الفهرس 
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Abstract
Trichinella species are worldwide foodborne nematodes that cause trichinellosis in many species of mammals and birds. Human infections are often caused by T. spiralis after eating undercooked meat, e.g., meat of pigs, horses, and bears, containing the infective larvae (Rostami et al., 2017). Approximately 11 million patients worldwide are chronically infected with Trichinella in addition to the economic burden to the livestock industry and trade that are sequalae of animal infection with Trichinella (Zhang et al., 2018).
Clinical manifestations vary according to number of ingested living larvae, age, gender, health status and ethnic group of the host. It often starts by nonspecific intestinal manifestations which relate to the presence of adult worms in the small intestine. Once the larvae are laid and find their way to the circulation, this short enteral phase ends and the parenteral phase begins. The most common manifestations of this phase are myalgia, and periorbital oedema. This phase ends when the larvae reach their target in the skeletal muscles of the host (Sharma et al., 2014).
Under normal conditions muscles have a high regenerative ability that enable it of self-repair after injury. In the regeneration process the muscle progenitors, satellite cells first exit their normal quiescent state to start proliferating. After several rounds of proliferation, most of the satellite cells differentiate and fuse to form new myofibers or to repair damaged ones (Wu et al., 2008).
Injury of muscles by the invading larvae initiates a process of repair, just like after any trauma. However, Trichinella borrows only the initial part of this repair process to construct its own home for a long-lasting infection in skeletal muscles of the host without killing it (Ilic et al., 2012).
A septum is formed between the injured and intact fibers and differentiation of satellite cells is stimulated with increased expression of myogenic regulatory factors (MyoD and myogenin) (Narayanappa and Nandeesh, 2021). Unlike other causes of muscle injury, the satellite cells mis-differentiates to the nurse cells. Infected muscle cells become withdrawn from the resting phase and re-enter the cell cycle and arrest before differentiation of satellite cells to new myofibers. The satellite cells otherwise de-differentiate to form the nurse cells. Formation of nurse cells occurs through a finely orchestrated set of cellular responses, forming a well-innervated, fully vascularized, and contractile muscle apparatus (Wu et al., 2008), after about 20-30 days post infection (García et al., 2013).
To stop muscle injury, treatment must be initiated during the first few days after infection to prevent onset of the parenteral phase of the disease. However, treatment is usually started only after the larvae reach the muscles and start to cause muscle pain. Unfortunately, neither mebendazole nor albendazole are fully effective in the treatment of invading larvae. However, because no major side effects are detected with ALZ treatment it is usually used to treat symptomatic patients. Till now, no anthelminthic drug has total efficacy against newborn larvae or maturing first-stage larvae (Shimoni and Froom, 2015). The intestinal absorption rate of oral ALZ is about 1–5%. Using higher doses or prolongation of treatment can lead to toxicity for example, neutropenia due to myelosuppression (Chai et al., 2021).
The vascular network that surrounds the nurse cell is a vital structure that regulates propre transport of nutrients and wastes for maintenance of larvae‟s metabolism. Therefore, a drug that can effectively suppress angiogenesis around the encysted larvae is expected to be a good candidate for treatment of muscular trichinosis (Wu et al., 2008).