Chapter 291 Trichinosis (Trichinella spiralis)
Human trichinosis (trichinellosis) is caused by consumption of meat containing encysted larvae of Trichinella spiralis, a tissue-dwelling nematode with a worldwide distribution. After ingestion of raw or inadequately cooked meat containing viable Trichinella larvae, the organisms are released from the cyst by acid-pepsin digestion of the cyst walls in the stomach and then pass into the small intestine. The larvae invade the small intestine columnar epithelium at the villi base and develop into adult worms. The adult female produces about 500 larvae over 2 wk and is then expelled in the feces. The larvae enter the bloodstream and seed striated muscle by burrowing into individual muscle fibers. Over a period of 3 wk, they coil as they increase about 10 times in length and become capable of infecting a new host if ingested. The larvae eventually become encysted and can remain viable for years.
Despite veterinary public health efforts to control and eradicate the parasite, reemergence of the disease has been observed in many areas of the world in the past 10-20 yr. Trichinosis is most common in Asia, Latin America, and Central Europe. Swine fed with garbage may become infected when given uncooked trichinous scraps, usually pig meat, or when the carcasses of infected wild animals such as rats are eaten. Prevalence rates of T. spiralis in domestic swine range from 0.001% in the USA to ≥25% in China. The resurgence of this disease can be attributed to translocations of animal populations, human travel, and export of food as well as ingestion of sylvatic Trichinella (T. brivoti, T. nativa, T. pseudospiralis, and T. murrelli) through game meat. In the USA from 1997 to 2001, wild game meat (especially bear meat) was the most common source of infection. Most outbreaks occur from the consumption of T. spiralis–infected pork (or horse meat in areas of the world where horse is eaten) obtained from a single source.
During the 1st 2-3 wk after infection, pathologic reactions to infection are limited to the gastrointestinal tract and include a mild, partial villous atrophy with an inflammatory infiltrate of neutrophils, eosinophils, lymphocytes, and macrophages in the mucosa and submucosa. Larvae are released by female worms and disseminate over the next several weeks. Skeletal muscle fibers show the most striking changes with edema and basophilic degeneration. The muscle fiber may contain the typical coiled worm, the cyst wall derived from the host cell, and the surrounding lymphocytic and eosinophilic infiltrate.
The development of symptoms depends on the number of viable larvae ingested. Most infections are asymptomatic or mild, and children often show milder symptoms than adults who consumed the same amount of infected meat. Watery diarrhea is the most common symptom corresponding to maturation of the adult worms in the gastrointestinal tract, which occurs during the 1st 1-2 wk after ingestion. Patients may also complain of abdominal discomfort and vomiting. Fulminant enteritis may develop in individuals with extremely high worm burdens. The classic symptoms of facial and periorbital edema, fever, weakness, malaise, and myalgia peak about 2-3 wk after the infected meat is ingested as the larvae migrate and then encyst in the muscle. Headache, cough, dyspnea, dysphagia, subconjunctival and splinter hemorrhages, and a macular or petechial rash may occur. Patients with high intensity infection may die from myocarditis, encephalitis, or pneumonia. In symptomatic patients, eosinophilia is common and may be dramatic.
The Centers for Disease Control and Prevention diagnostic criteria for trichinosis require positive serology or muscle biopsy for Trichinella with 1 or more compatible clinical symptoms (eosinophilia, fever, myalgia, facial or periorbital edema). To declare a discrete outbreak, at least one person must have positive serology or muscle biopsy. Antibodies to Trichinella are detectable about 3 wk after infection. Severe muscle involvement results in elevated serum creatine phosphokinase and lactic dehydrogenase levels. Muscle biopsy is not usually necessary, but if needed, a sample should be obtained from a tender swollen muscle. A history of eating undercooked meat supports the diagnosis. The cysts may calcify and be visible by radiograph.
Recommended treatment of trichinosis is mebendazole (200-400 mg tid PO for 3 days then 400-500 mg tid PO for 10 days, for all ages) to eradicate the adult worms if a patient has ingested contaminated meat within the previous 1 wk. An alternative regimen is albendazole (400 mg bid PO for 8-14 days, for all ages). There is no consensus for treatment of muscle stage trichinosis. Systemic corticosteroids along with mebendazole may be used, although evidence for efficacy is anecdotal. Thiabendazole (25 mg/kg bid PO for 10 days) and mebendazole (200 mg bid PO for 10 days) are effective against muscle larvae; mebendazole may have been less active but thiabendazole was poorly tolerated.
Trichinella larvae can be killed by cooking meat (≥55°C) until there is no trace of pink fluid or flesh, or storage in a freezer (−15°C) for ≥3 wk. Freezing to kill larvae should only be applied to pork meat, as larvae in horse, wild boar, or game meat can remain viable even after 4 wk of freezing. Smoking, salting, and drying meat are unreliable methods of killing Trichinella. Strict adherence to pubic health measures including garbage feeding regulations, stringent rodent control, prevention of exposure of pigs and other livestock to animal carcasses, constructing barriers between livestock, wild animals, and domestic pets, and proper handling of wild animal carcasses by hunters can reduce infection with Trichinella. Current meat inspection for trichinosis is by direct digestion and visualization of encysted larvae in meat samples. Serologic testing does not have a role in meat inspection.
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