope with an interference filter. limited because florescent microscopes are expensive. 5) buffy coat method the benefit of testing is in early treatment |
| Treatment of malaria infection | Depends on the stage of the reproductive cycle exo-erythrocytic stage/ tissue schizonticiedes: PRIMAQUINE ERYTHROCITIC STAGE/ BLOOD SCHIZONTICIDE: CHLOROQUINE PHOPSHATE. if resistant to chloroquine, use ; MEFLOQUINE, DOXYCYCLINE, QUININE, PYREMETHAMINE HALOFANTINE ARTEMISININ, ATOVAQUONE GEMETOCYTOCIDAL: USE QUININE GLUCONATE, ARTESUNATE, QUININE DIHYDORCHLORIDE, ARTEMETHER |
| TREATMENT IN THE ERYTHOCITIC STAGE | ERYTHROCITIC STAGE/ BLOOD SCHIZONTICIDE: CHLOROQUINE PHOPSHATE. if resistant to chloroquine, use ; MEFLOQUINE, DOXYCYCLINE, QUININE, PYREMETHAMINE HALOFANTINE ARTEMISININ, ATOVAQUONE |
| GEMETOCYTOCIDAL TREATMENT | USE QUININE GLUCONATE, ARTESUNATE, QUININE DIHYDORCHLORIDE, ARTEMETHER |
| TISSUE SCHIZONTICIDES TREATMENT | PRIMAQUINE |
| COMPLICATION Of malaria | Anaemia: very severe in P falciparum cns involvement: present and usually sever in P. flacilparum nephrotic syndrome: always present in P. malariae hypoglycemia pulmonary edema, respiratory distress, metaboloc acidosis malaria pregnancy |
| Prevention; | Chomoprophylaxis, ppe, avoidance and vaccines use trimethroprine/ cortimoxazole in hiv patients |
| The group that P.vivax does not infect? | Individual who lack Duffy antigens on the surface of their rbc, especially black people |
| Prevention of malaria infection in hiv patients? | Use trimethroprine/ cortimoxazole in hiv patients |
| The diseases caused by these parasitic flagellate protozoans arw ebdemic or enzootic in different parts of the world and constitute serious medical and economical problems | Trypanosoma and leishmania. they are also called hemoflagellates bceause require hematin from blood hemoglobin for aerobic respiration. |
| In their life cycle, which stage occur in vertebrate host | Amstigote and trypomastigote |
| Stages that may occur in invertebrate | Promastiogte, paramastigote and epimastigote |
| Leishamaniasis affects people in which regions of the world? | Tropic and subtropics |
| Location of majority of cases of viscreal leishmaniasis | 90% of cases occur in india, bangladesh, nepal, sudan and brazil |
| Chagas disease/ american trypanosomiasis: | Begins as a localized infection and followed by colonizationof internal organs and tissues. |
| Evidence of infection | As a small tumor( chagoma) of the skin or as Romana's sign if port of entry is conjunctiva, accompanied by welling of satellite lymph nodes that persists for 1/2 months |
| Signs and symptoms of chagas disease | Fever, generalised edema, adenopathy, hepatosplenomegaly, myocarditis with or without enlargement and sometimes minigoencephalitis; |
| Acute chagas disease | Acute disease is frequently subclinical and may become lifelong asymptomatic carriers |
| Chronic disease phase of chagas disease | May result after 10-20 years in cardiopathy and enlargement of parts of GI tract: megaesophagus, megacolon |
| Transmission of chagas disease | Bite from infected phlebotomite sandflies when infective stage promastigote is injected |
| Life cycle of trypanosoma | 1)promastigote injected 2)phagocytosis of promastigote in macrophages and other phagocytic cells 3)promastigote in cells transform into amastigote which divide and infect more cells. 4) sandflies become infected by ingesting amastigote in cells during blood meals 5) amastigote transform into promastigote and migrate to proboscis. |
| Where do the transformation from amastigote to promastigote occur for different leishmania organisms | In the hind gut for vianna subgenus in the mid gut for leishmania subgenus |
| Diagonistic stage of leishmaniasis | Promastigote |
| Cutaneous and muco-cutaneous diagnostic test | Pcr, antigen detection, biopsy, touch prep, culture , serological test |
| Visceral test for leishmaniasis | Pcr, antigen detection,, touch preparation, culture serologucal test, lymph node biopsy, bone marrow or splenic aspiration |
| Lab diagnosis for chagas disease | Fresh blood and stained smear, pcr, xenodiagnosis, selological test for chronic disease. |
| Lab test for african sleeping sickeness | Blood smear, pcr, serological tests. |
| Treatment of cutaneous leishmaniasis | 1)sodium stibogluconate (pentostam) 2)meglumine antimoniate 3)oral antifungal drugs : fluconazole, ketoconazole and itraconazole 4)pentamidine 5)liposomal amphotericin B |
| Visceral leishmaniasis treatment | Visceral leishmaniasis from indian subcontinent is prone to drug resistance: 1) liposomal amphotericin B 2) sodium stibogluconate and meglumine antimoniate 3) conventuional amphotericin B deoxycholate 4) parenteral paromomycin and miltefosine 5) pentamidine isethionate |