The larvae then use their piercing mouthpart, called the "stylet", to pass through the intestinal mucosa and enter the lymphatic vessels, and then enter the bloodstream.The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst. The larval host cell becomes a nurse cell, in which the larva will be encapsulated, potentially for the life of the host, waiting for the host to be eaten. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the parasite does not lay eggs, nor can it survive long outside a host. Diagnosis
Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing. Exposure history
An epidemiological investigation can be done to determine a patients exposure to raw infected meat. Often, an infection arises from home-preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal, or sharing of a common exposure with a laboratory-confirmed infected human. Clinical diagnosis
Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness, splinter hemorrhage, nonspecific gastroenteritis, and muscle pain.
In case of iatrogenic perforation common site is cervical esophagus just above the upper sphincter whereas spontaneous rupture as seen in Boerhaaves syndrome perforation commonly occurs in the lower one-third of esophagus. Signs and symptoms
The classic history of esophageal rupture is one of severe retching and vomiting followed by excruciating retrosternal chest and upper abdominal pain. Odynophagia, tachypnea, dyspnea, cyanosis, fever, and shock develop rapidly thereafter.Physical examination is usually not helpful, particularly early in the course. Subcutaneous emphysema (crepitation) is an important diagnostic finding but is not very sensitive, being present in only 9 of 34 patients (27 percent) in one series. A pleural effusion may be detected.Macklers triad includes chest pain, vomiting, and subcutaneous emphysema, and while it is a classical presentation, it is only present in 14% of people.Pain can occasionally radiate to the left shoulder, causing physicians to confuse an esophageal perforation with a myocardial infarction.It may also be audibly recognized as Hammans sign. Pathophysiology
Esophageal rupture,  in Boerhaave syndrome, is thought to be the result of a sudden rise in internal esophageal pressure produced during vomiting, as a result of neuromuscular incoordination causing failure of the cricopharyngeus muscle (a sphincter within the pharynx) to relax. As the intra-oesophageal pressure increases, the bolus within the oesophagus has nowhere to go superiorly (as the cricopharyngeus fails to relax) which causes the oesophagus to rupture.