Parasitology

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  1. What are the four vertically transmitted parasites?
    • Toxoplasmosa spp.
    • Plasmodium spp.
    • Trypanosoma spp. 
    • Trichomonas vaginalis
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    Triatoma (reduviid)

    vector for American Trypanosomiasis (Chagas disease)
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    • Trypanosoma cruzi
    • (Trypomastigote phase)
    • found in bloodstream
  4. What is another name for triatomas?
    vector for American Trypanosomiasis (Chagas disease)

    "kissing bugs"
  5. How is Trypanosoma cruzi transmitted?
    via feces of triatomas
  6. What are the reservoir hosts of Trypanosoma cruzi?
    • armadillo
    • agouti
    • rats
    • opossum
    • dogs/cats
  7. What is the growth cycle of Triatomas?
    • hemimetabolous growth
    • egg --> nymph --> bigger nymph --> adult
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    • Typanosoma cruzi amastigote stage
    • after invasion of muscle/nerve tissue
    • destroys tissue during binary fission 
  9. What are the predilection sites for Trypanosoma cruzi?
    • muscle/nerves
    • specifically:
    • myocardial tissue
    • myenteric plexus (peristalsis)
  10. How is Trypanosoma cruzi diagnosed?
    • in acute stage
    • Direct:
    • blood smear (thin/thick)
    • xenodiagnosis (use triatoma for PCR)
    • serology Ag
    • DNA probes

    • Indirect:
    • Serology Ab
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    • Trypanosoma rangeli
    • apathogenic
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    • changoma (Romana's sign)
    • first sign of Trypanosoma cruzi
  13. What is the acute clinical presentation of Trypanosoma cruzi?
    • fever
    • anemia
    • edema
    • lymphadenopathy
    • hepatosplenomegaly
    • EKG abnormalities
    • CNS involvement
  14. What can occur after the acute phase of Trypanosoma cruzi?
    • Indeterminate phase (asymptomatic)
    • Chronic phase (30%)
  15. What are the clinical manifestations of chronic Trypanosoma cruzi?
    • fever
    • loss of myenteric plexus:
    • constipation
    • abdominal distention
    • megacolon/megaesophagus
    • loss of myocardium:
    • EKG abnormalities
    • Cardiomegaly
    • apical aneurysm
  16. How is Trypanosoma cruzi transmitted?
    • Triatoma bites
    • blood transfusion
    • congenital transmission
    • lab transmission
    • organ transplant
  17. Where to Triatomas live?
    • South/Central American rainforests
    • Trinidad
    • *houses built in rainforests
  18. How is Trypanosoma cruzi treated?
    • Benzimadazole
    • Nifurtimox
    • - treatment in acute phase
    • - Tryptomastigotes only
  19. What are the two types of African Trypanosomiasis?
    • Trypanosoma brucei rhodensiense
    • (Rhodesian sleeping sickness)

    • Trypanosoma brucei gambiense
    • (West African/Gambian sleeping sickness)
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    • Tsetse fly
    • - "meat cleaver" on wing
    • - holometabolous growth (egg --> larva --> adult)
    • vector for African trypanosomiasis (sleeping sickness)
  21. What is the reservoir for T.b. rhodesiense (Rhodesian sleeping sickness)?
    • wild animals (antelope/bushbuck)
    • does not cause clinical symptoms

    causes disease in domestic animals
  22. What is the reservoir for T.b. gambiense (West African/Gambian sleeping sickness)?
    • Pigs
    • (humans are main reservoir)
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    • trypanosomal chancre
    • erythematous tsetse bite
    • clinical symptom of African trypanosomiasis
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    • Winterbottom's sign
    • enlarged cervical lymph nodes
    • first clinical sign of African trypanosomiasis
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    • Trypanosoma brucei 
    • rhodesiense/gambiense

    ONLY as trypomastigotes
  26. How is African trypanosomiasis diagnosed?
    • Direct:
    • T.b. rhodensiense/gambiense
    • in blood smear/buffy coat
    • gland juice aspiration
    • CSF
    • PCR
    • Indirect:
    • IgM ELISA (not useful)
  27. What are the clinical manifestations of African trypanosomiasis?
    • T.b. rhodensiense - acute (weeks)
    • T.b. gambiense - chronic (months)
    • fever
    • anemia
    • wasting
  28. What is the treatment for African trypanosomiasis?
    • I.V. Suramin
    • I.V. Eflornithine (expensive!)
    • both do not cross BBB
  29. What is the treatment for African trypanosomiasis with CNS involvement?
    • Suramin
    • Eflornithine
    • Melarsoprol (crosses BBB)
  30. How is African trypanosomiasis controlled?
    • biconical traps for tsetse flies
    • insecticide
  31. What are the different types of Leishmania?
    • Kala-azar (black fever)
    • Old world cutaneous
    • New world mucocutaneous
  32. What are the parasites that cause Kala-azar?
    • type of Leishmaniasis
    • Leishmania donovani
  33. What are the parasites that cause old world cutaneous Leishmaniasis?
    • Leishmania tropica
    • L. major
    • L. aethiopica
  34. What are the parasites that cause new world mucocutaneous Leishmaniasis?
    • aka "Espundia"/"Uta"
    • Leishmania braziliensis
  35. What are the predilection sites for Leishmania spp?
    • Vertebrate host:
    • WBC (amastigotes)
    • --> migrate to skin macrophages/inner organs (4-6 days)

    • Vector:
    • Saliva (promastigote)
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    • Leishmania spp. in WBC
    • --> lysis after 48 hours
    • --> migrate to skin (cutaneous)
    • --> 4-6 days - migrate to organs (visceral)
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    Leishmania promastigotes in saliva of sand flies
  38. How is L. donovani (Kala-azar) diagnosed?
    • spleen/bone marrow aspirate
    • to visualize amastigotes
    • rK39 dipstick
  39. What are the clinical symptoms of Kala-azar (L. donovani)?
    • early:
    • double daily fever spikes
    • anemia/leukopenia
    • diarrhea
    • joint pain
    • late: hepatosplenomegaly
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    • Fever spikes of Kala-azar
    • (L. donovani)
    • visceral leishmaniasis
  41. What is the treatment for L. donovani (Kala-azar)?
    • Amphoteracin B
    • --> highly toxic and expensive
    • Pentostam (antimonial compound)
    • --> cheaper/not well tolerated
    • --> developed by One World Health via Bill & Melinda Gates
    • Paramomycin
    • Miltefosine (oral)
  42. Where are sandflies found?
    • vector for L. donovani
    • Ethiopia, South Sudan, Kenya
    • near termite hills
  43. What are the clinical symptoms of Leishmania major?
    • old world cutaneous Leishmaniasis
    • small red papule
    • ulcerates (2 weeks)
    • serous exudate
  44. What are the clinical symptoms of Leishmania tropica?
    • Old world cutaneous Leishmaniasis
    • small red papule
    • ulcerates (2-4 months)
    • dry ulcer
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    • Leishmania major
    • ulceration in 2 weeks
    • with serous exudate
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    • Leishmania tropica
    • ulceration in 2-4 months
    • dry exudate
    • immune response
  47. What is another name for L. tropica exudates?
    oriental sore
  48. How are L. tropica and L. major diagnosed?
    • fluid aspiration from ulcer
    • look for amastigotes
  49. What is another name for Leishmania braziliensis?
    Espundia or Uta
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    • Lesions from L. braziliensis
    • oral or nasal appear in 3-20 years
  51. What are the clinical signs of L. braziliensis?
    • new world mucocutaneous
    • small cutaneous papule
    • ulcerates in a few months
    • leaves asymptomatic scar
  52. What are the differential diagnoses for L. braziliensis?
    • fungi
    • syphillis
    • yaws
    • leprosy
    • malignancy
  53. What are the treatments for L. tropica, L. major, L. aethiopica, and L. braziliensis?
    • Amphoteracin B
    • --> toxic/expensive
    • Pentostam (antimonial compound)
    • --> cheaper/not well tolerated
    • --> One World Health (Gates foundation)
    • Paramomycin
    • Miltefosine (oral)
  54. What are the reservoir hosts of Leishmaniasis?
    • sloths, rodents, dogs
    • found in rainforests
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    • Trichomoniasis
    • Trichomonas vaginalis
  56. How is Trichomonas vaginalis transmitted?
    • sexual transmission
    • mother --> infant
  57. What are the clinical symptoms of Trichomonas vaginalis?
    • vaginitis
    • burning
    • thick yellow discharge
    • vulvular/vaginal erythema
    • males asymptomatic
  58. How is Trichomonas vaginalis diagnosed?
    • Direct:
    • trophozoites in urine or vaginal discharge
  59. How is Trichomonas vaginalis treated?
    Metronidazole (Flagyl)
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    • Giardia lambia
    • Giardiasis
    • trophozoite form
    • found in diarrhea
    • not infective
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    • Giardia lambia
    • Giardiasis
    • cyst form
    • found in normal stool
    • infective
  62. What is the prevalence of Giardia lambia?
    • "traveller's diarrhea"
    • 2-7% USA, Canada, Europe, Australia
    • 40% developing countries
    • common in day-care centers
  63. What are the animal reservoirs for Giardia lambia?
    • beavers
    • dogs
    • animal form doesn't last as long
  64. When should G. lambia be suspected?
    • chronic (intermittent) diarrhea
    • unexplained weight loss
    • unresponding malnutrition
    • malabsorption
  65. How is G. lambia diagnosed?
    • Direct: stool microscopy
    • --> low specificity/sensitivity (cysts not always present)
    • Indirect: ELISA
    • Immunofluorescent slide
    • --> expensive
    • --> high sensitivity/specificity
    • Therapeutic Trial
    • = treat it!
  66. What are the symptoms of G. lambia?
    • pale loose stools 3-8x daily
    • flatulence
    • abdominal distention
    • abdominal pain
    • weight loss
    • "sulphorous belching"
    • +/- malabsorption syndrome
  67. How is G. lambia treated?
    • Metronidazole (Flagyl)
    • Tinidazole (Tindamax)
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    • Cryptosporidium parvum 
    • in GI tract (enterocytes)
  69. How is cryptosporidium transmitted?
    • water-borne epidemic
    • 1-3% diarrheas in developed countries
    • 17% diarrheas in developing countries
  70. What are the animal reservoirs of cryptosporidium?
    • humans
    • bovine
    • dog-like genotypes
    • mostly in young animals
  71. How does autoinfection occur with cryptosporidium?
    • thin walled oocysts reinvade gut
    • oocysts excreted
    • --> fecal-oral contamination

    anti-diarrheal drugs
  72. How is cryptosporidium diagnosed?
    • Oocysts in stool (modified Ziehl-Neelsen stain)
    • ELISA (Ag test)
    • Immunofluorescent test (IFAT)
    • --> most sensitive
  73. What are the clinical symptoms of cryptosporidium?
    • 1-2 weeks after exposure
    • --> explosive diarrhea 2-10x daily
    • --> fever, abdominal pain, anorexia, vomiting 
    • 1 day - several weeks
  74. What are the clinical symptoms of cryptosporidium for immunodeficient individuals?
    • large volume diarrhea
    • --> hypovolemic shock
    • weight loss
    • malabsorption
    • villous atrophy
  75. How is cryptosporidium parvum treated?
    it's not

    no anti-diarrheal drugs
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    • Amoebiasis
    • Entamoeba histolytica
  77. What are the two types of Amoebiasis (Entamoeba histolytica)?
    • Intestinal amoebiasis =
    • amoebic dysentary

    • Liver amoebiasis =
    • Amoebic liver abscess (ALA) 
  78. What is the prevalence of Amoebiasis?
    • one of most prevalent 
    • affects 10% world population
    • mostly in tropics
  79. How is Amoebiasis transmitted?
    • Fecal-oral ingestion
    • (fluid, fingers, flies, fields)
    • not zoonotic 
  80. How is intestinal amoebiasis diagnosed?
    • Direct:
    • cysts in stool
    • trophozoites in RBC (blood smear)
    • ELISA (highly sensitive/specific)
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    • Entamoeba histolytica cysts
    • found in stool samples
  82. What are the clinical manifestations of intestinal amoebiasis?
    • 95% asymptomatic
    • diarrhea (inconsistant; <12x daily) 
    • flatulence 
    • abdominal pain
    • no fever

    • blood/mucus in stool
    • tear drop ulcers in gut
  83. What are the clinical manifestations of amoebic abscesses?
    • amoebic abscesses in:
    • liver, brain, skin, lungs, orbit, spleen, genitals
    • fever
    • liver pain/tenderness
    • hepatomegaly
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    • liver abscess 
    • 2* to Entamoeba histolytica
    • detect via ultrasound
  85. How is amoebiasis diagnosed?
    • Direct:
    • abscess aspiration under US
    • trophozoites

    • Indirect:
    • imaging with serological confirmation
    • -ultrasound (liver)
    • -X-ray/CT/MRI (brain/lung)
  86. How is intestinal amoebiasis treated?
    • metronidazole (Flagyl)
    • paromomycin (Humatin)
  87. How are amoebic liver abscesses treated?
    chemotherapy with metronidazole (Flagyl)

    drainage of abscess via ultrasound
  88. How is Entamoeba histolytica controlled?
    • hygiene
    • boiling/filter water
    • no "night soil" fertilization
  89. What is the life cycle of Toxoplasmosa gondii?
    • cat ingests bradyzoites (meat) or tachyzoites (raw milk)
    • --> cat sheds unsporulated oocyst
    • oocyst sporulates in 1-5 days
    • all forms infective
  90. What is the prevalence of Toxoplasmoa gondii?
    • zoonotic
    • >30% world population infected
    • 3-20% AIDS patients die of toxoplasmosa associated encephalopathy
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    • Toxoplasma gondii
    • oocysts
    • sporocysts
    • sporozoites
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    • Toxoplasma gondii
    • tachyzoites (raw milk)
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    • Toxoplasma gondii
    • bradyzoites (meat)
    • no inflammation present around cyst
    • tachyzoites already present in WBC
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    • Tachyzoites transported via leukocyte
    • predilection sites: brain/eye
  95. What is the largest risk factor of toxoplasmosis?
    eating raw lamb, pork, goat
  96. When is a fetus most at risk for contracting toxoplasma gondii?
    • Transmission rate:
    • increases with time (more placental development)
    • % severe infections:
    • decreases with time (development of fetal immune system)
  97. What are the severe outcomes of fetal toxoplasm gondii?
    • chorioretinitis
    • hydrocephalus
  98. How does hydrocephalus occur with toxoplasma gondii?
    • bradyzoites enter periventricular areas
    • --> obstruction of 3rd ventricle 

    treat with ventriculoperitonel shunt
  99. How is toxoplasma gondii detected?
    • IgG, IgM serology
    • IgM present at initial infection

    • CT with contrast
    • MRI
    • tissue biopsy (bradyzoites)
  100. When should maternal testing occur for toxoplasma gondii?
    • (-) IgG --> test monthly for IgM
    • (+) IgG --> r/o recent or active infection
    • (+) IgM --> prophylaxis and f/u with infant
  101. How is toxoplasma gondii prevented?
    Prophylaxis with spiramycin
  102. How does Plasmodium spp. enter mosquitos?
    gametocytes formed by merozoites in the bloodstream ingested by mosquitos
  103. What form of Plasmodium spp. enters humans from mosquitos?
    sporozoites in mosquito salivary glands
  104. Where do Plasmodium spp. sporozoites go once inside human?
    • liver parenchyma
    • occurs within 30 minutes
  105. What happens to Plasmodium spp. in the liver?
    • sporozoites can either:
    • 1. asexual reproduction -->
    • merozoites within schizont
    • 2. formation of hypnozoite (P. vivax/ovale)
  106. How long does the liver cycle last for Plasmodium spp.?
    • 8 days
    • for P. falciparum
  107. How is Plasmodium spp. infection passed onto the blood?
    • 1. schizont releases merozoites
    • 2. merozoites invade erythrocytes
  108. What happens in the erythrocytic cycle of Plasmodium spp.?
    • in erythrocytes:
    • 1. merozoites --> tropnozoites --> schizonts
    • 2. erythrocyte lysis
    • 3. merozoites released
  109. How long does the erythrocytic cycle take for Plasmodium spp.?
    36 hours for P. falciparum
  110. What happens in the mosquito life cycle of Plasmodium spp.?
    • 1. gametocytes liberated --> micro/macrogamete
    • 2. micro/macrogamete unite --> zygote
    • 3. zygote --> ookinete
    • 4. ookinete penetrates gut wall
    • 5. ookinete --> oocyst
    • 6. oocyst --> oocyte
    • sporozoites created within oocyte
  111. How long is the mosquito stage of Plasmodium spp.?
    5 days
  112. How long does it take to get symptoms of Plasmodium spp. after a bite?
    • 8 days of hepatic cycle
    • 36 hours of erythrocytic cycle
    • => 11 days total
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    • Anopheline mosquito
    • vector for Plasmodium spp.
    • (P. falciparum, P. vivax, P. ovale, P. malariae)
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    • Plasmodium falciparum
    • - rings with double chromatin dots
    • - marginal forms
    • - RBC not enlarged
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    • Plasmodium falciparum
    • gametocytes
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    • Plasmodium malariae 
    • - band shaped
    • - RBC not enlarged
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    • Plasmodium ovale
    • - "oval" red cell
    • - enlarged RBC
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    • Plasmodium vivax
    • - thick (signet) ring
    • - enlarged RBC
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    hypnozoite in liver

    • dormant form of Plasmodium vivax/ovale
    • allows for reoccurrence 
  120. How does the anopheline mosquito reproduce?
    • gonotrophic cycle
    • egg --> larvae --> adult
    • eggs laid in standing water
  121. Where is Plasmodium falciparum found?
    • Africa
    • New Guinea
    • Haiti
  122. Where is Plasmodium vivax found?
    • Central America
    • Southern Asia
  123. Where is Plasmodium ovale found?
    • West Africa
    • **instead of Plasmodium vivax
    • --> P. vivax merozoites cannot infect 2* to "duffy" blood group
  124. Where is Plasmodium malariae found?
    widespread
  125. What are the clinical signs of Plasmodium spp. infection?
    • anemia
    • hepatosplenomegaly
  126. How does the fever cycle relate to the life cycle of Plasmodium spp.?
    • 1. release of merozoites --> decreased body temperature
    • 2. immune response --> fever spike
    • 3. immune response maintenance --> sweating phase
  127. Why does the body temperature decrease when merozoites of Plasmodium spp. are released?
    • Immune system shunts blood to core (protection)
    • skin dry, pale, cold
    • pulse rapid, low volume
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    • P. falciparum fever chart
    • persistant fever
    • fever decreases every 2 days
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    • P. malariae fever chart
    • slight peaks every 24 hours
    • large peak at 72 hours
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    • P. vivax/ovale fever chart
    • fever peaks every 2 days
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    • microcirculatory arrest
    • 2* to P. falciparum infection
    • hemolysis --> dead tissue aggregation
  132. What organs are affected by Plasmodium spp.?
    • kidneys --> renal failure
    • liver --> jaundice/fever
    • lungs --> pulmonary edema
    • stomach/intestines --> vomiting/diarrhea
    • brain --> delirium, stupor, disorientation, coma, convulsions
  133. When is cerebral malaria suspected?
    Patient suspected of malaria shows reduced consciousness 
  134. How does cerebral malaria manifest?
    • coma (eyes open; unseeing)
    • convulsions
    • abnormal posturing
    • dysconjugate gaze
    • retinal hemorrhages
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    • Cerebral malaria
    • schizont adhered to brain endothelium
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    • Decerebrate rigidity
    • 2* to cerebral malaria
    • --> rigidity of extensors
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    • Decorticate rigidity
    • 2* to cerebral malaria
    • --> rigidity of flexors
  138. What is the fatality of cerebral malaria?
    • 20% fatal
    • 10% of children with lingering neuropsychological deficits
  139. What are the risks of malaria with pregnant women?
    • maternal mortality
    • abortion
    • stillbirth
    • premature delivery
    • low birthweight
    • vertical transmission
  140. What are the direct effect of malaria on pregnant women?
    • depressed immunity
    • parasitization of placenta --> movement hindered
    • premature delivery
  141. What is the treatment for P. falciparum?
    • chemotherapy ASAP!
    • **resistance to chloroquine 
  142. What is the function of quinine (Quinadine)?
    • destroys blood stages of Plasmodium spp. 
    • - no resistance
    • - reserve drug
  143. How is Plasmodium malariae treated?
    • Chloroquine
    • destroys all blood stages
    • "magic bullet"
  144. How are Plasmodium ovale/vivax treated?
    • Chloroquine (blood stages)
    • Primaquine (hypnozoites)
    • --> prevents relapse/reoccurrence
  145. What is the treatment for Plasmodium falciparum?
    • Quinine, Quinadine
    • Artemether/lumefantrine (coartem)
    • **ACT - Artemisinin-based Combination Therapy
  146. How is malaria treated prophylactically?
    • Mefloquine (Lariam)
    • Doxycycline
    • Chloroquine (Aralen)
    • Atovaquone/proguanil (Malarone)
    • **P. falciparum resistant to chloroquine
  147. What are the side effects of malaria prophylaxes?
    • Mefloquine - neuropsychiatric problems
    • Chloroquine - itchy skin
    • Pauladrine - mouth ulcers
  148. What are the differences between stable and unstable malaria?
    • unstable:
    • seasonal transmission
    • epidemics
    • low immunity
  149. How does the sickle cell AS phenotype protect against malaria?
    • RBC sequestered in RE system
    • low pH area --> hinders parasite growth
    • fast splenic clearance
  150. How was malaria eliminated in Grenada?
    • swamp, drain, fish filling
    • DDT spraying
  151. What are autocthonous cases of malaria and why are they a problem?
    • imported malaria (especially from Jamaica)
    • merozoites must be present in blood prior to screening
  152. How is malaria diagnosed?
    • clinical:
    • fever
    • anemia
    • hepatosplenomegaly 
    • direct:
    • PCR to detect DNA
    • Rapid tests: parasite antigen
    • Parasites in blood smear
  153. When do anopheline mosquitos bite?
    • at night
    • (put up nets with pesticides as prevention)
  154. For trematodes, what form infects snails?
    miracidia
  155. For trematodes, what form infects crabs/fish/fluke?
    • cercaria 
    • fluke also infected by metacercaria
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    • Schistosoma haematobium
    • terminal spine
    • not zoonotic - only infects bulinus snails
    • found mostly Africa and Middle East

    leads to urinary syndromes
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    • Bulinus snail
    • host of Schistosoma haematobium
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    • Schistosoma masoni
    • egg has lateral spine
    • leads to liver pathologies
    • infects biomphalaria snail
    • mostly Africa and South America
  159. How widespread is Schistosoma masoni?
    • South America, Caribbean islands, Africa
    • reservoirs: humans, rodents, baboons
    • causes intestinal schistosomiasis (most important)
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    • biomphalaria snail
    • host of Schistosoma masoni
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    • Schistosoma japonicum  
    • leads to liver pathologies
    • infects oncomelania snails
    • Southeast Asia
  162. Where does reproduction occur for the schistosomes?
    • in the liver
    • --> migrates to final predilection site
  163. How is Schistosoma haematobium diagnosed?
    • direct:
    • eggs in urine

    • indirect:
    • serology
    • gross hematuria
    • dipstick
    • imaging
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    • Ultrasound of Schistosoma haematobium
    • check for areas of bladder wall thickening/polyps
  165. How are Schistosoma mansoni/japonicum diagnosed?
    • direct:
    • eggs in stool
    • rectal biopsy
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    • pipe-stem fibrosis
    • Schistosoma masoni/japonicum
    • 2* to eggs being swept back into liver
    • (normally --> mesenteric veins)
    • become calcified
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    • Phnom Pehn-Vientiane
    • Schistosoma japonicum
    • calcification of capillaries
    • --> "fishnet" appearance
  168. Which of the Schistosomas lead to the highest morbidity/mortality?
    Schistosoma japonicum
  169. What is the progression of schistosomiasis?
    • 0-3 days: swimmer's itch
    • (penetration of schistosomulum)
    • 3-10 days: schistosomular pneumonitis
    • (migration of schistosomulum)

    3-6 weeks: acute schisto (Katayama Fever)
  170. What are the characteristics of acute schisto (Katayama Fever)?
    • 2* to egg laying
    • acute febrile reaction
    • eosinophilia
    • lasts 3-8 week
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    • Chronic Schistasomiasis
    • --> eggs trapped
    • --> inflammation (granulomatous/fibrosis)
  172. What are the characteristics of chronic infection by Schistasoma haematobium?
    • thickened bladder wall
    • polyps (--> cancer)
    • ureter obstruction
    • hydronephrosis
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    • hydronephrosis 
    • 2* to chronic Schistasoma haematobium
  174. What are the manifestations of chronic Schistasoma masoni/japonicum?
    • periovular granuloma
    • - hepatosplenic inflammation
    • - hepatosplenomegaly
    • - liver fibrosis
    • - portal hypertension
    • 2* to eggs trapped in mesenteric veins/portal vein and branches
  175. How are Schistasoma spp. treated?
    • Praziquantel
    • --> effective for children

    existing fibrosis not reversible
  176. What factors influence the prevalence of schistasomiasis?
    • Schistasoma spp. favor:
    • - low altitude
    • - rainy area
    • - proximity to lake
  177. How was Schistasoma japonicum eliminated in Japan?
    • water buffalo are intermediate hosts
    • --> start using tractors

    • China control program:
    • treat/vaccinate water buffalo
  178. When are schistasoma spp. cercaria shed?
    in the midday
  179. What are methods for controlling Schistasoma spp.?
    • kill parasite (Praziquantel)
    • - treat school-age children 2-3x
    • kill snails
    • prevent contamination (drinking water/latrines)
    • protect from infection

    funded by Gates Foundation/World Bank
  180. Why are children more likely to get Schistasomiasis?
    • reinfection for adults lower
    • - possible immune response
    • children more likely to play in water (behavioral difference)

Card Set Information

Author:
akl273
ID:
193967
Filename:
Parasitology
Updated:
2013-01-23 22:26:57
Tags:
parasitology
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Description:
parasitology
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