BLOOD FLUKES ((SCHISTOSOMES((

Dr. Muntaha M. Hassan

• The Schistosomes are blood trematodes

belonging to the Phylum Platyhelmintha.
commonly known as blood-flukes
• Schistosomiasis is considered by the World
Health Organization as the second most
socioeconomically devastating parasitic disease,
(after malaria), with hundreds of millions
infected worldwide.
• Shistosomes: dioecious trematodes (blood flukes)
• Sexes are separated: two sexes are dissimilar
• The males broader than the female, females longer
than males, females are cylindrical while males are
flattened.
• The males have gynocophoric canal to held the
female during copulation.
• Thin female is adapted to an intravascular existence
• Provided by oral and ventral sucker.
• The secum bifurcate and reunite again at the
posterior end.
• The infection is acquired by direct penetration of
cercaria through the skin to invade the
circulatory system.

Schistosomes Other trematodes

• 1-Dioecious • Hermaphroditic
(monocious)
• 2- lack muscular • Have muscular
pharynx pharynx
• 3- The seca reunite • The seca have dead
after bifurication . end.
• 4-Produce non- • Produce operculated
operculated eggs. eggs.
• 5- Have not redial stage • Have redia stage.
.
• 6- The cercariae have • The cercariae have
forked tail unbranched tail.
 258

Schistosoma spp- Cercaria

Schistosoma spp- Miracidium

Fig 208 : stages from the life cycle of the schistosoma spp.

Schis. haematobium
• The common name is Vesical blood fluke.
• Cause :urinary schistosomiasis
• Live in the vesical and pelvic plexuses of veins
• Called Bilharzia haematobium
• Endemic in the Nile valley in Egypt
• 10-15mm long x1mm thick
• Covered by finely tuberculated cuticle
• Ovary located in posterior part of female
• 4-5 testes in male
• The female laid 20-300 eggs daily.
• The egg have terminal spine
 Schist. mansoni,
• Called mesenteric blood flukes ,
• Cause intestinal bilhariziasis or schist. Dysentery.
• Live in inferior mesenteric veins.
• Covered by coarse tuberculated cuticle
• Endemic in Africa, south America and India.
• The female laid few eggs daily.
• 6-12mm X 1.1mm.
• Ovary in anterior part of females.
• 6-9 testes in male. (in cluster)
• The eggs have lateral spine.
 Schistosoma japonicum
• Known as oriental blood flukes.
• cause oriental schistosomiasis or katayama fever.
• Found in china, Japan, Taiwan, Philippines.
• Live in superior mesenteric vein.
• Doesn’t have cuticular tuberculations. (smooth)
• Females laid 3500 eggs daily.
• 10-20mm X 0.5mm.
• Ovary in middle part of female.
• 6-7 testes in males.
• The eggs have lateral knob.
e s. Saline s. Iodine s.
243
( in stool )

Schistosoma japonicum Egg

Schistosoma haematobium Egg Schistosoma mansoni Egg

( in urine ) ( in stool )

Fig 193 : Ova of Schistosoma spp.

 246

244

Oral sucker Female

Schistosoma mansoni Male-Female Copula

Male Ventral
sucker

eosin s.

Schistosoma mansoni Male-Female Copula Section

Fig 194 : Schistosoma mansoni female and male in copula
 247

258

Schistosoma spp- Cercaria

Schistosoma spp- Miracidium

Fig 208 : stages from the life cycle of the schistosoma spp.
 259
Sch.h Sch. j

Oncomelania
Sch.m

Biomphalaria
Fig 209 : the intermediate hosts of schistosoma spp.
240
 Table 7 241
Morphological differentiation between

The species of schistosomes of man

Male adult worm :

S. haematobium S. mansoni S. japonicum

Length 10 – 15 mm 6 – 10 mm 12 – 20 mm
Integument finely tuberculated coarsely tuberculated smooth
No of testes 3–5(4) 6 – 9 ( 7 ) in (cluster) 7 – 9 ( 7 ) (in column)
Ceca reunite late reunite early reunite very late

Female adult worm :

Length 15 – 20 mm 10 – 14 mm 15 – 30 mm
Position of the ovary posterior half anterior half middle
Length of the uterus long short long

No. of ova in the uterus 20 – 50 1 –4 50 – 300

Ova :
Spine terminal spine lateral spine short lateral spine (rudimntary)

Present in urine, less, frequenitly in stool in stool rarely in urine in stool

Habitat in human :
Body vesical plexus of urinary bladder in ferior mesentric vein, superior mesentric vein, less
less frequently superior frequently interior

Snails :
(intermediate host) Bulinus truncatus Biomphalaria spp. Oncomelani spp.

Clinical features:
• 1. Initially, at the site of entry of larvae, there is
skin rash with pruritis, lasting for 1-2 days.
• 2. After 3-8 weeks of symptom-free period, there
appear allergic manifestations, known
as (Katayama Syndrome, or Katayama fever)
specially in Sch. Japon characterized by:
• i) Fever, chills, sweating, headache & cough.
• ii) Urticaria, muscle & abdominal pain and
patches of pneumonia ;
• iii) Splenomegaly
 (swimmer’s itch)

• Cercarial dermatitis: Erythematous papules on the exposed areas of

a swimmer. is a skin rash caused by an allergic reaction to an
infection with certain microscopic parasites of birds and animals.
• Symptoms of cercarial dermatitis or swimmer's itch include
burning, tingling, and itching of the infected skin. Small reddish
pimples appear within 12 hours of exposure. The pimples may
develop into small blisters. Itching may last up to a week or more
but will gradually go away. Cercarial dermatitis (swimmer's itch) is
not contagious.
• Treatment includes corticosteroid creams, anti-itch or Calamine
lotions, or other creams.
 Acute schistosomiasis, or Katayama
fever
occurs with the beginning of oviposition, usually 20 to 50 days
after primary exposure and infection with S. mansoni and S.
japonicum. It rarely follows infection with S.haematobium.
Although asymptomatic in endemic areas, acute schistosomiasis
is becoming a frequent and major clinical problem in non-
immune individuals from urban regions who are exposed for
the first time to a heavy infection in an endemic area.
This febrile condition is thought to be a hypersensitivity
reaction to schistosomal antigens.
Patients complain of a flu like illness with fatigue, headache,
arthralgia and night sweats, sometimes with
hepatosplenomegaly, cough, dyspnea and chest pain. Acute
schistosomiasis is a self-limiting condition and most
symptoms resolve without any treatment within 4-6 weeks.

• 3. Chronic cases:
• i) Portal hypertension with esophageal varices
& hemorrhoids causing hemorrhagic
manifestations.
• ii) Pulmonary hypertension
• iii) Immune-complex Glomerulonephropathy
• iv) Transverse myelitis- due to involvement of
spinal cord.
 Pathogenesity
• Schistosomiasis has been referred to as an immunologic disease. The
pathogenesis of acute and chronic schistosomiasis appears to involve
immunologic mechanisms, either humoral or cell mediated.
• Delayed type of cell-mediated hypersensitivity is due to secretion of
soluble enzyme by the ova. DTH helps ova to escape from intestinal
blood capillaries into gut lumen.
• Schistosomes evade host immunity by covering its surface with host
protein (red-cell glycoproteins, MHC molecule & IgG). in veins provoke
no inflammation.

• It lives in mesenteric vessels of host, in spite of blood containing

antibodies, It develops two outer cytoplasmic lipid-layers, which are
resistant to immune damage.

• Dead worms become entangled as emboli to be arrested in liver or

lung causing intense reaction

pathology
I. Skin lesion: Pruritic papular rashes.
II. Intestinal Schistosomiasis:
Distal rectosigmoid colon is most commonly
involved.
.
Mucosa of involved part shows granulation tissue
with ova, causing polypoid hyperplasia of
mucosa, which often bleeds and ulcerates.
Ulcers with dense fibrosis cause narrowing of
gut lumen.
Ova are deposited in minute vessels of submucosa.
*Miracidia are released from ova by mechanical pressure &
cytolytic enzymes, into gut lumen to be excreted in stool.
*If ova cannot be excreted through intestine it may be carried
through portal vein to liver producing portal tract fibrosis.
*If ova are retained in the intestinal tissue, miracidia are
disintegrated with fibrosis at the site
• The eggs penetrate blood vessels wall by :
• 1-piercing action of the spine
• 2-by mounting pressure within the venules
• 3-by lytic substances produced by egg. And by DTH

Hepatosplenic Schistosomiasis:

• Reticuloendothelial cell hyperplasia &

granulomas are often seen in liver & spleen
• Liver : Ova lodged in the small intrahepatic
portal radicles contain a living embryo that can
survive for a period of 2-3 weeks. It secretes
soluble antigen and induce granulomatous
reaction, that occludes the lumen.
• Acute endophlebitis finally lead to intrahepatic
vascular block.
• Inflammation and destruction of the coats of
blood vessel lead to thrombosis.
• Due to prominent vascular and fibrotic changes,
the portal area is moderately broadened.
• Grossly liver is enlarged & slightly nodular.
• Intrahepatic portal fibrosis causes portal
hypertension. Esophageal varices complicate the
picture of portal hypertension.
• Death in patients with hepatosplenic involvement
is usually due to rupture of these varices.
• Spleen: Enlarged with fibrosis .

IV. Cardiopulmonary lesion:

• , portal hypertension with collateral venous channels must be

present to allow direct passage of eggs to the right-side of
the heart and from there to the pulmonary arterial tree.
• Thus cardioovascular bilharziasis almost always occurs in
patients with hepatosplenic schistosomiasis.
• There are granulomas around ova which may extend into the
lumen of pulmonary vessels. Wall of the artery may be
destroyed by the inflammatory process.
• Newly formed arteries causing dilation of veins.
• Pulmonary obstructive arteriolitis causes pulmonary
hypertension with right-sided heart Failure (cor-pulmonale).
 • V. Immune complex Glomerulopathy of kidney:
Majority of cases have histopathologic findings
consistent with a diffuse membrano-
proliferative glomerulonephritis.
• VI. Ectopic lesions:
single granulomas around ova may involve any
organ or tissue, without any clinical effect.
Solitary lesions are composed of numerous
eggs, pseudotubercles, granulation tissue and
varying amount of fibrous tissue.
• VII. CNS lesion:
May affect brain causing symptoms of cerebral
irritation and spinal cord causing transverse
myelitis.

Schistosoma mansoni
Schistosoma japonicum
• In human host the habitat of the organism is the lower
mesenteric venous system. It may also be found in the veins of
the small and large intestine.
• In general Schistosoma Japonica is characterized by similar but
more serious symptoms than Schistosoma mansoni probably
because of the larger number of eggs.
 Schistosoma heamatobium
Clinical features:
• i) Painless hematuria is the earliest symptom.
• ii) Other symptoms are, more or less, similar
to Schistosoma mansoni.
• iii) Lesions in uterine cervix may simulate
carcinoma of cervix.

-Tissue proliferation and repair

• In chronic stage there is generalized hyperplasia and
fibrosis of the vesical mucosa with a granular
appearance. The entire mucosa becomes inflammed,
thickened and ulcerated.
• There may be obstructive hyperplasia of the ureters
and urethra.
• There may be a secondary bacterial infection leads to
chronic cystitis.
• Deposition of ca oxalate and uric acid around the eggs
and blood clots.
• Association with bladder cancer.
• The disease may also affect the prostate, seminal
vesicles, spermatic cord, epididymis, testes, penis,
penile urethra and female urethra.
the estimated incidence of urinary bladder cancer was higher
in areas with a high prevalence of S. haematobium
infection than in areas with a low prevalence;
Other malignancies that have been reported in association
with S. haematobium infection
include:
• squamous cell cancer of the female genitals,
• ovarian cystadenocarcinoma,
• teratoma and Brenner tumours,
• uterine leiomyosarcoma,
• male breast cancer,
• hepatocellular carcinoma, lymphoma, bladder sarcoma,
rectal carcinoid tumour, and renal cell carcinoma.

Laboratory Diagnosis
schist. haematobium
• The definitive diagnosis of urinary schistosomiasis is made by
finding the characteristic ova of S. haematobium in urine.
• Terminal urine should be collected as the terminal drops
contain a large proportion of the eggs.
• The urine can be centrifuged and the deposit examined
microscopically for ova.
• Eggs can sometimes be found in seminal fluid in males.
• A bladder biopsy may be used in some cases.
• Laboratory Diagnosis
• Laboratory confirmation of S. mansoni
infection can be made by finding the eggs in
the feces after an iodine stained, formol-ether
concentration method.

Epidemiology

• -The disease (contact with fresh water)

• 1-Higher in rural area (agricultural
population).
• 2-Sex: more in males than in females
(occupational hazard).
• 3-More common in lower socio-economic
communities (bathing and washing clothes).
• 4-Infection may last years
 Control and prevention of
schistosomiasis
1-Education of people in endemic areas.
2-Proper disposal of urine and feces.
3- Snail control (chemical and biological eradication).
4- Treatment of infected persons.
• It is difficult to control schistosomiasis because:

1- The intermediate host (snail) is difficult to kill by any chemical or

biological
agents.
2- In some species (S. japonicum), the snails are amphibious
(semiaquatic). So,
eradication of snails from water is virtually useless.
3- Some species (S. japonicum) have wide range of reservoir hosts
(domestic and wild). So, treatment of human cases is virtually
useless.