Except for members of the order Taeniidae, the first intermediate host is an arthropod, and except for in the case of Archigetes spp. (which can attain sexual maturity in freshwater oligochaeta), the second host is usually a fish, but can be another invertebrate or vertebrate. After the scolex has differentiated and matured in the larval stage, growth will stop until a vertebrate eats the intermediate host, and then the strobila develops. Adult tapeworms often have a high final host specificity, with some species only found in one host vertebrate. Common infective species
Medical importance
Taeniasis
Taeniasis is an infection within the intestines by adult tapeworms belonging to the genus Taenia. It is due to eating contaminated undercooked beef or pork. There are generally no or only mild symptoms. Symptoms may occasionally include weight loss or abdominal pain. Segments of tapeworm may be seen in the stool. Cysticercosis
Cysticercosis is a tissue infection caused by the young form of the pork tapeworm. Infection occurs through swallowing or antiperistaltic contractions during regurgitation carrying eggs or gravid proglottids to the stomach. At this point, larvae hatch when exposed to enzymes and penetrate the intestinal wall, travelling through the body through blood vessels to tissues like the brain, the eye, muscles, and the nervous system (called neurocysticercosis).At these sites, the parasites lodge and form cysts, a condition called cysticercosis, producing inflammatory reactions and clinical issues when they die, sometimes causing serious or fatal damage.
Approximately 50% of ERMS is associated with RAS mutations, with NRAS mutations more common in adolescent cases and HRAS and KRAS mutations occurring in 70% of infant cases. Embryonal rhabdomyosarcoma is commonly driven by a mutation in the RAS family of proto-oncogenes, creating a powerful signal which is now known to promote tumor growth by preventing muscle lineage progression by blocking expression of the transcription factor myogenin. Inhibition of this signaling pathway with a cancer medication, trametinib, has been recently shown to overcome this differentiation block and reduce tumor progression in animal models of embryonal rhabdomyosarcoma.Tumor suppressor gene mutations, such as TP53 mutations, were shown in about 13% in the mutations and MYOD1 mutations were seen in about 3% of the mutations. Tumor suppressors signal the cell to stop the cell cycle and start apoptosis, known as programmed cell death, when the cell senses damage or irregular cell cycle growth patterns. Approximately 10% of ERMS cases include a loss of function mutation at TP53, which results in anaplasia, poor cellular differentiation that can be identified through nuclei that are larger and darker-colored than normal. An international study of more than 600 people with RMS showed worst outcomes in cases with anaplasia, regardless of fusion-status. Predisposing Conditions
Genetic conditions such as Gorlin syndrome, neurofibromatosis type 1, Beckwith-Wiedemann syndrome, Li-Fraumeni syndrome, Noonan syndrome, Costello syndrome, and DICER1 syndrome have been shown to predispose individuals to embryonal rhabdomyosarcoma. Risk factors associated with embryonal rhabdomyosarcoma include cigarette smoking, older age of birth parent, x-ray exposure, and maternal drug use.