Transcript Classification of Protozoa

Kingdom Protista
▪ Subkingdom Protozoa
▪ automonous unicellular eucaryotic organisms
possessing various degrees of cellular
specialization and some type of motility
▪ Organelles specialize in nutrient storage,
excretion, digestion, motility
▪ Phylum = based upon motility
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Size 2 - 100 micrometers
Parasitic protozoa are most facultative anaerobes;
 Mostly heterotrophic, chemoorganotrophs
▪ Nutrients assimilated via phagocytosis, pinocytosis,
diffusion
▪ Digestion may be both extracellular and intracellular
Two life stages
 Trophozoite
active pathogenic vegetative stage
 Cyst
latent survival form
Sites of pathogenesis
▪ Intestinal, Urogenital, Blood and Tissue
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Phylum Sarcodina
 Motility via Pseudopoda
▪ Extensions of the cell membrane into which the
cytoplasm flows
▪ Cyclosis
▪ No cell wall; thus, no uniform shape
▪ Shape changes with movement
▪ Reproduce asexually by mitosis; sexually by meiosis
 Trophozoite
▪ Motile vegetative stage
 Cyst
▪ Latent survival stage
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Phylum Ciliata
 Motility via cilia
▪ Cilia surround the cell; their co-ordinated movement
▪ Uses energy from the cell membrane
▪ Synchronized ciliary movement
 Two nuclei per cell
▪ Small micronucleus governs sexually reproduction
▪ Large macronucleus governs metabolism and
growth
▪ Both nuclei divide during asexual mitosis
 Intracellular organelles
▪ Function in digestion and excretion
Only one ciliate pathogen affects humans
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Phylum Mastigophora
 Motility via flagella
▪ One or more whip-like filaments move in counterclockwise fashion creating rapid movement
▪ A flagellum is a complex organelle composed of
many smaller tubules
▪ Flagella attach to the cell membrane and derive
energy from movement from this membrane
 Most numerous of the protozoan types
▪ Several are pathogens of humans
 All reproduce asexually; some reproduce sexually
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Phylum Sporozoa
 No established means of movement
▪ Thus, not motile
 All are intracellular parasites in a variety of hosts
▪ Several parasitic species affect humans
▪ Most are in the Class Coccidia
 All lack intracellular organelles
 All have three things in common
▪ No motility
▪ Sexual and Asexual mode of Reproduction
▪ Intracellular parasites
Intestinal
 amebiasis
Entamoeba histolytica
 giardiasis
Giardia lamblia
 balantidiasis
Balantidium coli
 crytosporidosis
Cryptosporidium parvum
 Urogenital
 trichomoniasis
Trichomonas vaginalis
 Blood and Tissue
 malaria
Plasmodium spp
 meningoencephalitis Naegleria fowleri
 toxoplasmosis
Toxoplasma gondii
 trypanosomiasis
▪ African Sleeping Sickness Trypanosoma brucei
▪ Chagas Disease
Trypanosoma cruzi
 leishmaniasis
▪ visceral leishmaniasis( Kala-azar) Leishmania donovanii
▪ cutaneous leishmaniasis
Leishmania topica/braziliensis
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Amebiasis( Amebic dysentery)
colitis with
diarrhea(somtimes bloody) accompanied by
abdominal
pain and cramping: numerous bloody stools
per day
 extraintestinal amebiasis a complication of intestinal amebiasis
in
which the trophozoites enter the blood and
are carried to other
organs; most often the liver
▪ these patients have fever, leukocytosis, rigors
Parasite
Entamoeba histolytica
 trophozoite
sarcodine protozoa which slowly
move among the
crypts of the large intestine and are
shed into the feces
 cyst
latent survival stage which is significant in
transmission;
spherical containing four
characteristic nuclei; infective stage
Pathogenesis
the trophozoites bind to colonic
epithelial cells
and secrete a cytotoxin which alters cell
membrane permeability
causing the cells to take in calcium
and lyse; necrosis and
inflammation also
accompanies the lysis of neutrophils,
lymphocytes and
monocytes
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Diagnosis
microscopic observation of cyst in the feces
▪ the trophozoite is seen occasionally
▪ multiple concentrated stools specimens may be required since cysts are
distributed randomly
▪ pathogenic ameba must be distinguished from commensal ameba
 new test are designed to detect fecal antigen and trophozoite DNA
 extraintestinal complications can be confirmed via biopsy or serological
tests for antibody
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Epidemiology
 reservior is infected humans, both asymptomatic and symptomatic
▪ from 10 - 50 % of world population is infected
▪ prevalence of infection in the U.S. is 1 - 2 %
▪ asymptomatic individuals are chronic carriers
 person -to - person, indirect, fecal-oral mode of transmission
▪ food, water, fomites
▪ fecal comtamination of fresh vegetables, water
▪ flies and cockroaches also transmitt the cysts mostly to food and fomites
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Amebiasis
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Disease
meningoencephalitis
▪ destruction of the brain tissue causeing symptoms of frontal headache, sore
throat, fever, stiff neck, blocked nose with alter senses of taste and smell,
and Kernig’s sign(a sign of meningitis in which the patient cannot flex the
leg)
▪ cerebrospinal fluid is purulent and may contain erythrocytes
▪ leads to rapid death in 4 - 5 days
▪ Acanthomoeba can also enter the eye and cause keratitis and corneal ulcers
Parasite
Naegleria fowleri or Acanthamoeba spp.
▪ trophozoite is a free living amoeba found in soil and water
▪ cyst
Pathogenesis
most infections occur when trophozoites in
water enter the nasal passages when people swim; they
then
envade the nasal mucosa and extend into the brain
Diagnosis trophozoites( in wet mounts or stained smears) in nasal discharge,
cerebrospinal fluid, or corneal scrapings
Epidemiology
- this organism is an envronmental opportunist acquired
via
contact with water, soil , or dust
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Balantidiasis
a dysentery (watery stools with blood and
pus)
accompanied by nausea, anorexia, tenesmus,
and
abdominal pain and tenderness
Parasite
Balantidium coli
 trophozoite
an actively motile ciliate; highly
specialized for
reproduction and
food intake (cytostome)
 cyst
a latent survival stage is significant in transmission;
infective
stage with one large nucleus
Pathogenesis
ulceration of the intestinal mucosa
especially in the large intestine sometimes compounded by
bacterial infection
 no extraintestinal invasion as seen in amebiasis
Epidemiology
reservoir is swine and humans
 fecal-oral transmission involving water and food
Diagnosis
microscopic observation of cysts in the feces
 this trophozoite is very large and often seen also
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Giardiasis
mild diarrhea to severe malabsorption syndrome;
sudden onset of watery diarrhea, often foul-smelling,
with abdominal cramps, flatulence, and
stearorrhea.
Blood and pus are rarely present.
Parasite
Giardia lamblia
 Trophozoite - flagellate protozoan( 10 x 10 um) having two large
nuclei, a large sucking disc, and many flagella; face like appearance
 cyst
slightly smaller the trophozoite with four nuclei and
parabasal body
Pathogenesis
gastric acid stimulates excystation
and releases trophozoite into small intestine where it attaches via
the sucking disc to the intestinal villi; the alteration of the villi and
inflammation of the mucous causes maladsorption,
but not
obvious tissue necrosis; spontaneous recovery
occurs in 10 -14
days, but relapse may occur; chronic infection
is especially a
problem in patients with IgA
deficiency and diverticula
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Diagnosis
cyts and trophozoites in the feces with the onset of
symptoms; cyts occur in”showers” and are not present
every day, so stoo should be examined every three
days
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 in the absence of observable cysts, new tests for fecal
antigen are now available
Epidemiology
sylvatic and domestic reservoirs,
both human
and animals(mostly those around
lakes and
streams;
▪ fecal - oral transmission via contaminated water is most
common mode of transmission; in U.S. domestic setting, fecaloral fomites transmission is very common in day care settings;
also uncooked contaminated vegetable and fruits may serve as
a source of the cysts
▪ cyst are resistant to traditional chlorination methods
▪ other than day-care centers, most recent outbreaks have
involved contaminated water from reservoirs
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Giardiasis
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Vaginitis and urethritis
itching, burning, and painful
urination
sometime accompanied by scant watery vaginal
discharge
Parasite
Trichomomas vaginalis
 only a flagellate trophozoite with four flagella and undulating
membrane
 this flagellate has not cyst stage
Pathogenesis
extensive inflammation and erosion
of the vaginal or urethral epithelium causing itching, burning, and
painful urination; also sometimes a scanty watery vaginal discharge
Epidemiology
human reservoir with many
asymptomatic
carriers especially in males- females
may also be asymtomatic
 trophozoite is sexually transmitted
Diagnosis
microscope examination of vaginal or urethral
discharge
 stained smear show trophozoites
 also parasite is detected in fluorescent antibody stains and
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Trichomoniasis
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Cryptosporidosis
enterocolitis characterized by water diarrhea
without blood - self limiting in immunocompetent people
Parasite
Cryptosporidium parvum
 Sporozoan(coccidian) parasite exhibits both asexual(schizogony)
and sexual(gametogony) in the brush border of the intestinal
epithelium
 Oocyts are released from the cells and transmitted
Pathogenesis
In immunocompromised patients, an
unremitting enterocolitis with as many as 50 water stools per day
caused by the intracellular multiplication of the parasite
Epidemiology
reservoir is a variety of mammals,
fish, reptiles
 this host seed the environment especially water with oocyts
 a-p, indirect, fecal-oral, contaminated water/fecal droplets
 p-p, indirect, fecal-oral/oral-anal - fomite/direct contact
▪ high risk groups = homosexuals, day care children/adults,
animal handlers
Diagnosis
oocysts in the feces: concentrated and stained
 also assay for fecal antigen
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Cyclosporiasis -water diarrhea accompanied by nausea,anorexia,
abdominal cramping: sometime bloating and
flatulence
Parasite
Cyclospora cayetanensis
 a sporozoan(coccidian) parasite of the small intestine
 asexual and sexual cycle similar to Cryptosporidium but oocysts
are larger
Pathogenesis
inflammatory changes in the jejenum
resulting from the intracellular multiplication of the parasite = villous
atrophy
Epidemiology
reservoir is a variety of mammals,
birds, reptile
 source to humans is fecally contaminated water and some fresh
fruits like strawberries
Diagnosis
detection of oocysts in the stool:
concentrated and stained by a variety of methods including
immunofluorescence
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Cryptosporidiosis
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Sporozoan(coccidian)
 malaria
Plasmodium spp
 toxoplasmosis
Toxoplasma gondii
Flagellates
 trypanosomiasis
Trypanosoma cruzi
 African Sleeping Sicknes
Tyrpanosoma brucei
 leishmaniasis
Leishmania spp
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Malaria - influenza-like symptoms( fever, chills) with headache,
muscle pain, photophobia, anorexia, nausea, vomiting
Parasites
 Plasmodium vivax - benign tertian malaria
 Plasmodium falciparum - malignant tertian malaria
 Plasmodium malariae - quartan malaria
Pathogenesis
infection begins in the
liver(exoerythocytic)
but becomes a disease of
RBC’s (erythrocytic)
 merozoites released every 48 hrs in benign tertian malaria
 merozoites released every 36-48 hrs in malignant tertian malaria
 merozoite released ever 72 hrs in quartan malari
Epidemiology
reservior in infecte humans and wild
primates
 arthopod-borne transmission, via Anopheline mosquitos where
sporogamy produces infectious sporozoites
Diagnosis
trophozoites(schizonts) in blood smears
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Malaria
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Toxoplasmosis
infectious mononucleosis -like
symptoms of fever, chills, headache, myalgia, lymphadenitis, and
fatigue;
chronic form = hepatitis, encephalomyelitis, mycocarditis
Parasite
Toxoplasma gondii
 intracellular coccidian(sporozoan) parasite infecting various
tissues(systemic) but confined to intestines in felines
 infected tissues release pseudocysts containing bradyozoites
 feline intestines release oocyts containing tachyzoites
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Pathogenesis
muliplication
cerebral tissues
Epidemiology
birds
cellular death due to intracellular
of trophozoites especially severe in fetal and
reservoir is a variety of mammals and
including humans
 fecal-oral transmission of oocyst from felines
 common source transmission of pseudocyts in poorly cooked meat esp beef
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Diagnosis
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Risk Groups
serological detection of antibody: Elisa test for
IgM antibodies is most reliable
Pregnant females and immunocompromised
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Toxoplasmosis
African Sleeping SicknessCNS infection progressing to
lethargy, tremors, meningoencephalitis, convulsions, coma,
and death
 Parasites Trypanosoma gambiense- West/Central Africa
 Trypanosoma rhodesiense- East Africa
 Pathogenesis - trypanomastigote multiplies in the blood,
lymph, and cerebrospinal fluid; deprives the brain of amino
acids
 Epidemiology
T. gambiense - human reservoir
 T. rhodesiense - cattle and wild game reservoir
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 arthropod-borne transmission via the tsetse fly
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Diagnosis
for
trypanosomes in the blood, serological test
antigens in the blood
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American Trypanosomiasis/Chagas Disease -systemic
infection beginning with fever, chills, malaise, myalgia,
fatigue, and chagoma; progressing to involve heart and
brain
Parasite = Tryanosoma cruzi
 flagellate tryanosome exhibiting both the intracellular
amastigote(leishmanial) form and the extracellular
trypanomastigote(tryupanosmal) form
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Pathogenesis - the intracellular amastigote multiplies in
cells
and destroys the cells
Epidemiology- wild and domestic animal reservoirs
 arthropod-borne via the cone-nosed (reduviid) bugs which live in the
cracks of domestic dwellings
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Diagnosis
trypanosomes in the blood; amastigotes
in biopsy; also xenodiagnosis and gene probes
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Leishmaniasis
;Visceral - gradual onset of fever, chill, sweating,
diarrhea, anemia which progresses to enlargement of liver and spleen
with weight loss and emaciation: later kidney damage and
granulomatous skin lesion = also called kala-azar
 cutaneous form -ulcerative skin lesions which contain parasite: become
infected with secondary bacteria and scar formation disfigures
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Parasites
Leishmania donovani - visceral- amastigote stage
multiplies in visceral cells causing lysis
 Leishmania tropica - cutanous: Leishmania braziliensis - mucocutaneous
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Pathogenesis
- cells in infected visceral and cutaneous tissues
are destroyed by intracellular amastigote multiplication
Epidemiology
- animal reservoirs including dogs and cats
 arthropod-borne via the bite of sandflies: the amastigote stage becomes a
motile promastigote in the sandfly gut
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Diagnosis - amastigote is observed in tissue biopsy, body fluid
aspirates, and in the blood: also serology for antibody presence