Flashcards in Intestinal Protozoa Deck (62)
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1
List medically important protozoa and their diseases
(a) Amoebas: Entamoeba histolytica, Naegleria,
Acanthamoeba.
(b) Flagellates: Trypanosoma cruzi
(c) Sporozoa: Toxoplasma gondii
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Protozoa - classify by motility
(a) Mastigophora (flagella) - Trypanosoma cruzi, Giardia lamblia
(b) Sarcodina (pseudopodia) - Amoebas
(c) Apicomplexa (microtubule complex, commonly
referred to as sporozoa) - Toxoplasma gondi, Plasmodium
(d) Ciliophora (ciliates) - Balantidium coli
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Ciliophora spp
Balatidium coli
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Apicomplexa spp
Split into two categories
Coccidia
Isospora belli
Toxoplasma gondii
Sarcocystis spp.
Cryptosporidium parvum
Pneumocystis carinii
Piroplasma
Plasmodium falciparum
Plasmodium vivax
Plasmodium malariae
Plasmodium ovale
Babesia microti
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Kinetoplastida spp
(Flagellated)
Trypanosoma gambiense
Trypanosoma rhodiense
Trypanosoma cruzi
Leishmania spp
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Amoebic abscess (amoebiasis, amoebic dysentery) agent, epidemiology
Agent: Entamoeba histolytica
E. dispar (non invasive)
Epidemiology
Contaminated water
Poor sanitation - daycares
Close proximity places - military barracks, nursing home, prisons
Human waste as fertilizer
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Entamoeba coli, E. hartmanii, Endolimax nana, Iodamoeba bütschlii non pathogenic to humans (T/F)
True
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Amoebic abscess - transmission
–faeco-oral, food and water contaminated by flies/roaches, oral-anal sex
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All cases of amoebic abscess are symptomatic
False
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Amoebic abscess - Pathogenesis
1. Cysts pass in stool of infected person
2. Cysts ingested
3. Cysts pass through stomach ->
Gastric acid promotes trophozoite release in small intestine.
4. Trophozoites multiply
((may cause necrosis + ulceration in the large intestine))
5. Flask shaped ulceration = secondary bacterial infection/peritonitis due to damage to intestinal wall
If parasite moves to peritoneal cavity = goes to bloodstream -> goes to diff organs
(intermittent diarrhoea with abdominal pain and weight loss).
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Virulence factor of amoebiasis, explain
Trophozoites invade BVs of the portal system,
surviving lytic complement & neutrophils.
Result: Gain access to the liver parenchyma.
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What is second leading cause of mortality due to parasites?
Entamoeba histolytica
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Possible parasitic cause of diarrhea in infants
E. moshkovskii
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E. histolytica - host range
Mainly humans.
But: higher primates, dogs, cats and some rodents
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Which Trophozoite has the foll description:
Trophozoites are round with large,
lobular *pseudopodia* and a clock-face nucleus.
E. histolytica
-Central nucleus (most times)
- Erythrocytes seen in cytoplasm means digested erythrocytes
Active, feeding stage
16
Describe cyst stage of E. histolytica
Cysts are smaller than trophozoites.
They have 4 nuclei and chromatoid bars (tightly
packed mRNA with rounded ends).
-Infective stage
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What do E. histolytica and Entamoeba coli have in common?
They look alike
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Why is it important to distinguish between E histolytica and E coli?
E coli is not pathogenic in the GIT but E histolytica is; need to know if treatment is necessary
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E coli vs E histolytica
E. coli-coarser chromatin, eccentrically located
endosome (protein trafficking) and the absence of erythrocytes in the cytoplasm
-ingested erythrocytes appear as dark
inclusions.
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Entamoeba coli cyst
-8 nuclei (compared to 4 nuclei seen in E. histolytica)
and
-smaller chromatid bodies that are often filamentous
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E. histolytica - life cycle
1. Ingestion of cysts
2. Excystation in small intestine
3. Division of quadrinucleate cyst
into 4 and then 8 trophozoites
4. Trophozoites move to colonize the colon
5. Encystation
6. Excretion of cysts
7. Ingestion of cyst by the patient
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Epidemiologic factors
Events, characteristics, or other definable entities that have the potential to bring about a change in a health condition.
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Epidemiologic factors - Amoebiasis
(i)Strain virulence -
classic strain, non-classic strain; Laredo ,
Huff; pathogen zymodemes
(ii) Susceptibility of the host
(iii) Nutrition status
(iv) Immune-system.
• Breakdown of immunologic barrier
(tissue invasion)
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Virulence factors
Virulence factors:
- assist and promote colonization of the host e.g. adhesins, invasins, antiphagocytic factors.
- Bring damage to the host e.g. toxins, hemolysins, proteases
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Virulence factors - Amoebiasis
-Secreting proteolytic enzymes (histolysin)
and cytotoxic substances.
• Contact-dependent cell killing
• Cytophagocytosis
Necrosis in amoebiasis is caused by trophozoite division and cytotoxin produced by E histolytica.
Amoebic killing target cell:
• Receptor-mediated adherence of amoebae
to target cell
• Amoebic cytolysis of target cell
• Amoebic phagocytosis of killed target cell
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Intestinal and Extraintestinal Amoebiasis symptoms
Intestinal amoebiasis - Diarrhea or dysentery, abdominal
pain, cramping , anorexia, weight loss, chronic fatigue
Extraintestinal amoebiasis - Systemic signs - fever, leukocytosis, abscess formation in right lobe, pain over liver, hepatomegaly
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Liver abscess - due to Amoebiasis - causation
- seeding of infection from the bowel
- infectious agents are carried to the liver
from the portal venous circulation.
- Necrosis of hepatocytes due to toxins
of lysed neutrophils
- liver abscess pus = chocolate brown -‘anchovy paste’.
- Amoebas are to be found in the wall
of the abscess
Complications of liver abscess
Secondary bact infection
Rupture into pleural space - Empyema
Rupture into pericardium - Pericarditis
Rupture into peritonium - Peritonitis
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Lab ID - Amoebiasis
microscopy, culture, serologic testing, and (PCR) assay
29
Microscope and culture ID - Amoebiasis
Parasites concentrated in intestinal ulcers - one stool sample not as effective (need multiple stool samples)
Microscopic identification using:
Wet Mount (with or w/o iodine)
– a mature cyst has 4 nuclei, immature 1 – 3.
Trichrome stain
– Cysts, trophozoites can be stained for the location
of chromatoid bodies of the nucleus.
Culture: Using modified Locke-egg media
• culture less sensitive than microscopy
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