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61 Cards in this Set
- Front
- Back
How many vaccines are there for parasitic diseases?
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None. They're developing one for malaria, but it's not even 50% effective.
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Top 3 infectious/parasitic diseases in terms of deaths caused?
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HIV, TB, malaria
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2 big divisions in parasites:
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Protozoa (unicellular motile)
Helminths (worms) |
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2 big divisions of helminths:
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Nematodes (roundworms)
Platyhelminths (flat worms) |
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Two types of nematodes:
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Luminal (gut) nematodes
Tissue nematodes |
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Two divisions of platyhelminths:
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Trematodes (flukes; non-segmented)
Cestodes (tapeworms/cysts; segmented) |
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Two types of cestodes:
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Luminal cestodes (tapeworms)
Tissue cestodes (cysts) |
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List all the categories of parasites!
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8 types of protozoa:
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Amoeba
Babesia Giardia Leishmania Malaria Toxoplasma Trichomonas Trypanosomes |
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5 types of luminal nematodes:
5 types of tissue nematodes: |
Luminal nematodes:
Ascaris Hookworm Pin Worm Strongyloides Whip Worm Tissue nematodes: Dracunculus Filaria Loa Loa Onchocerciasis Trichinosis |
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5 species of trematodes:
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Schistosomes
Clonorchis Fasciola Opisthorchis Paragonimus |
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2 species of luminal cestodes:
2 species of tissue cestodes: |
Taenia and Diphyllobothrium
Cysticercosis and Hydatid disease |
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What are Neglected Tropical Diseases? 4
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-Serious bacterial & parasitic diseases that affect > 1 billion people worldwide
-Impair physical & cognitive development -Cause maternal and child morbidity & mortality -Impact earning capacity |
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11 examples of Neglected Tropical Diseases.
How might they be controlled? 2 |
-African trypanosomiasis (African sleeping sickness)
-Chagas’ disease (American trypanosomiasis) -cysticercosis -dracunculiasis (Guinea worm disease)* -echinococcus -fascioliasis -leishmaniasis -lymphatic filariasis* -onchocerciasis* -schistosomiasis* -soil‐transmitted helminths (ascaris, hookworm, whipworm)* *Disease is controllable by mass drug administration or effective intervention |
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Trypanosomiasis:
how widespread? new and old world carriers? 3 traits |
-widespread parasites
-“Old world” (Africa): cattle, sheep, goats, wild game, humans -New world (S. America): cats, dogs, armadillo, humans -unifying feature = kinetoplast (mitochondrial DNA) -flagella -Giemsa staining |
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Trypanosomiasis
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Trypanosome Distribution:
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West-African type
East-African type *distinguised by vectors--the type of flies involved South American type (Shaggar's disease) |
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East and West African tsetse flies. Why do we care about them?
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East: G. morsitans
West: G. palpalis *These are the vectors for Trypanosomiasis. |
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List the human (3) and tsetse fly (5) stages in the life cycle of Trypanosomiasis.
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Scientific names for the east and west African variants of Trypanosomiasis:
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East is T.b. rhodesiense (think rhodesia)
West is T.b. gambiense (aka sleeping sickness, think The Gambia) |
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Zoonosis:
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Infection that is naturally transferable between animals and humans.
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Trypanosomiasis, blood stage.
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Trypanosomiasis on EM.
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Characteristics of a tsetse bite?
How are they able to serve as vectors? |
-Usually painful and can have hypersensitivity.
-Tsetse are “pool feeders” (lacerate skin and suck up blood in lesion). -Metacyclic trypomastigotes in saliva enter bite wound |
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Acute symptoms and Blood Stage of African Trypanosomiasis:
-incubation period -characteristic mark -symptoms? -∆ between rhodesiense and gambiense |
-1-3 week asymptomatic incubation period
sometimes local inflammation -'trypanosomal chancre' -parasite replication at bite site -invasion of blood is characterized by irregular fever and headache *T. rhodesiense can quickly develop into fulminating infection *T. gambiense can be self-limiting or slowly progressing to more serious disease |
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Trypanosomal chancre
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Describe the Lymphatic Stage of Trypanosomiasis:
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-Disease progression often involves invasion of lymphatics
*Winterbottom’s sign (cervical adenopathy) *fever, continued febrile attacks itching edema weight loss (cachexia) weakness |
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Winterbottom’s sign (cervical adenopathy) in Trypanosomiasis, lymphatic stage.
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Describe the CNS disease course and symptoms in African Trypanosomiasis:
∆ b/t East and West African types? |
-parasites cross blood-brain barrier
*meningoencephalitis -increased apathy and fatigue -confusion and somnolence -motor changes --> tics, slurred speech, incoordination -convulsions, coma -progression to CNS involvement is rapid (weeks) in East African type and slow (6-12 months) in West African type -death results from disease (eg., convulsions, hyperpyrexia) or other infections |
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Describe the course of fevers in Trypanosomiasis:
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-parasitemia fluctuates
-peak parasitemia usually associated with intermittent fever or other symptoms -parasites from peaks are antigenically distinct i.e. variant antigenic types which produce variant surface glycoproteins (VSG; the basis for the high spiking fevers) |
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VSG:
general description: genetic traits: |
-Variant Surface Glycoprotein
-uniformly cover surface of parasite -form electron dense surface coat -100’s of VSG genes -they have conserved regions -Mutation rate = 10^-3 to 10^-5 per generation *they mutate a lot; that's the point. |
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What's the significance of VSG mutation in Trypanosomiasis?
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-VSG is immunogenic and host response clears parasites
-some trypanosomes will change VSG coat because of mutations -this population expands until host develops immunity against new VSG |
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How do you diagnose Trypanosomiasis?
clinically 6 what lab tests do you run? 2 |
Clinical Features:
-travel or residence in endemic area -history or scar of 'trypanosomal chancre' -irregular fever, enlarged lymph nodes (esp. posterior cervical), loss of weight -behavioral changes/mental symptoms Laboratory Diagnosis: serological tests microscopy trypanosomes in blood or CSF (especially during fever) *blood smear is key |
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How do you go about detecting African Trypanosomes in a blood smear?
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-examine on several days
-stained thin or thick smears (thick is best) -fresh (characteristic movement) -buffy coat (microhematocrit) -[inoculate rats or mice, xenodiagnosis, not often done] |
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Describe other ways to detect African Trypanosomes besides a blood smear: 2
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1) Lymph node aspirate- fresh or stained.
2) CSF- examine sediment; increased cells and PRO could indicate infection. Can also stain to see trypanosomes. |
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Describe early stage treatment of African Trypanosomiasis: 2
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Early Stage--no CNS involvement
-suramin -pentamidine *excellent prognosis if caught early |
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Describe late stage treatment of African Trypanosomiasis: 3
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Late Stage--CNS involvement
-Melarsoprol *arsenic based drug; highly toxic (4-12% mortality) -Eflornithine (DFMO) ± nifurtimox *expensive; 14 consecutive daily injections *oral formulation in phase 3 trials |
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Describe Prophylaxis and Control techniques for African Trypanosomiasis: 5
What's contraindicated? Why |
-insect repellants
-protective clothing -surveillance and treatment -traps, insecticides placed near livestock -habitat alteration drugs are contraindicated (mask infections, toxicity) |
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Describe Trypanosoma cruzi:
what does it cause? epidemiological info? |
-causes Chagas disease
-16-18 million infected -100 million at risk -50,000 deaths annually -leading cause of cardiac disease in S. and Central America |
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Talk about the bug that spreads Trypanosoma cruzi:
what is the bite like? what names is it known by? |
-painless bite, often around lips or face. The bugs defecate, and the feces gets into the skin via the bite.
-called triatomine bugs AKA reduviid bugs assassin bugs kissing bugs conenose bugs |
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-called triatomine bugs
AKA reduviid bugs assassin bugs kissing bugs conenose bugs -painless bite! |
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What's a simple intervention to reduce the number of triatomine bugs?
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-Replace thatch dwellings with another material. They live in thatch.
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Discuss the life cycle of Trypanosoma cruzi:
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-Have predilection for the heart
-Called amastigotes in heart because they will replicate there. |
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What stain do we use to find trypanosomes in a blood smear?
Can you distinguish b/t the African and S. American type? |
-Giemsa stain
-We won't be able to tell. Experts can. |
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What factors make triatomine bugs good transmitters of Trypanosoma cruzi? 4
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-defecation during triatomine feeding (their bite)
-colonization of human habitats *adobe walls *thatched roofs -para-domiciliary cycles *animal stalls adjacent to homes (live near livestock, which live near humans) -proximity to sylvatic cycle (live in the woods, which people go into) |
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triatomine bug
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Describe the Clinical Course of Chagas Disease:
Acute phase Indeterminate phase Chronic Phase |
-Acute Phase
*active infection (1-2 week incubation) *1-4 months duration *most are asymptomatic (children most likely to be symptomatic) -Indeterminate Phase *10-30 years of latency *relatively asymptomatic with no detectable parasitemia *seropositive -Chronic Phase *10-30% of infected exhibit cardiomyopathy or megacolon, -esophagus *This is the dangerous part! |
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Why is Chagas disease hard to diagnose and treat?
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-It's often asymptomatic at first
-Once it gets to the chronic phase it's hard to treat. |
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-To identify
-what do they become? -what are they spread by? |
-Amastigotes in heart muscle
-Will divide and become trypomastigotes once again in the blood. -Spread by triatomine bugs |
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Describe the acute phase of Chagas Disease:
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-1-2 week incubation period
-local inflammation -Romaña’s sign -chagoma (similar to African type) -symptoms: fever, malaise, lymphadenopathy, hepatosplenomegaly, nausea, diarrhea -acute, often fatal, myocarditis develops in a FEW individuals (uncommon) |
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-Romaña's sign and chagoma in Chagas disease.
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Describe Chronic Chagas' Cardiomyopathy:
clinical presentations? 3 |
-long latency characterized by seropositivity and no parasitemia
-progressive development of abnormalities -clinical presentations include: *Arrhythmias; heart block; conduction defects *congestive heart failure *thromboembolic phenomenon |
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What does this indicate?
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-Cardiomegaly, hypertrophy
-indicative of Chagas disease |
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List pathologies involved in Chagas Disease: 5
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cardiomegaly
apical aneurysm (left ventricle) extensive fibrosis hypertrophy ± cellular infiltration |
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Describe Megaviscerae in Chagas Disease:
-which organs most commonly affected? 2 -what signs/symptoms are involved? 3 -what happens to PS ganglia? |
-colon and esophagus most frequently affected
-megaesophagus --> painful swallowing, regurgitation -megacolon --> severe constipation *loss of parasympathetic ganglia |
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Megaviscerae in Chagas Disease.
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What's the basis of the Pathogenesis of Chagas Disease?
-Autoimmunity vs. Parasite-mediated destruction |
-Not quite clear.
-There IS an altered immune response; there's a Th1 to Th2 switch that happens. -No chagasic toxin has been identified. |
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How do you diagnose Chagas Disease?
3 broad methods |
-parasite detection
*direct examination *stained blood smears *in vitro culture *xenodiagnosis (not routinely done) -PCR -serological tests *hemagglutination *immunofluorescence *ELISA |
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Treatment in Chagas Disease:
acute (3 drugs) and chronic stages |
-acute stage
*nifurtimox *benznidazole *azole antifungal agents (experimental) -chronic stage *treat the symptoms; it's not going to get cured. |
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-Possible benefits of Chagas disease drugs?
-Cons of Chagas drugs? |
-One study showed good ECG ∆s, no worsening of clinical condition, and sero-negative conversion.
-Another study showed no benefits. -There are severe side effects of nitroderivatives and concomitant compliance issues. |
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What interventions can help control Chagas? 5
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-improvement of human dwellings
-separation of animal stalls from house -health education -insecticides -screen blood supply (it can be transmitted by transfusion) |