Trichinella spiralis - Life Cycle, Pathogenesis, Pathology

Life Cycle of Trichinella spiralis

The life cycle of Trichinella spiralis occurs in a single host which serves both as the definitive host and intermediate host i.e. a single host can harbor the adult as well as larva. However, to complete the life cycle, two different hosts are required.

Primary host: Pig

Natural hosts: carnivores, omnivorous animals including rodents, bears, and hyenas. Humans, which is an accidental hosts, are the dead end for Trichinella spiralis.

• Humans acquire the parasitic infection after consumption of raw or insufficiently cooked pork harboring viable encysted larvae

• the cyst wall is digested in the host stomach, freeing the Trichinella spiralis larvae

• the larvae penetrates the duodenal and jejunal mucosa

• further development of the larvae into males and females takes place within 2 days

• mating and fertilization take place within the intestinal mucosa as an intracellular parasite

• females burrow deep into the intestinal wall or mesenteric lymph nodes

• Trichinella spiralis females burrow deep into the host intestinal wall and within 6-7 days, deposit the larvae

• deposition of the larvae continues for several weeks

• each female can lay 1,500 to 2,000 newborn larvae during its lifespan

• male Trichinella spiralis die shortly after mating while the females die shortly after completion of laying larvae

• the newborn Trichinella spiralis larvae penetrate the mesenteric and lymphatic venules

• the larvae are carried by general circulation to various host organs and tissues – with a predilection for muscles of the tongue, diaphragm, eye muscle, masticatory muscles, muscles of arms and legs, and masticatory muscles

• inside the host muscle tissues, the larvae grow with an increase in size and encyst within 3 weeks

• in dead-end hosts like humans, calcification of the dead larvae begins in 6 to 18 months

• in other sites such as the myocardium, and central nervous system, dead larvae do not encyst

• transmission occurs after ingestion of raw or undercooked meat infested with viable cysts or larvae

• although infection in man is a dead end, the life cycle of Trichinella spiralis is maintained in nature

• primary host (pig) acquires infection after ingestion of other pig carcasses (pig-to-pig), rats (rat-to-pig)

• rats also acquire infection from infected rats (rat-to-rat) or from pigs (pig-to-rat)

Pathogeneis, Pathology of Trichinella spiralis

Both adult worms and larvae are pathogenic. Adult female Trichinella spiralis inhabitant the intestine results in gastrointestinal syndromes while migrating larvae cause allergic manifestations such as fever, eosinophilia, and edema of the face. Moreover, the encysted larvae present in the skeletal muscles cause muscular pain

Pathogenicity of adult worm

• adult Trichinella spiralis females present in the small intestine results in acute eosinophilia, inflammatory reactions, hyperemia, edema

Pathogenicity of migrating larva

• migrating Trichinella spiralis larvae cause profound lesions in the skeletal muscles such as myositis, basophilic granular degradation of muscle fibers

• associated with hyperemia, edema, hemorrhage

• in the muscle fiber cells, the larvae can induce a number of changes including:

  * hypertrophied nuclei

  * inactivation of transcription of muscle genes

  * reduced expression of certain muscle-specific proteins

  * infected muscle cell ceases to develop as it becomes arrested in the reproduction cycle of the cell at the gap 2 or M phase

Pathogenicity of encysted larva

• encysted larvae occur only in skeletal muscles

• since encapsulation of the Trichinella spiralis takes place between 21 to 90 days, pathological changes including the formation of a lemon-shaped sheath around the larva

• other clinical manifestations include fever, myalgias

• within 6 months to 2 years, the intramuscular cysts calcify

• although the growth or encapsulations do not take place in the myocardium, the encysted larva of Trichinella spiralis produces inflammation, necrosis, and fibrosis of myocardial fibers

• in the central nervous system, these larvae produce granulomatous nodules, and vascularisation of small arteries as well as capillaries which leads to frequent brain hemorrhage