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Two to 3 days after a family picnic and hog roast at which undercooked pork had been served, 2 members of a midwestern family developed malaise, nausea, vomiting, abdominal pain, and diarrhea. Fearing food poisoning or infection, they sought medical assistance. Physical and laboratory findings included mild fever, abdominal tenderness, and mild leukocytosis. Fecal specimens were submitted for bacterial culture, and the patients were given broad-spectrum antibiotics orally. The patients' intestinal symptoms improved over the next week, and no specific cause of their illness was identified.

About 3 weeks after initial evaluation, the patients felt weak, feverish, had headaches, difficulty sleeping, and muscular aches and pains. Physical examination revealed fever, myalgia, periorbital and facial edema, and hemorrhages in the bulbar conjunctiva and under the fingernails. Hematologic and serum biochemical evaluations indicated leukocytosis, eosinophilia (35% and 42%), and high serum creatine kinase activity. On the basis of these findings, especially the periorbital edema and eosinophilia, and history of eating undercooked pork, trichinellosis was suspected. Serum samples were sent to the Centers for Disease Control, Atlanta, GA, and were positive for antibodies against Trichinella sp, confirming the diagnosis of trichinellosis. After treatment with mebendazole, prednisolone, and aspirin, their symptoms and eosinophilia gradually subsided, although slight eosinophilia remained for 4 to 6 months.

After trichinellosis was diagnosed, the physician contacted the State Board of Health, which initiated an investigation of the problem. They found that 2 hogs had been purchased for the picnic from a local farmer who had a small hog operation, and that one hog had not been completely cooked, mainly in the more central portions of the carcass and hams. Specimens of leftover pork obtained from a person's freezer contained 200 to 300 Trichinella larvae/g of muscle, as determined by artificial digestion methods. Epidemiologists from the state health department traced 6 other cases of clinical trichinellosis, and another dozen subclinical cases, to ingestion of pork at the picnic.

After being contacted by the State Board of Health, the State Veterinarian's Office contacted the local veterinarian. The local veterinarian indicated that the farmer's hogs generally were in good health, except for occasional routine infections. The hogs sold for the picnic did not have any visible signs of disease.

The farmer was shocked and upset when made aware of the problem. He was concerned for the people who had contracted the disease from his pigs, for his own health and that of his family, and about possible legal actions by the people involved or by the state. Recently, he had marketed 2 dozen hogs through a USDA-inspected meat-packing facility; however, because there is no federal pork inspection program for trichinellosis, nothing was ever brought to his attention concerning this problem. Although state regulations did not prevent him from marketing the rest of his hogs however he wanted, the farmer voluntarily agreed to sell his hogs to a facility where they would be made into ready-to-eat products, because the processing involved would kill any trichinellae present.

The farmer had a number of questions concerning the disease, which he posed to the local veterinarian.

Q:What is trichinellosis?

A: Trichinellosis (also known as trichinosis) is a disease caused by parasitic worms (nematodes) in the genus Trichinella. A ubiquitous group of parasites, trichinellae have been reported from more than a hundred species of mammals (and a few species of birds), and have worldwide distribution.(1-4) The genus presently contains at least 5 closely related species, with different major host reservoirs and geographic distribution.(4) The most common cause of clinical trichinellosis in people is T spiralis acquired from domestic swine, although T britovi, T nelsoni, and T nativa from wild game, also are frequent causes of human disease episodes.(4)

Q: How is Trichinella transmitted?

A: Trichinella is transmitted through carnivorism (ie, by the ingestion of meat containing infective larvae). In animals, this occurs mainly through carrion-eating, cannibalism, and to some extent by predation.(2,4) Infected meat containing encysted larvae is ingested, and in about 2 days, the larvae develop to adult worms in the small intestine of the host. Beginning at about 5 days after infection, female worms shed hundreds of newborn larvae, which penetrate the intestine and migrate throughout the body via the circulatory system.(5) Although they invade various tissues, the larvae encyst only in striated skeletal muscle cells, where they become "mature" infective larvae in about 3 weeks.(5) Adult worms subsequently die and are shed from the intestine. The intestinal phase of infection may be prolonged in people, compared with some other animals, such as rodents.(4) This cycle is repeated as infected hosts containing muscle larvae are eaten by other hosts.

Q: How does Trichinella cause human disease?

A: The severity and clinical course of the disease are related to the intensity of infection (ie, the number of larvae ingested), the species of Trichinella involved, and host factors such as age, sex, ethnic group, and immune status.(4,6) Although most cases of trichinellosis are probably subclinical and related to low infection intensity, mild, moderate, and severe cases also occur in which clinical manifestations are of increasing severity and, in some cases, life-threatening.(6) Clinical trichinellosis is usually classified into an early abdominal syndrome and a later general trichinellosis syndrome.(4,6)

The abdominal syndrome, which begins 2 to 7 days after infection and may last many weeks, is related to trichinous enteritis, caused by developing and mature worms parasitizing the small intestine and by penetration of newborn larvae.(6) Patients may exhibit malaise, nausea, vomiting, anorexia, mild fever, abdominal pain and/or diarrhea; the latter may be persistent.(6) The general trichinellosis syndrome, which appears weeks to months after the abdominal syndrome, is related to systemic allergic reactions and inflammation caused by larval invasion of the skeletal muscles and other tissues. Patients develop allergic vasculitis, which is manifested as vascular leakage and hemorrhage, and is most visible as periorbital edema and conjunctival and subungual (nailbed) hemorrhages.(6) Myalgia and muscular weakness are common and are related to skeletal muscle invasion, inflammation, and related damage. Persistent, often marked eosinophilia is a characteristic sign of human trichinellosis, and patients may have leukocytosis and increased total IgE, creatine kinase, and lactate dehydrogenase values.(4,6) In severe cases of trichinellosis, patients may also develop immune-mediated myocarditis, pneumonitis, encephalitis, and other more serious complications.(6)

Q: How common is trichinellosis as a human disease in the United States?

A: Compared with other countries, particularly those in Europe, the United States continues to have a high rate of human trichinellosis.(4) Human trichinellosis has been a reportable disease in the United States since 1965.(7) Although many thousands of people may be exposed to infection in the United States each year (150,000 to 300,000 in 1970),(1) most exposures result in low-level, subclinical infections that are not specifically diagnosed or reported.(4,7) In recent years, the incidence of human infection has been decreasing, and the average annual number of reported cases has been 57, with only 3 fatalities reported during the period 1982-86.(7) Human infection is more common in the Northeast and especially in Alaska.(6) Most infections in the United States are outbreak-associated and tend to involve ethnic groups that prefer lightly cooked or raw pork or, in Alaska, wild game.(7)

Q: What are the main sources of human infection with Trichinella?

A: The primary source of human infection with Trichinella (spiralis) in the United States is infected pork. Pork products are incriminated in over two-thirds of reported cases and disease episodes, and are most often obtained through commercial outlets.(7) Pork dishes that are eaten lightly processed, partially cooked, or raw (eg, pork sausage and spiced pork) have been incriminated most often in reported human infections.(4,7) Since about 1980, there has been an annual decrease in the number of human cases of trichinellosis acquired from commercial pork products in the United States.(7) This is probably related to increased prevention and control activities at the national and state levels, as well as heightened awareness of this problem within the pork industry.(7) Home-raised or locally obtained swine continue to be an important source of human infection and have been incriminated in many episodes of trichinellosis. Interestingly, a number of large episodes have occurred in France and Italy that were associated with ingestion of horsemeat; most of these have involved infection with T britovi.(4)

Another important source of human infection is consumption of wild animals, especially bear, wild boar, and other carnivorous game.(1,2,7,8) At least 40 species of wild mammals have been found to be infected with Trichinella spp in the United States.(2,9) Most sylvatic species of Trichinella have moderate to high infectivity for humans, although their clinical manifestations differ somewhat from those caused by T spiralis.(4) In Alaska and other arctic regions, human cases involve T nativa, a freeze-resistant species that occurs in a wide variety of wild carnivores.(4,7,9) Focal epidemics of human trichinellosis attributable to T nativa have been linked most often to the consumption of bear and walrus meat.(4,7)

Q: What is the extent of the problem in the United States?

A: Traditionally in the United States, garbage-fed hogs were regarded as the primary source of human infection.(4) The prevalence of trichinellosis in American swine has decreased since the turn of the century, especially in garbage-fed hogs since 1952, when it became unlawful to feed uncooked garbage to swine.(1,4) In 1980, the Federal Swine Health Protection Act was passed, which further prohibited the feeding of garbage to swine unless it was first heat-treated to kill pathogens, including T spiralis.(7) Prevalence in slaughter hogs was estimated to be 0.95% in the 1930s, decreasing to 0.63% in 1952, and to 0.13% in 1970.(1) Despite this seemingly low prevalence in American swine, in 1974 to 1975, 0.1% translated into 105,000 infected carcasses being processed annually by the packing industry, resulting in about 40 million potentially infective pork meals for US consumers each year.(1) Today the prevalence in swine is less than 0.1% (possibly as low as 0.05%), indicating that far fewer Trichinella-infected swine are being processed annually. In some regions, however (eg, Middle Atlantic and New England states), the prevalence of trichinellosis in swine (0.58% and 0.73%, respectively) has traditionally been higher than the general prevalence in the United States.(10,11) It is commonly believed that this reflects the greater reliance on nonconfinement garbage feeding by eastern hog producers, in contrast to confinement grain-feeding practices in the midwestern "hog belt".(4)

Sylvatic trichinellosis is a common and widespread problem in the United States and is a potential source of human and porcine infection.(1,2,4,7,8,9,12) The true sylvatic species of Trichinella are poorly infective for swine; however, T spiralis from swine is highly infective for many wild animals.(4,13,14) Similar to sylvatic species of Trichinella, T spiralis could be maintained and propagated in the wild in a carrion-scavenger-cannibalism transmission cycle.(2,4) Such a cycle could be established in the vicinity of an infected swine herd, after transmission of T spiralis from discarded swine carcasses or rats to wild carnivores in the area.(13-15) Wild carnivores carrying T spiralis could then maintain and spread the parasite and serve as a source of infection for other swine, rats, and domestic carnivores.

Q: How do swine become infected with Trichinella?

A: Similar to other animals, swine become infected with Trichinella by ingesting infected meat containing larvae. Historically, meat scraps in garbage have been an important source of swine infection.(4) Where garbage cooking regulations are not properly enforced or adhered to, especially on small or poorly managed farms, meat scraps still pose a threat for introduction of this parasite to swine.(1,3,4,8)

Swine may also become infected with Trichinella by ingesting infected farm rats or wild animals carrying T spiralis. Rats are highly susceptible to T spiralis and may maintain the infection through cannibalism.(4,16,17) Because swine will readily eat rats, thereby becoming infected,(2,18) farm rats may represent an important source of this infection, especially on particular farms. Ingestion of wild animals infected with T spiralis also could introduce trichinellosis into a herd of swine.(1-4,8,13-15) Swine on a complete grain ration readily consumed infected coyote carcasses and became infected with T spiralis (KR Kazacos, unpublished data). Therefore, one should not intentionally feed wildlife carcasses to swine or otherwise let them have access to dead animals. (The farmer admitted that raccoon, fox, and coyote carcasses occasionally were fed to the hogs during the hunting/trapping season; on advice of his veterinarian, he has since stopped this practice).

Q: How is Trichinella maintained in swine herds?

A: Once introduced into a swine herd, the parasite may be propagated and maintained in several ways. Pig-rat-pig and rat-rat transmission cycles would serve to maintain and even amplify the infection in the farm environment.(2-4,16-18) Although less often considered, cannibalism among swine can be an important mode of on-farm transmission that can lead to rapid and extensive spread of T spiralis in a herd.(3,4,19) Cannibalism would be more likely on small, marginal farms with poor hog management practices and inadequate nutrition. Therefore, it is important that dead swine be promptly removed, not left in hog lots to be eaten by other swine. (The farmer admitted that cannibalism had indeed occurred in his herd, when he was unable to promptly remove dead pigs from the lot; on advice of his veterinarian, dead pigs are now promptly removed and properly disposed of). Another possible mode of transmission in a herd is via tail biting, a behavioral vice seen in swine that are under stress, such as from overcrowding or poor nutrition.(2)

Q: How can one tell that swine are infected with Trichinella?

A: Swine and other animals infected with Trichinella usually have subclinical infections and/or do not show obvious clinical signs of disease.(1) Even in very heavy infections, clinical signs are nonspecific and trichinellosis would not usually be considered.(1) Therefore, as in this case, infected pigs without other problems would appear healthy and act normally. Trichinellosis can only be detected in swine and other animals by either demonstrating or recovering larvae in/from the skeletal muscles or by detecting antibodies to Trichinella in the serum.(1,4,20-23) Larvae are recovered, using artificial digestion methods, performed on muscle specimens obtained after slaughter(1,20); such methods have been an integral part of successful control programs in Europe. Antibodies to Trichinella spp are detected, using various serologic tests, such as indirect immunofluorescence and ELISA.(4,21-23) These procedures, which compare favorably to direct detection methods, can be performed by various state and federal veterinary and public health laboratories. Serologic methods continue to be refined for possible use in the pork industry, and an ELISA is available commercially.(23)

Q: How can I prevent Trichinella infection in my family?

A: Trichinellosis can be contracted only by eating infected meat containing viable Trichinella larvae. Therefore, the most important preventive measure is to assume that pork and wild game may be infected and to prepare the meat accordingly. The USDA recommends that pork should be cooked to a uniform temperature of 140 F (60 C) throughout for at least 1 minute (USDA Food Safety Inspection Service regulations, 9CFR ChIII, 318.10).(4) However, consumers preparing pork at home are encouraged to cook to a temperature of 160 F (71 C), which ensures that all larvae present will be killed. Microwave cooking, which may result in "cold spots" in the meat, is considered less effective for killing of Trichinella larvae unless care is taken to ensure uniform heating.(3,20)

Trichinella larvae also can be killed by freezing, the temperature and duration required dependent on the thickness of the meat. The USDA recommends that meat less than 6 inches thick be frozen to 5 F (- 15 C) for 20 days, - 10 F (- 23 C) for 10 days, or - 22 F (- 30 C) for 6 days.(3,20) Generally, this is applicable to all meat, except meat from far northern regions (ie, Alaska or the Arctic), where a species of Trichinella (T nativa) exists that is resistant to freezing, but not to cooking.(3,4,8) Recently, the USDA and Food and Drug Administration approved gamma irradiation of pork for the control of trichinellosis and other food-borne pathogens.(4) Once adopted by the packing industry (and accepted by consumers), large-scale irradiation of pork may prove very important for safeguarding US consumers from infection with this parasite.

Q: If my swine are infected with Trichinella, how can I get rid of the problem?

A: Infected swine should be processed or disposed of properly, to prevent human infection as well as the spread of trichinellosis to other animals. Swine that are known to be infected should not be sold through channels where they will enter the human food chain as fresh pork products.

Infected swine should be sold only to a facility that will process them in such a way that the Trichinella larvae will be killed, namely a facility that prepares processed, ready-to-eat pork products.(3,20) Carcasses of infected swine should not be left in hog lots or otherwise discarded or disposed of so that other swine or wild animals will have access to them.(3,4) This would only perpetuate and spread the infection, and could lead to reintroduction of the parasite into the herd.

Q: What is the impact of trichinellosis on the pork industry?

A: Economically, the stigma of human disease acquired from pork has been detrimental to the pork industry. The main impact has been on consumer confidence in the safety of pork products, associated problems with pork preparation (such as overcooking), and loss of foreign markets. If trichinellosis could be eliminated from American swine, the industry would benefit by up to several hundred million dollars per year through increased domestic consumption and export of pork and by elimination of costly pork certification procedures.

Q: What is being done to control trichinellosis in the United States?

A: Several approaches are being pursued. There continues to be no federal pork inspection program in the United States, although inspection is mandatory for the export of horsemeat.(4) Therefore, emphasis has been placed on educating the consumer concerning the proper handling and cooking of fresh pork and wild game. Also important is continuing regulation of the commercial preparation of ready-to-eat pork products, as well as regulation of garbage feeding to swine.(3,20,24) Direct Trichinella-detection methods, such as pooled digestion, have been deemed too expensive for general implementation by the US meat packing industry, based on the very large number of animals processed in the US as well as the low prevalence of the parasite in swine.(3,24) Some packers, however, are examining pork for Trichinella and certifying it as "trichina-free" for sale in the United States and elsewhere at an increased cost. Preslaughter serologic diagnostic methods, such as the ELISA, may eventually prove more amenable for use by the meat packing industry. Certain states, such as Illinois, have passed laws to control trichinellosis in swine, enforcing state garbage-feeding regulations as well as quarantining, testing, and depopulating infected herds.(7) Commercial irradiation of pork will be an important step forward in the prevention and control of human trichinellosis in the United States.(3,4,20)

Discussion

Owing to its prevalence and maintenance in wild animals, trichinellosis may never be eliminated from the United States or wherever it is a problem. However, because most human infections are acquired from pork products, the human disease problem can be decreased by controlling trichinellosis in swine. With a decrease in trichinellosis in commercial swine in the United States in recent years, there has been a corresponding decrease in the incidence of human infections. As the prevalence of trichinellosis in commercial swine decreases, greater attention will have to be paid to small producers, who are less likely to use modern hog management practices and who would not be subject to normal enforcement programs.(4,7) Infected swine from small, marginal operations could still cause local episodes of human disease, could enter the general food distribution system, and could serve as a source of infection for other swine herds and for wildlife.

Practicing veterinarians can assist state and federal authorities and the swine industry in these control efforts by several means, most important of which is understanding the problem and making correct recommendations regarding trichinellosis. This would include stressing to swine producers, particularly small farmers, the potential problems associated with feeding food waste and/or wildlife carcasses to swine, the problem with swine cannibalism, and the benefits of controlling commensal rat populations. In addition, they can educate clients and other consumers about how to avoid trichinellosis from locally obtained or home-butchered swine and wild game. Veterinarians are in an important position to use their knowledge to help decrease the threat of this zoonotic disease.

References

1. Zimmermann WJ. Trichinosis. In: Libby JA, ed. Meat hygiene. Philadelphia: Lea & Febiger, 1975;187-204.

2. Campbell WC. Epidemiology I, Modes of transmission. In: Campbell WC, ed. Trichinella and trichinosis. New York: Plenum Press, 1983;425-444.

3. Murrell KD. Strategies for the control of human trichinosis transmitted by pork. Food Technol 1985;39:65-68, 110-111.

4. Murrell KD, Bruschi F. Clinical trichinellosis. In: Sun T, ed. Progress in clinical parasitology. vol 4. Boca Raton, FL: CRC Press, 1994;117-199.

5. Despommier DD. Biology. In: Campbell WC, ed. Trichinella and trichinosis. New York: Plenum Press, 1983;75-151.

6. Pawlowski ZS. Clinical aspects in man. In: Campbell WC, ed. Trichinella and trichinosis. New York: Plenum Press, 1983;367-401.

7. Bailey TM, Schantz PM. Trends in the incidence and transmission patterns of trichinosis in humans in the United States: comparison of the periods 1975-1981 and 1982-1986. Rev Infect Dis 1990;12:5-11.

8. Murrell KD. Preslaughter control of trichiniasis. Food Technol 1983;37:87-90.

9. Zimmermann WJ. The epizootiology of trichiniasis in wildlife. J Wildl Dis 1970;6:329-334.

10. Schad GA, Kelly M, Leiby DA, et al. Swine trichinosis in mid-atlantic slaughterhouses: possible relationship to hog marketing systems. Prev Vet Med 1985;3:391-399.

11. Schad GA, Leiby DA, Duffy CH, et al. Swine trichinosis in New England slaughterhouses. Am J Vet Res 1985;46:2008-2010.

12. Schad GA, Leiby DA, Murrell KD. Distribution, prevalence and intensity of Trichinella spiralis infection in furbearing mammals of Pennsylvania. J Parasitol 1984;70:372-377.

13. Dame JB, Murrell KD, Worley DA, et al. Trichinella spiralis: genetic evidence for synanthropic subspecies in sylvatic hosts. Exp Parasitol 1987;64:195-203.

14. Murrell KD, Stringfellow F, Darne JB, et al. Trichinella spiralis in an agricultural ecosystem. II. Evidence for natural transmission of Trichinella spiralis from domestic swine to wildlife. J Parasitol 1987;73:103-109.

15. Minchella DJ, Branstetter BA, Kazacos KR. Molecular characterization of sylvatic isolates of Trichinella spiralis. J Parasitol 1989;75:388-392.

16. Schad GA, Duffy CH, Leiby DA, et al. Trichinella spiralis in an agricultural ecosystem: transmission under natural and experimentally modified on-farm conditions. J Parasitol 1987;73:95-102.

17. Leiby DA, Schad GA, Duffy CH, et al. Trichinella spiralis in an agricultural ecosystem: transmission in the rat population. J Parasitol 1990;70:360-364.

18. Murrell KD, Gamble HR, Schad GA. Experimental transmission of Trichinella spiralis to swine by infected rats. Proc Helminthol Soc Wash 1984;51:66-68.

19. Hanbury RD, Doby PB, Miller HO, et al. Trichinosis in a herd of swine: cannibalism as a major mode of transmission. J Am Vet Med Assoc 1986;188:1155-1159.

20. Kotula AW. Postslaughter control of Trichinella spiralis. Food Technol 1983;37:91-94.

21. Ruitenberg EJ, van Knapen F, Elgersma A. Control III, Surveillance in swine by immunodiagnostic methods. In: Campbell WC, ed. Trichinella and trichinosis. New York: Plenum Press, 1983;529-550.

22. Despommier DD. Trichinellosis. In: Walls KW, Schantz PM, eds. Immunodiagnosis of parasitic diseases, volume 1, helminthic diseases. New York: Academic Press, 1986;163-181.

23. Gamble HR, Murrell KD. Swine trichinellosis: diagnosis and control. Agri-Pract 1987;8:12-15.

24. Leighty JC. Regulatory action to control Trichinella spiralis. Food Technol 1983;37:95-97.

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