PROTOZOANS

AMEBAE

● Single celled eukaryotes

● Not all amebae are pathogenic
● Cell is bounded by a Trilaminar unit membrane supported by a Sheet of Contractile Fibrils used for
movement and changing shape
● No fixed shape, always changing
○ 2 Cytoplasm Portion
■ ECTOPLASM / Outer Homogeneous Portion
● Organ for Movement and Engulfment of Food
■ ENDOPLASM/ Inner Granular Portion
■ Has Nucleus or Nuclei and other organelles
○ 2 Forms
■ CYST / Resting
● During ENCYSTMENT
○ Secretion of Cyst wall - for resistance/ survival during Unfavorable
conditions
○ Storage of food reserve eg. Starch or Glycogen
○ Projecting movement or locomotor organelles are partially / completely
resorbed
○ Nuclear Division (once or twice) → Multiple nuclei
■ TROPHOZOITE / Active Feeding
● Active and Feeding Stage
● Rapidly destroy outside the body
● Cannot survive the Gastric Environment exposure
● Pseudopodia
○ Formed by thrusting out ectoplasm followed by endoplasm
○ For Movement and Engulfment of food by Phagocytosis
○ Reproduction
■ By Binary Fission / Budding
 AMEBAE

Entamoeba Entamoeba coli Entamoeba Entamoeba Endolimax nana Iodamoeba

histolytica hartmanni gingivalis butschlii

General -Pseudopod ● Most common ● Occurs where ● Can be found ● Infects

description forming E. histolytica is in the mouth, humans,
around gingival tissues primates, pigs
-Non flagellated ● Most common
ameba of pigs
MOST INVASIVE
AMOEBA

-cause colitis and

liver abscess

Morphology ● No fixed ● Larger than E. ● Smaller than ● Characteristica ● Small ● Characterized

shaped histolytica E. histolytica lly have food trophozoite, by a large,
always vacuoles that sluggish chromatin-rich
changing ● Trophozoites: ● Trophozoites: contain cellular motility, large karyosome
● Contains ○ 15-50 μm 3-13 μm, no debris mostly karyosome surrounded by
RBCs ○ contains RBCs WBCs ● Oval cyst with a layer of
● Trophozoit bacteria ● Cysts: 4-10 four nuclei achromatic
es: 12-60 ○ No RBCs μm, may globules and
μm ○ Broader resemble anchored to
● quadrinucl pseudopod Endolimax the nuclear
eated ia nana membrane by
○ Thicker, achromatic
irregular ● Quadrinucleate fibrils
chromatin d with rod- ● Trophozoite:
○ Eccentric shaped large vesicular
karyosome chromatoid nucleus, with
● To differentiate material large central
from E. ● Less vigorous karyosome
histolytica motility surrounded by
 troph: achromatic
○ More granules
vacuolated ● Cyst:
or uninucleated
granulated with large
but no glycogen body
RBCs
○ Narrower,
less
differentiat
ed
ectoplasm
○ Broader,
blunter
pseudopod
ia (feeding
>
locomotion
)
○ Sluggish,
undirected
movement
s
○ thicker ,
irregular
peripheral
chromatin
with large,
eccentric
karyosome
● Cysts:
○ Large with
prominent
glycogen
mass
○ Eight
 nuclei
● E. coli cyst vs
E histolytica
○ Larger (10-
35 μm
○ Eight
nuclei
○ More
granular
○ sphincter -
like
chromatoid
al bodies

Intermediate -
Host

Definitive Host Human

Infective Stage Cyst Form Trophozoite Cyst form

Transmission -Fecal - Oral Fecal-oral transmission Direct Fecal-oral transmission

transmission:
-Ingestion of kissing, droplet
Mature Cyst in spray, sharing of
contaminated utensils
food, water or
hands

-Sexual
Transmission

Life cycle Cyst in Formed ● Same with E. ● Same with E. ● Lives in the
Stool histolytica but histolytica but: large intestine,
↓ remains ○ No cyst mainly near
Ingestion of commensal stage the cecum
 Contaminated without tissue ○ Does not
food, water or invasion inhabit the
hand small
↓ intestines
Forms Metacysts ● Remain
(mature - 4 commensal
nuclei)
↓
Excystation
occurs in Small
Intestine
↓
Cysts undergoes
nuclear &
cytoplasmic
division
↓
forms 8 Metacystic
Trophozoites
↓
Migrates to Large
Intestine
↓
Multiply via Binary
Fission
↓
Undergoes
Encystation (still
in Large Intestine)
↓
Forms Pre-Cysts
(1 nucleus)
↓
Passed in feces
↓
1.Trophozoite
 (diarrheal/invasive
form)

2.Cysts (infective/
survival form)

Signs and -Flask-shaped

symptoms Lesion due to
killing of Mucosal
cells by
trophozoite
adherence

-Hepatic
Amebiasis due to
its ability to break
through the
different muscle
layers, allowing it
to be carried into
the bloodstream
going to different
organs eg Liver

-Ameboma which
results from
cellular responses
to active
trophozoite after
obstruction of the
intestinal wall due
to Granulomatous
mass formation

-Perforation of the
Bowel →
 Secondary
Bacterial
Peritonitis
-Most Serious
Complications

Diagnostics and -Microscopic

results detection of Cyst
and Trophozoite in
> 3 stools
collected on
different days

-Trophozoite
detection using
Fresh Stool
collected within 30
mins after
defecation; E.
histolytica
trophozoites with
ingested RBCs is
diagnostic of
Amebiasis

-E. Dispar - non

invasive; can only
be detected with
PCR

Imporatnce of
Differentiating
-To avoid
unnecessary
medication
-To avoid NOT
 giving the
necessary/
appropriate
medication

Treatment -Metronidazole
-Luminal Agent
(usually added)

PROTOZOANS
FREE LIVING AMEBAE
[general description here]

FREE LIVING AMEBAE

Naegleria fowleri Acanthamoeba spp.

General description ● Brain-eating ameba ● Opportunistic

● heat-loving ameba ● Found in water and soil
○ Found in warm freshwater or lakes

Morphology ● 2 forms ● Trophozite - single large nucleus,

○ Trophozite - cytoplasm is granular + vacuoles, large centrally located nucleolus, finely
single nucleus granulated cytoplasm, small fine
■ Ameboid ( found in humans) filaments
● 10-35 micrometer in size (but 10-15 ○ Replicate by mitosis
micrometer when rounded)
■ Flagellate
○ Flagellate (swimming form)
IH

DH

Infective Stage ● Tropozoite - by penetrating the nasal mucosa and migrating to Trophozoites and cysts may enter the body,
the brain via olfactory nerves but Trophozoite is the Infective stage

Transmission ● Amoeba penetration to the nasal mucosa Inhalation, ingestion, through skin/eyes

Life cycle Three Stages 2 stages

● Cyst - not seen in brain tissue ● Cyst
● Trophozoite (replicate by promitosis) ● Trophozite
● flagellates

Signs and ● Causes Primary Amebic Meningoencephalitis (PAM) ● Granulomatous Amebic Encephalitis
symptoms ● Fever ○ Destruction of brain tissue
● Nausea ○ Miningeal irritation
● Vomiting ○ Fever
● Headache ○ Malaiseanorexia
● Nuchal rigidity ○ Increased sleeping time
● Mental status changes ○ Severe headache
● Rapid progression to coma ○ Changes in mental status
 ● death ○ Epilepsy
○ Coma
○ Hemiparesisblurring of vision
○ Diplopia
○ Ataxia
○ Inc intracranial pressure
○
● Acanthamoeba keratitis
○ Associated with improper
disinfection of contact lenses
○ Severe ocular pain
○ Blurring of vision
○ Corneal ulceration with
infiltration
○ Hypoyopon formation
○ Scleritis
○ Iritis
○ Vision loss

Diagnostics and ● Trophozoite in CSF ● Biopsy

results ● Elevated WBC in CSF, neutrophilic predominance, high protein ● Wet mount
and low glucose ● Culture
● Post mortem oexam of infected brain shows hemorrhagic ● Corneal scrapings with histologic analysis
necrosis particularly the olfactory bulbs, congestion and edema ● pcr
of neural tissue

Treatment ● Indistinguishable from bacterial meningitis For AK

● Amphotericin B plus Cotrimoxazole ● Surgical excision of cornea with corneal
transplantation
● Clotrimazole with pentimidine,
isethionate, neosporin
● Other agents such as
polyhexamethylene biguanide,
propamidine, dibropropamidine
isethionate, neomycin, paromycin,
 polymyxin b, ketoconazole,
minakonazole, itraconazole
● Topical corticosteroids should be
avoided
For GAE
● Amphotericin b, pentamidine
isethionate, sulfadiazine, flucystocine,
fluconazole, itraconazole,

PROTOZOANS
 FLAGELLATES
[general description here]

FLAGELLATES

Giardia lamblia Trichomonas vaginalis

General description ● Intestinal flagellate Causes Trichomoniasis

● Earliest protozoan parasites recorded ● STD; observed in purulent secretions of
● Aka Giardia duodenalis or Giardia male and female urogenital tracts
intestinalis ● The most prevalent non-viral sexually
● Lives in the duodenum and upper jejunum transmitted infection

Morphology Vegetative trophozoite ● Pyriform shape; 7-23um

● Heart-shaped ● 4 free anterior flagella, 5th flagellum
● Concave sucking disk for attachment embedded in the undulating membrane
● Bilaterally symmetrical ● Single nucleus
○ One pair of nuclei ● Exist only as Trophozoite, no cyst stage
○ Four pairs of flagella
○ One pair of axostyle
● Falling leaf motility
Infective cyst
● Small, oval, surrounded by hyaline cyst
wall
● Immature: 1 pair of nuclei
● Mature: 2 pairs of nuclei
● Axostyle forming dividing line

IH - Human

DH Human

Infective Stage Cyst Trophozoite

Transmission Ingestion of contaminated water and cysts Person to person, usually sexual intercourse
through contaminated water and food
Life cycle Ingestion of cysts → excystation → trophozoites
multiply through binary fission → adhere to small
intestine → can be passed out in feces

Signs and symptoms Causes “Traveller’s diarrhea” FEMALE:

Steatorrhea Liquid vaginal secretions
● Greenish or yellow
● Very irritating, intense itchiness,
burning sensation
Postpartum Endometriosis
Complication: UTI

MALE:
Latent, asymptomatic
Urethritis
Complication: Prostatitis

Diagnostics and results Trophozoites or cysts in stool Culture

● Gold Standard
● 2-5 days
● Stains: Giemsa, Papinicolau,
Romanowsky, Acridine orange stains
Saline Preparation of Vaginal Fluid
● Quickes, most inexpensive
● Sensitivity: 60-70%

Treatment Metronidazole ● Metronidazole or Tinidazole 2g

Tinidazole single dose
● If failed and reinfection is ruled out..
○ 7 day regimen 500 mg
Metronidazole 3x/day
● If failed…
○ Metronidazole or Tinidazole 2g
daily dose for 5 days
In pregnancy
● Metronidazole
 PROTOZOANS
TRYPANOSOMA
[general description here]

TRYPANOSOMA

Trypanosoma cruzi Trypanosoma brucei Leishmania spp.

General description ★ Etiologic agent of Chagas ★ Human African ★ Leishmaniasis - infection of

disease (S. American Trypanosomiasis (HAT) / diploid protozoa
trypanosomiasis) African sleeping sickness
★ Stercoraria group ★ Trypanosoma brucei
★ Intracellular parasite w/ complex
myocytes ○ T. brucei
★ Cells of reticuloendothelial gambiense (West
system - heavily infected African)
★ Other tissues infected - ○ T. brucei
skin, gonads, intestinal rhodesiense (East
mucosa, placenta African)
○ T. brucei brucei
(cattle)
★ Salivaria Family

Morphology 4 Developmental Stage 2 Developmental Stage ★ Amastigotes - ovoid or

★ Amastigotes - round or ★ Trypomastigote - rounded, 2 to 3 um in
ovoid shape, 1.5 to 4 um in polymorphic (slender, length, live intracellularly in
 diameter; (+) muscular &
nervous tissue and RES
★ Promastigote
★ Trypomastigotes - long,
slender, 16 to 20 um in
length; posterior end is
pointed; C-shaped
(stained), U or S-shaped w/
kinetoplast
★ Epimastigote
IH Human, Reduviid bug
DH RH - domestic animals, armadillos, RH - domestic cattles, primates,
raccoons, rodents, marsupials, ungulates
primates
Infective Stage Metacyclic trypomastigotes
Transmission Arthropod vector:
★ Triatoma, Panstrongylus,
Rhodnius
○ Reduviid bugs
Life cycle Infected triatomine vector→ takes
blood meal & release metacyclic
trypomastigotes in its feces near bite
wound → trypomastigotes enter host
thru wound or conjunctiva → it
invade the cells & differentiate into
amastigotes → binary fission →
differentiates into trypomastigotes
then released in bloodstream → infect
other cells & transform into
amastigotes → infected
trypomastigotes transform into
short, stumpy); flattened
and fusiform in shape, 14
to 33 um in length, 1.5 to
3.5 um in width, centrally
located nucleus w/ large
karyosome, single
flagellum
★ Epimastigote
Human, Tsetse fly
Metacyclic trypomastigotes
Vector:
★ Glossina spp.
○ Tsetse fly
Infected tsetse fly→ takes blood meal
injects metacyclic trypomastigotes in
skin tissue → enter lymphatic system
and pass into blood stream →
transform into blood trypomastigotes
carried thru out the body → binary
fission → tsetse fly gets infected
when taking blood meal on infected
mammalian host → parasite transform
to procyclic trypomastigotes (fly’s
midgut) → binary fission → leave the
midgut → transform into
monocytes, PMNs, or
endothelial cells; has large
nucleus
★ Promastigotes - single free
flagellum (15 to 20 um in
length, 1.5 to 3.5 um in
width)
★ proboscis
Human, Sandfly
Promastigote
Vector:
★ Phlebotomus (Old world),
Lutzomiya (New world)
○ Sandfly
Infected sandfly takes a blood meal →
injects promastigotes into skin →
promastigotes are phagocytosed by
macrophages → transforms into
amastigotes inside macrophages →
multiply in cells → sandfly ingested
infected macrophages when taking
blood meal →ingestion of parasitized
egg → amastigote transform
promastigote in midgut → divide in
midgut and migrate to proboscis
 epimastigotes in vector’s midgut → epimastigotes → it reach the fly’s
parasite multiply and differentiates in salivary gland → binary fission →
the midgut → infective metacyclic transform into metacyclic
trypomastigotes in hindgut trypomastigotes

Signs and symptoms ★ Acute phase ★ Acute phase ★ Cutaneous leishmaniasis

○ Focal or diffuse ○ Local, painful, ★ Diffuse Cutaneous
inflammation in pruritic, Leishmaniasis
myocardium erythematous ★ Mucocutaneous
○ Fever, malaise, chancre at bite site leishmaniasis
nausea, vomiting, ○ Irregular fever, ★ Visceral leishmaniasis
generalized headaches, joint &
lymphadenopathy muscle pain,
○ Romaña’s sign - malaise
eyelid swelling ○ Anemia, MI, DIC,
★ Chronic phase renal insufficiency
○ Fibrotic reactions ○ Posterior cervical
(myocardium, lymph nodes are
cardiac conduction enlarged non-tender,
network, enteric and rubbery
NS) (Winterbottom’s
○ Cardiomegaly, sign) → T.
CHF, gambiense
thromboembolism, ★ Chronic phase
arrhythmia ○ Meningoencephaliti
○ Chest pain, c stage
palpitations, ○ Apathy, behavioral
dizziness, syncopal changes,
episodes, abn. headache, sleep
ECG, achalasia, pattern changes
chronic constipation ○ Convulsions,
tremors, speech
defects, paralysis,
somnolence, coma

Diagnostics and results ★ History ★ CSF, tissue sample, lymph ★ Giemsa & hematoxylin-
 ★ Acute phase ★ Thick and thin blood eosin stains
○ Definitive: Direct smears (Giemsa stain) ★ NNN medium
visualization of ★ Buffy coat concentration ★ Schneider’s medium
parasite in thick and method ★ Montenegro skin test
thin blood smears ★ ELISA, indirect ★ ELISA and rk39 antigen
(Giemsa stain) hemagluttination, indirect dipstick, direct
○ CSF, tissue immunofluorescence and hemagglutination, urine
sample, lymph mini-anion exchange antigen assay, flow
○ Microhematocrit, centrifugation technique, cytometry, PCR, RFLP
blood culture, PCR PCR analysis
★ Chronic Phase ★ CATT
○ ELISA, indirect
hemagluttination,
indirect
immunofluorescenc
e and PCR
NOTE: WHO recommends use of
2 techniques w/ concurrent (+)
result to confirm disease

Treatment ★ Nifurtimox & Benznidazole ★ West early - Pentamidine
★ West CNS - Eflornithine
(Melarsoprol)
★ East early - Suramin
★ East CNS - Melarsoprol
★ Antimony compounds (Sb)
○ Pentavalent
antimonials (Na
stibogluconate, n-
methyl-glucamine)
★ Amphotericin B - if
antimony fails
★ Pentamidine - 2nd line
 PROTOZOANS
CILIATES
[general description here]

CILIATES

Balantidium coli

General description ★ Paramecium coli - initially

★ Causative agent of balantidiasis, balantidiosis, or balantidial
dysentery
★ Largest protozoan affecting human
★ Only ciliate known to cause disease

Morphology ★ Trophozoite - 30 to 150 um long , 25 to 120 um wide

★ Cilia arranged in longitudinal pattern

IH Human

DH RH: Pigs

Infective Stage Cyst form

Transmission Fecal - oral contamination

Life cycle Cyst shed in formed stool → ingestion, excystation occurs in small intestine →
trophozoite reside in large intestine & appendix → binary fission →
encystation to produce infective cyst → some trophozoite invade colon and
multiply causing ulcer → mature cyst are passed in feces

Signs and symptoms 3 forms of clinical manifestation:

★ Asymptomatic carrier
★ Fulminant balantidiasis - bloody diarrhea, mucoid stool,
abdominal pain, N/V
★ Chronic form - diarrhea alt with constipation, abdominal pain or
 cramping, anemia, cachexia

Diagnostics and results Direct examination or concentration techniques

Bronchoalveolar washing

Treatment Tetracycline

PROTOZOANS
SPOROZOA
[general description here]

SPOROZOA

Plasmodium Toxoplasma gondii

General description Plasmodium Falciparum, P. Vivax, P. Ovale,
and P. Malariae
● Group of parasites causing malaria

Morphology Oocyst
● Ovoid, has a thin wall, and measures
10-13um by 9-11um

IH Humans Humans and other mammals

DH Anopheles Mosquito Domestic Cat

Infective Stage Sporozoites Tachyzoite (Trophozoites)

Bradyzoite (Trophozoites)
Oocyst

Transmission Bite of an infected female mosquito Ingestion of Oocyst

belonging to genus Anopheles

Life cycle ASEXUAL CYCLE (Occurs in humans)
● Schizogony (The parasite multiplies by
division or splitting in RBC [erythrocytic],
and Liver cells [Exoerythrocytic]) →
merozoites → gametogony →
gametocytes
SEXUAL CYCLE (Occurs in mosquito)
● Sporogony → Sporozoites
○ Sporogony
Gametocytes that originate from
human RBC but they undergo
maturation and fertilization in the
mosquito → Sporozoites
https://www.cdc.gov/malaria/images/graphs/
Merozoites multiply and differentiate into →
Gametocytes (macro and micro) → undergo
fertilization → Oocyst → Passed out in cat feces →
Can be ingested with contaminated food or water
→ Oocyst sporulate → Sporozoites → upon
reaching the intestine of the new host → excyst
(release of sporozoites) → Sporozoites can then
penetrate the lamina propria of the intestine →
enters the lymphatics → Spread to different tissues
and organs in the body → as sporozoites enter a
new cell → Tachyzoite (fast multiplying) → as host
immunity to the parasite develops → Bradyzoites
(slow multiplying)
https://www.cdc.gov/parasites/toxoplasmosis/
biology.html
 life_cycle/Malaria_LifeCycle_1.gif

Signs and symptoms Prodromal Symptoms ● Asymptomatic as long as the immune

● Feeling of weakness and exhaustion, a system is functioning well
desire to stretch and yawn, aching ● Illness = ↓ immune system
bones, limbs, and back, loss of ● Brain – ring enhancing lesions
appetite, nausea, and vomiting, and a ● Pregnancy
sense of chilling ○ Result in stillbirth/abortion when
At onset infection happens in the first 3
● Malaise, backache, diarrhea, epigastric months
discomfort ○ If pregnancy is successful, the
1. Cold stage (15 - 60 minutes) neonates manifest with
● Sudden inappropriate feeling of intracranial calcification on
coldness and apprehension imaging studies
● Mild shivering → violent teeth chattering
and shaking of the entire body
● May vomit and febrile convulsion
2. Hot Stage (2-6hrs)
● Headache, palpitations, tachypnea,
epigastric discomfort, thirst, nausea,
and vomiting
● May become confused or delirious, skin
is notable flushed and hot
3. Sweating Stage (8-12hrs)
● Defervescence or diaphoresis, profuse
sweating
● Temperature lowers over the next 2-
4hrs
● Symptoms diminish accordingly

Diagnostics and results Microscopic identification of the malarial IgM antibody testing
parasite in thick and thin blood smears Giemsa Staining
● Stains: Giemsa or Wright’s Stain
● Gold Standard
● Falciparum malaria: Only the ring forms
may be found
 ● 10 days after symptoms begin,
gametocytes may be found

Obtaining smears every 6-8hrs (to monitor

treatment response) until malaria is ruled
out

Treatment ANTIMALARIAL DRUGS Sulfadiazine + Pyrimethane

● Protective (prophylactic), curative
(therapeutic), preventive
Casual Prophylactic Drugs
● Prevent the establishment in the Liver
Blood Schizonticidal Drugs
● Attack the parasite in the RBC,
preventing or terminating clinical attack
Tissue Schizonticides
● Act on pre-erythrocytic forms in the
Liver
Sporonticidal Drugs
● Inhibit the development of the oocysts
on the gut wall of the mosquito

DEPENDS ON THE SPECIES

● P. falciparum & P. malariae:
Chloroquine
● P. vivax & P. ovale: Chloroquine +
Primaquine
● P. falciparum w/ no complications
(Chloroquine resistant): Quinine +
Doxycycline/Clindamycin
● P. falciparum (severe): Artesunate +
Doxycycline/Clindamycin; Artesunate +
Mefloquine/Malarone;Artesunate +
Quinidine
 CESTODES
INTESTINAL CESTODES

TAENIASIS

Taenia saginata Taenia solium Taenia asiatica

General description Beef tapeworm Pork tapeworm Closely related to T. Saginata

Intestinal and Tissue Infection
(common tissues affected: brain,
eyes, striated muscles, lung, etc)

IH Cattle (muscle fiber - ova, Human Liver of: pig, cattle, goat, wild boar,
cysticerus bovis) monkey (cysticerus
larva/viscerotropica)

DH Human (jejunum, small intestine - Human

encysted larvae)

Infective Stage Encysted larvae Larvae

Transmission Fecal-Oral

Life cycle Eggs -> Oncospheres -> Cysticerci -> Larva

● Eggs are ingested by animal (animal depends on type of parasite)

● Animal infected with parasite is ingested by human

Signs and symptoms Intestinal Obstruction: weakness, Cerebral Cysticercosis, Ocular

weight loss, loss of appetite Cysticercosis

Diagnostics and results Eggs in stool Eggs and/or proglottids in stool

Treatment Praziquantel, Niclosinamide Praziquantel, Albendazole Praziquantel

(Cerebral Cysticercosis), Surgery
(Ocular Cysticercosis)

CESTODES
OTHER INTESTINAL CESTODES

OTHER INTESTINAL CESTODES

Hymenolepis Diphyllobothrium Sparaganosis Hymenolepis Dipylidium Raillietina

nana latum diminuta caninum garrisoni

General “dwarf tapeworm” “Fish tapeworm” or Diphyllobothrium “Rat tapeworm” Aka “double pored Tapeworm of Rats
description smallest “Broad tapeworm” latum infection tapeworm”
tapeworm infecting with plerocercoid Accidental human Common parasite Common in
 man 2 Types larva infection of dogs and cats. children
1. Diphyllobothri
Found in ileum asis: intestinal Diff from H. nana Common in
infection with Larvae commonly by morphology children
the adult worm found around the and requirement
2. Sparganosis: eyes, of an
tissue infection subcutaneous intermediate host
with the larva and muscular
tissues, inguinal
region, and in the
viscera

Morphology Spherical with the Eggs are yellowish procercoid larva Adult worm is Narrow proglottids Gravid segments
oncosphere, a thin brown with develops in the larger than H. with 2 sets of appear like white
outside & thick moderately thick copepod. nana male and female grains of rice
inner shell and an reproductive organ when passed out
membrane, and inconspicuous Retains the three in feces
with conspicuous operculum hooklets in the Bilateral genital
bipolar thickenings cercomer, pores
Has two bothria or a caudal
only human sucking grooves, attachment organ “Pumpkin seed -
tapeworm which located dorsally shaped” proglottid
can complete its and ventrally
entire life cycle in
a single host

IH -exemption of Humans insects like fleas, Dog and cat flea Flour beetle
intermediate host Fish beetles, or louse (Tribolium
bec it can Copepod cockroaches, meal Human flea (Pulex confusum)
complete its entire moths, and irritans)
life cycle in a earwigs
single host

DH Humans dogs, cats, and Humans and other Rats / Humans Dogs, Rodents, Human
 Accidental - other mammals mammals Cats,Human (accidental)
Arthropods (Humans) (accidental)
(rice/flour beetles)

Infective Stage Adult worm Plerocercoid larva Cysticercoid Cysticercoid

Transmission Direct: ingestion of Ingestion of raw Drinking water Ingestion of Ingestion of Ingestion of
eggs fish with freshwater rats/humans of an infected flea infected insect
Indirect: accidental copepods insect with
ingestion of infected w/ cysticercoid larvae
infected arthropod procercoid larva
(intermediate host)
Eating frogs,
snakes, or rodents
w/ plerocercoid
larva

Applying
plerocercoid
infected flesh of
frogs and
snakes as poultice
in sores

Life cycle

Signs and Allergic reaction Asymptomatic Painful edema Minimal and Slight intestinal Asymptomatic
symptoms Heavy infections: Digestive (due to the nonspecific discomfort,
enteritis disorders, migrating larvae) epigastric pain,
 Abdominal Local indurations pruritus and
discomfort, weight Urticarial allergic reactions
loss, weakness Chills
Pernicious Fever
anemia (Vit B12) High eosinophilia

Diagnostics and Stool exam: Operculated white larvae in the identification of Gravid proglottid Proglottids or ova
results demonstration of eggs/proglottids in lesion eggs in stools recovery (does not in stool
the eggs stool disintegrate in the
Whole worm may intestine)
be expelled -
scolex’
morphology can
be used for
diagnosis

Treatment Praziquantel Praziquantel Praziquantel Praziquantel Praziquantel

CESTODES
EXTRAINTESTINAL CESTODES
Family: Taeniidae; Order: Cyclophyllidea
Human Echinococcosis is regarded as an emerging/ re- emerging zoonotic disease. Disease is caused by the larval stage of the parasite which is
caused when eggs of this parasite are ingested.

EXTRAINTESTINAL CESTODES

Echinococcus granulosus Echinococcus multilocularis

General description ● Small intestines of canines are (+) Alveolar hydatid cyst
inhabited by adult worm
● Eggs are swallowed by suitable IH and Liver is the most common site of infection
hatch in the duodenum
 ● Development is completed when cyst in Cyst wall is not delineated from surrounding
tissues are ingested by carnivores or tissue
omnivores where protoscolices
evaginate and develop into adults

(+) Hydatid cyst

● Contains daughter cysts with brood
capsules -> rupture of brood capsule
releases protoscolices + free capsule =
“Hydatid sand”
● 2 million protoscolices in 1 cyst

Morphology Scolex: prominent rostellum with double row of Adult is similar to E. granulosus
20 to 40 large and small hooklets 1.2 mm-3.7 mm

Segments: 1 immature, 1 elongated mature, 1 Cyst:

long gravid ● thin outer wall; grows and infiltrates into
surrounding tissues
Ova: spherical with a brown radially striated
embryophore ; cannot be differentiated with
Taenia eggs

IH Sheeps, goats, swines Mice and Voles

DH Dogs and other canines Foxes and cats

Infective Stage Embryonated eggs that hatch in the duodenum Embryonated eggs that hatch in the duodenum
and release oncospheres and release oncospheres

Transmission Ingestion of raw plants contaminated with Ingestion of raw plants contaminated with
feces, contacts with dogs feces
Life cycle

Signs and symptoms Affects primarily the liver 66%(inferior right Disease is called “Alveolar hydatidosis”
lobe); presents as hepatomegaly, right Alveolar Cyst, (+) hepatomegaly
epigastric pain and jaundice. Cyst may rupture
from coughing, muscle strain , aspiration and ● Cyst grow very slowly and metastases
operative procedure. occur by direct extension or via blood/
Other involved organs: lungs (22%), lymphatic system
kidneys (3%)
● Rupture of cyst = metastasis and
formation of secondary cyst after 2-8
years with higher mortality rates

Diagnostics and results CLINCAL ● Radiological studies

● Insidious cystic tumor ● ELISA
● Residence in an endemic area
● Close assoc. With dogs

LAB
● Demonstration of protoscolices, brood
 capsules or daughter cyst after surgery
● Hydatid cyst in sputum or urine

Treatment ● Surgery and chemotherapy ● Surgery as the definite treatment

● High dose mebendazole : halts
progression of pathologic process

TREMATODES
BLOOD, LUNG, INTESTINAL, LIVER FLUKES
[general description here]

TREMATODES

BLOOD FLUKES LUNG FLUKES

Schistosoma japonicum Paragonimus westermani

General Oriental Blood Flukes

descripti
on Endemic in the Ph

Adults worms are parasites of the PORTAL VEIN

Morphol Males are smaller than females

ogy

IH Snail 1st: Antemelania sp Snails

2nd: Mountain Crab Sundathelphusa philipina

DH Wide Range Carnivorous Animals, Felines, Canines

- Carabaos, Cows, Pigs, Dogs, Cats, Rodents & Monkeys

Infected by SKIN PENETRATION when in contact with

CERCARIA which leaves the snail (Oncomelania quadrasi)

Infective Mature Cercariae Metacercaria

Stage

Transmis Nocturnal Release by the snails Raw or insufficiently cooked crabs

sion
Skin Penetration

Life Feces → Eggs

cycle

Signs Swimmer’s Itch - Dermatitis w/ Pruritus Hemoptysis

and
symptom 2-12 Weeks after penetration Granulomatous rxn in the lungs → fibrotic encapsulation → Rust
s ● Easy fatiguability colored/ blood-stained sputum (MORNING)
● Respi symptoms
● Arthralgias Chest pain, dyspnea, fever, fatigue, myalgia → MISDIAGNOSIS
● Malaise OF PTB
● Eosinophilia
● Fever Complication: CEREBRAL INVOLVEMNT
 ● Abdominal Pain
● Hepatosplenomegaly

KATAYAMA FEVER or SNAIL FEVER

Migration to pulmonary syste can cause coughing and

wheezing

Patho: Host’s GRANULOMATOUS REACTION TO EGGS

→ Portal hyprtension

Chronic Disease is ASYMPTOMATIC

Complication: HEPATOSPLENIC DISEASE in chronic

Schistosiomiasis
-Splenomegaly
-Portal HTN
-Ascitis
-Development of collateral circulation leading to gastric or
esophageal varices

Diagnost Stool exams are usually (-) unless eggs are deposited in the Radiographs
ics and intestines
results Difficult to differentiate with PTB (+) Bunch of Grapes
Merthiolate-iodine-Formalin : Mod-Heavy Infxn
Definitive Dx: detection of Eggs in sputum, or aspirate
Kato-Katz: Egg counting material from pleural effusions

Circumoval Precipitin Test (COPT) : Definitive Dx in Ph ELISA

-Formation of BLEB or septate precipiates
Loop mediated isothermal amplification (LAMP) → used for
Rectal Snips & Imprints - specialized personnel but very epidemiologic surveys
sensitive; also the most invasive bc of biopsy
 Treatmen Praziquantel Praziquantel
t Tricabendazole
Alternative: Bithionol

TREMATODES
INTESTINAL FLUKES
Fasciolopsis Buski Echinostoma ilocanum Heterophyes heterophyes

General Parasite of the intestine of human and Endemic in Northern Luzon, Leyte, live in the intestines of fish eating
description pigs Samar, and some provinces in Mindanao hosts

No locally acquired infections yet

Morphology

IH 1st:Segmentina or Hippetis snail
2nd: Aquatic plants –caltrop, water
chesnut, morning glory, kangkong and
lotus
1st: Snail Gyralus convexiuculus & snails (freshwater, brackish, marine
Heppitus umbilicalis) species)
2nd: Pila conica (kuhol) & Vivipara
angularis (susong pampang)

DH Pigs and Human Rat is an important reservoir Many fish in PH

Dogs, Cats, Pigs, Human E.g. bangus, balanak, hito, dalag,

danggit, tilapia, kitong

Excyst: duodenum - metacercariae

Attach: intestinal wall- larvae
Inhabit: small intestine - adult worm
Infective Stage Metacercariae

Transmission Ingestion of ENCYSTED Ingestion of Metacercariae encysted Ingestion of Metacercariae encysted

Metacercariae on aquatic plants SNAILS in fish

Life cycle Adults develop in the SI → Eggs in Feces Egg → miracidum → Giraulus → Free ●
→ Hatches and larva enters the snail → cercaria → Metacercaeria → Eaten
Cercariae exits the snail and encyts on plant
→ ingested plant → Adult development in
human

Signs and Inflammation and Ulceration
symptoms
Intestinal obstruction if heavy infections
Intoxication and allergies on the face,
abdominal wall, lower limbs
Inflammation at the site of attachment to the
intestinal wall → ulceration, Diarrhea,
Abdominal pain
GENERAL INTOXICATION: If
metabolites from worms are absorb
inflammation at site where worm is
attached in intestinal mucosa
Colicky pain & mucus diarrhea
Can be deposited in various organs
(heart & brain)

Diagnostics and Detection of eggs in the stool Detection of eggs in stool (+) eggs in stool
results Indistinguishable to that of Fasciola
eggs

Treatment Praziquantel Praziquantel Praziquantel

TREMATODES

LIVER FLUKES
 Clonorchis sinensis & Fasciola hepatica &
Opisthorchis spp Fasciola gigantica

General Parasites of the bile duct and gallbladder Parasites Found In Biliary passages of the Liver Of humans
description of humans and fish-eating mammals. and herbivorous mammals

Morphology

IH 1st IH: operculate snails 1st. IH)Snails ( Lymnaea sp. & F. Gigantica)
2nd IH: Fish (cyprinidae) 2nd IH) Aquatic plants

DH Humans Humans, sheeps, cattle

Infective Stage Metacercaria Metacercariae

Transmission ingestion of metacercaria of the parasite ingesting metacercariae

Edible aquatic plants / drinking water

Life cycle ● eggs in feces ● unembryonated eggs in feces

● ingested by snails
● release of cercariae
● encystation of cercariae to fish
● metacercariae ingested by
human host
● excyst in duodeum
● adults - biliary duct
● embryonated eggs in water
● Miracidia hatch
● penetrate snails
● sporocysts -> rediae -> Cercariae
● Cercariae encysts on water plants
● Metacercariae ingested
● excyst in duodenum
● adults in hepatic biliary ducts

Signs and cholangiocarcinoma Acute & Invasive phase (intestine to liver)

symptoms
Formation of gallstones Traumatic & necrotic lesions (produced when parasites burrow
thru the liver parenchyma)

Triad of Diagnostic Sig.:

● High fever
● Hepatomegaly.
 ● Eosinophilia

Chronic/ latent Phase (bile ducts)

Inflammation -> fibrosis

Heavy infection: liver atrophy & periductal cirrhosis

Diagnostics (+) egg in stool (+) eggs in stool

and results
Clonorchis & opisthorchis can’t be Early diagnosis:
differentiated ● ELISA
● Western blot
Difference:
Morphology & arrangement of testes Hepatic sonography:
● Small clustered hypoechoic lesions
● Nodular lesions

Ultrasound:
● Biliary lesions (oval shaped,, leaflike, no acoustic
shadowing)

Treatment Praziquantel Triclabendazole

Alt: Bithionol