8 schistosomiasis

8/6/2019 8 schistosomiasis

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Once known as bilharzia/bilhariasis. It was named after

Theodor Maximilian Bilharz.

1st to describe the ailment in men in 1851 at the Kasr-el-Aini in

Cairo, Egypt.

Schistosome eggs were found in ancient Chinese and Egyptian

mummies by Sir Armand Ruffer in 1910 (SRG).

S. haematobium, first species to be discovered.

S. japonicum, named by Fijiro Katsurada, Professor of

Medicine at Okayama Medical School. S. mansoni, discovered in 1907.

S. mekongi, officially named in 1978.

S. intercalatum, officially named in 1934.


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Species Geographicaldistribution

Intestinal S. S. mansoni Africa, Middle East,Caribbean, Brazil,Venezuela, Suriname

S. japonicum China, Indonesia,Philippines

S. mekongi Cambodia, Lao

S. intercalatum Rainforests of centralAfrica

Urogenital S. S. haematobium Africa, Middle East


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They belong to Genus Schistosoma, live in blood vessels and cause

schistosomiasis. People call them blood flukes. There are four species

infecting human body. They are:

1. Schistosoma japonicum is prevalent in Far East. In china, it is

prevalent in Yangtze valley and south of Yangtze except Guizhou Province.

The adults live in the portal vein system, causing liver cirrhosis and portal

vein hypertension syndrome.

22. Schistosoma mekongi is merely distributed in Mekong River Valley,resembles Schitosoma japonicum except intermediate host.

3. Schistosoma haematobium widely spreads in Africa, chiefly in Nile

River valley. The adults live in the vesical and pelvic plexus causing painless

terminal haematuria, renal failure complicated by the ureter obstruction. In

the endemic area infection is so common that hematuria is accepted as a sign

of manhood in young boy.

4. Schistosoma mansoni is distributed in Africa and focal area in Latin

America. Lives in the portal and hemorrhoidal vein plexus, causing stool with

fresh blood, liver cirrhosis and portal vein hypertension.


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I. Morphology

1. Adult worms are elongated cylindrical in shape,unlike other flukes. Two sexes are separate, gray white

in color, but the female is much dark and slender, the

male is shorter and thicker, sickle-like. In human body

the male usually embraces the female into itsgynecophoral canal, appears K like (or the female

usually resides in males gynecophoral canal).

Schistosoma japonicum


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Female: Longer and slender than the male, much dark colored thread-like,

12-26 x 0.1-0.3mm in size. The digestive system is similar to that of male.

The vitellaria are located in the posterior part of the body surrounding

the cecum. The unbranched, oval ovary lies in the mid-portion of the body.

The uterus lies in the anterior portion of the body filled with 50-300 eggs

arranged in a single row, arising from ootype to genital pore behind the

ventral sucker.

Male: 10-20 x 0.5-0.5 5mm in size, oral sucker at top near by ventral sucker. Just

behind the ventral sucker there is a longitudinal groove-gyncophoral canal in

which the female normally resides. The esophagus is divided into two branches in

front of the ventral sucker, and then unite to form a cecum at the posterior third

part of the body. Seven testes are situated one by one, each has a delicate efferens

which combine to form the vas deferens and dilate to become a seminal vesical

opening in the genital pore just behind ventral sucker.


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Paired male and female adult worms. The

female schistosomulum is the darker, curledworm within the male's gynacophoric canal.


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2. Mature egg is oval in shape, slight yellow in color, 89 x 67,

shell is thin without an operculum but with a lateral spine.

The content is a miracidium. Under the electron microscope

there are many micro-tubules on the shell, through which the

soluble egg antigen (SEA) is secreted by a miracidium.

3. Cercaria is infective stage. It is composed of the body and

forked tail (including tail stem and fork) and has 5 pairs of

penetrating glands in the body (2 pairs of preacetabular and 3

pairs of postacetabular glands)


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Oval in shape, slight

yellow in color, 89 x

67 , shell is thin

without an

operculum but with

a lateral spine.


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The small spine is

generally not visible as

the egg surface is often

covered with facal

debris.


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Forked cercaria of S.

japonicum


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1. Site of inhabitation: the portal vein system, mainly in theinferior mesenteric vein.

2. Infective stage: cercaria

3. Infective route: by skin

4. Intermediate hosts: Oncomelania snail5. Reservoir hosts: mammals such as buffalo, cattle, wild

rodents, goat, monkey, pig, fox.

6. Eggs are main pathogenic factor: (They are inlaid in theliver and intestinal wall. Some of them are discharged in feces

to complete its life cycle).7. The development in human body requires 25-30 days.

Cercaria can live 1-3 days. Life span of the adults is about 20-30 years.


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88. Blood fluke is a special kind of flukes because of

following characters:

(1) The adult worms look like nematodes, elongated

cylindrical in shape.

(2) Two sexes are separate.(3) Egg without operculum, but with a lateral spine.

(4) Only one intermediate host required.

(5) The infective stage is cercaria.

(6) The infective route is by skin.

(7) The eggs are main pathogenic stage.


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Three major factors responsible for theoccurance of schistosomiasis:

The method of disposal of human excreta

The presence of the snail intermediate host

The contact with cercaria-infected water


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adult worm passing eggs

egg into fresh water

cercariae

miracidia

penetrate into the body of the snail

(intermediate host)

oncomelania


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The intermediate host of S. japonicum: Oncomelania

snail


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1. Pathogenic mechanism of blood fluke

(1) Due to the cercaria and schistosomulum ( adolescent ) :

When human schistosome cercaria repeatedly penetrate the

human skin, type I allergy takes place. The cercarial dermatitis appears ,

petechiae and rashes ensue. The migration of the adolescents may inducelocalized pneumonitis and urticaria

(2) Due to adults:

The mechanical effect and toxic effect of adults and their

metabolites cause mesenteric phlebitis, hepatitis, and abdominal pain; the

immune complex may cause the damage to the kidney, schistosome

nephritis results from type III allergy, the esinophils increase in

peripheral blood.

III. Pathophysiology and clinical manifestation


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(3) Due to eggs:

The most serious damage is done by eggs. Colon and liver are most

seriously involved.

1) In liver: Soluble egg antigen Eosinophilic infiltration

Granuloma Eosinophilic abscess formation Fibrosis

Liver cirrhosis (pipestem fibrosis)

splenomegaly

Portal vein hypertension ascites esophageal varicosity

hemorrhoid varicosity

varicosity varicosity surrounding

the umbilicus


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2) In intestine

Soluble egg antigen Eosinophilic

infiltration Granuloma

Eosinophilic abscess UlcerationFibrosis or polyp


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(1) Initial phase: It is characterized by fever, dry cough

(pneumonitis), urticaria, eosoniphilia. These phenomena are due toadolescents migration.

(2) Acute stage: The characteristics symptom is dysentery.The patient may pass stool with blood, pus and mucus 5-10 timesper day, in which a large number of eggs can be found. Chills, fever,and malaise occur.

(3) Chronic stage: Chief manifestations of the patients are

interval diarrhea or dysentery. The patients experience fatigue,general condition and strength deteriorate, loss of weight andinterest, retardation of both physical and mental growth in children.Spleen and liver enlargement, anemia, in women menopause,sterility and abortion may occur. This stage may last from several

years to 20 years.

2. Clinical manifestation (symptoms and signs)


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(4) Terminal stage is characterized by portal vein

hypertension syndrome, common saying, abdomendistention looks like a big drum, emaciation looks like a

fire wood. Ascites, emaciation, varicosity, splenomegaly

and anemia are commonly found. The patients die of

secondary infection, upper digestive tract bleeding,

hepatic coma.

(5) Ectopic lesion: The damage to the central nervous

system ( brain, spinal ) may cause paralysis (monoplegia,

hemiplegia ).


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abdomen distention looks

like a big drum, emaciationlooks like a fire wood. Ascites, emaciation,varicosity, and splenomegaly


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Acute stage: eosinophilia is characteristic change.WBC raise to 10-

30G/L

Chronic stage: eosinophil ia (slightly or moderate rise in eosinophils)

Terminal stage: WBC and platelets are lower

Acute stage: rise in serum globulin, slight rise in ALT

Chronic stage: most patients have a normal liver function,

especially asymptomatic

Terminal stage: serum ALB descends caused by liver cirrhosis


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The discovery of eggs in stool is the evidence of

diagnosis by direct smear or other methods

Imaging testB-ultrasound: the degree of liver cirrhosis

CT: the image of liver and brain

X-ray: chest; esophagus; and gastrointestinal tract


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Immunological Tests

Intracutaneous test

Circumoval precipition test

ELISA and IHA etc.

Monoclonal antibody technique


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Varicosity of esophagus-fundus-stomach

Hemorrhage of upper gastrointestinal tract

Hepatic encephalopathy (HE)Spontaneous bacterial peritonitis (SBP)

Complications of intestinal tractAppendicitis

Intestinal obstruction and cancroid change


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1. Epidemiological investigation: Investigate whether

Oncomelania snail can exist in local natural environment; local

residents are used to defecate, work and play in the same water;

and examine the pathogen: Examine the feces from local

residents and domestic animals; also can dissect the suspicious

reservoir hosts, such as buffalo, goat, wild rodents and etc. If

the source of infection, intermediate hosts, transmitting route

and susceptible crowd exist at same time and local, an endemic

area of schistosomiasis can be confirmed.


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2. Eliminate the source of infection

Treat the patients, carriers and domestic animals. Drug of

choice for man: Praziqantel is pretty effective, side effects are

very light. The other effective drugs, such ashexachloroparaxylol, bithionol may be used.

Kill the wild animals which may be infected.

3. Prevention

(1) Health education is in progress, give up habits.(2) Control and deal with night soil.

(3) Avoid directly contacting with the water contaminated by

cercariae, lay up water in a container for 3 days, exposed to sun

shine; put on protective clothes; apply some chemical repellenton the skin (dibutyl phthalate)

(4) Kill the intermediate hosts and wild reservoir hosts.

(5) Change the bad environment, realize modernization of

agriculture.


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1. Geographical distribution: The disease is prevalent in

China, Japan, Philippines, Indonesia. In China, this

disease is found in 13 provinces, city and autonomic

regions along the Yangtze River Valley and south of the

Yangtze ( north from Jiangsu, Baoying county to southend Guangxi, Heng County ). In Taiwan, only animals, no

humans are infected by S. japonicum.


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33.. Social factors:

(1) Habits: residents are used to defecate, work

and play in the same water. The people whowork on catching fish, planting rice, washing

commodes, vegetables and clothes get

infection easily.

(2) Local economy and culture fall behind..


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Geographical

distribution of

mansoni

schistosomiasis

Schistosoma Mansoni


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Life Cycle


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infective form

cercaria

intermediate host:

snail Biomphalaria

swims freely in

infected waters penetrates the skin

of a definitive host:

man and other

mammals 0,5 cm


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Pathogenic form

adult female: 1.2 to1.6cm

adult male: 0.6 to 1.4cm

mature female inside

male walls of venules of

sigmoid and rectum

superior hemorrhoidal

plexus branches of inferior

Mesenteric vein


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Pathogenic form egg

300 eggs / day length: 150

width: 65

lateral spine


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Clinics

1. Acute phase

cercarial dermatitis

Schistosoma mansoni or other species

2/3 days: localized pruritus, urticarial rash,papuloerythematous exanthem

15 to 25 days: abrupt onset of fever, headache,

shivering, anorexia, myalgia, right upper quadrant

pain, less comonly nausea, vomitting, diarrhea, cough hypersensitivity: urticaria, generalized pruritus,

facial edema, erythematous plaques, purpuric lesions

weight loss, hepatosplenomegaly


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Clinics

2. Chronic phase

more common forms

intestinal (fatigue, vague abdominal pain,

diarrhea, alternating with constipation,

dysentery-like illness with bloody bowel

movements) hepatosplenic: 4 to 5% severe lesions

(portal hypertension, ascites, pdal edema,

hepatosplenomegaly)

cardiopulmonary


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Cutaneous mansoni schistosomiasis

Genital or vulvar forms

physiopathology

through hemorrhoidal plexus

periovular or

schistosomatic granuloma

Ectopic location of mansoni schistosomiasis

physiopathology unknown

how do eggs/adult worms reach theabdominal wall or other areas ? unknown

erythematous

linear arrangement

almost zosteriform


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Histopathological examination

Epidermis

papillomatous epithelial hyperplasiaDermis

granulomatous tuberculoid reaction

chronic inflammatory infiltrate

foreign body giant cell

large ovoid structures

Histopathological examination

Dermisovoid structures with

lateral spine dead

and viable eggs

ofS. mansoni


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Diagnosis

Clinics

Parasites

eggs in fecesbiopsy: rectal, liver and granuloma

Immunology

complement fixation, periovular andcercarial reaction, ELISA, intradermal

reaction, immunofluorescence, PCR


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Treatment

niridazol

hycanthone

oxamniquine

praziquantel

Prophylaxis

water source

sanitary facilities

control of snails

sanitary education


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SchistosomaSchistosoma

HaematobiumHaematobium Infects over 111 million people

Mostly in Africa and the Middle East

Most common cause of urinary schistosomoasis

Definitive host: human

Intermediate host: Bulinus species snail


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Life Cycle


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Life Cycle


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Signs and Symptoms

Immediate manifestations:

Cercarial dermatitis:maculopapular blistering eruption

1-2 days after exposure

Lasts for a few days Self-limited


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Acute Schistosomiasis: Fever, lymphadenopathy, hepatosplenomegaly, blood eosinophilia

Initial allergic hypersensitivity to the parasite as well assubsequent formation of soluble immune complexes

Chronic schistosomiasis: Chronic form develops as many S.haematobium eggs remain

trapped in the host tissues and become surrounded by delayed-type

hypersensitivity granulomatose inflammation

Inflammation is associated with collagen deposition and scar

formation

Gradual accumulation of the scar within bladder and ureterscan lead to hydroureter, hydronephrosis, ascending bacterial

infection

Inflammation can result in local ulceration and significant blood

loss in the urine

Inflammation may be associated with dyserythropoesis


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For those with less intense exposure the early signs

include: dysuria, proteinuria, bladder polyps

Later signs and symptoms include:

hydronephrosis, hydroureter, bladder calcification,urinary tract infection and squamous cell carcinoma

of the bladder

For hosts with eggs in the bladder and lower

ureters, 50% ofpatients have symptoms of dysuria,frequency and terminal hematuria

Cor pulmonale

Central nervous system disorders

Signs and Symptoms


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Diagnosis:

Finding of parasite egg in urine or feces

Concentration methods, sedimentation

or membrane filtration techniques

Serologic testing

Radiologic testing

Treatment: praziquantel

Eggs are spindle-shaped,

usually 140-150 by 60

micrometres, they have a

terminal spine


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8 schistosomiasis