2. At the end of this unit, the student
is able to:
 Classify the Protozoans
 Describe the morphology of each protozoa
 Explain the pathophysiology, life cycle, infective stages,
modes of transmission, epidemiology, prevention and
control
 Describe the diagnostic features of each parasite.
 Enumerate the different specimens used for identification
 Identify correctly the diagnostic features of each parasite.

3.  Perform the laboratory tests
 Discuss specimen collection,transport, processing,
preservation and disposal

4. General Characteristics
 They are single-celled organisms which are generally
classified according to their organelles of locomotion.
 Cilia, flagella & pseudopodia
 Considered as the simplest forms of animals

5. Organelles
 Nucleus
 Nucleulos
 Mitochondria
 Locomotory Organelles

6. Kingdom Protista
 Phylum Sarcomastigophora
 Subphylum Mastigophora
 (Superclass Rhizopoda)
Flagella (whip-like) = organ of locomotion
 Subphylum Sarcodina
 (Class Zoomastigophora)
Pseudopodia (hyaline foot like)= organ of locomotion
 Phylum Ciliophora
Cilia (hair like) = organ of locomotion
 Balantidiasis (Balantidium coli)

7. Kingdom Protista
 Phylum Apicomplexa
 w/ apical complex at the anterior end (apicoplast)
 Babesiosis (Babesia)
 Malaria (Plasmodium)
 Coccidian diseases including:
 Cryptosporidiosis (Cryptosporidium parvum)
 Cyclosporiasis (Cyclospora cayetanensis)
 Toxoplasmosis (Toxoplasma gondii)
 Phylum Microspora
 Spore-forming parasites

11. Giardia lamblia Amoeba Amoeba feeding

12. 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
Classification of Protozoa and Descriptions

13.  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
 Trophozoiteactive pathogenic vegetative stage
 Cyst latent survival form
 Sites of pathogenesis
 Intestinal, Urogenital, Blood and Tissue
Pathogenic Protozoa - Characteristics

14.  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
Protozoa - Amoeba

15.  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
Protozoa - Ciliates

16.  Phylum Mastigophora
 Motility via flagella
 One or more whip-like filaments move in counter-
clockwise 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
Protozoa - Flagellates

17.  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
Protozoa - Sporozoans

18. Classification of Protozoan Parasites:
Sarcomastigophora
Sarcodina Acanthamoeba castellani, Endolimax nana
Entamoeba coli, Entamoeba dispar
Entamoeba gingivalis, Entamoeba histolytica
Iodamoeba butschlii, Nagleria fowleri
Mastigophora Chilomastix mesnili, Dientamoeba fragilis
Giardia lamblia,Trichomonas (homini, tenax
,vaginalis)
Leishmania (braziliensis, donovani, tropica)
Trypanosoma brucei complex, Trypanosoma cruzi
Ciliophora Balantidium coli
Apicomplexa Bebesia spp., Cryptosporidum hominis, Cyclospora
cayetansis, Isospora belli, Plasmodium spp.,
Toxoplasma
Microspora Enterocytozoon bineusi, Encephalitozoon spp.
Vittaforma cornea,Trachipleistophora hominis
Pleistophora spp., Brachiola vesicularum,
Microspordium spp.

19. 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 donovani
 cutaneous leishmaniasis .......... Leishmania topica/braziliensis
Protozoan Diseases

20. AMOEBAS

21. Intestinal and Luminal Protozoa
 Constantly changing shapes, move by
ending out fingerlike extensions of their cell
membranes called pseudopods or “false-
feet” projections
 the name comes from the Greek word for
“change” is an example of a sarcodine,
found in fresh water or salt water

22.  six species have been established as parasites of man:
Entamoeba histolytica
Entamoeba coli
Entamoeba gingivalis
Dientamoeba fragilis
Endolimax nana
Iodamoeba butschlii

23. Intestinal and Luminal Protozoa
 Stages of Development
Cyst – infective stage
Trophozoite – vegetative stage

24. General Statements:
 All amoebas are capable of producing cyst and
trophozoite except for Entamoeba gingivalis
and Dientamoeba fragilis.
 Found in the colon except Entamoeba
gingivalis which is found in the oral cavity
 All are commensals except Entamoeba
histolytica.

25. Entamoeba histolytica
A) Trophozoite Stage (I & H preparation)
 shape: irregular
 shape: 10– 60 micra
 structures:
- cytoplasm is grayish violet with a clear
demarcation between the ectoplasm
and endoplasm

30. Entamoeba histolytica
B. Cystic Stage
 shape: spherical
 size: 5 – 20 micra
 structures:
- smooth, definite, relatively thin cystic
wall

31. Entamoeba histolytica
B. Cystic Stage
the number of nuclei range from 1-4,
rarely more, with a centrally located
karyosome
in the younger cyst, the chromatoidal
bars with rounded ends and glycogen
mass may be present

35. Entamoeba histolytica
Diseases:
Amoebiasis
Amebic dysentery
Amebic hepatitis
Pulmonary amoebiasis

36. Entamoeba histolytica

37. Entamoeba histolytica
Diagnosis:
 Microscopy
 Antigen detection
 Serology
 PCR
 Imaging studies

38. Entamoeba histolytica
Treatment:
 metronidazole
 tetracycline with diiodohydroxyquin

39. Entamoeba coli
A. Trophozoite Stage (I & H
preparation)
 shape: condensed, thickened,
rounded mass
 size: 15 – 50 micra

40. Entamoeba coli
A. Trophozoite Stage (I & H preparation)
 structures:
 cytoplasm is grayish violet; there is no clear
demarcation between the ectoplasm and
endoplasm
 the endoplasm is highly vacuolated containing
bacteria
 the nucleus is spherical with thick nuclear
membrane lined with coarse, irregular chromatin
granules or plaques; the karyosome is moderately
large and eccentrically located

43. Entamoeba coli
B. Cystic Stage
 shape: spherical
 size: 10 – 33 micra

44. Entamoeba coli
B. Cystic Stage
 structures:
 smooth, definite, thick cystic wall
 number of nuclei range from 1 – 8 rarely
more with an eccentric karyosome
 in younger cysts, chromatoidal bars with
splintered ends and glycogen mass

46. Endolimax nana
A.Trophozoite Stage (I & H preparation)
 shape: irregular
 size: small, 6 – 15 micra

47. Endolimax nana
A.Trophozoite Stage (I & H preparation)
 structures:
 cytoplasm is grayish-violet, vacuolated
which may contain bacteria
 there is small, spherical, single nucleus
with a large irregular, central or eccentric
karyosome

49. Endolimax nana
B. Cystic Stage
 shape: oval
size: 6 – 10 micra

50. Endolimax nana
B. Cystic Stage
 structures:
 smooth, definite cystic wall
 number of nuclei ranges from 1-4
 I & H preparation
 cytoplasm is grayish, granular
 nuclei are visible as darkly stained dots
 chromatoidal bodies occasionally seen as
deeply stained, small, slightly curved rods

53. Entamoeba gingivalis
A.Trophozoite Stage (I & H preparation)
 shape: irregular
 shape: 5 – 35 micra
 structures:
 clear demarcation between the clear
ectoplasm and granular endoplasm

54. Entamoeba gingivalis
 endoplasm contains food vacuoles with
bacteria and rarely rbc
 possesses a single nucleus which is
spherical in shape, karyosome is near the
center
 have multiple pseudopodia with
progressive directional movement similar
to E. histolytica

56. Dientamoeba fragilis
A.Trophozoite Stage (I & H preparation)
 shape: irregular
 size 3 – 22 micra

57. A.Trophozoite Stage (I & H preparation)
 structures:
cytoplasm is granular with vacuoles
containing bacteria
nuclei, commonly 2 in number, with
karyosome consisting of 4-8 chromatin
granules
Dientamoeba fragilis

59. Iodamoeba buetschlii
A.Trophozoite Stage (I & H preparation)
 shape: irregular
 shape: 6 – 25 micra

60. Iodamoeba buetschlii
A.Trophozoite Stage (I & H preparation)
 structures:
 granular, vacuolated cytoplasm and
vacuoles may contain bacteria and yeast
cells
 single, spherical nucleus with a large
central or eccentric karyosome
surrounded by an unstained halo

62. Iodamoeba buetschlii
B. Cystic Stage
 shape: irregular
 size: 6 – 15 micra

63. Iodamoeba buetschlii
B. Cystic Stage
 structures:
smooth, definite cystic wall
have a single nucleus, rarely with 2
nuclei
large glycogen vacuole

64. Iodamoeba buetschlii
B. Cystic Stage
I & H preparation
violet-gray granular cytoplasm
nucleus is visible
large glycogen vacuole is unstained
chromatoidal bodies are usually
absent; if present, they are seen as
deeply stained small rods

67. Soil andWater Amoebas

68. A) Trophozoite Stage (I & H preparation)
endoplasm is briefly granular with
ingested rbc which are bluish black in
color
single, spherical nucleus; nucleus
membrane is lined by fine, regularly
arranged chromatin granules;
karyosome is relatively small and
centrally located

69. Symptoms:
intermittent diarrhea
abodominal cramps
vomiting
general body malaise

70.  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
Pathogenic Protozoa - Entamoeba histolytica

71.  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 amoeba must be distinguished from commensal amoeba
 new test are designed to detect fecal antigen and trophozoite DNA
 extraintestinal complications can be confirmed via biopsy or
serological tests for antibody
 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 transmit the cysts mostly to food and
fomites
Entamoeba histolytica

72.  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
Naegleria fowleri/ and Acanthamoeba

73.  Pathogenesis most infections occur when trophozoites in
water enter the nasal passages when people
swim; they then invade 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 environmental opportunist
acquired via contact with water, soil , or dust

74.  major cause of a disease called PAM
 has 2 long flagella at one end
 most cases are contracted in lakes and
swimming pools
 probably the flagellated trophozoites are
forced deep into the nasal passages
when the victim dives in water
 found in USA, Czechoslovakia, Mexico,
Africa, New Zealand, Australia

76. PAM

77.  cause chronic infection of the skinor CNS in
immunocompromised persons
 has small spiky acanthopodia
 causes keratitis
 GranulomatousAmoebic Encephalitis

80. Naegleria Acanthamoeba
Trophozoite with
broad pseudopods
Actively motile
Forms the flagellate
stage
Single-walled cyst
Does not encyst in
tissues
Trophozoite with
filamentous pseudopods
Sluggishly motile
Does not form flagellate
stage
Double-walled cyst
May encyst in tissues

82. Prevention and Control
 Avoid swimming or jumping into bodies of warm
fresh water
 Avoid swimming in thermally polluted water (water
around power plants)
 Do not swim in areas posted as "no swimming."
 Hold the nose shut or use nose clips when jumping
or diving into bodies of fresh water.

83. Balantidium coli

84.  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
Pathogenic Protozoa - Balantidium coli

85.  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

88. Cysts

89.  Trophozoite

90. Giardia lamblia

91. Scientific classification
Domain:Eukaryota
Phylum: Metamonada
Order: Diplomonadida
Family: Hexamitidae
Genus: Giardia
Species: G. lamblia
species
Giardia agilis
Giardia ardeae
Giardia lamblia
Giardia muris
Giardia microti
Giardia psittaci

93.  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
Pathogenic Protozoa - Giardia lamblia

94.  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

95.  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
 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,
fecal- oral 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
Pathogenic Protozoa - Giardia lamblia

96. Trichomonas vaginalis

97. Scientific classification
Domain: Eukaryota
(unranked):Excavata
Phylum: Metamonada
Class: Parabasalia
Order: Trichomonadida
Family: Trichomonadidae
Genus: Trichomonas

99. Incubation Period is typically 5 to 28 days
Trichomonas vaginalis is pathogenic in the
genitourinary tract
In women, it lives in the vagina and the
Skene's glands (of the urethra)
In men, it lives in the urethra
Multiplies when vaginal conditions become
more basic than usual (normal pH is 3.8 to
4.2)
No known cystic form
May survive in a host for 2+ years

100.  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
Pathogenic Protozoa - Trichomonas vaginalis

101.  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
nucleic acid probes

102. Cryptosporidium parvum

103. Scientific classification
Domain: Eukaryota
Kingdom:
Chromalveolata
Superphylum: Alveolata
Phylum: Apicomplexa
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiorida
Suborder: Eimeriorina
Family: Cryptosporidiidae
Genus: Cryptosporidium
Species
Cryptosporidium andersoni
Cryptosporidium bailey
Cryptosporidium bovis
Cryptosporidium canis
Cryptosporidium cichlidis
Cryptosporidium cuniculus
Cryptosporidium felis
Cryptosporidium galli
Cryptosporidium hominis
Cryptosporidium meleagridis
Cryptosporidium muris
Cryptosporidium nasoris
Cryptosporidium parvum
Cryptosporidium pestis
Cryptosporidium reichenbachklinkei
Cryptosporidium saurophilum
Cryptosporidium scophthalmi
Cryptosporidium serpentis
Cryptosporidium suis
Cryptosporidium varanii
Cryptosporidium wrairi

106.  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
Pathogenic Protozoa - Cryptosporidium
parvum

107.  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

108. Cyclospora cayetanensis

110.  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
Pathogenic Protozoan -Cyclospora
cayetanensis

111.  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

112. Blood andTissue
Protozoa

113.  Sporozoan(coccidian)
 malaria Plasmodium spp
 toxoplasmosis Toxoplasma gondii
 Flagellates
 trypanosomiasis Trypanosoma cruzi
 African Sleeping SicknessTyrpanosoma brucei
 leishmaniasis Leishmania spp
Blood and Tissue Protozoa

114. Malarial Species

115.  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 malaria
Pathogenic Protozoa – Plasmodium spp

116.  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

118. Liver stage
Sporozoites
Mosquito Salivary
Gland
Malaria Life Cycle
Gametocytes
Oocyst
Red Blood Cell
Cycle
Zygote

119. RING FORMS GAMETOCYTE

120. RING FORMS SCHIZONT
GAMETOCYTE

121. Species Stages found in the circulating blood
P. vivax All stages. Wide range of stages may be seen
on given film
P. malariae All stages. Wide variety of stages usually not
seen. Relatively few rings, gametocytes
generally present
P. ovale All stages
P.
falciparum
Rings and or gametocytes. Other stages develop in
blood vessels of internal organs but are not seen in
peripheral blood except in severe infections

122.  Trophozoite or ring forms
young form is globose in shape with a
central vacuole, a red chromatin mass
and a blue cytoplasm
- in stained smear, they appear signet
rings

123. b) Growing form
- single chromatin
mass with a more
abundant cytoplasm
- cytoplasm may
appear compact or
irregular (ameboid)
c) Mature form
- single
chromatin mass but
with an increase
amount of cytoplasm
that partially fills the
erythrocyte

124.  Early trophozoites have
the characteristic
signet ring shape.
 Also, unique to P.
falciparum is the
presence of multiple
trophozoites in one
cell.

125. RING FORMS GAMETOCYTE

126.  The gametocytes of P.
falciparum have a
crescent or banana
shape.

127.  Red blood cells
infected by P. vivax are
often larger than
uninfected red blood
cells.
 They are
approximately 1.5
times the size of a
normal cell.

128. RING FORMS SCHIZONT
GAMETOCYTE

129.  A schizont showing the
large number of
merozoites typical of
this species (16-24).
 Also note the larger
size compared to a
normal red blood cell.

130.  Characteristic
trophozoites of P.
malariae showing the
ring shape and the
tendency of infected
cells to be of normal or
smaller size (arrows).

131.  A schizont containing
merozoites (6 to 12)
giving a coarse
granular appearance.

132. Species rbc stage Size of rbc Schauffner’s
stippling
P. vivax Young rbc enlarged +
P. malariae Mature rbc normal -
Ziemann’s
dots
P. ovale Young rbc enlarged +
P. falciparum rbc of all
stages
Normal/
Multiple
infection
_
Maurer’s dots

133.  A red blood cell
showing the
Schauffner's dots
characteristic of cells
infected by
Plasmodium vivax and
Plasmodium ovale.
Schauffner’s dots

134. Species Cytoplasm Pigment No. of
merozoites
Gametocytes
P. vivax Irregular,
ameboid in
trophozoite,
has spread
out
appearance
Golden
brown,
incons-
picuous
12-24
Average is
16
rounded

135. Species Cytoplasm Pigment No. of
merozoites
Gametocytes
P.
malariae
Rounded,
compact
trophozoite
with dense
cytoplasm/
band form
troph are
rarely seen
Dark
brown,
cons-
picuous
6-12
Average is 8,
“rosette”
schizonts are
sometimes
seen
rounded

136. Species Cytoplasm Pigment No. of
merozoites
Gametocytes
P. ovale Rounded,
compact
trophozoite
with dense
cytoplasm/
band form
troph are
rarely seen
Dark
brown,
cons-
picuous
6-12
Average is 8,
“rosette”
schizonts are
sometimes
seen
rounded

137. Species Cytoplasm Pigment No. of
merozoites
Gametocytes
P.
falciparum
Young rings
are small,
delicate,
often with
double
chromatin
mass
Black
coarse and
cons-
picuous in
gametocyte
6-32
Average is
20-24
Crescent,
sausage-
elongate
shape

138. Toxoplasma gondii

139.  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
 Pathogenesis : cellular death due to intracellular muliplication
of trophozoites especially severe in fetal and cerebral
tissues
Pathogenic Protozoa - Toxoplasma gondii

140.  Epidemiology : reservoir is a variety of mammals and birds
including humans
 fecal-oral transmission of oocyst from felines
 common source transmission of pseudocyts in poorly cooked meat
esp. beef
 Diagnosis : serological detection of antibody: Elisa test for
IgM antibodies is most reliable
 Risk Groups : Pregnant females and immunocompromised

143.  Enteroepithelial cycle
asexual schizogony
Sexual gametogony
*immature oocyst passed in the cat’s feces
 Immature oocyst mature to the infective stage
2 sporocysts with 4 sporozoites each (2-21 days)

144.  Ingestion of inadequately cooked meat, esp
lamb or pork
 Ingestion of infective oocysts from material
contaminated by cat feces
 Drinking contaminated water or unpasturized
goat’s milk
 Organ transplantation
 Blood transfusion
 Transplacental

145.  When mature oocyst is ingested, sporozoites
are released forming trophozoites
*tachyzoites- actively growing trop
*bradyzoites- latent or slow growing
trophozoites

146.  Active infection (all nucleated cells)
fever
lymphadenopathy
 Congenital
depends on the age of gestation when the
infection is acquired

147.  1st half pregnancy
- intrauterine death
- microcephaly
- hydrocephaly with intracranial calcification

148.  2nd half of pregnancy
-usually assymptomatic at birth though fever,
hepatosplenomegaly and jaundice may
appear
-choriorenitis, psychomotor retardation and
convulsive disorders may appear months or
years later

149.  Immunocompromised individuals
-present CNS involvement
-pneumonitis, myocarditis, retinitis,
pancreatitis or orchitis

150.  Examination of tissues, blood, and body fluids
- Demonstration of tachyzoites or tissue cysts
- Animal inoculation to uninfected mice
- PCR
- Sabin-Feldman dye test
- IFA
- EIA

151. Babesiosis

152.  Infection of rbc often producing febrile illness
 Transmitted by ticks (Ixodes scapularis, Ixodes
pacificus)
 Caused by Babesia microti
 mulitiply in rbc by schizogony but do not produce
gametocytes
 Appear as delicate ring forms that may easily
confused with malaria

153.  The organisms
resemble
P.falciparum
 they vary more in
shape and in size;
and they do not
produce pigment
 evidence of
Maltese cross
formation

157.  TICK vector of
Babesia
 The organism
belongs to the
genus Ixodes

158. The vector: Dog tick

160. MALARIA BABESIOSIS
Multiple rings _ +
Large
trophozoite
+ _
Gametocytes + _
Hemozoin
pigment
+ _

161. Patients with spleen only 25% of RBCs could be parasitized
Patients withoutspleen higher parasitemia fever, muscle aches,
chills, fatigue, headache and loss of appetite Capillary microvascular stasis
RBC fragments Hemolytic anemia liver, spleenic, renal and
Central Nervous System involvement.

162.  Indirect Fluorescent Antibody
 PCR

163.  antimicrobial drugs such as clindamycin*
plus quinine or atovaquone* plus
azithromycin are often used.
Prevention/Control
- wearing appropriate light-colored clothing
-using tick repellent in areas where the diseases
are endemic
-if possible test blood to be transfused for possible presence
of Babesia species

164. Blood and Tissue Flagellates

165. Trypanosomes

166. Species Disease Portal of Entry and
Final Site
Vector
Trypanosoma cruzi
Trypanosoma brucei
gambiense
Trypanosoma brucei
rhodesiense
American
Trypanosomiasis or
Chagas’ Disease
Gambian or West
African Sleeping
Sickness
Rhodesian or East
African Sleeping
Sickness
Breaks in skin or intact
mucous membranes,
later any organs and
blood stream; Heart and
GIT in chronic form
Skin for both
Lymph nodes, blood,
and brain
Infected
Triatomine
bug
Infected
tse-tse flies

167.  African Sleeping Sickness CNS 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
Pathogenic Protozoa - Trypanosoma brucei

168.  Epidemiology : reservoir is a variety of mammals
and birds including humans
 fecal-oral transmission of oocyst from felines
 common source transmission of pseudocyts in poorly
cooked meat esp. beef
 Diagnosis : serological detection of antibody:
Elisa test for IgM antibodies is most reliable
 Risk Groups : Pregnant females
and immunocompromised

169.  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(trypanosmal) form
 Pathogenesis - the intracellular amastigote multiplies in cells
and destroys the cells
Pathogenic Protozoa - Trypanosoma cruzi

170.  Epidemiology- wild and domestic animal reservoirs
 arthropod-borne via the cone-nosed (reduviid) bugs
which live in the cracks of domestic dwellings
 Diagnosis : trypanosomes in the blood; amastigotes
in biopsy; also xenodiagnosis and gene probes

173. Local inflammation at the site of
inoculation.
CHAGOMA = reddish painful nodule
Trypanosmes may enter the conjunctiva
= edema of eyelid & conjunctiva =
ROMAÑA’S SIGN

177. Winterbottom's sign
is the swelling of
lymph nodes
(lymphadenopathy)
along the back of the
neck, in the posterior
cervical chain of
lymph nodes, as
trypanosomes travel
in the lymphatic fluid
and cause
inflammation.

178. w/ CNS invasion = chronic disease known as sleeping sickness stage is
initiated
(Kerandel’s sign) = delayed sensation to pain indicative ofAfrican
trypanosomiasis
Untreated infection may lead to death

179. Leishmania

180. Species Disease Portal of Entry and
Final Site
Vector
Leishmania
donovani
Leishmania
tropica
Leishmania
brazilienses
Visceral Leishmanisis
or KALAAZAR
Cutaneous
Leishmaniasis
Mucocutaneous
Leishmaniasis
or ESPUNDIA
Skin/ Macrophages and
monocytes of spleen,
liver, bone marrow
Skin/ Macrophages of
the skin and mucosa
Infected
Phlebotomus
Fly

181.  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
 Parasites : Leishmania donovani - visceral- amastigote stage
multiplies in visceral cells causing lysis
 Leishmania tropica - cutanous: Leishmania braziliensis –
mucocutaneous
 Pathogenesis - cells in infected visceral and cutaneous tissues
are destroyed by intracellular amastigote
multiplication
Pathogenic Protozaa - Leishmania

182.  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
 Diagnosis : amastigote is observed in tissue biopsy, body
fluid aspirates, and in the blood: also serology for antibody
presence

183. Species Amastigote Promastigote Epimastigote Trypomastigote
Leishmania
Animal Host
Vector
Macrophages
-
-
midgut and
pharynx of
sandfly
-
-
-
-
Trypanosoma
Animal Host
Vector
-
-
-
-
-
salivary gland and
gut of flies/
culture
Blood, lymph
nodes, brain, CSF
-
Trypanosoma cruzi
Animal Host
Vector
Intracellular,
esp. striated
and smooth
muscle, brain
Cell cultures
-
-
-
-
Intestine of vector
bugs
Blood and tissues
of mammals
Rectum of vector
bug/culture and
cell cultures

188. Kalaazar

189. Cutaneous Leishmaniasis
1. Skin ulcers, w/ painless lesions = ugly scar
2. Subcutaneous nodules

190. Mucocutaneous Leishmaniasis
Metastatic spread to the oronasal and pharyngeal mucosa
(ESPUNDIA) = highly disfiguring leprosy like tissue destruction &
swelling (“TAPIR NOSE”)

191. Espundia

192. The current standard treatment for first stage
disease is:
 Intravenous pentamidine (for T.b. gambiense);
or
 Intravenous suramin (for T.b. rhodesiense)
 Eflornithine

193. To HIM we LIFT the HIGHEST PRAISE