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Taenia and Other Tapeworm Infections
SECTION II: PATHOGENS
PART J: Cestode Infections
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CHAPTER 121 Taenia and Other Tapeworm Infections Murray Wittner • A. Clinton White, Jr • Herbert B. Tanowitz
TAENIASIS INTRODUCTION The pork tapeworm, Taenia solium, and the beef tapeworm, T. saginata, are parasites of humans that have been known since ancient Greece.1 However, it was not until 1782 that Goeze differentiated the two species. The larval stage was clearly described by Aristotle and Aristophenes from the tongue of hogs, but it remained for Leukart (1856) and Kuchenmeister (1855) to prove that human infection with the adult worm resulted from eating pork containing viable larvae.1,2 More recently, a third species, T. asiatica, has been identified.
THE AGENT (Fig. 121.1) T. saginata adult worms vary in size from 4 to 12 m and may be composed of 1000–2000 proglottids. When mature proglottids become gravid, the testes, ovaries, and other reproductive organs degenerate and are replaced by the enlarging egg-filled uterus (Fig. 121.2). The scolex of T. saginata is distinctive, being approximately 1.5–2.0 mm wide and possessing four simple sucking disks, and is “unarmed” (i.e., without hooklets; Fig. 121.3). T. asiatica appears similar to T. saginata, except that it has a rostellum (also unarmed) and the proglottids have a posterior protuberance. In contrast, T. solium is somewhat smaller, varying from 2 to 8 m, with a total of approximately 1000 proglottids. The scolex possesses a welldeveloped crown or rostellum upon which is a double row of hooklets; that is, it is “armed”3 (Fig. 121.4). Following the ingestion of viable metacestodes (cysticerci) in insufficiently cooked or raw beef or pork, the scolex evaginates and attaches to the upper jejunum by its well-developed holdfast organs, and strobilation occurs. Infection with adult tapeworms causes few pathologic changes. However, intestinal mucosal biopsies in patients harboring T. saginata have shown a minimal inflammatory reaction, suggesting that the worms can have an “irritative” effect, perhaps causing clinical symptoms. Proglottids, that develop initially from the neck of the scolex, mature further as they are replaced by newer proglottids. Gravid proglottids contain thousands of ova. The ova are 30–40 µm in diameter, radially striated, and, when mature, contain a six-hooked (hexacanth) embryo called the oncosphere. The eggs of the three Taenia species are morphologically indistinguishable (Fig. 121.5). Cattle or pigs become infected by ingesting mature eggs contaminating pastures or barnyards. Hatching is initiated by the action of gastric juice, intestinal enzymes, bicarbonate, and bile on the eggs. Liberated embryos penetrate the intestinal mucosa, attach to intestinal cells via elongated microvillae,4 enter the circulation, and are transported throughout the body. Both T. saginata and T. solium oncospheres produce excretory-secretory peptidases, including serine and cysteine endopeptidases, and aminopeptidase, which may play a role in invasion of the intestinal mucosa.5,6 Larval encystment usually occurs
in a wide range of tissues, but is most commonly identified in striated muscle and the central nervous system; within 8–11 weeks the larvae become infectious. In muscle, cysticerci are ellipsoid, translucent bladderlike cysts in which an inverted scolex has developed. In humans who ingest a cysticercus, the scolex evaginates, attaches to the jejunal wall, and develops proglottids at the base of the scolex. T. solium becomes a mature tapeworm in 5–12 weeks, whereas it takes approximately 10–12 weeks for T. saginata to mature. The adult tapeworm may live for a few years.3
EPIDEMIOLOGY Taenia infections have worldwide distributions, but there are few reliable data on prevalence due to the insensitivity of available diagnostic tests. T. saginata is common in cattle-raising areas of Africa and the Middle East, found throughout Latin America, but rare in the United States and Europe. T. asiatica is endemic in much of east and Southeast Asia, including Taiwan, Korea, Indonesia, Vietnam, Thailand, and China. Currently, there are only reliable data on intestinal T. solium infections from a relatively small number of nations, especially Mexico, Guatemala, Peru, India, China, and some African countries. Thus, the extent of the endemicity of the infection is largely unknown. More data are available on the prevalences of human and porcine cysticercosis, which are common in Mexico, Central and South America, sub-Saharan Africa, Eastern Europe, China, South Asia, and Southeast Asia7–10 (see Chapter 119).
THE DISEASE Most people with taeniasis are either asymptomatic or have minor complaints.The most frequent complaint in T. saginata infection is spontaneous egress of proglottids per rectum. Since proglottids of T. saginata are motile, the patient may have a sensation of the worms moving. Taeniasis may be associated with abdominal pain, nausea, weakness, loss of appetite, increased appetite, headache, constipation, dizziness, diarrhea, pruritis ani, and hyperexcitability. Children are more frequently symptomatic than adults. Eosinophilia may be present but is usually mild. Serum immunoglobulin E levels may be increased. Only occasionally do these infections result in serious, life-threatening illness from intestinal,11 biliary, or pancreatic obstruction (Fig. 121.6).
DIAGNOSIS Taeniasis is usually diagnosed by identification of ova or proglottids. Although ova can be identified in stool, stool examination is an insensitive method for diagnosis of intestinal tapeworms. T. saginata gravid proglottids often emerge spontaneously per anus, depositing eggs on the perianal and perineal region. Thus, anal swabs, such as the “Scotch tape” method, as usually done for the diagnosis of pinworm (see Chapter 113), may be
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Scolex evaginates and attaches to intestine
Worm segments (sometimes motile) passed between bowel movements
PART J: Cestode Infections
Adults (to 10 m) in small bowel
Gravid proglottids and infectious eggs appear in stool ~2 months after infection
PATHOGENS
Beef tapeworm Taenia saginata
Cysticercus in muscle eaten with uncooked beef (<50°C)
Cattle eat embryonated eggs or gravid proglottids and oncospheres hatch and penetrate the intestinal wall and circulate to muscle over 2 months
Figure 121.1 Beef tapeworm (Taenia saginata) life cycle.
Figure 121.2 Taenia solium proglottid.
(Courtesy of the American Society of Tropical Medicine and
Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.3 Taenia saginata scolex. Note the four suckers and no hooks. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
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diagnostic. While the morphology of ova of the three species is identical, differentiation of the Taenia species can be accomplished based on proglottid morphology by pressing the segment between two glass microscope slides and counting the main lateral branches on one side of the uterus.12 T. solium has fewer primary branches, usually 7–13 on each side; T. saginata and T asiatica usually have more than 15 lateral primary branches per side12 (Fig. 121.7). An electrolyte-polyethyleneglycol purgative can enhance the recovery of the scolex and proglottids, which could aid in species identification.13
Figure 121.4 Taenia solium scolex. Four suckers and hooks are seen. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.5 Taenia ovum.
(Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman:
A Presentation of Pictorial Parasites.)
Newer immunodiagnostic and molecular approaches have been developed for the diagnosis of taeniasis,7,14–16 including the detection of coproantigens, copro-DNA, and serum antibodies to adult-stage antigens. Some of these methods were shown to be highly sensitive and specific.17–20
TREATMENT AND PROGNOSIS Treatment of taeniasis, identical for all three species, is with praziquantel (a single dose of 10–20 mg/kg). For treatment of T. solium, precautions
Figure 121.9 Proliferating cysticercus of Taenia crassiceps presenting as a large subretinal mass in the right fundus. (Courtesy of Drs GJ Weil, RS Chuck, and RJ Olk, Washington University School of Medicine, St Louis, MO.)
A
B
Figure 121.7 (A) Taenia solium proglottid and (B) Taenia saginata proglottid (India ink-stained).
temperatures of 65°C (150°F) or if the pork is frozen at approximately –20°C (–38°F) for at least 12 hours, whereas pickling in brine or salting of pork is not always sufficient. T. saginata cysticerci are killed by thorough cooking at 56°C (131°F) or freezing at –10°C for 5 days. Pickling of beef in 25% brine for 5–6 days is said to render the beef safe. Treatment of all infected people would eliminate the source of soil and sewage pollution with Taenia eggs and therefore reduce porcine and bovine infection. Meat inspection would help reduce transmission to humans who fail to prepare meat properly. Investigations are underway to develop vaccines against cysticercosis in pigs and cattle. Encouraging results have been obtained,21 but are not yet commercially available.
Taenia and Other Tapeworm Infections Chapter 121
Figure 121.6 Taenia proglottid in intestine.
TAENIA CRASSICEPS T. crassiceps, a tapeworm of canids, is transmitted by the oral–fecal route only rarely to humans. Since humans are not the usual hosts, it presents as a cysticercus in the brain, eye, or subcutaneous tissue.22–26 Medical therapy has been disappointing. One case of subretinal T. crassiceps has been managed by surgery (Fig. 121.9).
DIPHYLLOBOTHRIASIS INTRODUCTION Diphyllobothriasis occurs in areas where uncooked fresh water fish as well as brackish water and marine fish are consumed.27–30
THE AGENT Figure 121.8 Scanning electron microscopy of Taenia solium scolex, showing effect of praziquantel. (Reproduced from Thomas H, Andrews P, Mehlhorn H. New results on the effect of praziquantel in experimental cysticercosis. Am J Trop Med Hyg. 1982;31:803–810.)
should be taken to prevent autoinfection or dissemination to others. In addition, since praziquantel kills the worm (Fig. 121.8) but does not inactivate the eggs released from the disintegrating gravid segments, cysticercosis is theoretically possible following treatment. Niclosamide, as a 2-g oral dose, is also effective, but less widely available. Nitazoxanide 500 mg twice daily for 3 days has also been used for T. saginata. Posttreatment follow-up stool examination should be performed after approximately 5 weeks in the case of T. solium and 3 months for T. saginata infections. The prognosis of treated taeniasis is excellent.
PREVENTION AND CONTROL Education is an important aspect of the prevention of taeniasis.8 Beef and pork tapeworm infection can be prevented by adequate cooking or freezing of beef and pork. T. solium cysticerci are killed by moderate
The distinction between Diphyllobothrium, the broad or fish tapeworms, and Taenia appears to have been well known to medieval physicians. Diphyllobothrium was the earliest tapeworm to be scientifically recognized by Linnaeus in 1758.1 The life cycle of Diphyllobothrium (Fig. 121.10) requires three hosts: (1) the definitive hosts are predominantly humans and fish-eating carnivores; (2) the first intermediate hosts are a large number of copepod species (crustaceans); and (3) the second intermediate hosts are freshwater, anadromous, and marine fish. Diphyllobothrium is a large tapeworm, often consisting of 3000–4000 segments or proglottids measuring from 3 to 12 m, that inhabits the ileum and jejunum. Diphyllobothrium tapeworms possess a scolex that is characteristically elongate or spoonshaped with a ventral and dorsal sucking groove or bothrium (Fig. 121.11). Egg production takes place in many proglottids simultaneously over a relatively extended period. The mature proglottid is broader than it is long and contains both testes and uterus. In the center of the mature proglottid is a characteristic dark rosette: the egg-filled uterus that aids in its recognition (Fig. 121.12). The uterus leads to a muscular uterine pore through which eggs pass into the feces. Typically, proglottids do not break off and migrate out of the body, but a million eggs are extruded daily into the small intestinal lumen by contractions of the uterine pore.
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Section II PATHOGENS
PART J: Cestode Infections
Diphyllobothrium (latum, pacificum, et al) Vague abdominal pain, bloating, diarrhea Rarely obstruction, megaloblastic anemia Adults (3–12 m) with scolex develop in small intestine
Humans (or fox, mink, bear, cat, dog, pig, walrus, seals, marine birds) ingest raw or undercooked infected fish (salmon, gefiltefish, ceviche)
Proglottids release immature eggs
Predator fish eats infected small fish
Unembryonated eggs passed in feces
Infected crustaceans ingested by small freshwater fish Procercoid larva released from crustacean develops into plerocercoid larva Eggs embryonate in water Procercoid larvae in body cavity of crustaceans
Coracidia hatch from eggs and are ingested by crustaceans
Figure 121.10 Diphylloborthrium (latum, pacificum et al.) life cycle.
Figure 121.11 Diphyllobothrium latum. Immature proglottids and scolex. The scolex bears grooves. (Courtesy of the American Society of Tropical Medicine and
Figure 121.13 Diphyllobothrium latum. Ovum.
(Courtesy of the American Society of Tropical
Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
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Figure 121.12 Diphyllobothrium latum. Proglottid. Note the rosette shape of the uterus. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Spent proglottids eventually disintegrate and pass out of the body. Occasionally, a long chain of proglottids is passed with the stool.12 The most widely recognized species, D. latum, has characteristic lightyellow eggs, which are 42–50 µm wide by 59–75 µm long, with an operculum or lid at one end and a characteristic tiny knob at the abopercular end (Fig. 121.13).12 In fresh water, the unembryonated egg requires approximately 10–14 days to mature at 15–25oC. After the operculum opens, a ciliated hexacanth, or six-hooked, embryo (coracidium) emerges; the swimming embryo must be ingested within 6–12 hours by one of many crustacean species of copepods (Cyclops sp. and Diaptomus sp.) or perish. The larva penetrates the midgut and enters the hemocoel of the copepod and in 10–21 days transforms into an elongated procercoid larva, reaching approximately 0.5 mm in length. It remains in the copepod until ingested by one of many species of small fresh-water plankton-eating fish (second intermediate host). The procercoid larva next makes its way
EPIDEMIOLOGY
and mild leukopenia. The development of pernicious anemia is usually associated with attachment of the tapeworm within 145 cm of the mouth. In this situation, more than 80% of vitamin B12 is absorbed by the worm, with a differential absorption pattern of 1000 : 1 in favor of the worm. Anemia associated with diphyllobothriasis is most frequently encountered in Scandinavia, likely due to differences between parasite species. Approximately 40% of people harboring the worm in Scandanavia have reduced serum vitamin B12 levels, but fewer than 2% develop anemia. Neurologic lesions due to vitamin B12 deficiency include subacute combined degeneration of the dorsal and lateral columns and peripheral nerve degeneration. The anemia and neurologic manifestations respond to vitamin B12 and do not recur after the worm has been expelled.
D. latum biotypes are mostly shallow fresh-water littorals with vegetation favoring the development of copepods and fish. Infection with this parasite is most prevalent in areas of the north temperate and subarctic zones, where fresh-water fish are commonly consumed.30–32 The estimated worldwide prevalence is approximately 9–10 million people. In North America, endemic foci have been found among Native Americans in Alaska and Canada. In the United States, fish from the lakes of the north-central region and from Florida and California are found to be infected. In highly endemic regions of Finnish and Russian Karelia, prevalences ranged from 25% to 100%.28 In North America, human cases have declined, whereas in South America there have been increased reports from fish, especially salmonids. Transmission has been brought under control in western Europe, and only a few cases now occur in Finland, where nearly 20% of the population was infected in the 1950s. However, areas of Sweden, France, Switzerland, northwestern Russia, the Danube and lower Volga basins, and the lake regions of northern Italy and Switzerland contain infected fish. Humans are the primary definitive host and most important reservoir of infection. Secondary intermediate hosts can be species of brackish and fresh-water fish, including anadromous fish that spawn in fresh water (e.g., salmon). Salmon has been the cause of the transmission of this parasite in Japan (D. nihonkaiense) and the west coast of the United States where sushi has been prepared with infected salmon.30 Eating raw, insufficiently cooked, or lightly pickled fish or fresh roe can transmit infection. In northern Minnesota and Michigan, where large numbers of people of Scandinavian background live, raw and pickled fish are still eaten, although infection with D. latum has now become less common. Other diphyllobothriids can cause disease. D. pacificum has been reported from Japan and is endemic in coastal areas of Peru. Unlike D. latum, infection with this parasite is acquired from eating marine fish that has been prepared in lime juice (e.g., ceviche). Diplogonoporus grandis, another member of this group, is found in Japan and thought to be acquired by consumption of raw anchovies and sardines. Other species of Diphyllobothrium, such as D. dendriticum, D. klebaanovskii, D. cordatum, D. dalliae, D. ursi, and D. nihonkaiense, are found as occasional human parasites.31,32
INTRODUCTION
THE DISEASE
Two species of Hymenolepis infect humans: H. nana and H. diminuta. They are cosmopolitan in distribution. H. nana is common in warmer climates whereas H. diminuta only occasionally infects humans.36
Infection is usually associated with few symptoms or pathologic changes in the intestinal mucosa. Often, infection is first recognized in an asymptomatic patient as a result of a stool examination carried out for other reasons. However, some patients complain of vague abdominal pain and others describe the sensation that “something is moving inside.” Others describe bloating, sore tongue, sore gums, allergic symptoms, headache, hunger pains, loss of appetite, or increased appetite. Rarely, mechanical intestinal obstruction may occur as a result of several worms becoming entangled. Diarrhea may also occur. Almost all patients become aware of the infection when spontaneously passing a large section of the spent proglottids; most often this startling event brings the patient to the office or clinic. Unlike the proglottids of T. saginata, those of D. latum do not spontaneously crawl through the anus.33 In a small proportion of patients, D. latum causes pernicious anemia, a hyperchromic, macrocytic, megaloblastic anemia with thrombocytopenia
DIAGNOSIS The infection can be diagnosed readily by finding characteristic ova in the feces (see Fig. 121.10).12 The eggs can usually be identified without concentration due to the large number of eggs. However, species recognition or differentiation usually requires recovery of the scolex. Molecular methods have been employed for the diagnosis of Diphyllobothrium sp.34 Thus, restriction fragment length polymorphism has been used to speciate D. latum from D. nihonkaiense. It is not uncommon to find mild eosinophilia in patients with D. latum infection.
Taenia and Other Tapeworm Infections Chapter 121
through the tissues of the fish and settles in almost any organ or tissue of the second intermediate host where it transforms into a plerocercoid (sparganum) larva. The latter has the characteristic rudiments of a scolex but is unsegmented. Next, these fish are eaten by larger carnivorous fish, such as perch, wall-eyed pike, or the burbot (paratenic or transport hosts). The plerocercoid larvae later reinvade the tissues of these fish and if consumed raw or inadequately cooked by a suitable host (i.e., humans, carnivorous mammals), the larva attaches to the wall of the small intestine and becomes a mature tapeworm in approximately 5 or 6 weeks.
TREATMENT AND PROGNOSIS The treatment of choice is praziquantel, which is administered as a single dose of 5–10 mg/kg for both adults and children.35 Alternatively, niclosamide is given as a 2-g dose once for adults and 50 mg/kg for children. The prognosis for treated individuals is excellent.
PREVENTION AND CONTROL Careful cooking of fresh-water fish would eliminate all possibility of human infection. The sale of fish originating in heavily infected lakes should be regulated because freezing at –10°C for 24 hours suffices to kill the plerocercoid larva. In the United States, smoked salmon is usually brined before smoking and is not considered a source of infection. Other control measures include the education of cooks regarding the sampling of raw fish during preparation. In addition, sanitary sewage disposal rather than the dumping of raw sewage into fresh-water lakes would prevent viable eggs from contaminating various intermediate hosts.
HYMENOLEPIASIS
THE AGENT (Fig. 121.14) The adult H. nana is approximately 0.5 cm long and is found attached to the mucosa of the ileum by a scolex that has four suckers and a retractable, armed rostellum (Fig. 121.15). The entire worm usually consists of a scolex and approximately 200 proglottids. The uterus in a gravid proglottid contains approximately 100–200 mature eggs that are 30– 60 µm in diameter (Fig. 121.16).36 The eggs are passed in the feces and ingested by a new human or the same host (autoinfection). The embryo hatches in the small intestine and penetrates a villus, where it becomes a cysticercoid larva (Fig. 121.17). Upon maturation, in 3 or 4 days, it emerges from the tissue and attaches to the intestinal mucosa by its scolex. In 2 or 3 weeks, the new worm is producing eggs. Hyperinfection can occur when eggs liberated in the small intestine hatch and
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Section II
Hymenolepis nana Abdominal pain, mucoid diarrhea, especially in children; Rarely pruritus, seizures
PATHOGENS
Oncosphere hatches; cysticeroid develops in intestinal villus
Eggs released through the genital atrium of gravid proglottids Gravid proglottids can also disintegrate, releasing eggs that are passed in stools
PART J: Cestode Infections
Adult worm (2–4 cm) with scolex develop in ileum
Embryonated eggs ingested by humans from contaminated food, water, or hands or from ingestion of infected insects (by children or rodents)
Autoinfection can occur if eggs remain in the intestine The eggs then release the hexocath embryo, which penetrates the intestinal villus continuing the cycle Direct ingestion of eggs (person to person)
Cysticercoid develops in insect
Eggs ingested by insects
Figure 121.14 Hymenolepis nana life cycle.
Figure 121.15 Hymenolepis nana scolex and proglottids. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.17 Hymenolepis nana cysticercoid stage in the small intestine. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
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Figure 121.16 Hymenolepis nana ovum. and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
(Courtesy of the American Society of Tropical Medicine
immediately penetrate a villus to undergo a new cycle. As a result of hyperinfection, children may harbor many hundreds or even thousands of adult worms.The entire life history from ingestion of the egg to adulthood requires approximately 10–14 days. Eggs are first seen in the stools in approximately 25–30 days. H. nana is spread from hand to mouth. The closely related species, H. diminuta, which commonly parasitizes the rat and mouse, infrequently infects humans.36 Most of the more than 200 reported human infections have been in children younger than 3 years of age. The adult worm is 3–5 mm and possesses a club-shaped scolex that has a rudimentary apical unarmed rostellum with four small suckers. The ova are spherical and 60–86 µm in diameter.12 In contrast to the eggs of H. nana, there are no polar filaments. Development of this tapeworm requires an intermediate host. Presumably, infected rat fleas (Nosopsyllus
EPIDEMIOLOGY The dwarf tapeworm, H. nana, is found in most warm regions of the world. It is the most common cestode infection worldwide with endemic foci in Latin America, southern Europe, Russia and the former Soviet republics, the Indian subcontinent, and southeastern United States.36
THE DISEASE
The proglottids have a double set of reproductive organs with genital pores midway on each lateral margin (Fig. 121.20). The gravid proglottids are packed with 15–25 eggs. Each egg is 35–60 µm in diameter and contains an oncosphere with six hooklets. The strobila can migrate several centimeters per hour and pass out of the anus spontaneously or with the feces. Eggs are expelled by contraction or disintegration of the proglottid.39
EPIDEMIOLOGY Most infections occur in children younger than 8 years old as well as infants younger than 6 months of age.40–44 The ova of Dipylidium are ingested by the larval dog or cat flea, in which they become cysticercoid larvae. Infection occurs following accidental ingestion of the infected flea.
Most cases are asymptomatic. Young children may develop symptoms when many worms are present.37,38 These patients may have loose bowel movements or occasionally frank diarrhea with mucus but no blood. Diffuse, persistent abdominal pain is the most common complaint. Pruritus ani and nasi are occasionally encountered. Many children have sleep and behavioral disturbances that resolve after successful therapy. Serious neurologic disturbances such as seizures have been reported. Many patients with hymenolepiasis have a moderate eosinophilia of 5–10% and skin eruptions.37
Infection is often asymptomatic. The most common symptom is noting proglottids in stool, which are similar in size and color to grains of rice. Some children have intestinal disturbances, including abdominal pain and diarrhea (Fig. 121.21).40–42 Allergic manifestations such as urticaria and pruritus ani have been reported; intestinal obstruction has been a rare complication.1,2
DIAGNOSIS
TREATMENT AND PREVENTION
The diagnosis of hymenolepiasis rests on finding the characteristic ova by stool examination. Stools of the entire family must be checked before therapy is initiated because other members of a household are commonly infected, and they must also be treated for therapy to be successful. Posttreatment stool examinations should be done after 5 weeks and again after 3 months.1–3
Treatment is with 5–10 mg/kg of praziquantel once for both adults and children. An alternative therapy is 2 g of niclosamide once for adults and 25 mg/kg once for children. Children should not be allowed to fondle and kiss dogs and cats. Periodic treatment of pets for tapeworm infection and periodic use of insecticides to kill ectoparasites will control the spread of this infection.
TREATMENT AND PROGNOSIS
SPARGANOSIS
Praziquantel is the drug of choice for the treatment of hymenolepiasis and is highly effective in a single dose of 15 mg/kg. It not only eliminates adult worms but also, unlike other anthelminthics, is efficiently absorbed and kills the larval stages (cysticercoids) in the submucosa.2 Treated individuals have an excellent prognosis. Niclosamide (2 g in a single dose) and nitazoxanide (500 mg PO twice daily for 3 days) are alternative therapies. Recently nitazoxianide has been evaluated in field trials in Peru.38
INTRODUCTION
THE DISEASE
Sparganosis is an uncommon parasitic infection usually caused by the migration of larval tapeworms of the genus Spirometra.
THE AGENT
The dog tapeworm, Dipylidium caninum, is also a frequent parasite of cats and wild carnivores worldwide. It is an occasional parasite of the small intestine of humans.
Human sparganosis may occur following ingestion of species of Cyclops that are infected with the procercoid larva of various pseudophyllidean tapeworms of the species Spirometra.1,45 The procercoid penetrates the intestinal wall and migrates to various sites, including subcutaneous tissues, the central nervous system, and muscle, where they develop to second-stage larvae or plerocercoids. This condition is called sparganosis. Ingestion, either deliberately or accidentally, of infected uncooked flesh of an amphibian, reptile, bird, or mammal harboring plerocercoid larvae may also be a source of infection. All the spargana are morphologically indistinguishable. Since these worms cannot mature in humans, they migrate into the tissues and remain as plerocercoid larvae. However, in the few instances in which the larvae were allowed to complete their life cycle in dogs or cats, they were identified as members of the genus Spirometra. In some cases in the United States, they were identified as S. mansoni. Molecular approaches have been applied to this parasite that may aid in the diagnosis of this infection.46
THE AGENT (Fig. 121.18)
EPIDEMIOLOGY
The adult worm is approximately 15–20 cm long and usually has approximately 60–175 proglottids. The scolex is characteristic, being rhomboid with four oval suckers and an armed retractable conical rostellum containing 30–150 thorn-shaped hooks arranged in transverse rows (Fig. 121.19).
Sparganosis is reported in many areas of the world, including China, Japan, Southeast Asia, and South and Central America, and has occasionally been reported in various areas of the United States and Europe.47,48
PREVENTION AND CONTROL This infection is spread from person to person and therefore extremely difficult to control. Education in hygiene is probably the only practical way to reduce the incidence.
DIPYLIDIASIS INTRODUCTION
Taenia and Other Tapeworm Infections Chapter 121
and Xenopsylla) and mealworms (Tenebrio) are accidentally ingested, and the mature adult develops in approximately 3 weeks. Cockroaches may also serve as intermediate hosts and become infected by ingesting eggs passed in rodent feces.
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Adults (15–20 cm) with scolex develop in intestine
PART J: Cestode Infections
PATHOGENS
Section II
Dipylidium caninum Abdominal pain, mucoid diarrhea, Occasional urticaria, pruritus ani, rarely obstruction
Gravid proglottids are passed intact in the feces or emerge from perianal region of either animal or human hosts Human (usually children) or animals ingest infected fleas
Oncospheres hatch from the eggs and penetrate the intestinal wall of the larvae Cysticercoid larvae develop in the body cavity of adult flea
Egg packets containing embryonated eggs are ingested by larval stage of flea
Figure 121.18 Dipylidium caninum life cycle.
Figure 121.19 Dipylidium caninum scolex. Three of the four suckers and the retracted armed rostellum can be seen. (Courtesy of the American Society of
Figure 121.21 Egg pockets of Dipylidium caninum in an infant.
(Courtesy of
Dr Patrick Adegboyega, Department of Pathology, University of Texas Medical Branch, Galveston, TX.)
Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
THE DISEASE
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Figure 121.20 Dipylidium caninum proglottid. Note the two genital pores and the massing of the ova. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
The presence of plerocercoids in subcutaneous tissues is typically associated with a nodular mass consisting of tissue necrosis and a granulomatous inflammation with lymphocytes, plasma cells, and eosinophils (Fig. 121.22).49–51 Swelling and edema are often painful (Fig. 121.23). Any part of the body may be involved, including the neck, breast, scrotum, and pleura.50–55 Raw amphibian poultices harboring plerocercoid larvae applied to the eye have also been a cause of ocular sparganosis and may impair vision.56,57 Cerebral sparganosis is a rare complication of this infection. In the brain, the presence of the parasite evokes an intense inflammatory
(Courtesy of the American Society of Tropical
Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.24 Sparganum removed from the right occipital cortex. (Reproduced from Kim DG, Paek SH, Chang KH, et al. Cerebral sparganosis: clinical manifestations, treatment, and outcome. J Neurosurg. 1996;85:1066–1071, with permission of the Journal of Neurosurgery and the authors.)
unknown genus and species proliferate in the tissues as independent organisms. In several instances, thousands of spargana have been found in the subcutaneous tissues.45
DIAGNOSIS
Figure 121.23 Sparganosis: computed tomography scan of the thigh showing a circular hyperlucent lesion with inflammatory response of adjacent tissues. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation
In general, the diagnosis is based on pathological examination of biopsy or autopsy specimens and/or direct visualization of the parasite (Fig. 121.24). In the case of cerebral sparganosis, magnetic resonance imaging is most helpful in the diagnosis and is usually followed by stereotactic biopsies.61,62,67 Serodiagnosis using monoclonal antibodies in a competition enzyme-linked immunosorbent assay has been reported.68,69 Falsepositive results may occur when Clonorchis and Paragonimus infections are present.
Taenia and Other Tapeworm Infections Chapter 121
Figure 121.22 Sparganum: abscess in muscle.
of Pictorial Parasites.)
TREATMENT AND PREVENTION response. Pathological and radiographic (computed tomography and magnetic resonance imaging) studies demonstrate white-matter degeneration, cortical atrophy, ventricular dilatation, punctuate calcifications, irregular or nodular enhancement, vasculitis, and hemorrhage.58–66 An unusual manifestation of sparganosis is a condition known as sparganum proliferum, in which larvae of a pseudophyllidean tapeworm of
Treatment of sparganosis has been surgical removal of the larvae. Ocular sparganosis is sometimes treated by killing the larvae and allowing the organisms to resorb, although surgical removal has come into favor. Mebendazole, albendazole, and praziquantel have not been demonstrated to be useful. Spargana are destroyed by flash freezing at 10°C for 24 hours.
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PART J: Cestode Infections
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CHAPTER 121 Taenia and Other Tapeworm Infections Murray Wittner • A. Clinton White, Jr • Herbert B. Tanowitz
TAENIASIS INTRODUCTION The pork tapeworm, Taenia solium, and the beef tapeworm, T. saginata, are parasites of humans that have been known since ancient Greece.1 However, it was not until 1782 that Goeze differentiated the two species. The larval stage was clearly described by Aristotle and Aristophenes from the tongue of hogs, but it remained for Leukart (1856) and Kuchenmeister (1855) to prove that human infection with the adult worm resulted from eating pork containing viable larvae.1,2 More recently, a third species, T. asiatica, has been identified.
THE AGENT (Fig. 121.1) T. saginata adult worms vary in size from 4 to 12 m and may be composed of 1000–2000 proglottids. When mature proglottids become gravid, the testes, ovaries, and other reproductive organs degenerate and are replaced by the enlarging egg-filled uterus (Fig. 121.2). The scolex of T. saginata is distinctive, being approximately 1.5–2.0 mm wide and possessing four simple sucking disks, and is “unarmed” (i.e., without hooklets; Fig. 121.3). T. asiatica appears similar to T. saginata, except that it has a rostellum (also unarmed) and the proglottids have a posterior protuberance. In contrast, T. solium is somewhat smaller, varying from 2 to 8 m, with a total of approximately 1000 proglottids. The scolex possesses a welldeveloped crown or rostellum upon which is a double row of hooklets; that is, it is “armed”3 (Fig. 121.4). Following the ingestion of viable metacestodes (cysticerci) in insufficiently cooked or raw beef or pork, the scolex evaginates and attaches to the upper jejunum by its well-developed holdfast organs, and strobilation occurs. Infection with adult tapeworms causes few pathologic changes. However, intestinal mucosal biopsies in patients harboring T. saginata have shown a minimal inflammatory reaction, suggesting that the worms can have an “irritative” effect, perhaps causing clinical symptoms. Proglottids, that develop initially from the neck of the scolex, mature further as they are replaced by newer proglottids. Gravid proglottids contain thousands of ova. The ova are 30–40 µm in diameter, radially striated, and, when mature, contain a six-hooked (hexacanth) embryo called the oncosphere. The eggs of the three Taenia species are morphologically indistinguishable (Fig. 121.5). Cattle or pigs become infected by ingesting mature eggs contaminating pastures or barnyards. Hatching is initiated by the action of gastric juice, intestinal enzymes, bicarbonate, and bile on the eggs. Liberated embryos penetrate the intestinal mucosa, attach to intestinal cells via elongated microvillae,4 enter the circulation, and are transported throughout the body. Both T. saginata and T. solium oncospheres produce excretory-secretory peptidases, including serine and cysteine endopeptidases, and aminopeptidase, which may play a role in invasion of the intestinal mucosa.5,6 Larval encystment usually occurs
in a wide range of tissues, but is most commonly identified in striated muscle and the central nervous system; within 8–11 weeks the larvae become infectious. In muscle, cysticerci are ellipsoid, translucent bladderlike cysts in which an inverted scolex has developed. In humans who ingest a cysticercus, the scolex evaginates, attaches to the jejunal wall, and develops proglottids at the base of the scolex. T. solium becomes a mature tapeworm in 5–12 weeks, whereas it takes approximately 10–12 weeks for T. saginata to mature. The adult tapeworm may live for a few years.3
EPIDEMIOLOGY Taenia infections have worldwide distributions, but there are few reliable data on prevalence due to the insensitivity of available diagnostic tests. T. saginata is common in cattle-raising areas of Africa and the Middle East, found throughout Latin America, but rare in the United States and Europe. T. asiatica is endemic in much of east and Southeast Asia, including Taiwan, Korea, Indonesia, Vietnam, Thailand, and China. Currently, there are only reliable data on intestinal T. solium infections from a relatively small number of nations, especially Mexico, Guatemala, Peru, India, China, and some African countries. Thus, the extent of the endemicity of the infection is largely unknown. More data are available on the prevalences of human and porcine cysticercosis, which are common in Mexico, Central and South America, sub-Saharan Africa, Eastern Europe, China, South Asia, and Southeast Asia7–10 (see Chapter 119).
THE DISEASE Most people with taeniasis are either asymptomatic or have minor complaints.The most frequent complaint in T. saginata infection is spontaneous egress of proglottids per rectum. Since proglottids of T. saginata are motile, the patient may have a sensation of the worms moving. Taeniasis may be associated with abdominal pain, nausea, weakness, loss of appetite, increased appetite, headache, constipation, dizziness, diarrhea, pruritis ani, and hyperexcitability. Children are more frequently symptomatic than adults. Eosinophilia may be present but is usually mild. Serum immunoglobulin E levels may be increased. Only occasionally do these infections result in serious, life-threatening illness from intestinal,11 biliary, or pancreatic obstruction (Fig. 121.6).
DIAGNOSIS Taeniasis is usually diagnosed by identification of ova or proglottids. Although ova can be identified in stool, stool examination is an insensitive method for diagnosis of intestinal tapeworms. T. saginata gravid proglottids often emerge spontaneously per anus, depositing eggs on the perianal and perineal region. Thus, anal swabs, such as the “Scotch tape” method, as usually done for the diagnosis of pinworm (see Chapter 113), may be
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Section II
Scolex evaginates and attaches to intestine
Worm segments (sometimes motile) passed between bowel movements
PART J: Cestode Infections
Adults (to 10 m) in small bowel
Gravid proglottids and infectious eggs appear in stool ~2 months after infection
PATHOGENS
Beef tapeworm Taenia saginata
Cysticercus in muscle eaten with uncooked beef (<50°C)
Cattle eat embryonated eggs or gravid proglottids and oncospheres hatch and penetrate the intestinal wall and circulate to muscle over 2 months
Figure 121.1 Beef tapeworm (Taenia saginata) life cycle.
Figure 121.2 Taenia solium proglottid.
(Courtesy of the American Society of Tropical Medicine and
Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.3 Taenia saginata scolex. Note the four suckers and no hooks. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
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diagnostic. While the morphology of ova of the three species is identical, differentiation of the Taenia species can be accomplished based on proglottid morphology by pressing the segment between two glass microscope slides and counting the main lateral branches on one side of the uterus.12 T. solium has fewer primary branches, usually 7–13 on each side; T. saginata and T asiatica usually have more than 15 lateral primary branches per side12 (Fig. 121.7). An electrolyte-polyethyleneglycol purgative can enhance the recovery of the scolex and proglottids, which could aid in species identification.13
Figure 121.4 Taenia solium scolex. Four suckers and hooks are seen. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.5 Taenia ovum.
(Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman:
A Presentation of Pictorial Parasites.)
Newer immunodiagnostic and molecular approaches have been developed for the diagnosis of taeniasis,7,14–16 including the detection of coproantigens, copro-DNA, and serum antibodies to adult-stage antigens. Some of these methods were shown to be highly sensitive and specific.17–20
TREATMENT AND PROGNOSIS Treatment of taeniasis, identical for all three species, is with praziquantel (a single dose of 10–20 mg/kg). For treatment of T. solium, precautions
Figure 121.9 Proliferating cysticercus of Taenia crassiceps presenting as a large subretinal mass in the right fundus. (Courtesy of Drs GJ Weil, RS Chuck, and RJ Olk, Washington University School of Medicine, St Louis, MO.)
A
B
Figure 121.7 (A) Taenia solium proglottid and (B) Taenia saginata proglottid (India ink-stained).
temperatures of 65°C (150°F) or if the pork is frozen at approximately –20°C (–38°F) for at least 12 hours, whereas pickling in brine or salting of pork is not always sufficient. T. saginata cysticerci are killed by thorough cooking at 56°C (131°F) or freezing at –10°C for 5 days. Pickling of beef in 25% brine for 5–6 days is said to render the beef safe. Treatment of all infected people would eliminate the source of soil and sewage pollution with Taenia eggs and therefore reduce porcine and bovine infection. Meat inspection would help reduce transmission to humans who fail to prepare meat properly. Investigations are underway to develop vaccines against cysticercosis in pigs and cattle. Encouraging results have been obtained,21 but are not yet commercially available.
Taenia and Other Tapeworm Infections Chapter 121
Figure 121.6 Taenia proglottid in intestine.
TAENIA CRASSICEPS T. crassiceps, a tapeworm of canids, is transmitted by the oral–fecal route only rarely to humans. Since humans are not the usual hosts, it presents as a cysticercus in the brain, eye, or subcutaneous tissue.22–26 Medical therapy has been disappointing. One case of subretinal T. crassiceps has been managed by surgery (Fig. 121.9).
DIPHYLLOBOTHRIASIS INTRODUCTION Diphyllobothriasis occurs in areas where uncooked fresh water fish as well as brackish water and marine fish are consumed.27–30
THE AGENT Figure 121.8 Scanning electron microscopy of Taenia solium scolex, showing effect of praziquantel. (Reproduced from Thomas H, Andrews P, Mehlhorn H. New results on the effect of praziquantel in experimental cysticercosis. Am J Trop Med Hyg. 1982;31:803–810.)
should be taken to prevent autoinfection or dissemination to others. In addition, since praziquantel kills the worm (Fig. 121.8) but does not inactivate the eggs released from the disintegrating gravid segments, cysticercosis is theoretically possible following treatment. Niclosamide, as a 2-g oral dose, is also effective, but less widely available. Nitazoxanide 500 mg twice daily for 3 days has also been used for T. saginata. Posttreatment follow-up stool examination should be performed after approximately 5 weeks in the case of T. solium and 3 months for T. saginata infections. The prognosis of treated taeniasis is excellent.
PREVENTION AND CONTROL Education is an important aspect of the prevention of taeniasis.8 Beef and pork tapeworm infection can be prevented by adequate cooking or freezing of beef and pork. T. solium cysticerci are killed by moderate
The distinction between Diphyllobothrium, the broad or fish tapeworms, and Taenia appears to have been well known to medieval physicians. Diphyllobothrium was the earliest tapeworm to be scientifically recognized by Linnaeus in 1758.1 The life cycle of Diphyllobothrium (Fig. 121.10) requires three hosts: (1) the definitive hosts are predominantly humans and fish-eating carnivores; (2) the first intermediate hosts are a large number of copepod species (crustaceans); and (3) the second intermediate hosts are freshwater, anadromous, and marine fish. Diphyllobothrium is a large tapeworm, often consisting of 3000–4000 segments or proglottids measuring from 3 to 12 m, that inhabits the ileum and jejunum. Diphyllobothrium tapeworms possess a scolex that is characteristically elongate or spoonshaped with a ventral and dorsal sucking groove or bothrium (Fig. 121.11). Egg production takes place in many proglottids simultaneously over a relatively extended period. The mature proglottid is broader than it is long and contains both testes and uterus. In the center of the mature proglottid is a characteristic dark rosette: the egg-filled uterus that aids in its recognition (Fig. 121.12). The uterus leads to a muscular uterine pore through which eggs pass into the feces. Typically, proglottids do not break off and migrate out of the body, but a million eggs are extruded daily into the small intestinal lumen by contractions of the uterine pore.
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Section II PATHOGENS
PART J: Cestode Infections
Diphyllobothrium (latum, pacificum, et al) Vague abdominal pain, bloating, diarrhea Rarely obstruction, megaloblastic anemia Adults (3–12 m) with scolex develop in small intestine
Humans (or fox, mink, bear, cat, dog, pig, walrus, seals, marine birds) ingest raw or undercooked infected fish (salmon, gefiltefish, ceviche)
Proglottids release immature eggs
Predator fish eats infected small fish
Unembryonated eggs passed in feces
Infected crustaceans ingested by small freshwater fish Procercoid larva released from crustacean develops into plerocercoid larva Eggs embryonate in water Procercoid larvae in body cavity of crustaceans
Coracidia hatch from eggs and are ingested by crustaceans
Figure 121.10 Diphylloborthrium (latum, pacificum et al.) life cycle.
Figure 121.11 Diphyllobothrium latum. Immature proglottids and scolex. The scolex bears grooves. (Courtesy of the American Society of Tropical Medicine and
Figure 121.13 Diphyllobothrium latum. Ovum.
(Courtesy of the American Society of Tropical
Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
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Figure 121.12 Diphyllobothrium latum. Proglottid. Note the rosette shape of the uterus. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Spent proglottids eventually disintegrate and pass out of the body. Occasionally, a long chain of proglottids is passed with the stool.12 The most widely recognized species, D. latum, has characteristic lightyellow eggs, which are 42–50 µm wide by 59–75 µm long, with an operculum or lid at one end and a characteristic tiny knob at the abopercular end (Fig. 121.13).12 In fresh water, the unembryonated egg requires approximately 10–14 days to mature at 15–25oC. After the operculum opens, a ciliated hexacanth, or six-hooked, embryo (coracidium) emerges; the swimming embryo must be ingested within 6–12 hours by one of many crustacean species of copepods (Cyclops sp. and Diaptomus sp.) or perish. The larva penetrates the midgut and enters the hemocoel of the copepod and in 10–21 days transforms into an elongated procercoid larva, reaching approximately 0.5 mm in length. It remains in the copepod until ingested by one of many species of small fresh-water plankton-eating fish (second intermediate host). The procercoid larva next makes its way
EPIDEMIOLOGY
and mild leukopenia. The development of pernicious anemia is usually associated with attachment of the tapeworm within 145 cm of the mouth. In this situation, more than 80% of vitamin B12 is absorbed by the worm, with a differential absorption pattern of 1000 : 1 in favor of the worm. Anemia associated with diphyllobothriasis is most frequently encountered in Scandinavia, likely due to differences between parasite species. Approximately 40% of people harboring the worm in Scandanavia have reduced serum vitamin B12 levels, but fewer than 2% develop anemia. Neurologic lesions due to vitamin B12 deficiency include subacute combined degeneration of the dorsal and lateral columns and peripheral nerve degeneration. The anemia and neurologic manifestations respond to vitamin B12 and do not recur after the worm has been expelled.
D. latum biotypes are mostly shallow fresh-water littorals with vegetation favoring the development of copepods and fish. Infection with this parasite is most prevalent in areas of the north temperate and subarctic zones, where fresh-water fish are commonly consumed.30–32 The estimated worldwide prevalence is approximately 9–10 million people. In North America, endemic foci have been found among Native Americans in Alaska and Canada. In the United States, fish from the lakes of the north-central region and from Florida and California are found to be infected. In highly endemic regions of Finnish and Russian Karelia, prevalences ranged from 25% to 100%.28 In North America, human cases have declined, whereas in South America there have been increased reports from fish, especially salmonids. Transmission has been brought under control in western Europe, and only a few cases now occur in Finland, where nearly 20% of the population was infected in the 1950s. However, areas of Sweden, France, Switzerland, northwestern Russia, the Danube and lower Volga basins, and the lake regions of northern Italy and Switzerland contain infected fish. Humans are the primary definitive host and most important reservoir of infection. Secondary intermediate hosts can be species of brackish and fresh-water fish, including anadromous fish that spawn in fresh water (e.g., salmon). Salmon has been the cause of the transmission of this parasite in Japan (D. nihonkaiense) and the west coast of the United States where sushi has been prepared with infected salmon.30 Eating raw, insufficiently cooked, or lightly pickled fish or fresh roe can transmit infection. In northern Minnesota and Michigan, where large numbers of people of Scandinavian background live, raw and pickled fish are still eaten, although infection with D. latum has now become less common. Other diphyllobothriids can cause disease. D. pacificum has been reported from Japan and is endemic in coastal areas of Peru. Unlike D. latum, infection with this parasite is acquired from eating marine fish that has been prepared in lime juice (e.g., ceviche). Diplogonoporus grandis, another member of this group, is found in Japan and thought to be acquired by consumption of raw anchovies and sardines. Other species of Diphyllobothrium, such as D. dendriticum, D. klebaanovskii, D. cordatum, D. dalliae, D. ursi, and D. nihonkaiense, are found as occasional human parasites.31,32
INTRODUCTION
THE DISEASE
Two species of Hymenolepis infect humans: H. nana and H. diminuta. They are cosmopolitan in distribution. H. nana is common in warmer climates whereas H. diminuta only occasionally infects humans.36
Infection is usually associated with few symptoms or pathologic changes in the intestinal mucosa. Often, infection is first recognized in an asymptomatic patient as a result of a stool examination carried out for other reasons. However, some patients complain of vague abdominal pain and others describe the sensation that “something is moving inside.” Others describe bloating, sore tongue, sore gums, allergic symptoms, headache, hunger pains, loss of appetite, or increased appetite. Rarely, mechanical intestinal obstruction may occur as a result of several worms becoming entangled. Diarrhea may also occur. Almost all patients become aware of the infection when spontaneously passing a large section of the spent proglottids; most often this startling event brings the patient to the office or clinic. Unlike the proglottids of T. saginata, those of D. latum do not spontaneously crawl through the anus.33 In a small proportion of patients, D. latum causes pernicious anemia, a hyperchromic, macrocytic, megaloblastic anemia with thrombocytopenia
DIAGNOSIS The infection can be diagnosed readily by finding characteristic ova in the feces (see Fig. 121.10).12 The eggs can usually be identified without concentration due to the large number of eggs. However, species recognition or differentiation usually requires recovery of the scolex. Molecular methods have been employed for the diagnosis of Diphyllobothrium sp.34 Thus, restriction fragment length polymorphism has been used to speciate D. latum from D. nihonkaiense. It is not uncommon to find mild eosinophilia in patients with D. latum infection.
Taenia and Other Tapeworm Infections Chapter 121
through the tissues of the fish and settles in almost any organ or tissue of the second intermediate host where it transforms into a plerocercoid (sparganum) larva. The latter has the characteristic rudiments of a scolex but is unsegmented. Next, these fish are eaten by larger carnivorous fish, such as perch, wall-eyed pike, or the burbot (paratenic or transport hosts). The plerocercoid larvae later reinvade the tissues of these fish and if consumed raw or inadequately cooked by a suitable host (i.e., humans, carnivorous mammals), the larva attaches to the wall of the small intestine and becomes a mature tapeworm in approximately 5 or 6 weeks.
TREATMENT AND PROGNOSIS The treatment of choice is praziquantel, which is administered as a single dose of 5–10 mg/kg for both adults and children.35 Alternatively, niclosamide is given as a 2-g dose once for adults and 50 mg/kg for children. The prognosis for treated individuals is excellent.
PREVENTION AND CONTROL Careful cooking of fresh-water fish would eliminate all possibility of human infection. The sale of fish originating in heavily infected lakes should be regulated because freezing at –10°C for 24 hours suffices to kill the plerocercoid larva. In the United States, smoked salmon is usually brined before smoking and is not considered a source of infection. Other control measures include the education of cooks regarding the sampling of raw fish during preparation. In addition, sanitary sewage disposal rather than the dumping of raw sewage into fresh-water lakes would prevent viable eggs from contaminating various intermediate hosts.
HYMENOLEPIASIS
THE AGENT (Fig. 121.14) The adult H. nana is approximately 0.5 cm long and is found attached to the mucosa of the ileum by a scolex that has four suckers and a retractable, armed rostellum (Fig. 121.15). The entire worm usually consists of a scolex and approximately 200 proglottids. The uterus in a gravid proglottid contains approximately 100–200 mature eggs that are 30– 60 µm in diameter (Fig. 121.16).36 The eggs are passed in the feces and ingested by a new human or the same host (autoinfection). The embryo hatches in the small intestine and penetrates a villus, where it becomes a cysticercoid larva (Fig. 121.17). Upon maturation, in 3 or 4 days, it emerges from the tissue and attaches to the intestinal mucosa by its scolex. In 2 or 3 weeks, the new worm is producing eggs. Hyperinfection can occur when eggs liberated in the small intestine hatch and
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Section II
Hymenolepis nana Abdominal pain, mucoid diarrhea, especially in children; Rarely pruritus, seizures
PATHOGENS
Oncosphere hatches; cysticeroid develops in intestinal villus
Eggs released through the genital atrium of gravid proglottids Gravid proglottids can also disintegrate, releasing eggs that are passed in stools
PART J: Cestode Infections
Adult worm (2–4 cm) with scolex develop in ileum
Embryonated eggs ingested by humans from contaminated food, water, or hands or from ingestion of infected insects (by children or rodents)
Autoinfection can occur if eggs remain in the intestine The eggs then release the hexocath embryo, which penetrates the intestinal villus continuing the cycle Direct ingestion of eggs (person to person)
Cysticercoid develops in insect
Eggs ingested by insects
Figure 121.14 Hymenolepis nana life cycle.
Figure 121.15 Hymenolepis nana scolex and proglottids. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.17 Hymenolepis nana cysticercoid stage in the small intestine. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
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Figure 121.16 Hymenolepis nana ovum. and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
(Courtesy of the American Society of Tropical Medicine
immediately penetrate a villus to undergo a new cycle. As a result of hyperinfection, children may harbor many hundreds or even thousands of adult worms.The entire life history from ingestion of the egg to adulthood requires approximately 10–14 days. Eggs are first seen in the stools in approximately 25–30 days. H. nana is spread from hand to mouth. The closely related species, H. diminuta, which commonly parasitizes the rat and mouse, infrequently infects humans.36 Most of the more than 200 reported human infections have been in children younger than 3 years of age. The adult worm is 3–5 mm and possesses a club-shaped scolex that has a rudimentary apical unarmed rostellum with four small suckers. The ova are spherical and 60–86 µm in diameter.12 In contrast to the eggs of H. nana, there are no polar filaments. Development of this tapeworm requires an intermediate host. Presumably, infected rat fleas (Nosopsyllus
EPIDEMIOLOGY The dwarf tapeworm, H. nana, is found in most warm regions of the world. It is the most common cestode infection worldwide with endemic foci in Latin America, southern Europe, Russia and the former Soviet republics, the Indian subcontinent, and southeastern United States.36
THE DISEASE
The proglottids have a double set of reproductive organs with genital pores midway on each lateral margin (Fig. 121.20). The gravid proglottids are packed with 15–25 eggs. Each egg is 35–60 µm in diameter and contains an oncosphere with six hooklets. The strobila can migrate several centimeters per hour and pass out of the anus spontaneously or with the feces. Eggs are expelled by contraction or disintegration of the proglottid.39
EPIDEMIOLOGY Most infections occur in children younger than 8 years old as well as infants younger than 6 months of age.40–44 The ova of Dipylidium are ingested by the larval dog or cat flea, in which they become cysticercoid larvae. Infection occurs following accidental ingestion of the infected flea.
Most cases are asymptomatic. Young children may develop symptoms when many worms are present.37,38 These patients may have loose bowel movements or occasionally frank diarrhea with mucus but no blood. Diffuse, persistent abdominal pain is the most common complaint. Pruritus ani and nasi are occasionally encountered. Many children have sleep and behavioral disturbances that resolve after successful therapy. Serious neurologic disturbances such as seizures have been reported. Many patients with hymenolepiasis have a moderate eosinophilia of 5–10% and skin eruptions.37
Infection is often asymptomatic. The most common symptom is noting proglottids in stool, which are similar in size and color to grains of rice. Some children have intestinal disturbances, including abdominal pain and diarrhea (Fig. 121.21).40–42 Allergic manifestations such as urticaria and pruritus ani have been reported; intestinal obstruction has been a rare complication.1,2
DIAGNOSIS
TREATMENT AND PREVENTION
The diagnosis of hymenolepiasis rests on finding the characteristic ova by stool examination. Stools of the entire family must be checked before therapy is initiated because other members of a household are commonly infected, and they must also be treated for therapy to be successful. Posttreatment stool examinations should be done after 5 weeks and again after 3 months.1–3
Treatment is with 5–10 mg/kg of praziquantel once for both adults and children. An alternative therapy is 2 g of niclosamide once for adults and 25 mg/kg once for children. Children should not be allowed to fondle and kiss dogs and cats. Periodic treatment of pets for tapeworm infection and periodic use of insecticides to kill ectoparasites will control the spread of this infection.
TREATMENT AND PROGNOSIS
SPARGANOSIS
Praziquantel is the drug of choice for the treatment of hymenolepiasis and is highly effective in a single dose of 15 mg/kg. It not only eliminates adult worms but also, unlike other anthelminthics, is efficiently absorbed and kills the larval stages (cysticercoids) in the submucosa.2 Treated individuals have an excellent prognosis. Niclosamide (2 g in a single dose) and nitazoxanide (500 mg PO twice daily for 3 days) are alternative therapies. Recently nitazoxianide has been evaluated in field trials in Peru.38
INTRODUCTION
THE DISEASE
Sparganosis is an uncommon parasitic infection usually caused by the migration of larval tapeworms of the genus Spirometra.
THE AGENT
The dog tapeworm, Dipylidium caninum, is also a frequent parasite of cats and wild carnivores worldwide. It is an occasional parasite of the small intestine of humans.
Human sparganosis may occur following ingestion of species of Cyclops that are infected with the procercoid larva of various pseudophyllidean tapeworms of the species Spirometra.1,45 The procercoid penetrates the intestinal wall and migrates to various sites, including subcutaneous tissues, the central nervous system, and muscle, where they develop to second-stage larvae or plerocercoids. This condition is called sparganosis. Ingestion, either deliberately or accidentally, of infected uncooked flesh of an amphibian, reptile, bird, or mammal harboring plerocercoid larvae may also be a source of infection. All the spargana are morphologically indistinguishable. Since these worms cannot mature in humans, they migrate into the tissues and remain as plerocercoid larvae. However, in the few instances in which the larvae were allowed to complete their life cycle in dogs or cats, they were identified as members of the genus Spirometra. In some cases in the United States, they were identified as S. mansoni. Molecular approaches have been applied to this parasite that may aid in the diagnosis of this infection.46
THE AGENT (Fig. 121.18)
EPIDEMIOLOGY
The adult worm is approximately 15–20 cm long and usually has approximately 60–175 proglottids. The scolex is characteristic, being rhomboid with four oval suckers and an armed retractable conical rostellum containing 30–150 thorn-shaped hooks arranged in transverse rows (Fig. 121.19).
Sparganosis is reported in many areas of the world, including China, Japan, Southeast Asia, and South and Central America, and has occasionally been reported in various areas of the United States and Europe.47,48
PREVENTION AND CONTROL This infection is spread from person to person and therefore extremely difficult to control. Education in hygiene is probably the only practical way to reduce the incidence.
DIPYLIDIASIS INTRODUCTION
Taenia and Other Tapeworm Infections Chapter 121
and Xenopsylla) and mealworms (Tenebrio) are accidentally ingested, and the mature adult develops in approximately 3 weeks. Cockroaches may also serve as intermediate hosts and become infected by ingesting eggs passed in rodent feces.
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Adults (15–20 cm) with scolex develop in intestine
PART J: Cestode Infections
PATHOGENS
Section II
Dipylidium caninum Abdominal pain, mucoid diarrhea, Occasional urticaria, pruritus ani, rarely obstruction
Gravid proglottids are passed intact in the feces or emerge from perianal region of either animal or human hosts Human (usually children) or animals ingest infected fleas
Oncospheres hatch from the eggs and penetrate the intestinal wall of the larvae Cysticercoid larvae develop in the body cavity of adult flea
Egg packets containing embryonated eggs are ingested by larval stage of flea
Figure 121.18 Dipylidium caninum life cycle.
Figure 121.19 Dipylidium caninum scolex. Three of the four suckers and the retracted armed rostellum can be seen. (Courtesy of the American Society of
Figure 121.21 Egg pockets of Dipylidium caninum in an infant.
(Courtesy of
Dr Patrick Adegboyega, Department of Pathology, University of Texas Medical Branch, Galveston, TX.)
Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
THE DISEASE
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Figure 121.20 Dipylidium caninum proglottid. Note the two genital pores and the massing of the ova. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
The presence of plerocercoids in subcutaneous tissues is typically associated with a nodular mass consisting of tissue necrosis and a granulomatous inflammation with lymphocytes, plasma cells, and eosinophils (Fig. 121.22).49–51 Swelling and edema are often painful (Fig. 121.23). Any part of the body may be involved, including the neck, breast, scrotum, and pleura.50–55 Raw amphibian poultices harboring plerocercoid larvae applied to the eye have also been a cause of ocular sparganosis and may impair vision.56,57 Cerebral sparganosis is a rare complication of this infection. In the brain, the presence of the parasite evokes an intense inflammatory
(Courtesy of the American Society of Tropical
Medicine and Hygiene/Zaiman: A Presentation of Pictorial Parasites.)
Figure 121.24 Sparganum removed from the right occipital cortex. (Reproduced from Kim DG, Paek SH, Chang KH, et al. Cerebral sparganosis: clinical manifestations, treatment, and outcome. J Neurosurg. 1996;85:1066–1071, with permission of the Journal of Neurosurgery and the authors.)
unknown genus and species proliferate in the tissues as independent organisms. In several instances, thousands of spargana have been found in the subcutaneous tissues.45
DIAGNOSIS
Figure 121.23 Sparganosis: computed tomography scan of the thigh showing a circular hyperlucent lesion with inflammatory response of adjacent tissues. (Courtesy of the American Society of Tropical Medicine and Hygiene/Zaiman: A Presentation
In general, the diagnosis is based on pathological examination of biopsy or autopsy specimens and/or direct visualization of the parasite (Fig. 121.24). In the case of cerebral sparganosis, magnetic resonance imaging is most helpful in the diagnosis and is usually followed by stereotactic biopsies.61,62,67 Serodiagnosis using monoclonal antibodies in a competition enzyme-linked immunosorbent assay has been reported.68,69 Falsepositive results may occur when Clonorchis and Paragonimus infections are present.
Taenia and Other Tapeworm Infections Chapter 121
Figure 121.22 Sparganum: abscess in muscle.
of Pictorial Parasites.)
TREATMENT AND PREVENTION response. Pathological and radiographic (computed tomography and magnetic resonance imaging) studies demonstrate white-matter degeneration, cortical atrophy, ventricular dilatation, punctuate calcifications, irregular or nodular enhancement, vasculitis, and hemorrhage.58–66 An unusual manifestation of sparganosis is a condition known as sparganum proliferum, in which larvae of a pseudophyllidean tapeworm of
Treatment of sparganosis has been surgical removal of the larvae. Ocular sparganosis is sometimes treated by killing the larvae and allowing the organisms to resorb, although surgical removal has come into favor. Mebendazole, albendazole, and praziquantel have not been demonstrated to be useful. Spargana are destroyed by flash freezing at 10°C for 24 hours.
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