Giardiasis is a major diarrheal disease found throughout the world. The flagellate protozoan Giardia intestinalis­­ (previously known as G lamblia or G duodenalis), its causative agent, is the most commonly identified intestinal parasite in the United States[1, 2] and the most common protozoal intestinal parasite isolated worldwide.[3, 4, 5, 6, 7] Infection is more common in children than in adults.[8, 9]

G intestinalis can cause asymptomatic colonization or acute or chronic diarrheal illness. The organism has been found in as many as 80% of raw water supplies from lakes, streams, and ponds and in as many as 15% of filtered water samples.[10, 11] It is a common cause of chronic diarrhea and growth retardation in children in developing countries.

Giardiasis usually represents a zoonosis with cross-infectivity between animals and humans. Giardiaintestinalis has been isolated from the stools of beavers, dogs, cats, and primates. Beavers may be an important reservoir host for G intestinalis.[12, 13, 14] Other Giardia species include G muris in rodents; G agilis in amphibians; G psittaci and G ardeae in birds; and G microti in voles and muskrats.[15, 16, 17]

Giardia species are endemic in areas of the world that have poor sanitation. In developing countries, the disease is an important cause of morbidity. Water-borne and food-borne outbreaks are common. Because ingestion of as few as 10 Giardia cysts may be sufficient to cause infection, giardiasis is common in daycare center attendees and institutionalized patients in developed countries. G intestinalis is a particularly significant pathogen for people with malnutrition, immunodeficiencies, or cystic fibrosis.

High-risk groups for giardiasis include travelers to highly endemic areas, immunocompromised individuals, and certain sexually active homosexual men. Cyst passage rates as high as 20% have been reported among certain groups of sexually active homosexual men. These individuals were frequently symptomatic.[12, 18]

The traditional basis of diagnosis is identification of Giardia intestinalis trophozoites or cysts in the stool of infected patients via a stool ova and parasite (O&P) examination. Stool antigen enzyme-linked immunosorbent assays also are available. (See Workup.) Standard treatment for giardiasis consists of antibiotic therapy. Metronidazole is the most commonly prescribed antibiotic for this condition; however, tinidazole is also approved in the United States and is considered a first-line agent outside the United States. (See Treatment.)

A G intestinalis cyst is seen in the image below.

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A Giardia intestinalis cyst.

See Common Intestinal Parasites and 5 Cases of Food Poisoning: Can You Identify the Pathogen?, Critical Images slideshows, to help make an accurate diagnosis.

Historical background

Giardia was originally observed by von Leeuwenhoek in 1681, in his own diarrheal stool, and was described by Vilem Dusan Lambl in 1859 and by Alfred Giard in 1895. The organism’s previous name, honoring the contributions of Giard and Lambl, was bestowed in 1915.

Although G intestinalis was the first protozoan parasite described, its role as a pathogenic organism was not recognized until the 1970s, after community outbreaks and after the appearance of the disease in travelers returning from endemic regions. Prior to that time, the organism was thought to be a harmless commensal organism of the intestine.


Infection with Giardia intestinalis most often results from fecal-oral transmission or ingestion of contaminated water. Contaminated food is a less common etiology. Person-to-person spread is common, with 25% of family members with infected children themselves becoming infected.

Most infections are asymptomatic. The rate of symptomatic infection in the natural setting varies from 5-70%. Giardia is found in healthy people in endemic areas, and asymptomatic carriage with excretion of high numbers of cysts in stools is common.

Predisposing factors to symptomatic infection include hypochlorhydria, various immune system deficiencies, blood group A, and malnutrition. The incubation period averages 1-2 weeks, with a mean of 9 days. The average duration of symptoms in all ages ranges from 3-10 weeks.

Giardia life cycle

Giardia has one of the simplest life cycles of all human parasites. The life cycle is composed of 2 stages: (1) the trophozoite (see the first image below), which exists freely in the human small intestine; and (2) the cyst, which is passed into the environment. No intermediate hosts are required.

Upon ingestion of the cyst (see the second image below), contained in contaminated water or food, excystation occurs in the stomach and the duodenum in the presence of acid and pancreatic enzymes. The trophozoites pass into the small bowel where they multiply rapidly, with a doubling time of 9-12 hours. As trophozoites pass into the large bowel, encystation occurs in the presence of neutral pH and secondary bile salts. Cysts are passed into the environment, and the cycle is repeated.

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Giardia lamblia, cyst form.

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Giardia lamblia trophozoites in culture.

The trophozoite form of G lamblia is teardrop-shaped and measures 9-21 micrometers long by 5-15 micrometers wide. The trophozoite has a convex dorsal surface and a flat ventral surface that contains the ventral disk, a rigid cytoskeleton composed of microtubules and microribbons. The trophozoite also contains 4 pairs of flagella, directed posteriorly, that aid the parasite in moving. Two symmetric nuclei with prominent karyosomes produce the characteristic facelike image that appears on stained preparations.

The ventral disk, which is often referred to as the sucking or adhesive disk, provides the parasite with powerful adhesion, catching, and holding abilities. In the murine model of giardiasis, the ventral disk adhesion imprints are marked but less impressive than in the human small intestine. However, this direct injury is an unlikely cause of the more extensive reduction in microvillus surface area, the reduction in disaccharidase activities, and the more pronounced abnormalities of villous architecture that are seen in giardiasis.[19, 20]

The cyst form of the protozoan is smooth-walled and oval in shape, measuring 8-12 micrometers long by 7-10 micrometers wide. As the cyst matures, nuclear division occurs and readies the cyst to release 2 trophozoites upon excystation. Once the host is infected, trophozoites may appear in the duodenum within minutes.[21] Excystation occurs within 5 minutes of exposure of the cysts to an environment with a pH between 1.3 and 2.7.

After infection, the trophozoites attach to the enterocytes via the ventral adhesive disk. This may occur through the presence of lectin on the surface of the trophozoite or through other mechanical means. Encystation is a continuous process during infection.

As the trophozoites encounter neutral pH and/or secondary bile salts, encystation-specific secretory vesicles (ESVs) appear. After 15 hours, cyst wall proteins are visible. Within 24 hours after the appearance of ESVs, the trophozoite is covered with these cyst wall proteins, the form of the cyst has emerged, and new antigenic differences are present.

Mechanism of injury

The mechanisms by which Giardia causes diarrhea and intestinal malabsorption are probably multifactorial and not yet fully elucidated.[19] Postulated mechanisms include damage to the endothelial brush border, enterotoxins, immunologic reactions, and altered gut motility and fluid hypersecretion via increased adenylate cyclase activity.

Adhesion of trophozoites to the epithelium has been demonstrated to cause increased epithelial permeability. Giardia- induced loss of intestinal brush border surface area, villus flattening, inhibition of disaccharidase activities, and eventual overgrowth of enteric bacterial flora appear to be involved in the pathophysiology of giardiasis but have yet to be causatively linked to the disease's clinical manifestations.

Marked or moderate partial villous atrophy in the duodenum and jejunum can be observed in histologic sections from asymptomatic individuals who are infected. In addition to disrupting the mucosal epithelium, effects in the intestinal lumen may contribute to malabsorption and the production of diarrhea.[8, 22] Nevertheless, diarrhea can occur in individuals in the absence of obvious light microscopic changes in small intestinal structure.

Varying degrees of malabsorption of sugars (eg, xylose, disaccharides), fats, and fat-soluble vitamins (eg, vitamins A and E) may contribute to substantial weight loss. The histopathologic response to giardiasis varies and imperfectly correlates with the clinical symptoms.[13, 23]

G intestinalis may release cytopathic substances that damage the intestinal epithelium. Giardia species contain thiol-dependent and thiol-independent proteinases, which may find substrates in the microvillus membrane. A 2018 report suggests that three main cysteine proteases (CP14019, CP16160 and CP16779) secreted by G intestinalis disrupt intestinal epithelial cell junctional complexes and degrade chemokines.[24] In addition, the surface mannose-binding lectin of G intestinalis may contribute to epithelial damage. Whatever the mechanism by which G intestinalis damages villous epithelial cells, the result consistently appears to be an increase in crypt length and crypt cell proliferation.[25]

Enterocytic injury is mediated by activated host T lymphocytes. Pathophysiological activation of lymphocytes is secondary to Giardia -induced disruption of epithelial tight junctions, which, in turn, increases intestinal permeability. Loss of epithelial barrier function is a result of Giardia -induced enterocyte apoptosis.[22, 26, 27]

Epithelial barrier dysfunction in cases with chronic giardiasis is associated with increased rates of enterocyte apoptosis. Consistent with these observations, microarray analyses of the effects of G intestinalis on human CaCo2 cells found that the parasite–host interactions lead to a pronounced up-regulation of genes implicated in the apoptotic cascade and the formation of reactive oxygen species.

Panaro et al demonstrated that Giardia trophozoites induce cell apoptosis by activation of both intrinsic and extrinsic apoptotic pathways, down-regulation of the antiapoptotic protein Bcl-2, and up-regulation of the proapoptotic Bax. These findings suggest a possible role for caspase-dependent apoptosis in the pathogenesis of giardiasis.[28]

Giardia can also prevent the formation of nitric oxide, a compound known to inhibit giardial growth, by consuming local arginine, which effectively removes the substrate needed by enterocytes to produce nitric oxide. This mechanism may contribute to Giardia -induced enterocyte apoptosis because arginine starvation in these cells is known to cause programmed cell death.[19, 29]

G intestinalis is genetically heterogeneous with 8 genetically distinct genotypes or assemblages, designated A-H; assemblages A and B can infect humans. Genotypes vary within group A and B, which could explain why the role of animals in the epidemiology of human infection remains poorly understood.[30, 31] Some strains appear more biologically suitable than other strains. This feature is potentially important in giardiasis pathogenesis.[32, 33] Genotypically diverse isolates of Giardia species may vary in their ability to produce morphologic changes in the small intestine epithelium and to impair fluid, electrolyte, and solute transport.[34]


Giardiasis is caused by the flagellate protozoan Giardia intestinalis (formerly known as G lamblia) . Infection is transmitted through ingestion of infectious G lamblia cysts.[35] The organism is known to have multiple strains with varying abilities to cause disease, and several different strains may be found in one host during infection. The infective dose is low in humans; 10-25 cysts are capable of causing clinical disease in 8 of 25 subjects. Ingestion of more than 25 cysts results in a 100% infection rate.

Person-to-person transmission, often associated with poor hygiene and sanitation, is a primary means of infection. Diaper changing and inadequate hand washing are risk factors for transmission from infected children. Children attending day care centers, as well as day-care workers, have a higher risk of infection secondary to fecal-oral transmission.

Water-borne transmission is responsible for a significant number of epidemics in the United States, generally following ingestion of unfiltered surface water. Giardia cysts retain viability in cold water for as long as 2-3 months. Giardia was implicated in 90 waterborne outbreaks in the United States from 1964-1984, affecting 23,500 persons.

Venereal transmission occurs through fecal-oral contamination. Food-borne epidemics have been reported, most commonly secondary to contamination by infected food-handlers.[36, 37] Pets frequently harbor Giardia in their GI tracts, but they are not thought to be a significant cause of outbreaks in humans.


United States statistics

Giardia remains the parasite most commonly identified in stool specimens, causing about 1.2 million annual episodes of illness.[2] From 1964-1984, G lamblia caused at least 90 water-borne outbreaks of diarrhea, affecting more than 23,000 people. These outbreaks typically involved small water systems using untreated or inadequately treated surface water.

Most water-borne outbreaks in the United States have occurred in western mountain regions (eg, Rocky Mountains, Sierra Nevada, Cascades) where giardiasis must be considered endemic. The incidence of giardiasis is high among individuals who camp and backpack in mountainous Western states. Other groups at increased risk for infection include children, homosexual men, and individuals with immunoglobulin deficiency states (inherited or acquired).

Yoder et al reported that the incidence is greatest in northern states,[38] but this may be related to the differences in individual state surveillance systems and may not necessarily reflect an actual higher incidence.[38]  Because water-borne giardiasis outbreaks have been reported in every region in the United States, the diagnosis must be considered anywhere in the country.

Endemic infection occurs most commonly from July through October among children younger than 5 years and adults aged 25-39 years. Carrier rates as high as 30-60% have been documented among children in day care centers, institutions, and on Native American reservations.

The asymptomatic carriage rate in children may be as high as 20% in southern regions and in children younger than 36 months who attend daycare centers. Asymptomatic carriage may persist for several months. Many children with giardiasis are symptomatic, have been shown to spread the disease within their homes, and may contribute to high endemic rates in their communities.[18]

In the 46 states reporting giardiasis, the mean number of cases per 100,000 population varies by state, with a range of 0.1-23.5 cases. Most cases are reported between June and October and are associated with the summer recreational water season and camping.[39]

International statistics

Giardia has a worldwide distribution, occurring in both temperate and tropical regions. It continues to be the most frequently identified human protozoal enteropathogen. Prevalence rates vary from 4-42%. In the industrialized world, overall prevalence rates are 2-5%. In the developing world, G intestinalis infects infants early in life and is a major cause of epidemic childhood diarrhea. Prevalence rates of 15-20% in children younger than 10 years are common.[32, 40]

Giardia is the most common gut parasite in the United Kingdom, and infection rates are especially high in Eastern Europe. Prevalence rates of 0.94-4.66% and 2.41-10.99% have been reported in Italy.[41]

A 2005 study demonstrated a Giardia infection rate of 19.6 per 100,000 population per year in Canada.[42] While the yearly incidence of the disease was stable, a significant seasonal variation was observed, with a peak in late summer to early fall, which correlates with the pattern found in the United States.[42] New Zealand reports more than 30 cases of giardiasis per 100,000 population every year, which is one of the highest among the industrialized countries.[43]

Giardiasis accounts for a relatively small percentage of traveler's diarrhea. It is more likely to be found as the cause of diarrhea that occurs or persists after returning home from travel to developing regions of the world due to its relatively long incubation period and persistent symptoms. Giardia has been identified as the causative agent in a large percentage of cases among travelers to the region of St. Petersburg, Russia, where tap water is the primary source.

The highest prevalence of G intestinalis reached 73.4% in Western Nepal. In Bangladesh, a disparity between health prevention and health spending is observed. The Dhaka study performed within the urban areas had identified G intestinalis in 11% of diarrheal stool specimens.[44]

In Ethiopia, the prevalence has been reported to range from 2.0% to 11.4%.[45] Prevalence of G intestinalis has been reported 13.9% in Côte d'Ivoire.[46]

Race-, sex-, and age-related differences in incidence

Giardiasis does not have any race predilection. Native American populations residing on reservations can have high carrier rates.

Giardiasis is slightly more common in males than in females.[42] A Canadian population study demonstrated infection rates of 21.2 per 100,000 per year versus 17.9 per 100,000 per year for males and females, respectively, resulting in a relative risk of 1.19.[42]

Giardiasis affects people of all ages. Infection is rare during the first 6 months of life in breastfed infants, but infants and young children have an increased susceptibility to giardiasis. Age-specific prevalence of giardiasis continues to rise through infancy and childhood and begins to decline only in adolescence.[18, 47]

Children are particularly at risk for infection through exposure at day-care centers. Many of the epidemics documented over the last 2 decades have originated in day-care centers. Estimates of the prevalence of infection, defined by the presence of cyst passage, have been as high as 20-25% in children younger than 3 years.[48, 49]

According to 2003–2005 data from the Centers for Disease Control and Prevention, the greatest number of reported cases occurred among children aged 1-4 and 5-9 years and adults aged 35-44 years.[38]


The prognosis for patients with giardiasis is generally excellent. Most patients are asymptomatic, and most infections are self-limited. Giardiasis is not associated with mortality except in rare cases of extreme dehydration, primarily in infants or malnourished children.

Several antibiotic agents are available with good efficacy rates to shorten the disease course, although drug resistance has been observed in clinical experience. Untreated, giardiasis can last for weeks.

The parasite persists in the stool.[8, 26] Reinfection is possible.

Weight loss, disaccharidase deficiency, malabsorption, and growth retardation are possible complications.[50, 51]  G intestinalis has been implicated as the chief cause of growth retardation in infected children, even after other diarrhea-causing agents are controlled.[18, 26]

Some patients may experience persistent symptoms (eg, chronic diarrhea/steatorrhea, malabsorption) despite apparently effective antibiotic treatment, although these usually subside over weeks to months.[21, 39, 47] However, Hanevik et al found symptoms consistent with irritable bowel syndrome (IBS) and/or functional dyspepsia in 76 of 82 patients at least 6 months after eradication of Giardia infection.[52] Patients reported bloating, diarrhea, and abdominal pain, which were exacerbated by specific foods or by physical or mental stress. Another study by Hanevik and colleagues associated giardiasis with the presence of IBS and chronic fatigue even 6 years after infection.[53]

Similarly a longitudinal cohort study (2006-2010) of data from the MarketScan commercial database that evaluated the relationship between a diagnosis of giardiasis and that of IBS found that, even accounting for confounding factors, patients with giardiasis had a greater 1-year incidence of IBS than those without giardiasis.[1]  The study included a matched cohort of 3935 patients with giardiasis and 19,663 without giardiasis.

Patient Education

Patients and at-risk individuals should be instructed regarding appropriate hygiene methods and signs/symptoms of infection. Emphasis should be placed on measures such as careful hand washing after changing diapers. Day-care workers should use meticulous hygiene and careful hand washing to reduce spread between children and to staff. Personal hygiene education to minimize person-to-person transmission in high-risk settings such as residential institutions is helpful.

Patients should be advised that oral-anal and oral-genital contact increase the risk of venereal transmission.

Hikers and travelers to areas where the disease is endemic should be educated. Before drinking surface water, they should disinfect it by boiling or the use of halogenating compounds (eg, chlorine) or filtration devices.


Clinical signs and symptoms of giardiasis include the following[8, 9, 18] :

The nature of the overall clinical manifestations in affected patients is influenced by numerous factors, including the parasite load, virulence of the isolate, and the host immune response.

Diarrhea is the most common symptom of acute Giardia infection, occurring in 90% of symptomatic subjects. Abdominal cramping, bloating, and flatulence occur in 70-75% of symptomatic patients.

Symptoms of chronic infection include chronic diarrhea, malaise, nausea, and anorexia. Weight loss, as extensive as 10-15 pounds in an adult, occurs in approximately 66% of symptomatic patients. Chronic sporadic diarrhea may continue for months. Postinfection lactase deficiency also is a common finding, occurring in 2-40% of cases.

Extraintestinal manifestations are rare and include allergic manifestations such as urticaria, erythema multiforme, bronchospasm, reactive arthritis, and biliary tract disease. The etiology of such extraintestinal symptoms is likely a result of host immune system activation and cross-reactivity/molecular mimicry.

Gastrointestinal manifestations

A small number of persons develop abrupt onset of explosive, watery diarrhea, abdominal cramps, foul flatus, vomiting, fever, and malaise; these symptoms last 3-4 days before transition into the more common subacute syndrome. Most patients experience a more insidious onset of symptoms, which are recurrent or resistant.

Stools become malodorous, mushy, and greasy. Watery diarrhea may alternate with soft stools or even constipation. Upper GI symptoms, often exacerbated by eating, accompany stool changes or may be present in the absence of soft stools. These include upper and midabdominal cramping, nausea, early satiety, bloating, substernal burning, and acid indigestion.

Constitutional symptoms

Anorexia, fatigue, malaise, and weight loss are common. Weight loss occurs in more than 50% of patients and averages 10 pounds.

Chronic illness may occur. Adults may present with long-standing malabsorption syndrome and children, with failure to thrive.

Physical Examination

Physical examination does not contribute to the diagnosis of giardiasis. Weight loss may be evident, but no known unique physical findings are attributable to giardiasis.

On abdominal examination, patients may have nonspecific tenderness without evidence of peritoneal irritation. Rectal examination should reveal heme-negative stools. In severe cases, evidence of dehydration or wasting may be present.


Complications of giardiasis may include the following:

Approach Considerations

The traditional basis of diagnosis is identification of Giardia intestinalis trophozoites or cysts in the stool of infected patients via a stool ova and parasite (O&P) examination. However, in more recent years, the advent of more objective techniques (eg, immnoassays, nucleic acid amplification techniques [NAATs]) has led to an increase in their use versus those that rely on subjective microscopic examination of fecal specimens for Giardia cysts.[55]

Stool examination may be performed on fresh specimens or after preservation with polyvinyl alcohol or 10% formalin (with appropriate staining). Ideally, 3 specimens from different days should be examined because of potential variations in fecal excretion of cysts. G intestinalis is identified in 50-70% of patients after a single stool examination and in more than 90% after 3 stool examinations.

Stool O&P testing aids in the diagnosis of giardiasis in 80-85% of patients. It remains the diagnostic method with which other tests are compared. Aspiration of duodenal contents and demonstration of trophozoites also have been used for diagnosis but this is more invasive than stool examination and, in direct comparison studies to stool microscopy, may have a lower diagnostic yield.

Stool antigen enzyme-linked immunosorbent assays also are available.[56] These tests are similar to the stool O&P test in terms of cost and have a sensitivity of 88-98% and a specificity of 87-100%. These tests are best used as a screening test in high-incidence settings such as day-care centers or for identification of subjects during an epidemic, but they should not take the place of stool microscopy.

If the results from 3 O&P tests are negative and giardiasis is still suspected, stool antigen enzyme-linked immunosorbent assay (ELISA) may be helpful. If both of these methods result in negative findings but the patient has symptoms consistent with small bowel diarrhea/malabsorption, upper endoscopy with biopsies and duodenal aspirate is a reasonable alternative.

Stool culture is not routinely used because of the difficulty of reproducibly isolating Giardia from patient fecal samples. However, stool cultures are beneficial in ruling out other pathogens as the cause of a patient's symptoms.

Routine laboratory tests (eg, CBC count, electrolyte levels) usually show normal results. Eosinophilia is an uncommon feature of infection.

Because immunoglobulin G (IgG) levels remain elevated for long periods, they are not beneficial in making the diagnosis of acute giardiasis. Serum anti-Giardia immunoglobulin M (IgM) can be beneficial in distinguishing between acute infections and past infections.

Stool Examination

Stool examination (see the images below) for trophozoites or cysts is the traditional method for diagnosing giardiasis. At least 3 stools taken at 2-day intervals should be examined for ova and parasites. Trophozoites may be found in fresh, watery stools but disintegrate rapidly. If the stool is not fresh or is semiformed to formed, trophozoites will not be found.

Cysts are passed in soft and formed stools. Fresh stool can be mixed with an iodine solution or methylene blue and examined for cysts on a wet mount. If not immediately examined, stool should be preserved in polyvinyl, alcohol, or 10% formalin, with subsequent trichrome or iron hematoxylin staining. Cyst passage is extremely variable, not related to clinical symptoms, and may lag behind the onset of symptoms by a week or more.

Cysts are smooth walled and oval, measuring 8-12 μm long and 7-10 μm wide. Iodine stains the cysts brown and accentuates their intracystic structures, especially their curved median bodies, axonemes, and nuclei. By focusing through the plane of the sample, 4 nuclei may be visualized, representing 2 daughter trophozoites.

Trophozoites are leaf-shaped, measuring 9-21 μm long and 5-15 μm wide. Stained organisms have a characteristic facelike image with 2 nuclei and 4 pairs of flagella.[26]

Because many antibiotics, enemas, laxatives, and barium studies mask or cause the disappearance of parasites from the stools, microscopic examination should be postponed for 5-10 days following these interventions.

Fecal leukocytes should not be visualized in stool samples of patients with giardiasis.

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Giardia intestinalis trophozoites on stool examination from a patient with diarrhea.

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Giardia cyst.

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Giardia trophozoite

Stool Antigen Detection

Several tests to detect Giardia antigen in the stool are commercially available.[15, 37, 57] These utilize either an immunofluorescent antibody (IFA) assay or a capture enzyme-linked immunosorbent assay (ELISA) against cyst or trophozoite antigens. These tests have a sensitivity of 85-98% and a specificity of 90-100%.

Polymerase chain reaction (PCR) techniques may detect giardia in stool samples with parasites concentrations as low as 10 parasites/100 mcL. PCR may also be a valuable tool for screening of water supplies.[58] Real-time PCR has also the advantage of being able to detect both mild and asymptomatic infections.[59]

While more sensitive than stool examination, these examinations are limited to the detection of Giardia; isolated use might result in missing an alternative or concurrent parasitic infection.

A 2009 study evaluated a screening test for Giardia and Cryptosporidium on 136 fecal samples. The results showed the test to be 98.4% sensitive and 100% specific; the positive and negative predictive values were 98.7% and 99.3%, respectively.[60]

Abdominal Radiography

No imaging studies are required in the workup of giardiasis. Small-bowel plain films may show nonspecific thickening and distortion of the mucosal folds of the duodenum and jejunum, hypersecretion, and hypermotility.[13, 37] These changes are reversible with therapy. Barium studies should be avoided because barium can obscure identification of parasites for as long as 10 days.

String Test

The string test (Entero-test) consists of a gelatin capsule containing a nylon string with a weight attached to it. The patient tapes one end of the string to his or her cheek and swallows the capsule. After the gelatin dissolves in the stomach, the weight carries the string into the duodenum.

The string is left in place for 4-6 hours or overnight while the patient is fasting. After removal, it is examined for bilious staining, which indicates successful passage into the duodenum. The mucus from the string is examined for trophozoites in an iodine or saline wet mount or after fixation and staining.

Other Tests

Fecal fat quantification or a qualitative fecal fat analysis with Sudan stain may confirm steatorrhea. Serum carotene, folate, and vitamin B-12 levels may be variably depressed as a result of malabsorption. The findings from D-xylose absorption tests may be abnormal.

Disaccharidase deficiency is common during and after treatment and can be diagnosed with the aid of a lactose tolerance breath test.[61]

Serum electrophoresis can help diagnose immunoglobulin A, immunoglobulin M, and, occasionally, immunoglobulin G deficiency states.

Serologic studies are being investigated.

Endoscopy and Biopsy

Esophagogastroduodenoscopy (EGD) may be employed in patients in whom the diagnosis is suspected but unproven after stool microscopy and ELISA. This also may be used for patients who continue to manifest symptoms of malabsorption after adequate therapy.

Endoscopy may be used to assess the small bowel architecture and obtain a duodenal aspirate or biopsy. While rarely necessary, duodenal biopsy may be the most sensitive test. This has several benefits over the string test. An aspirate can be cultured to assess for overgrowth of the small intestine. Other small bowel parasites, such as microsporidia and cryptosporidia, may be detected in biopsy samples. Spruelike lesions, which may occur with giardiasis, can be detected with this technique.

Biopsy can also be used to visualize changes in histologic features. Intestinal biopsy shows flattened, mild lymphocytic infiltration and trophozoites on the surface.[22, 29]

Biopsy specimens from duodenum are often teeming with sickle-shaped Giardia trophozoites, which are tightly bound by the concave attachment disc to the villus surface of the intestinal epithelial cells. In cases where trophozoites are difficult to recognize in biopsy samples, specific anti-Giardia immunoperoxidase stains aid in the detection of the organisms, although these stains are not readily available.

Many patients exhibit atrophy of the small intestinal villi with a mixed inflammatory infiltrate in the lamina propria. The brush borders of the surface absorptive epithelial cells are irregular, and virtual absence of villi may be noted, as in celiac disease.

Histologic Findings

No classic universal histologic abnormalities result from infection with G intestinalis. Patients with giardiasis who undergo endoscopy and small bowel biopsy are likely to have similar findings compared to controls.

Patients with immunoglobulin deficiency states and giardiasis may demonstrate various degrees of villous atrophy that bear a striking resemblance to celiac sprue. These conditions can be differentiated from sprue by the absence of plasma cells in the lamina propria.

Approach Considerations

Standard treatment for giardiasis consists of antibiotic therapy.[62]  Metronidazole is the most commonly prescribed antibiotic for this condition.[35, 63, 64]  However, metronidazole use has been associated with significant failure rates in clearing parasites from the gut and with poor patient compliance.[65]  In addition, an increasing incidence of nitroimidazole-refractory giardiasis has been reported, particularly in travelers from India[66]  and other regions in Asia.[67]  An optimal treatment strategy for refractory giardiasis remains to be determined, and no standard treatment regimen for nitroimidazole-refractory giardiasis exists yet.[67]

In a systematic review and meta-analysis of 7 trials comprising 639 patients to evaluate the efficacy of mebendazole in children with giardiasis, investigators found no clinical difference in parasitologic cure between mebendazole and metronidazole, with a relative risk of 0.81 but high heterogeneity.[7] The researchers indicated clinicians should use caution in interpreting and using these results in clinical practice

Real-time polymerase chain reaction (PCR) may aid in the evaluation of treatment success. van den Bijllaardt et al showed it took about 1 week for samples to become negative after treatment of a G lamblia infection, indicating rapid clearance of the parasitic DNA following successful therapy.[68]

Appropriate fluid and electrolyte management is critical, particularly in patients with large-volume diarrheal losses.[9]

Treat children with acute or chronic diarrhea who manifest a failure to thrive, malabsorption, or other GI tract symptoms in whom Giardia organisms have been identified.[60]

Generally, do not treat asymptomatic persons who excrete the organism, except to prevent household transmission (eg, from toddlers to pregnant women or to patients with hypogammaglobulinemia or cystic fibrosis) and to permit adequate treatment in individuals with possible Giardia intestinalis –associated antibiotic malabsorption who require oral antibiotic treatment for other infections.[39, 69]

Routine treatment of infected persons in highly endemic areas where water supplies continue to be contaminated is of questionable value because reinfection may readily occur.[18, 70] Treat all infected persons who are in nonendemic areas.[71]

Ensure that close contacts of the patient are also examined for giardiasis and treated if infected.

Severely dehydrated or malnourished patients should be admitted for further care.

Diet and Activity

No special diet is required. A significant portion of patients have symptoms of lactose intolerance (cramping, bloating, diarrhea), and maintenance on a lactose-free diet for several months may be helpful. Acquired lactose intolerance occurs in as many as 20-40% of cases.[12]

Activity restrictions are not indicated. However, infected subjects who are at risk of spreading the infection should be isolated and treated.

Pregnant Patients

No consistent recommendations exist for the treatment of pregnant patients because of the potential adverse effects of anti-Giardia agents on the fetus. If possible, treatment should be avoided during the first trimester. Mildly symptomatic women should have treatment delayed until after delivery. If treatment is necessary, paromomycin can be used as systemic absorption is poor.[70] If the patient is left untreated, adequate nutrition and hydration maintenance are paramount.

Failed Treatment

Documenting the continued presence of Giardia in patients who appear unresponsive to treatment is important. A significant number of patients develop post-Giardia lactose intolerance and present with symptoms consistent with persistent infection. These patients usually improve with time and with the institution of a lactose-free diet.

If Giardia is found in the patient, a careful history should indicate whether this is a reinfection or a treatment failure. A second course of the same drug, for a longer period or a higher dose, should be effective in reinfections, whereas the use of an alternative drug should be effective in true treatment failures. A combination therapy may have to be implemented in certain cases of treatment failure.

Patients who fail repeated courses of treatment should be evaluated for hypogammaglobulinemia and may require combination therapy or chronic suppressive therapy.


Infected persons and persons at risk should carefully wash their hands after they have any contact with feces. Careful hand washing is important, especially for caregivers of diapered infants in daycare centers, where diarrhea is common and carriers of Giardia organisms are numerous.

Chlorination, sedimentation, and filtration methods should be implemented to adequately purify public water supplies. Effective chlorine inactivation of Giardia cysts in water requires an optimal chlorine concentration, water pH, turbidity, temperature, and contact time. These variables cannot be appropriately controlled in all municipalities, and they are particularly difficult to control in swimming pools.

Advise travelers to endemic areas to avoid eating uncooked foods that may have been grown, washed, or prepared with contaminated water.

Drinking water can be purified by using filtration (pore size, < 1 µm) or by briskly boiling water for at least 5 minutes. Chlorine or iodine water treatments are less effective than boiling or filtration, but they may be used as alternatives when other methods are not available.

Infected individuals should refrain from using recreational water venues (eg, swimming pools, lakes, rivers) until they are symptom-free for few few weeks.

Breastfeeding appears to protect infants from Giardia intestinalis infection.[12, 18, 20] Breast milk contains detectable titres of secretory IgA, which is protective for infants, especially in developing countries. A study from Egypt[72] showed breast-fed infants had a lower incidence of symptomatic and asymptomatic infection. Furthermore, infected infants who were exclusively breast-fed had fewer clinical manifestations than those who were not exclusively breast-fed.

Medication Summary

Antibiotic therapy is standard in the treatment of giardiasis.[49, 73] Antimicrobial resistance has been reported.

Metronidazole is the antimicrobial agent most commonly used in the treatment of giardiasis in the United States. It has a cure rate of 85-90%.

Tinidazole is also approved in the United States and considered a first-line agent outside the United States. It is given in a single dose, the efficacy is reported at 90%, and it is believed to have fewer side effects than metronidazole. A common adverse effect is GI upset. A meta-analysis of 5 trials comprising 403 children regarding the efficacy of tinidazole versus albendazole treatment for pediatric giardiasis showed that tinidazole significantly outperformed albendazole.[65]

Paromomycin has been recommended for use in pregnancy because systemic absorption is low, but the cure rate is lower than with other agents.

Some drugs not available in the United States are considered effective therapeutic alternatives. Quinacrine achieves a cure rate of 90-95% but is available as an orphan drug in the US. The most common adverse effects include nausea, vomiting, and abdominal cramping. Occasional yellow discoloration of the skin, urine, and sclerae may occur. This medication should not be used in patients with documented hypersensitivity to this medication or related products, those diagnosed with psoriasis, or those with a history of psychosis.

Metronidazole (Flagyl)

Clinical Context:  Metronidazole is a nitroimidazole that, once concentrated within the organism, is reduced by intracellular electron transport proteins. The formation of free radicals causes disruption of cellular elements and subsequent death of the organism. It is the most commonly prescribed antibiotic for giardiasis. The recommended adult dose is 250 mg PO tid for 5-7 days.

Albendazole (Albenza)

Clinical Context:  This agent decreases adenosine triphosphate (ATP) production in worms, causing energy depletion, immobilization, and, finally, death. To avoid an inflammatory response in CNS, the patient also must be started on anticonvulsants and high-dose glucocorticoids.

Nitazoxanide (Alinia)

Clinical Context:  This agent inhibits growth of Cryptosporidium parvum sporozoites and oocysts and Giardia lamblia trophozoites. It elicits antiprotozoal activity by interfering with pyruvate-ferredoxin oxidoreductase (PFOR) enzyme-dependent electron transfer reaction, which is essential to anaerobic energy metabolism. It is available as a 20-mg/mL oral suspension.

Tinidazole (Tindamax)

Clinical Context:  Tinidazole is a nitroimidazole antiprotozoal agent. The mechanism by which tinidazole exhibits activity against Giardia and Entamoeba species is not known. The recommended adult dose is 2 g PO once; for children, the recommended dose is 50 mg/kg PO once.


Clinical Context:  Paromomycin is a poorly absorbed aminoglycoside that may be considered for use in severe infection in pregnant patients. The most common adverse effects include nausea, increased GI motility, abdominal pain, and diarrhea.


Clinical Context:  This agent, available as an orphan drug in the United States is indicated to treat giardiasis and cestodiasis. It is occasionally used to treat and suppress malaria. The recommended adult dose is 100 mg PO tid for 5-7 d; for children, the recommended dose is 2 mg/kg PO tid for 5-7 d.

Class Summary

The therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.[60] The 2 major classes of drugs that have proven benefit in the treatment of giardiasis are nitroimidazole derivatives and acridine dyes.

Although most experts recommend metronidazole and tinidazole as the drugs of choice because the brief treatment periods encourage good patient adherence, treatment failures occur in as many as 20% of cases, probably because of resistance. Therefore, treatment with a second-line drug (eg, mepacrine) may be necessary.

The effectiveness of quinacrine is similar to that of nitroimidazole derivatives; however, it is less tolerated because of its adverse effects. These include the following: mild and transient headache, dizziness, and GI complaints (diarrhea, anorexia, nausea, abdominal cramps, vomiting [rare]), pleomorphic skin eruptions, and neuropsychiatric disturbances (nervousness, vertigo, irritability, emotional change, nightmares, transient psychosis).

Nitazoxanide is approved by the US Food and Drug Administration for the treatment of children and adults for diarrhea from giardiasis.

What is giardiasis?Which patient groups are at high risk for giardiasis?How is giardiasis diagnosed?When was giardiasis first identified?What is the pathophysiology of giardiasis?What is the life cycle of Giardia during transmission of giardiasis?What is the mechanism of injury in giardiasis?What is the role of epithelial barrier dysfunction in the pathogenesis of giardiasis?What causes giardiasis?What is the prevalence of giardiasis in the US?What is the asymptomatic carriage rate of giardiasis in children?What is the global incidence of giardiasis?Which geographic areas have the highest prevalence of giardiasis?Which patient groups have the highest incidence of giardiasis?What is the prognosis of giardiasis?What should be included in patient education about giardiasis?What are the signs and symptoms of giardiasis?What are the signs and symptoms of chronic giardiasis?What are the extraintestinal signs and symptoms of giardiasis?Which clinical history findings suggest giardiasis?Which physical findings are characteristic of giardiasis?What are the possible complications of giardiasis?What are the differential diagnoses for Giardiasis?Which tests are performed in the workup of giardiasis?What is the role of stool exam in the diagnosis of giardiasis?What is the role of stool antigen detection in the diagnosis of giardiasis?What is the role of imaging studies in the workup of giardiasis?How is the string test performed in the workup of giardiasis?What is the role of lab testing in the evaluation of giardiasis?What is the role of endoscopy and biopsy in the diagnosis of giardiasis?Which histologic findings are characteristic of giardiasis?How is giardiasis treated?Which dietary and activity modifications are used in the treatment of giardiasis?How is giardiasis treated during pregnancy?How is treatment-resistant giardiasis managed?How is giardiasis prevented?What is the role of medications in the treatment of giardiasis?Which medications in the drug class Antibiotics are used in the treatment of Giardiasis?


Hisham Nazer, MBBCh, FRCP, DTM&H, Professor of Pediatrics, Consultant in Pediatric Gastroenterology, Hepatology and Clinical Nutrition, University of Jordan Faculty of Medicine, Jordan

Disclosure: Nothing to disclose.

Chief Editor

Burt Cagir, MD, FACS, Clinical Professor of Surgery, The Commonwealth Medical College; Director, General Surgery Residency Program, Robert Packer Hospital; Attending Surgeon, Robert Packer Hospital and Corning Hospital

Disclosure: Nothing to disclose.


Manoop S Bhutani, MD Professor, Co-Director, Center for Endoscopic Research, Training and Innovation (CERTAIN), Director, Center for Endoscopic Ultrasound, Department of Medicine, Division of Gastroenterology, University of Texas Medical Branch; Director, Endoscopic Research and Development, The University of Texas MD Anderson Cancer Center

Manoop S Bhutani, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Institute of Ultrasound in Medicine, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Brooks D Cash, MD, FACP Director of Clinical Research, Assistant Professor of Medicine, Division of Gastroenterology, National Naval Medical Center

Brooks D Cash, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michelle Ervin, MD Chair, Department of Emergency Medicine, Howard University Hospital

Michelle Ervin, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, National Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Glenn Fennelly, MD, MPH Director, Division of Infectious Diseases, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Clinical Associate Professor of Pediatrics, Albert Einstein College of Medicine

Glenn Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Murat Hökelek, MD, PhD Technical Consultant of Parasitology Laboratory, Professor, Department of Clinical Microbiology, Ondokuz Mayis University Medical School, Turkey

Murat Hökelek, MD, PhD is a member of the following medical societies: Turkish Society for Parasitology

Disclosure: Nothing to disclose.

Mark H Johnston, MD Associate Professor of Medicine, Uniformed Services University of Health Sciences; Consulting Staff, Lancaster Gastroenterology Inc

Mark H Johnston, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Michael D Nissen, MBBS, FRACP, FRCPA Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Michael D Nissen, MBBS, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia

Disclosure: Nothing to disclose.

Andre Pennardt, MD, FACEP, FAAEM, FAWM Clinical Associate Professor of Emergency Medicine, Medical College of Georgia; Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Departments of Emergency Medicine, Aviation Medicine and Dive Medicine, Womack Army Medical Center

Andre Pennardt, MD, FACEP, FAAEM, FAWM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Association of Military Surgeons of the US, International Society for Mountain Medicine, National Association of EMS Physicians, Special Operations Medical Association, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment


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A Giardia intestinalis cyst.

Giardia lamblia, cyst form.

Giardia lamblia trophozoites in culture.

Giardia intestinalis trophozoites on stool examination from a patient with diarrhea.

Giardia cyst.

Giardia trophozoite

Giardia lamblia, cyst form.

Giardia lamblia trophozoites in culture.

A Giardia intestinalis cyst.

Giardia intestinalis trophozoites on stool examination from a patient with diarrhea.

Giardia trophozoite

Giardia cyst.