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AMEOBA- unicellular

Trophozoite: non-infectious, motile, feeding stage. Susceptible

to freezing and heat.
cyst: quiscent, resistant, infectious stage. Develops when envi
is not favourable or moisture drops

cyst: spherical. tick walled. Have 1-4 nuclei.

Boiling and drying can kill cyts.

Trophozoite: has
1 nucleus. irregular
Trophozoite causes ameobiasis.
Spread to body parts. For diagnosis,
fresh stool must be examined
immediately or kept at 4oC

movement by pseudopods
enteameoba hiltolytica: human pathogen
enteameoba dispar: commensal
10% of world is infected by E. dispar / histolytica. Majority is by
E. dispar.

Virulent form; E. histolytica: within ingested RBCs are observed.

Causes ameobiasis parasitic dysentery: diarhoea and bloody
3 forms of the disease: carrier/aymptomatic, intestinal,
extraintestinal (hepatic/genitourinary/cerebral/pulmonary)

Pathogenesis: E.histolytica is ingested and gastric acid results in

release of trophozite forms in duodenum. Trophozites attach to
epithelial cells in LARGE INTESTINE, invade mucosa and then

destroy them. They also lyse neutrophils, lymphocytes and

monocytes. This causes tissue destruction, lesions and necrosis.
They can multiply indefinetly within cyrpts feeding on starch
and mucus secretions.
If continue to invade deeper mucosa, E.histolytica enter
bloodstream and cause infections in other organs such as
spleen, liver, lungs, brain and heart.
If asymptomatic, it can continue for weeks and months and it is
self limiting. This type is caused either nonpathogenic dispar or
pathogenic histolytica.
Intestinal ameobiasis is in two forms; acute dysenteric (causes
dysentery) or chronic nondysenteric (self limited, porter state)
Dysentery: colitis is most commonly seen. Abdominal pain and
tenderness, diarhoea with mucus and blood. Ulcer formation is
seen with NO FEVER. Ulceration leads to complications including
peritonitis, hemorrhage, intussuseption, ameoboma (mass
under edemeatous mucosa - can be misdiagnosed with cancer)
Chronic ameobiasis: 40% symptomatic. Abdominal pain,
intermittent diarhoea with mucus and weight loss.

*If soft stools: look for trophozoites.

*If hard stools; look for cyst forms.

Main sources:
1) water and food contamination by CYST from asymptomatic
2) fecal-oral route
3) anal inoculation
4) arthropods


trophozoite/cyst examination of stool under microscope. Stained

with trichrome.
If complications occur, radiology is needed to examine
Examination of aspiration fluid.
serology : stool antigen test by ELISA (against E.histolytica
Molecular : PCR
Treatment: metranidazole followed by idoquinol, paromomycin,

FLAGELLATES : GIARDIA (lamblia/intestinalis/duodunalis) +


Inhabit small intestine (duodenum and jejunum)
Like ameoba; trophozoite and cyst forms. Detected in fecal
specimens of infected people.
Divide by binary fission.
Transmission: contaminated food and water
Causes: water borne infection: diarhoea and malabsorption.
Trophozoites: badmington racket in shape. 2 nuclei. 4 flagellae.
Adhesive disc
Cyst: Oval shaped. 4 nuclei at anterior end. Flagella and
adhesive disc are lost.
Can survive in cold water for several months.

Pathogenesis: When cysts are ingested, gastric acid causes

excystation and release of trophozoites in duodenum and

jejunum. They start multiplying by binary fission. Attach to

intestinal villi. Prevent fat absorption so that deficiency of fat
soluble vitamins (ADEK) occurs.
Abdominal pain, bloating, nausea, vomitting and anorexia.
Causes severe watery and fatty diarhoea without blood, and
(steattorhea: fatty diarhoea)
Giardia do not penetrate the surface
Identification: trophozoite and cysts in feaces. Trophozoites can
be found in fresh stools but they get disintegrate rapidly so
must be stained with trichrome and examined quickly.
Diagnosis: Several samplings are needed since giardia attach to
enterocytes which get slaughed off every 72 hours.
Duodenal biopsies. Antigen detection with ELISA or
immunoflourescence microscopy.

T.vaginalis No cyst forms.
Pathogenesis: Inhabit genitourinary tract and multpily by binary
fission. Causes degeneration and desquamation of local tissue.
Only form Trophozite is sensitive to and cannot survive in
external environmental conditions.
Only known HOST: HUMANS
Transmsion : Sexual and direct contact with contaminated
urine. Can live in moist clothes for 1 day and so sharing clothes
causes transmission.
Males are asymptomatic but are MAIN VECTORS. May cause
mild uretritis and prostatis.

Females are more commonly affected. Experience itching,

yellow-green creamy vaginal discharge with strong odor. Causes
discormfort during sexual intercourse and urination
Diagnosis: From vaginal and urethral
discharge in females and from
urethral and prostatic secretions in
males. With wet mounts, actively
motile trophozites can be seen. It
can be detected with/without stain
under microscope. Culturing is the
most sensitive method but takes time.
BALANTIDIUM only CILLIATE that infect humans.
Have cyst and trophozoite forms (like ameoba, giardia but
unlike trichomonas)
Largest protozoa. Have cillia all around the surface. Have
cytostome, 1 kidney-shaped nucleus and micronucleus.
Zoonotic but infect humans.
Resorvoir: PIGS, primates, humans
Pathogenesis: Pig borne cysts contaminate water/food. Upon
ingestion, excystation takes place in small intestine. COLONIZE
IN LARGE INTESTINE (like ameoba). Replicate by binary fission
and undergo excstation to produce
infectious cyst forms. Affect illium,
colon and rectum.
Causes a disease indistinguishable
from dysentery; persistent diarhoea
with blood, abdominal pain, weight
loss, ulcers in submucosa. Main
complication is perforation.

Diagnosis: Stools must be examined

immediately since once its outside, they
get destroyed. Trophozoites can be seen in
tissue biopsy/endoscopy.

1) Crytosporidium
2) Isospora
3) Cyclospora
4) Microsporidia

Causes waterborne and food borne diseases
2 oocyst forms:
1) thick walled: resistant to environmental conditions.
Excreted from the host. Does not suspend in water and
moves to everywhere. Has no surface tension.
2) Thin walled: causes autoinfection and infect other parts of
*Oocyts are very resistant to environmental stressors and
chemical disinfectants. Can cause comtamination and infection

Tranmission: fecal-oral route. Waterborne, foodborne,

arthroponotic, zoonotic.
Pathogenesis: Invade microvilli borders of GI tract in
During defecation, 4 nuclei oocysts are excreted. Transmission
occurs via contamination of water so many outbreaks occur in
swimming pools, water parks and day care centres. Zoonotic
and arthroponotic transmission occur upon exposure to infected
Symptoms: watery diarhoea, dehydration, weight loss,
abdominal pain, vomitting, nausea, FEVER
In immunecompetent people, duration is 1-2 weeks. But in
immunocompromised people, infection becomes chronic and
life cycles of the protozoa can be seen in gall bladder, plancreas
and liver.
Diagnosis: acid fast stained stool under microscope.
Immunoflourescence and enzyme immunoassays. PCR.
Treatment: spiramycin, paromycin. rehydration.

Unlike cyrptosporidium, does not infect immediately. Needs
Transmission: Sporulated oocytes are ingested in contaminated
food and water. Affect SMALL INTESTINE
Symptoms: watery diarhoea and steatorrhea (like giardia),
abdominal pain, weight loss, malaise, villus athropy.
Diagnosis: stool or biopsy examination. They are
autoflourescence - modified acid resistant staining.


Oocyts are not infective for 28-72 hours.

Tranmission: ingestion of contaminated water or food with
sporocysts that contain oocyts
Have sexual and asexual
reproduction cycles in epithelial
Symptoms: watery diarhoea,
abdominal pain, weight loss,
malabsorption, eosinophilia.
*In AIDS patients, cause serious
Extraintestinally can pass to lymph nodes and gall blader.
Diagnosis: stool and bisopsy examination. They are
autoflourescence. Modified acido resistant staining.

Causes severe infections in AIDS and immunocompromised
Transmission: by small spores.
Penetrates host cells and can be find in any viscera.
Symptoms: severe diarhoea
Diagnosis: special staining under electromiscroscopy

Vector: anopheles mosquito
4 main types: falciparum, vivax, maleriae, ovale
Generally they are found in tropical, subtropical and temperate
regions of the world.
Falciparum: tropical and subtropical regions. The most
dangerous. More common worldwide
Maleriae: subtrpical and tropical regions
Ovale: Africa, more prevalent than vivax.
Vivax: the most prevalent of human plasmodia. widest
geographical distribution including tropical, subtropical and
temperate regions. cyprus

Definitve host: Anopheles mosquito sexual reproduction

Intermediate host: humans/animals asexual reproduction

Life cyle: mosquitos have sporozoites in their saliva and when

they bite humans late at night and early in morning, they
transfer the sporozoites into human. Sporozoites migrate to
liver first hepatic stage. They reproduce and merozoites enter
into blood stream to infect RBCs. Within RBCs, they digest
hemoglobin. They reproduce and lyse RBCs to release more of
themselves erytrocytic stage. Every species take different
forms in RBCS used to diagnose and identify. In blood, some
merozoites become gametocytes. These gametocytes are
transferred to mosquito when they take a blood meal from
infected humans.
***Vivax and ovale can remain in the liver and produce dormant
HYPNOZOITES which do not divide and are responsible relapses
of the infection.
***Tranfussion maleria is the infection in which sporozoites
direclt enter into bloodstream before liver.

P. falciparum is the most dangerous since it can infect RBCs at

any shape, size, type and age. Infected RBCs have spikes on
them. They stick to each other and walls of endohelium of blood
vessels. Occlusions occur leading to organ failure. Causes
cerebral maleria and massive intravascular hemolysis.
Falciparum infections are fatal!



Symtoms: 9-14
incubation period for vivax,
and falciparum.


characteristic febile paroxysim. Chills, fever and sweating.

For falciparum, ovale and vivax, 48
hour periocity of paroxysim
For maleriea, it is 72 hours
Common symptoms are;
1) fever,
2) malaise,
3) headache,
4) rigors,
5) muscle pain,
6) anorexia
7) anemia
8) hepatosplenomegaly
*Can be misdiagnosed with a viral infection or typhoid fever.
LAB: giemsa stained blood samples
treatment: chloroquine for intraerythrotic phase.
primaquine for hypnozoites

Zoonotic infection: affects cows, sheeps etc.
Thick borne.
Fatal in splenectomized spleen.
No sucessful treatment
Can be misdiagnosed with maleria.

Vector: female sandfyl PHLEBOTOMUS
Zoonotic infection but affects humans.
2 types
1) old world: visceral and cutaenous
2) new world: visceral, cutaneous and mucocutaneous

Life cycle: When phelebotomus bites humans, promastigotes

are transferred. Promastigotes enter macrophages and
reproduce to form amastigotes which invade macrophages and
hide there. When macrophages die, amastigotes are released.
When infected humans are bitten by phelebotomus,
amastigotes are transferred to them. Amastigotes reproduce in
phelebotomus and form

Visceral leishmaniasis Zoonotic KALA AZAR

*DOGS are main resorvoir.

Affects children and malnurished people.

Causes hepatosplenomegaly and irregularly reoccuring fever
(difference from malaeria). Anorexia, weight loss, malaise,
diarhoea and abdominal pain are seen.
Involves bone marrow and lymph nodes.
*Darkening of the skin
If not treated fatal!
Can be seen cyprus.

Cutaneous leishmaniasis
Lesions are found at the site infection. Starts with erythamatous
painless itchy papules. Then lesions enlarge and ulcerates
ulcers resemble to volcano with crusted margins and necrotic
base. Sample must be taken from the margins.
Self limited
If not treated, scars are formed.

Mucocutaneous leishmaniasis
Affects mucocutaenous junctions in pharynx and then
disseminate to nose, palate and mouth. Some spread
throughout the skin leading to disseminated cutaneous

LAB: Giemsa stained samples

In cutaneous leishmaniasis, samples must be taken from

margins of ulcerated leasion
In visceral leishmaniasis, liver and spleen biopsies are best but
since they are fragile and can rupture, bone marrow biopsy is
Amastigotes in
Cryotherapy for CL

2 types:
1) African : sleeping sickness
2) American : chagas disease
African trypanosomiasis sleeping sickness
Vector: Tse tse fly
Resorvoir: antilopes and pigs - Zoonotic
2 forms:
*Epimastigotes are in tse tse fly.
*Trypomastigotes are formed in human bloodstream, CNS and
lymph nodes.

3 phases;
1) 1st phase: tsetse fly bites from upper site of the body, next
to head. Chancre, fever, headache, joint pain and itching.
2) 2nd phase: BBB is broken reaches brain tissue and
infects CNS. day time sleeping, confussion, sensory
disturbances, poor coordination and coma
3) 3rd phase: coma
escape immune system.

American trypanosomiasis
Vector : triatomine bug / kissing bug
Triatomine bug takes a blood meal and defacates
trypomastigotes. Chagoma, a local lesion, appears at the site of
inoculation. Organism enters the body by scratching the wound
or through intact skin such as conjuctiva. They transform into
amastigotes in CNS, lymph nodes and bloodstream. Acute
phase is asymptomatic but fever, anorexia,
hepatosplenomagaly and lymphadenopathy can be observed.
When amastigotes reach heart and invade cardiac tissues,
myocarditis occurs. Then disease progresses to chronic
symptomatic stage in which heart enlarges, cannot function
properly and cardiomyopathy occurs.
Transmission: by triatomine bugs, blood transfussion, organ
transplantation, transplacentally or lab accidents.

LAB: Giemsa staining of fresh

anticoaglulated blood for motile
parasites or thick/thin blood smears
for visualization of parasites

Zoonotic disease
Main resorvoir and definitve host: cats (sexual reproduction
takes place in intestine)
intermediate host: humans and wild animals
1) cat feaces contaning oocyst
2) ingestion of contaminated raw meat/egg which contain
tissue cysts..
3) Outbreaks occur when humans inhale contaminated dust
or food/water
4) blood/organ transfussion
5) lab accidents
Infective stage occurs when contaminated food/water remains
at least for 2 days for maturation of oocytes.
Oocytes or trophozoites / TACHOZOITES infect nucleated cells
intracellular pathogens. During acute infection, proliferation of
tachozoites kills the cell and results in tissue damage.
Very damgerous for babies since the organisms can pass
transplacentally. If infected in 1st trimester, abortion occurs. If
infected before the pregnancy, it is not a problem since
antibodies against toxoplasma are already produced.
2 types of toxoplasmosis;

1) congenital: when mother gets infected during gestation.

Results in sequela or stillbirth. If infection is acquired in
first half, intrauterine death, microcephaly or hydrocephaly
with intracranial calcification occur. If infection is in the
second half, it could be asymptomatic or may present
hepatosplenomegaly, fever and jaundice. Blindness,
psychomotor retardation and convulsive disorders are
seen in the baby months/yeasr later. Ocular toxoplasmosis
occurs in both eyes years later.
2) Postnatal toxoplasmosis: in immunocompetent people, flu
like symptoms; fever and ymphoadenopathy can be seen.
self healing. However, in immunocompromised people,
CNS is involved. Myocarditis, retinitis, orchitis and
pancreatitis can be seen. Occurs either from reactivation
of latent infection or from primary infection. ocular
toxoplasmosis occurs only in one eye yearslater.

LAB: Giemsa/H&E stained tissue, blood or body fluids. For

culturing, tissue culture or uninfected mice can be used.
Serology is the primary approach. With PCR, intrauterine,
disseminated and encepeolapathy toxoplasmosis can be
Treatment: drugs not effective against tissue cysts.
for pregnancy. Transplacental damagess cannor be reversed.
1) do not eat uncooked meal, raw eggs, raw milk
2) cook meat at 66oC and freeze in -20oC
3) wash vegetables
4) do not touch cat feaces