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PROTOZOA FLAGELLATA

dr. Paramita Septianawati

Departemen Parasitologi Kedokteran


Fakultas Kedokteran
Universitas Muhammadiyah Purwokerto
PROTOZOA

 jasad renik (mikro organisme) hewani, satu sel, hidup sendiri/ dalam bentuk koloni
 satu kesatuan yang lengkap yang sanggup melakukan semua fungsi kehidupan
 Definisi Protozoa berasal dari kata protos/proteus yang berarti pertama dan
zoon artinya hewan. Jadi, protozoa adalah hewan invertebrata pertama yang
bersel satu. Protozoa termasuk mikroorganisme (mikros=kecil,
organism=makhluk hidup), besarnya antara 3 mikron sampai 1000 mikron,
sehingga untuk melihatnya diperlukan mikroskop.
KARAKTERISTIK
 1. Bersel satu, berkoloni, simetris tubuh tidak ada, bilateral, radial atau spherical
 2. Bentuk sel umumnya tetap kecuali Rhizopoda
 3. Inti jelas, satu atau lebih, tidak memiliki organ atau jaringan
 4. Pergerakan dengan flagella, cilia, atau pseudopodia atau dengan sel itu sendiri
 5. Beberapa species memiliki pelindung/cangkok, banyak di antaranya yang membentuk kista
 6. Hidup bebas, komensalisme, mutualisme, atau parasitisme
 7. Nutrisi: holozoik (memakan organisme hidup lain secara utuh yang ukurannya lebih kecil dari tubuhnya),
saprozoik (memakan organisme yang telah mati), holofitik atau autotrof (dapat membentuk makanan sendiri
melalui fotosintesis), saprofitik (menyerap zat yang terlarut di sekitarnya).
 8. Reproduksi vegetatif dengan binary fission atau multiple fission sedangkan generatifnya melalui persatuan
gamet, konyugasi, atau autogami.
 9 . Ukuran dan bentuk tubuh: mikroskopik (10 – 200 mikron)
KARAKTERISTIK Lanjutan ..............
 10. Struktur dan fungsi tubuh: a. membran plasma  pelindung, pengatur
pertukaran makanan dan gas, b. Sitoplasma, c. vakuola makanan  mencerna
makanan, d. vakuola kontraktil  mengeluarkan sisa makanan (cair) melalui
membran sel (secara kontraksi) serta mengatur kadar air dalam sel
(osmoregulator), e. inti sel  mengatur aktivitas sel.
 11. Hidup pada daerah yang lembab/berair
 12. Ada yang menguntungkan dan ada yang merugikan
 13. tipe nutrisi dan nutriennya berbeda-beda
 14. tipe respirasinya berbeda-bedaTipe Respirasinya yaitu:a. Obligat aerob,
yaitu penting adanya udara.b. Obligat anaerob, yaitu: penting jika tidak
adaudara.c. Fakultatif aerob: akan lebih baik jika ada udarad. Fakultatif
anaerob : akan lebih baik jika tidakada udara.
Klasifikasi Protozoa

Protozoa dibagi menjadi 4 kelas berdasarkan adaatau tidaknya alat gerak, yaitu:
1.RHIZOPODA / SARCODINA. alat gerak berupa PSEUDOPODIA
2. FLAGELLATA / MASTIGOFORA. alat gerak berupa FLAGEL
3. CILIATA. alat gerak berupa cillia atau rambut getar
4. SPOROZOA -- TANPA ALAT GERAK
PROTOZOA FLAGELLATA
 Kelas Flagellata
 Flagel = cambuk, lata = berjalan
 Flagellata/Mastigopora ialah hewan bersel satu yang berjalan dengan cambuk.
 Classis Flagellata atau Mastigophora mempunyai struktur tubuh yang khas yaitu adanya bulu cambuk
(flagellum: tunggal,flagella: jamak).
 Kelompok ini mempunyai bentuk tubuh tetap karena memiliki selaput elastis yang disebut pelikel.
 Flagellata dijumpai di laut dan di air tawar. Ada pulayang hidup parasit, namun jarang yang saprofit
(parasit).
 Protozoa yang termasuk dalam kelas Mastigofora (Flagellata) memiliki satu atau lebih flagel yang
mempunyai peranan untuk bergerak. Berdasarkan tempat hidupnya maka Flagellata ini dapat
dikelompokkan menjadi hemoflagellata yang berhabitat di dalam sistem peredaran darah dan jaringan, dan
kelompok yang lain adalah flagellata usus, mulut dan genital. Termasuk dalam kelompok hemoflagellata di
antaranya adalah genus Trypanosoma dan Leismania, sedangkan yang termasuk dalam kelompok flagellata
usus adalah Chilomastix mesnili, Trichomonas hominis, Enteromonas hominis, Embadomonas
intestinalis dan Giardia lamblia. Sedangkan Trichomonas tenax termasuk flagellata mulut dan Trichomonas
vaginalis termasuk kelompok flagellata genital.
GIARDIA LAMBLIA
Overview
 Organism
 History
 Epidemiology
 Transmission
 Disease in Humans
 Disease in Animals
 Prevention and Control

Center for Food Security and Public Health, Iowa State University, 2013
Organism
Organism

 Giardia intestinalis
 Protozoal parasite
 Also known as:
 Giardia lamblia
 Lamblia intestinalis
 Giardia duodenalis
 Isolated from humans, domestic animals, and wild animals

Center for Food Security and Public Health, Iowa State University, 2013
Organism

 Human infections
 Humans are main reservoir
 Interspecies/zoonotic transmission
 Importance of animal reservoirs unclear
 Non-zoonotic Giardia spp. found in:
 Rodents
 Birds
 Reptiles
 Amphibians

Center for Food Security and Public Health, Iowa State University, 2013
History
History

 1681
 van Leeuwenhoek, the “Father of Microbiology,” observes Giardia trophozoites in
his own stool
 Doubt common regarding pathogenicity of Giardia organisms
 1970s
 Symptomatic travelers from Soviet Union increased awareness

Center for Food Security and Public Health, Iowa State University, 2013
Epidemiology
Geographic Distribution

 Giardia intestinalis
 Occurs worldwide
 Most common in warm climates

Center for Food Security and Public Health, Iowa State University, 2013
Morbidity and Mortality: Humans

 Populations affected
 Children
 Travelers, hikers
 Swimmers
 Prevalence
in developed countries
 2% of adults
 6-8% of children
 Up to 15% in developing countries

Center for Food Security and Public Health, Iowa State University, 2013
Morbidity and Mortality: Humans

 Naïve populations
 Morbidity rate up to 20%
 Infections often resolve spontaneously
 Chronic infections occur
 May contribute to decreased lifespan in immunodeficient individuals

Center for Food Security and Public Health, Iowa State University, 2013
Morbidity and Mortality: Animals

 Young animals most affected


 Reported prevalence rates
 Puppies: 20-35%
 Kittens: 10-15%
 Foals: 17-32%
 Calves: 5-90%
 Lambs: 6-80%
 Pigs: 7-44%
 Usually not life threatening

Center for Food Security and Public Health, Iowa State University, 2013
Giardiasis Incidence, 2011

Center for Food Security and Public Health, Iowa State University, 2013
Giardia Case Reports, by Age, 2006-
2008

Center for Food Security and Public Health, Iowa State University, 2013
Transmission
Parasite Stages
 Two stages of the parasite: cyst and trophozoite

Center for Food Security and Public Health, Iowa State University, 2013
Transmission

 Cysts
 Direct transmission
 Fomites
 Contaminated water and/or food
 Ingested cysts release trophozoites
 Trophozoites multiply and encyst in intestines
 Excreted in feces

Center for Food Security and Public Health, Iowa State University, 2013
Survival

 Cysts
 Survive well in cool, moist conditions
 Remain viable for months in cold water
 Two months at 8oC
 One month at 21oC
 Can also survive freezing
 Susceptible to desiccation and direct sunlight

Center for Food Security and Public Health, Iowa State University, 2013
Life Cycle

 Cysts responsible for transmission


 Cysts and trophozoites found in
feces
 Ingested by host
 Importance of animal reservoirs
unclear

Center for Food Security and Public Health, Iowa State University, 2013
Disease in Humans
Disease in Humans

 Incubation period: 1-25 days


 Most infections asymptomatic
 Symptoms of clinical disease
 Mild to severe gastrointestinal signs
 Sudden onset diarrhea
 Foul-smelling stools
 Abdominal cramps
 Bloating, flatulence
 Nausea, fatigue
 Weight loss

Center for Food Security and Public Health, Iowa State University, 2013
Disease in Humans

 Illness usually lasts for 1-2 weeks


 Chronic infections reported
 May last months to years
 Immunodeficient and immunocompetent individuals
 May lead to malabsorption syndromes, vitamin deficiencies, severe weight loss,
and debilitation
 Disaccharide intolerance

Center for Food Security and Public Health, Iowa State University, 2013
Diagnosis

 Direct observation in feces


 Trophozoites
 “Tear drop” shape
 Two nuclei and tumbling mobility
 Cysts
 Approximately 13 microns long
 Oval, with 2-4 nuclei

 Immunofluorescence
 ELISA, PCR

Center for Food Security and Public Health, Iowa State University, 2013
Treatment
 Anti-protozoal drugs
 Metronidazole
 Tinidazole
 Ornidazole
 Chronic cases
 May be resistant
 Prolonged therapy may be necessary

Center for Food Security and Public Health, Iowa State University, 2013
Disease in Animals
Species Affected

 Domestic animals
 Dogs, cats, ruminants
 Horses, pigs (infrequently)
 Others
 Wild animals
 Beavers
 Others

Center for Food Security and Public Health, Iowa State University, 2013
Disease in Animals

 Most infections asymptomatic


 Clinical signs may include:
 Acute, chronic, or intermittent diarrhea
 Poor hair coat
 Flatulence
 Weight loss/failure to gain
 Light-colored mucoid stools
 May contain undigested fat

Center for Food Security and Public Health, Iowa State University, 2013
Post Mortem Lesions

 No gross lesions usually found

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Diagnosis

 Microscopic exam of feces


 Stained preparations
 Unstained wet mounts
 Cysts or trophozoites may be identified

Center for Food Security and Public Health, Iowa State University, 2013
Treatment

 Infections may be self-limiting


 Consider treatment due to zoonotic potential
 Fenbendazole
 Albendazole
 Metronidazole
 Tinidazole
 Others

Center for Food Security and Public Health, Iowa State University, 2013
Prevention and Control
Prevention and Control

 Water
 Do not drink contaminated water
 Untreated lakes, rivers, shallow wells
 Treat potentially contaminated water
 Heat (rolling boil for one minutes)
 Filter (absolute pore size of one micron)
 Chlorinate

 Food
 Wash raw fruits and vegetables

Center for Food Security and Public Health, Iowa State University, 2013
Prevention and Control

 Practice good hygiene


 Hand washing
 Don’t swim in recreational
waters for at least two
weeks after symptoms end
 Avoid fecal exposure

Center for Food Security and Public Health, Iowa State University, 2013
Prevention and Control

 Limit environmental contamination


 Clean and promptly remove feces from surfaces
 Keep pets indoors
 Vaccination
 Dogs and cats
 Use is controversial

Center for Food Security and Public Health, Iowa State University, 2013
Haemoflagellates
Leishmaniasis

Leishmaniasis is a zoonosis.
Transmitted among mammalian hosts by
female sand flies.
Leishmaniasis
Species Pathogenic in Humans
Leishmania donovani (complex) (VL)
Leishmania tropica (CL)
Leishmania major (CL)
Leishmania aethiopica (CL)
Leishmania mexicana (Complex) (CL)
Leishmania brazilliensis (complex) (MCL)
Three important Species
Leishmania donovani (VL )
VISCERAL LEISHMANIASIS : involving endothelial tissue liver,
spleen, and bone marrow.

Leishmania tropica (CL)


OLD WORLD CUTANEOUS LEISHMANIASIS : involving epithelial cells
the skin at the site of a sand fly bite.

Leishmania brazilliensis (MCL)


NEW WORLD MUCO CUTANEOUS LEISHMANIASIS : involving mucous
membranes of the mouth and nose after spread from a
nearby cutaneous lesion.
Leishmaniasis in the Middle East
 90% of all visceral leishmaniasis occurs in
Bangladesh, Brazil, India, and Sudan.
2893 cases were reported in Iraq in 2001
90% of cutaneous leishmaniasis occurs in Afghanistan,
Iran, Saudi Arabia, Syria, Brazil and Peru
8,7% cases were reported in Iraq in 1992
 Sore is commonly called the Baghdad boil

 90% of mucocutaneous leishmaniasis occurs in


Bolivia, Brazil and Peru
Life Cycle of
Promastigote
leishmaniasis
Amasitgote
Transformation
Promastigote stage
Promastigote stage inside the Sandfly

Sand fly : Vectors Intermediate host,


flagella transmitted disease
Promastigotes in
rosettes in a culture of
an orient sore on N.N.N.
medium (Giemsa stain).
Leishmania sp.

amastigote stage
Ovoid small intracellular parasites in a bone marrow
aspirate. The typical rod shaped kinetoplast is seen besides
the nucleus.(Giemsa stain).
Life cycle
Leishmania Morphology Amastigote stage
_Mammalian stage
_Non-motile
_Intracellular
Bite of sand fly

Digenetic Life Cycle

Promastiogte stage
_inside the Insect Bite of sand fly
_Motile form
_infectious stage
Transmission of Leishmaniasis
_ by sand flies.

_ artificial transmission of leishmania via the


sharing of contaminated syringes and
needles, from one intravenous drug user to
another.

Rarely, Leishmaniasis is spread from a pregnant


woman to her baby (Materno-fetal transplacental
transmission).
Blood transfusion or contaminated needles also can
spread Leishmaniasis.
Disease
Cutaneous Leishmaniasis

Cutaneous forms of the


disease normally produce
skin ulcers on the
exposed parts of the body
such as the face, arms
and legs. The disease can
produce a large number
of lesions
A cutaneous leishmaniasis lesion on the arm.

Some people have swollen


lymph glands near the sores. The skin sores will heal by
For example, the glands themselves, but this can take
under the arm can swell if months or years. The sores can
the sores are on the arm or leave ugly scars.
hand.
Cutaneous Leishmaniasis
The Baghdad boil
Baghdad-boil, 2004

Several hundred US soldiers


in Iraq.
 Causes ulceration of the
skin called Cutaneous
Leishmania tropica Leshmaniasis
 Dry or urban C.L.
 Dry sore that may persist for
several months before
healing, then person is
immune
 Some people “vaccinate”
their children against
Leshmaniasis.
 Rarely can cause infections
of the viscera
Mucocutaneous Leishmaniasis
Mucocutaneous leishmaniasis (Espundia)

Leishmania braziliensis & L .


maxicana
Mucocutaneous Leishmaniasis
Nasal stuffiness, runny nose , bleeding of
mucocutaneous forms of nose, rectum &vagina.
leishmaniasis , lesions Ulcer & erosion of mouth, nose, rectum, lips,
can lead to partial or gums, vaginal
total destruction of the
mucosa membranes
of the nose, mouth and
throat cavities and
surrounding tissues.
Visceral Leishmaniasis
Visceral disease (Kala-azar)
Visceral disease (Kala-azar)
Most severe form of disease, the disease typically starts with irregular bouts of
fever, chills, and general anemia

Since leishmaniasis is primarily a disease of the reticulo-endothelial system,

replacement of infected cells produces hyperplasia and consequent enlargement of

Hepatosplenomegaly
the visceral organs associated with the system (e.g., spleen and liver) .
Post Kala Azar Dermal Leishmanoid

Normally develops <2 years after recovery


Restricted to skin, rare but varies geographically
 Some people recover spontaneously
 Some people who were treated later develop Post-Kala- azar dermal
leishmanoid
Hepatosplenomegaly Post Kala Azar
Dermal
Leishmanoid
Dogs can act as reservoirs
of Leishmania parasites.
They also exhibit
symptoms of infection.
Diagnosis
Diagnosing Leishmaniasis can be difficult Sometimes
the Lab tests are negative even if a person has
Leishmaniasis.
Diagnosis

1. Clinical Diagnosis: signs & symptoms

Patient history (travel, vectors)

2. Laboratory Diagnosis
Laboratory Diagnosis of leishmaniasis :

Cutaneous leishmaniasis :
 Tissue sample (scraping, aspirate or punch biopsy) for
smear and culture
Visceral leishmaniasis :
 Bone marrow biopsy or splenic aspirate for smear and
culture.(N.N.N) V.L.(anemia , leukopenia ,
glubuline/albumine is high (Hypergammaglobulinia)
 Serology ( ELISA ) ( IFAT ).
 PCR

 Skin test
 Inoculate serum of infected person in lab. animals.
Treatment:
 Pentavalent antimony (Pentostam)
 Amphotericin B

Treatment of complications:
 Anaemia
 Bleeding
 Infections etc.
African Trypanosomiasis (Sleeping
Sickness)
Background

 Human African trypanosomiasis (HAT), also called sleeping sickness, is an illness


endemic to sub-Saharan Africa. It is caused by the flagellate protozoan
Trypanosoma brucei, which exists in 2 morphologically identical subspecies:
Trypanosoma brucei rhodesiense (East African or Rhodesian African
trypanosomiasis) and Trypanosoma brucei gambiense (West African or Gambian
African trypanosomiasis). Both of these parasites are transmitted to human hosts
by bites of infected tsetse flies (Glossina palpalis transmits T brucei gambiense and
Glossina morsitans transmits T brucei rhodesiense), which are found only in Africa.
Causes

 A bite from an infected tsetse fly causes African trypanosomiasis .


 Blood transfusions are a rare cause of parasitic transmission.
 In rare cases, accidental transmission in the laboratory has been implicated.
•The reservoirs of infection for these vectors are exclusively human in West
African trypanosomiasis. However, East African trypanosomiasis is a
zoonotic infection with animal vectors.
Life cycle

 Trypanosomes are parasites with a 2-host life cycle: mammalian and


arthropod. The life cycle starts when the trypanosomes are ingested during a
blood meal by the tsetse fly from a human reservoir in West African
trypanosomiasis or an animal reservoir in the East African form. The
trypanosomes multiply over a period of 2-3 weeks in the fly midgut; then, the
trypanosomes migrate to the salivary gland, where they develop into
epimastigotes. The metacyclic trypomastigotes infect humans.
Current situation in endemic countries

 In the last 10 years, over 70% of reported cases occurred in the Democratic
Republic of Congo (DRC).
 In 2008 and 2009 only the DRC and Central African Republic declared over
1000 new cases per year.
 Angola, Chad, Sudan and Uganda declared between 100 and 1000 new cases
per year.
 Countries such as, Cameroon, Congo, Côte d'Ivoire, Equatorial Guinea,
Gabon, Guinea, Kenya, Malawi, Nigeria, United Republic of Tanzania,
Zambia and Zimbabwe are reporting fewer than 100 new cases per year.
 Countries like Benin, Botswana, Burkina Faso, Burundi, Ethiopia, Gambia,
Ghana, Guinea Bissau, Liberia, Mali, Mozambique, Namibia, Niger,
Rwanda, Senegal, Sierra Leone, Swaziland and Togo have not reported any
new cases for over a decade. Transmission of the disease seems to have
stopped but there are still some areas were it is difficult to asses the
exact situation because the unstable social circumstances and/or remote
accessibility hinders surveillance and diagnostic activities.
Mortality/Morbidity

 The symptoms of East African trypanosomiasis develop more quickly (starting


1 mo after bite) than the symptoms of West African trypanosomiasis, which
can begin months to a year after the first bite
 Both types of African trypanosomiasis cause the same generalized
symptoms, including intermittent fevers, rash, and lymphadenopathy.
Notably, individuals with the East African form are more likely to
experience cardiac complications and develop CNS disease more quickly,
within weeks to a month. The CNS manifestations of behavioral changes,
daytime somnolence, nighttime insomnia, stupor, and coma result in
death if untreated.
 In West African trypanosomiasis, the asymptomatic phase may precede
onset of fevers, rash, and cervical lymphadenopathy. If unrecognized, the
symptoms then progress to weight loss, asthenia, pruritus, and CNS
disease with a more insidious onset. Meningismus is rare. Death at this
point is usually due to aspiration or seizures caused by CNS damage.
 Exposure can occur at any time. Congenital African trypanosomiasis occurs
in children, causing psychomotor retardation and seizure disorders.
Pathology and clinical picture

1. Skin stage: chancre.


2. Haematolymphatic stage: generalized lymphadenopathy, anaemia,
generalized organ involvement.
3. Central nervous system stage (CNS): Meningoencephalitis.
(Development of the disease more rapid in Trypanosoma brucei rhodesiense)
chancre
Winterbottom’s stage
3rd stage CNS
Lymph node aspirate
trypanosoma
CSF
TREATMENT
African trypanosomiasis
For early infection
 pentamidine
 suramin

For late infection


 eflornithine (Diflouromethylornithine- DFMO)

American trypanosomiasis (Chaga’s disease)


 benznidazole
 nifurtimox
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