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Parisitology Exam 2
| Question | Answer |
|---|---|
| Name the structures found in protozoan eukaryotic cells. | Cell membrane, Centrioles, Endoplasmic reticulum (rough and smooth),Flagellum, Golgi apparatus, Nucleolus, Nucleus, Pellicle, Ribosomes, Water Valcuole |
| What is the function of the Cell membrane in a protozoan cell? | Controls things going in and out of the cell. |
| What is the function of the Flagellum in a protozoan cell? | This structure controls motion. |
| What is the function of the Ribosomes in a protozoan cell? | This structure is responsible for converting amino acids into proteins. |
| What is the function of the Endoplasmic reticulum (rough and smooth) in a protozoan cell? | Rough synthesizes proteins and smooth synthesizes lipids, metabolizes carbs and steroids, and regulates calcium concentration. |
| What is the function of the Pellicle in a protozoan cell? | This is a thin layer that supports the cell membrane. |
| What is the function of the Nucleolus in a protozoan cell? | This the structure within a nucleus that is composed of protein and RNA and is involved in ribosomal RNA synthesis and the formation of ribosomes |
| What is the function of the Nucleus in a protozoan cell? | This is the organelle where all of cell's genetic material is found. |
| What is the function of the Golgi apparatus in a protozoan cell? | This organelle acts like a post office, processing and packaging macromolecules such as proteins and lipids after their synthesis and before they make their way to their final destination. |
| What is the function of the Water vacuole in a protozoan cell? | It functions in removal of water in the protozoan cell. |
| What is an amastigote? | This is a cell that does not have any flagella or cilia. |
| What is an promastigote? | Basal body anterior of nucleus, with a long detached flagellum. |
| What is an epimastigote? | A developmental stage in trypanasomes. The undulating membrane is shortened and axoneme and kinetoplast are anterior to the nucleus. |
| What is a trypomastigote? | Basal body posterior of nucleus, with a long flagellum attached along the cell body. |
| Stumpy trypomastigote | A trypomastigote with very short flagellum. |
| What is a Leishman-Donovan body? | It is another name for amastigote in Trypanosome species. |
| Name two flagelattes that are commensal to humans. | Chilomastix mesnili & Dientamoeba fragilis |
| What is hemozoin or "malignant malaria"? | This is a bi-product of parasite's consumption of Hb. |
| Why is hemozoin deposited in cells and not excreted by the host? | It precipitates in large particles, it is deposited into cells because it can't be filtered out of the blood. In blackwater fever, the disease progression is so fast that the precipitate is in very small particles, which are filtered out in the kidneys. |
| What is the common name for Trypanosoma cruzi? | American trypanosomiasis. Chaga's disease. |
| What is the common name for Trypanosoma brucei brucei? | Animal sleeping sickness. Nagana - Zulu word "to be depressed" |
| What is the common name for Trypanosoma brucei gambiense? | Trypanosomiasis - African sleeping sickness..CHRONIC |
| What is the common name for Trypanosoma brucei rhodesiense? | Trypanosomiasis - African sleeping sickness..ACUTE |
| What is the common name for Leishmania donovani? | Leishmaniasis (visceral). |
| What is the common name for Leishmania tropica (includes L. major, L. braziliensis)? | Leishmaniasis (cutaneous). |
| What is the vector for Trypanosoma cruzi? | Tse tse fly (Glossina) |
| What is the reservoir if any for Trypanosoma cruzi? | Mammals, wild or domestic, including humans. |
| How is Trypanosoma cruzi diagnosed? | Parasites in blood, ELISA. |
| What is the common name for Leishmania donovani? | Leishmaniasis (visceral). |
| What is the common name for Leishmania tropica (includes L. major, L. braziliensis)? | Leishmaniasis (cutaneous). |
| What are the symptoms of Trypanosoma cruzi? | Acute phase: Usually asymptomatic-swelling & inflamation at bitesite, fever, anorexia, lymphadenopathy, myocarditis, mild hepatosplenomegaly, Romana's sign. Chronic may not show for years, cardiomyopathy, megaesphogus, megacolon, weight loss. |
| Describe the disease progression of Trypanosoma cruzi? | Acute phase fever, swelling, edema , pain, pseudocysts in organs, heart damage, death (3-4wks) Chronic phase - destruction of nerves cells & ganglia, pseudocysts in muscle, mega-esophagus, heart damage, death. |
| What is the vector for Trypanosoma cruzi? | Triatomine bug (Kissing bug, Cone-nosed bug). |
| What is the reservoir if any for Trypanosoma cruzi? | Rodents, dogs, cats, armadillos. |
| How is Trypanosoma cruzi diagnosed? | Observation of megacolon and megaesophagus in individuals from endemic areas indicate present or former infection. Can only see trymastigote stage in blood. More often in acute, rare in chronic. |
| What is the treatment for Trypanosoma cruzi? | No curative therapy. Most drugs are either ineffective or highly toxic. Recently 2 experimental drugs-Benznidazol and Nifurtimox promising-acute stage of dz, however, side effects limit their prolonged use in chronic cases. |
| What are the symptoms of Trypanosoma brucei brucei? | IN ANIMALS - high temp., lethargy, which lead to weight loss and anemia, muscular wasting. Also see discharge from eyes and nose. |
| Describe the disease progression of Trypanosoma brucei brucei? | In some animals the disease is fatal unless treated. |
| What is the vector for Trypanosoma brucei brucei? | Tse tse fly (Glossina palpalis). |
| What is the reservoir if any for Trypanosoma brucei brucei? | |
| How is Trypanosoma brucei brucei diagnosed? | By detecting trypomastigotes in the blood (the only stage found in patients). |
| What is the treatment for Trypanosoma brucei brucei? | Pentamidine isethionate, Melarsoprol for late disease with CNS. |
| What are the symptoms of Trypanosoma brucei gambiense? | Winterbottom's sign, Chancres, blood-lymph phase=fever, swelling, weakness, pain, CNS phase=apathy, sleepiness, coma, death (2-3yrs.) |
| Describe the disease progression of Trypanosoma brucei gambiense? | Slow (~1 year)acute ⇒ chronic =10 -20 year. |
| What is the vector for Trypanosoma brucei gambiense? | Tse tse fly (G. palpalis) |
| What is the reservoir if any for Trypanosoma brucei gambiense? | Domestic animals. |
| How is Trypanosoma brucei gambiense diagnosed? | By examining chancre fluid, lymph node aspirates, blood, bone marrow, and in later stages, cerebralspinal fluids for trypanosomes. |
| What is the treatment for Trypanosoma brucei gambiense? | Pentamidine isethionate, Melarsoprol for late disease with CNS. |
| What are the symptoms of Trypanosoma brucei rhodesiense? | Winterbottom's sign, chancers,blood-lymph phase=parasitemia, organ-heart damage, death (3-9 months) |
| What is the disease progression of Trypanosoma brucei rhodesiense? | Rapid, often fatal. |
| What is the vector for Trypanosoma brucei rhodesiense? | Tse tse fly (Glossina moristans) |
| What is the reservoir if any for Trypanosoma brucei rhodesiense? | Wild animals. |
| How is Trypanosoma brucei rhodesiense diagnosed? | By examining chancre fluid, lymph node aspirates, blood, bone marrow, and in later stages, cerebralspinal fluids for trypanosomes. |
| What is the treatment for Trypanosoma brucei rhodesiense? | Suramin, penlamidine and berenil: Can cure ifection if given before invasion of nervous system. Difluoromethylomithine (DFMO) even if parasite has invaded the brain. ARSENICALS NOT PREFERRED. |
| What are the symptoms of Leishmania donovani? | Open sores. |
| Describe the disease progression of Leishmania donovani? | System of liver, spleen - fever, malaise, bleeding, hepatosplenomegaly, with anemia, emaciation, death usually 2-3 years. |
| What is the vector for Leishmania donovani? | Sandfly. |
| is the reservoir if any for Leishmania donovani? | Dogs |
| How is Leishmania donovani diagnosed? | Examine chancre fluid for parasite. |
| What is the treatment for Leishmania donovani? | Pentavelent, antimony compounds. |
| What are the symptoms of Leishmania tropica (includes L. major, L. braziliensis)? | Papule - Open sores, volcano shaped, large dermal lesions. |
| What is the disease progression of Leishmania tropica (includes L. major, L. braziliensis)? | Mucocutaneous lesions and degeneration. (L. braziliensis - espundia); may persist for decades. |
| What is the vector for Leishmania tropica (includes L. major, L. braziliensis)? | Sandfly - Lutzomyia spp. |
| What is the reservoir if any for Leishmania tropica (includes L. major, L. braziliensis)? | Dog (?) |
| How is Leishmania tropica diagnosed (includes L. major, L. braziliensis)? | Examine chancre fluid for parasite. |
| What is the treatment for Leishmania tropica (includes L. major, L. braziliensis)? | Pentavelent, antimony compounds. |
| What is the common name for Giardia lamblia? | Giardiasis |
| What is the common name for Trichomonas vaginalis? | Thrichomoniasis - Vaginitis in women and urethritis in men and women. |
| What are the symptoms of Giardia lamblia? | Mucous production, diarrhea, cramps, flatulence, dehydration, weight loss. |
| Describe the disease progression of Giardia lamblia? | Range from total latency (ie, asymptomatic), to acute self-resolving diarrhea, to chronic syndromes associated with nutritional disorders, weight loss and failure to thrive. Incubation is generally 1-2 weeks, but ranges of 1-75 days have been reported. |
| What is the reservoir if any for Giardia lamblia? | Beaver, livestock, dogs, cats. |
| How is diagnosed Giardia lamblia diagnosed? | Fecal exam to check for cysts. |
| What is the treatment for Giardia lamblia? | Quinacrine, metronidazole. |
| What are the symptoms of Trichomonas vaginalis? | Painful urination, discharge, itching. |
| Describe the disease progression of Trichomonas vaginalis? | Damage to vaginal endometrium increases women's chance to becoming infected by the HIV virus. |
| What is the reservoir if any for Trichomonas vaginalis? | None. |
| How is Trichomonas vaginalis diagnosed? | Diagnosis is confirmed by the demonstration of trophozoites in vaginal, urethral, prostatic secretions |
| What is the treatment for Trichomonas vaginalis? | Metronidazole. |
| Describe the morphology of Entamoeba histolytica. | Trophozoite-ameboid~15-30um diameter, one nucleus w/distinct small central karyosome, fine granular endoplasm may see ingested RBCs, Cysts-spherical, w/refractile wall; cytoplasm contains dark staining chromatoidal bodies, 1-4 nuclei w/central karyosome |
| How is the nucleus of Entamoeba histolytica unique to other protozoans studied? | It contains a central endosome w/wagon wheel appearance. |
| What are the stages or forms in which Entamoeba histolytica can be found. | Trophozoite and cyst forms. |
| How do the different stages or forms of Entamoeba histolytica cause disease? | TROPHOZOITE form can invade intestinal epithelium causing flask shaped ulerated lesion. CYST form causes amoebic dysentery or abebiasis. |
| Which stage of Entamoeba histolytica is the major form of transmission? | The CYST stage form is the major form of transmission. |
| What are the symptoms of amebiasis and how does amebiasis cause the symptoms? | Acute-Dysentery w/necrotic mucosa and painful abdomen. Chronic-Recurrent dysentery w/blood & mucus. GI upset & no poo. Cysts in stool. Organism may invade liver, lung and brain, will see abscesses resulting in liver dysf., pneumonitis, and encephalitis. |
| What is hepatic amebiasis? | A result of Entamoeba histolytica trophozoites, from ingested water or food contaminated with human feces, that enter mesenteric venules and travel to the liver through the hepatoportal system. There they form abscesses. |
| What is pulmonary amebiasis? | Infection of the thoracic space with Entamoeba histolytica. Most cases originate when a liver abscess ruptures through the diaphragm. |
| How does Entamoeba histolytica differ (in terms of effects on host cells/tissues) from E. gingivalis, E. coli, and Endolimax nana? | Entamoeba histolytica is pathogenic and attacks the epithelial cell. |
| Why don't E. gingivalis, E. coli, and Endolimax nana cause disease? | Because they are commensals, non-pathogenic organisms. |
| Where are E. gingivalis, E. coli, and Endolimax nana found? | E. gingivalis, E. coli and E. nana feed on bacteria in the body. |
| What do E. gingivalis, E. coli, and Endolimax nana feed on? | E. gingivalis is found in the oral cavity, E. coli and E. nana are found in the digestive tract. |
| What are the forms of Naegleria fowleri? | Amoeba form found in soil and cyst form. |
| Describe the life cycle of Naegleria fowleri. | Trophozoites replicate by promitosis, Tand can turn into temp non-feeding flagellated forms reverting back to trophozoite stage. |
| How does Naegleria fowleri cause disease? | They infect humans or animals by penetrating the nasal mucosa and migrating to the brain via olfactory nerves causing (primary amebic meningoencephalitis) PAM. |
| How does Naegleria fowleri enter the body? | Through nasal passages. |
| Describe the disease progression of Naegleria fowleri. | Once into brain they destroy tissues rapidly leading to death. |
| What are the symptoms of Naegleria fowleri? | Severe headache, fever, vomiting and focal neurologic deficits. |
| What are the distinguishing characteristics of the phylum Apicomlexa? | Apical complex typical of this group as well as conoid and rhoptry. |
| Define apical complex. | Dense ring and conelike structure, along with assoiciated microtubles, micronemes, and rhoptries, at anterior end of an apicomplexan sporozoite. (apical = at the apex.) |
| Define rhoptries. | These are elongated, electron dense bodies extending within the polar rings of an apicomplexan. Aid entering cell. |
| Define polar rings. | These are electron-dense organelles of unknown function, located under the cell membrane at the anterior tip of sporozoites and merozoites. |
| Define conoid. | This is a truncated cone of spiral fibrils located within the polar rings of some Apicomplexa. |
| Describe the infectious cycle of Toxoplasma gondii. | Unsporulated cysts shed in cat feces, sporulate, become infective, consumed by intermediate host (bird, rodent) become infected. Oocyst to tachyzoites. This form localize in neural, muscle tissue and develop into tissue cyst bradyzoites. |
| How do humans pick up Toxoplasma gondii? | Blood transfusion, organ transplant, changing litter box, eating undercooked meat of animals harboring tissue cysts, and transplacentally from mother to fetus. |
| What is a tachyzoite? | A RAPIDLY multiplying stage in the development of the tissue phase of certain coccidial infections, as in toxoplasma gondii development in acute infections of toxoplasmosis. |
| What is a bradyzoite? | A SLOWLY multiplying encysted form of sporozoan parasite typical of chronic infection with Toxoplasma gondii. It has also been called a merozoite or zoite; |
| What is a sporocyst? | Stage of development of sporozoan protozoan, usually with an enclosing membrane, the oocyst. |
| What is a sporozoite? | Daughter cell from sporogony. Able to infects new hosts. Ex. Plasmodium, sporozoites are cells that develop in squeeter salivary glands. They enter new host liver X. Cells infected with sporozoites burst, releasing merozoites into the bloodstream. |
| What is an oocycst? | Cystic form of Apicomplexa , resulting from sporogony. An oocyst may be covered by a hard resistant membrane as in Eimeria, or it may not as in Plasmodium. |
| What is a zoitocyst? | Tissue phase in some coccidia of the Isospora group. The cyst containing the parasites is called a zoitocyst. It contain thousands of bradyzoites. Also called sarcocyst or Miescher's tubule. |
| What is the definitive host of Toxoplasma gondii? | The cat. |
| What are the symptoms of Toxoplasmosis gondii? | Immunocompetent persons is usually an asymptomatic infection. |
| Describe the disease progression Toxoplasmosis gondii? | Usually self limiting, symptoms resolving in a few weeks. Patients with AIDS, toxoplasmic encephalitis most common cause of intracerebral mass lesions. |
| What occurs during acute infections of Toxoplasmosis gondii? | Tachyzoites are disseminated throughout the body via the lymphatics and hematogenously. This acute stage will persist for several weeks as immunity develops. 10-20% of patients may develop cervical lymphadenopathy and/or a FLU LIKE ILLNESS. |
| What occurs during subacute infections of Toxoplasmosis gondii? | Latent infections due to IMMUNOSUPRESSION associated with ORGAN TRANSPLANTSand certain cancer treatments. |
| What occurs during chronic infections of Toxoplasmosis gondii? | 25-50% of AIDS patients with chronic toxoplasmosis will develop encephalitis. Occurs when CD4 cells drop below 100 cells/um. Early symptoms of toxoplasmic encephalitis are headache, fever, lethargy, and altered mental status, |
| What occurs during congenital Toxoplasmosis gondii? | The dz is transmitted congenitally (i.e., transplacentally) if the mother acquires the infection during pregnancy. Severe birth defects are the result. |
| Describe the infectious cycle of Sarcocystis spp.. | Oocytes from definitive host are injested by the intermediate host where the oocytes sporulate. The released sporozoites infect various tissues and rapidly undergo endodyogeny to form merozoites, aka tachyzoites. |
| How do humans pick up Sarcocystis spp.? | Humans pick up Sarcocystis spp. by injesting undercooked meat. |
| What organism(s) act as definitive host for Sarcocystis spp.? | Humans. |
| Why is sarcocystis spp. becoming more of a concern? | Because more than 50% of adult swine, cattle, and sheep probably infected with Sarcocystis spp. |
| Describe the infectious cycle of Cryptosporidium parvum. | Invades intestinal epithelium, respiratory tract; sporozoite is enveloped into parasitophorous vacuole, transforms into trophozoite which gives rise to merozoites |
| How do humans pick up Cryptosporidium parvum? | By consuming contaminated water and produce. |
| What organism(s) act as definitive host for Cryptosporidium parvum? | Humans. |
| What are the symptoms of Cryptosporidium parvum? | Diarrhea which is self-limiting in normal individuals; often fatal in immunosuppressed individuals. Respiratory issues if cycsts are inhaled. |
| Describe the disease progression of Cryptosporidium parvum. | AIDS patients-water diarrhea lasting several months. BMs range from 6-25/day. Much less severe in immunocopetent patients, some asymptomatic, self limiting diarrhea, abdominal cramps lasting 1-10 days. |
| Why is Cryptosporidium parvum on the rise? | High numbers of infected animals. Swimming pools a potential source of infection. It is a zoonotic dz. |
| Describe the infectious cycle of Pneumocystis carnii. | Trophic form replicates to Sexual phase: haploid trophic forms conjugate produce a zygote or sporocyte (early cyst) zygote undergoes meiosis and subsequent mitosis to produce eight haploid nuclei, spore release occurs through a vent in the cell wall. |
| How do people pick up Pneumocystis carnii? | Immunosuppressed individuals more susceptible to contracting. |
| Describe how Pneumocystis carnii differs from Toxoplasma gondii, Sarcocystis spp., and Cryptosporidium parvum. | |
| What are the four species of Plasmodium that cause malaria? | Plasmodium falciparum, P. ovale, P. malariae, P. vivax. |
| What kind of malaria does Plasmodium falciparum cause (begign tertian etc.)? | Malignant tertian Every 3rd day. TID. |
| What kind of malaria does Plasmodium ovale cause (begign tertian etc.)? | Mild tertian - Every 3rd day. TID. |
| What kind of malaria does Plasmodium malariae cause(begign tertian etc.)? | Quartan - Every 4th day. QID. |
| What kind of malaria does Plasmodium vivax cause(begign tertian etc.)? | Benign tertian - Paroxysms - Every 3rd day. TID. |
| How does the periodicity and timing (day-night) of the malarian paroxysms relate to the habits of the Plasmodium vector? | |
| Describe the life cycle of the malaria parasite in both the human and squeeter host. | Squeeter inoculates sporozoites into human, infect liver cells, mature into schizonts, rupture and release merozoites, parasites undergo asexual X in the RBCs, infect RBCs, ring stage trophozoites mature into schizonts, rupture releasing merozoites. |
| explain the exoerythrocytic cycle and the erythrocytic cycle of the malaria parasite in humans and relate what the parasite is doing to the symptoms of the disease. | This is where initial replication in the liver (exo-erythrocytic schizogony) by Plasmodium spp takes place. Erythrocytic cycle is when parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony). |
| What is gametogony? | Process by which gametes are produced in protozoa. Especially seen in Apicomplexa lifecycle. |
| What is a schizont? | A cell undergoing schizogony or asexual reproduction. The nuclear divisions have occurred but not cytokenesis is not yet completed. |
| What is a merozoite? | This is a daughter cell resulting from schizogony. |
| What is a trophozoite? | This is an active feeding protozoan. this stage is called the vegetative state. |
| What is a cryptozoite? | A malaria parasite that develops in tissue cells and gives rise to the forms that invade blood cells. This is a pre-erythroritic schizont of Plasmodium spp. |
| What is a gametoyte? | A cell by which gametes develop by meiosis. Oocyte is a gametocyte. |
| What is a hypnozoite? | This is a dormant exoeurthrocytic form found in certain Plasmodium species. |
| What is a ookinete? | This is an elongated motile zygote of a Plasmodium or related species. |
| In relation to Plasmodium spp., what is meant by relapse and which species is associated with this? | Reappearance of parasitemia wfrom mnerozoites (cryptozoites) in liver. P. vivax, and P. ovale are associated with this. |
| In relation to Plasmodium spp., what is meant by recrudescence and which species is associated with this? | Reappearance of parasitemia from merozoites reactivated in RBCs. P. malariae is associated with this. |
| What makes falciparum malaria a particularly pahtogenic form of the disease? | Because P. falciparum possesses antigen variation. |
| What is unique about falciparum in terms of RBCs that are infected? | Anopheles squeeter innocs sporozoites into human host, they travel to liver and replicate exo-erythrocytic schizogny, parasite undergoes asexual X into schizonts which rupture releasing merozoites. |
| What is pulmonary edema? | Swelling of lung associated organs. |
| What is cerebral malaria? | Swelling of the cerebral portion of brane. |
| What is algid malaria? | Caused by P. falciparum, long-term effect, will see shock, circulatory collapse, hemorrage and death. |
| What is blackwater fever? | Caused by P. falciparum, long-term effect, massive hemoloysis with fever, jaundice, renal failure. Renal failure causes black urine. |
| How can malaria be controlled clinically? | There isn't a true way clinically. Bednets. |
| How can malaria be controlled epidemiologically? | Malaria can be controlled epidemiologically by keeping the number of breeding places to a minimum. No standing water. |
| Why is the malaria resistant to drugs? | Incorrect doses are given making stronger strains develop and weaker strains die out. |
| Why is the malaria parasite vector resistant to insecticides? | Overuse of the pesticides. |
| What drugs have been used to treat malaria and do they still work? | Chloroquine and it is not effective due to over usage. |
| Why isn't a vaccine available for malaria? | It is difficult to develop a vax d/t parasite too complex. And d/t Variant Surface Glycoprotein (VSG) VSG expression sites are polycistronic transcription units, also a # of groups of expression site associated genes of unknown function. |
| Why aren't antbodies effective against the malaria parasite? | Parasite has a pleated sheet protein on surface, it sloughs off so antibody binding is ineffective. |
| Differ between sporotzoite and merozoite vaccine. What are the requirements for clinical trials of malaria vaccines according to the film "Malaria: Battle of the Merozoites"? | |
| What are the requirements for field trials of malaria vaccines according to the film "Malaria: Battle of the Merozoites"? | |
| How does sickle cell anemia confer resistance to malaria? Describe cellular level. | Parasitized RBCs=low pH, cell membrane breaksdown losing K+. K+ kills parasite. |
| How does thalassemia confer resistance to malaria? Describe cellular level. | The breakdown of the cell do to a change in amino acid. This causes H2O2 which oxidizes cell membrane. K+ leaks out killing parasite. |
| What are the effects of Balantidium coli on its host(s). | Diarrhea, stomach cramps. |
| How do humans get Balantidium coli? | By fecal transmission, injesting the parasite in the cyst form. |
| Describe the life cycle of the malaria parasite in the squeeter host. | Some formed gametocytes ingested by squeeter, X go through sporogonic cycle, in mid-gut, the microgametes penetrate the macrogametes=zygotes, become motile invade midgut wall=oocytes, rupture, and release sporozoites migrate to squeeters salivary glands. |
| What is kDNA? | DNA circles that forms the kinetoplast. |
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