Abdominal parasitic infection
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]
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Abdominal parasitic infection Main page |
Overview
Ascaris lumbricoides
Mode of infection
- Ingestion of eggs secreted in the feces of humans or pigs
- Ingesting uncooked pig or chicken liver bearing larvae of A. suum [13].
Epidemiology and demographics
- Approximately 800 million people are infected [2,5].
- Majority of individuals with ascariasis live in Asia (73 percent), Africa (12 percent), and South America (8 percent); some populations have infection rates as high as 95 percent [2,14].
- Ascariasis is most common among children 2 to 10 years of age, and the prevalence of infection diminishes among individuals >15 years of age. Infections tend to cluster in families [15].
Clinical manifestations
- During the late phase of infection (six to eight weeks after egg ingestion), symptoms of ascariasis may consist of nonspecific symptoms such as abdominal discomfort, anorexia, nausea, vomiting, and diarrhea. Macroscopic adult worms are passed in the stool.
Complications
- Intestinal obstruction: In endemic areas, 5 to 35 percent of all bowel obstructions are due to ascariasis [22]. Approximately 85 percent of obstructions due to ascariasis occur in children between one and five years of age. The overall incidence of obstruction associated with ascariasis in children is approximately 1 in 500. Obstruction occurs most commonly at the ileocecal valve.
- Migration of adult Ascaris worms into the biliary tree can cause biliary colic, biliary strictures, acalculous cholecystitis, ascending cholangitis, obstructive jaundice, liver abscesses, and bile duct perforation with peritonitis [43-45].
Laboratory findings
- The diagnosis of ascariasis is generally established via stool microscopy for evaluation of Ascaris ova (the eggs of A. lumbricoides and A. suum are indistinguishable).
- Characteristic eggs may be seen on direct examination of stool or following concentration techniques.
- Peripheral eosinophilia may be observed during the late phase of infection but is more likely to be observed during the early phase [30].
Imaging findings
- Barium swallow may also demonstrate adult Ascaris worms, which manifest as elongated filling defects of the small bowel. The worms may ingest barium; in such cases, the worm's alimentary canal appears as a white thread bisecting the length of the worm's body (image 3) [21].
- Computed tomography (CT) scanning or magnetic resonance imaging (MRI) may demonstrate worms in the bowel.
- Imaging the worm in cross-section demonstrates a "bull's eye" appearance.
- CT or MRI may demonstrate adult Ascaris worms in the liver or bile ducts. Magnetic resonance cholangiopancreatography (MRCP) may detect adult worms in bile or pancreatic ducts.
Treatment
| Drug | Dosage |
| Albendazole | 400 mg orally once |
| Mebendazole | 100 mg orally twice daily for 3 days or 500 mg orally once |
| Ivermectin | 150-200 mcg/kg orally once |
Necator americanus
- Approximetly 800 million people are infected with hookworms worldwide [3,5].
- The prevalence of hookworm infection in rural areas of the southeastern United States in the early 20th century was high; extensive control efforts have diminished the prevalence.
Acute gastrointestinal symptoms
- Patients may experience gastrointestinal symptoms at the time of larval migration to the small intestine. Nausea, diarrhea, vomiting, midepigastric pain (usually with postprandial accentuation), and increased flatulence have been observed in individuals with naturally acquired infections [6] and in experimentally infected volunteers [11,12].
- Initial infections may be associated with gastrointestinal symptoms more frequently than subsequent infections. In one individual who was experimentally infected on four occasions, gastrointestinal symptoms and diarrhea were marked with the first infection, mild after the second, and absent after the third and fourth infections [11].
Chronic nutritional impairment
- The major impact of hookworm infection is on nutritional status. This is particularly important in endemic areas where children and pregnant women may have limited access to adequate nourishment. In addition, maternal hookworm infection is associated with low birthweight.
- Hookworms cause blood loss during attachment to the intestinal mucosa by lacerating capillaries and ingesting extravasated blood. This process is facilitated by the production of anticoagulant peptides that inhibit activated factor X and factor VIIa/tissue factor complex [14] and inhibit platelet activation [15]. Each N. americanus and A. duodenale worm consumes about 0.3 mL and 0.5 mL of blood per day, respectively. The daily losses of blood, iron, and albumin can lead to anemia and contribute to impaired nutrition, especially in patients with heavy infection [10,16].
Stool examination
- Stool examination for the eggs of N. americanus or A. duodenale is useful for detection of clinically significant hookworm infection.
- Fecal egg excretion becomes detectable about eight weeks after dermal penetration of N. americanus infection and up to 38 weeks after dermal penetration of A. duodenale [8].
- Stool examination is not helpful prior to established intestinal tract disease, including during early stages of dermal, pulmonary, or intestinal involvement.
- Eosinophilia has been attributed to persistent attachment of adult worms to the intestinal mucosa.
- In untreated infections, eosinophilia slowly diminishes in magnitude but can remain elevated for several years [9].
Treatment
- Anthelminthic treatment of hookworm infection consists of albendazole. [26,27].
- Mebendazole is an acceptable alternative therapy; 100 mg twice daily for three days is more effective than a single dose of 500 mg.
- An alternative therapy is pyrantel pamoate (11 mg/kg per day for three days, not to exceed 1 g/day). [26,27,29,30]
Giardia lamblia
- High-risk groups include infants, young children, international adoptees, travelers, immunocompromised individuals, and patients with cystic fibrosis [2]. [1].
- The prevalence of giardiasis has been reported to be as high as 20 to 40 percent [1]. The highest rates of infection in resource-limited areas occur among children <5 years.
- Many individuals with G. duodenalis identified in stool samples are asymptomatic, a point highlighted by studies that identified Giardia more commonly in the stool of asymptomatic individuals than among individuals with acute diarrhea [3].
- In the United States in 2012, a total of 15,223 cases were reported [7].
- Transmission of infectious Giardia cysts to humans may occur via three routes: waterborne, foodborne, or fecal-oral transmission [11].
- Water is a major source of giardiasis transmission. Giardia cysts survive readily in mountain streams, as they are hardy in cold water. Water-dwelling mammals, such as beavers, can become infected and may serve as ongoing sources of water contamination [12]. For these reasons, giardiasis is an important cause of diarrheal illness among hikers in wilderness areas who drink water that has not been adequately filtered, treated, or boiled.
- Deep well water is usually safe because filtration of water through soil removes Giardia cysts. Giardia cysts are resistant to chlorination; therefore, bacterial coliform counts are not a reliable measure of Giardia contamination in chlorinated water sources.
- Transmission of giardiasis can occur via ingestion of raw or undercooked food contaminated with cysts or via food that is contaminated after cooking [13,14].
- Person-to-person transmission can occur in settings in which there is fecal incontinence and poor hygiene, such as childcare centers [15]. The risk of acquisition and transmission is greatest for young children who are not yet toilet trained; such children can also serve as a source for secondary cases within households [15].
- Giardiasis can be transmitted via heterosexual or homosexual anal-oral sexual contact [16,17].
Clinical presentation
Asymptomatic infection
Asymptomatic infection occurs in both children and adults, and asymptomatic cyst shedding can last six months or more [30,31].
Acute giardiasis
- Symptoms of acute giardiasis include diarrhea, malaise, steatorrhea, abdominal cramps and bloating, nausea, and weight loss.
- Symptoms usually develop after an incubation period of 7 to 14 days. Onset of acute gastrointestinal symptoms within one week of exposure is not likely attributable to infection with Giardia. Symptoms may last two to four weeks.
Chronic giardiasis
Symptoms of chronic giardiasis may include oose stools, steatorrhea, profound weight loss, malabsorption, malaise, and fatigue.
Complications
- In a small number of patients, persistent infection is associated with development of malabsorption and weight loss [38].
- Chronic giardiasis may resemble other diseases associated with malabsorption, including inflammatory bowel disease [39].
Laboratory diagnosis
Antigen detection assays
- A number of immunoassays using antibodies against cyst or trophozoite antigens have been developed for stool analysis. Available kits include direct immunofluorescent assays (DFA) that use fluorescein-tagged monoclonal antibodies, immunochromatographic assays, and enzyme-linked immunosorbent assays (ELISAs).
- These methods have greater sensitivity and faster turn-around time than conventional stool microscopy methods. Specificity and cost are usually relatively comparable. Some studies have shown DFA to have the highest sensitivity [46,47].
Nucleic acid amplification assays
- Nucleic acid amplification assays (NAAT) have been developed to detect Giardia in stool samples [45,52,53]; some remain research tools.
- The Luminex xTAG Gastrointestinal Pathogen Panel can detect various viral, bacterial, and protozoan (including G. duodenalis) intestinal pathogens [55,56].
Stool microscopy
- Stool microscopy to detect Giardia can be specific and may also be useful for detecting other potential parasitic causes of gastrointestinal symptoms.
- Limitations include intermittent excretion of Giardia cysts (necessitating up to three stool exams), cumbersome processing procedures, and technician expertise.
Treatment
Preferred agents
- Preferred agents for initial treatment of giardiasis include tinidazole and nitazoxanide [5,10-16]. For treatment of patients ≥3 years of age, we favor tinidazole since it has a longer half-life than nitazoxanide and may be administered as a single dose with high efficacy (>90 percent).
- For treatment of patients 12 to 36 months of age, we favor nitazoxanide. Given limited data regarding use of tinidazole and nitazoxanide for patients <12 months of age, we favor metronidazole for these patients. Drug dosing is summarized in the table (table 1).
Tinidazole
- Tinidazole is approved by the US Food and Drug Administration (FDA) for treatment of giardiasis in patients ≥3 years of age; dosing is summarized in the table (table 1) [21,22]. Tinidazole is available only in tablet form. For children unable to swallow tablets, the tablets may be crushed by a pharmacist and mixed with flavored syrup; the suspension should be shaken before use and is good for seven days at room temperature [23].
Schistosoma
- The prevalence of schistosomiasis is highest in sub-Saharan Africa.
- It has been estimated that more than 200 million people are infected, and schistosomiasis may cause up to 200,000 deaths annually [9,10]
Clinical presentation
Acute schistosomiasis syndrome
- Clinical manifestations of acute schistosomiasis syndrome include sudden onset of fever, urticaria and angioedema, chills, myalgias, arthralgias, dry cough, diarrhea, abdominal pain, and headache [52-56]. Only one or a few of the above symptoms may be observed, and fever is not an essential component of the illness [57]. The symptoms are usually relatively mild and resolve spontaneously over a period of a few days to a few weeks. Occasionally persistent manifestations are observed including weight loss, dyspnea, and chronic diarrhea. In rare cases, neurologic symptoms suggestive of encephalitis can occur [58].
Chronic infection
- Chronic infection related to schistosomiasis is most common among individuals in endemic areas with ongoing exposure.
- The severity of disease is related to the number of eggs trapped in tissues, their anatomic distribution, the duration and intensity of infection, and the host immune response [17,63].
Intestinal schistosomiasis
- Intestinal schistosomiasis is caused by infection due to S. mansoni, S. japonicum, S. intercalatum, S. mekongi, and, occasionally, S. haematobium. The most common symptoms include chronic or intermittent abdominal pain, poor appetite, and diarrhea. In heavy infection, chronic colonic ulceration may lead to intestinal bleeding and iron deficiency anemia [66-68]. Intestinal polyps and dysplasia can arise due to granulomatous inflammation surrounding eggs deposited in the bowel wall (picture 1) [69,70]. Bowel strictures can also develop. In rare cases, an inflammatory mass can lead to obstruction or acute appendicitis [71,72].
Hepatosplenic schistosomiasis
- Among adults with chronic infection, the left liver lobe is enlarged with a sharp edge, and splenomegaly may extend below the umbilicus and into the pelvis in some cases [36,73,74].
- The predominant pathological process consists of collagen deposition in the periportal spaces, which causes periportal fibrosis. [20,74,76,77]
- This leads to occlusion of the portal veins, portal hypertension with splenomegaly, portocaval shunting, and gastrointestinal varices. On physical examination, the liver is firm and nodular. Hepatocellular liver function is not impaired.
Pulmonary complications
- Pulmonary manifestations of schistosomiasis occur most frequently among patients with hepatosplenic disease due to chronic infection with S. mansoni, S. japonicum, or S. haematobium [82].
- Progression of disease may be associated with cardiac enlargement and pulmonary artery dilatation. These manifestations represent end-stage disease and are generally irreversible.
- Dyspnea is the primary clinical manifestation [84].
- Chest radiography demonstrates fine miliary nodules.
Genitourinary schistosomiasis
- In early infection, eggs are excreted in the urine and patients present with microscopic or macroscopic hematuria and/or pyuria [41,92-94]. Blood is usually seen at the end of voiding terminal hematuria, although in severe cases hematuria may be observed for the entire duration of voiding [17].
- In early chronic infection, the eggs provoke granulomatous inflammation, ulcerations, and development of pseudopolyps in the vesical and ureteral walls, which may be observed on cystoscopy and mimic malignancy. [41,92,93].
Laboratory findings
- Eosinophilia is observed in 30 to 60 percent of patients [123-125]. Eosinophilia is very common among patients with acute schistosomiasis infection syndrome, a hypersensitivity that occurs most frequently among travelers with new infection [46,57,126].
- Thrombocytopenia may be observed in patients with portal hypertension due to hepatosplenic schistosomiasis secondary to splenic sequestration in an enlarged spleen.
- Liver enzymes are rarely elevated, even in established hepatic fibrosis due to schistosomiasis.
- Hematuria and/or leukocyturia are common in the setting of S. haematobium infection [129-133].
Microscopy
- Identification of schistosome eggs in a stool or urine sample via microscopy is the gold standard for the diagnosis of schistosomiasis. It can also be used for species identification and to measure the parasite burden (picture 1). The sensitivity of microscopy is low in light infections and in acute infection.
Infection intensity
- Determining the intensity of infection is important in endemic settings, since parasite burden correlates with the likelihood of complications. The intensity of intestinal schistosomiasis is classified as light (up to 100 eggs per gram), moderate (100 to 400 eggs per gram), or severe (>400 eggs per gram). The intensity of urinary schistosomiasis is classified as light to moderate (up to 50 eggs/10 mL) or severe (>50 eggs/10 mL) [22].
Serology
- The assays available include ELISA, radioimmunoassay, indirect hemagglutination, Western blot, and complement fixation [27,28]. Serologic tests use a broad array of schistosome antigens including extracts of adult worms, cercarial antigens, or egg extracts such as the S. mansoni soluble egg antigen (SmSEA). Most commercially produced antibody test assays are not species specific; therefore, these assays are generally used as screening tests for schistosome infection.
Molecular tests
- Some PCR assays facilitate species identification [57]. One study of PCR on urine samples noted sensitivity and specificity of 94 and 100 percent, respectively; use of an assay specific for S. mansoni was notable for sensitivity and specificity of 100 and 90 percent, respectively [49]. Another assay for S. haematobium is promising for use with serum, urine, or stool [55]. More elaborate schistosome genome sequencing techniques are also used to determine the epidemiology of schistosome hybrids occasionally found in humans [58].
Biopsy
- Histopathology of superficial rectal biopsies is more sensitive than stool microscopy and may demonstrate eggs even when multiple stool specimens are negative. In one study of 135 British expatriates with S. mansoni infection, eggs were detected on rectal biopsy in 61 percent of patients and on stool examination in 39 percent of patients [21].
Treatment
Praziquantel
- Praziquantel alters the tegument structure of adult worms and increases calcium ion permeability. Calcium ions accumulate in the cytosol, leading to muscular contractions and subsequent paralysis. Damage to the tegument membrane also induces a host immune response to parasite antigens [39]. Therefore, the efficacy of praziquantel depends on both the parasite burden of infection and the host immune defense [40].
- Praziquantel is readily absorbed when taken orally with food [9]. Adverse effects of praziquantel occur in approximately one-third of patients and are generally mild. They include dizziness, headache, vomiting, abdominal pain, diarrhea, and pruritus. These symptoms may be attributable to the drug itself and/or to the host immune response to dying parasites.
Alternative therapies
- Oxamniquine has been used for refractory schistosomiasis infection and may be as effective as praziquantel; it is contraindicated in pregnancy and in general is not as effective as praziquantel [56,57].
- Mefloquine has limited action on mature worms. The addition of mefloquine or artesunate to praziquantel is not beneficial [59]. Combination praziquantel with artemether may offer some benefit [60].
Strongyloidis Stercoralis
- In tropical and subtropical regions, the overall regional prevalence may exceed 25 percent.
- The highest rates of infection in the United States are among residents of the southeastern states [3,4] and among individuals who have been in endemic areas.
Gastrointestinal symptoms
Patients may also experience diarrhea, anorexia, nausea, and vomiting. Epigastric pain may mimic a duodenal ulcer, except that food ingestion may aggravate the pain of strongyloidiasis. Chronic enterocolitis and malabsorption can result from a high intestinal worm burden.
Hyperinfection syndrome
The most common manifestations of the hyperinfection syndrome include [28,34,37]:
●Fever
●Nausea and vomiting
●Anorexia
●Diarrhea
●Abdominal pain
●Dyspnea
●Wheezing
●Hemoptysis
●Cough
Diagnosis
- Standard stool examination is notoriously insensitive for detecting Strongyloides (<50 percent sensitivity) [86].
- Aspiration of duodenojejunal fluid or the use of a string test (Enterotest) is sometimes used to detect Strongyloides larvae in patients with negative stool samples [85].
- Polymerase chain reaction (PCR) tests have also been developed for detection of Strongyloides in stool samples and have been found to be more sensitive and more reliable in detection of S. stercoralis compared with parasitological methods [97,98]. However, PCR tests are not yet widely available.
Serology
- Diagnosis of strongyloidiasis by enzyme-linked immunosorbent assay (ELISA) has proven useful in immunocompetent individuals, both in symptomatic and asymptomatic strongyloidiasis [99,100]. The ELISA for detecting S. stercoralis infection detects immunoglobulin (Ig)G to filariform larvae. Negative test results in immunocompetent individuals decrease the likelihood that infection is present; however, some ELISA serologies run by commercial laboratories are of variable reliability. In addition, ELISA results can be falsely negative in immunocompromised hosts [96]. False-positive results may occur in the presence of other helminth infections [90].
Endoscopy
- Upper endoscopy is not usually needed to establish a diagnosis of strongyloidiasis. However, it may be performed in patients with gastrointestinal symptoms with unsuspected disease. Strongyloidiasis has a broad range of endoscopic features [105]:
- In the duodenum, the findings included edema, brown discoloration of the mucosa, erythematous spots, subepithelial hemorrhages, and megaduodenum.
- In the colon, the findings include loss of vascular pattern, edema, aphthous ulcers, erosions, serpiginous ulcerations, and xanthoma-like lesions.
- In the stomach, thickened folds and mucosal erosions are seen [106].
Treatment
Ivermectin
Ivermectin is usually administered as two single 200 mcg/kg doses of ivermectin administered on two consecutive days [109,112].
Albendazole
Albendazole (400 mg by mouth on empty stomach twice daily for three to seven days) also has activity against Strongyloides [113,114]. the efficacy of albendazole has been lower than that of ivermectin, with a mean of 60 percent effectiveness for three days of albendazole versus 92 percent for ivermectin [115].
E. Histolytica (Amebiasis)
- Areas with high rates of amebic infection include India, Africa, Mexico, and parts of Central and South America. The overall prevalence of amebic infection may be as high as 50 percent in some areas [3].
- Infection with E. dispar occurs approximately 10 times more frequently than infection with E. histolytica [3].
Clinical presentation
- The majority of entamoeba infections are asymptomatic; this includes 90 percent of E. histolyticainfections.
- Clinical amebiasis generally has a subacute onset, usually over one to three weeks. Symptoms range from mild diarrhea to severe dysentery, producing abdominal pain (12 to 80 percent), diarrhea (94 to 100 percent), and bloody stools (94 to 100 percent), to fulminant amebic colitis. Weight loss occurs in about half of patients, and fever occurs in up to 38 percent. Amebic dysentery is diarrhea with visible blood and mucus in stools and the presence of hematophagous trophozoites (trophozoites with ingested red blood cells) in stools or tissues [24]. Fulminant colitis with bowel necrosis leading to perforation, and peritonitis has been observed in approximately 0.5 percent of cases; associated mortality rate is more than 40 percent. Toxic megacolon can also develop.
- Amebic colitis has been recognized in asymptomatic patients. Among 5193 asymptomatic individuals in Japan undergoing colonoscopy for evaluation of positive fecal occult blood tests, for example, four were found to have amebic ulcerative lesions in the cecum or ascending colon [25].
Diagnosis
Stool microscopy
- The demonstration of cysts or trophozoites in the stool suggests intestinal amebiasis, but microscopy cannot differentiate between E. histolytica and E. dispar or E. moshkovskii strains. In addition, microscopy requires specialized expertise and is subject to operator error [29].
Antigen testing
- Stool and serum antigen detection assays that use monoclonal antibodies to bind to epitopes present on pathogenic E. histolytica strains (but not on nonpathogenic E. dispar strains) are commercially available for diagnosis of E. histolytica infection [30]. Antigen detection kits using enzyme-linked immunosorbent assay (ELISA), radioimmunoassay, or immunofluorescence have been developed [31-33].
- Antigen detection has many advantages, including ease and rapidity of the tests, capacity to differentiate between strains, greater sensitivity than microscopy, and potential for diagnosis in early infection and in endemic areas (where serology is less useful).
Serology
- Antibodies are detectable within five to seven days of acute infection and may persist for years.
- Approximately 10 to 35 percent of uninfected individuals in endemic areas have antiamebic antibodies due to previous infection with E. histolytica [3].
- Negative serology is helpful for exclusion of disease, but positive serology cannot distinguish between acute and previous infection.
Molecular methods
- Techniques can detect E. histolytica in stool specimens [32,35,36]. Studies have shown that PCR is significantly more sensitive than microscopy and that it was 100 percent specific for E. histolytica [37,38].
- PCR is about 100 times more sensitive than fecal antigen tests [39].
TREATMENT
- All E. histolytica infections should be treated, even in the absence of symptoms, given the potential risk of developing invasive disease and the risk of spread to family members [1,3].
- The goals of antibiotic therapy of intestinal amebiasis are to eliminate the invading trophozoites and to eradicate intestinal carriage of the organism.
Taeniasis
Taeniasis
There are two main species of Taenia for which humans are the only definitive hosts. These are Taenia saginata, the beef tapeworm, and Taenia solium, the pork tapeworm. T. saginata occurs worldwide but is most common in areas where consumption of undercooked beef is customary, such as Europe and parts of Asia. The third species, T. asiatica, is found among pigs in Taiwan, Korea, China, Vietnam, Indonesia, Thailand, the Philippines, and Japan [1-5]. Concurrent infections with more than one Taenia species have been described [6].
Issues related to T. saginata are discussed here. The epidemiology, transmission, clinical manifestations, diagnosis, treatment, and prevention of cysticercosis due to T. solium are discussed separately. (See "Epidemiology, transmission, and prevention of cysticercosis" and "Clinical manifestations and diagnosis of cysticercosis" and "Treatment of cysticercosis".)
Life cycle — Humans are the only definitive hosts for T. saginata, T. solium, and T. asiatica (figure 1). Eggs or gravid proglottids are passed in human stool; eggs can survive for days to months in the environment. Cattle (T. saginata) and pigs (T. solium and T. asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids. In the animal's intestine, the oncospheres hatch, invade the intestinal wall, and migrate hematogenously to striated muscles, where they develop into cysticerci. Cysticercus contains protoscolices; they usually measure 5 by 10 mm and can survive for several years in the animal.
Humans become infected by ingesting raw or undercooked infected meat containing cysticerci. In the human intestine, protoscolices are released from the cysts and attach to the intestinal wall via suckers and hooks. Each protoscolex can become the head of an adult tapeworm, which develops by forming proglottids that arise from the caudal end of the scolex; this occurs over about two months, and the adult tapeworm can survive for years in the small intestine. Most human infections are with only one or a few adult tapeworms.
The length of an adult worm is usually ≤5 m for T. saginata (however, it may reach up to 25 m) and 2 to 7 m for T. solium. The adult worms produce proglottids that mature, become gravid, detach from the tapeworm, and are passed in the stool (approximately six per day). T. saginata adult worms usually have 1000 to 2000 proglottids, while T. solium adult worms have an average of 1000 proglottids. The eggs in the gravid proglottids are released after the proglottids are passed in the stool. T. saginata may produce up to 100,000 eggs per proglottid, and T. solium may produce 50,000 eggs per proglottid.
Clinical manifestations — Most human carriers of adult tapeworms are asymptomatic. Intermittently, patients may pass proglottids in the stool (T. solium) or spontaneously (T. saginata) or may notice segments in their stool or sense the movement of proglottids through the anus. There may be associated symptoms including nausea, anorexia, or epigastric pain. Anxiety, headache, dizziness, and urticaria can also occur. A peripheral eosinophilia (up 15 percent) may be observed.
Occasionally, segments can enter the appendix, common bile duct, or pancreatic duct and cause obstruction [7,8]. Rarely, proglottids can be aspirated or regurgitated.
Diagnosis — The diagnosis is generally established by identifying eggs or proglottids in the stool. The eggs of Taenia species are morphologically indistinguishable (picture 1); they are round with a double-walled, radially striated membrane and measure 30 to 40 micrometers. T. saginata eggs have an acid-fast shell; T. solium eggs are not acid fast.
The proglottids and scolices of T. solium and T. saginata are morphologically distinguishable and can be used to establish a species diagnosis (picture 2 and picture 3). The T. saginata proglottids have 12 or more primary uterine branches; T. soliumproglottids have ≤10. These branches can be seen on direct examination or by injecting India ink into the segment via its lateral genital opening.
The scolex usually remains in the intestine when proglottids are passed; it is rare for the entire worm to be eliminated spontaneously. Following antiparasitic therapy, however, the scolex of a fully evacuated worm may be identified in the stool. T. saginata has a scolex with four lateral suckers and no hooks ("unarmed"). T. solium has a scolex with a well-developed rostellum (crown) that has four suckers and a double row of hooks ("armed").
The sensitivity of stool examination is limited since elimination of eggs and proglottids is intermittent. To increase the diagnostic yield, repeat specimens should be examined, and concentration techniques can be used. In addition, T. saginata eggs may be deposited on perianal areas and be detected by anal swabs.
Laboratory workers must exercise caution when performing stool examinations; T. solium eggs are infectious if ingested [9,10]. (See "Clinical manifestations and diagnosis of cysticercosis".)
Immunologic and molecular methods have been developed to improve diagnostic sensitivity, including an enzyme-linked immunosorbent assay (ELISA) for the detection of T. solium antigens in fecal samples and DNA hybridization techniques for the detection of eggs in stools [11-17]. In addition, several polymerase chain reaction (PCR) assays targeting various genomic regions have been developed for distinguishing between species of human Taenia infections, including PCR-restriction fragment length polymorphism (RFLP) methods [18,19], species-specific DNA probes [14], loop-mediated isothermal amplification (LAMP) [20-22], and nested/multiplex PCR [23-27]. Primers targeting the mitochondrial cytochrome c oxidase subunit 1 (cox1) gene of the three Taenia species have been developed and show promise for more routine use to distinguish between the three Taenia species [5]. In general, these assays are not yet suitable for routine diagnosis or field studies and are not widely available.
Diagnosis of taeniasis has also been made by visualizing the worm on capsule endoscopy [28].
Praziquantel is the treatment of choice for all of the tapeworm infections discussed above [41,42]. Dosing depends upon the species [43]. Dosing for taeniasis and diphyllobothriasis is 5 to 10 mg/kg orally (single dose), although excellent efficacy against T. saginata infections has been reported at doses as low as 2.5 mg/kg [44]. Dosing for hymenolepiasis is 25 mg/kgorally (single dose), followed by repeat dose 10 days later.
Praziquantel is a synthetic heterocyclic isoquinolone-pyrazine derivative that induces ultrastructural changes in the teguments of parasites, resulting in increased permeability to calcium ions. Calcium ions accumulate in the parasite cytosol, leading to muscular contractions and ultimate paralysis of adult worms [45]. By damaging the tegument membrane, praziquantel also exposes parasite antigens to host immune responses [46]. These effects lead to dislodgement of worms from their intestinal sites and subsequent expulsion by peristalsis.
Niclosamide is an acceptable alternative treatment for tapeworms if praziquantel is not available. Niclosamide comes in 500 mg tablets that need to be chewed; it is not available in the United States. Dosing consists of four tablets (500 mg) in a single dose (2 g) for adults, two tablets (1 g) for children 11 to 34 kg, and three tablets (1.5 g) for children >34 kg.
Nitazoxanide has been used to treat hymenolepiasis with 75 to 85 percent efficacy [47,48]. Dosing consists of 500 mg twice daily for three days for patients >11 years of age, 200 mg twice daily for three days for patients 4 to 11 years of age, and 100 mg twice daily for three days for patients 1 to 3 years of age [47,48].