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Schistosomiasis (bilharziasis) is a parasitic infection caused by blood flukes (Trematodes).
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Three main
species cause human infection: 1.
Schistosoma haematobium, ; 2. Schistosoma mansoni ;
3. Schistosoma japonicum.
Epidemiology: Existence of
Schistosomiasis about 5000 years back is evidenced from the DNA
studies of Egyptian mummies . Schistosomiasis is increasing in prevalence, affecting
nearly 10% of the world’s population and ranking second only to
malaria as a cause of morbidity & mortality.
S. haematobium
are found in tropical Africa & part of southwest Asia.
S. mansoni
are found in tropical Africa, part of southwest Asia, south America &
Caribbean islands.
S. japonicum
are found in parts of Japan, China, Philippines, India & part of
southeast Asia.
Blood flukes are known as
schistosomes because of the "split body" on the ventral side of the
male , in which the female is held during insemination and egg laying.
Man
is the definite host
harbouring adult parasites, and fresh water snails
are intermediate hosts.
Life
Cycle: 
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The schistosome egg
hatches in water, liberates a miracidium that penetrates a snail,
and develops through two stages to sporocyst to form the final
larval stage,the cercaria.
(1)
The cercaria escapes from the snail into water, "swims" and
penetrates the skin of a human host.
(2) The cercaria loses its forked tail to become a schistosomule which
migrates through the tissues, penetrates a blood vessel.
(3) Then
it is carried to the lung and later to the liver. In hepatic
portal venules the schistosomule becomes sexually mature and
forms pairs, each with a male and a female worm. The organism
causes lesions in the liver, including granulomas, portal( "pipestem"
) fibrosis, and portal hypertension.
(4) The
female worm deposits immature eggs in small venules of the
intestine and rectum (S. mansoni and S. japonicum) or of
urinary bladder ( S. haematobium ). The bladder infestation leads
to obstructive uropathy, ureteral obstruction, chronic cystitis,
and bladder cancer. |
S. mansoni:
Clinical features:
1. Initially,
at the site of entry of larvae, there is skin rash with pruritus,
lasting for 1-2 days.
2.
After 3-8
weeks of symptom-free period, there appear allergic
manifestations, known as
Katayama Syndrome, characterized by:
i) Fever, chills, sweating,
headache & cough. ; ii) Urticaria, muscle &
abdominal pain and patches of pneumonia ; iii) Splenomegaly
3. Chronic
cases :
i) Portal hypertension with
esophageal varices & hemorrhoids causing hemorrhagic manifestations. ii) Pulmonary hypertension
causing cor-pulmonale iii ) Immune-complex Glomerulonephropathy iv) Transverse myelitis- due
to involvement of spinal cord.
Pathogenesis:
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. Delayed type of hypersensitivity 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). It lives in mesenteric vessels of host, in spite of blood containing
antibodies. It also develops two outer cytoplasmic lipid-layers, which
are resistant to immune damage. Adult living schistosomes in veins
provoke no inflammation. Dead worms become entangled as
emboli to be arrested in liver or lung causing intense reaction.
Pathology:
Classic bilharzial granuloma:
Basic lesion is a
circumscribed granuloma consisting of a centrally located round ova
together with epithelioid cells, fibroblasts, giant cells and some plasma
cells & eosinophils.
I. Skin lesion:
Pruritic popular rashes.
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II. Intestinal
Schistosomiasis:
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Distal rectosigmoid colon is most commonly involved.
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.
Mucosa
of involved part shows granulation tissue with ova, causing polypoid
hyperplasia of mucosa, which often bleeds & ulcerates. Ulcers with
dense fibrosis cause narrowing of gut lumen.
III. Hepatosplenic
Schistosomiasis: Reticuloendothelial cell hyperplasia & granulomas
are often seen in liver
& spleen
Liver
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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.
Intrahepatic portal radicle
is totally replaced by a granuloma that occludes the lumen.
Acute endophlebitis of the
intrahepatic radicles may be noted. This may finally lead to
intrahepatic vascular block.
Inflammation and destruction
of the coats of blood vessel lead to thrombosis.
The thrombi
become recanalized and the newly formed blood vessels communicate
through the wall of the vein with adjacent vessels outside ,forming
telangiectasias in the portal area.
Due to prominent vascular
and fibrotic changes, the portal area is moderately broadened.
Grossly liver is enlarged &
slightly nodular. On cross section portal fibrosis stand out , termed
as "pipestem" fibrosis.
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 & contain Gamma-Gandy bodies.
IV.
Cardiopulmonary lesion:
For sufficient numbers of
ova to reach the lungs, 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 in
both intra-arterial & para-arterial granulomas , form anastomoses with
pulmonary veins 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:
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Solitary 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.
S. japonica:
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 S. Japonica is characterized
by similar but more serious symptoms than S. Mansoni probably because
of the larger number of eggs.
S. japonicum
produce similar lesions
like S. mansoni except: Involvement of small
intestine is more frequent ; Fibrotic and stenotic lesions of bowel
are more common; Intestinal polyps are more frequent; Lesions in liver
& lungs are more serious.
S.
hematobium:
Vesical and pelvic venous
plexuses constitute the habitat of S. haematobium. In some cases
the parasite may be retained in the haemorrhoidal plexus of
veins or terminal tributaries of inferior mesenteric vein.
Clinical features:
i) Painless hematuria is the
earliest symptom. ii) Other symptoms are, more
or less, similar to S. mansoni. iii) Lesions in uterine
cervix may simulate carcinoma of cervix.
Pathological changes in Urinary bladder:
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Ova are deposited in
submucosa of urinary bladder producing granulomas. Ova are excreted
with urine.
Mucosal changes - Initial hyperemia &petechae ;
Polypoid or elevated areas covered with granular mucosa ;
Glandular hyperplasia (cystitis cystica) ; Squamous metaplasia (leukoplakia);
Ulceration ;
Epithelium over calcified ova, appears as "sandy patch" at the base of
bladder. ; Marked fibrosis around ureteric orifice causes bladder-neck
obstruction with hydronephrosis and hydroureter. ;
Calcification may eventually occur. ; In many
patients carcinoma of the urinary bladder may develop.
The disease may also affect
the prostate, seminal vesicles, spermatic cord, epididymis, testes,
penis, penile urethra and female urethra.
Diagnosis:
1.Ova in stool, urine & tissue section.
2.
Endoscopic findings of Intestine & urinary bladder.
3.
Serodiagnosis:
i) Indirect
immunoflourescence.
ii)
Radioimmunoassay ; iii) ELISA.
4.
Ultrasonography.
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