This site is 100% ad supported. Please add an exception to adblock for this site.

Parasitology Lecture 3

Terms

undefined, object
copy deck
Trypanosomatids Types
1.African Trypanosomasis(sleeping sickness)
2.American Trypanosomasis (Chagas' disease)
3.Leishmaniasis (cutaneous, mucocutaneous, visceral)
Trypanosomatids Characteristics
1.Asexual reproduction
2.Single Flagella and Kinetoplast
3.Usually Vector-borne
Trypanosomatids Life cyle Forms
1.Amastigote(Mammal)(intracellular)
2.Promastigote(Vector)
3.Epimastigote(Vector
4.Trypomastigote(Mammal)
Trypanosomatids' Kinetoplast
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
Human/animal
-Trypomastigote
Tsetse Fly
-Epimastigote
-Metacyclic
-Trypomastigote
African Trypanosomatids Epidemic
Sudan, Uganda, Congo, Angola
>100,000 new cases/yr
African Trypanosomatids in West africa
T. Gambiense
-Reservoir=human
-Glossina Palpalis group, lives by rivers
-Chronic Disease-years to develope
African Trypanosomatids in East Africa
T. Rhodesiense
-Reservoir=wild animals
-Glossina Morsitans group, lives in savanna
-Acute Disease-developes in months
African Trypanosomatids Disease stages
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
1.Variant Surf Glycoprot-protective coat
2.parasite may have >1000 VSG genes
3.NO Vaccine possible
African Trypanosomatids Treatment
new=Eflornithine, DB 289
old(toxic)=suramin, pentamidine, melarsoprol
American Trypanosomatids cause by/disease
1.Caused by Trypanosoma Cruzi
2.Chagas' disease
American Trypanosomatids life cycle forms (Human/animal)
1.Trypomastigote
2.Amastigote
American Trypanosomatids Life cycle forms (Reduviid)
1.Epimastigote
2.Metacyclic
3.Trypomastigote
American Trypanosomatids Amastigote form characteristics
1.Live in MACS or Muscle cells
2.Fuse w/ Phagolysosome then ESCAPE to cytoplasm
3.Transform to trypomastigotes intracytoplasmically
American Trypanosomatids Spread by?
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
1.Romano's sign
2.parasitemia, febril illness
3.trypomatigotes in blood
American Trypanosomatids Chronic Disease
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)
1.parasites usually not in peripheral blood
2.Xenodiagnosis(old)
American Trypanosomatids Diagnosis (immunologically)
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
1.Dermatotrophic strains(only one in europe/asia)
2.Viscerotropic Strains(only one in Indai/mediterranean)
Leishmanial lifecycle types
Human/animal=Amastigote
Sandfly=Promastigote
Leishmanial Lifecylce specifics
1.Amastigotes
-Live in Phagolysosome
-Release when cell ruptures
2.NO trypomastigote form
Leishmaniasis, The disease
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
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)
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
1.Culture
2.Leishmanin
3.PCR
4.Serology(ELISA/DAT)
5.Immunohistochemistry
Leishmaniasis Treatment
1.Antimonials(pentostam, glucantine, long course)
2.Pentamidine
3.Amphotericin B(liposome)
Anaerobic Protozoa
1.Trichomonas Vaginalis
2.Entamoeba Histolytica
3.Giardia Lamblia
Generic anaerobic life cycle
Environment
1.Cyst:durable daughter cells
Host
2.Trophozoites:Motile reproductive, destructive
Parasites In MACS
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)
1.NO cyst
2.Most common STD in world
3.Easily trans. sexually
4.Diagnosis-wet smear
Trichomiasis in men/women
1.Women
-yellow vag discharge(mimics yeast)
-itching
-burning
2.Men
-usually asympt
-may cause non-gonococcal urethritis
Trichomiasis Pathogenesis
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
1.cysteine proteases
2.adhesins
Trichomiasis and the Hydrogenosome
-reduces protons to H2 instead of reducing O2 to H2O
-Metronidazole(Flagyl) is reduced this way, often makes free rads
Entamoeba Histolytica life stages
1.Trophozoite-pathogenic, 1 nucleus w/ central nucleolus
2.Cyst-infective, survive in envior, 1-4 nuclei
Amebiasis Pathogenesis
1.Lumenal(noninvasive)
2.Invasive(hepatic) disease
Invasive Amebiasis
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
1.Eat bact/dead cells
2.NO mito or Hydrogenosome
3.Virulence factors:
-amebapore
-cysteine proteases
Diagnosis of Amebiasis intestinal disease
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
1.Serology
2.Aspiration-most amoebae in wall of abscess
Giardia Lamblia Life cycles
1.Trophozoites
2.Cysts
Giardia Lamblia characteristic
NO mito or hydrogenosome
Giardia Lamblia trophozoites characterisctics
Inhabit Small Intestine, DON'T Invade
1. 4 pairs of flagella
2. 2 nuclei
3. Adhesive disc
4. Lectins
Giardia Lamblia Cysts characteristics
Highly infectious(10cysts can cause infection)
1. 4 nuclei
2. resistant to Chlorine
3. Viable for months in Water
Giardiasis Epidemiology
1. Most common intestinal parasite in world
2. usually kids
3. 2-44% of acute diarrhea
Giardiasis Transmitted by?
1.usually by watter
2. or person to person
3. rarely in food
Giardiasis Reservoir
1.Beaver
2.Rats, dogs, cats, pigs
Giardiasis in US/control
1. 100 outbreaks since '65
-local water systems
-daycare centers
2. Control-latrines, boil/filter water
Giardiasis Pathology (acute)
1-Lots of Trophs in stool
2-diarrhea
3-steatorrhea
4-nausea
5-flatulence
6-weight loss
Giardiasis Pathology (Chronic)
1. Intermittent
2. Hard to Find
-Repeat O&P 3times
-duodenal aspiration to diagnose
Giardiasis in kids
1.intestinal malabsorption of Vit B12&A,Iron,Fat,Sugar
-impaired devel of kids
2.Human Breast milk kills Trophozoites

Deck Info

57

permalink