Schistosomes are a group of closely related flukes that inhabit
the portal vascular system.
Schistosomes are therefore known as Blood flukes.
Of the seven species known to infect humans, S.haematobium,
S.mansoni and S.japonicum are of primary importance.
S.mansoni and S.japonicum usually affect the gastrointestinal
tract. S.haematobium affects the urinary tract.
Schistosomiasis is a major cause of debilitating illness in the
world with about 10% having a chronic disease with significant
impaired liver function.
The deposition of schistosome eggs within the host is the
principal pathological vause of chronic schistosomiasis.
In contrast to other Trematodes, Schistosomes are not hermaphrodites.
They exist as separate sexes with the female residing in the groove of
the male known as the “schist” and hence the name.
The three species can be distinguished by the morphological features of
S.mansoni eggs have a prominent lateral spine, S.japonicum have a
small lateral spine, and S.haematobium eggs are with a terminal spine.
Schistosomes have evolved a remarkable process to avoid host
defences by absorbing host molecules, including immunoglobulins,
blood group glycolipids, and HLA antigens. These limit the ability of the
immune system to recognize them as foreign.
Includes and requires one intermediate host (specific
species of snail for the different S.species).
Humans are the definitive host harboring the adult
flukes that lay eggs passes out in the stool eggs
have miracidia Miracidia hatch in fresh water and
penetrate a specific species of snail sheds its
epithelium and develops into a mother sporocyst that
give rise to daughter sporocysts the cercaria larva
(forked tailed) emerge from the daughter sporocysts
and exit the snail.
The cercariae are the infectious stage and have a
strong attraction for skin secretions especially
arginine penetrate the skin transform into
schistosomules (little schistosomes) within 24
hours enter the peripheral circulation enter the
heart exit the heart through the pulmonary
capillaries enter the left side and thereby into the
A small number leave the mesenteric arteries ,
traverse the intestinal capillary bed and reach the
liver by the hepatic portal system.
After about three weeks of development in
the liver sinusoids, the young parasites use
their suckers to ascend the superior
mesenteric vessels against the blood flow
and migrate to the walls of the gut
copulate and produce eggs.
The eggs are release via stools.
The pathogenesis is almost entirely due to the eggs
and not the adult worm.
The eggs located in the liver, spleen or the walls of
the gut or the bladder liberate antigens over a
considerable period of time that ultimately induce
granulomas leading to fibrosis, hepatomegaly and
The primary lesion however, begins with a delayed
type Hypersensitivity (DTH) around the egg.
Pathogenesis divided into 3 stages:
I) Early stage:
A large number of schistosomules usually die within 24 hours of
the cercariae entering the skin.
Immediate and DTH to the parasitic antigens results in an
intensely pruritic papular skin rash reulting in characteristic
itching and local edema that resolves within around 4 days. This
is called Cercarial dermatitis.
Fever, abdominal pain and headache indicate the migration of
the schistosomula to the liver.
Fever may be due to the secretion and excretion materials of the
migrating schistosomules allergic reaction not as severe as
with their egg antigens.
II) The Intermediate stage:
After about 1-2 months of primary exposure, the patient may
experience the onset of acute febrile illness bearing a striking
resemblance to serum sickness.
This may be due to the egg antigens, now in excess results in
soluble immune complexes being deposited in the tissues.
Antigen-antibody complexes do correlate with the severity of the
illness and may induce glomerulonephritis.
Besides, fever, chills, arthralgia, lymphadenopathy,
splenomegaly, abdominal pain, diarrhea with inflamed colonic
mucosa and petechial hemorrhages.
Typically, leucocytosis,marked peripheral eosinophilia and
elevated levels of IgG, IgM and IgE antibodies are present.
This symptom complex is termed as Katayama syndrome.
III) The chronic stage:
The eggs retained in the intestines, liver and the bladder initiate the final and the most
morbid stage of Schistosomiasis. They induce inflammation and scarring and finally
Soluble antigens excreted by the eggs stimulate the formation of T-lymphocyte mediated
eosinophilic granulomas often marked by the inflammatory signals or lymphokines from
the T cells bringing about a host of cell types like macrophages, eosinophils, meutophils,
As the granuloma around each egg or cluster of eggs contain large number of eosinophils
and macrophages that get degenerated or die, these are termed as eosinophilic
These eosinophilic abscesses involving many cell types around the eggs in the granuloma
is called the Hoeppli phenomenon.
Fibroblasts stimulated by factors released by both the retained eggs and the granulomas
now lay down scar tissue and the earlier granuloma induced vascular obstruction is
This inflammatory reaction leads finally to the development of periportal fibrosis and
hepatic enlargement. Splenomegaly also is the resultant manifestation.
The circulating immune-complexes may cause nephropathy.
The severity of the tissue damage is directly related to the number of eggs retained.
Papules and erythema on the skin. Cercarial dermatitis.
Fever, peaking in the late evenings and recedes by midnight or
Rigors, sweating, headache, cough, muscular pain and
gastrointestinal disturbances like diarrhea, nausea, mucous and
bloody stools etc… usually associated.
Liver and spleen slightly enlarged.
Leucocytosis, eosinophilia, urticaria etc.. Can be the additional
Acute can become chronic if not treated
adequately or on time.
Generally the symptoms are not pronounced
except with a slightly large liver and spleen
and intermittent chronic diarrhea or dysentry
that is significant especially after tiredness or
other mild infections.
Mild anemia is common with an increase in
A portal hypertension syndrome after hepatic fibrosis, severe
growth retardation or granulomatous disease of the colon usually
defines Advanced schistosomiasis.
This is usually after untreated cases for 3-5 years.
Hepatosplenomegaly, ascites, portal hypertension, abdominal
collateral vein dilation and esophagogastric varices are the
Severe cases include upper gastrointestinal bleeding, hepatic
coma may lead to death.
S.haematobium infections can also lead to the carcinoma of the
Eggs carried around the liver may get lodged in the
small pulmonary arterioles where they produce
interstitial scarring, pulmonary hypertension, fibrosis
of the pulmonary bed and right ventricular failure.
Pulmonary involvement often seen with heavy worm
If the underlying schistosome infection is not
treateed , Salmonella infections will continue to
recur and this association is most frequently seen in
males between 15-30 years of age.
Characteristic eggs in the feces or urine.
Serological tests, detecting the circulating
Ag-Ab complexes, Antigens and antibodies,
do not differentiate between active and
inactive infection and hence not useful.
These are however, very sensitive and can
be a useful and economic epidemiological
Treatment and prevention:
Praziquantel is the treatment of choice.
Prevention proper disposal of human waste,
eradication of intermediate host, the snail
species and education.
Flukes of genera Clonorchis, and Fasciola
infect the human biliary tract and at times
produce manifestations of ductal obstruction.
Clonorchis sinensis, the chinese liver fluke is
the most important.
Is a long and narrow bodied fluke with a
cone-shaped anterior pole.
The mature egg is yellowish-brown and its
operculum is small and fits into the broad rim
of the eggshell. The eggs urn-shaped and
have a discernible shoulder at their
operculum ring and a tiny knob on the
broader posterior pole.
C.sinensis has a typical life cycle:
Human flukes mature in the bile-ducts of the
definitive host – eggs discharged and pass
down the bile duct into the fecal stream.
The egg contain a well developed Miracidium
– reach fresh water – ingested by the
intermediate host ( snail) – the miracidium
hatch in the snail – transforms into a
sporocyst – number of embryos develop
asexually to become Rediae.
Additional embryos develop within the redia –
transforms into Cercariae. Each redia
produces 5-50 cercariae.
Cercariae emerge from the snail and contact
the second intermediate host, the fresh-water
fish. It attaches to the fish epithelium with its
sucker, cast off its tail and penetrates the
tissue of the fish in which it encysts to form a
Metacercariae. Thousands of metacercariae
can accumulate in the fish.
The definitive host infected on eating the raw
or undercooked fish containing the encysted
The larvae are released in the duodenum,
ascend the common bile-duct – migrate to
the liver and mature around 30 days.
The hermaphrodite adult can now produce
Pathogenesis and clinical symptoms:
Pathological consequences of C.sinensis infection is mainly in
the intra-hepatic secondary bile-ducts and its neighboring tissue.
The basic pathogenesis is the erosion of the epithelial lining of
the bile ducts.
The adult worm induces proliferation of epithelial cells,
desquamation of the biliary epithelium, epithelial hyperplasia,
adenoma formation, bile-duct hyperplasia, periductal fibrosis,
inflammation and gradual thickening and occlusion of the ducts.
Infiltrating eggs become surrounded by granulomas, thereby
interfering with the liver function.
Can lead to obstructive jaundice, cholangitis, cholelithiasis, and
Acute stage: Migration of larvae from the duodenum to bile ducts
may produce fever, chills, gastrointestinal discomfort, nild
jaundice and hepatomegaly.
Leucocytosis, eosinophilia and elevation of Alkaline phosphatase
levels usuall seen.
Numerous reinfections may produce worm loads of 500-1000,
resulting in the formation of bile stones. Bile-duct carcinoma in
long-standing severe infections.
Occasionally, adult worms in the pancreatic duct may result in
duct obstruction or acute pancreatitis.
Typical eggs of C.sinensis demonstrated in
the stool specimen.
Treatment and Prevention:
Treatment of choice : Praziquantel.
Prevention is adequate cooking of fish and
proper human waste disposal.
Fasciola hepatica is the sheep-liver fluke.
Definitive host : sheep, Humans.
Humans infected when eat contaminated
( with metacercaria) aquatic plants or raw
sheep liver – excyst in the duodenum –
penetrate the gut wall, reach liver – mature
into adults – adults in the bile-ducts produce
eggs – excreted – hatch in fresh water –
miracidia enters snail – cercariae – cercariae
encyst on aquatic plants.
Pathogenesis and clinical symptoms:
Adult worms in the biliary ducts cause the symptoms
– right-upper-quadrant pain, fever- hepatomegaly.
Chronic cases may develop obstructive jaundice.
Adult flukes on the posterior pharyngeal wall,
acquired by eating raw-sheep liver may cause a
painful pharyngitis, typically called Halzoun.
Treatment of choice: Triclabendazole.
Surgical removal of adult flukes in the
pharynx and larynx.
Prevention: Avoid raw liver and contaminated
Scientifically known as the largest intestinal
fluke in humans. Also named as Giant Asian
Definitive hosts: Humans, pigs.
F.buski is an elongated-oval shaped adult fluke. It
has a visible cone-shaped acetabulum, larger than
the oral sucker and located close to it.
The eggs are ellipsoidal, with a small but distinct
operculum having a fertilized ovum inside and many
Eggs passed through feces – enter fresh-water and
hatch into miracidia – Miracidia penetrate snails, the
intermediate host – sporocyst – rediae – cercariae.
Cercariae released from the snail and encyst as
metacercariae on various aquatic plants like water
chestnut, lotus, water bamboo etc…
Humans infected on ingestion of these raw
vegetables – metacercaria excyst in the
duodenum – and attach to the intestinal walls
and develop into adult worms.
Pathogenesis and clinical manifestations:
Pathogenesis due to the damage of the intestinal mucosa by the
No noticeable symptom during the developmental period of the
fluke ( 3 months).
The condition resulting after, is traumatic, obstructive and toxic.
Irritation at the site of attachment provokes inflammation,
ulceration, hemorrhage and abscess of the intestinal wall with
excess mucous secretion accompanied by chronic diarrhea are
the typical symptoms.
Profound toxemia caused by absorption of the allerginic
metabolite of the fluke may also lead to prostration and death,
particularly in children.
Lab diagnosis based on the typical egg
findings in the stool specimen.
Treatment usually effective in early or light
infected cases. Praziquantel, the drug of
Prevention: proper disposal of human waste
and avoid undercooked, raw aquatic
vegetation and elimination of the intermediate
More than 50 different species known to be
human parasites. P.westermani is the most
Also known as Lung Fluke causes
The adult fluke is reddish-brown, thick with a flat
ventral and protuberant back, like a semi-peanut.
The oral and ventral suckers are almost equal in
size. Adult flukes are characteristically found
encapsulated in the lung parenchyma.
The eggs are yellowish-brown, oval, a fertilized
ovum inside with 10 vitelline cells and surrounded
by a thick shell.
Definitive host: Humans and also pigs, dogs and
The eggs are often trapped in the surrounding
tissues and cannot leave the lungs – the capsule
erodes into a bronchiole – eggs are coughed up –
spat out or swallowed and passed in the stool.
The eggs reach the fresh water – hatch into
miracidia – enter snails (first intermediate host) –
develop into sporocyst, rediae, cercariae - leave the
snail – invade the gills, musculature and viscera of
certain cray-fish or fresh-water crabs – the larval
forms transform into metacercariae – eaten raw or
undercooked by humans get infected.
The metacercariae excyst in the duodenum burrow through the gut wall into the peritoneal cavity
– majority continue migration through the diaphragm
and reach maturity in the lungs after 5-6 weeks.
Some retained in the intestinal wall wander to other
foci such as liver, pancreas, kidney, skeletal muscle
or subcutaneous tissue.
Some young worms migrating through the neck and
the jugular foramen may encyst in the brain.
Pathogenesis and clinical manifestations:
The presence of adult worms in the lungs elicits an eosinophillic
inflammatory reaction and eventually the formation of fibrous
capsule that surrounds and encloses one or more parasites. The
infected patient may harbour as many as 25 lesions.
With the onset of oviposition, the capsule swells and erodes into
a bronchiole, resulting in expectoration of the brownish eggs,
blood and an inflammatory exudate.
Secondary bacterial infection of the evacuated cysts is common,
producing a clinical picture of chronic bronchitis or
If cysts rupture into the pleural cavity, chest pain and effusion
can result. Eventually, cystic rings, fibrosis and calcification
occur, closely resembling a clinical picture of pulmonary
tuberculosis (these two diseases often coexist).
Adult flukes in the intestines produce pain,
bloody diarrhea and on occasion, palpable,
abdominal or cutaneous masses.
Parasites lodged in the brain may produce, a
variety of neurological manifestations like
epilepsy, paralysis, optic atrophy etc…
Typical operculated eggs in sputum or feces.
Treatment of choice:
Avoid undercooked crabs.
Intestinal parasite. Endemic in Africa and
Definitive host: humans.
Intermediate hosts: Primary: snail
Eggs from the adult pass into feces –reach
brackish water – ingested by snails –
sporocyst, rediae, cercariae – cercariae leave
snail and encyst under scales of fishes as
metacercariae – raw fish containing cysts
eaten – larvae excyst in the small intestine –
attach to the mucosa – develop into adults –
lay eggs – passes out in the feces.
Pathogenesis and clinical symptoms:
Presence of the adult fluke causes
inflammation of the intestinal epithelium.
Most infections are asymptomatic, but
abdominal pain and diarrhea may be
Demonstration of typical eggs in the feces.
Treatment of choice : Praziquantel.
Prevention: proper disposal of human
sewage, elimination of the primary host and
to avoid undercooked or raw fish.