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    Current Diagnosis

    Signs and Symptoms

    • Watery diarrhea—Most protozoal infections: Giardia, Blastocystis, Dientamoeba, Cryptosporidium, Cyclospora, Cystoisospora, Microsporidia

    •   Dysentery—Most commonly Entamoeba histolytica; less commonly Balantidium coli, Trichuris trichiura (whipworm)

    • Eosinophilia—Throughout chronic infection: Strongyloides, schistosomiasis, Cystoisospora; usually only in early infection: Ascaris, hookworm, whipworm

    • Prolonged or severe diarrhea in HIV infection—Spore-forming protozoal infections: Cryptosporidium, Cyclospora, Cystoisospora, Microsporidia

    •   Visible worms passed in stool—Ascaris, Taeniasis, Diphyllobothrium

    Diagnosis of Parasitic Infections

    •   Stool antigen assay—Entamoeba histolytica, Giardia, Cryptosporidium

    •   Serology*—Strongyloides, schistosomiasis

    • Stool for ova and parasites—All intestinal parasites. Sensitivity increased with repeat examinations if necessary. Concentration, preservation, and staining improve diagnosis of certain pathogens.

    Note: Key features of intestinal parasitic infection may overlap with other conditions, including nonparasitic infections, and extra- intestinal parasites.

    Intestinal parasites are a diverse group of pathogens with local and global significance. Immigration, international adoption, travel, and the frequency of HIV/AIDS and other immune-compromising conditions (e.g., malignancy, organ transplantation) have all contributed to a need for ongoing or increased awareness of parasitic infections in the United States. Persons who reside in chronic care facilities, children in daycare, and persons whose sexual practices increase the likelihood of fecal–oral contact are also at risk for acquiring intestinal parasitic infection.

    Globally, intestinal parasites are responsible for an enormous burden of disease. Although these pathogens are rarely fatal, ongoing exposure to intestinal parasites among persons in endemic areas exacerbates malnutrition, carries multiple morbidities, and causes stunting of growth and development in children, all of which have far-reaching consequences.

    Patients who present with diarrheal illness (especially prolonged or travel-associated), unexplained eosinophilia, or expulsion of worms should be evaluated for intestinal parasites. In such cases, a careful history should focus on the patient’s country of origin, detailed travel and recreational activities, dietary habits and new or unusual food exposures, occupation, sexual history, sick contacts, and risks for or known immunodeficiency. Some specialists advocate obtaining a complete blood count with differential to assess eosinophil count in all international adoptees and immigrants from areas where parasitic infections are common. If eosinophilia is present, antibody testing for schistosomiasis and strongyloidiasis—two chronic parasitic infections with potentially serious consequences—should be performed, and appropriate therapy should be administered if infection is discovered. For key features of common intestinal parasitic infections, see the Current Diagnosis box.

    Diagnosis of intestinal parasites has improved recently with the advent of quick, simple, and accurate stool antigen tests for some major pathogens, such as Entamoeba, Giardia and Cryptosporidium species. However, the fecal examination for ova and parasites is still the mainstay of diagnosis in many cases. Whenever possible, stool specimens should be sent to a laboratory with clinical expertise in parasitology, where wet preparation, concentration, or staining can identify most pathogens. Evaluation of fresh specimens and repeated examinations improve diagnostic sensitivity. Key diagnostic points are summarized in the Current Diagnosis box.

    This review focuses on basic understanding, recognition, diagnosis and treatment of common intestinal parasites in the United States and throughout the world. Within each section, parasites are listed in order of relative clinical significance.

    * Optimal method of diagnosis in returned travelers and immigrants from endemic to nonendemic areas. Does not distinguish between active and resolved   infections.

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  2. 2
    Protozoa: Amoebae, Flagellates, Ciliates

    Entamoeba histolytica

    Entamoeba histolytica, the cause of amoebic dysentery and amebic liver abscess, is a worldwide pathogen of major clinical significance.

    Approximately 10% of the world’s population and up to 60% of children in highly endemic areas show serologic evidence of infection, and E. histolytica is estimated to cause 100,000 deaths per year globally. In the United States, infection is almost exclusively found among returned travelers, immigrants from endemic areas (especially Mexico and Central and South America), men who have sex with men (MSM), and institutionalized persons. E. histolytica exists in only two forms, the hardy cyst characterized by four nuclei, and the trophozoite, which has a single nucleus and survives poorly outside the human body. It is important to note that Entamoeba dispar and Entamoeba moshkovskii, which are morphologically identical to E. histolytica in stool microscopy, are now thought to be largely nonpathogenic species. Other Entamoeba, including Entamoeba hartmanni, Entamoeba coli, Entamoeba polecki, and others, can be individually identified on microscopy but are of uncertain pathogenicity and generally considered benign.

    E.histolytica infection is acquired by ingestion of cysts in contaminated water or food or by fecal–oral contact, as can occur in chronic care facilities or with anal–oral sexual practices. Acquisition of the parasite can result in asymptomatic infection (most common), diarrheal illness, or extraintestinal infection, the latter most commonly manifest as amebic liver abscess. An appropriately robust layer of colonic mucin may be protective against symptomatic infection, whereas attachment to intestinal epithelium results in penetration of the organism into the submucosal layer, where extensive tissue destruction can take place in the form of apoptosis and lysis of cells, hence the name “histolytica.”

    Symptoms of classic amebic dysentery begin insidiously 1 to 2 weeks after infection. Diarrhea is almost universal and typically consists of numerous small-volume stools that can contain mucus or frank blood, or both. Stools are almost always heme positive if not grossly bloody. Abdominal pain and tenesmus are common; fever is present in approximately 30% of cases. Some persons have a chronic course characterized by weight loss, intermittent loose stools, and abdominal pain. Rare presentations of amebic dysentery include amebomas, which can mimic malignancy, and perianal ulcerations or fistulae. Severe disease can occur in the form of fulminant colitis or toxic megacolon; the latter almost universally requires colectomy.

    Young age, pregnancy, and corticosteroid use predispose to severe infection. Although persons with HIV infection or AIDS can develop invasive disease, E. histolytica does not appear to be a common opportunistic infection, and infection is curable in this population.

    Amebic liver abscess is the most common extraintestinal complication of E. histolytica; cerebral and ocular amebiasis have also been reported. Amebic liver abscess affects children of both sexes equally, but it is up to nine times more common in men, indicating that hormonal milieu likely plays a role. Amebic liver abscess almost always manifests within 3 to 5 months of initial infection, but it can surface years later. Illness is characterized by fever and abdominal tenderness that worsen over several days to weeks. Weight loss, jaundice, and cough from diaphragmatic irritation can also occur.

    Symptoms of dysentery usually are not present, and diarrhea is reported in less than one third of cases. Laboratory abnormalities include leukocytosis, transaminitis, elevated alkaline phosphatase, and elevated sedimentation rate. Chest radiograph often demonstrates elevation of the right hemidiaphragm, and pleural effusion may be present. Rupture of the abscess can occur into the abdomen or pleuropulmonary space, manifesting as acute abdomen or empyema.

    Diagnosis of intraintestinal E. histolytica infection has classically relied on stool microscopy, and this remains the only available method in much of the world. At least three stool specimens should be examined to improve sensitivity. Cysts visualized in stool might or  might not indicate active infection and cannot be distinguished from E.dispar and E. moshkovskii. Presence of trophozoites with ingested red blood cells on stool preparation is diagnostic of dysentery secondary to E. histolytica, as are mobile amebae if seen within freshly examined biopsy material.

    Diagnosis of E. histolytica infection has improved greatly with the advent of antigen tests, now available as enzyme-linked immunosorbent assays (ELISAs) and immunofluorescent probes. The Techlab ELISA antigen test is highly sensitive and specific and can be used on a freshly passed stool specimen, serum, or hepatic abscess material. It becomes positive with onset of symptomatic disease and resolves on treatment of infection. Other available antigen tests appear to function well but have not been as rigorously studied. Aspirate of liver abscess material may be necessary to distinguish from pyogenic liver abscess; a negative stool examination for E. histolytica does not preclude amebic liver abscess. In a patient at high risk for amebic liver abscess (e.g., young male immigrants), a trial of antimicrobial therapy can help in diagnosis because infection typically responds rapidly.

    All patients who have confirmed E. histolytica infection and reside in nonendemic areas should be treated regardless of whether they are symptomatic, because invasive disease can develop in the future.

    Asymptomatic cyst passers may be treated with an intraluminal agent alone, such as paromomycin (Humatin) or iodoquinol (Yodoxin). In the United States, the most readily available effective treatment for patients with amebic colitis or liver abscess is metronidazole (Flagyl). It can be given intravenously for patients unable to tolerate oral medications. Experts recommend that a course of therapy with an intraluminal agent be given following the completed course of the systemic agent for all cases of invasive E. histolytica. See Table 1 for medications and doses.

    Table 1

    Pharmacologic Treatment of Major Protozoan Infections

    Adapted from World Health Organization. Drugs for parasitic infections. Med Lett Drug Ther 2010: 8 (Suppl.).

    Abbreviations: DS = double strength; GI = gastrointestinal; HAART = highly active antiretroviral therapy; max = maximum; tab = tablet; TMP-SMX = trimethoprim- sulfamethoxazole.

    1  Not FDA approved for this indication.

    *  Should be taken with meals.

    †  Should be taken after meals.

    ‡ The drug is not available commercially, but as a service it can be compounded by Panorama Compounding Pharmacy, 6744 Balboa Blvd., Van Nuys, CA 91406 (800-247-9767) or Medical Center Pharmacy, New Haven, CT  (203-688-6816).

    • A nitroimidazole similar to metronidazole, tinidazole is FDA approved and appears to be as effective and better tolerated than metronidazole. It should be taken with food to minimize Gl adverse effects. For children and patients unable to take tablets, a pharmacist may crush the tablets and mix them with cherry syrup. The syrup suspension is good for 7 d at room temperature and must be shaken before use. Ornidazole, a similar drug, is also used outside the United States. Dosing recommendations are only available for children ≥3 years of   age.

    ” Contraindicated in pregnant and breastfeeding women and children <8 y.

    ¶ Clinical significance of these organisms is controversial; metronidazole 750 mg tid × 10 d, iodoquinol 650 mg tid × 20 d, or TMP-SMX11 double-strength tab bid × 7 d are   effective.

    Metronidazole resistance may be common. Nitazoxanide is effective in  children.

    **  Should be taken with liquids after a meal.


    Giardia lamblia, also known as Giardia intestinalis or Giardia duodenalis, is the most commonly identified diarrheal parasitic infection in the United States, with an estimated 100,000 to 2.5 million cases per year. It is globally distributed and found in fresh water throughout mountainous regions of the United States and Canada. The organism is a flagellated aerotolerant anaerobe that exists in a cyst and trophozoite form. Cysts can survive for several weeks in cold water. Contaminated food and water are the most common sources of infection, but the organism can also be passed by person-to-person contact. In the United States, giardiasis is primarily diagnosed among international travelers, persons with recreational water exposure, institutionalized persons and children in day care, and persons with anal–oral sexual practices.

    Illness can result from ingestion of as few as 10 to 25 cysts, which transform into trophozoites in the small intestine and attach to and damage the small bowel wall. Symptomatic disease begins insidiously over approximately 2 weeks in 25% to 50% of persons who ingest Giardia cysts. Others become asymptomatic cyst passers (5%–15%) or have no signs of infection (35%–50%). Hallmarks of infection are watery diarrhea, bloating, gas, abdominal pain, and weight loss; less commonly, patients have nausea, vomiting, or low-grade fever.

    Steatorrhea and malabsorption, particularly secondary to Giardia– induced lactase deficiency, can be observed. Chronic Giardia infection should be considered in the differential diagnosis for a long-standing diarrheal illness, especially if there is history of exposure to possibly contaminated water. Patients with common variable immune deficiency, X-linked agammglobulinemia, and IgA deficiency syndromes are at risk for fulminant and sometimes incurable disease, suggesting a significant role for humoral immunity in control of infection. Persons with HIV infection or AIDS have symptoms similar to those in patients without HIV and typically can be cured of infection with standard therapy.

    Diagnosis of giardiasis is made by examination of fresh or preserved stool or by stool antigen assays. In the case of fecal examination, trophozoites may be directly visualized in fresh liquid stool; semiformed and preserved stool should be stained before examination. Currently, there are immunochromographic, direct fluorescence antibody, and ELISA tests for diagnosis of Giardia, including the ImmunoCard STAT! Cryptosporidium/Giardia Rapid Assay (Meridian Bioscience, Cincinnati, Ohio), which tests for both pathogens simultaneously. Although it is rarely necessary, the diagnosis can sometimes be made on duodenal biopsy.

    For details of treatment options, see Table 1. Metronidazole1 is the most commonly prescribed treatment in the United States and should be given for a 10-day course. Tinidazole (Tindamax), recently approved in the United States, appears to have excellent efficacy and improved tolerability over metronidazole. Nitazoxanide (Alinia) has also been shown to eradicate infection well and can be used as an alternative or in patients who fail a first course of treatment. Patients who fail first-line therapy might have a persistent source of infection (contaminated water source, close contact with an infected person), immune deficiency predisposing to difficult eradication, or persistence of cysts. Once possible sources of reinfection have been investigated and eliminated, relapsed infections should either be re- treated with a longer course of therapy (21–28 days) or treated with a different agent. Patients who fail more than one course of therapy should undergo immunologic work-up.

    Prevention of Giardia infection, as with other parasitic infections, involves primarily close attention to personal hygiene, hand washing, and avoidance of ingestion of fresh unfiltered water. Boiling water or use of a 0.2- to 1-µm water filter offer optimal protection against Giardia and other parasitic pathogens, although such filters still might not protect against Cryptosporidium.

    Blastocystis hominis

    Blastocystis hominis, formerly considered a protozoan, has been reclassified as a fungus. It has a worldwide distribution found most commonly in tropical regions; it is present in humans and several other animals. In temperate regions, B. hominis is detected at a high rate among MSM. B. hominis was long thought to cause only asymptomatic colonization, but there is some evidence to suggest a role in human disease, although this remains controversial. Ongoing molecular analysis might elucidate subtypes of B. hominis with varying degrees of pathogenicity in humans.

    B. hominis has four forms: vacuolated, amoeba-like, granular, and cyst, the latter of which is likely to be the infectious form. It appears to be transmitted via the fecal–oral route, possibly from waterborne sources.

    As suggested previously, the majority of infections appear to be entirely asymptomatic, and number of organisms does not appear to accurately predict severity of illness. Symptoms consist mainly of watery diarrhea, bloating, and abdominal cramps. There are typically no pathologic findings on colonoscopy and there are no reports of invasive disease. Infection is diagnosed by stool microscopy with use of a trichrome or hematoxylin-stained preserved specimen. The organism is susceptible in vitro to numerous antimicrobials. Bactrim1 or metronidazole is the treatment of choice; details are listed in Table 1.

    Dientamoeba fragilis

    Dientamoeba fragilis was originally classified as an amoeba, but it is more closely related to the flagellates such as Trichomonas vaginalis. It is distributed worldwide, including in Western nations, and has only recently been recognized as a clinically significant pathogen, possibly because it is difficult to visualize without specific staining techniques. Illness has commonly been found in travelers and MSM, but it can affect anyone.

    The parasite exists only in the trophozoite form. Despite its genetic relationship to the flagellates, D. fragilis does not have a flagellum and is immotile. Trophozoites range in size from 4 to 20 µm and are binucleate. Patients in the United States who have D. fragilis were found in some studies to harbor other intestinal parasites as well, such as E. vermicularis and B. hominis, and in general D. fragilis is more prevalent in areas of the world with limited public sanitation. These features support a fecal–oral mode of transmission for D. fragilis.

    Most patients are asymptomatic; however, numerous case reports and small series describe patients with no other organisms identified to cause their symptoms who improve significantly after treatment and documented clearance of D. fragilis from their stool. Illness is typically subacute to chronic, characterized by abdominal pain, watery diarrhea, anorexia, fatigue, and malaise. Diagnosis can be difficult, because the parasite is fastidious. If D. fragilis is suspected, stool should be preserved with polyvinyl alcohol and quickly stained with iron–hematoxylin and trichrome. Polymerase chain reaction (PCR) has been used for diagnosis as well, but it is not readily available for use in most clinical settings.

    For full treatment information, see Table 1. Iodoquinol (Yodoxin)1 and metronidazole1 have both been used successfully to treat D. fragilis.

    Balantidium coli

    Balantidium coli is the largest protozoan that infects humans, and the only ciliate. Balantidiasis is a relatively rare cause of illness and is found primarily in rural agrarian communities in Southeast Asia, Central and South America, and Papua New Guinea. B. coli is highly associated with animal farming, in particular, pigs; humans are incidental hosts. The parasite is transmitted by direct contact with animals or on ingestion of water or food contaminated by animal excrement. Persons with malnutrition or immune deficiency are particularly susceptible to infection.

    B.coli invades the intestinal mucosa from the terminal ileum to the rectum. About one half of infections are asymptomatic; the other one half result in a subacute or chronic diarrheal illness with abdominal cramping, nausea, vomiting, weight loss, and occasional low-grade fever. Fewer than 5% of patients present with severe or even fulminant dysentery, and rare cases of colonic penetration with peritonitis, mesenteric lymphadenitis, or hepatic infection have been reported.

    Diagnosis is made by visualization of trophozoites in fresh stool specimens or preserved and permanently stained samples. The trophozoite is large and ciliated; cysts are difficult to distinguish. It displays a distinct spiraling motility that can be seen under low power. On stained sample, visualization of B. coli‘s characteristic macronucleus and spiral micronucleus can help confirm the diagnosis. All patients should be treated regardless of symptoms. Tetracycline1 (Sumycin and others) is the therapy of choice; the infection also responds to metronidazole1; see Table 1 for dosing information.

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  3. 3
    Spore-Forming Protozoa and Microsporidia


    Cryptosporidium is a pathogen with worldwide distribution that is endemic to the United States. Humans are most commonly infected by the recently reclassified Cryptosporidium hominis, but Cryptosporidium parvum, primarily a bovine pathogen, also causes human disease.

    Cryptosporidium has caused multiple waterborne outbreaks in the United States and can be acquired secondary to recreational water exposure (e.g., swimming pools, water parks). The best-known outbreak occurred secondary to heavy rains that brought farm runoff into the drinking water supply in Wisconsin in 1984. It resulted in 430,000 documented cases of cryptosporidiosis and contributed to the deaths of dozens of persons with advanced HIV infection or malignancy.

    Cryptosporidium is a coccidian, part of a group of spore-forming protozoa with a complex life cycle and a structure that allows mechanical penetration into host cells. Cryptosporidium can mature and reproduce entirely within human hosts, thereby enabling infection to occur both from environmental sources and by direct person-to-person contact. Its oocysts, the source of infection on ingestion, are markedly hardy; they can withstand heavy chlorination, survive for months in cold water, and are small enough to occasionally evade even the smallest available water filtration systems.

    All persons are susceptible to infection, which usually is self- limited. Fulminant or chronic infection, or both, can be seen among patients with immune compromise secondary to HIV infection (especially those with CD4 <50), in patients with malignancy, and in malnourished children. As few as 100 oocysts can cause infection, which results when the parasite penetrates small bowel epithelium and replicates just beneath its surface. Villous flattening and small bowel wall edema are seen on pathologic examination from infected persons.

    Asymptomatic infections occur but are relatively rare. Symptoms begin within several days to 1 week of ingestion of oocysts. The hallmark of infection is explosive watery diarrhea, which can be so voluminous as to resemble cholera and can cause significant dehydration and electrolyte imbalance. Abdominal discomfort, nausea, vomiting, fever, malaise, and myalgia can also be present, and weight loss is common. Illness lasts 1 to 2 weeks, but a substantial percentage of patients report a relapse of symptoms after initial improvement. The biliary tract can be involved, particularly in patients with HIV infection, and infection at other distant sites, such as the lungs, has rarely been reported.

    Diagnosis of Cryptosporidium has improved dramatically in recent years with the advent of antigen tests, which are highly sensitive and specific and can be used on a single sample of fresh stool. The ImmunoCard STAT! Cryptosporidium/Giardia Rapid Assay is useful because it can detect both pathogens. When such tests are not available, stools submitted for examination should be fixed in formalin and stained for trophozoites or cysts; availability of multiple stool specimens improves the diagnostic sensitivity. Luminal fluid or biopsy specimens obtained during endoscopy can also reveal the organism.

    Infection with Cryptosporidium is typically a self-limited illness in otherwise healthy persons, but symptoms can be improved and the course shortened with the antiparasitic nitazoxanide. Cryptosporidium remains an extremely challenging and potentially devastating infection in immunocompromised patients, especially those with HIV and a low CD4 count (counts <200 increase risk of severe illness, and counts <50 markedly increase risk). Although anticryptosporidial therapies in this population have shown very limited efficacy, restoration of immune function with HAART often effects cure.

    Limited data suggest a trial of nitazoxanide may be reasonable in this circumstance as well. Appropriate supportive measures are also crucial in all patients with Cryptosporidium, including fluid and electrolyte replacement; avoiding lactose products is likely to be beneficial during the first 2 weeks after infection as the brush border regenerates. Appropriate treatment doses for nitazoxanide are listed in Table 1.

    Prevention of Cryptosporidium infection requires a highly developed public water purification system including flocculation, sedimentation, and filtration. Use of 0.2- to 1-µm personal water filters for campers and hikers greatly reduces but does not eliminate risk of infection, whereas boiling water before drinking kills oocysts. Close attention to hygiene and avoidance of fecal–oral contact is the mainstay of prevention in the settings of institutional and community outbreaks.

    Cyclospora Species

    Cyclospora cayetanensis is a coccidian with structure similar to that of Cryptosporidium. Unlike Cryptosporidium, C. cayetanensis requires a period of development outside the human body, thereby eliminating the possibility of close person-to-person contact as a means of acquiring the infection. C. cayetanensis is distributed worldwide, most commonly in the tropics and subtropics where infection tends to exhibit seasonality. It has also been associated with food (e.g., raspberries) and waterborne outbreaks in temperate regions, including the United States, and in recent years it has become increasingly recognized as a cause of infectious diarrhea in returned travelers.

    All persons are susceptible to infection, but those with HIV are at risk for more severe and prolonged disease, as seen with cryptosporidiosis and isosporiasis. Symptomatic disease appears to be most common in adults who do not have previous exposure to Cyclospora, such as travelers or persons who have relocated to endemic areas. Illness begins about a week after ingestion of sporulated oocysts and is characterized by watery diarrhea, abdominal cramping, bloating, anorexia, and weight loss. Low-grade fever can occur; marked fatigue is common and can last weeks or even months, and untreated infections can relapse after apparent resolution. Biliary involvement can occur in patients with HIV coinfection, as with cryptosporidiosis. Cyclosporiasis, similar to infection with other coccidians, causes damage to the small bowel epithelium, with resultant crypt flattening, edema, and inflammatory infiltrate. Lactose deficiency can remain for months following initial infection.

    Diagnosis is made by stool examination. As with diagnosis of other parasitic infections, multiple stool specimens improve sensitivity. In the case of Cyclospora, concentration of the stool specimen also increases yield. If cyclosporiasis is suspected, specific testing should be requested, because the organism exhibits unique properties.

    Organisms are about two times the size of Cryptosporidium and can be seen with Kinyoun acid-fast stain. They also autofluoresce and can be visualized under ultraviolet microscopy. Currently there is no stool antigen assay, but PCR testing has been used in experimental and limited clinical settings to assist in diagnosis.

    Cyclosporiasis is best treated with trimethoprim-sulfamethoxazole (Bactrim)1; ciprofloxacin1  may be effective for patients who have a sulfa allergy. Patients with HIV infection can require longer courses of treatment or chronic suppressive therapy; appropriate antiretroviral therapy is also important in the treatment of severe or relapsing infections. See Table 1 for details.

    Cystoisospora Species

    Cystoisospora belli, formerly Isospora belli, is a large coccidian native to tropical areas. Similar to Cyclospora, it requires a period of maturation outside the human body and therefore cannot be spread directly from person to person. It appears to cause largely asymptomatic or mild infection in tropical areas to which it is endemic; the exception is among patients coinfected with HIV and particularly those with AIDS, in which it is a very common cause of chronic diarrhea in the Caribbean and Central America. Currently in wealthy countries it is found primarily in travelers returning from endemic areas.

    Illness is typically mild and self-limited, consisting primarily of watery diarrhea. However, some immunocompetent persons can develop a chronic spruelike syndrome with malabsorption, and those with HIV infection or AIDS often have severe and prolonged diarrhea. Cystoisospora can invade to the lamina propria and can cause eosinophilia, which is different from other coccidian infections.

    Diagnosis is made by observation of cysts in stool. As with Cyclospora, they can be visualized with acid-fast stains or ultraviolet microscopy. Stool may also contain Charcot–Leiden crystals. Infection in immunocompetent hosts responds well to antimicrobials; persons coinfected with HIV can require longer courses of therapy or chronic suppression, and appropriate antiretroviral therapy may be helpful as well. Trimethoprim-sulfamethoxazole (Bactrim)1 is the treatment of choice. Ciprofloxacin (Cipro)1 or pyrimethamine (Daraprim)1 may be used in cases of sulfa allergy. Doses are listed in Table 1.


    Microsporidia are eukaryotic organisms that have been recently reclassified as fungi based on molecular genotyping. They are distributed globally, and more than 100 genera have been identified, seven of which contain species known to be pathogenic in humans: Encephalitozoon, Enterocytozoon, Trachipleistophora, Pleistophora, Nosema, Vittaforma, and Microsporidium. These pathogens cause a wide variety of systemic and focal illness throughout the world.

    Many immunocompetent patients in wealthy nations exhibit positive serology for certain types of microsporidial infections without a history of disease or travel. Microsporidia are most commonly associated with systemic infection in immunosuppressed persons, particularly those with HIV and a CD4 count of less than 100 or patients with organ transplants. Mode of transmission is not entirely clear, but the pathogen likely is spread both from water sources and possibly from close household contact.

    Encephalitozoon intestinalis and Enterocytozoon bieneusi are responsible for intestinal microsporidial infections. E. bieneusi has been associated with self-limited diarrheal illness; E. intestinalis is commonly found in stool specimens throughout the developing world, but its pathogenicity is often not certain. Symptomatic infections, most often in patients coinfected with HIV, typically include a gradual onset of watery diarrhea, which may be worse in the morning and after oral intake. Significant volume and electrolyte depletion can occur, as well as fatigue, anorexia, weight loss, and malabsorption. E. intestinalis can disseminate and cause acute abdomen with peritonitis, cholangitis, nephritis, and keratoconjunctivitis, and E. bieneusi infection can result in cholangitis and nephritis as well as rhinitis, bronchitis, and wheezing. Other microsporidia are implicated in a wide variety of illness both in previously healthy and immunosuppressed hosts and include several ocular pathogens.

    Diagnosis of microsporidiosis is attained by visualization of spores in stool or in tissue specimens. As suggested by their name, microsporidial spores are much smaller than those produced by spore-forming protozoal infections; most are approximately 1 µm in length and can easily be confused with bacteria or debris on slides.

    Special staining techniques have been described, but electron microscopy is required for species identification. See Table 1 for details of treatment. Albendazole (Albenza)1 is the treatment of choice for Encephalitozoon intestinalis.

    Treatment of Enterocytozoon bieneusi is more challenging. Although some response to albendazole has been reported, oral fumagillin2 may have more efficacy. Unfortunately, it is not currently commercially available in the United States. Use of appropriate antiretroviral therapy is perhaps the most important treatment for patients with HIV infection or AIDS and chronic microsporidial infections.

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  4. 4


    Nematodes (roundworms) are cylindrical nonsegmented organisms that are found throughout the world both as free-living species and as human and animal pathogens. Nematodes are the most common type of human parasitic infestation, found in approximately one quarter of the world’s population; often, susceptible hosts carry multiple different pathogenic nematodes. There are at least 60 species that have been shown to infect humans and 10 times that many that cause disease in other animals, but a few pathogens account for the bulk of human infections, in particular Ascaris, hookworm, and whipworm.

    These three organisms all require a period of maturation outside the human body—typically in warm, moist soil—underscoring the fact that repeated contact with fecally contaminated soil or food and water is necessary to sustain the cycle of infestation. Strongyloides and Enterobius are unique in that they can both complete their life cycle on or within human hosts and therefore can cause chronic infection and be transmitted directly by close person-to-person contact where there is the possibility of fecal–oral contamination.


    Ascaris lumbricoides, the most common human helminthic infection, is estimated to affect 20% to 25% of the world’s population. Up to 80% of community members are infected in heavily endemic areas, namely in Africa, Asia, and Central and South America. Cases of Ascaris infestation are also seen in rural areas in the southeastern United States. A. lumbricoides are white to pinkish worms that range from 10 to 40 cm in length; the infectious eggs are oval white bodies with an adherent mucopolysaccharide capsule that clings to multiple surfaces and aids in transmissibility of the parasite. Eggs are also remarkably durable, capable of surviving up to 6 years in moist soil and able to weather brief droughts and periods of freezing.

    Fecal contamination of water, food, and environmental surfaces such as doorknobs and countertops provide the means of transmission for Ascaris, and recurrent infection occurs as long as living conditions that predispose people to infection remain unchanged. Lack of adequate public sanitation, use of human feces as fertilizer (night soil), and frequent contact with soil or shared contaminated surfaces among close household members are risk factors for infection. Persons who move to environments with improved sanitation typically lose their infection within 2 years as all the adult worms die. Eggs excreted by an infected person must mature outside the human body for approximately 2 weeks. On ingestion by a susceptible host, mature eggs hatch in the small intestine and release larvae, which penetrate the intestinal wall and travel through the venous circulation to the lungs, where they are coughed up and swallowed. They then undergo maturation into adult worms in the intestine and produce eggs by 2 to 3 months after initial infection. The eggs are excreted in the feces and mature outside the body to continue the cycle.

    Most persons with Ascaris infection are asymptomatic.

    Approximately 15% of infected people have morbidity, which is associated with young age, large burden of worms, coinfection with other intestinal parasites, and genetic predisposition. In children, infection contributes to malabsorption of protein, fat, and vitamins A and C, and treatment of heavily infected children can improve their nutritional status. Ascaris infection can also cause intestinal, pancreatic, or biliary obstruction as a result of worm mass or worm migration. Despite the low incidence of obstructive complications per infected person, the Ascaris-related acute abdomen is a significant problem on a global level given the enormous number of people infected. Some patients with intestinal Ascaris infection report vague abdominal complaints, such as abdominal discomfort, nausea, vomiting or diarrhea, but these are relatively rare. Pulmonary migration of a large quantity of worms can produce Loeffler’s syndrome, or eosinophilic pneumonitis.

    Diagnosis is easily attained with standard saline stool preparation, and large numbers of eggs are typically seen. Larvae or worms can also sometimes be seen in sputum or stool samples. In cases of intestinal obstruction, worms may be visualized on upper gastrointestinal series, computed tomography, and even ultrasound. Eosinophilia with Ascaris infection is found only during the larval migratory phase, but not at all times. Chronic eosinophilia in an at- risk person suggests another parasitic infection, often Strongyloides.

    All persons documented to carry Ascaris who have migrated to nonendemic areas should be treated to prevent complications in the future; in endemic areas, adults need only be treated if they are symptomatic. Children have been shown to benefit from intermittent anthelminthic therapy in heavily affected areas of the world.

    For patients with intestinal obstruction, bowel rest and intravenous hydration are usually sufficient to relieve the obstruction, at which time anthelminthic therapy can be administered. In such cases, gastroenterology consultation should be obtained. In rare cases, surgical intervention is required. Treatment of pulmonary infection is controversial; however, most experts recommend steroid therapy for severe infections followed 2 to 3 weeks later (at the time full-grown worms will have migrated to the intestine) by administration of anthelminthic therapy.

    The benzimidazoles (mebendazole [Vermox], albendazole [Albenza],1 levamisole [Stromectol], and pyrantel pamoate [Pin-X]) all exhibit excellent activity against Ascaris. Doses and other options are listed in Table 2. Although albendazole and mebendazole carry a pregnancy class B label, they have been used in pregnant women, adolescent girls, and women of reproductive age without demonstrable effects on fetuses; most experts recommend holding treatment until the second trimester whenever possible.

    Table 2

    Pharmacologic Treatment of Nematode, Trematode, and Cestode Infections

    Adapted from World Health Organization. Drugs for parasitic infections. Med Lett Drug Ther 2010: 8 (Suppl.).

    1  Not FDA approved for this indication.

    • Should be taken with a fatty

    † Safety of Ivermectin in young children (<15 kg) and pregnant women not yet established. Ivermectin should be taken on an empty stomach with  water.

    ‡  Limited availability; can be mixed with juice or water to improve  palatability.

    • Should be taken with liquids during a meal.

    ” Limited or no availability in the United States.

    ¶  Available in the U.S. only from the manufacturer. Must be chewed or crushed thoroughly   and swallowed with a small amount of water. Limited or no availability in the United  States.

    Sanitary conditions that allow for proper management of human feces are crucial in control and prevention of Ascaris infection; boiling water kills the eggs.

    Whipworm (Trichurasis)

    Trichuris trichiura has become recognized in recent years as a worldwide pathogen with a scope similar to that of Ascaris. Sanitary conditions that predispose to ingestion of food and water contaminated with human feces place people at risk for infection; in many communities infection is hyperendemic, with almost universal carriage of the pathogen.

    The adult organism is a small worm about 4 cm in length with a unique whip-like structure that allows its thin tail to become embedded in colonic crypts. Whipworm eggs have a characteristic barrel shape with mucous plugs at either end. Infection is acquired by ingesting Trichuris eggs that have undergone embyronation in the soil for 2 to 4 weeks after excretion from a previous host. Larvae emerge from eggs in the intestine and migrate into crypts, where they begin to mature. Egg production begins approximately 3 months later.

    Most persons with whipworm carry few worms (approximately 20) and are asymptomatic. As with many other intestinal parasites, children are at greater risk for symptomatic infection, which can cause failure to thrive, anemia, clubbing, inflammatory colitis, and rectal prolapse. Adults with a high worm burden can also experience inflammatory colitis characterized by frequent—often bloody— diarrhea and tenesmus. Infection has been shown to result in production of tumor necrosis factor (TNF)-α by lamina propria cells in the colon, which can contribute to poor appetite and wasting that can be seen with significant infection.

    Diagnosis is made by standard stool microscopy without a need to concentrate stool, because large numbers of eggs are excreted. Worms can also be seen on colonoscopy, or they can be visualized grossly in cases of rectal prolapse. Eosinophilia may be seen.

    Treatment of symptomatic infections can be accomplished with mebendazole, albendazole,1 or ivermectin (Stromectal)1; see Table 2 for details.

    Hookworm (Necator americanus and Ancylostoma duodenale)

    Like other helminthic infections, hookworm affects a substantial portion of the world’s population, particularly in rural subtropical and tropical communities where human feces is used as a component of fertilizer. Infection results primarily from parasite penetration into the skin; therefore persons with an agrarian lifestyle and significant soil contact are at greatest risk.

    Two species are responsible for the majority of human hookworm: Necator americanus and Ancylostoma duodenale. Ancylostoma braziliense, a canine intestinal pathogen, causes cutaneous larval migrans in humans because the pathogen cannot penetrate the human dermis. Of the two common forms of human hookworm, N. americanus is smaller and a less aggressive pathogen with a longer life span than A. duodenale. Both parasites are found in warm climates throughout the world; A. duodenale exists in smaller pockets, whereas N. americanus is widely distributed throughout impoverished rural areas of the tropics in the Americas, Asia, and Africa.

    Hookworms are small helminths, between 0.5 and 1 cm in length. Infection results from larval penetration of the skin on contact with contaminated soil. An intensely pruritic, erythematous, papulovesicular rash called ground itch can develop at the site of entry. Parasites then enter the venous or lymphatic circulation and travel to the lungs, at which point an urticarial rash with cough can develop.

    The larvae are swallowed and migrate to the small intestine, where they attach to the bowel wall with teeth or biting plates and take a continuous blood meal by sucking with strong esophageal muscles. As the hookworms lodge in the small intestine, peripheral eosinophilia peaks, and gastrointestinal discomfort with or without diarrhea can result. Large oral ingestion of A. duodenale can cause Wakana syndrome, characterized by cough, shortness of breath, nausea, vomiting, and eosinophilia. The most important clinical manifestation of hookworm infection is iron-deficiency anemia, which can be mild or severe and may be accompanied by malabsorption of protein in hosts with heavy burden of disease. Infants and pregnant women can become extremely ill or even die as a result of the anemia.

    Hookworm may be difficult to diagnose because light infections often do not produce enough eggs to be readily seen on stool examination; stool should therefore be concentrated if infection is suspected. Eggs do not appear in stool until approximately 2 months after infection, so patients with pulmonary complaints will not yet have a positive stool examination.

    Hookworm infection can be eradicated with benzimidazole antihelminthics; see Table 2 for details. Prevention of hookworm infection, as with other parasites, lies in improved sanitary conditions; wearing shoes is especially important because the majority of infections are acquired through the skin. Mass anthelminthic treatment campaigns have shown some efficacy in reducing disease in children; however, reinfection and concern for development of resistance continue to present significant challenges. Candidate vaccines are currently under investigation.


    Strongyloides stercoralis is a global pathogen that is estimated to affect as many as 100 million people, mostly in tropical regions of the world. In recent years, it has become more commonly recognized in the United States among immigrants as a cause of chronic eosinophilia as well as symptomatic infection.

    Strongyloides infection results when filariform larvae dwelling in fecally contaminated soil penetrate the skin or mucous membranes of a susceptible host. Larvae move to the lungs and subsequently to the trachea, where they are coughed up and swallowed. Females, about 2 cm in length, lodge in the lamina propria of the duodenum and proximal jejunum where they begin to oviposit. Rhabditiform larvae emerge from these eggs and either repenetrate the intestinal wall or are passed into the feces, at which point they can begin a free-living cycle and reproduce sexually, or can molt directly into an infectious form ready to enter a subsequent susceptible host.

    Persons infected with Strongyloides are typically asymptomatic. Those who have symptoms might report abdominal discomfort, diarrhea alternating with constipation, or, rarely, blood-tinged stool. Severe intestinal infections can occur and are manifest by chronic watery or mucousy diarrhea. In such cases, colonoscopy reveals excessive bowel wall thickening and copious secretions, or edema (catarrhal enteritis or edematous enteritis). Parasite migration through the dermis can manifest as serpiginous, erythematous, and pruritic patches along the buttocks, perineum, and thighs, known as larvae currens.

    Strongyloides appear to attain a balanced state in their host, with similar numbers of adult worms throughout the many years of infection. During periods of host immunocompromise, in particular in patients taking corticosteroids, Strongyloides can enter into a state of rapid autoinfection and rampant reproduction called hyperinfection syndrome, which results in devastating illness. Persons with HIV infection do not seem to be at particular risk for symptomatic disease or hyperinfection, but hyperinfection has been linked to HTLV-1 infection. Strongyloides has also caused hyperinfection in organ transplant patients whose donor had been infected asymptomatically with the parasite. Although it has long been thought that steroid- induced immune compromise was the major trigger for hyperinfection, growing evidence suggests that steroids themselves may be the culprit by directly inducing the accelerated life cycle in the parasite.

    The hyperinfection syndrome is characterized by systemic illness with fever, cough, hypoxia, patchy or diffuse pulmonary infiltrates with alveolar microhemorrhages, and dermatitis; it can include myocarditis, hepatitis, splenic abscess, meningitis and cerebral abscess, and endocrine organ involvement. Larvae migrating out of the intestines can drag bacteria with them, resulting in gram-negative or polymicrobial sepsis. The prognosis of Strongyloides hyperinfection syndrome is grave even with highly effective anthelminthic treatment given the diffuse nature of this disease. However, earlier recognition and intensive supportive care result in cure.

    Diagnosis of uncomplicated Strongyloides infection in endemic areas can be challenging because few larvae are passed in stool, and numerous examinations may be necessary to detect them. ELISA is available and is highly sensitive, but it does not distinguish between active and past infections. It is, however, the test of choice for persons who have migrated to nonendemic areas, and all persons in this setting should be treated. Ivermectin is the treatment of choice; see Table 2 for dosing. During the first days of treatment, patients can experience intense dermal pruritis as parasites die. Eosinophilia and positive ELISA can persist for months even after effective therapy.

    Enterobius vermicularis

    Human pinworm infection, caused by the thread-like nematode Enterobius vermicularis, is found throughout the world and continues to be diagnosed commonly in the United States, especially in children. Its persistence is likely related to the fact that pinworm does not require a period of maturation outside the human body, and autoinfection or transmission by very close contact sustains the parasite within communities. E. vermicularis is at maximum 1 cm long with a tapered tail, and dwells in the cecum, appendix, and adjacent colon. At night, female worms travel to the anus and lay small (25–50µm), double-walled oval eggs in the perianal skin. Within 6 hours, the eggs embryonate within their capsule and are infectious. In scratching the perianal area and subsequently bringing his or her hand to the mouth, the host ingests the embryos, which then hatch in the bowel about 2 months later and continue the cycle of infection. Embryonated eggs can also attach to bedclothes, thereby placing other household members with close contact at risk for infection. In family groups, infection is associated with close living quarters, poor hand washing, and infrequent washing of clothes and sheets. It can also be prevalent in among institutionalized persons.

    Infection is often asymptomatic, but it can cause perianal itching, which helps to facilitate persistent infection by encouraging frequent touching of the perianal area. Rarely, worms migrate into ectopic foci and produce painful genitourinary tract disease with granulomatous inflammation; pinworm infection rarely results in pain that mimics acute appendicitis.

    Pinworm infestation is best diagnosed by the classic Scotch tape test, which involves placing and immediately removing a piece of sticky tape firmly across the perianal area early in the morning when the eggs have been deposited. The tape can then be brought into a physician’s office or laboratory, where it is placed sticky-side down for microscopic examination to detect the eggs. Three specimens should be examined if necessary to improve the sensitivity. It is also sometimes possible to see the worms directly on the perianal region, although they are so small that they may easily be mistaken for residual bits of toilet paper. E. vermicularis is susceptible to standard anthelminthic therapies as listed in Table 2. All household contacts should be empirically treated with the same regimen to avoid reintroducing infection from family members who may be asymptomatically carrying the parasite. Careful laundering of all bedclothes is recommended as well.


    Anisakiasis is a descriptive term for human infection with parasites of two distinct genera: Anisakis and Pseudoterranova. Humans are incidental hosts for these roundworms that inhabit multiple species of fish and other marine animals (tuna, mackerel, hake, cod, sardines, and cephalopods) as intermediate hosts, and marine mammals such as whales, seals, sea lions, and walruses as final hosts. Humans acquire the parasite in its larval stage by eating raw fish (e.g., sushi, ceviche), and therefore the condition predominates in cultures where uncooked fish is consumed. Cases are most commonly reported from Japan but are seen throughout the world in other coastal nations and among restaurateurs.

    On consumption of fish with anisakid larvae embedded in its musculature, humans can experience immediate symptoms in the form of itching or burning in the throat, which can provoke coughing that expels the parasite. If the parasite is swallowed, the larva attempts to embed in the gastric musculature at the pylorus. This can produce acute, short-lived epigastric abdominal pain and possibly immediate vomiting, at which point the parasite might again be ejected. If the larva does manage to penetrate gastric tissue, it dies because it is incapable of further tissue invasion in humans. An intense inflammatory response to the dead pathogen can then result, with gastric pain, nausea, and occasionally diarrhea with blood or mucus if a gastric ulcerative lesion has resulted.

    Rare cases have been reported in which the larva penetrates the peritoneum, causing focal peritonitis and abscess formation.

    Pseudoterranova appears to cause milder symptoms and less tissue invasion, and the worm might simply be vomited several days after initial ingestion and presented to a physician, often by an alarmed patient. Because the vast majority of infections are caused by a single organism, vomiting of the parasite results in a definitive cure and patients can be reassured. Diagnosis in patients with ongoing symptoms related to an embedded parasite is ultimately endoscopic. Effective cure results on endoscopic or surgical removal of the worm.



    Schistosomes are freshwater pathogens with areas of endemicity in Africa, South America, Southeast Asia, and parts of the Middle East. These small trematodes cause varied, often chronic infections that can carry significant morbidity, although some species cannot invade beyond the dermis in humans and result strictly in cercarial dermatitis or swimmer’s itch. There are five species of schistosomes known to cause disease in humans: Schistosoma haematobium, found through much of Africa and parts of the Middle East; Schistosoma mansoni, also native to Africa and the Middle East as well as Latin America; Schistosoma japonicum, present in China, Southeast Asia, and the Philippines; Schistosoma mekongi, found only in the Mekong River basin in Southeast Asia; and Schistosoma intercalatum, endemic only in West Africa.

    All persons who come in contact with schistosomes are at risk for infection, even after only very brief exposure to fecally contaminated freshwater in which the intermediate hosts of the pathogen (snails) reside. Frequency and degree of infection tend to be highest in children in endemic areas and then level off in the early teenage years, likely secondary to level of environmental exposure and possibly to host immunity. S. haematobium causes disease in the genitourinary system; the others cause intestinal, hepatic, and sometimes pulmonary diseases.

    Infection is acquired rapidly on contact with freshwater (including brief swims or by repeated splashing, as can occur during river rafting), when free-living fork-tailed schistosomal larvae penetrate human skin and lose their tail. These schistomorula can cause intense itching and a papulovesicular, pruritic rash at the site of penetration, swimmer’s itch. Invasive schistomorula then enter the venous bloodstream and ultimately lodge in gut mesenteric and portal venules, where maturation occurs, and male and female forms join and mate for life. Females begin to oviposit, and the resultant inflammatory response to the eggs can cause either acute illness or chronic fibrosis and granulomatous inflammation of the tissues in which they reside.

    Acute illness, called Katayama fever, is more common among hosts who have not been previously exposed to the organism and can be quite severe, even fatal. Katayama fever begins 4 to 8 weeks after exposure to the schistosomes, with fever, cough, abdominal pain, hepatomegaly, and lymphadenopathy. Eggs might not yet be present in the stool at the time of diagnosis. Chronic schistosomiasis is a slowly progressive illness. S. haematobium infection is manifest by gross or microscopic hematuria, urinary symptoms, and chronic bacterial urinary tract infections; ultimately ureteral fibrosis, hydronephrosis, and granulomatous genital lesions also can ensue. In infection with other invasive schistosomes, chronic illness can manifest as abdominal pain and diarrhea, which is often bloody, with associated iron-deficiency anemia. Hepatomegaly is often the first clinical finding in chronic intestinal schistosomiasis. Over many years, hepatic congestion and fibrosis can result in liver failure, and the pulmonary vasculature can be involved as well, which causes pulmonary hypertension and cor pulmonale.

    Diagnosis of schistosomiasis is by observation of eggs in stool (intestinal disease), urine (urinary tract disease), or biopsy specimens, or by serum antibody testing. Concentration of stool may be necessary to detect the pathogen. The eggs of the three most common species of schistosomes can be readily identified microscopically: S. haematobium has an inferior spine, S. mansoni an inferolateral spine, and S. japonicum lacks a spine. Eosinophilia is a hallmark of chronic infection and is a common cause of asymptomatic eosinophilia among immigrants from schistoendemic regions of the world. Serology is highly sensitive and specific but cannot distinguish acute, chronic, or cleared infection; it is very useful when attempting to diagnose infection in returned travelers.

    All patients with schistosomiasis should be treated, and those with chronic manifestations might experience significant regression of even late-stage organ-specific disease. Treatment of choice is with praziquantel; see Table 2 for details.

    Prevention of schistosomiasis involves improving access to treated water and exploration of avenues to eliminate the intermediate snail hosts. Host immunity does appear to occur, and efforts are underway to better understand and induce such immunity in the form of a vaccine.



    Human tapeworm infection has long been implicated in North American oral folklore as a cause of insatiable appetite and excessive weight loss. In reality, despite their impressive size of up to 12 meters, tapeworm infection tends to be minimally symptomatic.

    Taenia solium, pork tapeworm, and Taenia saginata, beef tapeworm, are the two most common flatworm infections of humans worldwide and occur in any setting in which raw or undercooked meat is served and cattle and pigs have access to feed contaminated with human feces. T. saginata is still found in areas of North America and Europe, as well as in Central and South America and Africa; T. solium is common throughout Mexico, Central and South America, Africa, China, and the Indian subcontinent. Although humans are the definitive hosts for both parasites, T. solium is best known for its pathogenicity in the form of cysticercosis. Cysticercosis is not an intestinal parasitic infection.

    Domesticated animals acquire infection on ingestion of eggs excreted by humans; the eggs mature in their musculature and develop a scolex. When humans consume infected meat, the scolex attaches in the small intestine, and the adult tapeworm develops over approximately 2 months. Adult tapeworms are made up of hundreds to thousands of gravid proglottids and can live for up to 25 years.

    Symptoms tend to be mild or absent but can include nausea, abdominal pain, loose stools, anal pruritus, and occasionally weakness or increased appetite, especially in children. Serious illness rarely results when a tapeworm becomes lodged in the biliary or pancreatic ducts or is coughed up and aspirated. Some patients come to medical attention when the worm is noted emerging from the anus or on extrusion of proglottids in the stool.

    Diagnosis of taeniasis can be made on visualizing the round eggs in stool; however, the species cannot be determined unless a segment of the worm is examined. Serum antibody and antigen tests, as well as stool PCR, have been developed for diagnosis but are not widely used in clinical practice. Eosinophilia and elevated IgE levels may be present. Single-dose praziquantel1 (see Table 2) is curative in almost all cases, but infectious eggs can still be released in the feces for a time; ingestion of these could result in the subsequent development if cysticercosis, so patients should be counseled to avoid fecal–oral contact.

    Proper cooking of meat is the mainstay of prevention; disposal of human waste away from animals would also be effective in interrupting the life cycle.


    Diphyllobothrium latum is the longest parasite known to infect humans (10–12 m). It is found in freshwater lakes in areas of the Americas, Northern Europe, Africa, China, and Japan and has a complex life cycle involving two intermediate hosts: crustaceans and small fish.

    Humans and other fish-eating mammals are the definitive hosts and acquire the infection on ingestion of raw fish or roe.

    The organism attaches within the small intestine, and hosts are usually asymptomatic. Infected persons might complain of increased appetite, nausea, or abdominal discomfort. Many present after passage of portions of the tapeworm in stool, as with taeniasis; in others, diagnosis is on stool examination done for other purposes or during screening colonoscopy. As with other worms, the parasite occasionally migrates into biliary ducts or causes intestinal obstruction. Attachment of the parasite higher in the intestine can result in decreased levels of vitamin B12. Rarely, pernicious anemia develops as a result (tapeworm anemia).

    Diagnosis is made either by seeing eggs in unconcentrated stool or by encountering the adult worm. Eosinophilia is present in a minority of cases. Treatment with praziquantel1 is curative; see Table 2. Vitamin B12 supplementation is necessary in cases of severe or symptomatic deficiency, but it will not recur once the tapeworm is eliminated.

    Prevention involves not ingesting undercooked fish.

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    Concha R., Hartington Jr. W., Rogers A.I. Intestinal strongyloidiasis: Recognition, management, and determinants of outcome. J Clin Gastroenterol. 2005;39(3):203–211.

    Drugs for Parasitic Infections. In: Treatment Guidelines from the Medical Letter. 2013:e1–e31 (11).

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    Guerrant R., Walker D., Weller P., eds. Tropical Infectious Diseases: Principles, Pathogens, and Practice. Philadelphia: Churchill Livingstone; 1999.

    Huang D.B., White A.C. An updated review on Cryptosporidium and Giardia. Gastroenterol Clin North Am. 2006;35:291–314.

    Mandell G., Bennett J., Dolin R., eds. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases. 5th ed. Philadelphia: Churchill Livingstone; 2005.

    Pardo J., Carranza C., Muro A., et al. Helminth-related eosinophilia in African immigrants, Gran Canaria. Emerg Infect Dis. 2006;12(10):1587–1589.

    Stark D., Beebe N., Marriott D., et al. Dientamoebiasis: Clinical importance and recent advances. Trends Parasitol.


    1 Not FDA approved for this indication.

    1 Not FDA approved for this indication.

    1 Not FDA approved for this indication.

    2  Not available in the United  States.

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