MedicalProtozoology PPTPresentationIAUK

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Medical Protozoology Presentation
Presentation · May 2019

DOI: 10.13140/RG.2.2.10696.98566
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Farokh Rokhbakhsh Zamin

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Medical Protozoology
Protozoology lecture for Bsc. Students by

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Dr. Farokh Rokhbakhsh Zamin
Chapter 1:
Introduction

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Protozoology:
• (Pro: Primary; zoan: Animal; Logy: denoting of a subject)
• Protozan: One celled animals (1. free living 2. Parasite)
• Classification: (5 kingdoms):
• (kingdom, Phylum, class, Order, Family, Genus, Species)
1. Monera Prokaryote
2. Protista
3. Animaliae Eukaryote
4. Plantae
5. Fungi

3
Table 1. Classification of Medically important parasites: (According locomotory system)
Kingdom Subkingdom Phylum Organisms
Protista Protozoa Sarcomastigophora Amoeba, Flagellates
ciliophora Cilliates
Apicomplexa Sporozoa, Coccidia
Structure:
• Size: most human parasites are less than 50 Microns;
smallest 1-10; largest 150
• Unicellular eukaryotes
• Nucleus: other than ciliates, nucleus is vesicular, with scattered chromatin
Vesicular nucleus contains central body, called endosome or karyosome
Ciliates: Micronucleus & Macronucleus (quite homogenous)
• Plasma membrane: Enclosing the cytoplasm 7 locomotory structures
(Pseudopoda, cillia, flagella)
• Cytoplasm: I.Ectoplasm : outer transparent layer.
II. Endoplasm: inner layer containing organells.
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• Mouth:
I. Temporary mouth
II. Permanent mouth = Cytostome

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• Contractile vacuole: Osmoregulation eg. Naegleria & Balantadium
• Subpelicular microtubules: In Apicomplexa (no locomotor) slow motion
• Flagella: movement eg. Trypanosoma > Undulating membrane
• Cilliata: movement eg: Balantidum
• Prabasal body: Some : Rod shape bodies (DNA & Phosphate)
(cellular fission & Food storage)
• Pellicle: the outer surface layer of some protozoa
Rigid to maintain distinctive shape eg: Trypanosoma & Giardia
• Mitochondria
• Lysosomes
• Food vacuole
• Golgi apparatus

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• Shapes of a single protozoan:
1. Trophozoite:
2. Cyst

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• Life cycle of parasites:
1. Direct life cycle: (Single host)
Transmission from one individual to another of the same species
I. Direct physical contact eg. Tichomonas
II. By means of resistant forms eg. Giardia
III. By means of vectors
Mechanical vector : an instrument of passive transfer
(fly feeding on faecal matter containing cyst of Entamoeba or Giardia
2. In direct life cycle: (Complex) Parasite has 2 or more hosts
Definitive host: sexual reproduction of parasite : Cat Toxoplasma
Intermediate host: Asexual reproduction of parasite :Human
Definitive host: Biological vector :Anophel Plasmodium
Intermediate host: :Human
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 Reproduction:
• (Amoeba & Flagellates: Asexual)
• (Apicomplexa: Asexual & Sexual)
I. Asexual reproduction:
1. Binary fission: (organells duplicated & ptozoan divides into
Two complete organisms)
A) Longitudinal BF (flagellates)
B) Transverse BF (Cilliates)
C) Irregular BF (Amoeba)
* Endodyogeny : 2 daughter cells form within the parent cell:

rupture after maturation & releasing the
smaller progeny

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2. Multinuclear dividing: protozoan grow to full size
A) Schizogony: a nucleus divides a number of times & then the cytoplasm
divides into smaller uninucleated merozoites (in Apicomplexa)

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B) Sporogony: the nucleus of oocyst divides & form infective sporozoites
within the oocyst (in Apicomplexa)

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II. Sexual reproduction:
1. Syngamy (Fertilization):
(Combination of male & female gametes leading to zygote)
A) Isogamy- 2 fusing gametes that are structurally & functionally simillar
eg. Monocytosis
B) Anisogamy- 2 fusing gametes are dissimillar eg. Ceratium
C) Oogamy- large non motile female gamete is fertilized with smaller
motile male gamete eg. Plasmodium
* After fertilzation, the diploid number of chromosomes (2n) is restored &
maintained constantly in a species.
2. Conjugation: Exchange of haploid nuclei

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Chapter 2:
Cilliates

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* Balantidium coli: (Balantidiasis)
• Largest among human pathogenic protozoa
• Invade intra intestinal tissue of large intestine.
• Oral-fecal transmission
• Water born epidemics

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Life Cycle:
@ Cyst ingestion by contaminated food & water > Excystation in small intestine >
Trophozoites colonize in large intestine > invading colon wall &
multiply by Binary fission & Conjugation > Encystation > cysts passing by faeces@
Clinical manifestations:
1. Opportunistic commensals
2. Mostly, secondary invaders
3. Produce hyalorunidase, superficial to deep ulceration,
4. similar to E.histolytica lesions but doesn’t invade extra intestinal tissues
5. mild entratitis
6. Diarrhoea & dysentery
Epidemiology:
1. Considered to be rare & occurs in less than 1% of human population
2. Most problems in area where water sources may be contaminated with human
or swine feces
Laboratory diagnosis:
• Demonstrating trophozoites or cysts in stool.

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Trophozoite:  Balantidiasis:
• Ovoid • Diarrhea or dysentry
• Covered with cillia • Abdominal pain
• Divide by binary fission • Nasusa
• Micro & Macro nucleus • Vomiting
Cyst: • Stool containing Blood, Mucus and Pus
• Spherical
Treatment:
• Tetracyclines
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Chapter 3:
Amoeba

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Amoeba:
• Life cycle- (Trophozoite: Motile feeding stage)
(Cyst: Quiescent resistant infective stage)
• Replication:
1. Binary fission-
2. Multinucleated cyst-
• Motility: extension of pseudopod (false foot) extrusion of cellular
ectoplasm, then drawing the rest cell (snail like movement)
• Pseudopoda types:
1. Lobopodium: large blunt extensions of body with ecto & endoplasm
2. Filopodium: Thin extensions of body containing only ectoplasm
3. Retculopodium: repeated branching of rejoining filopodia to form a net
4. Axopodium: can be extended or retracted, by addition or removal of
micro tubular material.

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Chapter 3-1:
Intestinal
Pathogenic
Amoeba
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A) Intestinal amoeba:
* Entamoeba histolytica: (Amoebiasis):
Life Cycle:
Cyst ingestion >>> stomach > duodenum
(troph) > local necrosis in large intestine
> hystolytica for tissue lysis by a cytotoxin
> lysosomal enzyme(phospholipase A2)
> Flask shaped ulcer >>> inflemation ,
Hemorrhagic, secoundary bacterial infection
> extension to deeper mucosa
> peritoneal cavity (80% death)
> secoundary involvement
> liver, lungs, brain, heart

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Clinical manifestations: Cyst
Excyst (Small intestine)
Commensal growth (Colon)

Magna (hematophage: invasive) Minota (noninvasive form)
Mucosal ulceration (colon) Continued commensal existence
Direct extension to skin Hematogenous spread to liver Desication

(sigmoid & rectum)
Cutaneous or perianal Hepatic abscess Encystation

amoebiasis
spread to brain & others Direct extension to cyst in feces

pleura, lung, pericardium
Brain abscess Lung or pericardial abcess

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Ingested mature cyst >>> Metacystic form >>> Trophozoite >>> Immature cyst
(4 nuclei) (8 nuclei) (1 nucleus) (1,2 or 3 nuclei)
<<< Mature cyst <<<

(4 nuclei)

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1. Trophozoites:
• 10-60 Micrometer, motile
• Karyosome: small, central
• Chromatin: fine, peripheral
2. Cysts:
• 10-20 micrometer, non motile, 1-4 nuclei
• Chromatoidals: ends rounded or square
• Infective stage
• Trophs:- anaerobic, no mitochondria, no cytochrome, no TCA

• It can be cultured in axenical medium (35-37oC) ; pH:7

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Epidemiology:
1. Greatest morbidity/mortality in the developing countries of central and
south America, Africa and India
2. Disease more sever in: very young, elderly, pregnant women
3. 40-50 milion symptomatic infections/year, 100 deaths annualy
4. In Dhaka, Bangladesh, 50% of children have serologic evidence of E.h infection
by 5 years
5. Groups at increased risk of amebiasis:
• Immigrants from endemic areas
• Long term visitors to endemic areas
• Institutionalized individuals
Treatment:
• Metronidazole
• Albendazole
• Tinidazole
----------------------------------------------------------------------------------------------------------------
Note: Entamoeba polecki:
Asia east Asia mostly in monkey & Pigs, rarely human, Shape similar E.histolytica
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Chapter 3-2:
Intestinal
commensal
Amoeba
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B) Commensal non pathogenic amoeba
1. Entamoeba hartmanni:
• (large intestine)
• Size : Trophozoite 4 -12
• Cyst 5 -10
• shapes similar to
E. histolytica

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2. Entamoeba coli:
Trophozoite Cyst
• 10 – 50 micrometer, sluggish • 10 – 35 micrometer, non motile
movement • 1 – 8 nuclei
• Karyosome: Large, eccentric • Chromatoidals: Ends Jugged
• Chromatin: Clumpy, peripheral
• Cytoplasm: no RBC, except in the
rare case of patients with intestinal
haemorrhage" that leads to blood
in the stools of these patients.
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3. Endolimax nana:
Trophozoite:
6 – 15 micrometer, sluggish movement
Karyosome: Large
Chromatin: little or not seen
Cyst:
4 – 14 micrometer, non motile
1 – 4 nuclei
Chromatidal bars: noting

33
4. Iodamoeba butsclii: (in large intestine)
Trophozoite:
6 – 25 micrometer ,
active motility
Karyosome: Large & central
Chromatin: Absent
Cyst:
6 – 20 micrometer,
non motile
1 Nucleus
Chromatidals: none
5. Entamoeba gingivalis:
Trophozoite: shape similar to E.hstolytica , size 5 – 35 micrometer
NO CYST Protozoology lecture for Bsc. Students by
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Chapter 3-3:
Tissue
Amoeba
35
• Naegleria fowlerii: (Amebic meningoencephalitis)
• Three morphological forms:
1. A feeding amoeboid trophozoite stage
2. A transitional flagellate stage
3. A dormant cyst stage
(It is the only pathogenic free-living amoeba with a flagellate state)
Life cycle
1. In the free-living state, the amoeboid trophozoite feeds on bacteria
and other organic materials. It reproduces by binary fission.
2. When deprived of nutrients, the trophozoite transforms into flagellate
state. This form is usually pear shaped with two flagella emerging from
the narrow portion. The flagellate form does not divide or feed.
3. It will revert back into the amoeboid form when nutrients are restored.
When conditions become adverse, such as diminished food supply or
colder temperatures, the trophozoite transforms into a resistant cyst
stage. It is the trophozoite stage that is infective.

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Pathogenesis:
• Incubation period : 3-15 days
• Young children > swimming in infected warm waters up to 46oC > via olfactory
tract > Brain
• Bifrontal or bitemporal headache, fever, nausea, vomiting, stiff neck, lethargy,
Confusion, coma
• 1/3 recorded cases > Death
• Examination 1 or 2 drops of fresh CSF by light microscope
• Treatment:
• Amphotereicin B & Miconazole / cholorinated swimming pools
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• Acanthamoeba:

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Life Cycle:
• Free living amoeba of soil & fresh and salt water
• Reproduction of trophozoites by binary fission
• Infective stage : Cyst transmitted by dust & Aerosols
Pathogenesis:
• Opportunistic pathogen > lung & skin infection in immunocompromised patients
• Infection hamatogenously spread to brain (Encephalitis) & Death
• Contaminated contact lens solutions is a source of infection
• Specimen from CSF, Eye,
Brain Biopsy
Treatment:
• No effective treatment for
lung , skin or brain

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Chapter 4:
Flagellates
Chapter 4-1:
Lumen Dwelling
Flagellates
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Giardia lamblia: (Giardiasis, Lambliasis)
Life Cycle:
@ Cyst ingestion by contaminated food & water > Excystation in small intestine >
Trophozoites remaining in small intestine > multiply by Binary fission >
cysts passing
by faeces@

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Incubation period: about 2 weeks
1. Silent cases without any symptoms (Asymptomatic)
2. Intestinal
• Malabsorption syndrome (Steatorrhoea)
• Mucus diarrhoea
• Dull epigastric pain
• Flatulence
• Chronic entrititis
• Acute entrocolitis
3. General:
• Fever
• Anemia
• Weight loss
4. Chronic cholecystopathy
Laboratory Diagnosis:
• Direct microscopic examination of faeces

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• Enterotest is performed when a physician suspects a parasitic infection, but
no parasites were found in stool samples.
Its sensitivity is comparable to duodenal aspiration.
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Epidemiology:
• Worldwide
• Most frequent protozoan intestinal disease
• Most common identified cause of water born disease
Treatment:
• Quinaqrine hydrochloride
• Metronidazole (Flagyl)
• Furazolidone (Furoxone)
• Probiotics could help the treatment
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Dientamoeba fragilis (the unflagellated human flagellate) :
• Despite its name, Dientamoeba fragilis is not an ameba but an intestinal flagellate, most
closely related to trichomonads.
• In human stool specimens, D. fragilis is almost always found solely as a trophozoite.
• The rare presence of putative cyst and precyst forms in clinical specimens has been
reported.

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Life Cycle:
Infective stage:
1. Trophozoites (transmission via helminth eggs
2. Possible involvement of precyst and cyst
@ Transmission by fecal-oral rout > infective stage ingestion > Trophozoites in lumen
of large intestine > Multiplication by binary fission > Shed in feces @
Note: Transmission via helminth eggs (eg. Ascaris, Enterobious) has been postulated
Laboratory Diagnosis:
• Trichrome staining; Trophozoites: 1 or 2 nuclei; cyst-like stages are rare.
• Pseudopodia are angular to broad-lobed and transparent.
• Most trophozoites are binucleate, some have only one nucleus.
• The nucleus typically has a fragmented karyosome with discrete chromatin
granules, and a thin nuclear membrane may be visible.
Protozoology lecture for Bsc. Students by 5 to 15 µm 47

• Diagnosis by detection of trophozoites in fecal smears stained with trichrome
or another permanent stain.
• The trophozoites are not usually detectable if stool concentration methods are
used.
• Trophozoites can easily be overlooked or misidentified because they are
pale-staining and their nuclei sometimes resemble those of Endolimax nana or
Entamoeba hartmanni.
• Mostly in children
• Both asymptomatic and symptomatic infection
(e.g., with various nonspecific gastrointestinal symptoms) have been reported.
1. Intestinal symptoms (Intermittent diarhea, Abdominal pain)
2. Other symptoms (nausea, anorexia, fatigue, malaise, poor weight gain
Epidemiology:
• Worldwide
• More common in children
Treatment:
• Carbarsone / Diphetrasone / Tetracyclines / Paromycin / erythromycin
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Trichomonas vaginalis: (Trichomoniasis, vaginitis)
• Most common prtozoal
urogenital tract infection
• Living 24 hrs in urine samples
or semen or water sample
• Living on a wet surface 1-2 hrs
Life Cycle:
• Direct life Cycle
• Only trophozoites
• Largely sexually transmitted

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1. Male: Asymptomatic carrier (symptomatic white discharge)
2. Female: fishy odor yellow or green discharge
Epidemiology:
• Worldwide.
• Over 170 million infections in women annually
• It is seen in all age groups.
• It is seen in both men & women.
• Women (Reservoir) / Men (Carrier)
Treatment:
• Metronidazole
• Tinidazole
* (The sexual partner should also be treated)

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Trichomonas tenax:
• Oral cavity of humans, dogs, cats
• Smallest Trichomonads
• Direct transmission (no cyst)
• Mostly in persons with periodontal disease
• Submaxillary glands
• May be found in oral cavity
• Unable to survive in intestinal tract
• Pathogenic role role in necrotizing ulcerative gingivitis &
necrotizing ulcerative periodontitis
• May be found in respiratory tract
of humans with chronic disease
• Diagnosis: Microscopic, PCR,
Culture on media

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Trichomonas hominios:
Pentatrichomonas (T.intestinalis):
• Non pathogenic
• Direct transmission
• 7-15 micrometer long
• Occures in Cecum & Colon of Mouse, Cat, Dog
• Cross transmitted among these species to human
• Non pathogenic to human
--------------------------------------------------------------------------------------------------
The pathology caused by Trichomonas may enhance the efficiency of HIV transmission. T. vaginalis
infection typically elicits a local cellular immune response with inflammation of the vaginal epithelium
and cervix in women and the urethra of men. This inflammatory response includes the infiltration of
potential HIV target cells such as CD4+ bearing lymphocytes and macrophages. T. vaginalis can cause
punctate hemorrhages on the vaginal walls and cervix. This leukocyte infiltration and the genital lesions
may increase the number of target cells for the virus and allowing direct viral access to the bloodstream
through open lesions. In addition, the hemorrhages and inflammation can increase the level of virus in
body fluids and the numbers of HIV-infected lymphocytes and macrophages present in the genital area
in persons already infected with HIV. This increase of free virus and virus-infected leukocytes can
increase the probability of HIV exposure and transmission to an uninfected partner. Increased cervical
shedding of HIV has been shown to be associated with cervical inflammation, and substantially increased
viral loads in semen have been documented in men with trichomoniasis. Moreover, since many patients
with Trichomonas infection are asymptomatic, or only mildly symptomatic, they are likely to remain
sexually active in spite of infection.
Sorvillo F, Smith L, Kerndt P, Ash L. (2001) Trichomonas vaginalis, HIV, and African-Americans.
Emerg Infect Dis. 7:927-32. Protozoology lecture for Bsc. Students by
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 Chilomastix mesnili:
• Worldwide
• Non pathogenic
@ Cyst ingestion (Infective stage) > Excystation in Large (and possibly small)
intestine > Presence of trophozoites in
cecum and/or colon > Cyst in faeces @

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Chapter 4-2:
Blood & Tissue
Flagellates
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Hemoflagellates: 2 Genera: Trypanosoma & Leishmania
• They require hematin for aerobic respiration from hemoglubin
• Different cycle stages > placement & origin of flagella
Leishman body Leptomonad crithidia

• Kinetoplast: A special part of mitochondrion > rich of DNA, controls certain
heriditary functions eg. Morphogenesis
• Kinetoplast in Geimssa staining: reddish purple & darker than nucleus in pale blue
cytoplasm Protozoology lecture for Bsc. Students by
55
Trypanosoma cruzi: (Chagas disease)
• Kissing bug = mostly bite people around
the month > infected human blood
ingestion > Epimastigote (mid gut) >
Trypomastigote (hind gut) >
biting new human > Trypo leave bug
in the faeces > human blood by
patient rubbing or scraching >
migration to tissues (cardiac, muscle,
liver, brain) > lose flagellum & undulating
membrain > become smaller, intracellular
(Amastigote form) & multiplication >
destroy the host cells >
return to blood in Trypomastigote form >
attack to other cells or ingested by bug
 Diagnosis:
• Thin blood smear for acute stage
• In progressive infections: trypomastigotes leave bloodstream > difficult finding
• Culture of blood & biopsy of lymph nodes > detecting Amastigote
• Serologic tests Protozoology lecture for Bsc. Students by
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 Trypanosoma brucei: (African Trypanosomiasis : Sleeping sickness)
• Agents:
1. Trypanosoma brucei rhodesiense (East AT)
2. Trypanosoma brucei gambiense (West AT)
• Vector:
• TSE TSE Fly (Glucina Species)

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Life Cycle:
@ TSE TSE bite > Trypomastigote (in salivary glands) infective stage for human >
Blood & Lymphs > invade CNS > Reproduction (Blood, lymph, spinal fluid) >
TSE TSE Bite > infected fly > Reoroduction in mid Gut (Epimastigote) >
Transfer to Salivary glands > Changing Epimastigote to Trypomastigote >
Infective stage for human@
• Thick & Thin smear
• Using concentrated anticoagulated
blood
• Aspiration from lymph nodes &
concentrated spinal fluid
• 2 subspecies are indistinguishable
• Pleomorphic, 12-42 micrometer long
(mean 30)
• Small kinetoplast, well developed
undulating membrane
• Posterior end is more rounded than
T.cruzi
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1. Initial chancre (lymph adenitis) > T.b rodesiense , seldom T.b gambiense
2. Enlargment the posterior cervical chain of lymph nodes
mostly in T.b gambiense (Winterbottom’s sign)
3. Lesions persist weeks > multiplication > Trypanosomes > Circulation >
Recurrent fever, Head ache, lymph adenopathy, spleenomegaly
Comma, Death.
Epidemiology:
Vector: Glucina species
1. In west Africa :
• Riverrine TSE TSE (Palpalis group) > living in Bush
• Man-Fly-Man Cycle , some times domestics
• Transmission Day time
• Vector: TSE TSE (Glusina species)
2. In East Africa:
• Open Savanah
• Animal-Fly-Human Cycle
• Vector: TSE TSE (Morsitans group)
Treatment Protozoology lecture for Bsc. Students by
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• Pentamidine & Arsenical suramin / control: insecticides
 Leishmania: (Leishmaniasis)
1. L. tropica (Cutaneous Leishmaniasis)
2. L.donovani (Visceral Leishmaniasis)
3. L.braziliensis (Mucocutaneous Leishmaniasis)
• Vector: Sandfly : Genera (Phlebotomus / Lutzomyia)

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Life Cycle:
• Life cycles of all Leishmania are common
• Differences: epidemiology, tissues affected, clinical manifestation
@ Infected sandfly bite human > Transfer Promastigote via saliva > penetration to
skin > changing to Amastigote > invade to different tissues (according to
species) > uninfected sandfly bite infected human > ingestion Amastigotes >
changing to promastigote > migration to proboscis > new infection by biting @
1. Leishmania donovani:
(Visceral Leishmaniasis: Kalaazar or Dumdum fever Black disease)
Epidemiology:
• Asia, South east Asia
• Vector: Sandfly (Plebotomus)
Clinical syndrome:
• First: Chills, sweating similar to Malaria
• Late: Enlargment of reticuloendothelial organs, weight loss
Post kalaazar dermal leishmaniasis (deeply pigmented granolomatous areas of skin)
A. Chronic disease
B. Lethal Protozoology lecture for Bsc. Students by
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• Diagnostic stage: Amastigote in Tissue biopsy
• Aspiration of bone marrow, lymph nodes,
• Culture of blood, bone marrow
Treatment:
• Stibigluconate
• Protection from sandfly
2. Leishmania tropica:
(Cutaneous Leishmaniasis: Old World Leishmaniasis, Aleppo boil,
oriental or lahore sore, Baghdad button )
Physiology & Structure:
• Same to L.donovani
Epidemiology:
• Asia, Africa, Mediterranean Europe, Southern Russia
• Vector: Phlebotomus sandfly
• Reservoir: Dog
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Clinical syndrome:
• Incubation period: weeks to 2 months
1. Red papule (on bited skin)
2. Irritation & enlarge & ulcerate (hard ulcer & exudated)
3. Secondary bacterial infections
4. Lesion may be heal after months
5. Scar

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1.L.tropica: (City form or Dry lesion)
• Vector: Phelobotomus sergenti, Reservoir: Human, Dog
2. L.major: (Village form or moist lesion)
• Vector: Phlebotomus papatasii, Reservoir: Rodents
3. L.aethiopica (Village form or moist lesion)
• Vector: Phlebotomus longipes, Reservoir: Rock hyrax
• Giemsa Stained smear
from touch preparation
• Biopsy & culture
from ulcer to see Amastigotes
• Serological tests
Treatment:
• Stibogluconate
• Applying heat directly to lesion
• Protection from sandfly

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3. Leishmania braziliensis:
(American Leishmaniasis: Mucocutaneos Leishmaniasis : Old world Leishmaniasis :
Chiclero Ulcer : Espundia : UTA)
Physiology & Structure:
• Same to L.donovani
Epidemiology:
• Central & South America (rain forest)
• Vector: Sandfly (Lutzomiya)
Clinical syndrome:
• Incubation period: similar to L.tropica
• Difference to L.tropica (Involvement & destruction of mucus membranes) with
Secondary bacterial infections
Laboratory diagnosis & Treatment:
• Similar to L.tropica
• Note:
Leishmania mexicana is similar to L.braziliensis
but only cutaneous:
DCL: Diffuse Cutaneous Leishmaniasis
65
Chapter 5:
Apicomplexa

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Sporozoa:
• Large group called Apicomplexa
 Kingdom: Protista
 Subkingdom: Protozoa
 Phylum: Apicomplexa
 Class: Sporozoa
 Order: Coccidia
 Genus / Species
 Reproduction:
1. Asexual (Schisogony)
2. Sexual (Gametogony)
Classification:
A) Intestinal parasites:
1. Isospora
2. Cryptosporidium
3. Sarcocystis
B) Blood and tissue parasites:
1. Plasmodium
2. Toxoplasma Protozoology lecture for Bsc. Students by
67
Chapter 5-1:
Intestinal
Sporozoa
68
A) Intestinal parasites:
1. Isospora belli:
• Diagnostic stage: Immature oocyst
• Infective stage: Mature oocyst
 Life cycle:
1. Mature cyst ingestion
2. Shedding in small intestine
3. Sporozoa penetrate intestinal cells
4. Asexual reproduction: Merozoites
5. Sexual reproduction:
• Micro + Macro gametes to Zygote
• Zygote turns to Immature oocyst in
intestine lumen
6. Immature oocysts in feces
 Pathogenesis:
• Acute, non bloody diarrhea with campy
abdominal pain can last for
weeks,Malabsrbtion and weight loss
• Sever diarrhea in immunodepressed
69
pataints & children. Maybe Eosinophilia
70
• Mild to sever gastro intestinal disease (Mimics to giardiasis)
 Diagnosis:
• Acid fast stain to observe immure oocysts
 Treatment, prevention and control:

• Trimethoprim – sulfometaxazole
• Personal hygiene

71
2.Cryptosporidium parvum:
Diagnostic stage: Immature oocyst
Infective stage: Mature oocyst
 Life cycle:
Mature cyst ingestion
Shedding in small intestine
Sporozoa penetrate intestinal cells
Asexual reproduction: Merozoites
Sexual reproduction:
Micro + Macro gametes to Zygote
Zygote turns to Immature oocyst in
intestine lumen
6. Immature oocysts in feces
 Pathogenesis:
• Mechanism: not known
• Non invasive but host cells
are damaged

72
73
 Treatment:
• Nitazoxanide
• Normal immunity recover spontaneously cryptosporidiasis
• Life treatening in immunocompromised patants
74
3. Sarcocysis lindemani:
• It can be detected in stool
• Isolated from pigs and cattle
• Identical in all aspects to Isospora
with 1 exception.:
Sarcocystis oocysts rupture before
passage in stool specimens and only
sporocysts will be present.

75
Chapter 5-2:
Tissue
Sporozoa
76
B) Blood and tissue parasites:
1. Toxoplasma gondii:
• Definitive host:
Cat family
• Intermediate host:
Mouse, Sheep, Goats, swine
Human
 Different forms of Toxoplasma:

1. Tachyzoites (Trophozoites)
2. Bradyzoites (in Tissue cyst)
3. Oocyst (resistant form in
cat feces via sexual reproduction)

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Parasites in definitive host (Cat):
1. Intra intestinal stage (Cat):
@ cat ingests mouse with tissue cysts:
releasing Bradtzoites in small intestine:
Penetration to epithelial cells:
I) Asexual reproduction= Tachyzoites
II) Sexula reproduction:
(Male+Female) gametes=
zygote with 2 walls: oocyst:
Excrete in feces
III) Sporulation outside the cat body
maturation after 1-5 days
simillar appearance to Isospora
remain infectious in soil for months

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2. Extra intestinal stage (Cat):
• cat ingests (mouse) or herbivores
with tissue cysts:
• releasing Bradtzoites in small
intestine:
• Penetration to lamina propria:
• Asexual reproduction= Tachyzoites
• Transfer by Lymph & blood
• Enter any types of cat cells
• Multiplication
• Host cells filled by tachyzoites & die
• Tachyzoites released & enter new cells
• Tissue necrosis
• Cat immunity overcome this stage
• Changaing to Bradyzoites in
cysts in different tissues
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 Human infection by Toxoplasma gondii:
 Only Extra intestinal stage (all intermediate hosts)
1. Tissue cyst ingestion in herbivores : Bradyzoites
2. Oocyst ingestion via food contaminated with cat feces : Sporozoites
tissue necrosis by intracellular multiplication of Tachyzoites
3. Congenital toxoplasmosis : Tachyzoites
• Ocular disease (posterior chamber) sometimes entire eye
• proliferation in retina
• Inflamation of chroid
• Retinochoroiditis
lesions yellow, white,
cotton like patches

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Epidemiology:
• Worldwide spread (0.5 bilion of human have antibody to T.gondii)
 Diagnosis:
I. Serologic examination:
Sabin-feldman test:
Tachyzoites (Ag) : dilutions of test serum (sensitive, high cost)
Titration:
[Human serum – Antibody – (live virulent Toxoplasma )]
If : Ab (high) > Toxoplasma (to be killed) > not stainable in blue field
If : Ab (low) > Toxoplasma (Alive) > highly stainable in blue field
Indirect fluorescent antibody test (IFAT):

Titration
A) [Human serum – Antibody – (Killed Toxoplasma )] commercially available
Microscopic observation by UV light
B) Finding Ab in undiluted serum > indicates ocular Toxoplasmosis

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II. Histocytologic examination:
Host tissue biopsy > impression smears of lesions
• on glass slides : 10-30 min smear fixed in methyl alcohol & stained with Geimssa
In this section > Tachyzoites > oval to round
Cysts > spherical > silver positive walls
Bradyzoites > stain strongly with Acid Schiff stain
Electron microscopy
 Treatment:
• Sulfonamides & Prymethamine) synergistically blocking metabolic pathways
involving para amino benzoic acid and foilc acid cycle
• During drug using > Thorombocytopenia & Leukopenia
• Sulfonamides for acute stage of disease
• Spiramycin used for peregnant women
• No vaccine
 Control:
1. Meat > cooked (66oC) before eating
2. Hands, after handling meat > washing with soap & water
3. Cats feeding > not raw meat (canned food & cooked meat)
4. Keeping cats > Indoors, litter boxes change daily
5. Cat faeces > flushed down to toilet
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6. Garden working > with glowes
Chapter 5-3:
Blood
Sporozoa
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 Plasmodium: (P.vivax, p.malariae, p. ovale, p.falciparum)
• Sporozoan parasites of blood
• 2 Hosts:
I. Mosquito (Sexual reproduction stage) = gametocytes
II. Human (Asexual reproduction stage) = Schisogony
• Life cycle:

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• Life cycle:
I. Human stage:
1. Exoerythrocytic cycle (Preerythrocytic cycle= liver phase)
• Infected Anophel biting human > sporozoites > circulatory system >
liver paranchymal cells > Asexual reproduction : Schizogony)
Note: P.vivax & p.ovale > dormant hepatic phase > sporozoites change to
sleeping forms or Hypnozoites without dividing
After months to years > Relapsing Malaria
• Hepatocytes > rupture liberating plasmodia as Merozoites >
attach to receptors of RBC
2. Erythrocytic cycle:
• Asexual reproduction > series stages > trophozoite growth dividing > merozoites
RBC rupture > initiate another EC
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• Some merozoites inRBC > maleDr.&Farokh
female gametes
Rokhbakhsh Zamin in blood
II. Anophel stage: (sexual reproduction)

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 Ingestion of gametocytes by female Anophel
1. Anophel intestine lumen:
I. Male Microgametocte > dividing 3 times > 6 – 8 nuclei >
several flagellated Microgametes (Exflagellation)
II. Female Macrogamete > without division > Macrogamete
I + II > flagelated Microgamete + Macrogamete = zygote

Remaining inside intestine 12 – 24 hrs.
2. Anophel intestine cells:
• Ookinet (motile worm like) > oocyst containing sporozoites
3. Anophel body cavity:
• Releasing sporozoites > migration to salivary glands
• Pathway in Anophel : 10 – 17 days

• Clinical manifestation: (1 paroxysm 6 – 10 hours)
1. Cold stage: 1 hour
• Shivering, feeling colds (releasing merozoites from infected RBC)
2. Hot stage: 6 – 12 hours
• Fever up to 41oC, dry skin, headache, Nausea, vomiting
3. Wet stage: 2 – 4 hoursProtozoology lecture for Bsc. Students by
• Fever drops until entire sweating
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Pathogenesis:
1. 1st symptoms & signs > rupture of RBCs (after schizogony & maturation in RBCs)
> host immune response > cytokinins & other cellular products
> responsible for fever
2. P. falciparum causative most deaths > parasites adhere to endothelium capillaries
& post capillary venules > obstruction of microcirculation & local tissue anoxia
• In brain: Cerebral Malaria
• In kidney: Renal failure
• In intestine: Ischemia & ulceration > gastrointestinal bleeding > Bacteremia >
secondary infections in circulatory system
3. Severity of Malaria associated anaemia > degree of parasitemia >
haemolysis or phagocytosis of parasitized RBC >
phagocytosis of uninfected RBC > Autoimmune haemolytic anaemia >
Massive intravascular haemolysis > haemoglubinuria & renal failure >
Syndrome called Black water fever

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Host defences:
• Susceptibility to Malaria-
I. hereditary factors:
1. Sickle cell trait (sickle cell anemia) > protect against P. falciparum
2. Most blacks (no Duffy blood group antigens) > no receptor for P. vivax
3. G6PD deficiencies & thalassemia > protect to malaria
II. Acquired factors:
• In malaria areas > prevalence & severity of Malaria decrease with age >
Adults suffer repeated malaria infections
• Individuals mostly exposed to malaria > T helper & Abs against sporozoites, blood
stages, sexual stages
• These Abs decrease susceptibility to reinfections
• Abs against sexual stages (gametes) > decrease malaria transmission
• Cytokines against all stages ; cytotoxic T cells against liver stages
• Ab mediated immunity transfer from mother to fetus
• Immunity in new borns lost within 6 – 9 months
• Pregnant women > more susceptible

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Epidemiology: (anophele, patient, normal human)
1. Transmission mostly by female anophele in tropic & subtropic areas
2. Transmission by needle (intravenous drug abuser)
3. Congenitally > mother to offspring
• In many regions > P.falciparum > resistant to chloroquine
Control:
I. Blood schizonticides:
• For clinical cure (elimination of symptoms & signs of Malaria attack
1. Mefloquine
2. Pyrimethamine / sulfodoxin
3. Quinine
4. Quinidine
II. Tissue schisonticides: (eg. Primaquine)
• For radical cure (elimination of parasites from tissues)
• Specially for hypnozoites of P.vivax & P.ovale > therapy against liver stage
Prevention of Malaria:
I. Avoiding exposure to Anopheles: (From dusk to dawn)
1. Wearing protective cloths
2. Staying & Spraying in screened area
3. Insect repellent use (eg. N,N – diethyl
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Students by
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II. Chemoprophylaxis: using drugs Dr. Farokh Rokhbakhsh Zamin
against asexual erythrocytic stage
Diagnosis:
• Demonstration of plasmodia (1. Thin blood smear 2.Thick blood smear)
• Since p.falciparum sequestered in microcirculation of deep organs > blood smear

> every 6 – 12 hours for 48 hours
• Rapid , sensitive technique : flourescent staining
• Immunologic assay > detection of Ab
Protozoology &
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1
6
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The morphology of Malaria parasites:
Plasmodium vivax
1. Early trophozoite (Ring form)
2. Late trophozoite with ameboid cytoplasm (very typical of P.vivax)
enlarged RBC with schuffner’s dots
3. Immature schizont
4. Mature schizont with Merozoites (18) and clumped pigment
5. Microgametocyte with dispersed chromatin
6. Macrogametocyte with compact chromatin
Plasmodium falciparum
1. Early trophozoite (accole or applique form, Ring form, headphone configuration)
2. Late trophozoite with normal size RBC with Muer’s dots
4. Mature schizont with Merozoites (24)

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Plasmodium malariae
2. Early trophozoite in normal size RBC (Band form)
4. Mature schizont with Merozoites (9) arranged in a rosette
Plasmodium ovale
2. Late trophozoite in (enlarged RBC, fimbriated edges) with schuffner’s dots
4. Mature schizont with Merozoites (8) arranged irrigularly

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• Babesia microti: (Babesiosis)

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• Zoonosis infection : deer, cattle, rodent, human (Accidental host)
• Intracellular parasie resemble Plasmodia
• Vector: Ixoid Tick
Life Cycle:
@ Infected Tick > Human biting > Trophozoites attack to RBC > Binary fission > Tetrad >
RBC lysis > releasing Merozoites > Infect other RBCs (Erythrocytic cycle) >
Ingested by non infected thick > Intestinal epithelium > Asexual division >
Reproduction in hemocytes, Muscle cells > Salivary glands > Pyriform bodies >
Infective stage for human by biting@
• Transovarian transmission in thick
Pathogenesis:
• Incubation period: 1-4 weeks
• Malaise, fever without periodicity, headache, chills, sweating, fatigue, weakness
• Hemolytic anemia
• Hepatomegaly & spleenomegaly
Epidemiology:
• Transmission: Ixodes dominii
• Most infections: mild, Asymptomatic

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• Examination of Blood smears (should differentiate Babesia & Plasmodium
• Samples may be negative > low grades of parasites
• Inoculating samples to hamster
• Serologic tests
Treatment:
• Clindamycin & Quinidine

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The End

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Medical Protozoology Presentation

Presentation · May 2019

Farokh Rokhbakhsh Zamin

Iranian Date Palm germplasm View project

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* Endodyogeny : 2 daughter cells form within the parent cell:

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Excyst (Small intestine)

Commensal growth (Colon)

Mucosal ulceration (colon) Continued commensal existence

Direct extension to skin Hematogenous spread to liver Desication

Cutaneous or perianal Hepatic abscess Encystation

spread to brain & others Direct extension to cyst in feces

Brain abscess Lung or pericardial abcess

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<<< Mature cyst <<<

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• Trophs:- anaerobic, no mitochondria, no cytochrome, no TCA

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Protozoology lecture for Bsc. Students by 5 to 15 µm 47

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Leishman body Leptomonad crithidia

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 Treatment, prevention and control:

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 Different forms of Toxoplasma: