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parisitology exam 2
| Question | Answer |
|---|---|
| What are the 3 types of Leishmaniasis? | Visceral, Cutaneous, and Mucocutaneous |
| What is Visceral leishmaniases caused by? | Leishmania donovani |
| What is visceral leishmaniasis? | An infection of the reticulo-endothelial cells in visceral organs like the spleen and liver |
| What is Kala-azar? (Dum Dum fever) | A clinical manifestation of a type of visceral leishmaniasis |
| What is Cutaneous Leishmaniases? | Infection of macrophages of the skin |
| What is an Oriental sore caused by? | Leishmania tropica |
| What does Leishmania Mexicana cause? | Chiclero's Ulcer |
| What is mucocutaneous Leishmaniases? | An infection of microphages that occur in mucous layers |
| What mucous layers does mucocutaneous leishmaniasis seem to effect? | Mucous membranes around mouth, cartilage of nose and pharynx region |
| What is Espudia caused by? | Laishmania braziliensis |
| How many types of Kala-azar are important and pathogenic? | Three |
| ___ of infected people if not treated will die of Kala-azar | 90-99% |
| During the outbreak of Kala-azar in sudan, how many villages were eradicated? | 30-40% |
| Kala-azar is one of the big ___ in reference to _____ | three, feared tropical fevers |
| The agent that caused Kala-azar was found in __- | 1900 |
| What did Dr. Leishman discover? | amastigotes in macrophages of the liver |
| What did Sir Leonard Rogers discover? | He was working in Calcutta and put spleen tissue from infected person into a simple salt solution and found |
| What was discovered in the guts of bedbugs? | Promastigotes |
| What did Major John Sinton discover? | Kala-azar had a restricted range in eastern India so decided to overlay distribution maps of blood sucking insects |
| What are sand flies? | Small hairy flies with pointed elliptical wings that are 2-4 mm big |
| Where do Sand flies live, and why? | The larvae are terrestrial in burrows of small mammals and in the stone walls of human habitat. They stay close to these areas because they are weak fliers and can fly no more than 100 m |
| What was found in 1924 about sand flies? | They can become infected with Leishmania donovani, but they could not show that sand flies infected people |
| What did Henry Edward Short say? | The assumption was that a sand fly was like a small mosquito; in that both only the ladies are blood feeders |
| What did R.O. Smith find? | Female sand flies feed commonly on fruit, and once infected the sand flies fed on raisins. The promastigotes multiplied rapidly and formed plugs in the sand flies pharynx |
| What happens when the plugged host tries to feed on a human? | The clogged up pharynx gets pushed out and the promastigotes infect the human |
| in 1940, what did C.S. Swaminath do? | Critical experiment from human to sand fly back to human for Kala-azar |
| What two ways can sand flies become infected? | 1. Ingesting macrophages with amastigotes. 2. (less common) Ingesting already free amastigotes in the blood |
| When sandflies probe the skin for blood, what do they do? | Inject saliva that suppresses immunologic functions of macrophages which the promastigotes infect |
| What is the geographic distribution of sand flies? | Genus Phlebotomus occur on all continents except australia |
| What is the main genus of sand fly species in the Americas? | genus Lutzomyia |
| What are reservoir hosts for Kala-azar? | Foxes, Rodents, Dogs, (Hamsters) |
| Why are Hamsters good lab animals to study? | They are readily available and their system mimics what happens in humans |
| What is the distribution of Leishmania donovani? | Argentine, Brazil, Sudan, Eastern coast of India, Eastern and northern areas of China, Russia, countries along the Mediterranean. Of major concern in the muddle east |
| What is the distribution of Leishmania tropica? | Nigeria; Middle east: Turkey, Iraq, Iran, Pakistan, Afghanistan; Southern mexico |
| What is the distribution of Leishmania brazeiliensis? | S. America: Brazil, coastal Chilie, Central America and up to southern mexico |
| What are 6 symptoms of Kala-azar? | Headache, fever (both irregular) , wasting disease, bleeding from mucous membranes, dysentery, anemia |
| What is the Cardinal Symptom? | Hepatosplenomagaly |
| (pathology) What happens to RBC because of kala-azar? | They are not produced anymore and the energy goes towards making more reticuloendothelial cells |
| (Pathology) What happens when phagocytes are being destroyed because of kala-azar? | It causes physiological demand on the person and the body goes into overdrive b/c loss of these cells |
| (Pathology) What is Hypertrophy (caused by Kala-azar) | Increase in the size of an organ, not resulting from an increase in the number of cells or tissue elements (non-pathogenic) |
| (Pathology) What is Hyperplasia? (caused by Kala-azar) | It is the excessive proliferation of normal cells in the normal tissue of an organ (pathogenic) |
| What is the incubation period of Kala-azar? | As quick as 10 days and up to a year. Usually 2-4 months |
| What is the drug of choice for Kala-azar? (and one backup) | Pentostam. AmBisome if Pentostam does not work. 100$ for 30 days. Toxic but w/o treatment ends in fatality |
| What is the Post-Kala-Azar Dermal Leishmania? | Pustubules form on the skin when it has not been treated adequately enough, but if treatment resumes then face clears up |
| Why is Kala-Azar hard to diagnose? | There are not a lot of organisms present in the blood stream |
| What is the best way to find Kala-azar amastigotes? | Biopsy (which are invasive and uncomfortable. They are also dangerous because the hyperplastic tissue is "brittle" and can crumble causing hemorrhaging and even death) |
| What are two tests for Diagnosis of Kala-azar? | ELISA and IFA |
| What is IFA? | Indirect fluorescent antibody test. utilizes fluorescent dyes to identify the presence of antibodies bound to specific antigens |
| Where is cutaneous Leishmaniasis found? | Arid regions (Mediterranean, Middle east) |
| What is the vector of cutaneous leishmaniasis? | Phlebotomus sergenti, which lives in sandy areas, will hide in cracks, and needs moisture during mating |
| What is the incubation time for Cutaneous Leishmaniasis? | A month or two |
| What happens to the skin with cutaneous Leishmaniases? | An open sore occurs and will heal spontaneously within a year |
| What is the drug of choice for Cutaneous Leishmaniasis? | Pentostam |
| How is cutaneous Leishmaniasis transmitted? | Touch, and flies to other open wounds |
| What is the drug of choice for Leishmania braziliensis? (expundia) | Pentostam. (Most people are not treated) May have to have reconstructive surgery |
| Why would someone die of Espundia? (Leishmania braziliensis) | Difficulty breathing, eating, and bacterial infections. It will also cause a loss of voice if localized in the larynx |
| What is the causative agent of Chagas' Disease? (American trypanosomiasis) | Trypanosoma cruzi |
| Is Trypanosoma rangeli pathogenic in humans? (American trypanosomiasis) | No |
| How is trypanosoma transmitted? (American trypanosomiasis) | Biting insects in the order Hemiptera, family Reduvidae (Assassin bugs, Reduvids, or Kissing bugs) |
| What are 3 basic facts about kissing bugs? (American trypanosomiasis) | Up to 34 mm, some found in ground, trees, human dwellings, the eggs are laid and have 5 nymphal instars |
| Where are epimastigotes found on kissing bugs? (American trypanosomiasis) | Near the rectum |
| How do you get infected with the epimastigotes from kissing bugs? | Bugs deficate while eating, the epimastigotes must come in contact with mucous membranes or open wounds |
| Why are trypomastigotes not really found in the circulatory system? (African Trypanosomiasis) | They do not persist long there, and do not reproduce there |
| Where do trypomastigotes go in the body? (African) | They move into muscle cells and become amastigotes and reproduce by binary fission |
| What are the three steps of African Trypanosomiasis infection? | 1. Epimastigotes are transmitted through bug feces. 2. Trypomastigotes are found in the peripheral blood. 3. Amastigotes reproduce in muscle cells. |
| In American trypanosomiasis transmission is _____ or ____ | Stercorarian, Posterior station |
| What is the distribution of Trypanosoma cruzi | Primarily in the costal areas of S.A. and a few reports in southern U.S.A. |
| What are two vectors of trypanosomiasis? | Triatoma gerstaeckeri and Triatoma sanguisuga |
| How do the feeding habits of T sanguisuga and T gerstaeckeri differ from their latin American counterparts? | They are very cautious and neither will walk completely onto a host, reducing the chances of defecating on the host. Also, they do not generally defecate while feeding. |
| What are the 3 phases of American Trypanosomiasis course of infection? | 1 - Trypomastigotes in peripheral circulation, 2- Trypomastigotes enter cells (symptoms of 1 become absent or subside) 3. Amastigotes within cells |
| What cells do American Trypanosomiasis amastigotes generally invade? | Cells of reticuloendothelial system in the spleen, liver, cardiac muscle, smooth muscle, and skeletal muscle, also nervous system can be infected |
| Phase 3 of American Trypanosomiasis causes an Edema. What is this? | An abnormal accumulation of fluid in the tissue spaces (cellular level) |
| What does phase 3 of American trypanosomiasis cause? | Edema, inflamed lymph glands, hyperplasia of spleen and liver, heart problems |
| What heart problems does phase 3 of American trypanosomiasis cause? | The fibers separate, inflame, and weaken causing irregular heartbeat. There is an invasion of connect. tissue that enlarges the heart and nerve ganglia are destroyed causing cardiac arrest. Impulses into ventricles affected |
| What 5 things relate to the pathology of Trypanosoma cruzi? | Megaesophagus/megacolon, muscle tone and peristalsis destroyed, organs increase in diameter, victim may not be able to swallow and die from starvation, feces not formed effectively |
| What are the diagnosis tests for Trypanosoma cruzi? | Demonstration of trypanosomes in blood (difficult), ELISA, Xenodiagnosis |
| What is an Xenodiagnosis? | allowing a noninfected disease-carrying organism such as a mosquito to feed on an infected person's blood and then examining the organism for infection |
| What is the treatment for Trypanosoma cruzi? | No effective treatment but not all people die from it. Children have acute cases and die within a month. Adult infections are more chronic (shorter lifespan, 30% die) |
| What is the causative agent of Dourine? | Trypanosoma equiperdum |
| How is Dourine transmitted? | Sex |
| What are the symptoms of Dourine? | Unhappy genetalia ? |
| What is the causative agent of Surra or Murrina? | Trypanosoma evansi |
| How is Murrina (or surra) transmitted? | Mechanically, like with a fly |
| What are two groups of Trypanosomes? | African (transmitted by Tsetse flies belonging to Glossina) and New world (transmitted by bugs) |
| What three parasite types are correlated with African Sleeping sickness? | The trypanosome brucei group: T. brucei brucei, T. brucei gambiense, T. brucei rhodesiense |
| Where does T. b. brucei occur? (host) | Circulatory system of most native antelopes, ruminants, and other African wildlife (Nonpathogenic to these animals) Fatal to INTRODUCED livestock |
| What is Nagana caused by? | T. b. brucei |
| Where does T. b. gambiense occur?(host) | Occurs in people and fatal if not treated. It causes chronic infections. |
| How is T. b. gambiense transmitted? | Transmitted from person to person by the tsetse fly |
| Where does T.b. rhodiense occur?(host) | Acute infections in people (Usually fatal within a year). Recent colonizer of people and does not do well and kills them, not around long enough to adapt to host yet. Occurs in native animals but is not fatal to them |
| How is T. b. rhodiense transmitted? | Tsetse fly |
| What does it mean that the vector Glossina (fly) has a "host" seeking behavior? | It has a visual sense used to search for animals or humans to feed on, they spend most of their time resting on vegetation waiting to ambush prey |
| How is there stimulation of feeding with nets to catch Glossina? | Stimulate feeding with uric acid, leucine, valine, and lactic acid (HUMAN SWEAT) yummy. |
| What are the 2 important Glossina vectors to transmit? | Glossina palpalis -> T. b. gambiense, and Glossina morsitans -> T.b. rhodiense |
| What does the G. morsitans vector group tend to feed on? | Suids (like warthogs), and bovids (buffalo) and less so on people |
| What does the G. palpalis vector group tend to feed on? | reptiles and people |
| In Africa, where is G. morsitans vector found? | In savannahs |
| In Africa, where is G. palpalis vector found? | Associated with rivers and lakes |
| What are the 2 stages (general) of the life cycle of Trypanosoma brucei? | Epimastigote and trypomastigote. |
| What are the 6 steps of the Trypanosoma brucei life cycle? | Uninfected tsetse (glossina) fly bites infected host, trypomastigotes multiply with binary fission, they migrate to salivary glands and turn to epimastigotes/multiply. transform back to trypo. fly bites human and infects. trypo live/mult in blood |
| What is the African Typanosomiasis course of infection? (Africans) 4 phase | 1. incubation (lesions, itching, trypo in skin, 1-2 weeks), Trypo enter circulation (fever, headache, skin rash, duration variable), Trypo collect in lymph nodes and channels, invasion CNS (African sleeping sickness) |
| What are the symptoms of African Sleeping Sickness? | Headaches, Emaciation, mental dullness, apathy, drowsiness, death from asthenia, heart failure, meningitis, severe fall, etc |
| What is the pathology for T. brucei group | Parasites have toxic biproducts, causes hyper stimulated immune system (VATs constantly changing which compromises immune system), Host lyses it's own RBC (causing anemia) |
| How is the African Trypanosomiasis (t. brucei group) diagnosed? | Can be found in blood plasma, lymph nodes, very questionable to do lumbar puncture |
| What is the drug of choice for African Trypanosomiasis (t. brucei group) | Suramin(Bayer 205) However, does not defend against CNS forms. Also, Current drug of choice is Ornidyl (DFMO) but is expensive 2 wk is 150$ |
| What is the drug of choice for African Trypanosomiasis (t. brucei grouo) when the CNS is infected? | Melarsoprol used with Bayer 205. Causes vomiting and kidney damage and 10% patients die from treatment |
| Where is T. b. rhodiense distributed? | E. Africa |
| Where is T. b. gambiense distributed? | Costal W. Africa and in drainages of Congo and Niger rivers |
| What are the Big 3 tropical fevers to be feared? | 1. Malaria, 2. African Trypanosomiasis, 3. Kala-azar |
| What are 4 negative effects of African Trypanosomiasis? | Depopulation (social stability, lack of productivity, equality of life) and Agriculture, tsetse flies effect environment and climate, and aesthetics (how many wild animals can we live with?) |
| What are some main characteristics of Apicomplexa? | Shape maintained by pellicle, locomotion is gliding, asexual and sexual reproduction, apical complex, all intracellular parasites at some stage In the life cycle |
| What is a perkinsozoa | apicomplexan. Parasites of oysters; likely similar to the ancestor of current apicomplexans |
| What is a conoidasida | apicomplexan. gregarines and coccidians |
| What is an aconoidasida | apicomplexan. malaria parasites and piroplasms, usually blood parasites of vertebrates, with an arthropod host |
| What are three types of fission that protozoans can undergo? | Binary, repeated, multiple |
| What is Schizogony? | asexual process done by an organism that is itself asexual |
| What is Sporogony? | Formed by a sexual process |
| How are gametes made? | gametogenesis |
| What are the 3 main steps of sexual reproduction | Gametocyte -> gametogenesis -> gametes |
| What is Gamogony | sexual reproduction |
| What is sporogony | multiple fission of a zygote |
| How was malaria first found? | It was commonly found in swamps and thought to be contracted by breathing "bad air" (miasma theory) |
| What is the vector for malaria (general) | mosquito |
| What has a two host life cycle? | Malaria |
| What genus of mosquitos are vector host for malaria | Anopheles |
| What is Paroxysm? | Breaking of erythrocytes |
| What is the period for tertian? | 48 hr erythrocytes break; attacks every other day. P. vivax and P. ovale |
| What is the period for Quartan? | 72 hr erythrocytes break; attacks 3 days. P malariae |
| What is the period for P. falciparum? | Not as predictable. 36-48 hours |
| What re the 4 species of Plasmodium that infect humans? | P: vivax, falciparum, malariae, ovale |
| Where is P. vivax found? What period? | temperate areas, Asia, North Africa. (Tertian malaria) |
| Where is P. falciparum? What period? | Tropics. (Malignant tertian malaria) |
| Where is P. malariae?What period? | Rare, localized, but widespread (Quartan) |
| Where is P. ovale? What period? | Very rare. Africa, phillipenes, India, S. America, Vietnam. (Mild tertian malaria) |
| What happens in the human for malaria? | The parasite is in RBC. It reupts and the parasite gets into blood stream, causes pigment, and releases byproducts. 200 parasites per cc of blood. |
| What is the cardinal symptom of malaria? | Paraxysm |
| What is paraxysm? | First the chill (hour), then the fever (as high as 106; vomit rapid pulse), profuse sweating 204 hr, then symptoms subside until next cycle. |
| When is the primary attack of malaria over? | About 3 weeks. |
| What occurs after the primary attack of malaria? | A relapse. A true relapse is persistend exoerythrocytic schizogony produces merozoites that infect RBCs that produce more merozoites. P. vivax and ovale |
| What are the mechanisms for malaria relapse? | Can be dormant 3 years. Infect liver some turn to schizonts and other dormant called hynozoites. When sporozoites inoculates, not all genetically identical |
| When is there a reoccurance of P. malariae? | Reoccurance can happyen 50 yrs after primary attack, |
| When is there a reoccurance of P. falciparum? | No relapse. Same mechanism as P. malariae but will not last 50 yrs. |
| What are 2 major aspects during the erythrocytic cycle? | Host inflammatory response and Anemia |
| What is the pathology for malaria? | Destruction of RBC, accumulation of Fe in brain, liver, spleen |
| What is the most severe plasmodium? | P. falciparum (Infected cells clmp more, more cells infected, cause clogging) |
| What is blackwater fever? | makes the urine weird and black |
| What are some complications from P. falciparum? | Cerebral malaria: headache, coma, hypoxia, high temp. Pulmonary edema. Algid shock, Blackwater fever |
| What are 4 drugs to use for malaria? (why) | Quinine - no effect on sporozoites or exoerythroytic schizogony. Chloroquine -> DOC against non resistane malaria. Primaquine - acts on exoerythrocytic schizogony, not replace because toxic. Mefloquine - use for resistant strains P. falciparum. |
| What are some side effects of malaria? | Malnutrition, shuttding down of organs, stunts growth of children, affects growth of children, ancient disease, endemic that can turn to epidemics |
| What are two kinds of non malaria apocomplexans? | Gregarines and coccidians |
| What is the phylum apicomplexan named for? | Ultrastructural features of the infective stages |
| What infect all metazoan taxa? | Apicomplexans |
| What is the treatment for T. Gondii | Pyrimethamin (pregnant take spiramycin_ DOC - Latent - atovaquone |
| What can monocystic spp. do? | The cysts survive passage through a predators intestine and get distributed through the environment |
| For gregarine cuneata, the sexual reproduction occurs in the | gametocyst |
| For gregarine cuneata, ___ occurs only with the ____ inside the gametocyst | Schizogony, gametocytes |
| For gregarine cuneata, ____ contain haploid ____ | Oocysts, sporozites |
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