PARASITIC INFECTIONS

IN GASTROINTESTINAL
TRACT
Taniawati Supali
Department of Parasitology
Faculty of Medicine
University of Indonesia

Intestinal protozoa found in the gastrointestinal tract

Intestinal helminths found in the gastrointestinal tract

Mature egg

Adult worms

Ascaris lumbricoides
(roundworm)
Disease: Ascariasis

Epidemiology
z
z

Affecting about 1.3 billion people.

Distribution:
Asia, Africa, and Latin America.
Occurring in slum & shanty towns (poor socioeconomic conditions)
Most severe consequences of infection occur in
children who usually suffer from heavier worm
burdens than adults living under similar conditions.

Pathogenesis
z

Antigen released during molting process cause

inflammation associated with eosinophilic infiltration of
the tissues, peripheral eosinophilia, & an increase IgE
levels.

Heavy infections may lead to the formation of a large

bolus of adult worms that obstructs the lumen.

Adult worms secrete an anti-trypsin factor that

enables it to ingest a portion of any meal before its
absorbed.

Life cycle
Infection occurs when host ingests the
mature eggs. The eggs hatch in the small
intestine of host.
The immature parasite penetrates the
intestinal wall, enters the lamina propria,
penetrates a capillary, and is carried by
the portal circulation to the liver.
It then migrates via the blood stream to
the heart and into the pulmonary
circulation. The larva migrates up the
bronchi into the trachea and across the
epiglottis.
It is swallowed, finally reaching the lumen
of the small intestine again, then molts to
be adult worm.

Clinical Symptoms
z

Symptoms due to adult worms:

Diarrhea
Intestinal obstruction due to numerous of adult
worms

The worms can perforate the intestine and migrate

to the appendix or bile duct (ectopic infection)

Diagnosis:

Stool examination for eggs.

Recovery of adult or juvenile worms in stool
or vomit from infected human.

Egg

Treatment:

Albendazole
Mebendazole
Pyrantel pamoat
Piperazine citrate - used for intestinal
obstruction because it paralyzes the
worms

Ancylostoma duodenale

Hookworms

Necator americanus

Epidemiology
z

The distribution of those worms are not

overlapping but both species can be found in the
same regions in Africa, South America, and Asia.

It is estimated that 2150 million persons are iron

deficient and about half of them suffer from iron
deficiency anemia.

Route of infection
z
z

Necator americanus: percutaneous

Ancylostoma duodenale: percutaneous
and oral
larvae infect orally may
undergo two molts to adulthood without
leaving the gastrointestinal tract.

Life cycle
The filariform larvae penetrate the
cutaneous tissues, usually through a hair
follicle. Then the larvae enter capillaries
and are carried passively through the
bloodstream to the capillaries of the lungs.
The 3th stage larvae break out of the
alveolus capillaries and then crawl up the
bronchi and trachea, over the epiglottis,
and into the pharynx.
They are then swallowed, and proceed into
the stomach. Two molts take place in the
small intestine resulting in the
development of adult worms.

Pathogenesis
z

The adult worms move several times a day to different

attachment sites in the intestinal mucosa.

The worms eat villous tissue and also suck blood

directly from their site of attachment to the intestinal
mucosa and submucosa.

The worms secrete an anticoagulant that blocks the

action of host factor Xa and VII a/tissue factors. Blood
loss continues after the worms move to a new location.

Pathogenesis
z

The combination of constant blood loss due to

hookworm infection and poor iron intake in the
diet results in iron deficiency anaemia.

The severity of iron-deficiency anemia depends

upon the species of hookworms in the intestine
(A. duodenale ingests 4-5 times more blood
each day than N. americanus)

Clinical symptoms
Head of A. duodenale

Head of N. americanus

Rarely itch at skin entry site of larvae

Most infections are asymptomatic
Minor abdominal pain
Iron deficiency anemia
pregnant women,

z
z

menorrhagia women, children

Malnutrition

In a child, the continued daily loss of 10ml of blood can lead to

severe anaemia.
Heavy hookworm infection results in chronic haemorrhage from
the intestinal mucosa.

Diagnosis:

Finding eggs in stool by

microscopic examination.

Treatment:
-

Albendazole
Mebendazole

Adult worm

Egg

Trichuris trichiura
(Whipworm)
Disease: Trichuriasis

Epidemiology
It has a worldwide distribution.
The prevalence is estimated to be over 1 billion.
It is coincident with infections caused by Ascaris
lumbricoides and hookworms.
The whipworm is especially prevalent in areas of high
rainfall and high humidity.
It is a fecal oral transmission

Life cycle
The first stage of larva hatches in
the small intestine, penetrates
the columnar epithelium, and lie
just above the lamina propia.
The immature adult emerges and
is passively carried to the large
intestine, where it re-embeds itself
in the columnar cells and induces
its essential niche.
Adult worms live in the transverse
and descending colon.

Pathogenesis
z

Adult worms in the large intestine induces structural

defects in the epithelium.

To invade the colonic mucosa, the adult worm

releases protein which induces pores.

It may facilitate invasion and enable the parasite to

maintain its syncytial environment in the caecal
epithelium.

Diagnosis
z

Finding eggs by microscopic

examination.

Clinical symptoms

Most cases are asymptomatic

In heavily infected patients, the symptoms include:

Dysentery ( diarrhea containing blood and mucus)

Tenesmus which can lead to rectal prolapse
Abdominal pain

Treatment

Albendazole
Mebendazole

Prevention
Proper disposal of feces

Egg

Adult worm

Oxyuris vermicularis
(Pinworm)
Disease: trichuriasis

Epidemiology
z
z

It affects children < 12 years old

The transmission of enterobiasis is
especially frequent in elementary school
and daycare center.

Life cycle
The embryonated eggs are swallowed
& hatch into the 2nd stage larvae once
they reach the small intestine.
Development to the 3th & 4th stages
also occurs here.
The adult worms take up residence in
the large intestine.
Eggs can hatch on the skin at the site
of deposition, and the 2nd stage larvae
can crawl back through the anus into
the rectum, and the colon where they
develop into reproducing adults
Retro infection

Clinical symptoms
z

Most of infected individuals are asymptomatic.

Common symptoms found in children are loss of
appetite, insomnia and restlessness.

The most common symptom is itching in the

perianal region due to worms migrating to the area
around the rectum to lay their eggs.

Ectopic enterobiases have been described at the

vagina and the genital area.

Diagnosis

Finding eggs by microscopic

examination of a sticky tape

Anal swab

Treatment

Albendazole
Mebendazole
Pyrantel pamoat.

Prevention

Finger nail cleaning

Stop finger nail chewing
Wash bed sheet & cloths

Strongyloides stercoralis
Disease: Strongyloidiasis

Epidemiology
It is distributed in tropical
and subtropical countries
Fecal oral transmission

Life cycle
Free-living cycle: The rhabditiform larvae passed in
the stool becoming infective filariform larvae or free
living adult males & females that mate & produce
eggs from which rhabditiform larvae hatch. The
filariform larvae penetrate the human host skin to
initiate the parasitic cycle.
Parasitic cycle: Filariform larvae in soil penetrate
the human skin, & are transported to the lungs
where they penetrate the alveolar spaces; are
carried through the bronchial tree to the pharynx, are
swallowed & then reach the small intestine. In the
small intestine they molt twice and become adult
female worms. The females live threaded in the
epithelium of the small intestine and by
parthenogenesis produce eggs, which yield
rhabditiform larvae.
The rhabditiform larvae can either be passed in the
stool (Free-living cycle), or can cause
autoinfection. In autoinfection, the larvae become
infective filariform larvae, which can penetrate either
the intestinal mucosa (internal autoinfection) or the
skin of the perianal area (external autoinfection).

Pathogenesis
z

Most of the pathology is associated with

larval stages that moved through the
tissue.

Clinical symptoms
Cross-sections of female S. stercoralis
(blue arrows) in small intestine tissue

Itchy at the skin entry site of the infective larvae.

Most infections are asymptomatic.
Acute strongyloidiasis is characterized by a

marked IgE & blood eosinophil response with

the symptoms: abdominal pain, diarrhea.
In hyperinfection (Chronic form), the symptoms
are severe & bloody diarrhea.

Diagnosis

Stool culture for larvae

Serology test (ELISA)
z

Treatment

Albendazole
Ivermectin not registered for
human use in Indonesia

Larva

Adult worm

Proglotide

Egg

Taenia sp
(Tapeworm)
Disease: taeniasis

Taenia sp
z

There are two species infecting human:

Taenia saginata

Taenia solium (pork tape worm)

Epidemiology: cosmopolitan

Taenia sp
z

Taenia solium has a complex two host life cycle.

Human is the only definitive host and habour the adult
worm, whereas both people and pigs can act an
intermediate hosts and harbour the larvae or cysticerci.

For Taenia saginata, human is the only definitive host

and animals (cow, buffalo) are the intermediate hosts.

Infective stage for human:

T. saginata : bovine cysticercus
T. solium : pig cysticercus (cysticercus cellulosae)

Life cycle
Eggs or gravid proglottids are passed with
feces.
Cattle (T. saginata) and pigs (T. solium)
become infected by ingesting vegetation
contaminated with eggs or gravid
proglottids . In the animal's intestine, the
oncospheres hatch , invade the intestinal
wall, and migrate to the striated muscles,
where they develop into cysticerci.
Humans become infected by ingesting raw
or undercooked infected meat . In the
human intestine, the cysticercus develops
over 2 months into an adult tapeworm
which attach to the small intestine by their
scolex and reside in the small intestine.
The adults produce proglottids which
mature, become gravid, detach from the
tapeworm, and migrate to the anus or are
passed in the stool

Pathogenesis
Scolex of T. saginata with 4 large suckers

Scolex of T. solium with 4 large suckers &

rostellum containing 2 rows of hooks

The worm which is flexible and fragile live in a

large part of the lumen of the small intestine
therefore the bowel obstruction does not occur.

The worm attaches strongly to the mucosa of

the upper small intestine by means of its
suckers and hooks.

The adult causes only mild inflammation at the

implantation site, without substantial damage
to the intestine.

Clinical symptoms
z
z

z
z

Most taeniasis are asymptomatic.

Infected people become aware of
infection until discovering the proglotids
in stool.
Rarely nausea, vomiting, abdominal pain.
Unpleasant sensation due to active
moving proglottids discharge from anus.

Head of Taenia sp

Proglottide

Taenia solium taeniasis is less frequently

symptomatic than Taenia saginata
taeniasis.

Adult worm

Cercaria

Schistosoma japonicum
(blood fluke)
Disease: schistosomiasis

Diagnosis
z

Stool microscopy for eggs but can

not be used to differentiate between
T. saginata & T. solium.
Proglottid in feces used to
differentiate between T. saginata &
T. solium

Egg

z Treatment

Praziquantel

Proglottid

Epidemiology
z

Distribution: China, Japan, Taiwan, The Philippines,

Vietnam, Malaysia, Indonesia.

Indonesia:

It is found only in Central of Sulawesi (Lindu lake and

Napu valley)
limited by the distribution of
their snail intermediate host - Oncomelania hupensis
lindoensis (keong air)

Life cycle
Eggs hatch & release miracidia ,
which swim and penetrate specific
snail intermediate hosts.
The stages in the snail include 2
generations of sporocysts & the
production of cercariae .
Upon release from the snail, the
infective cercariae swim, penetrate
the skin of the human host becoming
schistosomulae which migrate
through several tissues and stages to
their residence in the veins. Adult
worms in humans reside in the
superior mesenteric veins of the
small intestine. The eggs are moved
progressively toward the lumen of the
intestine.

Pathogenesis
z

Adult worms living in the venous circulation

usually do not cause significant pathological
damage.

The attached bacteria on the surface of adult

worms can result in the introduction of enteric
bacteria in the blood stream
enteric
fever from non-thypoidal salmonellosis.

Pathogenesis
z

Deposition of eggs in the intestine and liver

result in intestinal and hepatic fibrosis
due
to granuloma formation around eggs.

Eggs secrete proteolytic enzymes which cause

erosion of the submucosa and villous tissue.

In heavy infection, gastrointestinal hemorrhage

results from damage to the submucosa.

Clinical symptoms
z

Acute manifestation commonly occur in

new immigrants frequently febrile and flulike symptoms.

Chronic manifestation:
Intestinal & hepatic dysfunction
Abdominal pain
Bloody diarrhea

Diagnosis:
Egg

Finding eggs by microscopic examination of stool

Serological test

Treatment:

Praziquantel administered in an oral form in one or two

doses from 40-60 mg/kg body weight

Control:

Sanitary disposal of sewage and destruction of snails

Adult worm

Egg

Fasciolopsis buski
(Intestinal fluke)
Disease: Fasciolopsiasis

Epidemiology
z

Distribution:

China, Vietnam, Thailand, India, Indonesia

z

Indonesia:

Kalimantan Selatan

Life cycle
Unembryonated eggs pass in feces
becoming embryonated in water &
release miracidia , which invade a
suitable snail intermediate host.
In the snail the parasites undergo
several developmental stages
(sporocysts, rediae, & cercariae ). The
cercariae are released from the snail
and encyst as metacercariae on
aquatic plants .
The mammalian hosts become
infected by ingesting metacercariae on
the aquatic plants. After ingestion, the
metacercariae excyst in the duodenum
and attach to the intestinal wall.

Pathogenesis
z
z

The worms attach the luminal surface.

They feed on columnar epithelial cells and
injure cells.

Clinical symptoms
z

Light infection does not cause any

clinical disease (asymptomatic)
Heavy infection causes continuous
diarrhea, abdominal pain, intestinal
hemorrhage

Diagnosis
z

Finding eggs by microscopic

examination of stool.

Treatment

Praziquantel

Egg

Trophozoite

Entamoeba histolytica
(Subphylum: sarcodina)

Disease : Amoebiasis

Morphology

Epidemiology
z
z

The infection is distributed world wide.

The higher rates of infection is in
underdeveloped countries.
Infection is associated with poor hygiene.
Humans are the principal host, although
dogs, cats and rodents may be infected.

Infection occurs by ingestion of mature

cysts in fecally contaminated food, water,
or hands. Excystation occurs in the small
intestine & trophozoites are released,
which migrate to the large intestine.
The trophozoites multiply by binary fission
& produce cysts. Both stages are passed
in the feces. Because of the protection
conferred by their walls, the cysts can
survive in the external environment & are
responsible for transmission. Trophozoites
passed in the stool are rapidly destroyed
once outside the body.
In some patients the trophozoites invade
the intestinal mucosa (intestinal disease),
or, through the bloodstream, extraintestinal
sites such as the liver, brain, and lungs (
extraintestinal disease), with resultant
pathologic manifestations.
Cysts & trophozoites are passed in feces. Cysts
are typically found in formed stool, whereas
trophozoites are typically found in diarrheal
stool.

Life cycle

Pathogenesis
z

Trophozoites penetrate the perimucosal space

and attach to epithelial cells using lectincarbohydrate interactions.
Amebapore (a channelforming protein)
Cysteine proteinases (tissue invasion)

Causing lysis of cells, then parasites grow and

divide by binary fusion
develop flaskshaped ulcer .

Amoebiasis
z

Clinical disease:

Intestinal amoebiasis
Extra-intestinal amoebiasis
Parasite erode the wall of the large intestine, enter
the blood circulation of the submucosa
The parasites spread to extra-intestinal through portal
system (liver, brain) or percontinuitatum (lung, rectum).

Amoebiasis
Clinical symptoms:
1. Most of the infected individuals are
asymptomatic and some of them go on
becoming carrier.
2. Symptomatic amoebiasis consists of
acute amoebic dysentry, amoebic liver
abscess and amoeboma.

Amoebic dysentry
z

Clinical symptoms
Bloody, mucous diarrhea
Fever
Abdominal pain

Diagnosis
Finding amoebic (hematophagous trophozoites) in stool

Detecting parasite by PCR or antigen capture from stool

sample.

AMOEBIC LIVER ABSCESS

z

Clinical symptoms:

persisting fever
epigastric pain
rarely diarrhea
z

Diagnosis
1. serology
2. aspirate microscopy to find trophozoites

Treatment
z

Tissue:

Metronidazole
Chloroquine
Emetin hidrochloride
z

Bowel lumen:

Paromomycin
Diloxanidefuroate

Cyst

Trophozoite

Giardia lamblia
(Subphylum mastigophora)

Disease: Giardiasis

Epidemiology
z
z
z

Fecal oral transmission

increased in travellers, backpackers.
found in most mammals (beaver,cattle,
cats, dogs,etc) -- Zoonotic

Life cycle
Infection occurs by the ingestion of
cysts in contaminated water, food, or by
the fecal-oral route (hands or fomites).
In the small intestine, excystation
releases trophozoites (each cyst
produces two trophozoites).
Trophozoites multiply by longitudinal
binary fission, remaining in the lumen of
the proximal small bowel where they
can be free or attached to the mucosa
by a ventral sucking disk . Encystation
occurs as the parasites transit toward
the colon.
The cyst is the stage found most
commonly in nondiarrheal feces.
Because the cysts are infectious when
passed in the stool or shortly afterward,
person-to-person transmission is
possible.

Pathogenesis
z

Covering of the intestinal epithelium by

the trophozoites and flattening of the
mucosal surface results in malabsorption
of nutrients.

trophozoite

Symptoms
z

Early symptoms include flatulence, abdominal

distension, nausea and foul-smelling bulky, often
watery, diarrhea.
The stool contains excessive lipids but very rarely
any blood or necrotic tissue.
The chronic stage is associated with vitamin B12
malabsorption, disaccharidase deficiency and
lactose intolerance.

Diagnosis
z

Finding either cysts or trophozoites in

fresh stool by microscopic examination.

ELISA test to detect G.lamblia antigen.

Treatment
z
z

Metronidazole
Tinidazole

Vegetative

Cyst

Balantidium coli
(ciliate protozoa)
Disease : Balantidiosis

Life cycle
Infection occurs when host ingests cysts
(parasite stage responsible for
transmission of balantidiasis) from
contaminated food or water. Following
ingestion, excystation occurs in the small
intestine, & the trophozoites colonize the
large intestine. The trophozoites reside
in the lumen of the large intestine of
humans and animals, where they
replicate by binary fission, during which
conjugation may occur. Trophozoites
undergo encystation to produce infective
cysts. Some trophozoites invade the
wall of the colon and multiply. Some
return to the lumen & disintegrated.
Mature cysts are passed with feces

Habitat
z
z

mucosa layer of large intestine (cecum)

lumen of large intestine

Pathogenesis
z

Balantidium coli usually resides in the lumen

of its host, trophozoites can invade the
mucosa of the large intestine (cecum and
colon) and cause ulcerations.
The parasite secretes a substance called
hyaluronidase enzyme, which helps degrade
intestinal tissue and facilitates penetration of
the mucosa.

Clinical symptoms
z
z

Asymptomatic
Symptomatic:
Chronic diarrhea, occasional dysentery
(diarrhea with blood or mucus), nausea,
colitis (inflammation of the colon),
abdominal pain, weight loss, deep
intestinal ulcerations, and possibly
perforation of the intestine (peritonitis)

Diagnosis
z

Finding either cysts in formed stool or

trophozoites in watery stool by microscopic
examination

Treatment
z

Tetracycline

Vacuolar form

Blastocystis hominis
Disease: blastocystosis

Blastocystis hominis

The epidemiology of B. hominis

remains almost totally unkonwn
because the status of the organism
z is still unclear.
z

B.hominis is a pathogenic or nonpathogenic organism ?

Life cycle is still unclear yet

Transmission: fecal-oral route through ingestion of contaminated water or food

Blastocystis hominis
z

B. hominis exists in 4 forms (vacuolar, granular, ameboid,

cyst)

B. hominis can be considered as the agent of infection

after all organisms causing diarrhea are negative in the
stool examination.

It should be > 5 parasites/LPF (large per field) in

microscopic examination.

Clinical Symptoms
z
z

Asymptomatic (commensal parasite)

Symptomatic :

Watery diarrhea
Abdominal pain
Perianal pruritis (itch)
Excessive flatulence

Treatment
z

The disease is self-limiting and therefore

should not be treated. However, upon
diagnosis with the disease, patients are
usually treated with Metronidazole,
which has been effective.

Cryptosporidium parvum
(Phylum apicomplexa)
Disease: cryptosporidiosis

Epidemiology
z

Infection can occur from animal reservoirs

sheep, cattle, birds) to human
Zoonotic.

Transmission occurs mainly through contact

with contaminated water

Life cycle
Infection begins when the host ingests
sporulated oocysts containing four sporozoites.
The sporozoites excyst when the oocyst
reaches the small intestine. Sporozoites
parasitize epithelial cells of the gastrointestinal
tract. In these cells, the parasites undergo
asexual multiplication (schizogony or
merogony) and then sexual multiplication
(gametogony) producing microgamonts (male)
and macrogamonts (female). Upon fertilization
of the macrogamonts by the microgametes,
oocysts, develop that sporulate in the infected
host. Two different types of oocysts are
produced, the thick-walled, which is commonly
excreted from the host , and the thin-walled
oocyst , which is primarily involved in
autoinfection. Oocysts are infective upon
excretion, thus permitting direct and immediate
fecal-oral transmission.

Pathogenesis
z

Diarrhea associated with Cryptosporidium appears to be

primarily osmotic in nature. Associated with this disruption of
enterocyte (i.e. intestinal epithelial cells) function is a blunting of
the villi and crypt cell hyperplasia.
A possible mechanism of pathogenesis is that the infection of
intestinal epithelial cells with Cryptosporidium damages the
enterocytes and eventually leads to their death.
This triggers cell division in the crypt region (i.e., hyperplasia) to
replace the damaged cells. The combination of destruction of
absorbtive cells at the tips of the villi and the increase in the Cl-secreting crypt leads to an overall enhanced secretion.

Clinical symptoms
z

In immunocompetent patients:

In immunocompromised patients:

Self limiting disease

In acute stage: abdominal pain, nausea, vomiting,
transient episode of diarrhea.

Diarrhea (chronic- lasting months & even years)

Cholecystitis extraintestinal infection in bile duct

Diagnosis
z

Finding oocysts in stool by microscopic

examination/ serological test/ PCR

Treatment
z

Nitazoxanide

The effectiveness of nitazoxanide in

immunosuppressed persons is unclear. For
persons with AIDS, anti-retroviral therapy,
which improves immune status, will also
reduce oocyst excretion and decrease diarrhea
associated with cryptosporidiosis.

Cyst

Cyclospora cayetanensis
(Phylum apicomplexa)
Disease: cyclosporiasis

Epidemiology
z

The epidemiology of Cyclosporiasis is still unclear.

Cyclosporiasis has been reported in many countries, in tropical
and subtropical areas.

The unsporulated oocysts passed in the stool are not infectve

stage of C. cayetanensis
Fecal-oral transmission can
not occur

An infective stage is a sporulated oocyst.

Contamination of food and water can serve as vehicles for
transmission. However, the potential mechanisms of
contamination of food and water are still unclear.

Life cycle
Infection starts when the
sporulated oocysts are
ingested.
The oocysts excyst in the
gastrointestinal tract, freeing the
sporozoites which invade the
epithelial cells of the small
intestine.
Inside the cells they undergo
asexual multiplication and
sexual development to mature
into oocysts, which will be shed
in stools.

Clinical symptoms
z
z
z

The disease is usually self-limiting.

Watery diarrhea
The loss of appetite, weight loss,
bloating, flatulence, stomach cramps,
nausea, vomiting.

Diagnosis
z

Finding oocysts in stool specimens by

light microscopy.

Oocyst

Treatment
z

Trimethoprim-sulfamethoxazole.

Patients with AIDS may need higher

doses and long-term maintenance
treatment.

Isospora belli
(Disease: Isosporiasis)

Epidemiology
z

It is distributed worldwide, especially in

tropical and subtropical areas.

Infection occurs in immunocompromised

individuals.

Life cycle
Infection occurs by ingestion of
sporocysts-containing oocysts: the
sporocysts excyst in the small intestine
and release their sporozoites, which
invade the epithelial cells and initiate
schizogony . Upon rupture of the
schizonts, the merozoites are released,
invade new epithelial cells, and
continue the cycle of asexual
multiplication.
Trophozoites develop into schizonts
which contain multiple
merozoites. After a minimum of one
week, the sexual stage begins with the
development of male and female
gametocytes . Fertilization results in
the development of oocysts that are
excreted in the stool .

Clinical Symptoms
z
z

Asymptomatic
Symptomatic : gastrointestinal complaints
(self limiting)

Diarrhea
Abdominal pain
Weight loss
Slight fever
Malabsorption of fat
Isospora belii

Diagnosis
z

Finding oocysts in stool using acid-fast

stain.

Oocyst

Treatment
z

Sulfamethoxazole-trimethoprim.

In immunocompetent individuals, the

symptoms disappear in 2-3 days with
treatment and longer without treatment.

Coccidian Parasites Found in Human Feces

Species

Excreted Form

Cryptosporidium sporulated
parvum
oocysts

Size (m) Oocyst Structure

4-5

4 sporozoites,
no sporocysts

8-10

2 sporocysts with
2 sporozoites each

Cyclospora
cayetanenis

unsporulated
oocysts

Isospora belli

unsporulated
2 sporocysts with
30 x 12
oocysts
4 sporozoites each

Microsporidium
Disease: Microsporidiasis

Life cycle
The infective form of microsporidia is the
resistant spore. The spore infects the host cell
The spore injects the infective sporoplasm
into the eukaryotic host cell through the polar
tubule. Then the sporoplasm undergoes
multiplication either by merogony (binary
fission) or schizogony (multiple fission). This
development can occur either in direct contact
with the host cell cytoplasm (E. bieneusi) or
inside a vacuole termed parasitophorous
vacuole (E. intestinalis). Either free in the
cytoplasm or inside a parasitophorous
vacuole, microsporidia develop by sporogony
to mature spores. During sporogony, a thick
wall is formed around the spore, which
provides resistance to adverse environmental
conditions. When the spores increase in
number and completely fill the host cell
cytoplasm, the cell membrane is disrupted &
releases the spores to the surroundings.
These free mature spores can infect new cells
thus continuing the cycle.

Organism(s)

Clinical presentation

Immunocompromised
host
Enterocytozoon
bieneusi

Chronic diarrhea, wasting,

cholangitis, acalculous
cholecystitis

Immunocompetent
host
Self-limiting diarrhea
and traveler's diarrhea;
asymptomatic carriers

Encephalitozoon
Chronic diarrhea;
intestinalis
cholangiopathy

Self-limiting diarrhea;
asymptomatic carriers

Encephalitozoon
cuniculi

Not identified

hepatitis; peritonitis;
symptomatic and
asymptomatic intestinal
infection

E. bieneusi and E. intestinalis are the most common microsporidia causing diarrhea.
Clinical presentations in immunocompromised and immunocompetent hosts are the
same, however the diarrhea in immunocompromised host is more severe and prolonged

The clinical symptoms resulting from the infection among

3 species are different based on the location of infection
Organism

Main sites of infection

Enterocytozoon bieneusi

Small intestinal epithelium, bile

duct epithelium

Encephalitozoon intestinalis

Epithelia of the gut from small

intestine to colon, gall bladder

Encephalititozoon cuniculi

Liver, peritoneum, intestine

Diagnosis
z

Finding spores in the fecal sample by

microscopic examination / PCR/
serological test

Treatment
z

Albendazole is the drug of choice.