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A 9-year-old boy from Lexington, Ky, was taken to his pediatrician because of discomfort in the right side of his abdomen and an intermittent cough. These symptoms had been evident for approximately 2 months, but had become bothersome 2 weeks before treatment was sought. The child and his mother denied any other associated symptoms, specifically fever, sweating, hemoptysis, vomiting, or diarrhea. The boy had been healthy otherwise. His exposure to animals was limited to the family pet, a Labrador Retriever. Three years before symptoms began, the boy's family had spent 3 months in Italy, visiting grandparents.

Physical examination revealed mild to moderate tenderness in the upper right abdominal quadrant and minimally decreased breath sounds at the right lung base. Results of urinalysis, CBC, and analysis of electrolyte, creatinine, and bilirubin concentrations were all normal. Hepatic transaminase activities were slightly higher than normal. Thoracic radiography revealed a well-circumscribed, 4-cm cystic lesion in the lower lobe of the right lung. Computerized tomography of the abdomen revealed a 5-cm cyst in the right lobe of the liver. Small cysts were visible within the lesion.

The boy's physician suspected cystic hydatid disease, and a serum sample was sent to the Centers for Disease Control to test for antibodies against Echinococcus granulosus. Results were reported as positive, and surgical consultation was requested. The boy underwent 2 surgical procedures to remove the pulmonary and the hepatic cysts. Six months after the second procedure, the boy was well, without recurrence of symptoms. The surgeon told the parents that the boy had probably acquired the infection from the family dog. The family veterinarian answered the following questions from the boy's parents.

Q: What is echinococcosis?

A: Echinococcosis, or hydatid disease, is infection with the larval (cystic) stage of tapeworms belonging to the genus Echinococcus. Cysts most commonly develop in the liver, but can also be found in the lungs, kidney, spleen, nervous tissue, or bone.

Q: Is there more than one type of hydatid disease?

A: Three species of Echinococcus are known to cause disease in human beings: E granulosus, E multilocularis, and E vogeli. Pathogenesis and disease manifestations vary according to the infecting species. Echinococcus granulosus, the most common and widespread species, causes cystic hydatid disease. A hydatid cyst enlarges slowly and is generally well tolerated by an infected person until it is large enough to cause a notable mass effect. Signs and symptoms depend on cyst size and location. Ruptured or leaking cysts, however, may result in severe anaphylactoid reactions and they may release protoscolices capable of producing secondary cysts. The most common definitive host for E granulosus is the domestic dog, but other hosts are the dingo, wolf, coyote, and jackal. With the exception of the African lion, most feline species (including the domestic cat) are not suitable hosts for E granulosus. Sheep appear to be the most common intermediate hosts in most areas of the world, but in some regions, other domestic ungulates, including goats, cattle, swine, buffalo, horses, and camels, serve as hosts.^1,2 Local populations of E granulosus may vary in morphologic and biologic features (such as infectivity to various species of final intermediate hosts, transmission patterns, and pathogenicity to human beings); the variations between strains may cause local differences in the epidemiology and clinical characteristics of the disease.³ Echinococcus granulosus has been found on all continents except Antarctica. Within areas of endemic echinococcosis, illness is most common among people who rear livestock with the use of dogs.

Echinococcus multilocularis causes alveolar hydatid disease, a highly invasive and destructive form of echinococcosis that causes solid, tumorlike masses and is commonly confused with hepatic cirrhosis or carcinoma. Unlike E granulosis, E multilocularis is largely restricted to wild animal hosts, including foxes (definitive hosts) and rodents (intermediate hosts). Domestic dogs and cats can become a source of human infection if allowed to feed on infected rodents such as voles. Echinococcus multilocularis is less widely distributed than E granulosus and is more common in northern latitudes. Hunters, trappers, and Alaskan natives of certain villages are at risk.¹

Echinococcus vogeli produces polycystic hydatid disease, which has characteristics of cystic and alveolar disease. Polycystic hydatid disease has been identified in Central and South America, where E vogeli exists in cycles that involve bush dogs, pacas, agoutis, and spiny rats. Human infection most often results from exposure to domestic dogs that have fed on the viscera of infected pacas.

Q: How do people become infected?

A: Adult-stage Echinococcus, which are only 5- to 10-mm long, are found in the intestines of the definitive hosts (canids) of the parasites. Eggs that contain infective embryos (oncospheres) are passed in the feces. When ingested by susceptible intermediate mammalian hosts, the eggs hatch and liberate the oncospheres, which penetrate the intestinal mucosa and migrate via venous or lymphatic vessels to distant sites. At these sites, the metacestode, or hydatid cyst, develops by vesiculation and production of thousands of protoscolices. When consumed by a dog or another susceptible definitive host, each protoscolex may develop into an adult tapeworm. People, especially children, acquire echinococcosis in the same way that intermediate hosts do--that is, by ingestion of Echinococcus eggs. This usually occurs by hand to mouth transfer of eggs after contact with infected dogs, but may also result from ingestion of food, water, soil, or fomites contaminated by infected dog feces. Also, flies can disperse tapeworm eggs after they feed on infected feces.¹

Q: Did the family dog cause our son's infection?

A: No. Echinococcosis is not known to develop in people residing in Kentucky. The boy was probably infected during his visit to Italy, where he lived for 3 months on a sheep farm owned by his grandparents. This case, as are approximately 98% of all hydatid infections diagnosed in the United States, was imported.^1,4 More cases are imported to the United States from Italy than from any other country.

Q: Does echinococcosis exist in animals and people in the United States?

A: Yes. Echinococcus granulosus is prevalent in sheep-raising regions of certain western states, including Utah, Arizona, New Mexico, and California.^4,6-8 Dogs in these regions are at risk for E granulosus if they have access to uncooked sheep viscera. In Alaska, echinococcosis exists in sylvatic cycles and dogs may be at increased risk if exposed to wild ungulates such as moose and caribou.⁹ Cystic hydatid disease is frequently diagnosed in Navajo and Zuni populations⁷ and in Alaskan natives,⁹ but may develop in anyone exposed to infected dogs. Echinococcus multilocularis develops in animals and human beings in north central states (North Dakota, South Dakota, Minnesota, Iowa, Nebraska, Montana, and Wyoming)^1,2 and western Alaska.⁹

Q: What are the signs of Echinococcus infection in animal hosts?

A: Echinococcus infection is remarkably well tolerated by lower animal hosts. Dogs and other definitive hosts may have thousands of tapeworms in their intestines without developing diarrhea or other signs attributable to the infection. Sheep and other intermediate hosts with hydatid cysts in their lungs and livers usually are indistinguishable from noninfected animals; however, results of some studies have suggested that infection reduces meat, milk, and wool production and the value of the animals is reduced because of condemnation of the infected viscera.¹

Q: How are Echinococcus spp identified in definitive and intermediate hosts?

A: Eggs are passed sporadically in the feces of infected dogs and other definitive hosts. Fecal examination is insensitive for diagnosis of echinococcosis, and Echinococcus eggs cannot be differentiated from other taeniid cestodes such as Taenia pisiformis, T hydatigena, T serialis, and others more commonly found in dogs in the United States.¹

Diagnosis in live animals usually is achieved by administering a taeniafuge such as arecoline hydrobromide (3.5 mg/kg of body weight), which causes fecal evacuation. Segments or entire tapeworms may be found in the mucous part of the purge produced 15 to 45 minutes after drug administration, although not all infected dogs pass worms.^1,10 Species identification of the worms requires expert assistance and is based on the lengths of the worms and the individual proglottids, size and shape of rostellar hooklets, and internal characteristics of the proglottids.¹ Because Echinococcus eggs are potentially infective for human beings, the handling of dog feces or intestines (at necropsy) must be done with precautions.

Hydatid cysts (E granulosus) in sheep and other intermediate hosts appear as thick-walled, spherical, fluid-filled cysts (1 to 10 cm in diameter) in liver and lungs. In human beings, detection of these cysts has been greatly facilitated by the availability of newer and more sophisticated radiographic imaging techniques such as computerized tomography and magnetic resonance. Examination of histologic sections of the cysts reveals the characteristic structure of the inner germinative membrane supported by a thicker, acellular, laminated membrane.¹ Protoscolices, contained in saclike brood capsules, look like sand when viewed macroscopically.

Human beings and animals infected with E multilocularis develop tumorlike nodules or masses in their livers that, on sectioning, reveal alveolar-like microvesicles with numerous protoscolices.^1,11

Q: How is echinococcosis treated?

A: Praziquantel (5 mg/kg of body weight) administered once orally or IM completely eliminates all juvenile and adult Echinococcus tapeworms from the intestines of dogs and other definitive hosts.¹⁰ Larval echinococcosis in intermediate hosts responds to benzimidazole carbamate compounds. Mebendazole and albendazole administered for 1 month have been shown to kill most hydatid cysts in infected sheep¹²; however, the cost of such treatment limits its applicability.

Surgery is the recommended treatment for human disease caused by E granulosus and E multiloculans; however, advances in medicinal treatment may offer alternatives to patients with irresectable disease and those who cannot tolerate surgery. Treatment with mebendazole has met with varied success, but results of recent studies of treatment using albendazole are more encouraging. This medication may soon be the preferred alternative to surgical intervention in patients for whom surgery is not an option.^5,13

Q: How can echinococcosis be prevented?

A: Together, animal control programs and personal protection prevent echinococcosis. The primary objective of control programs in most settings is to prevent dogs from feeding on infected intermediate hosts. For E granulosus, control measures include supervision of livestock slaughtering, safe disposal of infected viscera, dog control, and health education.^9,14 Mass treatment of dogs with praziquantel may be indicated in hyperendemic areas.

Personal protection requires education of people at risk and implementation of measures that prevent exposure to Echinococcus eggs. Handwashing, particularly for children, should be emphasized.

Q: Do veterinarians report cases of echinococcosis to tate officials?

A: Most US veterinarians will never diagnose a case in either definitive or intermediate hosts, although those who practice in western states and Alaska should be aware of the disease and of its public health importance. Statepublic health officials should be notified when the infection is diagnosed.

Q: Is the prevalence of echinococcosis increasing?

A: Since 1964, E multilocularis has been identified in animal hosts from an increasingly large area of central North America including North Dakota, South Dakota, Minnesota, Iowa, Montana, Wyoming, Manitoba, Saskatchewan, and Alberta. The important sylvatic hosts in these regions are red foxes, coyotes, deer mice, and field voles.^2,15 The availability of suitable hosts and the lack of ecologic barriers adjacent to this expanding focus may allow for further spread. Infection also occurs in cats; surveys of farm cats in North Dakota have measured infection rates from 1 to 5% from 1971 through 1976.^a At least one case of alveolar hydatid disease has been diagnosed in Minnesota,¹⁶ in a patient who had probably acquired infection some years earlier from pet cats or dogs that had become infected by ingesting infected rodents.

The introduction and spread of E multilocularis in the north central states has potentially serious implications. When the parasite is restricted to sylvatic hosts, human exposure is uncommon except for hunters and other people who handle foxes or their skins. However, the enzootic occurrence of the cestode in rodents provides a constant source of potential infection for cats and dogs in rural areas, and effective prevention can only be achieved by controlling the movement of such pets at all times--a measure that is often impractical.

Footnote

(a) Kritsky DC, Leiby P, Idaho Stale University, Pocatello, Idaho: Personal communication, 1977.

References

1. Schantz PM. Echinococcosis. In: Steele JH, ed. CRC handbook series in zoonoses. Section C: parasitic zoonoses. Vol 1. Boca Raton, Fla: CRC Press, 1982; 231-277.

2. Rausch RL. Life-cycle patterns and geographic distribution of Echinococcus species. In: Thompson RCA, ed. The biology of Echinococcus and hydatid diseases. London: George Allen Unwin, 1986; 44-80.

3. Thompson RCA, Lymberry AJ. The nature, extent and significance of variation within the genus Echinococcus. Adv Parasitol 1988; 27:210-263.

4. Pappaioanou M, Schwabe CW, Sard DM. An evolving pattern of human hydatid disease transmission in the United States. Am J Trop Med Hyg 1977; 26:732-742.

5. Schantz PM. Effective medical treatment for hydatid disease. JAMA 1985; 253:2095-2097.

6. Araujo PF, Schwabe CW, Sawyer JC, et al. Hydatid disease transmission in California: a study of the Basque connection. Am J Epidemiol 1975; 102:291-302.

7. Schantz PM. Echinococcosis in American Indians living in Arizona and New Mexico: a review of recent studies. Am J Epidemiol 1977; 106:370-379.

8. Crellin JR, Andersen FC, Schantz PM, et al. Possible factors influencing distribution and prevalence of Echinococcus granulosus in Utah. Am J Epidemiol 1982; 116:463-474.

9. Wilson JF, Diddams AC, Rausch RL. Cystic hydatid disease in Alaska: review of 101 autochthonous cases of Echinococcus granulosus infection. Am Rev Respir Dis 1968; 98:1.

10. Eckert J, Gemmell MA, Soulsby EJL, eds. FAO/UNEP/WHO guidelines for surveillance, prevention and control of echinococcosis/hydatidosis. VPH/81.28. Geneva: World Health Organization, 1981.

11. Wilson JF, Rausch RL. Alveolar hydatid disease. A review of clinical features of 33 indigenous cases of Echinococcus multilocularis infection in Alaskan Eskimos. Am J Trop Med Hyg 1980; 29:1340-1355.

12. Morris DL, Clarkson MS, Stallbaumer MF, et al. Albendazole treatment of pulmonary hydatid cysts in naturally infected sheep: a study with relevance to man. Thorax 1985; 40:453-458.

13. Davis A, Pawlowski ZS, Dixon H. Multicentre clinical trials of benzimidazole carbamates in human echinoccosis. Bull WHO 1986; 64:383-388.

14. Gemmell MA, Lawson JR, Roberts MG. Control of echinococcosis/hydatidosis: present status of worldwide progress. Bull WHO 1986; 64:333-339.

15. Ballard NB, Vande Vusse FJ. Echinococcus multilocularis in Illinois and Nebraska. J Parasitol 1983; 69:790-791.

16. Gamble WG, Segal M, Schantz PM, et al. Alveolar hydatid disease in Minnesota: first human case acquired in the contiguous United States. JAMA 1979; 241:904-906.

Addendum

In 1990, infection with Echinococcus mulfilocularis was diagnosed in a coyote in Indiana,^a thus extending its known range further south. In the same year, the parasite was found at necropsy of foxes confiscated in South Carolina, because they had been illegally translocated from Ohio and Indiana.^b The latter confirms a possible mechanism for introduction and establishment of E multilocularis infections in the southeastern United States.

Footnotes

(a) Kazacos KR, Purdue University, West Lafayette, Ind: personal communication, 1990.

(b) Brown J, Department of Health and Environmental Control, Columbia, SC and Nettles V, University of Georgia, Athens, Ga: personal communication, 1990.

Addendum (1994)

Prior to the 1960s, Echinococcus multilocularis spread from the northern tundra zone and became established in central North America in an endemic area centered in southern Manitoba and North Dakota. From this region, it has evidentally spread south and eastward. To date, the cestode has been documented in foxes, coyotes, and several species of rodents in all or part of 11 contiguous states and 3 Canadian provinces.^1-7a

Where surveys have been carried out repeatedly over time, the prevalence has tended to increase.^2,3,6,7,b Recently, rates of infections in samples of red foxes and coyotes have ranged from 69 to 90% in North Dakota and South Dakota to 19 to 35% in Illinois, Indiana, and Ohio. Given the abundance of suitable definitive and intermediate hosts throughout the United States, it may be assumed that the cestode will continue to spread and become established in contiguous states.

Footnotes

(a) Bates K, Storandt S, Green T, et al. Echinococcis multilocularis in foxes in Missouri. Unpublished data, 1993.

(b) Hildreth MB, Schneider D. Zoonotic helminths in red foxes from Southeastern South Dakota (abstr), in Proceedings. Annu Meet South Dakota Acad Sci 1989; 47:1.

References

1. Carney WP, Leiby PD. Echinococcus multilocularis in Peromyscus maniculatus and Vulpes vulpes from Minnesota. J Parasitol 1968; 54:714.

2. Leiby PD, Carney WP, Woods CE. Studies on sylvatic echinococcosis. III. Host occurrence and geographic distribution of Echinococcus multilocularis in the north central United States. J Parasitol 1970; 56:1141-1150.

3. Rausch RL, Richards, SH. Observations on parasite-host relationships of Echinococcus multilocularis Leuckart 1863, in North Dakota. Can J Zool 1971; 49:1317-1330.

4. Kritsky DC, Leiby PD. Studies on sylvatic echinococcosis. V. Factors influencing prevalence of Echinococcus multilocularis Leuckart 1863 in red foxes from North Dakota, 1965-1972. J Parasitol 1978; 64(4):625-634.

5. Ballard NB, Van deVusse FJ. Echinococcus multilocularis in Illinois and Nebraska. J Parasitol 1983; 69:790-791.

6. Ballard NB. Echinococcus multilocularis in Wisconsin. J Parasitol 1984; 70:844.

7. Storandt ST, Kazacos KR. Echinococcus multilocularis identified in Indiana, Ohio, and east-central Illinois. J Parasitol 1993; 79:301-305.