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89 Cards in this Set
- Front
- Back
what is mononucleosis characterized by?
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an increase in mononuclear leukocytes
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what is the etiologic agent for mononucleosis? what does it have an affinity for?
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EBV w/ an affinity for B-lymphocytes
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what would you see on a CBC differential of someone diagnosed w/ mononucleosis?
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increase in lymphocytes
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what does the reactive lymph in infectious mononucleosis look like?
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abundant cytoplasm; chromatin is not as dense as a resting lymphocyte. Remeber the blueing around the edges of the cytoplasm indicating a lot of RNA in the cytoplasm hugging the RBCs.
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what two types of lymphocytes can you see on blood smear that is indicative of mononucleosis?
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reactive lymphs and degenerated lymphocytes (smudge cells)
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what are the EBV antibodies associated with infectious mononucleosis? (4)
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EBV-VCA (IgM), EBV-VCA (IgG), EBNA, EBV-EA
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when do you use the viral capsid antigens test?
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when infectious mononucleosis is suspected, but the heterophile antibody test is negative
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In IM, when do you normally see the EBV-VCA (IgM)antibody? what does it indicate?
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during the 1st week of infection indicating best indicator of current infection
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In IM, when do you normally see the EBV-VCA (IgG) antibody? what does it indicate?
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about 7 days after exposure indicating either current or past infection.
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In IM, when do you normally see the EBNA antibody? what does it indicate?
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appears late in 1st month of infection and persists indefinitely; indicates past infection
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In IM, what is EBV-EA's indicative of?
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EBV-carrier state
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what is the first test you do in someone that you suspect has infectious mononucleosis?
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heterophil antibody test
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what happens when the ENV incorporates its genome into host cell DNA? what is potential outcome of this?
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it establishes a latent infection--> transforms B-cells into immortal, constantly dividing cells (potentially causing cancer)
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what virus is associated w/ causing Burkitt's lymphoma?
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EBV--genome detected in tumor cells
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what is the vector for yellow fever?
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mosquitos
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where does the yellow fever virus replicate inside of the body?
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liver
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How many phases are involved in yellow fever? what does each phase entail?
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3 phase: 1) slight fever, headache, muscle aches. 2) remission, 3) delirium, seizures, coma, jaundice, and black vomit
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how many phases are involved in dengue fever? what does each phase entail?
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3 phases: 1) Fever, severe pain in the head and muscles (breakbone fever), 2) remission - 24 hrs, 3) return of the fever and a bright red rash.
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how many strains are there of dengue virus?
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4
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what can cause fungemia?
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complications due to venous or arterial catherization
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what populations are most at risk for developing fungemia?
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AIDS/ immunocompromised; pts on antimicrobial therapy, radiation, antineoplastic drugs.
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what type of endocarditis are IVDA prone to? what is the most common cause?
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candida endocarditis; candida albicans
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candidemia is associated with significant ______ and _____ rates.
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morbidity, mortality
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what are the four overlapping forms of invasive candidiasis?
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catheter related candidemia, acute disseminated candidiasis, chronic disseminated candidiasis, deep organ candidiasis
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what is primary infection of catheter-related candidemia?
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is on the catheter or related to the fibrin clot which forms on the catheter
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where does acute disseminated candidiasis originate from?
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contaminated catheter
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what is another name for chronic desseminated candidiasis? when does it occur?
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hepatosplenic candidiasis; exclusively occurs following prolonged episodes of bone marrow dysfunction and neutropenia (leukemia tx)
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What is the only manifestation of deep organ candidiasis?
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focal infection of a specific organ
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name which disseminated form of fungi causes these infections:
1) Pericardium 2) myocarditis, pericarditis, endocarditis 3) lymphadenitis, endocarditis |
1) coccidioidomycosis (coccidioides immitus)
2) Crytococcosis (cryptococcus neoformans) 3) Histoplasmosis (Histoplasma capsulatum) |
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what is the infectious phase of malaria?
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the production of sporozoites that migrate from the gut to the salivary glands
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in malaria, where do the sporozoites invade inside of the human and what do they replicate into?
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liver cells; replicate many times into merozoites
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what happens to the RBCs in malaria when they are invaded by merozoites?
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the merozoites continue to replicate and lyse the RBCs and invade other RBCs
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what parasite causes the most severe form of malaria? what makes it the most severe?
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plasmodium falciparum; the parasite infects all erythrocytes any phase of an erythrocytic life cycle.
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what two parasites cause relapsing malaria? how does this happen?
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plasmodium vivax, and ovale; after tx, tx-resistant parasites reside dormant in the liver and later multiply in an exoerythrocytic cycle eventually invading RBCs and beginning a typical erythrocytic cycle.
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what is a complication of recurrent malarial infections?
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can cause severe anemia
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which plasmodium produces long-lasting infections and is most often asymptomatic?
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plasmodium malariae
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why are the clinical manifestations of malaria delayed?
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due to prophylaxis txs
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what is a key indicator of malaria found on a peripheral blood smear? what are they?
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schuffner's dots- small purplish red granules found in RBCs
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what are the physical findings of malaria? what physical findings are specific to P. falciparum?
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elevated temp, weakness, enlarged spleen.
P. falciparum: mild jaundice, heptomegaly. |
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what lab results are indicative of malaria, particularly malaria caused by P. falciparum?
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mild anemia, thrombocytopenia, elevated bilirubin, aminotransferases
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what are some complications of severe malaria?
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cerebral malaria, severe anemia, pulmonary edema, abnormal blood coags, CV collapse, kidney failure, acute kidney failure, hypoglycemia
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what are the four ways that you can diagnose malaria?
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blood smear, antigen detection, molecular diagnosis, serology
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what are the four groups of individuals who have resistance to malaria? why?
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sickle-cell: erythrocyte membrane is abnormal and becomes stiff under low oxygen tension making them resistant to plasmodium sp infection
hemoglobin C: homozygous (mechanism unknown) G6DPH deficiency: doesn't allow trophozoites to replicate intracellularly lack of blood antigens Duffy A and Duffy B: plasmodium parasite requires the Duffy antigen as the receptor site. |
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what population generally has a lack of blood antigens, duffy A and Duffy B?
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african americans
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what do the parasites in babesiosis invade and induce?
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invade RBCs and induce a febrile dz (hemolytic anemia, hemoglobinuria, shock, death)
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what are the 2 species responsible for the majority of human infections in babesiosis? what are the 2 hosts? which one is the vector?
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responsible: Babesia microti and divergens
Hosts: white footed mouse and deer tick (ixodes dammini- vector) |
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T/F
in babesiosis humans are accidental hosts and humans are considered dead end hosts because they cannot transfer from human to human. |
true
except in blood transfusions |
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where does babesiosis regionally occur?
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coastal areas of NE US, offshore islands of NY and mass
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what are the two ways in which you can diagnose babesiosis? which one is used just as a confirmatory test?
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direct blood smears and IFA (confirmatory)
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what does a direct blood smear of babesiosis look like?
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tetrad formation- parasites in RBCs.
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what other dz has the same vector as babesiosis?
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lyme
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how are individuals infected with schistosomiasis?
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through contaminated water;
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what form of schistosomiasis infects humans?
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cercariae
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which schistoma has a prediliction for the bladder? which two are found in fecal matter?
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bladder: hematobium
fecal: japonicum and mansoni |
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what are the organs infected by schistosomiasis? what does it cause?
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organs:
a) skin: swimmers itch b) bladder: granulomatous lesions, hematuria, and urethral occlusions c) intestines: polyp formation d) liver: eggs cause hepatomegaly (d/t periportal fibrosis and portal HTN) e) NS: headaches, disorientation, amnesia, coma f) heart: arteriolitis and fibrosis --> enlargement and failure of right ventricle. |
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what is a key diagnostic tool for schistosomiasis?
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eosinophilia
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what two types of schistoma cause katayama's fever?
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mansoni and japonicum
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what type of schistoma can can CNS lesions by depositing eggs in the brain? what about in the spinal cord?
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brain: japonicum
SC: mansoni, haematobium |
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what are the two host immune responses to schistosomiasis?
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IgE and eosinophil-mediated cytotoxicity
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how do you diagnose schistosomiasis? which one can you find in the urine?
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microscopy (stool and urine), and antibody detection.
Urine--> hematobium |
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what causes chagas disease? chronic form of african sleeping sickness? acute african sleeping sickness?
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trypanosoma cruzi; trypanosoma brucei gambiense; trypanosoma brucei rhodesiense
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what does chagas's disease primarily affect?
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NS and heart
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what can chronic infections of trypanosoma cruzi cause? what vectors spread it?
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dementia, damage to heart muscle and death; triatoma infestans, rhodnius prolixis, panstrongylus megistus
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what regions can you find chagas disease?
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central and south america
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what bug specifically infects individuals w/ chaga's disease? how do they do it?
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reduviid bug... the bugs poop on your face (usually when sleeping) and sometimes directly into eyes. Then you rub the infected fecal material into your eyes, mouth or open cuts. Or by eating uncooked food contaminated by that fecal material.
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what sign is closely associated with the acute stage of chagas's disease?
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romana's sign: eye on one side swellings
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how many stages are associated with chagas's disease? what are they?
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3;
1) acute phase: romana's sign 2) indeterminate stage: asymptomatic (8-10 weeks after infection) 3) chronic stage: cardiac problems, enlargment of esophagus or large bowl (10-40 yrs after infection) |
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T/F
Trypanosoma brucei gambiense is a rapidly progressing dz. |
false
trypanosoma brucei RHODESIENSE (acute african sleeping sickness) is rapidly progressing... Trypanosoma brucei GAMBIENSE (chronic african sleeping sickness) is slow-progressing |
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what are kinetoplastids?
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mitochondrial DNA
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what is the life cycle of african sleeping sickness?
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Metacyclic trypomastigotes (MT) --> Long slender (LS) --> Short Stumpy (SS) --> Procyclic trypamastigoes (PT) --> epimastigotes (E)
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which phase of the life cycle of african sleeping sickness resides in salivary glands? in what insect does the African sleeping sickness reside?
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metacyclic trypomastigotes-- tsetse fly
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how do the trypomastigoes of the african sleeping sickness elude the immune system?
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via antigenic variance (long slender, short stumpy)
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where are procyclic trypomastigotes develop in african sleeping sickness?
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in the gut
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why do relapses occur in african sleeping sickness?
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d/t antigenic variation of trypanosomal surface--> life cycle exhibits different morphologies
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what is the hallmark of african sleeping sickness? In which type of african sleeping sickness does this occur more quickly?
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invasion of the CNS-- NS impairment;
more quickly in trypanosoma rhodensiense |
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what transmits leishmaniasis? what type of dz is this? what parasite causes this?
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transmitted by sandflies--> vector-borne dz; leshmania donovani
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where are the amastigote forms of leishmaniasis found?
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in reticuloendothelial cells of the viscera
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what are the sxs of leishmaniasis?
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low grade fever, anemia, protrusion of abdomen d/t enlargement of spleen and liver, edema, diarrhea
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what are the possible complications of leishmaniasis?
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post kala-azar dermal lesihmanoid, badly disfigured face
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what is the diagnostic phase of the leishmaniasis life cycle?
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amastigoes in the various organs--> identified as LD bodies (Leshmania donovani)
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what is the geographical distribution of visceral leishmaniasis?
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south america (mostly), some africa and Mediterranean.
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what is caused by infections w/ nematodes?
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filariasis (roundworms)
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what three species are responsible for most of the morbidity due to filariasis?
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wuchereria bancrofti, brugia malayi, onchocerca volculus
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what is the geographical location of loa loa and onchocerca volvulus?
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Africa
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what two parasites infiltrate the subcutaneous tissues? lymphatics?
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subQ: onchocerca volvulus, loa loa
lymphatics: brugia malayi, wuchereria bancrofti |
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where do microfilariae develop into filariform?
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in arthropod
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what are the clinical manifestations of lymphatic filariasis?
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asymptomatic microfilaremia, lymphadema, elphantiasis, febrile lymphagitis
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what cell type of prominent in filarial infections?
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eosinophils
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what are the three diagnostic techniques that we can use for filariasis?
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microscopic examination, antigen detection, and antibody detection
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