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- Microsporidia are a group of spore-forming

PROTOZOAN PARASITES unicellular parasites. These spores contain an
extrusion apparatus that has a coiled polar tube
PROTOZOA
ending in an anchoring disc at the apical part of
• Provided with nucleus/nuclei, cytoplasm, outer the spore. They were once considered protozoans
limiting membrane, and cellular elaborations called or protists, but are now known to be fungi, or a
organelles. sister group to fungi.
• Locomotory apparatus: cilia, flagella and
pseudopodia.

• Require a wet environment for feeding, locomotion,

osmoregulation, and reproduction.

Stages:

• Cyst – infective stage

• Trophozoite – vegetative stage CLASSIFICATION OF PROTOZOAN PARASITES
Sarcomastigophora Entamoeba histolytica
Entaamoeba coli
Sarcodina Entamoeba dispar
Entamoeba hartmanni
Entamoeba polecki
Entamoeba gingivalis
Iodamoeba butschlii
Endolimax nana
Naegleria fowleri
Acanthamoeba spp.
Mastigophora Chilomastix mesnili
KINGDOM: PROTISTA Dientamoeba fragilis
Giardia lamblia
PHYLA: Pentatrichomonas hominis
(formerly Trichomonas hominis)
• Sarcomastigophora
• Ciliophora Trichomonas tenax
• Apicomplexa Trichomonas vaginalis
- They have a unique organelle called an apicoplast, Leishmania braziliensis
which is a non-photosynthetic plastid that helps them
penetrate host cells. Leishmania donovani
- They also have an apical complex structure that Leishmania tropica
contains several rings, including a conoid in some Trypanosoma brucei complex
species. They are spore-producing and lack
Trypanosoma cruzi
contractile vacuoles and locomotor processes.
Ciliophora Balantidium coli
• Microspora Apicomplexa Babesia spp.

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- apical complex at the anterior
end which consists of polar
rings, subpellicular tubules,
conoid, rhoptries, and
micronemes.
Microspora
consists of spore-forming
parasites of both vertebrates
and invertebrates.
Cryptosporidium hominis The resulting trophozoites proliferate by binary fission in the
lumen of the colon.
Cyclospora cayatanensis
Isospora belli Both cysts and trophozoites may be passed in feces, but only
mature cysts are infective.
Plasmodium spp.
Toxoplasma gondii Note:
Enterocytozoon bineusi
E. histolytica is the only amebic species capable of invading
Encephalitozoon spp. tissues and causing disease.
Vittaforma cornea
Trachipleistophora homimis
Pleistophora spp.
Brachiola vesicularum
Microsporidium spp.

INTESTINAL AMOEBA

7 species of amoebae that are commonly found in human fecal

specimens:

1) Entamoeba histolytica
2) Entamoeba dispar
3) Entamoeba hartmanni
4) Entamoeba coli
5) Entamoeba polecki
6) Endolimax nana
7) Iodamoeba butschlii

ENTAMOEBA HISTOLYTICA

• Subphylum: Sarcodina
3 genera of amebae may inhabit the intestinal tract: • Superclass: Rhizopoda
• Class: Lobosea
1) Entamoeba • Order: Amoebida
2) Endolimax • Family: Entamoebidae
3) Iodamoeba • Genus: Entamoeba
• Specie: Histolytica
Cysts are ingested and excyst in the small intestine

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TAKE NOTE:
The scientific names of species are italicized. The genus name
is always capitalized and is written first; the specific epithet
follows the genus name and is not capitalized.
There is no exception to this!
Example:
• Entamoeba histolytica
• Entamoeba histolytica

CONT. ENTAMOEBA HISTOLYTICA

• Pseudopod-forming nonflagellated parasite
• Most invasive of the parasites in the Entamoeba family MODES OF TRANSMISSION
• The only member of the family to cause colitis and
liver abscess a) fecal-oral contact
b) direct colonic inoculation through contaminated
enema equipment.

LIFE CYCLE OF E. HISTOLYTICA

• Infection by Entamoeba histolytica occurs

by ingestion of mature cysts in fecally contaminated
food, water, or hands.
• Excystation occurs in the small intestine and
trophozoites are released, which migrate to the large
2 STAGES IN THE LIFE CYLE: intestine.

• Cyst
- The quadrinucleate cyst is resistant to gastric
acidity and desiccation and can survive in a moist
environment for several weeks.

• Trophozoite

PATHOGENESIS AND CLINICAL MANIFESTATIONS

• may cause various clinical diseases:

- amebic dysentery
- amebic colitis
- liver abscess

STAGES OF DEVELOPMENT: AMEBIC DYSENTERY

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• Acute disease characterized by bloody diarrhea with
abdominal cramping.
• Invasion of the intestinal mucosa occurs, producing
ulceration that may lead to perforation and peritonitis.
AMEBIC COLITIS
• mimic ulcerative colitis.
• Less severe than amoebic dysentery (may include
non-bloody diarrhea, constipation, abdominal
cramping, and weight loss).
• Develops small, pinpoint mucosal ulcerations and
expand within the submucosa to form flask-shaped
ulcers.
AMEBIC LIVER ABSCESS
most common form of extraintestinal amebiasis (5% of patients
with a history of intestinal amebiasis)
Symptoms:
a) fever
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b) right upper quadrant pain (diagnosed by radiographic
scans, ultrasound, and serologic tests).
c) Rarely appear in other organs, such as the lung, brain,
or skin, either by hematogenous spread from the
intestine or by contiguous spread from a liver abscess.
PATHOLOGY
Invasiveness of the trophozoites is facilitated by:
a) Gal/Gal Nac lectin which mediates adherence to the
host cells
b) Amebapores which forms pores in host cell
membranes
c) cysteine proteinases which are cytopathic for host
tissues
IMMUNITY
• Natural immunity (intestines) – mucin inhibition of
amebic attachment to mucosal cells.
• Systemic circulation – complement-mediated killing
of trophozoites
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• Activated T-cells kill E.histo by:
a) directly lysing trophozoites in a contact-
dependent process
b) producing cytokines which activate macrophages
c) providing helper effect for B cell Ab production
EFFECTS OF AMEBIC MODULATION OF HOST IMMUNE
RESPONSES:
Infected subjects have been shown to be in a state of
immunosuppression during acute stage:
a) T cell hyporesponsiveness
b) suppressed proliferation and cytokine production
c) depressed delayed type hypersensitivity
d) macrophage suppression
• Minimum of 3 stool specimens collected in different
days should be examined.
• Fresh stool examination should be examined within 30
mins. (troph identification)
• DFS with saline – observe troph motility (unidirectional
movement)
• Saline and MB – differentiating Entamoeba from WBCs
• Saline and iodine – nucleus and karyosome can be
observed
- Karyosome – in the center of the nucleus
- Centrally locally (E. histolytica), ara sa kilid ang
nucleus (E. coli)
• E.histo troph with ingested RBC – diagnostic of
amebiasis

DIFFERENTIAL DIAGNOSIS:

BACILLARY DYSENTERY AMEBIC DYSENTERY

Maybe epidemic Seldom epidemic
Acute oneset Gradual oneset
Prodromal fever and malaise No prodromal features
common
Vomiting common No vomiting CONCENTRATION METHOD
Patient prostrate Patient usually ambulant
• Formalin ether concentration test (FECT)
Watery, bloody diarrhea Bloody diarrhea • Merthiolate iodine formalin concentration test (MIFC)
Odorless stool Fishy odor stool
Morphological structures are noted:
Stool microscopy: numerous Stool microscopy: few bacilli,
bacilli, pus cells, macrophages, red cells, trophozoites with - size of the cyst
red cells, no Charcot-Leyden ingested RBCs, Charcot-Leyden - number nuclei
crystals crystals
- location and appearance of karyosome
Abdominal cramps common Mild abdominal cramps - characteristic appearance of chromatoid bodies
and severe - presence of cytoplasmic structures such as glycogen
Tenesmus common Tenesmus uncommon vacuole.
Natural history: spontaneous Natural history: lasts for weeks,
recovery in few days, weeks, or dysentery returns after
more: no relapse remission, infection persists for
years
Side notes:
• Prostrate – sever exhaustion
• Ambulant – nagalakat lakat pa kuno ang patient
• Charcot-Layden Crystals – just the product of
integrated eosinophils
• Tenesmus – abi mo ma poop ka pero ubos na

DIAGNOSIS

Microscopic Diagnosis:

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NOTE:
Laboratories who do not use one of the immunologic or
molecular methods to differentiate E. histolytica from E. dispar,
and rely exclusively on morphologic analysis, must use a
reporting format – “E. histolytica/E. dispar” would be most
appropriate.

SEROLOGY

• Serum Abs – key in the dx of ALA (amoebic liver

abscess)

Able to detect Abs of past infection

- indirect hemagglutination (IHAT)

Short duration Abs detection

- counter immunoelectrophoresis (CIE)

- agar gel diffusion (AGD)
- indirect fluorescent antibody test (IFAT)
- enzyme-linked immunosorbent assay (ELISA)

TREATMENT AND PROGNOSIS

2 objectives:

• To cure invasive disease at both intestinal and extra-

intestinal sites
• To eliminate the passage of cysts from the intestinal
lumen
- Metronidazole (drug of choice)
- Nitroimidazole (tinidazole secnidazole)
- Diloxanide furoate (asymptomatic cyst
passers)

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