Protozoology

 Eukaryotic
 Unicellular
 Motile
 Generally has 2 stages: Trophozoite and Cyst
o Trophozoite: Actively feed and multiply
o Cyst: Protective stage – must survive outside host
 Reproduction: Binary fission; Asexual and sexual reproduction in
Apicomplexa
 Pathogenesis: Proliferation, Diffusion, Opportunistic parasitosis
 Habitats in Humans:
o Skin: Leishmania
o Eye: Acanthamoeba
o Mouth: Amoeba and flagellates
o Gut: Giardia, Entamoeba, Cryptosporodium, Isospora,
Balantidium
o Urogenital: Trichomonas
o Blood: Plasmodium, Trypanosoma
o Spleen: Leishmania
o Liver: Leishmania, Entamoeba
o Muscle: Trypanosoma cruzi
o Central Nervous System: Trypanosoma, Naegleria, Toxoplasma,
Plasmodium
Phylum Sarcomastigosphora

Class Zoomastigospora
o Motile by Flagella

Giardia Lamblia
Life cycle: Mature cyst ingested -> Hatch into trophozoites -> Binary
fission -> Colonization in duodenum [crypts of duodenal and jujenal
mucosa]
Infective dose: 10-100 cysts
Transmission: Ingestion, person-to-person in children, male homosexual,
and mentally ill person
Pathogenesis:
G. lamblia adhered to the intestinal epithelium using sucking disc -> cell
apoptosis and increased lymphatic infiltration -> villus atrophy and crypt
cell hypertrophy -> repopulation by immature enterocytes -> reduced
absorptive capacities
G. lamblia infection also leads to inflammation and lactase deficiency
Reduced digestion and absorption may lead to osmotic diarrhea and
malabsorption symptoms [fat malabsorption: Steatorrhea, can’t absorb
other fat-soluble substances as well]
Stool may be watery, semisolid, greasy, bulky, and foul smelling
Sometimes, colonize gall bladder -> biliary colic & jaundice
Treatment: Metronidazole
Prevention: Chlorination and filtration of water, disposal of waste water
and feces, personal hygiene
Lab diagnosis:

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 Formed feces -> Cyst
Diarrheic feces -> Trophozoites

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 Trichomonas vaginalis
Habitat: Urogenital system [vagina, bathrolin gland, urethra, urinary
bladder, epididymis, prostate gland, preputial sac]
Life cycle: No cyst stage [kaya entamoeba gingivalis]
Transmission: Hub sexual -> Ping Pong phenomenon; Handuk bersama;
Saat persalinan
Pathogenesis & Clinical Manifestation:
 Menginfeksi epital skuamous
 Adhesion, hemolysis, sekresi enzim
 Menyebabkan ptekiae (strawberry cervix/strawberry vagina),
perubahan metaplastic, desquamasi sel epitel
 Purulent discharge warna kuning kehijauan
 Gatal dan panas pada vagina, sakit saat BAK dan sex
Lab Diagnosis: Wet mount – if negative -> Kultur (gold standard)

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 Other species:
Trichomonas tenax – tartar and gums of the mouth; not pathogenic
Trichomonas hominis – not pathogenic; associated with diarrhea

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 Leishmania
 Amastigote -> in human inside endothelial cell of capillary, near
lymph node, and inside mononuclear phagocytic cells
 Promastigote -> in intestine of Phlebotomus (sandfly)
 Endemic: Turkey, Uganda, Africa
 Pathogenesis:
Leishmania tropica
o Infection in stratum corneum -> crateriform lesion -> ulcer.
Location of Leishmania: edge of crater region in lymph node
o Volcano-like lesion/Raised outline
Leishmania braziliensis
o Cutaneous lesions on lower extremities, face, earlobes
o Tend to migrate to muco-cutaneous junction; nasal septum,
cheek mucosa, nasopharynx mucosa, larynx
o Complications: fever, anemia, hepatosplenomegaly
o Diagnosis: PCR (braziliensis vs tropica); Montenegro skin test
Leishmania donovani [HIGHEST DEATH RATE]
o Visceral leishmaniasis
o Tropical splenomegaly
o Kala azar
o Dundum fever
o Anemia

Congenital Parasitic Infection: low birth weight, respiratory

distress, hepatomegaly, death.

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 Trypanosoma
Possess flagellate and kinetoplast
Cyclozoonoses
Cyclopropagative
Trypanosoma gambiense
 Vector: Glossina palpalis [tse-tse flies]
 Zoonotic
 Life cycle:
o In human:
Metacyclic trypomastigote injected into human by tse-tse fly ->
Bloodstream trypomastigote -> Binary fission
o In fly:
Trypomastigote in blood get ingested by fly -> Into procyclic
trypomastigote in midgut -> Binary fission -> Epimastigote ->
Multiply in salivary gland and transform into metacyclic
trypomastigotes -> infect other human
 Pathogenesis & Clinical Manifestation:
o Does not invade tissue cells, but inhabit connective tissue
spaces
o Haemo-lymphatic stage: trypanosomes multiply in subcutaneous
tissues, blood, and lymph
o Neurological stage: parasites cross Blood-Brain Barrier ->
Changes of behaviour, confusion, sensory disturbances, poor
coordination, disturbance of sleep cycle [Sleeping sickness]
o African typanosomiasis (Sleeping Sickness)
o Enlargement of spleen, liver, lymph node, postcervical triangle
(Winterbottom’s sign) -> Kerandel’s sign -> nephritis, anemia

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  Morphology: 1 form – trypomastigote
 Endemic area: Africa

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  Trypanosoma cruzi
 Vector: Reduviid bug [Triatoma, Rhodnius, and Panstrongylus]
 Cyclo-propagative, Zoonotic
 Pathogenesis & Clinical Manifestation:
o Chagas’ Disease: The disease can be mild, causing swelling and
fever, or it can be long lasting.
 Chagoma (lesion): block lymphatic capillaries and produce
edema of the area
 Edema eyelids = Romana’s sign
 Anemia
 Chronic: Congenital heart failure, Adam-Stokes
syndrome, other cardiac symptoms
 Deranged peristalsis
 Morphology: Amastigote in reticuloendothelial and other tissue cells.
Trypomastigote in blood

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Phylum Sarcomastigosphora

Class Lobosea
o Motile by Pseudopods & Amoeboid Movements

Entamoeba Histolytica | Pathogenic

o Transmission: Fecal-oral; Contamination of food and water
o Zooanthroponoses
o Life Cycle:

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 o Cysts:
o Resistant to chlorination
o Susceptible to drying, deep freezing, heated to 50o C for 5
minutes
o When excysted, release 4 trophozoites
o Pathogenesis, Clinical Manifestations:
o Intestinal:
 Diarrhea > 2 weeks, 6 to 8 motions a day
 At Mucosa

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  Lysosomal enzymes – cytopathogenic effect
 Active pseudopodal movement – penetrate intact
mucosa
 At Submucosa lateral
 Lysis and necrosis – flask-shaped or diamond-
shaped ulcer
 Mild: Amoebic appendicitis (tenderness in the caecal
region)
 Moderate-Severe: Blood and mucus in feces
 Severe: Peritonitis -> Sepsis, hypovolemia, perforation ->
Necrotizing colitis
 Repeated infection: granuloma
o Extraintestinal
 Amoebic Liver Abscess:
Process: Multiplication of trophozoites - obstruction –
thrombosis of sinusoids – necrosis of liver cells – liver abscess –
liquefaction of centre of abscess - “Anchovy sauce pus”
Rupture of abscess: metastasis to lungs, brain, skin, spleen
Trophozoite in peripheral zone of abscess
Symptoms: Fever, epigastric and/or shoulder pain, rarely diarrhea
 Lung: Fever, cough, dyspnea, pain, vomica
 Cutaneous: Perianal ulcers, urogenital
 Brain: Hematogenous
o Virulence Factors:
o Proteinase
o Amebapore
o GaI/GaINAc-binding lectin
o Lab Diagnosis:
o Liver aspirate & Stool (trophozoite)

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  Trophozoite with red blood cell in cytoplasm = Ulceration
 Stool taken 3-times, weekly interval
o Ultrasound
o Raised WBC
o Serology
o Therapy: Metronidazole
Entamoeba Coli| Non-Pathogenic
o Hosts: Man, Primates, Pigs
o Life cycle and habitat same as E. histolytica
o Does not invade tissue
Entamoeba gingivalis
o Hosts: Man, Primates, dogs and cats
o Habitat: Surface of teeth and gums
o Transmission: Mouth-to-mouth, droplet spray, sharing eating utensils
o Life cycle: Trophozoite, no cyst stage [kaya t vaginalis]
o Clinical manifestations: Dental caries
Naegleria Fowleri | Free-Living Amoeba | Potential Pathogen
o Life cycle: Amoeboid trophozoite, Flagellate, Cyst
o Infection: Inhaled while swimming in contaminated water
o Clinical manifestation:
o Primary Amoebic Meningoencephalitis
 Stiff neck
 Lethargy
 Haemorrhagic inflammation and necrosis of brain tissue
o Drug of choice: Amphotericin B

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 o Lab Diagnosis:
o CSF or brain tissue: Amoeba form

Acanthamoeba | Free-Living Amoeba | Opportunistic Pathogen

o Obligate or facultative intracellular in phagocytes
o Morphology:
o Trophozoite: spine-like projections of plasma membrane
o Cyst: Double wall – outer is wrinkled, many pores (osteoles)
o Infection:
o Invasion through broken skin
o Inhalation of aerosol or dust
o Prolonged use of contact lenses

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 o Clinical manifestation:
o Granulomatous Amoebic Encephalitis
 Only in immunocompromised patients
 Stiff neck, Seizures, Headache, Nausea
o Amoebic Keratitis
 Superficial corneal abrasions
 Ulcerative keratitis
 Because of contaminated contact lens
o Chronic granulomatous skin ulcers
o Lab Diagnosis:
o Brain tissue: Trophozoite, cyst, multinucleate giant cells
o Corneal tissue: Trophoize and cyst
o Drug of choice: Sulfasiazinem, penicillin, chloramophenicol
o Keratitis -> ketoconazole, miconazole, keratoplasty

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Phylum Apicomplexa

Class Sporozoa
Most have sexual and asexual stages
Adult forms are non-motile

Cryptosporidium
o Intestinal protozoa
o Obligate intracellular on microvilli of intestinal tract and respiratory
tract
o Zoonotic
o Transmission: Fecal-oral route; Ingestion
o Oocysts ingested -> sporozoites excyst & invade intestinal cells -> s
multiply asexually -> released -> infect other intestinal cells to begin a
new cycle
o They also reproduce sexually, forming male microgamonts and female
macrogamonts that fuse and develop into oocysts.
o Oocyst: Contain 4 sporozoites
o Resistant to chlorine, can survive in pH 3-10 > 24 hours
o Susceptible to drying, pasteurization, temperature >65oC for 30
minutes, freeze-drying, ozone, UV, ammonia, 10% formalin
o Pathogenesis:
o Immunocompetent: self-limiting disease;
 Intestinal – Profuse and watery diarrhea
 Respiratory cryptosporidiosis – bronchitis

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  Immune response: IFN-gamma, TNF-alpha, IL-12
o Immunodeficient:
 Cholera-like illness
 Sclerosing cholangitis-type lesion -> Acalculous cholecytis
 Severe respiratory cryptosporidiosis
o Lab Diagnosis:
o stool: oocyst [red, round formation – needs modified acid-fast
stain]

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 o

Plasmodium
o In blood
o 4 Species: Plasmodium vivax, Plasmodium ovale, Plasmodium
malariae, Plasmodium falciparum
o P. vivax & P. ovale has hypnozoites -> can relapse
o P. falciparum most pathogenic because it infects all kinds of RBC
lebih toxic -> induksi monocyte terus -> fever terus menerus

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 highest death rate
causes cerebral malariae
o P. malariae = longest incubation period
o P. falciparum = shortest incubation period
o P. malariae affect mature erythrocytes; P. vivax & ovale affect
reticulocytes; P. falciparum affects all
o Intermediate host: humans
o Definitive host: Mosquito (Anopheles)
o Endemic areas: Papua, Papua Barat, Maluku, NTT
o Clinical features: Anemia, parasitemia, splenomegaly, hepatomegaly
o Obstetric complication: Maternal anaemia, haemorrhage during
childbirth
o Congenital: Abortion, stillbirth, hepatomegaly, jaundice,
splenomegaly, anaemia, fever
o Histopathological changes in cerebral malariae: Sequestration
and Ring Haemorrhage
o Lab Diagnosis:
o Microscopic Examination
 Thick smear: No fixation; Giemsa; Screening
 Thin Smear: Fixation (+); Giemsa & Acridine Orange;
Species identification
o Therapy
o For uncomplicated malariae:
 1st Choice:
Dihydroartemisin + Piperaquine (3 days) + Primaquine (1st
day only for P. malariae & falciparum, 14 days for P. ovale
& vivax)

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  Alternative choice:
Quinine + Tetracycline or Clindamycin + Primaquine (1st
day only for P. malariae & falciparum, 14 days for P. ovale
& vivax)
o For pregnant women:
 1st trimester: Quinine + Clindamycin, alt: Artesunate +
Clindamycin
 2nd & 3rd trimesters: ACT or artesunate + clindamycin or
quinine + clindamycin
o For lactating women:
 Anything is okay except Tetracyclin and Primaquine
o

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 Toxoplasma gondii
o Obligate intracellular in phagocyte
o Intermediate host: humans, mammals, birds
o Definitive host: cat, felines
o Zoonotic
o Oocyst:
o Susceptible to temperature 45-55oC, drying, formalin, ammonia,
iodine
o Cyst:
o Not infective when heated to 66oC
o Transmission:
o Eating undercooked meat with tissue cyst
o Ingesting food or water contaminated by cat feces
o Blood transfusion [parasite is in phagocyte] or organ
transplantation [parasite as tissue cyst]
o Transplacentally [mother to fetus]
o Clinical:
o Pregnant women
 Chronic toxoplasmosis: menurunkan antibody ke bayi
 Acute toxoplasmosis: menularkan bayi
 1st trimester -> abortus
 2nd and 3rd trimester -> classic triad [hydrocephalus,
retinochoroiditis, intracranial calcification]
o Lab Diagnosis:
o Serology: IgG paling lama stay
o Therapy:

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 o 1st Trimester -> Spiramycin
o 2nd and 3rd Trimester -> Pyrimethamine
o Folic Acid
o Prophylactic therapy

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Phylum Ciliophora

Class Kinetofragminophorea
o Motile by Cilia

Balantidium coli
o Transmission: Fecal-oral; Contamination of food and water
o Endemic area: West Papua
o Zoonotic [pig to human]
o Life Cycle:
o Excystation in small intestine
o Binary fission in large intestine
o Pathogenicity & Clinical Features:
o Hyaluronidase -> flask-shaped ulcers -> diarrheic stools with
blood and mucus
o Genitourinary infections
o Peritonitis, colonization of nasopharynx
o Therapy: Tetracycline
o Diagnosis:
o Formed stool: Cyst
o Diarrheic stool: Trophozoites

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