The below mentioned article provides a study-note on the blood helminths.
Family Schistosomatidae
Genus Schistosoma
Species
Schistosoma hematobium
Schistosoma mansoni
Schistosoma japonicum
Schistosoma Hematobium:
(The vesical blood fluke causing schistosomiasis hematobia, vesical schistosomiasis, urinary bilharziasis, schistosomal hematuria). It is not intestinal trematode.
History:
This worm was first recovered by Bilharz (1851) from the mesenteric veins of a native of Cairo and was demonstrated by him to be the cause of haematuria.
Geographical distribution:
It is distributed in Africa, Egypt, Tanzania. In 1952, an autochthonous (cases contracted locally) focus has been found by Gadgil and Shah in Ratnagiri district about 140 miles from Mumbai (India). In Pondicherry (India), Panjarathinam, in 1972, observed for the first time the eggs of Schistosoma nasalis (animal trematode) from the nasal washing of the nasal granuloma of cattle.
Habitat:
Adult worm of Schistosoma haematobium live in the vesical and pelvic plexuses of the venous circulation.
Morphology:
The male adult worm is shorter, stouter organism, measuring 10 to 15 mm in length by 0.8 to 1 mm in breadth. It is covered with minute integumentary tuberculation’s and has two muscular suckers, of which the ventral sucker is larger. Behind the ventral sucker, the body of the male is folded all the way to the caudal extremity to form the gynaecophoric canal (gc), in which the female is held during copulation and oviposition (Fig.48.1).There is a bulbous cluster of glands around the esophagus.
The paired caeca fuse to form a single trunk which ends blindly near the caudal extremity. The testes are behind the ventral sucker. The female is long and slender, measuring about 20 by 0.25 mm. The suckers are small and are not muscular. The tuberculation’s are confined to the extremities of the worm. The digestive tract is similar to that of the male.
Egg:
1. It measures 112 to 170 microns by 40 to 70 microns;
2. It possesses a distinct terminal spine;
3. Egg shell is transparent and light yellowish brown, every time one sufferer urinates, he releases 20 to 40,000 eggs (Fig. 48.2).
Life cycle:
Schistosoma haematobium passes its life cycle in two hosts:
(a) Definite host —MAN;
(b) Intermediate host – Fresh water snail, particularly in India, Ferrissia tenuis.
The eggs are discharged in the urine of the infected man, usually at the end of micturition. When these eggs are diluted in the water, they hatch out the ciliated larvae (miracidium)—the first larval stage (Fig. 48.7). These ciliated larvae swim in the water with the help of cilia in search of a suitable intermediate host, snail (particularly in India), Ferrissia tenuis.
On contact with the appropriate species of snails, they infect the snails by penetrating into their soft tissues and ultimately in the liver, where they lose their cilia and other organs and in course of four to eight weeks, they develop into first and second generation of sporocysts (second larval stage) and finally a generation of fork tailed cercariae (Fig. 48.8) which break out of the snail daily in swarming in water over a period often to twenty five days.
When human beings bathe or wade in cercaria-infested water, the cercariae come in contact with the skin of man and, as the water on the skin evaporates, enter the skin, casting off their tails (cercariae without tails are called as metacercariae or schistosomules).
Skin (portal of entry) penetration is effected by their anterior ends followed by digestive action of penetration gland secretions and lasts for less than thirty minutes. The metacercariae (infective to man) enter the peripheral venules, are transported to the right heart, pass into pulmonary capillaries, then they are carried through the left heart into the systemic circulation. The majority of them are shunted into the abdominal artery, then gain access to the mesenteric artery, pass through mesenteric capillaries and enter the portal circulation.
In the intrahepatic portal vessels, the larvae begin to feed and grow, become sexually differentiated about twenty days after skin penetration, migrate against the blood stream. They pass through the inferior mesenteric veins, rectal venous plexuses, pelvic veins and, at last, enter the vesical plexus of veins, where they arrive after three months after the initial exposure of the skin.
Upon arrival in vesical venules (site of predilection), the worms become sexually mature. Male embraces and holds the female within the gynaecophoric canal, both of them mate and the fertile female begins to lay eggs in the smallest venules by extending its anterior end, one egg immediately followed by another egg after the first.
In this way, the venules are filled with eggs which are held in position by their terminal spines. Because of the contraction of vessels, the eggs work their way through the vessels and the mucosa of the urinary bladder, enter into the cavity and are discharged with the urine.
Pathogenesis:
During the period of development, the metabolites of Schistosoma haematobium are discharged and provoke allergic reaction in the patient. In vesical schistosomiasis, the damage occurs in the wall of the urinary bladder due to escape of the eggs. Infiltration of eggs in the tissues may proceed to fibrosis with resultant miliary pseudo tubercles formation.
This eventually causes fibrosis of the entire organ. Pathogenic effects of Schistosoma haematobium consist of
(1) Generalized and localised reaction to metabolite of growing and mature worms,
(2) Trauma with haemorrhage as eggs escape from the venules and
(3) Pseudoabscess and pseudo tubercle formation around eggs lodged in perivascular tissues.
Clinical Features:
The incubation period lasts about ten to twelve weeks. The earliest manifestations are irritation and minute haemorrhages at the site of entry of cercariae into the skin. Then there is a gradual onset of toxic symptoms, consisting of anorexia, headache, malaise, generalized pain in the back and the limbs, and fever followed by rigors and night sweating.
There is pronounced urticaria, at first on the limbs, later more generalized in distribution. The abdomen may be enlarged and tender, the liver and spleen may be hypertrophic and there may be difficulty in breathing. After several months, there is painless passage of small volume of blood at the end of micturition-haematuria. There is frequent burning sensation at the time of urination and increased desire to urinate.
Laboratory diagnosis:
Specific diagnosis can be made by:
(i) Microscopic demonstration of terminal spined eggs in the centrifuged deposit of urine;
(ii) A piece of biopsied vesical mucosa obtained through cystoscope is compressed between two slides and examined for eggs under microscope.
Serological tests:
Fairley’s complement fixation test in which antigens from cercariae and adult worms are used. This is group specific reaction and is sensitive in detecting acute infection. The intradermal, precipitin, haemagglutination, bentoniteflocculation tests are all group-specific for schistosome infection. The precipitin test is more sensitive in chronic than in acute infection. Recent ELISA test can be used for the diagnosis of schistosomiasis.
Treatment:
Specific chemotherapeutic agents are potassium antimony tartarate or sodium antimony tartarate. Trivalent antimony compounds: Neoantimosan (Fuadin) is better tolerated and less efficatious for Schistosomiasis haematobia; dimercaptosuccinate has high cure rates.
Miracil D (Nilodon) has a 55 per cent cure rate in Schistosoma haematobium infection. Niridazoleis effective; TAC Pomoate also exhibits activity against Schistosoma haematobium. Praziquantal is recently used anthelminthic agents. Successful treatment is indicated by the disappearance of eggs in urine and absence of haematuria.
Prophylaxis:
1. Eradication of snails by molluscicides;
2. Sanitary improvement of the environment to reduce the pollution of water;
3. Prevent the water pollution by infected persons;
4. Avoid swimming or wading in polluted water;
5. Proper disposal of human excreta.
Schistosomal Cercarial Dermatitis (Swimmer’s itch, cercarial itch):
There are three types of cercarial dermatitis:
1. First type of schistosome dermatitis. It is caused by Trichobilharziaocellata,a non-human schistosome developing in the snail Lymnaea. It is prevalent in Oregon, Washington, California, Canada, Germany, Switzerland, France, Burma, and India.
Clinical aspects:
As the water evaporates from the skin a pricking sensation is experienced, followed by urticarial wheals. After one-half hour the initial dermatitis subsides leaving only a few macules. Several hours later, intense itching of the area develops with edema and the papules transform into pustules grown itch.
2. The second type of schistosome dermatitis is caused by the cercarian of avian species of blood flukes, particularly Trichobilharzia.
3. The third type of schistosome dermatitis results from penetration into human skin by cercariae of mammalian species of blood fluke. Schistosoma spindalis. It has been reported in paddy field workers in Malaysia and Thailand.
Treatment:
Trimeprazine is given orally.
Schistosoma Mansoni:
(Manson’s blood fluke producing schistosomiasis mansoni or Manson’s intestinal schistosomiasis often called bilhaziarsis).
History:
Bilhaz first observed lateral-spined egg in female schistosoma recovered from a patient at Cairo.
Geographical distribution:
Schistosoma mansoni is common in the Nile Delta and is widespread in Sudan, East African coast, United States (New York).
Habitat:
Adult worms of Schistosoma mansoni are mostly found in the mesenteric veins of the sigmoid rectal area and live for 26 years. S. mansoni may be kept in the laboratory for the study.
Morphology:
Adult worms (Fig. 48.3) resemble those of S. hematobium; both the male (6.4 to 12 mm long) and female (7.2 to 17 mm long). S. mansoni are smaller. The integumentary tuberculation’s of the male S. mansoni are also more conspicuous and the testes number 6 to 9. In the female, the ovary is situated at the anterior half of the body. The uterus is short and contains only a few lateral spined eggs.
Eggs—They have:
(a) A yellowish brown transparent shell;
(b) A characteristic lateral spine;
(c) Measure 114 to 175 microns in length by 45 to 68 microns in diameter (Fig. 48.4). 
Miracidium:
It is larger than that of S.japonicum and S. haematobium and has larger anterior penetration glands and its life cycle in the snails is similar to that the S.japonicum and S. hematobium.
Life cycle:
It parallels that of 5. hematobium.
Definite host—Man; intermediate host—Fresh water snail, Biomphalaria glabrata in America.
Pathogenicity:
The lesions produced by S. mansoni are similar to those of S. haematobium and S.japonicum infections, except that the production of granuloma around the eggs in the tissues is delayed, because of smaller number of eggs produced by S. mansoni. The colon and rectum are mostly involved. In the liver, pathological changes are hepatic cirrhosis. A living immature male S. mansoni has been recovered from anterior chamber of the right eye.
Clinical features. Initially there is popular rash with pruritus over the skin of the feet. Liver is enlarged and tender accompanied by fever. In classical schistosomiasis dysentery, there are frequent stools with lateral spined eggs and abdominal pain. Dysentery becomes less conspicuous, as the tissue reaction takes place around the eggs in the intestinal wall. The incubation period is 7 to 8 weeks.
Laboratory diagnosis:
1. Diagnosis is readily accomplished by the recovery of the characteristic lateral spined eggs in the stool, which can be seen under microscope.
2. Microscopical examination of the rectal tissue obtained by rectal biopsy as in Schistosoma hematobium.
3. Serological tests. Complement fixation and slide flocculation tests are satisfactory and far superior to the intradermal test. ELISA and CIEP are used to diagnose 5. Mansoni ‘infection.
4. Blood examination. In early stage, there is leucocytosis with marked eosinophilia, later moderate leucopenia and macrocytosis may develop.,
5. Ultrasonography can be useful for the diagnosis.
Treatment:
The only effective drug is potassium antimony tartarate or sodium antimony tartarate. Niridazole (Ambilhan) is most effective. Praziquantel is current anthelminthic against S. mansoni infection.
Prophylaxis:
1. It is similar to that of S. hematobium;
2. Sodium pentochlorophenate has been used with considerable success to control the vector snails;
3. Patients should be treated with tartar emetic;
4. Construction of public bath, laundry tanks and sanitary drainage canals can control the infection;
5. Disinfection of night soil with ammonium nitrate may kill the eggs, before the night soil is used as fertiliser in the field.
Schistosoma Japonicum:
(The Oriental Blood Fluke, producing Schistosomiasis japonica or Oriental schistosomiasis):
History:
This disease was first mentioned by Fujii, a Japanese physician, in 1847 and Fuginami (1904) first found the female worm in the portal vein and Katsurada (1904) first described the adult worm from infected dogs and cats.
Geographical distribution:
This infection is confined to areas in Far East, Japan, China, Philippines.
Habitat:
Adult worms of Schistosoma japonicum inhabit mostly in the radicles of the superior mesenteric veins draining the ileocaecal region.
Morphology:
The adult worm of S.japonicum (Fig. 48.5) resembles S. haematobium and S. mansoni, but lacks integumentary tuberculation’s. The male measures 12 to 20 mm in length and 0.5 to 0.55 mm in diameter. There are seven testes. The female averages 26 mm. in length by 0.3 mm in diameter. The ovary lies behind the mid-plane of the body. The uterus is a long straight tube containing fifty eggs at a time.
Egg:
1. It measures 70 to 100 microns by 50 to 65 microns;
2. is hyaline, oval or biconvex;
3. Has an abbreviated spine on the upper right border of the shell (Fig. 48.6).
Life cycle:
It is similar to that of S. mansoni and s. haematobium and takes place in two hosts:
(a) Definite host — Man, cat, dog, pig and cattle,
(b) Intermediate host — Fresh water snail of the genus Oncomelania.
Eggs which are passed out in the feces, require only dilution of the faeces in the water to hatch, allowing the miracidium to escape from the egg and to swim in the water. This miracidium is smaller but similar to that of S. haematobium and S. mansoni. It enters the soft tissues of the snail (Oncomelania guadrasi) in Philippines and produces first and second generation of sporocysts, then fork-tailed cercaria.
On contact with the skin of man or animals wading through the polluted water, the cercariae cast off their tails, penetrate the skin and enter the venous circulation and carried through the right heart to the lungs; and through the pulmonary capillaries they are carried through the left heart into the systemic circulation, reach the intrahepatic portal circulation to feed, grow and migrate into the superior mesenteric venules where the adult worms mate and the females lay eggs which are passed out with the feces of man and animals.
Pathogenicity:
S.japonicum produces the lesions which are similar to those produced by S. mansoni and S. haematobium. Intestinal tract and liver are mostly involved. The pseudo tubercles around the eggs produce fibrosis and papillomata’s growths. The intestinal and hepatic schistosomiasis of the Orient is called as ‘Katayema disease’.
Patients with acute schistosomiasis japonicum had disappeared in Japan, but patients with chronic schistosomiasis japonicum are still alive in the previously endemic regions of Japan, they may develop hepatocellular carcinoma with association with hepatitis C virus (HCV) infection.
Clinical features. The manifestations include dysentery, hepatic cirrhosis, splenomegaly, appendicitis, intestinal obstruction, pneumonitis, cerebral syndrome and intoxication, urticarial rashes accompanied by fever may develop into characteristic wheals of varying sizes in the skin.
Laboratory diagnosis:
Specific diagnosis rests on the recovery of characteristic eggs in the stools. In proctoscopic aspiration and biopsy, the eggs can be demonstrated.
Complement fixation and slide flocculation tests along with the clinical history will support the diagnosis.
Treatment Potassium antimony tartarate or sodium antimony tartarate is the most effective drug. Fuadin and anthiomaline are not much effective. Praziquantel (recent anthelminthic) is also very effective.
Prophylaxis:
1. Proper disposal of night soil;
2. Treatment of night soil with ammonium nitrate to kill eggs before it is used as fertiliser;
3. Destruction of snails by molluscicides;
4. Avoid bathing and wading through polluted water;
5. In Philippines, cats, pigs, dogs, water buffaloes and wild rats are commonly infected. These reservoir hosts constitute an important handicap to the control of schistosomiasis japonica.