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Flashcards

Gut Protozoa

tate0295 Medical Parasitology MSc English 45 cards

Cards in this deck (45)

  1. 1Entamoeba histolytica/dispar epidemiologyUsed to be believed that 10% of world population had E. histolytica - but actually E. dispar; >90% cases are aymptomatic; Formal recognition of two different species in 1997 - differentiation is important in deciding whether to treat
  2. 2Differentiation of E. histolytica from disparNot possible from morphology; By antigen - in stool, most commonly targeting galactose specific lectin; By DNA - PCR usually on ribosomal subunits
  3. 3Entamoeba moshkovskiiMostly free living; First ID in humans in 1956, but now commonly found worldwide; Pathogen status uncertain, but causes a problem for histolytica/dispar diagnosis, as is very similar
  4. 4E. histolytica/dispar/moshkoskii trophozoitesRing and dot nuclei (unique to entamoeba); Food vacuoles; Uroid (where indigestible bacterial material is deposited); Have no fixed shape or dimensions
  5. 5E. histolytica/dispar/moshkoskii cystsAll forms cysts to be excreted in faeces to continue lifecycle; 10-15um; Mature cysts has 4 ring and dot nuclei; May have chromatoid bars
  6. 6E. histolytica/dispar lifecycleSpread due to poor hygiene; Cysts defacated and ingested, excyst in the large intestine and multiply by binary fission, encystation; May be 'accidental' tissue invasion in histolytica (intestinal wall, liver etc.)
  7. 7Asymptomatic E. histolytica infectionCysts in faeces only; Normal stool; May or may not be seropositive (could also be historical infection); Is the case for >90% infections
  8. 8Invasive E. histolytica infection in intestineAmoebic dysentery/colitis - bloody diarrhoea with mucus, colon has flask shaped ulcers, trophs with visible ingested RBCs; Not enough for diagnosis - may see E. dispar in a Shigella infection causing pathology
  9. 9Invasive E. histolytica infection in liverAmoebic liver abcess - One or more lesions, usually right lobe of liver; Filled with necrotic, liquified tissue; Few amoebae present except in periphery
  10. 10Invasive E. histolytica infection in other tissuesOccasional dissemination into other tissues including the brain, lungs, pericardium or spleen; Can invade almost any organ
  11. 11E. histolytica treatmentFor invasive disease - metronidazole, followed by a drug to treat lumenal infection; For lumenal infection - Diloxanide furoate, Paromomycin
  12. 12Process of E. histolytica tissue invasionNormally sits in mucosal layer; Likely that some kind of disruption allows amoebae to bind epithelial layer (lectin binding), release of lytic enzymes (normally directed to lysosome); Leads to recruitment of neutrophils and destruction, further contributing to tissue destruction; Crosses the mucosae 10% of the time
  13. 13Diagnosis of pathogenic amoebiasisSerology - good for liver abcess, but problems with historical infection; Ag detection - Can differentiate, but needs time for Ag levels to rise, not good for early detection; PCR - general pos and neg
  14. 14Causes of variability in pathogenicity of E. histolyticaPossibly: strain, immune response (modulation, variability), Genetic predisposition, diet, secondary infection, chance?
  15. 15BlastocystisVery common; Pathogenicity controversial, but possible link to IBS; Hard to ID
  16. 16Giardia intestinalis life cycleCysts passed in stool and ingested (in water or faecal-oral); Excyst in small intestine, probably triggered by gastric acids; Multiplication by binary fission; Encystation towards colon
  17. 17Giardia trophozoite morphologySmiley face; 8 Flagella; Axoneme - diagnostic feature; 2 nuclei; Ventral disk - point of attachment to lumen
  18. 18Giardia cyst morphology4 nuclei; Median bodies and axoneme; 8-12um
  19. 19Symptoms of GiardiasisDiahorrea; Malaise; Flatulence - malabsorption of food; Foul smelling faeces; Weight loss; Extraintestinal symptoms involving eyes, skin, joints, urinary tract
  20. 20Possible pathogenic mechanisms of GiardiasisApoptosis of enterocytes - loss of epithelial barrier; Hypersecretion of Cl-; Malabsorption of glucose, water & Na+; Immunopathology (T cells, mast cells, IgA, NO)
  21. 21Diagnosis of GiardiasisMostly by wet microscopy - 3 specimens, with 2 days between (intermittent shedding); Cysts easily recognisable; ELISA or card agglutination (RDT), PCR
  22. 22Epidemiology of GiardiasisTypical in developing countries; Many young children infected; Children shed many cysts, but adults fewer; Mainly person to person transmission
  23. 23Giardia immunologyDecline in cyst shedding into sdulthood suggests some immunity developing - but is not complete or rapidly acquired; Genome contains ~200 variants of VSP coats - vaccine target? Express all variants to induce complete protection
  24. 24Epidemiology of epidemic GiardiasisOccurs worldwide (unusual), even in UK; All ages affected; Transmission by food or person to person; Most big outbreaks are waterborne
  25. 25Reasons why Giardia is easily acquiredInfectious dose is very small - ~10 cysts; Cysts resist chlorine and other disinfectants; Cysts are viable even in cold water for weeks; Animal reservoirs for some species
  26. 26Giardia infective assemblagesAssemblage A - A1 mostly in livestock & pets, A2 mostly in humans; Assemblage B - Mainly in humans and other primates; Mixed infections are likely and gnetic exchange may occur; Globally, human infection is more likely with assemblage B
  27. 27Treatment of GiardiasisMetronidazole still widely used; Tinidazole may be more effective (longer half life); Paromomycin
  28. 28Human infective TrichomonadsT. vaginalis - most common & important; T. tenax - in mouth; Pentatrichomonas hominis - Found rarely in faeces
  29. 29Trichomonas tenaxInhabits crevices around teeth; Not generally believed to be pathogenic; Very rarely spreads to lungs; Most common in men with poor oral hygiene
  30. 30Pentatrichomonas hominisIhabits large bowel; No cycts, but trophs; Not believed to be pathogenic, but associated with diahorrea in dogs
  31. 31Clinical Trichomonas vaginalisMost common in women, but also in men; Most infections asymptomatic; In women - vaginal discharge, vaginal & vulvar erythema; In men - rarely urethral discharge
  32. 32Diagnosis of Trichomonas vaginalisWet film microscopy - most widely used, mjst be rapid, poor sensitivity but 100% specific; Culture - usually in prepared culture pouches, for at least 5 days; Some RDTs; Mostly relies on site of infection to distinguish
  33. 33Epidemiology of Trichomonas speciesAlmost exclusivelt sexually tranismitted - hard to detect conventionally in males, but PCR detects in 72% males with infected partners; Transmission theoretical by sharing clothes, bedding etc.; Very rare but genuine neonatal infections; Peaks of infection in women in later life (unlike all other STIs); Decline of infection in developed world
  34. 34Trichomonas and HIVA concensus that trichomoniasis increases risk of HIV tranmission; Is very common in HIV+ population; Bacterial vaginosis is also common in this population, synergistically increasing the risk
  35. 35Treatment of TrichomonasUsually metronidazole, but tinidazole more effective; Resistance rare, but real problem as no alternatives
  36. 36Dientamoeba fragilisFlagellate, but no flagella; Related to Trichomonas; Does not normally forms cysts; Pathogenicity is controversial, but probable; May be transmitted by enterobius eggs - very high levels of co-infection
  37. 37Balantidium coliCiliate - the only one to normally infect humans; Common in pigs; Can very rarely invade gut tissue, causing dysentery
  38. 38Retortomonadida - Chilomastix and RetortomonasCommon flagellates in humans; Neither thought to be paths;
  39. 39Free living pathogenic amoebaeRare; Naegleria fowleri, Acanthamoeba spp.; Balamuthia mandrillaris; Sappinia spp. (only 1 recorded infection); Usually very high mortality
  40. 40Naegleria fowleriIn warm, stagnant water, contaminated with sewage/organic matter; Infection by water entering nasal passages/sinuses; Migrates along olfactory nerve to brain, causing PAM
  41. 41Primary Amoebic Meningoencephalitis (PAM)Caused by N. fowleri; Often affects young, active people; Almost invariably fatal; Very rare - exposure must be frequent; Due to low infection rate and survival, treatment uncertain - amphotericin B current best choice
  42. 42Granulomatous Amoebic Encephalitis (GAE)Caused by Acanthamoeba spp., Balamuthia mandrillaris, Sappinia pedata; Linked almost exclusively to immunosuppression - HIV, alcoholics, diabetics; Chronic - slow deterioration; Usually fatal; Miltefosine & pentamidine most common treatments
  43. 43Acanthamoeba spp.Widely distributed - soil, water and air; Trophs and resistant double walled cysts; Can cause Granulomatous Amoebic Encephalitis or Amoebic keratitis (often in contact lense wearers); Infection is intranasal or break in the skin; Cysts form in tissue, making treatment diffiuclt
  44. 44Balamuthia mandrillarisFlagellate; Can cause GAE; Inects immunosupressed and immunocompetant; Manifest as skin lesions, followed by infection to brain; High mortality; Appears to be some asymptomatic infection, without GAE
  45. 45Trichomonas vaginalis virusType I strain T. vaginalis more sensitive to metronidazole than type II; Type II strain more likely to be infected with T. vaginalis virus; Shown that human epithelial cells induce inflammatory responses to TVV - complications in pregnant women, esp. as metronidazole exacerbates inflammation

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MSc Medical Parasitology Flashcards on Gut Protozoa, created by tate0295 on 01/05/2015.
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