Module 3: Protozoa ▪ filopodia (slender,

thread like)
- Unicellular animals without cell walls
- Flagella
- Metabolism and locomotion carried out
o filamentous
by organelles
- Cilia
- Majority are free living, found in almost
o Like short flagella
every habitat on land and in water
o Numerous
o Moist
o Commensalism/parasites Organelles for nutrition
o 5-250 um
- Pseudopodia
o Largest: 6.7 mm
o Gain food for protozoa
o High surface area rel’n to body
- Cytostome
volume
o Phagocytosis
▪ Active uptake diffusion
o Mouth → food vacuole
Structure - Food vacuoles
- Cytopyge
- Plasma membrane
o Excrete
- Mitochondria
o Anus
- Golgi apparatus
- Microbodies
- Cytoplasm
- Nucleus
- Locomotory organelles
o Flagella/flagellum
o Cilia

Reproduction

- Asexual
o Binary fission
▪ Lateral/transverse
▪ Division; controlled
mitotic replication of
chromosome

Movement

- Pseudopodia
o Amoeba-like
o 2 kinds
▪ Lobopodia (bulbous) -
rounded o Budding
▪ Portion
 o Products are of a completely
different life cycle stage
(sporozoites)
▪ Merozoites

o Multiple fission
▪ Many nuclear division
proceed to
differentiation of
organism
- Sexual
o Syngamy
▪ Normal
▪ 2 gametes fused to
form a zygote
- Conjugation
o Exchange genetic/nuclear
material
o reorganization

Multiple fission types

- Schizogony
o Large no. of cells reproduced
simultaneously;
o Cell is called a schizont,
meront, or segmenter
- Merogony
o Schizogony to produce
merozoites
o products are additional
parasites of the same life cycle
stage.
- Sporogony
o Another type of cell fission after
the union of gametes
 Phylum Sarcomastigophora Developmental stages

- Umbrella term for protozoans that - Amastigote

move either by one or more flagella o Intracellular, dividing form in
- Polyphyletic the cytoplasm of vertebrate
o Came from diff. ancestors but cells
are grouped together o Round/oval-shaped cell with no
protruding flagellum
Trypanosoma

- Phylum Sarcomastigophora
- Subphylum mastigophora
- Order kinetoplastida
- Family Trypanosomatidae

Description

- All parasitic
- Found in the blood and/or tissues of
mammals and birds
- Heteroxenous
- Promastigote
o Infect more than 1 host
o Motile, elongated, extracellular
form
- Epimastigote
o Found in the intestinal tract of
the insect vector
o Kinetoplast is found anterior
and adjacent to the nucleus
o Flagellum emerges in the
Structure middle of the cell

- Leaf-like in shape
- Single flagellum
o Attached to the body of the
organism by an undulating
membrane

kinetoplast

- Trypomastigote
o Leaf-like; 1 flagellum
o C-shaped
 o Found in the bloodstream of - Disease: Nagana
infected vertebrates o Anemia
▪ Non dividing ▪ Iron deficient
form/infectious o Edema
▪ Stained in blood smear ▪ Accumulation of liquid
o Non-dividing form that is in body
infectious for the reduviid bug. o Watery eyes and nose
o Fever
o Emaciation
▪ Weakness
o Incoordination, paralysis
▪ Reflexes
o Death

A. Section Salivaria (anterior station)

- Developmental stages multiply in the

gut of the arthropod and infective
stages accumulate in the mouth parts
or salivary glands so that infection is Vectors
transmitted when the arthropod takes
a blood meal - Glossina morsitans, G. pallidipes, G.
swynnertoni
Trypanosoma brucei brucei - Tse tse fly
- Hosts
o Antelopes
o Other African ruminants
o Livestock
▪ Sheep, goats, oxen,
horses, camel, pigs,
dogs, donkeys, and Clinical manifestation
mules
- Infection can lead to death, extreme
weight loss, reduced growth rate in
young animals, and organ damage.
- Fertility in males may also be decreased
due to testicular damage.
Trypanosoma brucei gambiese - Low endemic levels
o Benin, Burkina-Faso, Gabon,
- Host:
Ghana, Equatorial Guinea,
o Humans
Kenya, Mali, Nigeria, Togo, &
- Vectors:
Zambia.
o G. palpalis, G. tachinoides
- Poor disease surveillance and reporting
- Distribution
o Burundi, Botswana, Ethiopia,
o West and Central Africa
Liberia, Namibia, Rwanda,
- Disease
Senegal, & Sierra-Leone
o Chronic form of sleeping
sickness
▪ Long term and
reaccuring

Trypanosoma brucei rhodesiense

- Host:
o Humans
- Distribution
o Central and East Africa
- Vector
o Glossina morsitans, G.
pallidipes, G. swynnertoni Economic state
- Disease
- The Food and Agricultural Organization
o Acute form of sleeping sickness
of the United Nations states,
▪ Abrupt; brief (6
“Trypanosomiasis is probably the only
months)
disease which has profoundly affected
Distribution the settlement and economic
development of a major part of a
- Epidemic
continent.” Of the approximately 7-10
o Angola, Democratic Republic of
million km2 of land that are infested by
the Congo, Uganda & Sudan.
tsetse fly, only 20 million cattle are
- High levels endemicity
raised. Under different circumstances,
o Cameroon, Congo, Cote
this land could support more than 140
d’Ivoire, Central African
million cattle and increase meat
Republic, Guinea, Mozambique,
production by 1.5 million tons!
Tanzania, & Chad.
Barrier; affect continent

- “From the beginning of Arab and

European influence in the hinterland of
tropical Africa, trypanosomiasis of man
and animals has curbed the realization
of human ambitions and the
mobilization of the continent’s vast
resources.” --Herbert S. Gasser

Vector

- Tsetse flies – haematophagous

o Feed on blood
African sleeping sickness
- Different species of Glossina have
different preferences for the source of - Based on the report by Franco et al.
their blood meal with some specifically (2014)
preferring human blood and are
therefore important vectors of the
disease in human populations
- Both male and female flies feed on
blood and are both vectors of the
parasites

Transmission

- T.b.rhodesiense
o G. morsitans, G. pallidipes and
G. swynnertoni. It is primarily
transmitted from person-to- Clinical presentation
animal and then back to - First sign: chancre
person o Sore in skin → site where tse
- Reservoirs include domestic and wild tse fly hit
ungulates, plus other game and wildlife
- T. b. gambiense – person to person
transmission
- G. palpalis, which live near vegetation
associated with drainage lines, rivers
- Incubation Period:
and other permanent bodies of water.
o T.b. rhodesiense may be two to
three weeks
o T.b. gambiense may last several
weeks to months.
- Invasion of the blood characterized by
irregular fever and headache
- Disease progression characterized by
o invasion of lymphatics
 o weight loss
o weakness
o rash, itching and edema
o febrile attacks
o swollen lymph nodes.
- Chronic phase
o Apathy, Fatigue, Confusion,
Somnolence, Motor changes,
Tics, Slurred speech,
Incoordination, Convulsions,
Coma.
o Disinclination to work, mental
dullness
o Tremor, paralysis, sleepiness
increases with the patient
falling asleep even while eating
or standing.
o Coma. Death.
Immunology
- Trypanosomes escape host defenses by
the successive dominance of each of a
series of variant antigenic types (VAT).
→ like mutation
Pathogenesis
- The host’s immune system is greatly
stimulated
- Some antigens adsorb to the surface of
some host cells resulting to cell lysis
- Trypanosomes may have nutritional
requirements for tyrosine resulting in
interference in protein and
neurotransmitter synthesis
Diagnosis
- Detection of trypanosomes in the
blood, lymph node aspirations, or spinal
fluid
ELISA
- Detection of tryposome
- Card Agglutination Test for
Trypanosomiasis (CATT)
Treatment
- SURAMIN, PENTAMIDINE
o acute stage without CNS
involvement
- MELARSOPROL, TRYPARSAMIDE
o if CNS is involved, but
prognosis poor
- DFMO
o difluoromethylornithine
o drug of choice
Control
- Early detection and treatment of
infected individuals
- Limiting of human exposure to tsetse
flies in the form of fly traps

Reservoir control
- Poisoning and drainage of water
sources
Trypanosoma congolense
- DISEASE: Nagana
- HOSTS: all domestic animals and wild
game animals such as antelope, zebra,
warthog and elephant may serve as
reservoir host
o Sports and food animals
- VECTORS: Tse tse flies or mechanically
by biting flies
- DISTRIBUTION: East Africa
Trypanosoma vivax
- DISEASE: Nagana
- HOSTS: Cattle, water buffalo
- DISTRIBUTION: West Africa, Central and
South America
- VECTOR: Tse tse flies in Africa In south
America, transmission is mechanical by
biting flies
Trypanosoma evansi
- DISEASE: SURRA
- HOST: horse, dog, cattle, pig, camel,
elephant
- VECTOR: Mechanical transmission by
biting flies which go quickly from one
host to the other. In south America,
vampire bats are the vectors and the
disease is called MURRINA
- PATHOLOGY: Anemia, emaciation
- DISTRIBUTION India, Far East, North
Africa, Philippines, Central and South
America
Trypanosoma equinum
- Disease: Mal de Caderas
- Hosts : horses
- Vectors: mechanically by biting flies
- Distribution : South America
Trypanosoma equiperdum
- DISEASE: DOURINE
- HOST: Horses and donkeys
- DISTRIBUTION: Africa, Asia, Europe,
Russia, Mexico
- TRANSMISSION: mechanically during
coitus and rarely by biting flies
- PATHOLOGY: Venereal disease that
ends in generalized paralysis
 B. Section Stercoraria (POSTERIOR STATION) o inflammatory nodule at the bite
site of the reduviid bug which
- Infective stages accumulate in the hind
transmits Chagas disease
gut and are passed in the feces of the
arthropod. Infection occurs by
contamination of the skin or skin
wounds.

Trypanosoma cruzi

- DISEASE: Chagas Disease / American/

Human Trypanosomiasis
- HOST: Humans

- PATHOLOGY
o reference for the heart , muscle
nerve cells (esophagus, colon) 
Rupture of the pseudocyst is
accompanied by local
inflammatory response with
degeneration and necrosis of
- VECTOR: Cone nosed bugs (Hemiptera,
nerve cells in the vicinity
family reduviidae)
especially ganglion

- CLINICAL SIGNS
- Clinical manifestation o Anemia
o ROMANA’S SIGN o Loss of strength
o periorbital swelling, palpebral o Nervous disorders
edema and conjunctivitis o Chills, muscle and bone pain
o Heart failure
o Megaesophagus, megacolon
o Deranged peristalsis
- Distribution South and Central America
- EPIDEMIOLOGY
o Dogs and cats are the most
important reservoirs
o Primitive or poor quality
housing
- CHAGOMA
 o Coitus and breast milk are
possible means of transmission
o Mother to fetus through the
placenta
o Oral mucosa when bugs are
eaten as some believe they are
aphrodisiacs
o Blood transfusion
o Acute phase is most fatal to
children less than to years of
age
- DIAGNOSIS
o Demonstration in blood, CSF,
fixed tissues or lymph
o Immunodiagnostic tests (CFT)

- Treatment
o does not respond well to drugs
since intracellular parasites are
shielded
o Benzdinazole, Nifurtimox
 SARCOMASTIGOPHORA
- Other important flagellates
A. Phylum Metamonada
Giardia lamblia
- PHYLUM SARCOMSTIGOPHORA
- SUBPHYLUM MASTIGOPHORA
- CLASS ZOOMASTIGOPHORA
- ORDER DIPLOMONADIDA
- FAMILY HEXAMITIDAE
- GENUS GIARDIA
Median
bodies
- Parasites for dogs
MORPHOLOGY: Trophozoites
- 12 -15 µm long, rounded at the anterior
end and pointed on the posterior end.
- Dorsoventrally flattened, convex on the
dorsal side.
- Flattened ventral surface with a
concave, bilobed adhesive disc.
- 4 pairs of flagella arise from
kinetosomes
o 2 anterior; 2 posterior flagella;
medial (atleast 4)
- Behind the adhesive disc, there is a pair
of large, curved, transverse, dark
staining median bodies which are
unique to the genus Giardia
MORPHOLOGY: Cyst
- The ovoid cysts are 8-12 um by 7 to 10
um in size. Newly formed cysts have
two nuclei but older ones have four
HOST
- Humans. Commonly affects children.
- Cats, dogs and birds.
- Mammalian hosts also include cattle,
beaver, deer and sheep.
- Lives in the duodenum, jejunum, and
upper ileum (digestive tract & small
intestine)
DISEASE: Giardiasis
- Marked increase in mucus production,
diarrhea, dehydration, intestinal pain,
flatulence, weight loss
- Fatty stool but never contains blood
- Does not lyse the host cell but appears
to feed on mucous secretion
 - Dense coating of flagellates on the
intestinal epithelium interferes with
the absorption of fats and nutrients
- Gallbladder may be infected causing
jaundice (yellow) and colic (gallbladder
(gallstone) attack)
- Disease is not fatal but can be
discomforting
LIFE CYCLE
- duodenum, jejunum, and upper ileum
- adhesive disc fitting over epithelial cell.
- Binary fission
- parasites become dehydrated and
encyst in colon
- When swallowed by the host, they pass
safely though the stomach and excyst in
the duodenum
DIAGNOSIS, TREATMENT, EPIDEMIOLOGY
- Recognition of trophozoites or cysts in
stained fecal smears
o Fecal analysis
- Immunodiagnostic tests
- Highly contagious
o Prevent contamination
- Transmission by the swallowing of
mature cysts
o Like in fruits/water
- TREATMENT: Quinacrine or
metronidazole
TRANSMISSION
- Chief pathways of human infection
include ingestion of untreated sewage
- Contamination of natural waters also
occurs in watersheds where intensive
grazing occurs.
B. Phylum Ciliophora
Balantidium coli
- Class Kinetofragminophorea
- Subclass Vestibulifera
- Order Trichostomatida
- Family Balantidiidae
MORPHOLOGY
- Trophozoite – oblong, spheroid 30-150
um long by 25 to 120 um wide
o Swimming using cilia
- Cyst – spheroid or ovoid, 40-60 um in
diameter. macronucleus is a large
sausage shaped structure. Single
micronucleus is smaller and hidden
from view by the macronucleus. 2
contractile vacuoles, cytostome at the
anterior end
- HOST:
o humans, pigs, guinea pigs, rats
etc mammals
- LOCATION:
o cecum and colon (digestive)
- EPIDEMIOLOGY:
o common in the Philippines but
can be found almost anywhere
in the world especially those in
contact with pigs
- LIFE CYCLE

o Binary fission
- PATHOGENESIS (disease)
o Can produce proteolytic
enzymes that digest away the
intestinal epithelium of the
host
o Produces an ulcer
o Perforation of large intestines
or appendix
o Secondary foci include liver,
lungs, urogenital organs,
bladder
- TREATMENT
o Carbasone
o Diiodohydroxyquin
o Tetracycline
 Trichomonas

- Family Trichomonadidae

Trichomonas vaginalis

Costa

- unique in trichomonadidae
- rodlike structure with complex cross
striations which serves as a strong
,flexible support in the region of the
undulating membrane

Parabasal body (golgi body) LIFE CYCLE

- lies near the nucleus with the parabasal
filament running from the kinetosome
complex and ending in the posterior
portion of the body

Axostyle

- extends from the area of the

kinetosomes posteriorly to protrude
from the end of the body (covered by
cell membrane).

Pelta

- comprises a sheet of microtubules and

- sexual intercourse
appear to function in supporting the
- Lives in the vagina and urethra of
periflagellar canal, a shallow depression
women and in the prostrate, seminal
in the anterior end from which all
vesicles, and urethra of men.
flagella emerge.
- Divide by longitudinal fission and do not
Paracostal granules / Microbodies form cysts

- lie along its costa TRANSMISSION

- Sexual Intercourse
- Unlike most STDs, Trichomonas can
survive for some hours outside the
body on infected objects and can be
transmitted by sharing bodily fluids,
contaminated bedding , damp towels
,sheets ,toilet seats . Viable cultures
have been obtained from damp cloth as
long as 24 hours after inoculation.
- Has been found in newborn infants

PATHOGENESIS (disease)
- They feed on bacteria, leucocytes and
cell exudates and are themselves
ingested by monocytes.
- Most are of low pathogenicity that the
infected person is virtually
asymptomatic.
- Other strains cause an intense
inflammation with itching and a copious
white discharge (leukorrhea – white
discharge) that is swarming with
trichomonads
CLINICAL SIGNS
- Trichomoniasis infection frequently has
no symptoms.
- There have been rare cases where the
incubation period of the infection has
covered years, but usually symptoms
appear within 4-20 days of exposure
- In women:
o Blood spotting in vaginal
discharge
o Heavy, yellowish-green or gray,
frothy vaginal discharge
o Infection in the urethra
o Itching, burning or pain in the
vagina
o lower abdominal pain
o musty vaginal odor
o Pain and/or burning when
urinating
o Pain or discomfort during
sexual intercourse
(dyspareunia)
o Swelling in the groin
o Swollen and irritated vagina and
cervix
o Urinating more than usual
o Vaginal or vulval redness
o Worsening symptoms when
menstruating
- In men
o Men rarely have any symptoms,
however, if symptoms do occur.
They include:
o Infection of the urethra or
prostate gland
o Painful and/or difficult
urination
o Thin, whitish discharge from the
penis
o Tingling inside the penis
COMPLICATIONS
- It has been shown that Trichomoniasis:
o is associated with increased
risk of transmission of HIV
o may cause a woman to deliver a
low-birthweight or premature
infant
DIAGNOSIS
- Recognizing the trichomonad from
secretions
o discharge
- In vitro culture made from vaginal
irrigation
TREATMENT
- Metronidazole
 - Suppositories and douches are useful in
promoting an acid Ph of the vagina
- Sexual partners should be treated
simultaneously to prevent reinfection

PREVENTION

- Abstinence from sex until the infection

is cured
- Consistent and correct male, latex
condom use
- Spermicides and diaphragms which may
provide some protection
- Know your partner's sexual history
- Limit one's sexual relationship to a
single, uninfected partner
- Douching or urinating after sex does not
prevent STDs
 Entamoeba histolytica MORPHOLOGY: CYST

- SUBPHYLUM SARCODINA , - Ovoid or elongate but usually spheroid.

- ORDER AMOEBIDAE 10 to 20 um wide but may be as small
- FAMILY ENDAMOEBIDAE, as 5 um.
- GENUS ENTAMOEBA Divides twice to form two and four
nucleus stages.
CHARACTERISTICS

- Third most common cause of parasitic

death in the world
- 500 million people affected at any one
time
- 100,000 deaths per year
- Cysts are viable in a moist, cool
MORPHOLOGY: TROPHOZOITE environment for at least 12 days and in
water for up to 30 days.
- 20 to 30 um (10-60um in some) - They are rapidly killed by putrefaction,
- Clear, thin ectoplasm that is clearly desiccation and temperatures below 5
differentiated from the granular and above 40.
endoplasm. - Can withstand passage through the
o Ectoplasm -directs movement intestines of flies and cockroaches.
of the cell - Cysts are resistant to levels of chlorine
o Endoplasm -regulation of water normally used for purification.
inside the cell (have partial
membrane) LIFE CYCLE
- Nucleus is spherical and 1/5 to 1/6 the
diameter of the cell.
- Prominent endosome in the center of
the cell
o Membrane bound
compartment
o Regulation of trafficking in
proteinsa and other internal
compents of the cell

- Contaminated water/fruit
- Enters digestive tract
- Exestuation (trophozoites form)
 BIOLOGY - Acute amoebic dysentery: less
common, onset sudden after incubation
- Trophozoites live and multiply
period of 8 to 10 days or after an
indefinitely within the crypts of the
asymptomatic period as an
mucosa (l. intestine)
asymptomatic cyst passer.
- Feed on starches and mucous
o less common; sudden
secretions
o did not transform to trophozoic
- Interacts with enteric bacteria.
- headache, fever, cramps, prolonged
o Biota that exist on the digestive
ineffective straining at stool.
tract
- 15 to 20 stools per day consisting of
- Under optimal conditions, nonvirulent
liquid feces specked with bloody
E. histolytica becomes virulent and
mucus.
become invasive
- Death from peritonitis, cardiac failure or
exhaustion.
- Bacterial involvement may lead to
extensive scarring of the intestinal wall
with loss of peristalsis.
o Peristalsis – internal movement
during digestion
- Ectopic lesions typical of affected organ
- erode ulcers into the intestinal wall - Intestinal ulcer
eventually reaching the submucosa and
the underlying vessels
o enzyme to erode - cysteine
proteinase
- Travel with blood to other sites of the
body such as the liver, lungs, or skin.
- Unique in its ability to hydrolyze host
tissues.

- Amoeba can invade the following:

o Metastasis – 1st to secondary
site

DISEASE

- Amoebic diarrhea- bouts of abdominal INTESTINAL LESION

discomfort with 4 to 6 loose stools per
day but with little fever. - Cecum, appendix, or upper colon
- Ulcer
- The lesion may stop at the basement
membrane or at the muscularis mucosa
and then begin eroding laterally,
causing broad, shallow areas of
necrosis.
o Necrosis – death of tissue

- Early lesions

o usually not complicated by

bacterial insvasion

o little cellular response by the

host. SECONDARY LESIONS

- Older lesions - Hepatic amoebiasis

o amoeba, assisted by bacteria,
may break through muscularis
mucosa → submucosa →
muscle layers and serosa.
o enables trophozoites to be
carried by blood and lymph to
ectopic sites throughout the
body where secondary lesions
form
- Perforated colons with concomitant
peritonitis
- Early lesions usually not complicated by
bacterial invasion
- In older lesions, the amoebas, assisted
by bacteria, may break through the
muscularis mucosa, infiltrate the
submucosa and even penetrate the
muscle layers and serosa.
o liver
o form abscesses
o Lesions may be pinpoint size or
may continue to grow reaching
the size of a grapefruit.
o Center is filled with necrotic
fluid, a median zone consists of
liver stroma and outer zone
consists of liver tissue being
attacked by amoebas.
o Abscess may rupture, pouring
debris and organisms into body
cavity where they attack other
organs.
• lungs, pericardium,
genitalia, adrenals

- This enables trophozoites to be carried

by blood and lymph to ectopic sites
throughout the body where secondary
lesions form

- Perforated colons with concomitant DIAGNOSIS

peritonitis
- Demonstration of cysts or trophozoites
in feces
o fecalysis
 - Extraintesinal lesions often with no
intestinal infection
- X-ray and scanning of liver
GENERAL CHARACTERISTICS
- Immunological tests
- TREATMENT: Metronidazole preferred
drug
MORPHOLOGY
- -
EPIDEMIOLOGY
- Found throughout the world
- Age influences the prevalence of
infection.
o USA: highest in 26 to 30 yrs of
age.
- Tropics higher prevalence
- Recognized as a sexually transmitted
disease among gay men. Oral to anal
contact
- Manner of disposal of human waste
o Most important factor in the
epidemiology of this organism
o Transmission depends heavily
on contaminated water and
food
o Filth flies and cockroaches are
mechanical vectors
- Careless plumbing in which sanitary
drains were connected to freshwater
pipes have resulted into epidemics.
- Use of human feces as fertilizer
- Humans most important reservoir but
dogs, monkeys, pigs are also implicated
Entamoeba coli
- SUBPHYLUM SARCODINA ,
- ORDER AMOEBIDAE
- FAMILY ENDAMOEBIDAE,
- GENUS ENTAMOEBA
- It is a commensal that never lyses it’s
host’s tissues.
- Feeds on bacteria, other protozoa,
yeasts and occasionally blood cells that
may be casually available to it.
- More common than E. histolytica
because of it’s superior ability to survive
putrefaction.
Trophozoite
o 15 to 50 um in diameter
o superficially identical to that of
E. histolytica.
- Nuclei differ
o Endosome is eccentric whereas
E. histolytica is central.
- Chromatin lining the nuclear
membrane is coarser with larger
granules. Food vacuoles contain
bacteria.
- Encystment follows same pattern as E.
histolytica.
- Splinter shaped chromatoidal bars
rather than blunt as in E. histolytica.
- Cyst 8 to 16 nuclei
- TROPHOZOITE : 15 to 50 um
 o Endosome eccentric, chromatin
lining the nuclear membrane is
coarser with larger granules
- CYSTS : chromatoidal bars
- 8 to 16 nuclei
Entamoeba gingivalis
- SUBPHYLUM SARCODINA ,
- ORDER AMOEBIDAE
- FAMILY ENDAMOEBIDAE,
- GENUS ENTAMOEBA
MORPHOLOGY
- Only Trophozoite has been found
- 10 to 20 um in diameter
- transparent
- Moves quickly by means of blunt
pseudopodia.
- Spheroidal nucleus with a small, nearly
central endosome.
- Chromatin concentrated on the inner
lining of the nuclear membrane.
BIOLOGY
- Lives on the surface of the teeth and
gums, in the gingival pockets near the
base of the teeth and sometimes in the
crypts of the tonsils.
- Abundant in cases of gum or tonsil
disease but there is no evidence that
they cause these conditions.
- Transmission is direct by kissing, droplet
spray or sharing utensils
Endolimax nana
- SUBPHYLUM SARCODINA ,
- ORDER AMOEBIDAE
- FAMILY ENDAMOEBIDAE,
- GENUS ENTAMOEBA
MORPHOLOGY: TROPHOZOITE
- 6 to 15 um in diameter.
- Ectoplasm is a thin layer surrounding
the granular endoplasm.
- Small nucleus and contains a large
centrally or eccentrically located
endosome.
- Marginal chromatin is a thin layer.
- Large glycogen vacuoles often present
and food vacuoles contain bacteria,
plant cells and debris.
MORPHOLOGY: CYST
- 5 to 14 um ,
- 4 nuclei
- with glycogen vacuoles and
- Occasionally small, curved chromatoidal
bars
HOSTS, LIFE CYCLE
- HOSTS: Humans, mainly in the cecum
- Pseudopodia and blunt and moves
slowly “Dwarf internal slug”
 - LIFE CYCLE: Follow same pattern as E.
histolytica
- Commensal, cyst is more susceptible to
putrefaction and dessication than E. coli

Iodamoeba buetschlii

- HOSTS: humans, primates, pigs

- DISTRIBUTION: Worldwide
- Most common amoeba of swine
- Less common than E. coli and E. nana in
humans
- Feeds on intestinal flora

MORPHOLOGY LIFE CYCLE

- Trophozoite 9 to 14 um long but may
range from 4 to 20 um Ectoplasm is not
clearly demarcated from the granular
endoplasm.
o LARGE nucleus containing an
endosome that is surrounded
by lightly staining granules
about midway between it and
the nuclear membrane.
o Achromatic strands extend -
between the endosome and the
-----------
nuclear membrane which has
peripheral granules. Naegleria fowleri
o Food vacuoles contain bacteria
- PHYLUM PERCOLOZOA
and yeasts.
- CLASS DISCOBA
- ORDER MASTIGAMOEBIDA
- FAMILY VAHLKAMPHIDAE

MORPHOLOGY

- Diphasic
- Amoeboid
- Mature cyst has only one nucleus. A
o predominating stage
large conspicuous glycogen vacuole
o single blunt pseudopodia.
stains deeply with iodine.
- Flagellated stage
o with two long flagella at one
end
o Elongated
o No pseudopodia
- Transformation is very rapid
 - Nucleus is vesicular and has a large
endosome and peripheral granules.
LIFE CYCLE
- Cyst forms in freshwater ecosystems
and moist soils
- Form the trophozoite stage, reproduce
asexually
o Infective stage
- Transform to the flagellated phase,
rapidly swim in the substrate
- Water-related activities
- Enter through olfactory
neuroepithelium (nose)
- flagellated trophozoites are forced deep
into the nasal passages when the victim
dives into the water.
- After entrance into the nose, the
amoebas migrate along olfactory
nerves, through the cribriform plate
and into the cranium
EPIDEMIOLOGY
- Infection typically occurs when people
go swimming or diving in warm
freshwater places
- In very rare instances, infections may
also occur when contaminated water
from other sources enters the nose
DISEASE
- PRIMARY AMOEBIC
MENINGOENCEPHALITIS
- Affects the CNS
o changes in olfactory perception
o vomiting, nausea, fever,
headache,
o rapid onset of coma and death
in two weeks.
o Acute, fulminant , rapidly fatal
illness usually affecting children
and adults who have been
exposed to water harboring
free living N. fowleri.
o Most cases are contracted in
lakes or swimming pools.
- Death from brain destruction is rapid
and few cures have been reported.
- Multiplies rapidly as water temperature
rises, so thermal pools that are
 contaminated by rainwater are
particularly at risk
LOCATION
- Czech Republic
o Between years 1962–1965, 16
young people died of acute
meningoencephalitides in Ústí
and Labem as a consequence of
bathing in an indoor swimming
pool.
- United States
o According to the CDC, the
amoeba killed 23 people
between 1995 and 2004.
o In August 2005, two Oklahoma
boys, ages 7 and 9 were killed
by N. fowleri after swimming in
hot stagnant water of the lakes
in the Tulsa area.
o In 2007, six cases were reported
in the U.S., all fatal:
o In July, the amoeba caused the
deaths of three boys in lakes
around Orlando, Florida.
Possible causes of the infections
include higher temperature and
droughts in that area of
Florida.[9]
o In late summer, the amoeba
caused the death of a 12-year-
old boy and a 22-year-old young
man in Lake LBJ in Texas.[10][1]
o In September, a 14-year-old boy
was killed by the amoeba after
likely having caught it while
swimming in Lake Havasu in
Arizona. The doctors suspected
meningitis before the boy died,
but did not know the etiology
until the CDC confirmed it as N.
fowleri.[11][12]
o In August 2008, a 9-year-old
boy was killed after having been
exposed to the amoeba while
swimming several times in Lake
Elsinore in California. The boy
was the first ever confirmed
case in Riverside County.[13]
Morphological and Physiological
Characterization of Philippine Naegleria
Isolates
- Naegleria is a free-living amoeba with a
transient flagellate stage and a resistant
cyst in its life cycle. One species,
Naegleria fowleri, causes primary
amoebic meningoencephalitis (PAM) in
humans. Eight environmental isolates of
Naegleria were obtained from the
University of the Philippines in
Diliman, Mt. Arayat, Marikina, Taal
Island, and Calamba, Laguna. They
were subsequently maintained as clonal
cultures derived from single cells.
Together with the local clinical isolate
that was previously designated as N.
philippinensis (RITM-1) and a Japanese
clinical isolate of N. fowleri (IT9611) for
comparison purposes, all isolates were
characterized using morphological and
physiological parameters. Differences in
cyst morphology, rate of encystment,
rate of enflagellation, and thermal
tolerance at 45C indicate that the
Philippine isolates may actually belong
 to other species that have not yet been
described.

TREATMENT

- Amphoterecin B,
- Miltefosine
- Qinghaosu
- Most cases are diagnosed at autopsy.
Rare and course of brain destruction is
so rapid that only seldom has it been
diagnosed in time for treatment to be
attempted.
Plasmodium spp.

- Life cycle overview:

- GEOGRAPHICAL DISTRIBUTION:

- DISEASE: Malaria
- Asexual: fission
- Bloodstream → brain

- TRANSMISSION
o The bite of a mosquito
o Blood transfusion, syringes
o Congenital
- CLINICAL SIGNS
o Host inflammatory response
which produces chills
o Anemia arising from destruction
of RBC
o Malaise, muscle pain,
headache, loss of appetite
before the first paroxysm
▪ Sudden coldness
o Cold stage: Attack begins with a
feeling of intense cold, teeth
chatter and the bed may rattle
from shivering
o Hot stage: intense feeling of
heat, intense headache and
delirium. Temperature then
returns to normal until the next
paroxysm

- INTERMEDIATE HOST: Anopheles sp.

 - PATHOGENESIS CONTROL
o Anemia due to RBC destruction.
- Destruction of breeding places of the
Bilirubin increases producing
vector
jaundice
- Appropriate drug treatment of persons
o Blackening of the liver, spleen
with the disease
and brain due to pigment
- Prophylactic drug treatment of
deposition
newcomers to malarious places
o Macrophages suffer impairment
in phagocytic ability after TREATMENT
ingestion of hemozoin
- Primaquine
Plasmodium falciparum complications - Mefloquine
- Pyrimethamine
- Cerebral malaria
- Proguanil
- Pulmonary edema
- Sulfonamides
- Algid malaria
- Blackwater fever DIAGNOSIS
- Hemorrhage
- Clinical manifestations of the disease
Cerebral malaria - Demonstration of the parasites in
stained smears
- Sudden, progressive headache followed
- DNA Probe, ELISA
by coma, uncontrollable increase in
temperature, psychotic symptoms or
convulsions, death may ensue in a
matter of hours

Pulmonary edema

- Difficulty in breathing and death may

ensue in a few hours

Algid malaria

- Rapid development of circulatory

collapse with markedly low blood
pressure

Blackwater fever

- Acute, massive lysis of erythrocytes

with high levels of hemoglobin by
products in the urine and blood
- Dark colored urine
- Renal failure
o Kidney
Toxoplasma gondii

- CLASS: Sporozoea
- SUBCLASS: Coccidia
- ORDER: Eucoccidiorida
- SUBORDER: Eimeriinae - Tachyzoites- found during initial and
- FAMILY:Sarcocystidae acute stage of infection; rapidly
multiplying forms
HOST

- Warm blooded animals

- Humans
o Raw
o Digestion of cyst

4 DEVELOPMENTAL STAGES
- Bradyzoites – slowly multiplying forms
- oocysts
that form oocysts; seen during chronic
- schizonts
infections
- tissue cysts
- Asexual multiplication within host cells
- gamonts
by endodyogeny

LIFE CYCLE

- Infective stages: Tachyzoite, Bradyzoite,

Oocyst
- Complete life cycle occurs only in
members of the cat family
o Follows a typical coccidian life
cycle (schizogony, gametogony,
and sporogony) in intestinal
epithelium
o Extraintestinal stages: asexual
stages → tachyzoites and
bradyzoites
TOXOPLASMOSIS
- Intestines are the first site of infection.
- Tachyzoites destroy cells, causing
extensive lesions in the lung, liver,
heart, brain and eyes.
- Cyst break down releasing bradyzoites.
Death of bradyzoites causes
encephalitis with spastic paralysis,
blindness, myocarditis, pneumonia.
- immunosuppressed individuals:
organism disseminates rapidly, may
 lead to ocular toxoplasmosis and to
fatal CNS disorders
- Most are asymptomatic
- Hydrocephalus
- Intracerebral calcification
- Retinochoroiditis
- Mental retardation
- 30% Stillbirths and spontaneous
abortion 60%
- May develop Ocular Toxoplasmosis
later in life 9% MAY DIE
EPIDEMIOLOGY
- Chronic asymptomatic toxoplasmosis is
age related, increasing 0.5 to 1.0% per
year of age.
- Raw meat seems to be an important
source of infection (beef, pork and
lamb)
- Feral and domestic cats
- Filth flies and cockroaches carry oocysts
from cat feces to the dinner table.
- Tachyzoites have been isolated in
humans from nasal, vaginal and eye
secretions milk, saliva, urine, seminal
fluid and feces.
- Philippines .. 19,023,902 (extrapolated
prevalence)
- Serologic prevalence data indicate that
toxoplasmosis is one of the most
common of humans infections
throughout the world. Infection is more
common in warm climates and at lower
altitudes than in cold climates and
mountainous regions.
- About half of the toxoplasmosis-related
fatalities reported are thought to
involve exposure to Toxoplasma gondii
through the consumption of
contaminated meat, making the disease
one of the top causes of foodborne
deaths in the United States (only
foodborne infection with Salmonella
and Listeria are more deadly).
DIAGNOSIS
- Demonstration of the organism at
necropsy or biopsy
- Demonstration of specific antibody
- DNA Probes
TREATMENT
- PYRIMETHAMINE AND SULFONAMIDE
GIVEN TOGETHER
PREVENTION

- WASH HANDS / FOOD

- COOK MEAT THOROUGHLY
- IF IMMUNOCOMPROM
ISED/PREGNANT AVOID CAT LITTER
- CLEAN /PROTECT CHILDREN’S SAND
BOXES FROM FECES
- CLEAN CAT LITTER DAILY AND DO NOT
FEED RAW MEAT
 Leishmania o L. major : found in sparsely
inhabited regions
- Phylum Sarcomastigophora
- Subphylum Mastigophora
- Order Kinetoplastida
- Family Trypanosomatidae
- Genus Leishmania

Prosmatigote

- Hosts o 1.5 million cases every year

o Primarily humans, dogs,
rodents
- Vector
o Breed in forest areas, caves and
burrows in tropical and
subtropical regions.
o Sandflies, (blood sucking insects
in the Family Psychodidae,
Subfamily Phlebotominaea)
Epidemics occur when people
are displaced into affected
regions through war or
migration or when people in
affected regions experience
high rates of disease or
malnutrition.
- Life cycle

LEISHMANIA TROPICA AND LEISHMANIA MAJOR

- DISEASE: Oriental Sore, Cutaneous - Clinical manifestation

Leishmaniasis, Jericho Boil, Aleppo Boil, o Incubation period is from a few
New Delhi Boil, Old World Cutaneous days to several months
Leishmaniasis o First sign is a small red papule
which may disappear in a few
Cutaneous Leishmaniasis
weeks
- DISTRIBUTION: West Central Africa,
Middle East, Asia Minor
o L. tropica: found in more
densely populated areas
 - Heals within 2 months to a year in
uncomplicated cases, leaving a
depressed, unpigmented scar.
- Common for secondary infection to
occur
- DIAGNOSIS
o Usually it develops a thin crust o Demonstration of amastigotes
that hides a spreading ulcer from scrapings on the side or
underneath. Two large ulcers the edge of the ulcer
may coalesce to form a large o Cultures
sore.

- TREATMENT
o Pentavalent antimonials, such
as sodium stibogluconate or
meglumine antimoniate
- L. tropica - dry, persists for months
o Long courses of these drugs are
before ulcerating , and has numerous
often required.
amastigotes within it
- CONTROL AND PREVENTION
- L. major – ulcerates quickly, is of short
o Eliminating vectors
duration, contains few amastigotes
o Reducing reservoir
o Immunization

Leishmania braziliense

- DISEASE: Espundia, uta, mucocutaneous

leishmaniasis
- DISTRIBUTION: Central Mexico,
northern Argentina
- MORPHOLOGY: same
- VECTOR: Lutzomyia
- CLINICAL MANIFESTATION
o Bite causes a small red papule
on the skin which becomes an
itchy, ulcerated vesicle in 1 to 4
weeks
 o Lesion heals in 6 to 15 months o Amastigotes cannot be
differentiated from other
species of Leishmania.
o Live within the cells of RES cells
including spleen, liver,
mesenteric lymph nodes,
intestines, bone marrow.

- LIFE CYCLE
o Same except that
promastigotes develop in the
hindgut - LIFE CYCLE
o Parasite has a tendency to
spread to mucocutaneous
zones causing degeneration of
cartilaginous and soft tissues
o Affects the nasal system and
the buccal mucosa especially
the lips, palate, pharynx, larynx,
trachea and rarely the genitalia.
o Death from infection or
respiratory complications

- VECTOR

Leishmania Mexicana

- DISEASE: Chiclero ulcer

- DISTRIBUTION: Northern, Central - DISTRIBUTION
America, Texas, Dominican Republic, o Bangladesh, India, Nepal, Brazil
Trinidad and Sudan
- MORPHOLOGY :Same - Epidemiology
- VECTOR: Lutzomyia, Sandflies o Frequently fatal in infants and
small children
Leishmania donovani o More predominant in males
- DISEASE: Dum Dum Fever or Kala Azar / o Poor nutrition, stress, other
Visceral Leishmaniasis infections predispose to deaths
- MORPHOLOGY - Essentially a disease of the RES.
- Phagocytic cells
 o important in defending the host
against invasion
o habitat of parasites
- Spleen and bone marrow
o undergo compensatory
production of macrophages and
other phagocytes to the
detriment of red blood cell
production.
o Spleen and liver become
enlarged while the patient
becomes severely emaciated
Visceral leishmaniasis
- Asymptomatic to fully progressive
- Incubation period from 10 days to 1
year but 2 to 4 months average
- Fever, malaise, progressive wasting,
anemia, protrusion of the abdomen
from enlarged liver and spleen and
finally death in 2 to 3 yrs
- Acute with death in 6 to 12 months
Edema especially of the face, bleeding
of the mucous membranes, breathing
difficulty, diarrhea.
- Death from invasion of secondary
pathogens
- Rare in the Mediterranean and Latin
American areas but develops in 5 to
10% of cases in India.
- Reddish,
- depigmented nodules that can be
disfiguring.
- Develops 1 to 2 yrs after inadequate
treatment for kala azar.
- DIAGNOSIS
o Finding L-D Bodies in tissues or
secretions
o Spleen punctures, nasal blood
smears, bone marrow and other
tissues should be examined for
the characteristic parasites and
cultures from these and other
organs should be attempted.
o Immunodiagnostic tests, ELISA ,
IFA
o ▪ Differential diagnosis: typhoid,
paratyphoid, malaria, syphilis,
tuberculosis, dysentery,
relapsing fever
- TREATMENT
o Antimony compounds

Post kala azar dermal leishmanoid