Strongyloides stercoralis - Life Cycle, Pathogenesis, Pathology

Life Cycle of Strongyloides stercoralis

Although the life cycle of Strongyloides stercoralis is completed in a single host, it is complex. The life cycle of the parasite is unique due to its ability to auto-infection and multiply within the host.

The parasite has two distinct life cycles – one within the human body (including autoinfection) and another free-living in the soil.

Principle host: Man is the principal host while dogs, cats, and other animals can serve as reservoirs.

Host cycle

• Humans acquire the infection after the infectious form of the Strongyloides stercoralis parasite i.e. the filariform larvae penetrates the skin or buccal mucosa

• upon reaching the small blood vessels, these larvae are carried to the heart and then to the lungs via blood circulation

• the parasite leaves pulmonary capillaries to reach the alveoli and move upward to the trachea from where they are swallowed back into the intestine – the duodenum and the jejunum

• in the intestine, these larvae moult twice to mature into adult female worms

• these female Strongyloides stercoralis burrow deep into the intestinal mucosa where they begin lay eggs via parthenogenesis within 28 days

• these eggs immediately hatch to release non-infective Strongyloides stercoralis rhabditiform larvae that form

• these newly hatched larvae are passed out along with the host stool to follow the free-living cycle

• another path of the life cycle is the rhabditiform larvae migrating back to the intestinal lumen where they transform to filariform larvae to cause autoinfection (parasitic cycle)

• the autoinfection by Strongyloides stercoralis results due to the non-infective larvae, rhabditiform larvae transforming into the infective filariform larvae while still in the host intestine

• similar to other Strongyloides stercoralis infections, in autoinfection, the larvae penetrate the intestinal mucosa resulting in internal autoinfection of the skin of the perineal area resulting in external autoinfection

• in the above ways, the cycle is continued in a single host with a repeated migratory cycle

Free-living cycle

If the non-infective rhabditiform larvae present in the faeces reach the soil, the indirect life cycle (new free-living adults) of Strongyloides stercoralis begins or a direct cycle (infective filariform larvae) can take place.

Direct cycle (host-soil-host)

• in the soil, the Strongyloides stercoralis rhabditiform larvae undergo two moults to turn into the filariform larvae

• the transformation takes place within 3 days to 4 days

• these filariform larvae which come to human contact, penetrate the human skin to cause infection and the life cycle is repeated

• sexual phase is absent

• each rhabditiform larvae gives rise to one single filariform larvae

Indirect cycle

• within 24 to 30 hours of hatching of Strongyloides stercoralis rhabditiform larvae, it matures into free-living males and females

• the males fertilize the female and the gravid females begin to lay eggs

• eggs hatch to release the

• within 3 to 4 days, the larvae moult to form the infective Strongyloides stercoralis filariform larvae – each rhabditiform larvae hatching from the first batch of eggs gives rise to 30 filariform larvae

• these filariform larvae when coming into human contact, penetrate the human skin to cause infection and the life cycle is repeated

Pathogeneis, Pathology of Strongyloides stercoralis

Both the larval and the adult worms of Strongyloides stercoralis are pathogenic to their human hosts.

Pathogenicity of larva

• at the site of penetration by filariform larvae, macules and papules are produced

• in a sensitized host, the parasitic antigens can result in allergic reactions such as urticaria and pruritus

• in the lungs, the migrating larvae produce tissue damage, alveoli injury, and bronchial epithelium injury resulting in bronchopneumonia or pneumonitis

• pathological changes include inflammatory exudates of macrophages, epithelial cells, and minimal haemorrhage

Pathogenicity of adult worm

• in the host intestinal mucosa (duodenum and jejunum), mild to moderate levels of pathological changes take place

• common changes include oedema, cellular infiltration, partial villous atrophy, and in severe cases, ulcers and long-standing fibrosis is seen

• in cases of autoinfection and hyper infection syndrome, mucosal inflammation is severe with thickened and oedematous sigmoid colon and rectum