Parasites as a cause of acute diarrhea are seen most frequently in the traveler and the immigrant from developing countries where the prevalence of parasitic diseases is much higher due to problems with safe water and sanitation.1-2 Children are taken along on trips to foreign lands more frequently now than ever before.3 They are likely to have an increased chance of exposure to fecally contaminated soil and vegetation given their higher level of activity in play and difficulty with fastidious hygiene.4 They are also more apt to become symptomatic due to their size, potential for dehydration, and immature immune defenses. Indigenous parasitic causes of chronic diarrhea remain a problem in several areas of the United States. In addition, the recent recognition of new pathogens as a result of the acquired immunodeficiency syndrome (AIDS) epidemic has made the exotic seem more common in die clinic.
The most common pathogens shown to cause diarrhea in major developing countries are rotavirus, entetotoxigenic Escherichia coí, and shigella.5 These agents cause syndromes that are encountered routinely in clinical practice in developed countries as well.6 Most symptomatic diarrhea is either self-limited or responds to standard antibiotic therapy without further investigation. Persistent diarrhea mandates a révaluation of the patient while paying special attention to rehydration. Diagnosis of parasitic diarrhea depends on the consideration of the possibility in the differential, careful attention to historical details of exposure and symptoms, and evaluation of stool specimens. Children who have lived in an endemic area for some time are likely to be infected with multiple intestinal parasites, not all of which cause chronic symptoms.
Parasites are divided into two major groups: the single-cell protozoa and the helminths, commonly known as worms. The "typical" clinical picture associated with each of these human pathogens is often the best clue to diagnosis. Each one has a characteristic stage of the life cycle that usually can be seen on stool examination, although the stool occasionally has to be specially handled to find the source of the symptoms. Eosinophilia is almost always related to infection with helminths and is a consequence of tissue invasion, not just the presence of the worm in the gut. Knowledge of the organisms, their life cycles, and the associated clinical syndromes makes the diagnosis clear in most cases.
Protozoan Causes of Parasitic Diarrhea
PROTOZOAN CAUSES OF DIARRHEA
Intestinal protozoa depend on a simple fecal-oral mode of transmission. Most have developed a mechanism to survive the harsh environment of the outside world, undergoing encystment by a process that usually begins before being carried out of the body. Within the intestine, they tend to form colonies or pockets of infection in the most hospitable sites. A parasitic infection is, by definition, most successful when the host is unaware and minimally harmed by the presence of the stowaway. What triggers invasion beyond the mucosal wall and severe symptoms is largely unknown. Two clinical syndromes are typically seen in protozoan infections (Table 1 ). Secretory diarrhea may be caused by malabsorption or perhaps the histamine immune response to the parasites in the mucosal lining. Dysentery, usually a result of invasion of the deeper layers of the mucosa, is manifested by fever, severe abdominal pain, and tenesmus with liquid stool mixed with blood and mucus.
Giardiasis is probably the most common parasitic diarrhea in the developed world, causing problems in nurseries, day-care centers, homosexual men, and even in upscale ski resorts. Trophozoites are seen only in very fresh liquid stool having the characteristic "owl's face11 morphology with several pairs of flagella. A ventral sucking disk provides attachment to the wall of the duodenum and upper jejunum. The two nuclei that form the "eyes" in the trophozoite divide in the cyst, which retains many of the other internal structures. The stool contains no blood or white blood cell (WBC) counts. A duodenal aspirate or a swallowed string device give the highest diagnostic yield. Immunologie detection of Giardia antigen in the stool is highly predictive of infection but is not yet widely available.
Intestinal malabsorption and chronic intermittent diarrhea are the typical syndromes associated with infection. Villi shorten and inflammatory foci develop within the crypts by unclear mechanisms, resulting in steatorrhea, impaired absorption of vitamins, and abnormal function of digestive enzymes. Patients complain of flatulence, bloating, nausea, anorexia, foul-smelling stools, and weight loss. Quinacrine hydrochloride 5 mg/kg/day in three doses after meals (maximum: 300 mg/day) for 7 days was the preferred treatment, but this can cause dizziness, headache, vomiting, and diarrhea, and is not currently available. Metronidazole 15 mg/kg/day (maximum: 750 mg/day) is still considered investigational by the Food and Drug Administration. Furazohdone 6 mg/kg/day in four doses (maximum: 400 mg/day) is available in liquid form and tastes better than the other two drugs.
The amebas are the most primitive of the protozoa and move by forming pseudopods. They include seven species that parasitize the human gastrointestinal tract: Entamoeba histolyâca, Entamoeba coif, Entamoeba hartmanni, Entamoeba gingivolts, Dientamoeba fragiUs, EndoUmax nana, and lodamoeba biitscbhi. Stool examination techniques and comparative morphologies can be found in standard texts of parasi tology.7 All but E fustotytica are commensal amebas that live in the large intestine, except E gíngivoüs, which is found in the mouth. Dientamoeba fragilis can produce a moderate, persistent diarrhea in some individuals, but in most people there are no symptoms. The prevalence of each of the amebas ranges from 0.2% to more than 50% throughout the world, in direct correlation with the condition of sanitation.
The ingestion of as few as 10 E histoíyíca cysts can initiate an infection, although the average infectious dose is more than 1000 organisms. The cyst wall disintegrates in the small intestine where the quadrinucleate parasite divides to form eight trophozoites that are carried to the colon to multiply by binary fission. Colonization is heaviest in the cecum and rectosigmoid in areas of fecal stasis. Cytolytic enzymes dissolve the tissues to provide nutrients for absorption, causing the characteristic flask-shaped ulcérations. Trophozoites are seen most frequently in liquid stools, often containing ingested red cells, while cysts begin to develop and mature in formed stool. Infection with E histolytica is most frequently asymptomatic, but when it invades the bowel wall, significant illness can develop within 1 to 14 weeks.
Dysentery is common, characterized by intermittent, watery, foul-smelling diarrhea with mucus and blood, flatulence, and cramping abdominal pain. Fulminant symptoms develop with corticosteroid therapy or in women who are pregnant, and symptoms are abrupt in onset with a high fever, severe abdominal cramps, tenesmus, and profuse, bloody diarrhea. Marked rectosigmoid ulcération that commonly results in secondary bacterial infection is seen on sigmoidoscopy. Following extensive tissue destruction, postdysenteric colitis, bowel adhesions, and fistulas may form, occasionally requiring surgical correction.
About 5% of patients who develop symptoms can present with a liver abscess that is usually singular and in the upper outer quadrant of the right lobe. Onset of fever and tender hepatic enlargement can be acute or insidious. Extension can occur into the lung or through the left lobe of the liver into the pericardium. Aspiration reveals the classic reddish-brown, odorless fluid free of bacteria and polymorphonuclear leukocytes (WBCs), which are destroyed by the cytolytic enzymes of the ameba.
Diagnosis of dysentery is by identification of trophozoites or cysts through examination of fresh stool or sigmoidoscopic aspirates using wet mounts or stains of fixed specimens. Three or more samples may be required. Serology is positive only with tissue invasion, but may be diagnostic in evaluation of an hepatic abscess where the titers are often quite high. Metronidazole is the treatment of choice to eradicate invasive organisms, given as 35 to 50 mg/kg/day in three doses (maximum: 2250 mg/day) for 5 to 10 days, followed by the luminal agent iodoquinol 30 mg/kg/ day in three doses (maximum: 2 g/day) for 20 days. Extraintestinal amebic disease should be treated as above, followed by chloroquine 10 mg base/kg/day (maximum: 300 mg base/day) for 2 to 3 weeks plus iodoquinol.8 Stool from family members should be examined for cysts, as asymptomatic carriage can result in spread to others unless treated with iodoquinol.
Balantìdium coli is the only pathogenic citiate and the largest intestinal protozoan, with a clinical picture similar to E histolytica. Trophozoites colonize the lumen, mucosa, and submucosa of the cecum and terminal ileum in nests and small abscesses that become oval, irregular ulcers. Cysts are the infectious form and can survive outside the body for several weeks. While up to 90% of hogs are infected, the incidence of human infection is very low, even among hog farmers; human strains are thought to be the source of human infections.
Prognosis is best in asymptomatic infection and in chronic intermittent diarrhea that alternates with constipation, associated with a tender colon, anemia, and cachexia. Acute bloody dysentery can be complicated by bacterial superinfection requiring surgical intervention, but hepatic invasion is rare. Tetracycline 10 mg/kg/day administered in four doses (maximum: 2 g/day) for 10 days is the treatment of choice in adults and children over the age of 7. lodoquinol and metronidazole also can be used as in amebiasis.
Although the AIDS epidemic has highlighted this coccidian protozoan as an opportunistic parasite, the frequency of symptomatic diarrhea in the immunocompetent host has been recognized only recently. Infection is encountered commonly in travelers and locally in day-care centers since the distribution is worldwide. A large waterbome outbreak occurred in Milwaukee in 1993, presumably due to a breakdown in filtration (The New York Times. April 9, 1993:A15). Sporozoites, having escaped from oocysts in the upper gastrointestinal tract, invade the epithelial cells of the small bowel and undergo asexual multiplication to become merozoites. TT\e merozoites then can invade other cells or produce the sexual stage micro- and macrogametes. Fertilization results in the development of oocysts containing four naked sporozoites. Thick-walled oocysts are passed in the feces to initiate a new infection.
Persistent watery diarrhea, nausea, vomiting, abdominal cramps, and fever are the most common manifestations; the consequent severe dehydration can be iatal in children. Organisms can be found in the small bowel, gallbladder and pancreatic duct, and the stomach and colon. Acid-fast stain of concentrated stool is usually diagnostic, but the organism may be found only on biopsy. Intense research is ongoing to study the pathogenesis of this infection because all attempts at treatment have been unsuccessful.9 A new coccidian named Cydospara recently has been identified as causing a syndrome similar to infection with Cryptosporkíilcm, also affecting both immunocompetent and irnmunocompromised patients.10
The microsporidia are another new species of intracellular spore-forming protozoa recently recognized to cause severe enteritis in AIDS.11 An unusual coiled organelle, the polar filament, is extruded from a spore to inject the sporoplasm into the host cell and initiate the infection. Because of their small size and complex intracellular stages, electron microscopy of a duodenal aspirate or biopsy specimen is required to recognize and identify the organisms. Treatment has not yet been studied adequately; metronidazole may relieve symptoms without eradicating the parasite.
While this organism is usually considered a simple and common coinhabitant human protozoan, the pathogenicity of Bìastocystìs Komirus has yet to be proven. No toxin has been reported and no anatomic site of colonization or invasion found that would explain the occurrence of diarrhea.12 Large numbers of B hominis have been found in the stool of patients with severe diarrhea and no other apparent cause. When faced with this situation, a therapeutic trial of metronidazole or iodoquinol in doses used for amebiasis may be in order.
HELMINTHIC CAUSES OF DIARRHEA
When estimating the burden of parasitic diseases throughout the world, intestinal helminthic infections are among the most prevalent. However, diarrhea is not a prominent feature of most of these infections because the worms generally take up residence in the lumen of the gastrointestinal tract, using the normal fecal contents as their source of nutrition. Only when there is an invasive stage in the life cycle or when there is permanent close contact with the intestinal mucosa is there clinical diarrhea13 (Table 2-). While heavy infection with Ascaris htmbricoides can cause obstruction and even perforation, experimental infections and large surveys in the developing world have found no associated diarrhea. The tapeworms, Taenia soginata and Taenia solium, can cause significant abdominal discomfort, nausea, and vomiting, and may result in a frantic clinic visit after the passage of motile proglottides, but reports of diarrhea are rare. Likewise, pinworm infections (Enterobius vermicuiaris) will send the patient to the doctor for the pruritus, not for diarrhea.
Initial infection with the hookworms, Necator americanus and Ancyhstoma duodenale, may result in brief symptoms of diarrhea, yet the mechanism remains unclear since there is no mucosal penetration.14 Chronic infection can cause anemia but not diarrhea. Heavy infections with the dwarf tapeworm, Hymeno/epis nana, have been reported to cause diarrhea when large numbers of cysticercoids invade the mucosa and produce an inflammatory response and malabsorption, while light infections are asymptomatic. The pathology is not well studied in humans.
Helminthic Causes of Parasitic Diarrhea
Infection with this nematode, commonly called the whipworm, tends to be quite prevalent, up to 80% in some tropical countries with heavy warm rainfall. The problem persists in humid regions of the southern United States; humans are the principal reservoir and children are affected most commonly, although most people are asymptomatic. Once ova are ingested, activated larvae escape from the egg shell in the upper small intestine to mature and travel to the cecum. The worms resemble a whip 3 cm to 5 cm in length, with the narrow anterior three fifths embedded in the mucosa. Local inflammation results in erosion of the mucosa, pus formation, and the loss of about 0.005 mL blood per worm per day. Within 1 to 3 months, eggs can be found in the stool, although formalin-ether concentration may be required in light infections. A single female may lay up to 10 000 eggs per day that are unicellular, football-shaped, and have a translucent polar region at both ends. After stool is deposited, it takes about 3 weeks for embryonation to occur in favorable conditions when the mature larva, still in the egg shell, becomes infectious.
Heavy infections usually manifest as chronic dysentery with bloody stools, abdominal pain and tenderness, anemia, weight loss, and in the heaviest infections, rectal prolapse caused by straining at the frequent stools. TKe syndrome may be mistakenly labeled as chronic ulcerative colitis unless stools are examined carefully. The Hfespan of adult worms is 4 years or more. Treatment with mebendazole 100 mg orally twice a day for 3 days is recommended for all age groups, given the poor absorption, high efficacy, and minimal toxicity of the drug.
Humans are infected with TnchineUa spiroiis by eating raw or poorly cooked pork, beai; or other carnivorous or omnivorous animals that contain encysted larvae in striated muscle. The prevalence of human infection in the United States reached a peak of 15% to 20% in the 1930s, but is now less than 2%. Within a population, infection can be eradicated only by interruption of the life cycle; laws requiring the cooking of meat scraps before feeding them to swine are in force in most states. This is an unusual parasite because the success of transmission depends on the eventual death of the host and consumption of the larvae in meat.
Larvae are liberated from the ingested cyst in the upper small intestine and invade the mucosa to mature, marking the onset of the intestinal phase of infection. After being fertilized, the female burrows deeply into the mucosa throughout the small intestine. Larvae begin to be deposited into the lymphatics about 5 days after infection and then are carried to all parts of the body (the migration phase). The final phase is encystment, when the larvae mature in striated muscle, coil, and are encapsulated in oval microscopic cysts that become calcified over several months. Calcified cysts can be seen as fine opaque granules in heavily affected meat. The adult female continues to produce larvae until it is expelled from the intestine by immune mechanisms within several months. Pigs are infected by eating uncooked scraps of contaminated meat.
The intestinal phase is associated with an acute secretory gastroenteritis that may persist for about a week. Symptoms are most prominent in repeated infections, thought to be due to the immune response caused by the invasion of mature female worms. Eosinophilia that continues to rise despite the resolution of diarrhea may be a clue to the diagnosis. Orbital edema, muscular pain, tenderness, weakness, headache, and fever typify the migration phase in heavy infection. Diaphragmatic involvement will cause shallow, painful breathing. Muscle biopsy in the third week of illness is the most definitive diagnostic procedure. Supportive care and sedation are considered to be the mainstay of treatment. If there is myocarditis and congestive heart failure, steroids can be helpful for several days but generally are not indicated because their use can increase the number of larvae that penetrate the intestinal mucosa. Although treatment has not been found to be highly effective, thiabendazole 44 mg/kg/day in two doses for 5 days or moderately high doses of mebendazole 20 mg/kg/day in three doses (at least 1000 mg/day in adults) for 10 to 14 days may kill the parasite. Mebendazole is contraindicated in the first trimester of pregnancy.
Strongyloidiasis is common in the tropics and subtropical areas as well as in rural areas in the southern United States. The complicated lue cycle can be understood as following three paths of development. Slender infective filariform larvae can develop directly from the shorter rhabditiform larvae, which are already present in stool. Like the hookworm, they penetrate the skin of a passing human victim to enter the venous circulation and migrate to the lungs. There they penetrate the alveoli, move up to the glottis, and are swallowed to mature into adults in the mucosa of upper small intestinal villi. Females are capable of laying eggs within the intestinal mucosa about a month after infection. These quickly hatch into rhabditiform larvae that migrate back into the lumen to be passed in the stool. A second path is indirect, in that larvae can develop into sexually mature, free-living male and female adult worms in the soil. A greatly increased number of rhabditiform larvae can be generated after fertilization of the female and egg development. In favorable conditions, an additional indirect cycle of development may occur in the soil before the worm must reenter the host. Finally, autoinfection can occur within the host when the larvae rapidly develop into the filariform stage within the intestine to reinfect the mucosa or perianal skin. This is how infection persists in nonendemic areas, causing severe illness and even a hyperinfection syndrome if the host becomes immunocompromised, sometimes decades after exposure and initial infection.
Diarrhea, when present, alternates with constipation and is accompanied by burning midepigastric pain and focal tenderness. Chronic malabsorption, steatorrhea, and weight loss will follow heavy infection. Larva currens describes pruritus of the buttocks, lower back, and upper thighs that can be present in autoinfection. Asthmatic pulmonary symptoms may occur as a result of hypersensitivity to larvae passing through the lungs. Diagnosis is made by finding motile larvae in fresh feces or duodenal aspirate. Eosinophilia of 10% to 20% is frequently present, but is suppressed or absent in hyperinfection. With a typical syndrome and failure to find larvae, an enzymelinked immunosorbent assay (ELISA) may be diagnostic, since there are relatively few cross-reactions. Treatment with thiabendazole 50 mg/kg/day (maximum: 3 g/day) in two doses for 2 or 3 days is usually curative in the immunocompetent host.
Reports of capillariasis have increased in the 30 years since this infection has been recognized, mostly affecting residents of the Far East. This uncommon infection is remarkable for its relentless progression from asymptomatic passage of eggs, to malabsorptive diarrhea and cachexia, to death over a course of several months, without effective treatment.15 Like Strong^íoídes, Capitaria sp have an autoinfective cycle within the human host, but replication does not seem to be suppressed by immune mechanisms. Eggs that are passed in the stool embryonale in fresh or brackish water to hatch and develop into infective larval stages in the intestines of fish once they are eaten. Humans and birds are thought to be infected by eating small whole raw fish. Larvae and adults are found in the jejunal mucsoa where they cause inflammation and flattening of villi. Female worms can be oviparous or larviparous, which accounts for the potential for hyperinfection. Eggs in the stool must be differentiated from Tricfmris eggs, which they resemble. Albendazole 400 mg/day in two doses for 10 days is the treatment of choice, but must be obtained directly from the manufacture^ SmithKline Beecham. Relapses with thiabendazole and mebendazole are thought to be due to their inability to affect the larval stages.
While many trematodes can cause diarrhea, the blood flukes are the most prevalent. Eggs, deposited in the bowel by Schistosoma mansoni or Schistosoma japonicum, or in the bladder by Schistosoma hematobium, are excreted and hatch when they reach freshwater. Miracidia infect certain species of snails and multiply, then develop into cercariae that are released into the water. When they contact human skin, cercariae burrow into the capillary bed and lose their tails to become schistosomula. This form is carried in the circulation through the heart and lungs to the liver, where it matures over the next 3 weeks. Adolescent worms migrate against the portal vein flow to the mesenteric, vesical, and pelvic venules, where the female is embraced in the gynecophoric canal on the ventral surface of the male in constant copulation. The infection becomes "patent" 5 to 12 weeks later when eggs begin to appear in the stool or urine.
Initial penetration of the skin by cercariae can cause pruritus and a mild rash at the site of entry, known as swimmer's itch. Light infections will cause no further symptoms. Katayama fever is the acute systemic disease that may accompany a heavy primary infection during the prépaient and early egg-laying phases, possibly a result of an allergic response to migrating larvae and oviposition. The syndrome is manifested by fever, arthralgias, cough, marked eosinophilia, lymphadenopathy, hepatosplenomegaly, abdominal pain, and bloody diarrhea. These symptoms gradually subside, although abdominal pain and diarrhea, or periodic hematuria, dysuria, and urgency may persist. Hepatosplenic fibrosis only occurs after many years of chronic reexposure as a result of the immunemediated deposition of connective tissue around the eggs. Diagnosis is made by finding the characteristic eggs in the stool, filtered urine, or rectal biopsy. The most specific serological tests screen for immunoglobulin (Ig) M reacting with gut antigens of the worm or circulating antigen, but these tests are available only in specialized labs. Serodiagnosis using crude antigens is nonspecific and is not thought to be adequate for treatment decisions unless eggs also are found. Praziquantel 40 mg/kg/day taken with food divided into two doses 4 hours apart is the preferred treatment. This often is associated with mild dizziness, myalgia, headache, and abdominal discomfort.
Many etiologies may provoke an eosinophilic infiltrate in the intestinal wall, but a recent epidemic in Australia led to an association with the dog hookworm Ancy/ostoma caninum.16 "Accidental" infection of humans occurs when larvae penetrate the skin and migrate through the tissues, where most encapsule and remain dormant in skeletal muscles. When the occasional larva reaches the intestine and matures, it has been found in the distal small bowel causing a segmental allergic inflammation, severe abdominal pain and melena, moderate eosinophilia, and high serum IgE. Eggs are not seen in the stool; the parasite presumably is not able to attain full maturity in the human host. Treatment with mebendazole as in Trichuris seems adequate.
SPECIAL CONCERNS IN DIAGNOSIS AND TREATMENT
Most antidiarrheal compounds are not approved for children younger than 2 or 3 years old given the higher risk of adverse effects.8 Drugs that alter intestinal motility such as loperamide17 and atropinecontaining agents such as Lomotil (diphenoxylate hydrochloride with atropine, G. D. Searle & Co, Chicago, Illinois) are not recommended in infants. Instead, attention should be focused on rehydration and correcting electrolyte abnormalities. Specific treatment is a priority since parasites transmitted by the fecal-oral route are particularly troublesome in institutional settings and day-care centers.
Parasitic diarrhea is rarely life threatening. Given the plethora of potential etiological agents, every effort should be made to diagnose the infection before presumptive treatment. Fortunately, this is often easier with parasitic infections than with other causes of infectious diarrhea. A week should pass after barium or bismuth administration before attempting to examine stool. As is evident from the life cycles discussed above, additional time may need to elapse to find diagnostic eggs or larvae in the stool, even in the presence of peripheral eosinophilia. In the case of patients infected with multiple parasites, there is an added benefit of cross-sensitivity to many of the drugs. Protozoa, when treatable, can be managed with metronidazole. Its use is discouraged in pregnancy and during breast-feeding, and is contraindicated in the first trimester, given the theoretical teratogenicity. Most nematodes are susceptible to mebendazole. Trematodes and cestodes can be treated with praziquantel.
Chemotherapeutic advances have been dramatic over the past two decades, mostly as a result of learning about the life cycles of each parasite to discover points where treatment can be effected. Although infection with Cryptosporidium and microsporidia remain untreatable, we now have agents for most of the parasitic causes of diarrhea that are much less toxic and highly efficacious. We are just beginning to appreciate the cytokine interactions underlying the immune response to intestinal parasites in animal models of infection.18 Perhaps when these basic mechanisms are fully understood, we will discover new approaches to interruption of the life cycles that can be taken from the laboratory to the clinic, and out to the world.
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Protozoan Causes of Parasitic Diarrhea
Helminthic Causes of Parasitic Diarrhea