Schistosoma japonicum - Life Cycle, Pathogenesis, Pathology, Host Immunity
Life Cycle of Schistosoma japonicum
The life cycle of Schistosoma japonicum is completed in the following hosts.
Definitive host: Man, domestic animals (cat, dog, cattle, pig), and wild animals (mouse, monkey, feline, mustelid) is the only definitive host.
Intermediate host: Amphibian snails of the genus Oncomelania
man becomes infected with Schistosoma japonicum after coming in contact with water contaminated with cercaria – the infective stage
this cercaria penetrates the epidermis of the unbroken skin with the help of oral and ventral suckers
after losing its tail in the skin and another layer of glycocalyces, it becomes schistosomula
during development, schistosomula acquires:
a double-lipid bilayered tegument that is highly resistant to host immune response
host proteins, blood group antigens, and major histocompatibility complexes (MHCs) on its surface
the schistosomula then migrates to dermal veins through the skin and eventually to pulmonary capillaries over many days
after living in the host lung for a short while, the blood fluke reaches the portal veins in the liver through the systemic circulation
in the portal veins of the liver, they develop into adult worms where females are fertilized by the male Schistosoma japonicum
both males and females move out of the liver against the blood flow to reach the venules that drain the small intestine, ascending colon, and caecum
the fertilized Schistosoma japonicum eggs are now deposited and excreted out in the host faeces
the time between infection by cercariae and production of eggs i.e. pre-patent period ranges from 40 to 60 days
while these oviposited eggs are partially mature, by the time they are passed out through the urine, they each contain miracidium- a fully developed larvae
the stool upon gaining access to the water hatch to release free-swimming miracidium
Schistosoma japonicum miracidium has a lifespan of 2-3 weeks during which they infect must infect the intermediate host- amphibian snails of the genus Oncomelania; otherwise, they will die
in the snail host, the miracidium undergo asexual reproduction through first and second-generation sporocysts but lacks redial stage in its asexual cycle
after the asexual cycle, the larvae transform into fork-tailed cercariae - a single miracidium can give rise to nearly 100,000 cercariae
these infectious cercariae escape from their snail host and can survive in freshwater for up to 48 hours
if these cercariae can each another human skin or any susceptible mammal host, they will survive and the life cycle of Schistosoma japonicum is continued
Image: Schistosoma japonicum life-cycle (Source: CDC)
Pathology, Pathogenesis of Schistosoma japonicum
During oviposition, the adult Schistosoma japonicum causes a clinical syndrome known as Katayama fever. This fever is caused when high worm load and egg antigen stimuli result in the immune-complex formation and may lead to serum sickness-like disease.
Although Katayama fever is not caused by granuloma, the egg-induced granuloma is the key pathological lesion in the intestinal wall or in rare cases- the liver. Katayama fever due to Schistosoma japonicum is more severe and fatal.
The host central nervous system is more commonly infected by Schistosoma japonicum than other human Schistosoma species. Periportal fibrosis is another major pathology change observed.
Other important pathological changes in chronic cases include small liver with white Clay pipe-stem fibrosis, periportal fibrosis, perisinusoidal blockage, and symmers fibrosis. In such conditions, haemin pigments are found in Kupffer cells and phagocytic cells present in the granuloma.
Host immunity of Schistosoma japonicum
The host immunity in Schistosoma japonicum infection does not depend on antibodies or T lymphocytes.
Also, the egg granuloma is formed due to antigen-antibody complexes in the host.