SHISTOSOMA MANSONI: MORPHOLOGY, LIFE CYCLE, PATHOGENESIS - BIOLOGY - 2024

Shistosoma mansoni is a parasite of the trematode class that lodges in the venous portal circulation of the definitive host. It is the causal agent of mansonic schistosomiasis or bilharzia, an endemic disease in Africa, America and the Arabian Peninsula.

The disease is native to Africa, but was transported to Latin America in conjunction with the slave trade. The intermediate host is found in Africa, Brazil, Venezuela, Suriname, in certain areas of the Antilles, the Dominican Republic and Puerto Rico.

Electron microscopy of adult Shistosoma mansoni worms / S. mansoni egg.

In the world there are more than 200 million infected people, of which 130 million are symptomatic and 20 thousand die each year. Preventive measures are aimed at environmental sanitation, construction of latrines or toilets and treatment of sewage.

It also seeks to minimize the contact of the susceptible host with contaminated waters, through the construction of bridges, walkways, aqueducts, public toilets, among others.

Another way to prevent the disease is by controlling the population of intermediate hosts through the use of chemical substances or competing mollusks (Marisa and Thiara). The latter is more recommended and ecological.

Taxonomy

Animalia Kingdom

Phylum: Platyhelminthes

Class: Trematoda

Sub-class: Digenea

Order: Diplostomida

Family: Schistosomatidae

Genus: Shistosoma

Species: mansoni

Morphology

The evolutionary cycle of the parasite is complex, which causes it to present various evolutionary forms during the process.

Eggs

The eggs are large, measuring 116-180 µm long x 45-58 µm wide. They are elongated-oval in shape and have a prominent lateral spur, pointing backward.

Inside the egg is the developing miracidium. On some occasions, movements of the larva within the mature egg (flame cells) can be observed under the microscope. When it hatches it releases the miracidium.

Miracide

The miracidium is a mobile ciliated larva measuring 100-182 µm in length by 62 in width.

This larva does not feed and survives for a short time in water, being the maximum survival time (24 - 48 hours), but the vast majority die in 8 - 12 hours. During this time it must invade its intermediate host (mollusk of the genus Biomphalaria).

Mother sporocyst

It is a saccular stage that contains germ cells inside, formed by the transformation of the miracidium within the mollusk. This structure is capable of originating between 200-400 daughter or secondary sporocysts.

Secondary sporocysts

Structures from the primary sporocyst that later gives rise to the cercariae.

Cercarias

Larva with a head and a long tail forked at the distal end. This structure is very mobile. They have sexual differentiation (female and male cercariae).

Schistosomulus (adolescent worm)

Upon penetrating the skin of the definitive host, the cercaria loses its tail and the head transforms into a trilaminar and later heptalaminar structure, to give rise to the adolescent worm or schistosomulus.

Adult worm

The worms are flattened, not segmented covered by an integument that serves to absorb nutrients. It has a visible and incomplete digestive tract without an anus.

Male

The male is 10-12 mm in length and 0.11 mm in width. Its body is wide compared to that of the female and has two portions: the previous one is short and has two suction cups called oral and ventral respectively, which serve to adhere to the tissues.

The posterior part is long and there is the gynecophore canal, the place where the female enters for copulation.

The male has 6 to 9 testes attached to a vas deferens that ends in a seminal vesicle, located behind the ventral sucker.

Female

The female measures 12-16 mm long x 0.016 mm wide, being longer and finer than the male.

Like the male it has an oral and a ventral sucker. It has a single ovary located in the anterior half of the body, with a short uterus that can contain 1 to 4 eggs. The vulva is located behind the ventral sucker.

Occupying two-thirds of the rear body of the female are a large number of vitelline glands. The digestive tract is very well distinguished as black due to digested blood, also known as the pigment hemozoin.

Morphologies of the various stages of the Shistosoma mansoni parasite

Lifecycle

Hatching of eggs

When the female oviposits the egg is immature, therefore it needs approximately 10 days in the tissues to complete the development of the miracidium inside.

After maturing, the egg has an average life of 12 days to reach the intestinal lumen and be expelled by the feces, where it can remain 24 to 72 hours until it reaches a freshwater pond where it hatches, otherwise it perishes.

The eggs hatch in water, stimulated by the appropriate temperature of 28ºC and the presence of natural light (sunlight). The eggshell breaks and the miracidium comes out.

Invasion of the intermediate host

The miracidium has little time to swim and find its intermediate host, a snail of the genus Biomphalaria, found in slow-flowing freshwater rivers.

In this genus there are several species, including: B. glabrata, B. straminea, B. havanensis, B. prona and B. schrammi. B. glabrata is the main host for S. mansoni.

Miracidia are attracted to water-soluble substances secreted by mollusks. When found, they adhere to the soft parts of the snail (antennae, head and foot) by the secretions of the adhesive glands of the miracidium.

Then with the help of the secretion of the apical penetration gland, the miracidium accompanied by an optimal temperature of 18 to 26ºC, enters the interior of the snail.

Then the miracidium becomes a mother or primary sporocyst, from which 200 to 400 daughter sporocysts originate (asexual reproduction). These are released from the mother sporocyst and travel to the snail's hepatopancreas, where they settle.

Later, after 4 to 5 weeks, they have been transformed into numerous cercariae by a process called polyembryony. This process gives rise to approximately 300,000 cercariae for each miracidium entered into the mollusk. Later the cercariae are released by the soft parts of the snail.

Definitive host invasion

Cercariae do not feed, and can live up to 96 hours, however most die within 24 hours.

Before this time they must find their definitive host, the human. When they come into contact with the man's skin, they penetrate it through the lytic secretions of their penetration glands.

In this process it loses its tail and from that moment it is called a schistosomulus (adolescent worm).

These migrate to the skin venules and in a period of 2 days reach the right side of the heart and from there to the lungs. They then pass from the arteriolar channels to the venous channels and reach the left side of the heart to be distributed by the systemic arterial circulation.

It is necessary that they manage to pass through the portal system so that they can develop fully, those that do not die. Once located in the intrahepatic portal system after 1 to 3 months, they become adults and copulation begins.

The male migrates together with the female in the opposite direction to the bloodstream and goes towards the venules (hemorrhoidal plexus and mesenteric venules of the sigmoid and rest of the colon, where the female oviposits).

Release of eggs to the outside

For this purpose, the female, still mated, enters the capillaries of the submucosa and mucosa, depositing the eggs (300 / day / female). These should come out through the stool.

However, this is not always the case and the eggs can sometimes be carried by the bloodstream to the liver, lungs and other organs, being an important fact in the pathology.

The cycle in men lasts 6 to 8 weeks.

Shistosoma mansoni life cycle

Pathogenesis and pathology

This is divided into 3 stages:

Initial stage due to penetration of the schistosomulus

During penetration, a large percentage of schistosomuli die in the attempt, while others progress.

This produces an immediate and delayed hypersensitivity against the intruding parasite, causing a popular pruritic skin rash (dermatitis or Katayama syndrome), which is increased if the individual is exposed to cercariae frequently.

The rash disappears when viable schistosomuli begin to migrate to the liver, at which point fever, headache, and abdominal pain appear for 1 to 2 weeks.

Intermediate stage due to oviposition

Oviposition initiation 1 to 2 months after primary exposure induces the formation of immune complexes. Some remain circulating in the blood and others are deposited in the host's tissues.

This creates an acute febrile illness that can be accompanied by chills, cough, hives, arthralgia, lymphadenopathy, splenomegaly, abdominal pain, and diarrhea.

Immune complexes can induce glomerulonephritis.

Chronic stage due to the formation of granulomas

Only half of the eggs manage to reach the intestinal lumen, the rest are retained in the tissues, where they cause inflammation and scarring.

Eggs excrete soluble antigens that stimulate the formation of eosinophilic granulomas mediated by T lymphocytes. At first the granulomas are larger and exaggerated, with time the immune response is moderated, causing smaller granulomas.

Blockage of blood flow is common. The severity of tissue damage is directly proportional to the number of eggs retained and the organ affected.

In the liver they cause periportal fibrosis and hepatomegaly, while in the lungs interstitial scarring, pulmonary hypertension and right ventricular failure. Finally, in the central nervous system they can produce epilepsy or paraplegia.

This disease can cause the death of the patient.

Diagnosis

Eggs can be evidenced on stool examination by the Kato-Katz concentration method. If the load is low they can give negative results, for which a rectal biopsy is useful.

The eggs can remain in the tissues long after the adult worms have died, so to determine if the infection is active it is necessary to check if the egg is viable.

For this, they are observed under a microscope in order to detect the movement of the flame cells or their ability to hatch in water is studied (their hatching is stimulated in the laboratory).

There are other diagnostic techniques such as EIA (Immunoassay Assay) and RIA (Indirect Antibody Reaction), which look for antibodies against the parasite.

Treatment

For the initial phase there is no specific treatment, however antihistamines and corticosteroids can help. The existing treatment is aimed at avoiding oviposition of the female, destroying or sterilizing the adult worms.

The most frequently used drug is a derivative of pyrazinoisoquinoline called praziquantel in a single dose of 30-40 mg / kg weight.

However, if the parasite load is very high and the symptoms persist, a second dose may be considered 10 days after the first.

Unfortunately, in endemic areas, the parasite has become resistant to this drug, due to massive treatments, therefore in these cases oxamnaquine can be used, but not in pregnant women.

References

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