Helminths

Chapter 10

Helminths

Helminths (Helmins: worm) are parasitic metazoans from the phyla Platyhelminth (flatworms), Nematoda (roundworms), and Acanthocephala (thorny-headed worms). The organisms in this last phylum are of little significance as human parasites. provides a taxonomic overview of the groups covered in the text.

Platyhelmintha

General. Most of the trematode species that parasitize humans are dorsoventrally flattened with an oval to lancet shape, although others have different shapes such as the threadlike schistosomes. Suckers (trema: hole, opening) serve as attachment organs: an oral sucker around the mouth connected to the esophagus and the blind-ending intestine, and a ventral sucker. The body surface of adult trematodes is covered by a cellular tegument (composed of an outer annucleate, syncytial layer of cytoplasm connected by cytoplasmic strands to inner nucleated portions) through which substances can be absorbed from the environment. Most species are hermaphroditic, only the schistosomes have separate sexes. Snails are the first intermediate hosts; some species require arthropods or fish as second intermediate hosts.

Schistosoma 

• Schistosomosis (bilharziosis) is one of the most frequent tropical diseases with about 200 million infected persons. The occurrence of schistosomosis depends on the presence of suitable intermediate hosts (freshwater snails). Human infections result from contact with standing or slow-moving bodies of water (freshwater) when Schistosoma cercariae penetrate the skin. Schistosoma hematobium causes urinary schistosomosis; S. mansoni, S. japonicum, S. intercalatum, and S. mekongi are the causative agents of intestinal schistosomosis and other forms of the disease. Diagnosis can be made by detection of either Schistosoma eggs in stool or urine or of specific antibodies in serum.

• Parasite species and occurrence. Schistosomosis is also known as bilharziosis after the German physician Th. Bilharz, who discovered Schistosoma hematobium in human blood vessels in 1851. Schistosomosis occurs endemically in 74 tropical and subtropical countries of Africa, South America, and Asia. The number of persons infected with schistosomes is estimated at 200 million (WHO, 2004).

• The most important species pathogenic to humans are Schistosoma hematobium (Africa, the Near East, and questionable occurrence in India), S. mansoni (Africa, the Caribbean, the north-east of South America), and S. jap cum (Southeast Asia and the western Pacific, especially China, Indonesia, the Philippines, but no longer in Japan). S. intercalatum occurs focally in central and western Africa, S. mekongi in Laos and Cambodia.

• Morphology and life cycle. The various Schistosoma species can be differentiated morphologically. The relatively thick male forms a tegumental fold, the ventral groove (or canalis gynaecophorus) in which the threadlike female is enclosed. The male thus appears to be slit longitudinally (schizein: to split, soma: body).

• At the site of their deposition, the eggs lie in chainlike rows within small veins. Some penetrate through the vascular wall and surrounding tissue to reach the lumen of the urinary bladder or intestine (regarding the eggs that remain in the body see section on pathogenesis). Enzymes produced by the miracidium and secreted through micropores in the eggshell and granuloma formation (see below) contribute to the penetration process. The eggs are shed by the definitive host in stool or urine within a few weeks post infection (p.i.) (see below). If the eggs are deposited into freshwater, the miracidia hatch from the eggshell and begin their search for a suitable intermediate hose.

• Various genera and species of freshwater snails serve as intermediate hosts (Table 10.2) in which the invading miracidia reproduce asexually, producing mother and daughter sporocysts, and finally numerous cercariae, which begin to swarm into the water three to six weeks p.i. at the earliest. A characteristic feature of the approximately 340–520 lm long cercariae is their forked tail. The cercariae swim freely about or cling to the surface of the water. Upon contact with a human host, enzyme secretion and vigorous movements enable them to penetrate the skin within a few minutes, or less frequently the mucosa when ingested with drinking water. During the infection process, the cercaria loses its tail, sheds the surface glycocalyx, forms a new tegument, and transforms into the schistosomulum.

• Epidemiology. Schistosomosis occurs as an autochthonous infection in tropical and subtropical regions. Aquatic freshwater snails that prefer standing or slow-moving bodies of water are the intermediate hosts for S. hematobium, S. mansoni, S. intercalatum, and S. mekongi (Table 10.2). The intermediate hosts of S. japonicum are amphibious snails also found on moist ground and plants, e.g., in rice paddies. Although the cycles of all Schistosoma species can include animals as hosts, humans are the most important parasite reservoirs (Table 10.2). However, animals contribute significantly to the dissemination of the eggs of S. japonicum and S. mekongi. Travelers to endemic tropical areas can acquire the infection by a single instance of contact with water containing cercariae.

• Penetration phase: penetration of cercariae into the skin, either without reaction or—especially in cases of repeated exposure—with itching and skin lesions (erythema, papules), which disappear within a few days.

• In the acute phase, about two to 10 weeks after a severe initial infection, the symptoms may include fever, headache, limb pains, urticaria, bronchitis, upper abdominal pain, swelling of the liver, spleen and lymph nodes, intestinal disturbances, and eosinophilia (= Katayama syndrome). Due to release of Schistosoma antigens, the serum antibody levels (IgM, IgG, IgA) rise rapidly and immune complexes are formed that can cause renal glomerulopathies. These symptoms persist for several days to several weeks. Normally, Schistosoma eggs are not yet excreted at the beginning of this phase (see prepatent periods). In low-level infections this phase is usually inapparent or subclinical

• Urinary schistosomosis (urinary bilharziosis). Causative agent: S. hematobium. Incubation 10–12 weeks or longer, morbidity rate as high as 50–70%. Hematuria (mainly in the final portion of urine), micturition discomfort, hyperemia, increasing fibrosis, 1–2 mm nodules, necroses, ulcers and calcification of the bladder wall, pyelonephritis and hydronephrosis, urethral strictures, lesions in the sexual organs. In some endemic areas, an increased incidence of urinary bladder cancer has been associated with the S. hematobium infection.

• Other forms: the causative agents of the hepatosplenic form are mainly S. japonicum, less frequently S. mansoni. This fibrotic form is caused by eggs deposited around the branches of the portal vein in the liver (“pipestem” fibrosis according to Symmers) and results in circulatory anomalies, portal hypertension, splenomegaly, ascites, hemorrhages in the digestive tract, and other symptoms. Pulmonary schistosomosis is observed mainly in severe S. mansoni infections, more rarely in infections with other species (including S. hematobium). Cerebral schistosomosis is relatively frequent in S. japonicum infections.

• Cercarial dermatitis. Cutaneous lesions (itching, erythema, urticaria, papules) in humans, caused by (repeated) skin penetration of schistosomatid cercariae parasitizing birds (e.g., Bilharzial, Trichobothria) or mammals (e.g., Schistosoma spindale). The infection occurs worldwide in freshwater or brackish water and is known as “swimmer’s itch.” The symptoms generally abate after a few days. The cercariae of schistosomes from humans can cause similar, although usually milder, symptoms.

• Immunity. The prevalence and intensity of Schistosoma infections rise in endemic regions in children until the age of about 14, followed by a decline usually also accompanied by reduced egg excretion. This acquired immune status, known as “concomitant immunity,” is characterized by total or partial protection against cercarial infection. However, the schistosomes already established in the body are not eliminated and may persist for years or even decades.

• Diagnosis. Following the prepatent period, i.e., four to 10 weeks p.i. at the earliest, the eggs can be detected in stool specimens or in urine sediment. The eggs can also be found in intestinal or urinary bladder wall biopsies. Immunodiagnostic methods are particularly useful for detecting infections before egg excretion begins (important for travelers returning from tropical regions!). Detection of microhematuria with test strips is an important diagnostic tool in bladder schistosomosis. Clinical examination with portable ultrasonic imaging equipment has proved to be a highly sensitive method of detecting lesions in the liver and urogenital tract in epidemiological studies.

• Therapy. The drug of choice for treatment of schistosomosis is praziquantel, which is highly effective against all Schistosoma species and is well tolerated. Oxamniquine is effective against S. mansoni

• Control and prevention. Current schistosomosis control strategies are based mainly on regular drug therapy of specific population groups. Morbidity, mortality, and egg excretion rates are clearly reduced by such programs. Hygienic and organizational measures (construction of latrines, improvement of water supply quality, etc.) aim to reduce Schistosoma egg dissemination and contact with contaminated bodies of water. Individual preventive measures in Schistosoma-contaminated areas include avoidance of skin contact with natural or artificial bodies of water (freshwater). Drinking water that could be contaminated with cercariae must be decontaminated before use by boiling, chlorination, or filtration.

• Occurrence. Fasciola hepatica occurs worldwide as an important parasite in domestic ruminants that can also infect other animal species. Sporadic or endemic F. hepatica infections in humans have been reported from about 50 countries or regions on all continents (WHO,1999). In Asia and Africa, human infections with the 7.5 cm long giant liver fluke are also reported

• Clinical manifestations. The infection may run an inapparent course or, after an incubation period of four to six weeks, become symptomatic with abdominal pain, hepatomegaly, fever, leukocytosis and eosinophilia (acute phase), or hepatocholangitic symptoms (chronic phase) and anemia. Occasionally, the parasites also migrate into other organs than the liver.

• Diagnosis. The manifestations to be expected during the migration phase of the liver fluke include mainly leukocytosis, eosinophilia, and a rise in liverspecific serum enzymes. Detection of eggs in stool or duodenal fluid is not possible until at least two to three months p.i. In patients from Asia, differential diagnosis of the eggs of the small intestinal parasites Echinostoma and Fasciolopsis.

• Therapy and prevention. The drug of choice is triclabendazole, originally developed as a veterinary drug, is now registered ad usum humanum in several countries and is recommended by the WHO. The infection can be avoided by not eating raw watercress and other plants that may be contaminated with metacercariae.

Dicrocoelium

• Liver flukes of the genera Opisthorchis and Clonorchis occur mainly in river and lake regions of Asia and Eastern Europe; Opisthorchis is also found further westward as far as northern Germany. The life cycle of these organisms includes two intermediate hosts (aquatic snail, fish). Infections are contracted via raw fish containing infective stages (metacercariae). Diagnosis is based mainly on detection of eggs in stool or duodenal aspirate.

• Parasites and occurrence. The members of these genera resemble the lancet liver fluke (Dicrocoelium dendriticum) in size (length 1–2 cm) and form. The position and structure of the testicles (ophisten: posterior; orchis: testicle; clon: branch) allow the discrimination of genera (Fig. 10.6c). Opisthorchis and Clonorchis occur endemically in river and lake regions: Opisthorchis felineus in Eurasia (Russia, Kazakhstan, Ukraine; other endemic foci in the Baltic countries, northern Poland, and northern Germany), Opisthorchis viverrini in Thailand and Laos, Clonorchis sinensis in far-eastern Russia and other Asian areas (including China, Taiwan, Vietnam and Korea).

• Life cycle and epidemiology. The definitive hosts of Opisthorchis and Clonorchis species are fish-eating mammals (cats, dogs, pigs, etc.) and humans, in which these trematodes colonize the bile ducts. The life cycle of these organisms involves various species of aquatic snails (Bithynia, etc.) as the first intermediate hosts and freshwater fish species as the second intermediate hosts. The infective metacercariae are localized in the musculature of the fish and, when raw fish is ingested, enter the intestinal tract of the definitive host, from where they migrate through the common bile duct (ductus choledochus) into the intrahepatic bile ducts. The prepatent period is four weeks.

• Pathogenesis and clinical manifestations. Opisthorchis and Clonorchis infections cause proliferations of the bile duct epithelium, cystlike dilatation, inflammation, and fibrosis of the bile duct walls as well as connective tissue proliferation in the hepatic parenchyma. A high incidence of bile duct carcinomas has been reported from areas in which C. sinensis and O. viverrini are endemic. Clinical symptoms of more severe infections include variable fever, hepatocholangitic symptoms with hepatomegaly, leukocytosis, upper abdominal pains, and diarrhea.

Parag Onimus

• Occurrence. At least nine Paragonimus species are known to be parasites of humans. They are found in East and Southeast Asia (Paragonimus westermani, Paragonimus heterotremus, and Paragonimus uterobilateralis), in North America (Paragonimus kellicotti), and in Central and South America (Paragonimus mexicanus, etc.). The number of infected persons is estimated at about 21 million (WHO, 1995).

• Clinical manifestations. Typical cases are clinically characterized by pulmonary symptoms (chronic cough, bloody expectoration, thoracic pain). Parasites following the normal or deviant migration routes can also cause abdominal, hepatic, pancreatic or CNS symptoms, or skin lesions (swelling, nodules).

• Diagnosis, therapy, and prevention. An etiological diagnosis is based on detection of eggs in sputum or stool and of serum antibodies. Regarding the differential diagnosis especially tuberculosis must be kept in mind. The drug of choice is praziquantel, but triclabendazole can also be used (see Fasciola, p. 556). Cooking crustaceans before eating them is a reliable preventive measure.

Cestoda

• General. Various tapeworm species can parasitize in the small intestine of humans, including species from the “lower” (Pseudophyllida) and “higher” (Cyclophyllida) cestodes (from kestos = ribbon). These cestode species are hermaphrodites and consist of the head (scolex or “holdfast”), followed by an unsegmented germinative section (neck) and a posterior chain of segments (proglottids). There are no digestive organs, so nutrients are taken up through the absorptive integument. The life cycle of cestodes include one or two intermediate hosts.

• The eggs are released when a proglottid detaches from the tapeworm in the intestinal lumen or when a segment disintegrates outside the host. The eggs are small (diameter approx. 30–40 lm) and round. The outer shell forms a thick, brownish, radially striped embryophore enclosing an oncosphere with three pairs of hooks. The eggs are highly resistant and can remain infective in a moist environment for weeks or months (however, susceptible to desiccation!). Carried by feces of humans infected with Taenia, they contaminate pastures or feed either directly or via sewage. When cattle (or buffalo) ingest the eggs, the oncospheres hatch in the small intestine, migrate into the intestinal wall, and are transported with the bloodstream into the striated musculature, in which they develop into the infective metacestodes or cysticerci (= Cysticercus bovis) within three to four months.

• Pathogenesis and clinical manifestations. In some infected persons, T. saginata causes morphological changes (villus deformation, enterocyte proliferation, cellular mucosal infiltration, etc.) and functional disturbances. Blood eosinophilia may occur sometimes. The infection takes an asymptomatic course in about 25% of cases. Symptoms of infection include nausea, vomiting, upper abdominal pains, diarrhea or constipation and increased or decreased appetite. Infection does not confer levels of immunity sufficient to prevent reinfection.

• Diagnosis. A Taenia infection is easy to diagnose if the 1.5–2 cm long and 0.7 cm wide segments are eliminated in stool. Morphological species differentiation (T.saginata vs. T. solium) is often not possible based on the gravid proglottids but can be done by DNA-analysis (PCR). T. saginata eggs are shed irregularly in stool and cannot be differentiated morphologically from T. solium eggs. Using an ELISA, coproantigens are detectable in stool fluid even when neither proglottids nor eggs are being excreted.

• Therapy and prevention. The drug of choice is the highly effective praziquantel. Albendazole, mebendazole, and paromomycin are less reliable. The main prophylactic measures are sewage treatment and the detection of cysticercus carriers at inspection of slaughter animals. Meat containing numerous cysticerci (“measly meat”) has to be confiscated, but meat with small numbers of cysticerci can be used for human consumption after deep-freezing that is lethal to the parasites. Individual prophylaxis consists of not eating beef that is raw or has not been deep-frozen.

• Parasite and life cycle. T. solium (solium: from the Arabic word sosl: chain) is 3–4 m long and is thus smaller than T. saginata. The scolex of T. solium has a rostellum armed with two rows of hooks in addition to the four suckers (Fig. 10.8). Inside the gravid segments, the number of lateral uterus branches is usually 7–13, i.e., less than in T. saginata (usually >15). The life cycle is similar to that of T. saginata, except that T. solium uses the pig as intermediate host, in which the metacestode (Cysticercus cellulosae) develops to infectivity within two to three months.

• Diagnosis, therapy, prevention, and control. The recommendations made for diagnosis and therapy of T. saginata apply here as well. Infections with T. solium can be prevented by cooking or deep-freezing the pork (–20 8C for at least 24 hours). Control measures in endemic areas include mass treatment of the population with praziquantel, improvement of hygiene and slaughter animal inspection.

• Causative agent and epidemiology. The metacestodes of T. solium, known as Cysticercus cellulosae, can colonize various human organs (Fig. 10.8) and cause the clinical picture of cysticercosis. Infections occur under unhygienic conditions due to peroral ingestion of eggs stemming from the feces of tapeworm carriers (exogenous autoinfection or alloinfection). It is assumed that oncospheres hatching from eggs released from gravid proglottids in the human digestive tract may also cause an infection (endogenous autoinfection). In some countries of Latin America, Asia, and Africa, human cysticercosis is a public health problem. In Latin American countries, seroprevalences up to 10% and above have been found, and cysticerci were detected in 0.1–6% of the autopsy cases.

Echinococcus

• The most important species of the genus Echinococcus are Echinococcus granuloses (intestinal parasite of Canidae) and E. multilocular is (intestinal parasite of fox species, dogs, cats, and other carnivores). Both species occur in Europe. Their meta cestodes can cause cystic echinococcosis (CE, hydatid disease) or alveolar echinococcosis (AE) in humans. Humans are infected by peroral ingestion of Echinococcus eggs, from which in CE, liquid-filled cystic meta cestodes (the hydatids) develop, particularly in the liver and lungs. In AE the Meta cestodes primarily parasitize the liver, where the Meta cestodes proliferate like a tumor and form conglomerates of small cysts; secondary metastatic spread to other organs is possible. Clinical imaging and immunodiagnostic methods are used for diagnosis. Treatment involves surgery and/or chemotherapy.

• Parasite species. Echinococcus species are small tapeworms that parasitize the small intestine of carnivores and produce eggs that are shed to the environment by the host. Pathogenic larval stages (Meta cestodes) develop following peroral ingestion of such eggs by the natural intermediate hosts (various mammalian species), as well as in humans and other accidental hosts (which do not play a role in the life cycle). Four Echinococcus species are currently known, all of them pathogenic for humans (Echinococcus granulosus, E. multilocular is, E. Vogeli, and E. oligarthrus).

Echinococcus granulosus (Dwarf Dog Tapeworm)

• Occurrence. E. granulosus occurs worldwide, with relative high prevalence in eastern and southeastern Europe, the Mediterranean countries, the Near East, northern and eastern Africa, South America, and various parts of Asia and Australia. The parasite has become rare in northern and central Europe; most of the human cases of CE diagnosed in these areas are imported, in particular from Mediterranean countries. E. granulosus and E. multilocular is occur together in some areas.

Morphology and development

• Adult stage. E. granulosus is a 4–7 mm long tapeworm with a scolex (bearing Rosellar hooks) and normally three (two to six) proglottids. A notable characteristic is the uterus with its lateral sacculation, containing up to 1500 eggs (

• Definitive (final) and intermediate hosts. The most important definitive host for E. granulosus is the dog, whereby other Canidae (jackal, dingo, and other wild canids) are involved in certain regions. Herbivorous and omnivorous vertebrates function as intermediate hosts, in particular domestic animals (ruminants, pigs, horses, camels) and in some area's wild animals as well.

• Life cycle. The adult tapeworms live in the small intestine of the definitive host for about six months, a few for up to two years. Eggs are either released from gravid proglottids in the intestine and shed with feces or pass out of the host still enclosed in the tapeworm segments. The eggs (diameter approx. 30–40 lm) are nearly spherical, contain an oncosphere and feature a radially striped shell. They cannot be morphologically differentiated from the eggs of other Echinococcus or Taenia species. Infection of the intermediate hosts, humans, and other accidental hosts is by peroral ingestion of eggs, from which the oncospheres are released in the small intestine, penetrate into its wall and migrate hematogenous into the liver, as well as sometimes into the lungs and other organs. At first, the oncospheres develop into little vesicles, then gradually into meta cestodes.

• Epidemiology. There are a number of strains of E. granulosus that differ in morphological, biological, and genetic features and partially also in their infectivity to humans. Worldwide, for most of the human cases the sheep strain is responsible which develops in a cycle involving dogs and sheep (and other, less important, intermediate hosts). Humans are infected by peroral ingestion of Echinococcus eggs, either during direct contact with tapeworm carriers or indirectly by uptake of contaminated food or drinking water. Echinococcus eggs remain viable for months in a moist environment and can also survive the winter. They are killed rapidly by desiccation. They can also be killed by heat (75–100 8C) within a few minutes and by deep-freezing at –70 or –80 8C for four or two days, respectively. Standard chemical disinfectants have no effect. The mean annual incidence of CE varies in the countries and areas of the Mediterranean region between about one to 10 nonclinical cases per 100 000 inhabitants, although higher incidences (>40 cases/100 000 inhabitants) have been observed in other endemic areas (e.g., South America and China.

• Pathogenesis and clinical manifestations. Several clinical parameters of human CE and AE are presented and compared. The CE is always asymptomatic initially and it remains so for longer periods in a proportion of cases (up to 30%), especially when only small, well encapsulated or calcified cysts are present. Symptoms may appear after months or years when one or more cysts begin to disrupt organ functions due to their size, expansive growth, or localization. Acute symptoms may appear following spontaneous, traumatic, or intraoperative cyst ruptures, whereby the release of antigen containing hydatid fluid can cause symptoms of anaphylactic shock. There is also a risk that protosciences will be released and develop into new cysts in the human host (secondary CE). On the other hand, cyst rupture can also result in spontaneous cure.

• Diagnosis is based on detection of cysts using imaging techniques (ultrasonography, computer tomography, thoracic radiography, etc.) in connection with serological antibody detection. Specific antibodies occur in about 90–100% of patients with cystic hepatic echinococcosis, but in only about 60–80% of cases with pulmonary echinococcosis. Diagnostic cyst puncture is generally not advisable due to the risks described above (secondary echinococcosis, anaphylactic reactions).

• Therapy. The disease can be cured by removing the Echinococcus cysts surgically. Inoperable patients (e.g., with multiple cysts in lungs and liver) can be treated during several months with albendazole or mebendazole. Chemotherapy results in cure in about 30% of cases and in improvement in a further 30–50% (WHO, 1996). PAIR (puncture aspiration injection respiration) therapy is a new technique still under evaluation: after puncturing the cysts (not all cysts are suitable, e.g., pulmonary cysts!) under ultrasonic guidance, most of the hydatid fluid is aspirated, after which an adequate amount of 95% ethanol is injected into the cyst, left in it for 15 minutes and removed (respirated). If effective, the PAIR procedure often succeeds in killing the germinative layer and protosciences by ethanol. Since Longterm experience with this method is lacking, it is recommended that the procedure be accompanied by a short-term drug regimen (WHO, 1996).

• Control and prevention. Control of CE in humans includes regular mass treatment of dogs to eliminate E. granulosus, preventing access of dogs to viscera of domestic or wild animals, and dog population control. Special hygienic principles must be observed when handling dogs in endemic areas.

Echinococcus multilocular is (Dwarf Fox Tapeworm)

• Multilocular is widespread in the northern hemisphere with endemic regions in Europe, Asia (Turkey, Iran, Russia, and bordering countries all the way to Japan), and North America (Alaska, Canada, northern and central US states). In Central Europe, the parasite is widely distributed with prevalence levels in foxes exceeding 50% in some areas.

• Definitive hosts, intermediate hosts, and accidental hosts. The most important definitive hosts for E. multilocularis are red and polar foxes, although other wild carnivores (e.g., coyotes, raccoons, wolves) as well as dogs and cats can also carry this tapeworm species. The intermediate hosts are usually rodents (field mice, voles, muskrats, etc.). Accidental hosts include humans and various mammalian animals such as monkey species, domestic and wild pigs, horses, and even dogs.

• Life cycle. The E. multilocular is cycle is similar to that of E. granulose. In natural intermediate hosts, protosciences develop in the meta cestode (see description below) within 40–60 days. Ingestion of meta cestodes containing protosciences by a definitive host result in development of a new generation of tapeworms in its small intestine with infective eggs produced as early as 26–28 days.

• The meta cestode of E. multilocular is is a conglomerate with an alveolar structure comprised of small cysts (microscopical to 3 cm in diameter) surrounded by granulomatous or connective tissue. Each cyst is structured as in E. granulosus, but contains a gelatinous mass. E. multilocular is rarely produce (small numbers of) protosciences in humans.

• Epidemiology. In Europe, E. multilocular is develops mainly in a sylvatic cycle with the red fox as the definitive host and main source of human infections. Dogs and cats can become carriers of E. multilocular is by eating small mammals containing meta cestodes. In the environment, the eggs of E. multilocular is show resistance similar to that of E. granulosus. The eggs are transmitted to humans by various routes, but it is not yet clear which are the most important.

• athogenesis and clinical manifestations. The initial phase of an infection is always asymptomatic. Following a long incubation period, usually 10–15 years, the infection of the liver may present with symptoms resembling those of a malignant tumor (Table 10.3). The infection runs a slowly progressing, chronic course, lasting several weeks to several years. The lethality rate can exceed 94% in untreated patients. Spontaneous cure is possible, although no reliable statistics are available.

• Control and prevention. Trials are currently in progress to evaluate drug-based control of E. multilocular is in fox populations, but an established and effective control program is not yet available. Personal prophylaxis in endemic areas should include special precautions when handling potentially infected foxes and other definitive hosts. Thorough washing, and better yet cooking, of low growing cultivated and wild plants and windfall fruit before eating them and washing the hands after working with soil are further basic preventive measures. Persons known to have had contact with definitive hosts that are confirmed or potentially infected carriers, or who are in frequent contact with foxes or are exposed to other concrete infection risks can have their blood tested for antibodies to E. multilocular is, the objective being exclusion or early recognition of an infection.

Hymenolepis

• Occurrence, morphology, and life cycle. Hymenolepis nana, 1–4 cm long (rarely 9 cm) and 1 mm wide, is a small intestinal parasite that occurs worldwide, the highest prevalences being found in warm countries and in children. The final hosts are rodents and humans. Infection results from peroral ingestion of eggs, from which oncospheres hatch in the small intestine, penetrate into the villi, and develop there into larvae (cysticercoids). The larvae then return to the intestinal lumen, where they develop into adult tapeworms within two to three weeks. Alternatively, H. nana develops in a cycle with an intermediate host (insects: fleas, grain beetles, etc.). The closely related species Hymenolepis diminuta (10–60 mm) is not as frequent in humans. The developmental cycle of this species always involves intermediate hosts (fleas, beetles, cockroaches, etc.)