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Giardiasis: Epidemiology, clinical manifestations, and diagnosis

Giardiasis: Epidemiology, clinical manifestations, and diagnosis
Karin Leder, MBBS, FRACP, PhD, MPH, DTMH
Peter F Weller, MD, MACP
Section Editor:
Edward T Ryan, MD, DTMH
Deputy Editor:
Milana Bogorodskaya, MD
Literature review current through: Dec 2022. | This topic last updated: May 26, 2021.

INTRODUCTION — Giardia duodenalis (also known as G. lamblia or G. intestinalis) is a protozoan parasite capable of causing sporadic or epidemic diarrheal illness. Giardiasis is an important cause of waterborne and foodborne disease, daycare center outbreaks, and illness in international travelers.

The epidemiology, microbiology, pathogenesis, clinical manifestations, and diagnosis of giardiasis will be reviewed here. The treatment and prevention of giardiasis are discussed separately. (See "Giardiasis: Treatment and prevention".)

EPIDEMIOLOGY — G. duodenalis infection occurs worldwide [1]. High-risk groups include infants, young children, international adoptees, travelers [2], immunocompromised individuals, and patients with cystic fibrosis [3]. Giardia was included in the World Health Organization’s Neglected Disease Initiative in 2006.

Giardiasis is especially common in areas with poor sanitary conditions and limited water-treatment facilities. In resource-limited settings, the prevalence of giardiasis has been reported to be as high as 20 to 40 percent; in such settings, the rate of infection is highest among children <5 years [1]. Prevalence rates for giardiasis are generally reported to be 2 to 7 percent in developed countries [4]. Worldwide, G. lamblia is the third most common agent of diarrheal disease in children <5 (after rotavirus and Cryptosporidium spp); >300 million cases are reported annually [5]. Many individuals with Giardia in stool samples are asymptomatic; in some studies, Giardia has been observed more frequently in the stool of asymptomatic individuals than among individuals with acute diarrhea [6]. In resource-limited settings giardiasis may be associated with stunted growth in children, even in the absence of acute diarrhea [7].

Giardiasis is a well-recognized cause of enteric disease among international travelers in the United States, Canada, and Europe [8-10]. In the United States in 2018, over 15,000 cases were reported, equating to a rate of approximately 6 cases per 100,000 population [11]. In a study including 147 pediatric patients with acute nondysenteric diarrhea in the United States, giardiasis was the cause in 15 percent of cases, second only to rotavirus [12].

One case-control study in the United States identified the following risk factors for sporadic giardiasis: international travel (adjusted odds ratio [aOR] 13.9) drinking water from a river, lake, stream, or spring (aOR 6.5), swimming in a natural body of water (aOR 3.3), male-male sexual behavior (aOR 45.7), contact with children in diapers (aOR 1.6), antibiotic use (aOR 2.5), and presence of a chronic gastrointestinal condition (aOR 1.8) [13].

Giardia infections are commonly seen in domestic and wild animals, with young animals in particular demonstrating a high prevalence of infection.

Life cycle — Giardia species have two morphological forms: cysts and trophozoites. Cysts are the infectious form of the parasite; they are excreted in stool and can survive in moist environments for prolonged periods (figure 1). A low infective dose of 10 cysts is thought to be sufficient to facilitate infection. Following cyst ingestion, excystation occurs in the proximal small bowel with release of trophozoites.

Trophozoites are pear-shaped, binucleate, multi-flagellated parasite forms capable of division by binary fission; they localize principally to the proximal small bowel. An adhesive disk on the ventral surface of the trophozoite facilitates trophozoite attachment to the mucosal surface of the duodenum and jejunum, although the trophozoite does not invade the mucosal epithelium. Trophozoites that do not adhere to the small bowel move forward to the large intestine, where they revert to the infectious cyst form; conjugated bile salts appear to foster encystation. Cysts are passed back into the environment in excreted stool; in the setting of diarrhea, trophozoites can also be found in the stool.

Following cyst ingestion, infections have an incubation of a week or more before symptoms of acute giardiasis may develop. (See 'Clinical manifestations' below.)

Routes of transmission — Transmission of infectious Giardia cysts to humans may occur via three routes: waterborne, foodborne, or fecal-oral transmission [14].

Water is a major source of giardiasis transmission. Giardia cysts survive readily in mountain streams, as they are hardy in cold water. Water-dwelling mammals, such as beavers, can become infected and may serve as ongoing sources of water contamination. For these reasons, giardiasis is an important cause of diarrheal illness among hikers in wilderness areas who drink water that has not been adequately filtered, treated, or boiled [15].

Deep well water, in contrast with surface well water, is usually safe because filtration of water through soil removes Giardia cysts. Giardia cysts are resistant to chlorination; therefore, bacterial coliform counts are not a reliable measure of Giardia contamination in chlorinated water sources.

Foodborne transmission of giardiasis can occur via ingestion of raw or undercooked food (including raw vegetables, salad bars, and fresh fruit) contaminated with cysts and via food that is contaminated after cooking [16]. However, foodborne outbreaks have been difficult to document, likely because of limitations in detection methods [17].

Person-to-person transmission can occur in settings in which there is fecal incontinence and poor hygiene, such as childcare centers [18]. The risk of acquisition and transmission is greatest for young children who are not yet toilet trained; such children can also serve as a source for secondary cases within households [19].

Giardiasis can be transmitted via anal-oral sexual contact [20]. In addition, soil and environmental contamination can be a source of infection [21].

MICROBIOLOGY AND PATHOGENESIS — Species of the genus Giardia infect many hosts ranging from mammals to amphibians and birds [1]. Six known Giardia species are restricted to nonhuman hosts and are not recognized as causes of human disease. The species Giardia duodenalis consists of eight genetic groups (or assemblages); two assemblages are found in both humans and animals (A and B), and the remaining six are rarely found in humans, instead occurring mainly in nonhuman hosts, including canines, felines, rodents, and seals (assemblages C to H).

Genotypes vary even within assemblages A and B, and it is likely that only some genotypic variants have potential to cause infection in humans. Because of this heterogeneity, the role of animals in the epidemiology of human infection remains poorly understood [1]. Beavers have been clearly implicated in transmission of waterborne infection to humans, although the roles of domestic dogs and cats as sources of human infection remain to be ascertained [22].

The relative roles of Giardia assemblages and the human host responses that contribute to asymptomatic and symptomatic infections have not been fully determined. Ingestion of 10 to 25 cysts is thought to be sufficient to cause symptomatic giardiasis; some infections resolve by about three weeks, while others persist with milder symptoms [23,24]. In a subsequent study, no volunteers challenged with assemblage A Giardia became infected, whereas all challenged with assemblage B strain became infected, although only half of these individuals were symptomatic [25]. In one study, assemblage B isolates occurred more frequently in patients with chronic infection than assemblage A isolates [26]. In another study, assemblage A was associated with symptomatic infection, and genotype B was associated with asymptomatic infection [27]; this association was particularly evident in children <5 years, suggesting host factors also influence the nature of clinical manifestations.

Giardia is a noninvasive parasite, and the pathogenesis of symptoms that can occur in giardiasis (including acute diarrhea and longstanding malabsorption) is not fully understood. Trophozoites can attach to epithelial cells lining the intestinal tract (most commonly the proximal small intestine), leading to structural and functional abnormalities. Light microscopy may demonstrate no abnormalities, mild or moderate partial villous atrophy, or subtotal villous atrophy in severe cases. An increase in crypt depth may be seen, and microvilli shortening or disruption may occur. Intestinal epithelial tight junctions may be disrupted leading to increased permeability and altered epithelial cell survival. Consequent deficiencies in small bowel epithelial brush border enzymes, including disaccharidases such as lactase, may develop. Such local epithelial enzyme deficiencies likely contribute to symptoms such as malabsorption seen in acute and chronic giardiasis and are slow to recover even with effective treatment of the infection. Loss of intestinal barrier function and disruption of the commensal intestinal microbiota in the setting of infection are also though to contribute to symptoms [17,28]. In addition to affecting the composition of the intestinal microbiota, Giardia may also lead to a metabolic shift among the intestinal microbial community, thereby impacting on the virulence of other microbes [29].

Immunity — Chronic exposure to G. duodenalis may induce partial immunity; in endemic areas, children <10 years have higher rates of giardiasis than older individuals [30]. In addition, travelers to endemic areas have higher rates of symptomatic disease than long-term residents [31]. In endemic regions, however, reinfections can be frequent, so any acquired immunity is limited.

Humoral immunity appears to be important for host defense against giardiasis. Secretory immunoglobulin (Ig)A antibodies are an important humoral response to infection, since trophozoites are localized to the intestinal lumen. Patients with cystic fibrosis or immunoglobulin deficiencies (such as common variable immunodeficiency or X-linked agammaglobulinemia) tend to have more severe disease, perhaps because of deficiencies in secretory IgA and cell-mediated immunity [32].

Nonantibody host responses are also increasingly recognized as contributing to the host response to Giardia infections, in particular interleukin 17, although a range of cytokines are likely involved [29].

Patients with HIV infection have impaired immune response to the parasite but do not seem to develop more severe disease [33]. Asymptomatic infections occur in the presence of HIV, although with progressive immunosuppression, the risk of symptomatic infection increases [34,35].

CLINICAL MANIFESTATIONS — The severity of clinical manifestations associated with giardiasis is variable. In general, about half of exposed individuals clear the infection in the absence of clinical symptoms, approximately 15 percent of individuals shed cysts asymptomatically, and the remaining 35 to 45 percent of individuals have symptomatic infection [14,36]. The nature of clinical manifestations in an individual likely depends on a number of factors including the virulence of the isolate, the parasite load, and the host immune response.

Asymptomatic infection — Asymptomatic infection occurs in both children and adults, and asymptomatic cyst shedding can last six months or more [18,37].

It has been observed that in resource-limited settings, most children will have encountered Giardia by age two years without it being associated with diarrhea, but infected children may have impaired growth [38,39].

Acute giardiasis — Symptoms of acute giardiasis include [14]:

Diarrhea – 90 percent

Malaise – 86 percent

Foul-smelling and fatty stools (steatorrhea) – 75 percent

Abdominal cramps and bloating – 71 percent

Flatulence – 75 percent

Nausea – 69 percent

Weight loss – 66 percent

Vomiting – 23 percent

Fever – 15 percent

Constipation – 13 percent

Urticaria – 10 percent

Symptoms usually develop after an incubation period of 7 to 14 days. Onset of acute gastrointestinal symptoms within one week of exposure is not likely attributable to infection with Giardia. If acute symptoms occur, they generally last one to four weeks.

Chronic giardiasis — Chronic giardiasis may follow the acute phase of illness or may develop in the absence of an antecedent acute illness. Chronic symptoms can develop in up to half of symptomatic individuals [40]. In one study of experimentally infected individuals, 84 percent had a self-limited illness (mean duration 18 days); the remainder became chronically infected.

Symptoms of chronic giardiasis may include:

Loose stools but usually not diarrhea


Profound weight loss (10 to 20 percent of body weight)


Stunted growth




Abdominal cramping




The manifestations may wax and wane over many months. Some patients may have persistent infection after initial treatment, which may be associated with development of malabsorption and weight loss [41]. Even in cases of otherwise asymptomatic infection, malabsorption of fats, sugars, carbohydrates, and vitamins may occur. This can lead to hypoalbuminemia and deficiencies of vitamin A, B12, and folate.

Acquired lactose intolerance occurs in up to 40 percent of patients; clinically, this manifests with exacerbation in intestinal symptoms following ingestion of dairy products. Recovery can take many weeks, even after clearance of the parasite [42,43].

Complications — In children, chronic giardiasis may affect growth and development [38,44,45]. A study among Colombian children suggested that giardiasis was a strong predictor of stunted growth [44]. A longitudinal study including 597 children in Brazil found that growth was impeded among children with giardiasis, even among those with asymptomatic infection [45]. Likewise, in Bangladesh, a prospective longitudinal birth cohort study found decreased growth measures among children even without diarrhea [38].

Hypersensitivity phenomena such as rash, urticaria, aphthous ulceration, and reactive arthritis or synovitis have been described in the setting of giardiasis, although these manifestations are rare [40,46,47].

Rarely, Giardia can spread from the duodenum to the biliary and pancreatic ducts, leading to cholecystitis, cholangitis, or granulomatous hepatitis. Impaired exocrine pancreatic function with diminished secretion of trypsin and lipase has also been described.

Previously infected individuals may report symptoms even years after effective treatment. Following a large waterborne epidemic of giardiasis in Norway, a cohort study including more than 800 individuals exposed to Giardia noted that the prevalence of irritable bowel syndrome (39 percent) and chronic fatigue (31 percent) were significantly increased six years after exposure (relative to unexposed controls) and the frequency of these symptoms declined with time after the initial exposure [48]. Although the frequency of these symptoms declined with time after the initial exposure, at 10 years, those who had developed Giardia infection still had a lower Quality of Life score [49]. Another study in the United States noted individuals diagnosed with giardiasis were more likely to have a subsequent diagnosis of irritable bowel syndrome [50].

DIAGNOSIS — Tools for diagnosis of giardiasis include antigen detection assays, nucleic acid detection assays, and stool microscopy [51]. Antigen and nucleic acid detection tests are more sensitive than stool microscopy.

Antigen detection assays — A number of immunoassays using antibodies against cyst or trophozoite antigens have been developed for stool analysis. Available kits include direct immunofluorescent assays (DFAs) that use fluorescein-tagged monoclonal antibodies, immunochromatographic assays, and enzyme-linked immunosorbent assays (ELISAs). In general, these methods have greater sensitivity and faster turn-around time than conventional stool microscopy methods. Specificity and cost are usually relatively comparable. Many of the commercially available assays can detect both Giardia and Cryptosporidium simultaneously.

One study of 325 stool specimens demonstrated that an ELISA against a specific Giardia antigen (antigen 65) detected 30 percent more cases of Giardia than stool microscopy [52]. In a study of stool samples from patients with abdominal symptoms using different assays for detection of Giardia, the sensitivities obtained by Ridascreen Giardia, Rida Quick Giardia, Rida Quick Combi, and Giardia-Strip were 82, 80, 80, and 44 percent, respectively. The specificity of all tests was ≥98 percent [53]. In another study, the Ridascreen Giardia ELISA was reported to be 100 percent sensitive and 91.5 percent specific, including in children [54].

Another study that compared stool microscopy, DFA, and three immunodiagnostic techniques for diagnosis of Giardia found that there was agreement among the methods in 76 percent of cases and that immunologic methods detected more positive results than stool microscopy in 12 percent of cases [55].

Immunoassays are of limited use following treatment of infection. Loss of detectable stool antigens is suggestive of effective treatment, but continued stool antigen shedding could reflect shedding of killed parasites.

Polymerase chain reaction assays — Polymerase chain reaction (PCR) assays have been developed to detect Giardia in stool samples [51,56,57]. Many PCR tests are now commercially available, often as part of a panel for organism detection in stool samples [58-61]. However, PCR is of limited use following treatment of infection as residual detection might represent killed or viable parasites [57].

PCR-based tools have also been applied to detect Giardia and other pathogens in water and food supplies [62].

Whole-genome sequencing is also emerging as an increasingly used tool for the identification of novel genotypes and mixed infections and in the setting of outbreak investigations [63].

Stool microscopy — Giardia cysts are oval in shape, 8 to 12 microns in length, and contain four nuclei. Trophozoites contain two nuclei and have four pairs of flagellae and an adhesive disc for attachment to intestinal epithelial cells. Stool microscopy to detect Giardia is specific and may also be useful for detecting other potential parasitic causes of gastrointestinal symptoms. Limitations include intermittent excretion of Giardia cysts (necessitating up to three stool exams), cumbersome processing procedures, and technician expertise.

Laboratory processing of stool samples consists of a saline suspension to look for trophozoites and cysts (picture 1) and a polyvinyl alcohol and/or formalin preparation for permanent staining. Loose, watery stool is more likely to be positive for trophozoites; a semiformed or formed stool will likely contain cysts only (picture 2 and picture 3).

In a study among 100 patients with chronic diarrhea, all patients were evaluated by stool microscopy and nested PCR; 30 patients also had upper gastrointestinal endoscopy and duodenal biopsy performed [64]. Among these patients, 48 percent had evidence of Giardia infection; stool microscopy detected 65 percent, stool PCR detected an additional 27 percent, and duodenal biopsy PCR detected an additional 8 percent of cases.

Other tests — In general, patients with giardiasis do not have peripheral leukocytosis or eosinophilia. White cells in stool specimens are usually absent. Fecal fat excretion and other laboratory tests of malabsorption may be abnormal. Upper gastrointestinal series are usually normal but may demonstrate mucosal edema in some cases.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of giardiasis includes:

Travelers' diarrhea – Travelers' diarrhea can be caused by a range of pathogens, including enterotoxigenic Escherichia coli and Campylobacter spp; it consists of malaise, anorexia, and abdominal cramps followed by watery diarrhea in the setting of travel to a developing setting. The diagnosis is usually established based on clinical history; the illness is generally self-limited. Onset of travelers' diarrhea is usually within days, whereas symptomatic giardiasis develops only after a week or more after infection. Evaluation for Giardia is warranted in the setting of delayed onset (at least one week following exposure) of upper gastrointestinal manifestations (such as bloating, gas, or nausea) and in the setting of persistent symptoms. (See "Travelers' diarrhea: Treatment and prevention".)

Cryptosporidiosis – Cryptosporidium is similar to Giardia in that it can cause a diarrheal illness with associated malaise, nausea and anorexia, crampy abdominal pain, and low-grade fever. They may be distinguished via stool antigen testing, nucleic acid amplification testing, or fecal microscopy. (See "Cryptosporidiosis: Epidemiology, clinical manifestations, and diagnosis".)

Lactose intolerance – Clinical symptoms of lactose intolerance include diarrhea, abdominal pain, and flatulence after ingestion of milk or milk-containing products. The diagnosis is established by a lactose tolerance test. (See "Lactose intolerance and malabsorption: Clinical manifestations, diagnosis, and management", section on 'Diagnostic evaluation'.)

Tropical sprue – Tropical sprue is a chronic diarrheal disease that occurs in the tropics and involves the small intestine; it is characterized by nutrient malabsorption. The diagnosis is established by upper endoscopy with biopsy of the small bowel. (See "Tropical sprue".)

Crohn ileitis – Crohn disease is an inflammatory disease that may involve the entire gastrointestinal tract; most patients have small bowel involvement (usually the distal ileum); one-third have ileitis exclusively. The diagnosis is established by endoscopy with biopsy. (See "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults".)

Dientamoeba fragilis – The clinical manifestations of Dientamoeba fragilis are similar to those of giardiasis and include abdominal pain, flatulence, and diarrhea. It may be associated with eosinophilia; the diagnosis is established by stool microscopy. (See "Dientamoeba fragilis".)

Irritable bowel syndrome – Irritable bowel syndrome may present with a wide array of symptoms including chronic abdominal pain, diarrhea, and/or constipation and bloating. It is chronic in nature and the diagnosis is established based on diagnostic criteria (table 1). (See "Clinical manifestations and diagnosis of irritable bowel syndrome in adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute diarrhea in adults".)

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Beyond the Basics topic (see "Patient education: Giardia (Beyond the Basics)")


Life cycle Giardia duodenalis is a protozoan parasite capable of causing epidemic or sporadic diarrheal illness. It has two morphological forms: cysts and trophozoites. Cysts are the infectious form of the parasite; following cyst ingestion, trophozoites are released in the proximal small intestine. Trophozoites that do not adhere to the small intestine move forward to the large intestine where they revert to the infectious cyst form; these cysts are passed back into the environment in excreted stool. (See 'Life cycle' above.)

Epidemiology G. duodenalis infection occurs worldwide. High-risk groups include infants, young children, international adoptees, travelers, immunocompromised individuals, and patients with cystic fibrosis. Giardiasis is especially common in areas with poor sanitary conditions and limited water-treatment facilities. (See 'Epidemiology' above.)

Routes of transmission Transmission of infectious Giardia cysts to humans may occur via three routes: waterborne, foodborne, or fecal-oral transmission. Giardiasis is an important cause of diarrheal illness among hikers in wilderness areas who drink water that has not been adequately filtered, treated, or boiled. Transmission of giardiasis can also occur via ingestion of raw or undercooked food contaminated with cysts or via food that is contaminated after cooking. Person-to-person transmission can occur in settings in which there is fecal incontinence and poor hygiene, such as childcare centers. (See 'Routes of transmission' above.)

Clinical manifestations

The severity of clinical manifestations associated with giardiasis is variable. In general, about half of exposed individuals clear the infection in the absence of clinical symptoms, approximately 15 percent of individuals shed cysts asymptomatically, and the remaining 35 to 45 percent of individuals have symptomatic infection. (See 'Clinical manifestations' above.)

Symptoms of acute giardiasis include diarrhea, malaise, abdominal cramps, and weight loss. Malabsorption may be responsible for the significant weight loss that can occur in chronic giardiasis. Acquired lactose intolerance occurs in up to 40 percent of patients. (See 'Acute giardiasis' above and 'Chronic giardiasis' above.)

Diagnosis Tools for diagnosis of giardiasis include antigen detection assays, nucleic acid detection assays, and stool examination. Antigen and nucleic acid detection tests are more sensitive than stool microscopy. (See 'Diagnosis' above.)

  1. Feng Y, Xiao L. Zoonotic potential and molecular epidemiology of Giardia species and giardiasis. Clin Microbiol Rev 2011; 24:110.
  2. Takaoka K, Gourtsoyannis Y, Hart JD, et al. Incidence rate and risk factors for giardiasis and strongyloidiasis in returning UK travellers. J Travel Med 2016; 23.
  3. Roberts DM, Craft JC, Mather FJ, et al. Prevalence of giardiasis in patients with cystic fibrosis. J Pediatr 1988; 112:555.
  4. Dixon BR. Giardia duodenalis in humans and animals - Transmission and disease. Res Vet Sci 2021; 135:283.
  5. Lanata CF, Fischer-Walker CL, Olascoaga AC, et al. Global causes of diarrheal disease mortality in children <5 years of age: a systematic review. PLoS One 2013; 8:e72788.
  6. Muhsen K, Levine MM. A systematic review and meta-analysis of the association between Giardia lamblia and endemic pediatric diarrhea in developing countries. Clin Infect Dis 2012; 55 Suppl 4:S271.
  7. Rogawski ET, Liu J, Platts-Mills JA, et al. Use of quantitative molecular diagnostic methods to investigate the effect of enteropathogen infections on linear growth in children in low-resource settings: longitudinal analysis of results from the MAL-ED cohort study. Lancet Glob Health 2018; 6:e1319.
  8. Harvey K, Esposito DH, Han P, et al. Surveillance for travel-related disease--GeoSentinel Surveillance System, United States, 1997-2011. MMWR Surveill Summ 2013; 62:1.
  9. Boggild AK, Geduld J, Libman M, et al. Travel-acquired infections and illnesses in Canadians: surveillance report from CanTravNet surveillance data, 2009-2011. Open Med 2014; 8:e20.
  10. Schlagenhauf P, Weld L, Goorhuis A, et al. Travel-associated infection presenting in Europe (2008-12): an analysis of EuroTravNet longitudinal, surveillance data, and evaluation of the effect of the pre-travel consultation. Lancet Infect Dis 2015; 15:55.
  11. Centers for Disease Control and Prevention. Giardiasis NNDSS Summary Report for 2018.,local%20or%20state%20health%20departments (Accessed on May 05, 2021).
  12. Caeiro JP, Mathewson JJ, Smith MA, et al. Etiology of outpatient pediatric nondysenteric diarrhea: a multicenter study in the United States. Pediatr Infect Dis J 1999; 18:94.
  13. Reses HE, Gargano JW, Liang JL, et al. Risk factors for sporadic Giardia infection in the USA: a case-control study in Colorado and Minnesota. Epidemiol Infect 2018; 146:1071.
  14. Hill DR, Nash TE. Intestinal flagellate and ciliate infections. In: Tropical Infectious Diseases: Principles, Pathogens and Practice, 3rd ed, Guerrant RL, Walker DA, Weller PF (Eds), Saunders Elsevier, Philadelphia 2011. p.623.
  15. McClung RP, Roth DM, Vigar M, et al. Waterborne disease outbreaks associated with environmental and undetermined exposures to water - United States, 2013-2014. Am J Transplant 2018; 18:262.
  16. Conners EE, Miller AD, Balachandran N, et al. Giardiasis Outbreaks - United States, 2012-2017. MMWR Morb Mortal Wkly Rep 2021; 70:304.
  17. Buret AG, Cacciò SM, Favennec L, Svärd S. Update on Giardia: Highlights from the seventh International Giardia and Cryptosporidium Conference. Parasite 2020; 27:49.
  18. Pickering LK, Woodward WE, DuPont HL, Sullivan P. Occurrence of Giardia lamblia in children in day care centers. J Pediatr 1984; 104:522.
  19. Waldram A, Vivancos R, Hartley C, Lamden K. Prevalence of Giardia infection in households of Giardia cases and risk factors for household transmission. BMC Infect Dis 2017; 17:486.
  20. Escobedo AA, Almirall P, Alfonso M, et al. Sexual transmission of giardiasis: a neglected route of spread? Acta Trop 2014; 132:106.
  21. Capone D, Bivins A, Knee J, et al. Quantitative Microbial Risk Assessment of Pediatric Infections Attributable to Ingestion of Fecally Contaminated Domestic Soils in Low-Income Urban Maputo, Mozambique. Environ Sci Technol 2021; 55:1941.
  22. Bouzid M, Halai K, Jeffreys D, Hunter PR. The prevalence of Giardia infection in dogs and cats, a systematic review and meta-analysis of prevalence studies from stool samples. Vet Parasitol 2015; 207:181.
  23. RENDTORFF RC. The experimental transmission of human intestinal protozoan parasites. II. Giardia lamblia cysts given in capsules. Am J Hyg 1954; 59:209.
  24. Santin M. Cryptosporidium and Giardia in Ruminants. Vet Clin North Am Food Anim Pract 2020; 36:223.
  25. Nash TE. Unraveling how Giardia infections cause disease. J Clin Invest 2013; 123:2346.
  26. Franzén O, Jerlström-Hultqvist J, Castro E, et al. Draft genome sequencing of giardia intestinalis assemblage B isolate GS: is human giardiasis caused by two different species? PLoS Pathog 2009; 5:e1000560.
  27. Sahagún J, Clavel A, Goñi P, et al. Correlation between the presence of symptoms and the Giardia duodenalis genotype. Eur J Clin Microbiol Infect Dis 2008; 27:81.
  28. Allain T, Buret AG. Pathogenesis and post-infectious complications in giardiasis. Adv Parasitol 2020; 107:173.
  29. Singer SM, Fink MY, Angelova VV. Recent insights into innate and adaptive immune responses to Giardia. Adv Parasitol 2019; 106:171.
  30. Gilman RH, Brown KH, Visvesvara GS, et al. Epidemiology and serology of Giardia lamblia in a developing country: Bangladesh. Trans R Soc Trop Med Hyg 1985; 79:469.
  31. Istre GR, Dunlop TS, Gaspard GB, Hopkins RS. Waterborne giardiasis at a mountain resort: evidence for acquired immunity. Am J Public Health 1984; 74:602.
  32. Oksenhendler E, Gérard L, Fieschi C, et al. Infections in 252 patients with common variable immunodeficiency. Clin Infect Dis 2008; 46:1547.
  33. Smith PD, Lane HC, Gill VJ, et al. Intestinal infections in patients with the acquired immunodeficiency syndrome (AIDS). Etiology and response to therapy. Ann Intern Med 1988; 108:328.
  34. Stark D, Barratt JL, van Hal S, et al. Clinical significance of enteric protozoa in the immunosuppressed human population. Clin Microbiol Rev 2009; 22:634.
  35. Nash TE, Ohl CA, Thomas E, et al. Treatment of patients with refractory giardiasis. Clin Infect Dis 2001; 33:22.
  36. Nash TE, Herrington DA, Losonsky GA, Levine MM. Experimental human infections with Giardia lamblia. J Infect Dis 1987; 156:974.
  37. López CE, Dykes AC, Juranek DD, et al. Waterborne giardiasis: a communitywide outbreak of disease and a high rate of asymptomatic infection. Am J Epidemiol 1980; 112:495.
  38. Donowitz JR, Alam M, Kabir M, et al. A Prospective Longitudinal Cohort to Investigate the Effects of Early Life Giardiasis on Growth and All Cause Diarrhea. Clin Infect Dis 2016; 63:792.
  39. Kotloff KL, Nataro JP, Blackwelder WC, et al. Burden and aetiology of diarrhoeal disease in infants and young children in developing countries (the Global Enteric Multicenter Study, GEMS): a prospective, case-control study. Lancet 2013; 382:209.
  40. Cantey PT, Roy S, Lee B, et al. Study of nonoutbreak giardiasis: novel findings and implications for research. Am J Med 2011; 124:1175.e1.
  41. Mørch K, Hanevik K, Robertson LJ, et al. Treatment-ladder and genetic characterisation of parasites in refractory giardiasis after an outbreak in Norway. J Infect 2008; 56:268.
  42. Singh KD, Bhasin DK, Rana SV, et al. Effect of Giardia lamblia on duodenal disaccharidase levels in humans. Trop Gastroenterol 2000; 21:174.
  43. Rana SV, Bhasin DK, Vinayak VK. Lactose hydrogen breath test in Giardia lamblia-positive patients. Dig Dis Sci 2005; 50:259.
  44. Botero-Garcés JH, García-Montoya GM, Grisales-Patiño D, et al. Giardia intestinalis and nutritional status in children participating in the complementary nutrition program, Antioquia, Colombia, May to October 2006. Rev Inst Med Trop Sao Paulo 2009; 51:155.
  45. Prado MS, Cairncross S, Strina A, et al. Asymptomatic giardiasis and growth in young children; a longitudinal study in Salvador, Brazil. Parasitology 2005; 131:51.
  46. Halliez MC, Buret AG. Extra-intestinal and long term consequences of Giardia duodenalis infections. World J Gastroenterol 2013; 19:8974.
  47. Painter JE, Collier SA, Gargano JW. Association between Giardia and arthritis or joint pain in a large health insurance cohort: could it be reactive arthritis? Epidemiol Infect 2017; 145:471.
  48. Hanevik K, Wensaas KA, Rortveit G, et al. Irritable bowel syndrome and chronic fatigue 6 years after giardia infection: a controlled prospective cohort study. Clin Infect Dis 2014; 59:1394.
  49. Litleskare S, Rortveit G, Eide GE, et al. Quality of life and its association with irritable bowel syndrome and fatigue ten years after giardiasis. Neurogastroenterol Motil 2019; 31:e13559.
  50. Nakao JH, Collier SA, Gargano JW. Giardiasis and Subsequent Irritable Bowel Syndrome: A Longitudinal Cohort Study Using Health Insurance Data. J Infect Dis 2017; 215:798.
  51. Heyworth MF. Diagnostic testing for Giardia infections. Trans R Soc Trop Med Hyg 2014; 108:123.
  52. Rosoff JD, Sanders CA, Sonnad SS, et al. Stool diagnosis of giardiasis using a commercially available enzyme immunoassay to detect Giardia-specific antigen 65 (GSA 65). J Clin Microbiol 1989; 27:1997.
  53. Weitzel T, Dittrich S, Möhl I, et al. Evaluation of seven commercial antigen detection tests for Giardia and Cryptosporidium in stool samples. Clin Microbiol Infect 2006; 12:656.
  54. Jahan N, Khatoon R, Ahmad S. A Comparison of Microscopy and Enzyme Linked Immunosorbent Assay for Diagnosis of Giardia lamblia in Human Faecal Specimens. J Clin Diagn Res 2014; 8:DC04.
  55. Aziz H, Beck CE, Lux MF, Hudson MJ. A comparison study of different methods used in the detection of Giardia lamblia. Clin Lab Sci 2001; 14:150.
  56. Vasoo S, Pritt BS. Molecular diagnostics and parasitic disease. Clin Lab Med 2013; 33:461.
  57. Boadi S, Polley SD, Kilburn S, et al. A critical assessment of two real-time PCR assays targeting the (SSU) rRNA and gdh genes for the molecular identification of Giardia intestinalis in a clinical laboratory. J Clin Pathol 2014; 67:811.
  58. Buss SN, Leber A, Chapin K, et al. Multicenter evaluation of the BioFire FilmArray gastrointestinal panel for etiologic diagnosis of infectious gastroenteritis. J Clin Microbiol 2015; 53:915.
  59. Mengelle C, Mansuy JM, Prere MF, et al. Simultaneous detection of gastrointestinal pathogens with a multiplex Luminex-based molecular assay in stool samples from diarrhoeic patients. Clin Microbiol Infect 2013; 19:E458.
  60. Claas EC, Burnham CA, Mazzulli T, et al. Performance of the xTAG® gastrointestinal pathogen panel, a multiplex molecular assay for simultaneous detection of bacterial, viral, and parasitic causes of infectious gastroenteritis. J Microbiol Biotechnol 2013; 23:1041.
  61. Perry MD, Corden SA, Lewis White P. Evaluation of the BD MAX Enteric Parasite Panel for the detection of Cryptosporidium parvum/hominis, Giardia duodenalis and Entamoeba histolytica. J Med Microbiol 2017; 66:1118.
  62. Dreelin EA, Ives RL, Molloy S, Rose JB. Cryptosporidium and Giardia in surface water: a case study from Michigan, USA to inform management of rural water systems. Int J Environ Res Public Health 2014; 11:10480.
  63. Ryan U, Paparini A, Oskam C. New Technologies for Detection of Enteric Parasites. Trends Parasitol 2017; 33:532.
  64. Jangra M, Dutta U, Shah J, et al. Role of Polymerase Chain Reaction in Stool and Duodenal Biopsy for Diagnosis of Giardiasis in Patients with Persistent/Chronic Diarrhea. Dig Dis Sci 2020; 65:2345.
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