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List medically important protozoa and their diseases

(a) Amoebas: Entamoeba histolytica, Naegleria,
(b) Flagellates: Trypanosoma cruzi
(c) Sporozoa: Toxoplasma gondii


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


Ciliophora spp

Balatidium coli


Apicomplexa spp

Split into two categories
Isospora belli
Toxoplasma gondii
Sarcocystis spp.
Cryptosporidium parvum
Pneumocystis carinii

Plasmodium falciparum
Plasmodium vivax
Plasmodium malariae
Plasmodium ovale
Babesia microti


Kinetoplastida spp

Trypanosoma gambiense
Trypanosoma rhodiense
Trypanosoma cruzi
Leishmania spp


Amoebic abscess (amoebiasis, amoebic dysentery) agent, epidemiology

Agent: Entamoeba histolytica
E. dispar (non invasive)

Contaminated water
Poor sanitation - daycares
Close proximity places - military barracks, nursing home, prisons
Human waste as fertilizer


Entamoeba coli, E. hartmanii, Endolimax nana, Iodamoeba bütschlii non pathogenic to humans (T/F)



Amoebic abscess - transmission

–faeco-oral, food and water contaminated by flies/roaches, oral-anal sex


All cases of amoebic abscess are symptomatic



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).


Virulence factor of amoebiasis, explain

Trophozoites invade BVs of the portal system,
surviving lytic complement & neutrophils.
Result: Gain access to the liver parenchyma.


What is second leading cause of mortality due to parasites?

Entamoeba histolytica


Possible parasitic cause of diarrhea in infants

E. moshkovskii


E. histolytica - host range

Mainly humans.
But: higher primates, dogs, cats and some rodents


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


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


What do E. histolytica and Entamoeba coli have in common?

They look alike


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


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


Entamoeba coli cyst

-8 nuclei (compared to 4 nuclei seen in E. histolytica)
-smaller chromatid bodies that are often filamentous


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


Epidemiologic factors

Events, characteristics, or other definable entities that have the potential to bring about a change in a health condition.


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)


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


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


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


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


Lab ID - Amoebiasis

microscopy, culture, serologic testing, and (PCR) assay


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


Antigen detection - Amoebiasis

EIA kits.
Ag detection may be useful as an adjunct to microscopic
diagnosis in detecting parasites and to distinguish between pathogenic and nonpathogenic infections.