Parasitology Lecture 3
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- Trypanosomatids Types
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1.African Trypanosomasis(sleeping sickness)
2.American Trypanosomasis (Chagas' disease)
3.Leishmaniasis (cutaneous, mucocutaneous, visceral) - Trypanosomatids Characteristics
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1.Asexual reproduction
2.Single Flagella and Kinetoplast
3.Usually Vector-borne - Trypanosomatids Life cyle Forms
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1.Amastigote(Mammal)(intracellular)
2.Promastigote(Vector)
3.Epimastigote(Vector
4.Trypomastigote(Mammal) - Trypanosomatids' Kinetoplast
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1.w/in mitochondria
2.<20% of total DNA
3.mini/maxi-circles
4.produce mRNA for mito prots
5.RNA edited by inserting U's - African Trypanosomatids Lifecycle
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Human/animal
-Trypomastigote
Tsetse Fly
-Epimastigote
-Metacyclic
-Trypomastigote - African Trypanosomatids Epidemic
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Sudan, Uganda, Congo, Angola
>100,000 new cases/yr - African Trypanosomatids in West africa
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T. Gambiense
-Reservoir=human
-Glossina Palpalis group, lives by rivers
-Chronic Disease-years to develope - African Trypanosomatids in East Africa
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T. Rhodesiense
-Reservoir=wild animals
-Glossina Morsitans group, lives in savanna
-Acute Disease-developes in months - African Trypanosomatids Disease stages
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1.Primary-Lymphadenopathy (Winterbottom's sign)
2.Secondary-systemic disease (Fever, Wasting)
3.Advanced-CNS disease (Lethargy, insomnia, seizures, coma) - Glossina
- Tsetse fly
- African Trypanosomatids Antigenic Variation
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1.Variant Surf Glycoprot-protective coat
2.parasite may have >1000 VSG genes
3.NO Vaccine possible - African Trypanosomatids Treatment
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new=Eflornithine, DB 289
old(toxic)=suramin, pentamidine, melarsoprol - American Trypanosomatids cause by/disease
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1.Caused by Trypanosoma Cruzi
2.Chagas' disease - American Trypanosomatids life cycle forms (Human/animal)
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1.Trypomastigote
2.Amastigote - American Trypanosomatids Life cycle forms (Reduviid)
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1.Epimastigote
2.Metacyclic
3.Trypomastigote - American Trypanosomatids Amastigote form characteristics
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1.Live in MACS or Muscle cells
2.Fuse w/ Phagolysosome then ESCAPE to cytoplasm
3.Transform to trypomastigotes intracytoplasmically - American Trypanosomatids Spread by?
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1.Reduviid Bugs
2.Triatomes
-Domestic(cracks in mud, thatch)
-sylvatic(animals only)
3.Transfusions
4.Zoonotic in US (rodents, raccoons) - American Trypanosomatids Acute disease
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1.Romano's sign
2.parasitemia, febril illness
3.trypomatigotes in blood - American Trypanosomatids Chronic Disease
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1.occurs 10-20 yrs later
2.chronic cardiomyopathy(20-30%)
3.mega-colon/esophagus(8-10%) - American Trypanosomatids Treatment
- acute treated w/ nifurtimox(lampit)
- American Trypanosomatids Diagnosis (Normal)
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1.parasites usually not in peripheral blood
2.Xenodiagnosis(old) - American Trypanosomatids Diagnosis (immunologically)
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1.indirect fluoescent antibody (IFA)
2.Enzyme Immuno Assay (EIA) - American Trypanosomatids Pathogenesis
- PCR showed organisms in Lesion, could be direct effect
- Leishmanial organism types
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1.Dermatotrophic strains(only one in europe/asia)
2.Viscerotropic Strains(only one in Indai/mediterranean) - Leishmanial lifecycle types
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Human/animal=Amastigote
Sandfly=Promastigote - Leishmanial Lifecylce specifics
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1.Amastigotes
-Live in Phagolysosome
-Release when cell ruptures
2.NO trypomastigote form - Leishmaniasis, The disease
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1.Cutaneous/mucocutaneous(1-1.5mill cases/yr)
2.Visceral leishmaniasis(500,000/yr)
3.Most are epizootic(lots of animals in same region) - Leishmaniasis disease most often effects who?
- Malnourished kids
- Leishmaniasis disease manifestations
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1.Initially=painless skin lesion
2.most disappear spontaneously
3.May metastasize to Liver/Spleen/Bone marrow (Visceral Leishmaniasis)
4.Or to mucus membranes of face(mucocutaneous Leishmaniasis)
5.High death rate if untreated - Visceral Leishmaniasis (endemic/epidemic/opportunistic)
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1.Endemic
-worse in kids
-animal reserviors(dogs,other)
2.epidemic
-often human-fly-human transmition
-India, sudan
3.Opportunistic in AIDS
-S. europe, Brazil - Leishmaniasis diagnosis
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1.Culture
2.Leishmanin
3.PCR
4.Serology(ELISA/DAT)
5.Immunohistochemistry - Leishmaniasis Treatment
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1.Antimonials(pentostam, glucantine, long course)
2.Pentamidine
3.Amphotericin B(liposome) - Anaerobic Protozoa
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1.Trichomonas Vaginalis
2.Entamoeba Histolytica
3.Giardia Lamblia - Generic anaerobic life cycle
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Environment
1.Cyst:durable daughter cells
Host
2.Trophozoites:Motile reproductive, destructive - Parasites In MACS
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1.Toxoplasma Gondii-prevents fusion w/ lysosome
2.Trypanosoma Cruzi-fuse then escape to cyto
3.Leishmania-in phagolysosome - Trichomonas Vaginalis Characteristics (life cycle, epi, diagnosis)
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1.NO cyst
2.Most common STD in world
3.Easily trans. sexually
4.Diagnosis-wet smear - Trichomiasis in men/women
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1.Women
-yellow vag discharge(mimics yeast)
-itching
-burning
2.Men
-usually asympt
-may cause non-gonococcal urethritis - Trichomiasis Pathogenesis
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1.Lives in vaginal epithelium
2.Need pH=5-6 (usual vag pH=4-4.5)
3.Often coexists with yeast/bacterial overgrowths - Trichomiasis, possible virulence factors
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1.cysteine proteases
2.adhesins - Trichomiasis and the Hydrogenosome
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-reduces protons to H2 instead of reducing O2 to H2O
-Metronidazole(Flagyl) is reduced this way, often makes free rads - Entamoeba Histolytica life stages
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1.Trophozoite-pathogenic, 1 nucleus w/ central nucleolus
2.Cyst-infective, survive in envior, 1-4 nuclei - Amebiasis Pathogenesis
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1.Lumenal(noninvasive)
2.Invasive(hepatic) disease - Invasive Amebiasis
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1.Abscess in liver
-fever
-pain
2.can rupture,extend, or metastasize
3.Hard diagnosis-may be no sign in stool - Amebiasis Trophozoite characteristics/virulence factors
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1.Eat bact/dead cells
2.NO mito or Hydrogenosome
3.Virulence factors:
-amebapore
-cysteine proteases - Diagnosis of Amebiasis intestinal disease
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1.direct exam of stool
-can look like E. Dispar
-Need 3 specimins b/c low yeild
2.Sigmoidoscopically-obtained specimins
3.EIA-see E. Histolytica specific lectin - Diagnosis of Amebiasis Liver abscess
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1.Serology
2.Aspiration-most amoebae in wall of abscess - Giardia Lamblia Life cycles
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1.Trophozoites
2.Cysts - Giardia Lamblia characteristic
- NO mito or hydrogenosome
- Giardia Lamblia trophozoites characterisctics
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Inhabit Small Intestine, DON'T Invade
1. 4 pairs of flagella
2. 2 nuclei
3. Adhesive disc
4. Lectins - Giardia Lamblia Cysts characteristics
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Highly infectious(10cysts can cause infection)
1. 4 nuclei
2. resistant to Chlorine
3. Viable for months in Water - Giardiasis Epidemiology
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1. Most common intestinal parasite in world
2. usually kids
3. 2-44% of acute diarrhea - Giardiasis Transmitted by?
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1.usually by watter
2. or person to person
3. rarely in food - Giardiasis Reservoir
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1.Beaver
2.Rats, dogs, cats, pigs - Giardiasis in US/control
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1. 100 outbreaks since '65
-local water systems
-daycare centers
2. Control-latrines, boil/filter water - Giardiasis Pathology (acute)
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1-Lots of Trophs in stool
2-diarrhea
3-steatorrhea
4-nausea
5-flatulence
6-weight loss - Giardiasis Pathology (Chronic)
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1. Intermittent
2. Hard to Find
-Repeat O&P 3times
-duodenal aspiration to diagnose - Giardiasis in kids
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1.intestinal malabsorption of Vit B12&A,Iron,Fat,Sugar
-impaired devel of kids
2.Human Breast milk kills Trophozoites