Blood Fluke pdf - (Helminthes (Trematodes

Unit 3: Helminthes (Trematodes)

Lecture 5+6+7 - Blood Fluke

Schistosoma haematobium:



Schistosomes are digenetic trematodes that inhabit the

blood stream of vertebrate host. So referred as blood
flukes .Schistosome so called because of the (split body)

on the ventral side of the male in which the female is held

during insemination & egg laying.



Disease: Shistosomiasis haemotobia (urinary schistosomiasis



Natural habitat: vesical venules.



Geographical distribution: In Africa ,middle east

Biology:



Sexes are separated .adult worm are delicate & cylindrical



Male: about 10-15 mm in length &1 mm in diameter ,the

tegument is provided with fine tubercle .There is 4-5
small sub globose (testes) behind the acetabulum .There is

a gynecophoric canal on the ventral side of the body .The

muscular male is attached by its sucker to the wall of the
vessels holding the thread-like female in its sex canal.



Female: about 20mm in length &0.25 mm in width .The

genital organ exclusive of the vitellaria occupy the

median longitudinal field.

ovary in the posterior .half of the body.
Uterus –long containing 20-30 eggs



Egg: the mature egg is rounded at one pole &

has a terminal spine at the other .It measure

upto 170-µ--m in length by 70—µm in width
.Straw coloured & relatively transparent.



Holding the female in the sex canal of the

male enable the female to extend its anterior

.extremity into the smaller venules to deposite it ُs eggs.

  obstruction of the venules
  pressure exerted by the worm
  Increase in size  of the eggs
  hypermotility  of the parasitized organ cause the blood

vessel .to repture & discharge the egg into the

surrounding tissue .On oviposition ,the eggs are immature
but when shed from the tissue & excreated .they become

fully embryonated .(maturation takes about one week)

Then the egg is sloughed into the lumen of the bladder &
excreated in the urine.

Life cycle:

Egg appears in urine 10-12 weeks after skin penetration.
Sch.haematobium may live 20-30 years

Pathogenesis:

The pathologic changes are divided into 3 consecutive periods

1) Prepatent period: From the skin penetration to the

appearance of eggs in urine .In this period petechial
haemorrhage, popular pruritic rash ,small foci of

eosinophilic & inflammatory changes in the lung & liver

2) Acute stage: when we have active egg deposition &

extrausion

3) chronic stage: which consist of stable egg output, tissue

proliferation & repair

Prepatent period:

Schistosoma dermatitis ,  resulting from  contact with
cercaria  of Schistosomes.  The lesion composed of initial
Prickling  sensation accompanied by erythema and local or
general urticaria then irritation  subside leaving a macules ,
but in few hours there is intense itching and papules
formation.  The reaction reaches its maximu m  between the
2

and 3

day, then gradually decrease.

Acute stage:

Egg deposition and extrusion cause local  damage to the
tissue of the rectum or urinary bladder. Ulceration  and
irritation  of the epithelium  of the bladder lead to
formation  of Polyps which may undergo malignant
changes. Numerous eggs calcified  giving the inner surface
a "sandy appearance" and Calculi  may  form  in the lumen

Chronic stage:

Extensive fibrosis of the bladder wall leads to contraction
of the organ. Fibrosis of the bladder neck obstructs the

Unit 3: Helminthes (Trematodes)

flow of urine with the development of hydro ureter and
hydronephrosis which may be associated with bacteriuria.
In Female the vulva is hyper plastic and indurated.

Symptomatology:

During the prepatent period the patients may be
symptomless or may  have malaise  with late afternoon
fever, moderate hepatic pain or epigastric distress .
If worms  mature in the rectal veins there is severe
tenesmus with dysentery.
The first evidence of infection is the painless passage of
blood at the end of  micturition,  then discharge of pus
cells and necrotic tissue debris ,  decrease in the interval
between urination  and eventually incontinence or  Anuria
.

Diagnosis:

1) Urine examination for eggs

* Simple  sedimentation (centrifugation)
* Nucleopore filtration  method
* Miracidial  hatching.

2) Intradermal test:

By using purified extracts of adult worm

3) Serological and Immunological test:

* Indirect immunofluorescence
* Elisa
* Circumoval  precipitin
* Cercarien  _ hullen   reaction
* Radiologic  test
* Rectal and Bladder  mucosal Biobsy and Cystoscopy.

Epidemiology



Three factors must coincide for transmission to occur:

 Presence of the vector snail Bulinus. Man is the only

important definitive host of Sch.

 Presence of human infected with the parasite.
 Human habit, that lead to urine contamination of fresh

water and to water contact and expos ure to cercaria.



Schistosomiasis haematobia is endemic in Africa, Middle

east,. In Iraq it is distributed in southern parts . After the

extension of irrigation system other areas are included.



Prevalence increase with age peaking at age 15_2o years

then start to decline.

Treatment

Praziquantel (Biltricide) single oral dose 4o mg/ kg.
Side effect: Abdominal discomfort, headache, drowsiness,
backache, fever, sweating, giddiness.

Control:

Effective measures includes



Chemotherapy



Snail control: Biological & chemical



Environmental sanitation.



Health Education

Schistosoma mansoni

Disease: Schistosomiasis mansoni
Manson ُ s blood fluke is a parasite of man occur widely
in Africa, several foci of the Arabian in south America .It
is hyper endemic in the Nile delta (Egypt )

Biology & Life cycle:



Male of S.mansoni measure (6.4-9.9) mm in length &

female (7.2-14)mm



The tegument of the male is provided with numerous

warty excrescences



The number of testes (6-9) form a grape like cluster a

short distance behind the acetabulum.



The most striking internal feature of female is a short

uterus containing very few eggs



The adult worm usually reside in tributaries of the inferior

mesenteric vein adjacent to the lower colon ,they may be

found at higher level of the intestine , in intra hepatic
portal veins ,vesical venules , pulmonary arterioles.



Fully developed egg of Sch. mansoni are large ,rounded

at both ends &provided with a conspicuous lateral spine
near one pole .The egg range in size from (120 x 45)-µ--m

when laid to (170 x 65 )—µm when ready to hatch .

Unit 3: Helminthes (Trematodes)

Pathogenesis & Symptomatology:



Humeral & tissue changes caused by S. mansoni resemble

those of infection with other intestinal schistosome spp.but:

1) The incubation period is about 2 weeks longer.

2) The early intestinal lesions typically develop in the

colon rather than the small intestine.

3) The number of eggs produced by each female is less ,

there for fewer eggs extruded from the intestinal
wall& fewer that later become trapped in the

perivascular tissue of the intestine & liver



Thus intestinal & hepatic fibrosis develop more slowly in

Manson ۥs schistosomiasis.



The common manifestation with S. mansoni are:

Fever, chills,  weakness, weight loss,
headache, nausea, vomiting,  diarrhea
(at times  bloody)



There may be evidence suggestive of

peptic ulcer, malabsorption

syndrome, gastrointestinal bleeding,
marked eosinophilia, rectal polyps,

thrombophlebitis . hepatic fibrosis
which may lead to portal hypertension & splenomegaly.



Frank ascitis is less frequent.



pulmonary lesion & symptoms are relatively common

Diagnosis

1) Fecal examination.
2) Rectal biopsy.

3) Immuno diagnostic test.

a) circumoval precipitin test
b) cercarien-Hüllen reaction

c) Immuno diffusion

d) Immuno electrophoresis.
e) Fluorescent antibody test.

Treatment:

-Praziquantel (drug of choice) 40 mg/kg .once
-Oxamniquine.15mg/kg .once

Epidemiology:



S. mansoni is also a parasite of several spp. of mammals.

Ex: Rodent, monkey in Africa & brazil



Man is only definitive host.



Exposure result from contact with cercaria- infected water.

Control :

1) Chemotherapy

2) Snail control.

a) chemical (Niclosamide)
b) Biology Predators (Thiara spp)

Competitor (Marisa spp.)

3) Enviromental sanitation

4) Health education.

Schistosoma japonicum



Disease: Schistosomiasis japonicum



It occurs in the Far East mainly in china, Japan &

Philippines.

Biology &Life cycle:



adult male measure 12-20 mm by 0,5 mm



The tegument is smooth



Oral & ventral sucker are subequal.



There are 7 relatively large testes behind the ventral sucker



Female are delicate with a length (15-30) mm &width

(0.1-0.3)mm



Egg: are round measuring 70-100—m each contains

ciliated miracidium. Aminute blunt projection may be
seen on the outer surface.



The earliest habitat of the young adult is tributaries of the

superior .mesenteric vein. of small Intestine.



Later some worm migrate into the inferior. mesenteric vein.

In these location, female continue to lay eggs daily over a
period of years.

Intramolluscan phase 6-7 weeks. -4-5 weeks from
cercaria penetration & adult maturation & laying eggs.

Pathogenesis:



The prepatent period

is short 4-5 weeks

 Female Schistosoma japanicum produce large

number.of eggs.

 most of damage is born by the small intestine & liver
 Damage is produced as each egg escape from the

venule, filter through the tissue & extruded into the

lumen of the intestine through the ruptured mucosa

with accompanying hemorrhage.

 The worm metabolites causes systemic sensitization,

resulting in eosinophilic leukocytosis .over a period of

5 years in heavy infection there is evidence of fibrosis,

Unit 3: Helminthes (Trematodes)

papillomas, stenosis of small intestine, hepatic fibrosis

with ascitis, splenomegaly &pulmonary fibrosis.

 Towards the end of prepatent period: late

afternoon,fever ,night sweat &diarrhea ,enlarged

tender ,liver ,epigastric distress , pain in the back, groin

or legs .also sometime urticaria develop.



Acute stage:

characterized by :

 Diarrhea, eggs in feces, fever, epigastric pain,

enlargement of liver, loses of appetite & weight.

 After few weeks ,he may feel better & return to work,

but symptoms return on physical exertion

 the blood picture is one of anemia ,increase in serum

globulin level with high eosinophilia



Chronic stage

Liver  become increasingly fibrosed with multiple  minute
granulomas in the parenchyma &on the surface.
The mesentery & omentum  may be thickened so as to
bind down the colon & separate the abdomen into an
upper & lower  portion .Then increasing ascitis &
emaciation  develop dyspnea on slight exertion  ,dilatation
of the superficial   abdominal  veins ,myocarditis  due to
infiltaration  of eggs into the cardiac wall  .The patient
gradually goes into a decline & may  die of exhaustion or
supervening infection.

Diagnosis:



Is similar to that of Sch .mansoni



Sedimentation & Kato-thick smear technique may be

required to discover the eggs.

Notes about human blood fluke:



Schistosomiasis japonicum :

most pathogenic - least responsive to treatment.



Schistosomiasis haematobia

Least pathogenic - most responsive to treatment.

Treatment:

Praziquantel 30 mg/kg in one day.

Epidemiology:

Most mammals  are susceptible to infection .Exposure
occur when cercariae  come in contact with the skin during
washing .The principal  source of infection in the snail is
faecal contamination by man.

Control:

Is very difficult because other mammals is susceptible to
infection but it is similar to the control of Sch.haematobium

S.
haematobium

S. mansoni

S.
japonicum

length

10-15 mm
20 mm/adult

6.1-9.9 mm
7.2-14 mm

12-20 mm
15-30 mm

Male
tegument

Slightly
tuberculated

Warty
exerescence

smooth

Reproducti ve system
In male /
testes

4-5

6-9 grape
like cluster

Location
of uterus

Anterior two
third

Anterior
half

Position of
ovary

Posterior half

Anterior
half

Middle half

Location
of caecal
junction

middle

Anterior
half

Posterior
fourth

Schistosoma.dermatitis
Cercarial dermatitis (swimmerۥs itch)



Is the skin reaction that produced by the cutaneous

penetration of cercaria of non-human schistosoma.



They are cercaria of schistosome of aquatic birds

&mammals & may affects person exposing skin to fresh

or salt water, all over the world.



Avian schistosomes that are responsible for Cercarial

dermatitis belong to the genera Trichobilharzia,

ornithobilharzia, Gegantobilharizia, Microbilharzia,
Austrobilharzia



When human are attacked by bird or non-human

mammalian schistosome cercaria, the parasite become
trapped in the skin & fail to complete their circulatory

migration, initiate cercarial dermatitis & then die in

several day.

Clinical Aspect:

Consist of prickling sensation, erythema, urticaria &
macules & papules .The reaction reached into maximu m
within 48-72 hr after exposure then gradually decreases .

Treatment:

Application of palliative (calamine lotion), antihistamine
cream or orally to relieve itching or trimeprazine