WELCOME

TO

UNIT THREE
PROTOZOA

By: Ahmednur .A
 What are Protozoa?

 Single-celled eukaryotic organisms

 kingdom Protists

 Vary in size (1 to 150um)

 The cells consist of plasma membrane, cytoplasm,

ER, GB, ribosomes, nuclear membrane, nucleus and
chromosomes.

By: Ahmednur .A
 Protozoa…
In addition may possess
Pseudopodia,
Flagella &
Cilia as organ of locomotion.
Single protozoal cell performs all the functions of
 Respiration
 Digestion
 Excretion
 Locomotion and
 Reproduction
• These organisms occur generally as a single cell

By: Ahmednur .A
Reproduction types
Asexual multiplication:

• A. Simple binary fission

• In this process after division of all the structures, the
individual parasite divides either longitudinally or
transversally in to two more or less equal parts.

• B. Multiple fission or schizogony

• In this process, more than two individuals are produced,
• E.g. asexual reproduction in plasmodia.

By: Ahmednur .A
 Sexual reproduction
A. Conjugation
In this process temporary union of two individuals occurs
during which the interchange of nuclear material takes place.
Later on, the two individuals separate.

B. Syngamy
In this process, sexually differentiated cells, called gametes,
unite permanently and complete fusion of the nuclear
material takes place.
The resulting product is known as a zygote.
By: Ahmednur .A
 Cont’d…

• The protozoa are classified biologically according to their type

of
 Locomotory organelles or
 Their habitat in the body of the host.
• Locomotory organelles Habitat
– pseudopodia -Intestinal protozoa
– Flagellate -Tissue protozoa
– Ciliate - Blood protozoa.

By: Ahmednur .A
 Taxonomic classification of protozoa
Sub kingdom Phylum Sub-phylum Genus- examples Species- examples

Protozoa Sarcomastigop Sarcodina move Entamoeba E. histolytica

hora by pseudopodia
further divided into

Mastigophora Giardia G. Lamblia

move by flagella Leishemania
Trypanosma

Apicomplexa Plasmodium P. falciparum,

no organelle of P. vivax,
locomotion P. malariae,
P. Ovale
P. knowlesi

Ciliophora Balantidium B. coli

move by cilia

Microspora Enterocyto-zoa E. bienusi

Spore-forming

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 Intestinal protozoa
Amoeba: Flagellates:
* Entamoeba histolytica * Giardia lamblia
• Entamoeba dispar • Dientamoeba fragilis
• Entamoeba coli • Chilomastix mesnili
• Entamoeba hartmanni • Trichomonas hominis
• Endolimax nana • Enteromonas hominis
• Retortamonas intestinalis

Apicomplexa: Other:
**Cryptosporidium hominis • Blastocystis hominis
**Cryptosporidium parvum *Balantidium coli
**Cyclospora cayetanensis
**Isospora belli
* Pathogenic
** Opportunistic
By: Ahmednur .A
COMMON CHARACTERSTICS

TYPICAL FECAL-ORAL LIFE CYCLE

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 Sarcodina- amoeba

Characteristics:

Possess shapeless mass of cytoplasm (ectoplasm and endoplasm)

Move by means of pseudopodium

Reproduce by simple binary fission

Most species have two stages

Trophozoite- active, motile and feeding

Cyst -resistant and infective stage

7 species are found in the intestine and oral cavity

By: Ahmednur .A
 Six species in the large intestine
 E. histolytica
 E. coli
 E. dispar
 E. hartmanni
 Endolimax nana
 Iodamoeba bütschlii
One species in the oral cavity
 E. gingivalis
• Two species have been found as pathogenic free living
(facultative parasite) amoeba: Naegleria fowleri and
Acanthamoeba cephalus

By: Ahmednur .A
 Entamoeba histolytica
 Cause amoebiasis (amoebic dysentery and liver
abscess)
 Only a few strains are pathogenic
Morphology
 Trophozoite:
 Has one nucleus and pseudopodium
The invasive strain possess RBCs
 Cyst:
Immature cyst possess one or two nucleus and inclusion
bodies
Mature cyst possess four nuclei

By: Ahmednur .A
 Epidemiology
Distributed worldwide
Incidence is highest in tropical and sub tropical regions
90% of infections are asymptomatic

Transmission and life cycle:

Ingestion of infective cyst in food or water

contaminated with faeces

By: Ahmednur .A
 Life cycle
 After ingestion the cyst passes through the stomach, where
exposure to gastric acid stimulates the release of pathogenic
trophozoite in the duodenum.

 It divide and produce extensive local necrosis in large intestine.

Forms “flask-shaped” or “duct-tube” ulcer.

 Invasion into the deeper mucosa may result extra-

intestinal amoebiasis

 After a period of growth and multiplication, encystations occur in

the cecum and colon /large intestine.
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 Cont’d…

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Pathogenesis and pathology of amebiasis
• Non-invasive
• ameba colony on intestinal mucosa
• asymptomatic cyst passer
• non-dysenteric diarrhea, abdominal cramps, other
GI symptoms
• Invasive
• necrosis of mucosa  ulcers, dysentery
• ulcer enlargement  severe dysentery, colitis,
• peritonitis
• flasked-shaped ulcer
• Metastasis/ spreading  extra-intesinal
amebiasis
By: Ahmednur .A
 Clinical features

About 90% do not develop clinical symptoms

Some - exhibits amoebic dysentery and/extra intestinal

amoebiasis in liver, spleen, brain & lungs.

Amoebic dysentery occurs when the trophozoite

invades the intestinal wall.

Symptoms include abdominal pain and dysentery with

blood and mucus.

Multiplication of trophozoite forms ulcer.

By: Ahmednur .A
 Liver abscess

Trophozoite that reach the blood stream are carried to

the liver, lungs, brain & heart and can form ulcer.

The clinical features include:

 Pain,

 Tenderness in the region of liver,

 Wasting and

 Fever associated with chills and night sweat.

By: Ahmednur .A
flasked-shaped ulcer

By: Ahmednur .A
 Laboratory diagnosis

1. Stool examination
Examination of a fresh dysenteric fecal specimen
for motile E. histolytica trophozoite and cyst

2. Serologic studies: not common

3. Tissue examination: Sigmoidoscopic biopsy, aspiration

Treatment
Tinidazole (drug of choice)
Metronidazole (alternative drug)
By: Ahmednur .A
 Prevention and control

 Personal hygiene

 Safe water supply or prevents faecally contamination.

 Boiling drinking water (cyst killed at 55 oC)

 Vegetable should be cooked

 Food handlers should be checked

 Access of flies and cockroach to food must be prevented

 Health education

By: Ahmednur .A
 Flagellates

(Intestinal, (Blood & Tissue)

Urogenital & Oral) flagellates
flagellates

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 Intestinal,urogenital & oral flagellates

• Intestinal Flagellates:

• -Giardia lamblia - Dientamoeba fragilis

• Chilomastix mesnili - Trichomonas hominis
• Enteromonas hominis - Retortamonas intestinalis

• Urogenital flagellates

• Trichomonas vaginalis

• Oral flagellates

• Trichomonas tenax
By: Ahmednur .A
 General characterstics

• Usually posses 2-6 flagella (~ 8 flagella)

• Inhabit the intestinal, urogenital and oral cavity

• Direct life cycle/no biological vector

• All have trophozoites and cyst stage except the

Trichomonas species
• All are commensal/ non-pathogenic/except G.lamblia and T.
vaginalis

By: Ahmednur .A
 1. Giardia lamblia
Trophozoite stage
Typical Characteristics:
Size range: 8-20 um
Shape: Pear/teardrop
Motility : “Falling leaf”
Appearance: Bilaterally symmetrical
Nuclei: Two ovoidal-shaped, each
with a large Karyosome
No peripheral chromatin
Flagella: Four pairs arising from the ventral side:
-One pair anterior end
-One pair posterior end
-Two pairs central laterally
Habitat
• Small intestine ( duodenum & jejunum)
By: Ahmednur .A
 Epidemology

• Worldwide distribution

• higher prevalence in tropical or developing countries (20%)

• 1-6% in temperate countries

• Most common and easily recognized protozoa in stools

• ~200 million cases/yr

• Giardiasis

• Often asymptomatic

• Acute or chronic diarrhea

By: Ahmednur .A
 Transmission

*Giardia is transmitted via the cyst stage

1- Ingestion of faecally contaminated food

or water with cyst
2- Person to person among homosexuals (feco-oral
contact)

By: Ahmednur .A
 Fecal-oral transmission factors

• Poor personal hygiene

• Children
• Food handlers
• Developing countries
• Poor sanitation
• Endemic
• Water-borne epidemics/ outbreak common

By: Ahmednur .A
 Life Cycle of G. lamblia

1. Life cycle is direct - no intermediate host.

2. When cyst is ingested, the organisms escape from the cyst in the
duodenum.

3. Attach via adhesive disk to microvillar surface of epithelium of upper

two-thirds of the small intestine.

4.They divide by longitudinal binary fission.

5. Encystment occurs in lower intestinal tract.

6. Freshly passed cysts are infective

7. Trophozoites are found in diarrheic stools; cysts are found in formed

stools.
By: Ahmednur .A
 By:
Ahmednur .A
 Pathogenesis
• Epithelial damage
• Villus blunting
• Crypt cell hypertrophy/size
• Malabsorption develops
• Enzyme deficiencies
• Lactase (lactose intolerance)

Possible Mechanisms
• Mechanical irritation
• Obstruction of absorption
By: Ahmednur .A
 Out come of giardiasis May be :

 Asymptomatic/latent
 Acute short-lasting diarrhea
 Chronic/nutritional disorders

By: Ahmednur .A
 Acute symptoms
Develops after an incubation period of 1 to 14 days and usually lasts
1 to 3 weeks

Sudden explosive, watery diarrhea, bulky, frothy, greasy,

foul-smelling stools, no blood or mucus
Upper gastro-intestinal uneasiness, bloating, flatulence,
cramps, nausea, vomiting, anorexia
Usually clears spontaneously (undiagnosed), but can
persist or become chronic
Irregular excretion of cysts
By: Ahmednur .A
 Chronic symptoms

• Recurrent diarrheal episodes

• Anorexia, nausea frequent

• Can lead to weight loss and failure to thrive

• The more chronic stage is associated with vitamin B12

malabsorption, disaccharidase deficiency and lactose intolerance

• Stools become steatorrheic (fatty stool) containing large

amount of fats and mucus but no blood

By: Ahmednur .A
 Laboratory Diagnosis:

• Macroscopic examination
• Stool is usually offensive, bulky, pale, mucoid (fatty),
diarrheic (watery) but there is no blood in the stool.
• Microscopy
• Finding the trophozoite stages in fresh diarrheic stool
• Finding the trophozoite stages in duodenal aspirate…..for
children
• Finding cyst stage in formed stool
• Immunological methods
• Molecular methods…PCR
By: Ahmednur .A
 Treatment Prevention and Control

Drug of Choice • Avoid fecal-oral transmission

• metronidazole • Improve personal hygiene
• 750 mg/Tid/5d • Treat asymptomatic carriers
• >90% cure rate • Health education
• Protect water supply from
Alternatives
• tinidazole (single dose) contamination

• paromomycin (pregnancy) How to get rid/free of Giardia in water?

• quinicrine * Boiling (at least 1 minute)

• furazolidine * Filtration (1μm pores)

* Chemical treatment (Iodine)
By: Ahmednur .A
 Urogenital flagellates (Trichomonas vaginalis)

General feature
• Inhabit the urogenital tract of male and female

• Has only trophozoite stage

• Most frequent Sexually Transmitted pathogen longitudinal

binary fission

By: Ahmednur .A
 Trichomonas vaginalis

Distribution: World wide

Habitat: Uro-genital tract
Females: vagina
Males: urethra, prostate
Transmission:
sexual
Trophozoite stage transmitted during sexual
intercourse
intercourse

-Common STD
• Co-infection with other STDs
• More prevalent in at risk groups
• Both sexes equally susceptible
• symptoms more common in females

By: Ahmednur .A
 Life cycle

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 Pathology

 Inflammation

 Erosion

 Discharge

 Itching, burning

 Urethritis, dysuria

 Dermatitis

By: Ahmednur .A
 Clinical manifestations
In females:
• Ranges from asymptomatic to mild or moderate irritation, to
extreme vaginitis
• 50-75% abnormal discharge (frothy, yellowish or greenish)
• 25-50% pruritus
• 50% painful coitus
• Onset or exacerbation often associated with menstruation or
pregnancy
• Vaginal erythema, ‘strawberry cervix’

In males
• 50-90% are asymptomatic
• Mild dysuria or pruritus
• Minor urethral discharge
By: Ahmednur .A
 Laboratory diagnosis

• Finding the trophozoite in smear of vaginal or urethral discharge

• Occasionally in urine sediment of men and women

Treatment

• Metronidazole

-250 mg (Tid) for 5-7 days

• Simultaneous treatment of partner! (85-90% cure)

Prevention

• Limit number of sexual partners

• Use condoms
By: Ahmednur .A
 Blood and Tissue flagellates

• Belonging to the family Trypomastidae

• Six genera but only two of them are responsible to

cause disease to man
 Genus Leishmania
Genus Trypanosoma

By: Ahmednur .A
General Characteristics of blood and tissue flagellates

• Reproduces by simple longitudinal binary fission

• Transmission occurs through biological insect vectors

as intermediate hosts & human as definitive host

• The species are morphologically indistinguishable, but

they can be differentiated on the basis of on their
Clinical features, geographical distribution,

By: Ahmednur .A
 Genus Leishmania

• Causative agent of Leishmaniasis

• Obligate intracellular protozoa of the genus Leishmania

• Named after Leishman, who first described it in London in May 1903

• In the human host, Leishmania are intracellular parasites that infect the

mononuclear phagocytes

By: Ahmednur .A
 Geographical distribution

Distribution of leishmaniasis is limited by:

• The distribution of the sand fly,

• Its tendency to take blood from humans or animals only.

• Its capacity to support the internal development of specific

species of leishmania
By: Ahmednur .A
 • The incidence of leishmaniasis is increasing,
mainly because of:
• Man-made environmental changes
• Poverty and malnutrition
• Movement of susceptible populations into
endemic areas
• In Ethiopia
• Four species of Leishmania is found, namely,
• L. aethiopica,
• L.major
• L. tropica
• L. donovani
By: Ahmednur .A
Transmission and life cycle
• Common mode of transmission.
• Bite of sand fly
• Genera Phlebotomus in Old
world
• Lutzomyia in New world
• Uncommon modes of transmission:
• Congenital transmission,
• Blood transfusion,
• Rarely, inoculation of cultures.

By: Ahmednur .A
 The following are the main developmental forms

1. Amastigote (Leishmanial 3.Epimastigote forms

form) • Elongated body, single free
 no free flagellum, flagellum, single nucleus
 The only intracellular forms of • found in the invertebrate host and in
culture media (of Trypanosome
all leishmania species and species)
Trypanosome cruzi. 4. Trypomastigote
• 2. Promastigote  single Flagellum arises
posteriorly
 found in the invertebrate host, and in
 found in the peripheral blood of
culture media (of all Leishmania
species) and in man for Tryponosoma vertebrates and is the diagnostic
cruzi stage of Trypanosome species

By: Ahmednur .A
By: Ahmednur .A
 • Leishmaniasis can easily classified clinically as
• Visceral leishmaniasis
• Cutaneous leishmaniasis
• Mucocutaneous leishmaniasis
• Diffuse cutaneous leishmaniasis

By: Ahmednur .A
 These different forms of the disease is caused by the
different species of Leishmania
• 1.Cutaneous • 3.Mucocutaneous
leishmaniasis(CL) leishmaniasis (MCL)
• L. tropica
• L. major  L. panamensis
• L. aethiopica  L. guyanensis
• L. panamensis  L. Brazilliensis
 L. aethiopica
• L. guyanensis
• L. Peruviana
• 4. Diffuse cutaneous
• 2. Visceral leishmaniasis(VL)
leishmaniasis (DCL)
• L. donovani
• L. infantum  L. amzonensis
• L. Chagasi
By: Ahmednur .A
 L. aethiopica
 Clinical features and pathology

• Cutaneous leishmaniasis (CL): Most common form, and relatively

benign self-healing skin lesions (localized or simple)
• Diffuse cutaneous leishmaniasis (DCL): Rare cutaneous infection
with non- ulcerating nodules resembling lepromatous leprosy
• Mucocutaneous Leishmaniasis (MCL): Simple skin lesions that
metastasize to mucosa especially nose and mouth region
• Visceral Leishmaniasis (VL): Generalized infection of the
reticuloendothelial system, high mortality response

By: Ahmednur .A
 Cutaneous Leishmaniasis
• Caused by L. Mexicana)
• Incubation period: 2 weeks to
several months
• Initially, the lesion is a small,
red papule up to 2 cm in
diameter
• Chronic ulcerated, papular, or
nodular lesion
• Lesion is painless, non-
tender, non- pruritic and
usually clean(Chiclero
Ulcer)
By: Ahmednur .A
 Diffuse Cutaneous Leishmaniasis
• Caused by L.aethiopica
• Lesion develop over large
areas of the body
• Scaly, not ulcerated,
nodules
• Chronic and painless
• Numerous parasites in
lesions
• Seldom/ rarely heal
despite treatment

By: Ahmednur .A
Mucocutaneous Leishmaniasis (espudia)

 Caused by L. braziliensis
• Two stages
-Simple skin lesion
-2o mucosal involvement
• Metastasis via blood or lymphatic
systems
• Can occur long after primary lesion
(up to 16 years)
• Frequently in naso-pharyngeal
mucosa
• Junction of skin and mucosa
By: Ahmednur .A
 Visceral Leishmaniasis (Kalazar/dum dum fever )
 Caused by the Leishmania donovani complex,
• Reticuloendothelial system affected
• Spleen, liver, bone marrow, lymph nod

• Progressive disease
• 75-95% mortality if untreated
• death generally within 2 years

•Death usually occurs because of severe secondary

bacterial infections in advanced disease

• Pneumonia is the common complication

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 Clinical Presentation
• Incubation period
• generally 2-6 months
• can range 10 days to years
• Fever, malaise, weakness
• Wasting despite good appetite
• Hepatosplenomegaly, enlarged
lymph nodes
• Depressed hematopoiesis
• Severe anemia
• Leucopenia
• Thrombocytopenia

By: Ahmednur .A
• Profile view of a teenage boy
suffering from visceral
leishmaniasis.
• The boy exhibits splenomegaly,
distended abdomen and severe
muscle wasting.

By: Ahmednur .A
 Diagnosis of CL, MCL, DCL
• It is suspected because of:
• Geographical presence of parasite/ vector
• History of sand fly bite
• Positive skin lesion:
• Chronic, painless, ‘clean’ ulcer
• Nasopharyngeal lesions
• Nodular lesions
1. Demonstration of parasite amastigotes (skin snip
scrapings, biopsy, aspirates)
2. Culture from ulcer material
3. Serology

By: Ahmednur .A
 Diagnosis of Visceral leishmaniasis

I. Demonstration of parasite in tissues by

light microscopic examination of the stained specimen
-Culture(NNN media)
-Animal inoculation???????
II. Aspirates from spleen, bone marrow, lymph node
III. Immunodiagnosis by detection =RK39
I. Antigen detection
II. Antibody detection

By: Ahmednur .A
 Treatment
Treatment

• Sodium stibogluconate (Pentostam)

• Pentamidine isethionate

• Amphotericin B

By: Ahmednur .A
 Prevent and control

1. Early detection by serological diagnosis (VL) and treatment of

infected persons

2.Personal protection from sand fly bites by:

• Using insect replants
• Avoiding endemic areas especially at times when sand flies are
most active
• Use of pyrethroid impregnated bed nets and curtains /screen

3. Vector control by the use of light traps, sticky paper traps, or

residual insecticide spraying of houses

By: Ahmednur .A
 2. Genus Trypanosoma

General features
-Actively motile flagellated protozoa that live in blood and
lymph node
-Require insect vector : tsetse fly, bug

• Two distinct forms occur in humans:

• African Trypanosomiasis
• Trypanosoma brucei gambiense
• Trypanosoma brucei rhodesiense
• Transmitted by the Tsetse fly
• American Trypanosomiasis( Chagas diseases)
• Trypanosoma cruzi
• Transmitted by the Tritomine bug
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Human African Trypanosomiasis (Sleeping Sickness)

• It is caused by the flagellate protozoan, Trypanosoma brucei complex

• Exists in 2 morphologically identical subspecies:

 Trypanosoma brucei gambiense
• Disease: West African or Gambian African trypanosomiasis
• Geographical Distribution: Central & West Africa
 Trypanosoma brucei rhodesiense
• Disease: East African or Rhodesian African trypanosomiasis
• Geographical Distribution : Rift valley & East Africa

By: Ahmednur .A
 Habitat : blood, Lymph channel throughout the body, CSF,
Connective tissue, brain.

Vector : Tsetse fly (Glossina spp).

1. G. palpalis
T. b. gambiense
2. G. tachinoides
3. G. morsitans
4. G. pallidipes T. b. rhodesiense

Mode of Transmission:
1. Bite of infected tsetse fly
2. Congenital

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By: Ahmednur .A
Pathology and clinical features

Mechanism of pathogenesis

Mortality is due to over all disruption of normal physiological

process

Antigenic variation and hosts immune reactions (immuno

pathogenesis and inflammation)

• Monocytosis due to inflammation

• Brain edema due to hypoglycemia

• Host cell lysis

•By: Ahmednur
Anemia .A due to red blood cell lysis
The disease has generally three stages:

1. Bite stage

 Trypanosomes multiply in the tissue around the initial bite site

 This result in characteristic local inflammation trypanosomal

“chancre” usually not pain full

Itchy chancre will develop and lasts for1-2 weeks with out
leaving scare

From there they enter blood and lymphatic system

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 2. Parasitemia stage

• After 1-2 weeks period of asymptomatic incubation, parasite

invade blood

• This stage is characterized by progressive anemia.

• The presence of the parasite in blood and lymph node leads to

fever, malaise, headache, lymphadenopathy, nausea and
vomiting, edema and back pain.

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 3. CNS stage
In the later stage of infection parasites passes blood brain barrier
and infect CNS

Presence of parasite lead to meningo-encephalitis with

neurological involvement.

Patients may be immobilized for their own safety

This ultimately yields comma, drowsiness and uncontrolled desire

to sleep (sleeping sickness) .

 Death occur due to cardiac failure recurrent infection and comma.

Untreated trypanosomiasis is always fatal

By: Ahmednur .A
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Comparison of gambiense & rhodesiense sleeping sickness

West African East African

• Caused by T. b gambiense • Caused by T. b rhodesiense

• West and Central Africa • Rift valley and eastern Africa

• Tsetse fly (G. palpalis group) • Tsetse fly (G.morsitans group)

• Reservoir-human • Reservoir-wild animal

• Parasitemia-low/variable • Parasitemia-high
• Mortality -100% if left untreated • Mortality -100% if left untreated
• Asymptomatic carrier common • Asymptomatic carrier rare
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 Laboratory diagnosis

• A definitive diagnosis requires detection of

trypanosomes
 In blood (thick and thin smear)
 In bone marrow aspirate
 Lymph node aspirate
 Chancre aspirate
 CSF analysis
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• Treatment

Suramin and Pentamidine are the recommend drugs during the

acute stage without CNS involvement

whereas Melarsoprol or Eflornithine are recommend if the CNS

is involved.

Pentamidine is less toxic than Suramin. However, it is not

effective against T. rhodesiense.

All four of these drugs are provided free of charge by the World
Health Organization through public and private partnerships with
pharmaceutical firms.

The prognosis is generally excellent if treatment starts during the

acute stage.
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Control measures for African trypanosomiasis

o Removal of vegetation

o Killing of wild animals????

o Animal drug administration to kill trypanosomes

o Male sterile insect technique

o Spraying of insecticides

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 Quize
• 1. Intestinal amoebiasis in large bowel is characterized by:
A. Atrophy of villi. C. Constipation.
B. Obstruction of intestine. D. Flask-like ulceration
• 2. Which one is correctly matched regarding to the infective stages
trypanosomiasis parasitic infection
A. Trypomastigote – human
B. Metacyclic trypomastigote- human
C. Metacyclic trypomastogote - tsetsefly
D. Amastigote -tsetsefly
• 3. Bloody stool is a clinical presentation in infection with:
A. G. lambilia B. E. histolytica C. I. beli D. T.gondi

• 4.Mention the infective stage and diagnostic stage for T. vaginalis

• 5. List two protozoan intracellular parasitic infection (1pt)
By: Ahmednur .A
 •THANK YOU !!!

By: Ahmednur .A