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.
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