Flagellated Protozoa

Orders Retortamonadida &

Diplomonadida
Common Characteristics
1. No mitochondria
2. No dictyosomes (Golgi apparatus)
3. (+) a recurrent flagellum in a cytostomal
groove
4. Occupy an anoxic environment
 I. Order Diplomonadida
Family Hexamitidae
1. Genus Giardia
A. Giardia lambelia
2. Genus Enteromonas
Enteromonas hominis
 Il. Order Retortamonadida
Family Retortamonadidae
1. Chilomastix mesnili

2. Retortamonas intestinalis
Order Diplomonadida
Family Hexamitidae
 Giardia lamblia
(synonymous with Giardia
intestinalis and Giardia
duodenalis)

Habitat : duodenum, upper part

of small intestine, bile ducts and
gall bladder as trophozoites
attached to the mucosa.
D.H: man R.H: animals
Most common flagellate of
the human digestive tract
The distribution is
cosmopolitan. Children are
specially suspectible.
Transmission of Giardia is
predominantly by ingestion
of food or water
contaminated with cysts.
 The trophozoite of Giardia lamblia
Active metabolizing, motile
form, lives in the upper two-
thirds of the small intestine
(duodenum and jejunum)
9 to 21 m long, shaped like
a pear
Two nuclei
8 flagella (2 anterior, 2
posterior, 2 ventral, and 2
caudal)
 Morphology of Giardia lamblia trophozoite

Ventral surface bears

adhesive disk to adhere to
surface of intestinal cell.

Reproduction by binary
fission-asexual
reproduction
 2nd Stage is Giardia lamblia: cyst
The cyst forms as trophozoites become
dehydrated when they pass through the large
intestine

Morphology:
ovoid in shape; 8-14 m long
thin cyst wall
four nucleus, often concentrated at one
end (indicates that a nuclear division
occurs during encystment)
flagella shorten and are retracted within
cyst
axonemes
 Cyst may remain viable in the external environment
(usually water) for many months.

-14 billion cysts can be passed in 1 stool sample

-Moderate infections: 300 million cysts.
 Encystation and Excystation
Excystation:
In vivo occurs in the stomach/small intestine. Motile
trophozoites emerge in the small intestine.
In vitro: can be induced by:
Low pH
Protease treatment at pH 8
Encystation
In vivo occurs in the lumen of the small intestine.
Trophozoites starts synthesizing cyst wall components
and transport them to the outer surface.
In vitro: can be induced by:
High pH
High bile salts concentration
 LIFE CYCLE
Cysts are resistant and are
responsible for transmission. Both
cysts and trophozoites can be
found in the feces. The cysts can
survive several months in cold
water. Infection occurs by the
ingestion of cysts in contaminated
water, food, or by the fecal-oral
route. In the small intestine,
excystation releases trophozoites
(each cyst produces two
trophozoites). Trophozoites
multiply by longitudinal binary
fission, remaining in the lumen of
the proximal small bowel where
they can be free or attached to the
mucosa by a ventral sucking
disk. Encystation occurs as the
parasites transit toward the
colon. The cyst is the stage found
most commonly in non-diarrheic
feces
 Pathogenesis
Coats intestinal epithelium

Microvilli damage

Interference in absorption of fat & other
nutrients

Fatty stools, Mucus production, Dehydration
Intestinal pain, Flatulence & Weight loss
Adhesion of the trophozoite to the epithelial cells of the small intestine.

Note the impression left on the epithelia where a trophozoite has detached (upper left) and the
interaction between the ventral disk of the parasite and the brush boarder cells of the intestines
(lower right).
 Mechanism of Disease development
Pathogenesis is determined by:

1- Mechanical irritation Hyperemia / inflammation Duodenitis (mild illness)

2- Enterotoxin stimulate cytokine production inflammatory response

Permeability / hypermotility / hypersecretion (play an important role in production of
Inflammation & Diarrhea that may be mild or severe

3- Blunting of brush border Atrophy of villi related to

immunodeficiency (secretory IgA)

4- Malabsorption syndrome Malnourishment (due to interference with

absorption Atrophy of the villi)
Leads to:
* Fat Malabsorption---- greasy stool *Folic acid & fat soluble vitamin def.

*Accumulation of electrolytes ----- increase water content in intest. lumen

 Clinical Manifestations
Symptom Percent
Diarrhea 64-100
Malaise. Weakness 72-97
Abdominal distension 42-97
Flatulence 35-97
Abdominal cramps 44-81
Nausea 14-79
Foul-smelling, greasy stools 15-79
Anorexia 41-73
Weight loss 53-73
Vomiting 14-35
Fever 0-28
Constipation 0-17
 Immunity to Giardia lamblia
Cysts viable for 3 months in water at 4o C
Freezing does not eliminate infectivity completely
Human milk is lethal to Giardia trophozoites through the action of
fatty acids and lipase
Anti-Giardia IgA
Human milk protection against Giardia correlates with anti-
Giardia serum IgA
GIARDIA INTERACTION WITH THE HUMAN
INTESTINE
 Antigenic Variation
The ability of a parasite to change the proteins it presents to the
hosts immune system.
The surface of the Giardia trophozoite is covered by the Variant
Specific Protein (VSP) - only one is expressed per trophozoite.
Cysteine rich protein (about 12%), in CXXC motifs. TM proteins
Over 150 different VSP genes are encoded in the Giardia genome.
Expression of different VSPs results in the phenomenon of Antigenic
Variation
Mechanisms not known: may be changes in gene expression at the
mRNA level
 Diagnosis
Detection of trophzoites, cysts or antigens in stool or duodenal fluid

Stool specimens:
Examined within 1 hour after being passed or should be
stored in vials containing polyvinyl alcohol (PVA) or 10% formalin

Trophozoites are more likely to be found in unformed stools

(rapid transit time)

Cysts, but not trophozoites, are stable outside the GI tract

Aspiration of duodenal contents

Not always used because it is very invasive
 Giardia lamblia

10-25 cysts sufficient to initiate infection

Colonization morphologic damage to intestinal

epihelial cells and brush border may result in
normal microvilli or subtotal atrophy
 Treatment

Agent Pediatric Dose Adult Dose

Metronidazole 15 mg/k/d divided in 3 doses X 5d 250 mg tid X 5d

Nitazoxanide 12-47 mo: 100 mg bid X 3d 500 mg bid X 3d

4-11 yrs: 200 mg bid X 3d
(100 mg/5 ml)

Tinidazole, Furazolidone, Quinacrine , Paromomycin

 Epidemiology

Occurs worldwide

Age-specific prevalence:
Highest in children 0-5 years
Transmission is common in certain high risk populations:
Consumers of contaminated water
Travelers to certain areas of the world
Those exposed to domestic and wild animals (dogs,
cats, cattle deer, and beaver)
Major reservoir/vehicle for spread: Water contaminated
with cysts
 Enteromonas hominis
TROPHOZOITE:
SIZE: 4 to 10 mcm.
SHAPE : Pyriform.
NUCLEUS: Single, distinct nuclear membrane; large, central
karyosome.

Cyst:
Simular to Endolimax nana.
SIZE: 6 to 8 mcm.
SHAPE : Oval.
NUCLEUS:
NUMBER: 1 to 4, (predominant: binucleate form).
Order Retortamonadida
 2 species
1. Chilomastix mesnili

2. Retortamonas intestinalis
 Chilomastix mesnili

Non-pathogenic; endocommensal.
Trophs and cysts in the life cycle.
Lives in the cecum.
Divides by binary fission.
Water borne endocommensal infected
by contaminated water.
 Chilomastix mesnili - Troph
Motility
Stiff, rotary
1 Nucleus
Flagella
3 anterior
1 in cytostome
Features
Prominent cytostome
Shepherd's crook

Dr. RAAFAT MOHAMED

 Chilomastix mesnili

CYST is lemon-
shaped; 6 to 10 m in
diameter.

Contains single
nucleus, cytosome,
and retracted flagella.
 Life cycle of Chilomastix mesnili

Infection occurs by the

ingestion of cysts in
contaminated water,
food, . In the large (and
possibly small)
intestine, excystation
releases trophozoites.
Chilomastix resides in
the cecum and/or colon;
considered a
commensal organism
 Laboratory diagnosis

Trophozoite stage Cyst stage

 Retortamonas intestinalis
Location: coecum, colon
Trophozoite only has 2 flagella
 Cyst:
1. Ovoid to pear-shaped

2. W/ a single nucleus