| Trichinosis | |
|---|---|
| Other names | Trichinellosis, trichiniasis |
 | |
| Trichinellalarvae in pressed bear meat, partially digested withpepsin. The classic coil shape is visible. | |
| Specialty | Infectious disease |
| Symptoms | Initially:diarrhea,abdominal pain,vomiting[1] Later:swelling of the face,inflammation of the whites of the eyes,fever,muscle pains,rash[1] |
| Complications | Inflammation of heart muscle,inflammation of the lungs[1] |
| Causes | Trichinella from eating undercooked meat[1] |
| Diagnostic method | Antibodies in the blood, larvae ontissue biopsy[1] |
| Differential diagnosis | Measles,dermatomyositis,gastroenteritis[2] |
| Prevention | Fully cooking meat[3] |
| Medication | Albendazole,mebendazole[4] |
| Prognosis | Low risk of death[5] |
| Frequency | ~10,000 cases a year[6] |
Trichinosis, also known astrichinellosis, is aparasitic disease caused byroundworms of theTrichinella genus.[1] During the initial infection, invasion of theintestines can result indiarrhea,abdominal pain, andvomiting.[1] Migration oflarvae to muscle, which occurs about a week after being infected, can causeswelling of the face,inflammation of the whites of the eyes,fever,muscle pains, and arash.[1] Minor infection may bewithout symptoms.[1] Complications may includeinflammation of heart muscle,central nervous system involvement, andinflammation of the lungs.[1]
Trichinosis is mainly spread when undercooked meat containingTrichinellacysts is eaten.[1] Wild meat is more likely to contain the parasite.[7][8] In North America this is most often bear, but infection can also occur from pork, boar, and dog meat.[9] Severalspecies ofTrichinella can cause disease, withT. spiralis being the most common.[1] After the infected meat has been eaten, the larvae are released from their cysts in the stomach.[1] They then invade the wall of thesmall intestine, where they develop into adult worms.[1] After one week, the females release new larvae that migrate tovoluntarily controlled muscles, where they form cysts.[1] The diagnosis is usually based on symptoms and confirmed by finding specificantibodies in the blood, or larvae ontissue biopsy.[1]
The best way to prevent trichinosis is to fully cook meat.[3] Afood thermometer can verify that the temperature inside the meat is high enough.[3] Infection is typically treated with antiparasitic medication such asalbendazole ormebendazole.[4] Rapid treatment may kill adult worms and thereby stop further worsening of symptoms.[4] Both medications are considered safe but have been associated with side effects such asbone marrow suppression.[4] Their use during pregnancy or in children under the age of 2 years is poorly studied but appears to be safe.[4] Treatment with steroids is sometimes also required in severe cases.[4] Without treatment, symptoms typically resolve within three months.[5]
Worldwide, about 10,000 trichinosis infections occur a year.[6] At least 55 countries including the United States, China, Argentina, and Russia have had recently documented cases.[5] While trichinosis does occur in the tropics, it is actually less common there.[5] Rates of trichinosis in the United States have decreased from about 400 cases per year in the 1940s to 20 or fewer per year in the 2000s.[6][10] The risk of death from infection is low.[5]
The great majority of trichinosis infections have either minor or no symptoms and no complications.[11] The two main phases for the infection are enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species ofTrichinella, the quantity of encysted larvae ingested, age, sex, and host immunity.[12]
A large burden of adult worms in the intestines promotes symptoms such asnausea,heartburn,dyspepsia, anddiarrhea from two to seven days after infection, while small worm burdens generally are asymptomatic.Eosinophilia presents early and increases rapidly.[13]
The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the body's inflammatory response results inedema, muscle pain, fever, and weakness. A classic sign of trichinosis isperiorbital edema, swelling around the eyes, which may be caused byvasculitis.Splinter hemorrhage in the nails is also a common symptom.[14]
They may very rarely cause enough damage to produce serious neurological deficits (such asataxia orrespiratory paralysis) from worms entering thecentral nervous system (CNS), which is compromised by trichinosis in 10–24% of reported cases ofcerebral venous sinus thrombosis, a very rare form of stroke (three or four cases per million annual incidence in adults).[15] Trichinosis can be fatal depending on the severity of the infection; death can occur 4–6 weeks after the infection,[16] and is usually caused bymyocarditis,encephalitis, orpneumonia.[17]
The classical agent isT. spiralis (found worldwide in many carnivorous and omnivorous animals, both domestic andsylvatic (wild),[citation needed] but seven primarily sylvatic species ofTrichinella also are now recognized:
The typical lifecycle forT. spiralis involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcinecarrion or arat (sylvatic cycle). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, thecysts from infected undercooked meat are acted on bypepsin andhydrochloric acid, which help release the larvae from the cysts into thestomach.[12] The larvae then migrate to thesmall intestine, and burrow into theintestinal mucosa, where they molt four times before becoming adults.[12]
30 to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae.[12] Adult worms can only reproduce for a limited time because theimmune system eventually expels them from the small intestine.[12] The larvae then use their piercing mouthpart, called the "stylet", to pass through theintestinal mucosa and enter thelymphatic vessels, and then enter thebloodstream.[22]
The larvae travel bycapillaries to various organs, such as theretina,myocardium, orlymph nodes; however, only larvae that migrate toskeletal muscle cells survive andencyst.[16] The larval host cell becomes anurse 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 theparasite does not lay eggs, nor can it survive long outside a host.[5][23]
Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing.[citation needed]
An epidemiological investigation can be done to determine a patient's 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.[16]
Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness,splinter hemorrhage, nonspecificgastroenteritis, and muscle pain.[16] The case definition for trichinosis at the European Center for Disease Control states, "at least three of the following six:fever, muscle soreness and pain,gastrointestinal symptoms, facialedema,eosinophilia, and subconjunctival, subungual, and retinalhemorrhages."[16]
Blood tests andmicroscopy can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia,creatine phosphokinase activity, and various immunoassays such asELISA for larval antigens.[16]
In some cases, muscle biopsies are performed, where "0.2 to 0.5 grams of human or animal skeletal muscle tissue is collected and examined for Trichinella larvae via artificial digestion or histological analysis."[24]
Laws and rules for food producers may improve food safety for consumers, such as the rules established by theEuropean Commission for inspections, rodent control, and improved hygiene.[16] A similar protocol exists in the United States, in theUSDA guidelines for farms and slaughterhouse responsibilities in inspecting pork.[25]
Public education about the dangers of consuming raw and undercooked meat, especially pork, may reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of wild game, including bears. As such, many states, such as New York, require the completion of a course in such matters before a hunting license can be obtained.[26]
Testing methods are available for both individual carcasses and monitoring of the herds.[27] Artificial digestion method is usually used for the testing of individual carcasses, while the testing for specific antibodies is usually used for herd monitoring.[27]
Larvae may be killed by the heating orirradiation of raw meat. Freezing is normally only effective forT. spiralis, since other species, such asT. nativa, are freeze-resistant and can survive long-term freezing.[16]
Pork can be safely cooked to a slightly lower temperature, provided that the internal meat temperature is at least as hot for at least as long as listed in theUSDA table below.[30] Nonetheless, allowing amargin of error for variation in internal temperature within a particular cut of pork, which may have bones that affect temperature uniformity, is prudent. In addition, kitchen thermometers have measurement errors that must be considered. Pork may be cooked for significantly longer and at a higher uniform internal temperature than listed below to be safe.[31]
| Internal Temperature | Internal Temperature | Minimum Time |
|---|---|---|
| (°F) | (°C) | (minutes) |
| 120 | 49 | 1260 |
| 122 | 50.0 | 570 |
| 124 | 51.1 | 270 |
| 126 | 52.2 | 120 |
| 128 | 53.4 | 60 |
| 130 | 54.5 | 30 |
| 132 | 55.6 | 15 |
| 134 | 56.7 | 6 |
| 136 | 57.8 | 3 |
| 138 | 58.9 | 2 |
| 140 | 60.0 | 1 |
| 142 | 61.1 | 1 |
| 144 | 62.2 | Instant |
Unsafe and unreliable methods of cooking meat include the use of microwave ovens, curing, drying, and smoking, as these methods are difficult to standardize and control.[16]
Incidence of infection can be reduced by:[citation needed]
The USCenters for Disease Control and Prevention makes the following recommendation: "Curing (salting), drying, smoking, or microwaving meat does not consistently kill infective worms."[32]However, under controlled commercial food processing conditions, some of these methods are considered effective by the USDA.[33]
The USDA Animal and Plant Health Inspection Service (APHIS) is responsible for the regulations concerning the importation of swine from foreign countries. The Foreign Origin Meat and Meat Products, Swine section covers swine meat (cooked, cured, dried, and fresh). APHIS developed the National Trichinae Certification Program; this is a voluntary "preharvest" program for U.S. swine producers "that will provide documentation of swine management practices" to reduce the incidence ofTrichinella in swine.[34] The CDC reports 0.013% of U.S. swine are infected withTrichinella.[34]
As with most diseases, early treatment is better and decreases the risk of developing the disease. If larvae do encyst in skeletal muscle cells, they can remain infectious for months to years.[16]
Early administration ofanthelmintics, such asmebendazole oralbendazole,[35] decreases the likelihood of larval encystation, particularly if given within three days of infection.[14] However, most cases are diagnosed after this time.[16] In humans, mebendazole (200–400 mg three times a day for three days) or albendazole (400 mg twice a day for 8–14 days) is given to treat trichinosis.[36] These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age.[12]
Medical references from the 1940s described no specific treatment for trichinosis at the time, but intravenous injection of calcium salts was found to be useful in managing symptoms related to severe toxemia from the infection.[37]
After infection,steroids, such asprednisone, may be used to relieve muscle pain associated with larval migration.[citation needed]
Researchers trying to develop a vaccine forTrichinella have tried using either "larval extracts, excretory-secretory antigen, DNA, or recombinant antigen protein."[38] Currently, no marketable vaccine is available for trichinosis, but experimental mouse studies have suggested possibilities.
About 11 million humans are infected withTrichinella;T. spiralis is the species responsible for most of these infections.[42] Infection was once very common, but this disease is now rare in thedeveloped world, but two known outbreaks occurred in 2015. In the first outbreak, around 40 people were infected in Liguria, Italy, during a New Year's Eve celebration.[43][44] The second outbreak in France was associated with pork sausages fromCorsica, which were eaten raw, affecting 14 people in total.[45]The incidence of trichinosis in the U.S. has decreased dramatically in the past century from an average of 400 cases per year mid-20th century down to an annual average of 20 cases per year (2008–10).[10] The number of cases has decreased because of legislation prohibiting the feeding of raw meat garbage to hogs, increased commercial and home freezing of pork, and the public awareness of the danger of eating raw or undercooked pork products.[46]
China reports around 10,000 cases every year and is the country with the highest number of cases.[16][dubious –discuss] In China, between 1964 and 1998, over 20,000 people became infected with trichinosis, and more than 200 people died.[38]
Trichinosis is common in developing countries where meat fed to pigs is raw or undercooked, but infections also arise in developed countries in Europe where raw or undercooked pork, wild boar, and horse meat may be consumed as delicacies.[16]
In thedeveloping world, most infections are associated with undercooked pork. For example, inThailand, between 200 and 600 cases are reported annually around theThai New Year. This is mostly attributable to a particular delicacy,larb, which calls for undercooked pork as part of the recipe.[citation needed]
In parts of Eastern Europe, theWorld Health Organization reports, some swine herds have trichinosis infection rates above 50%, with correspondingly large numbers of human infections.[47]
Historically, pork products were thought to have the most risk of infecting humans withT. spiralis. However, a trichinosis surveillance conducted between 1997 and 2001 showed a higher percentage of cases caused by consumption of wild game (the sylvatic transmission cycle). This is thought to be due to the Federal Swine Health Protection Act (Public Law 96-468) that was passed by Congress in 1980. Before this act, swine were fed garbage that could potentially be infected by T. spiralis.[citation needed] This act was put in place to prevent trichinella-contaminated food from being given to swine. Additionally, other requirements were put in place, such as rodent control, limiting commercial swine contact with wildlife, maintaining good hygiene, and removing dead pigs from pens immediately.[48]
Between 2002 and 2007, 11 trichinosis cases were reported to the CDC each year on average in the United States, and 2008–10 averaged 20 cases per year;[10] these were mostly the result of consuming undercooked game (sylvatic transmission) or home-reared pigs (domestic transmission).[citation needed]
Thekashrut andhalal dietary laws ofJudaism andIslam prohibit eating pork. In the 19th century, when the association between trichinosis and undercooked pork was first established, this association was suggested to be the reason for the prohibition, reminiscent of the earlier opinion of medievalJewish philosopherMaimonides that food forbidden by Jewish law was "unwholesome". This theory was controversial and eventually fell out of favor.[49]
The disappearance of the pathogen from domestic pigs has led to a relaxation of legislation and control efforts by veterinary public health systems. Trichinosis has lately been thought of as a re-emergingzoonosis, supplemented by the increased distribution of meat products, political changes, a changing climate, and increasingsylvatic transmission.[50]
Major sociopolitical changes can produce conditions that favor the resurgence ofTrichinella infections in swine and, consequently, in humans. For instance, "the overthrow of the social and political structures in the 1990s" in Romania led to an increase in the incidence rate of trichinosis.[51]
As early as 1835, trichinosis was known to have been caused by a parasite, but the mechanism of infection was unclear at the time. A decade later,American scientistJoseph Leidy pinpointed undercooked meat as the primary vector for the parasite, and two decades afterward, this hypothesis was fully accepted by the scientific community.[52]
The circumstances surrounding the first observation and identification ofT. spiralis are controversial, due to a lack of records. In 1835,James Paget, a first-year medical student, first observed the larval form ofT. spiralis, while witnessing an autopsy at St. Bartholomew’s Hospital in London. Paget took a special interest in the presentation of muscle with white flecks, described as a "sandy diaphragm". Although Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor,Richard Owen, who is now credited for the discovery of theT. spiralis larval form.[22][53]
A series of experiments conducted between 1850 and 1870 by the German researchersRudolf Virchow,Rudolf Leuckart, andFriedrich Albert von Zenker, which involved feeding infected meat to a dog and performing the subsequent necropsy, led to the discovery of the lifecycle ofTrichinella. Through these experiments, Virchow was able to describe the development and infectivity ofT. spiralis.[54]
TheInternational Commission on Trichinellosis (ICT) was formed in Budapest in 1958. Its mission is to exchange information on the epidemiology, biology, pathophysiology, immunology, and clinical aspects of trichinosis in humans and animals. Prevention is a primary goal. Since the creation of the ICT, its members (more than 110 from 46 countries) have regularly gathered and worked together during meetings held every four years: theInternational Conference on Trichinellosis.[citation needed]
During 2008–2010, 20 cases were reported to CDC each year on average.
During 2002–2007, 11 cases were reported to CDC each year on average.
