Open access peer-reviewed chapter

Giardiasis Epidemiology

Written By

Antonio Marty Quispe Gutiérrez

Submitted: October 13th, 2016 Reviewed: July 7th, 2017 Published: December 13th, 2017

DOI: 10.5772/intechopen.70338

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Edited by Alfonso J. Rodriguez-Morales

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Giardiasis is the intestinal infection caused by Giardia lamblia, in which pathogenicity was cast doubted for decades but now is recognized as one of the most common causes of diarrheal disease worldwide. Originally described as waterborne transmitted, it has been broad described as of fecal-oral, person-to-person contact, and sexual transmission also. Although it is recognized as endemic throughout the world, most cases are reported from tropical countries with regular outbreaks commonly reported from developed countries. In humans, giardiasis normally produces a self-limited infection without symptoms, but some patients may present intestinal symptoms such as diarrhea and abdominal pain, and few show symptoms long after parasites clear up. Upon diagnosis, we may choose among several effective treatment alternatives, but not every patient responds to such therapies. Hence, having specific knowledge about the epidemiology of Giardia, it is critical for its prevention, which is the best strategy to protect us against such important disease.


  • giardiasis
  • Giardia
  • Giardia lamblia
  • epidemiology
  • life cycle stages

1. Introduction

Giardiasis is the intestinal infection caused by Giardia lamblia (also known as Giardia intestinalis or Giardia duodenalis). G. lamblia is a unicellular eukaryotic protozoan that was first described by Antonie van Leeuwenhoek in 1681—in his own stool sample [1]. For decades, it was considered of uncertain pathogenicity but now is recognized as common causes of diarrheal disease worldwide. Its clinical significance was broadly accepted after many symptomatic cases of giardiasis were diagnosed and reported among visitors to the Soviet Union in the early 1970s. Since then, giardiasis has been reported as responsible for many outbreaks throughout the world.

The epidemiology of giardiasis still is a matter of great discussion. From the original debates around its pathogenicity to the later ones about its speciation and biology, G. lamblia has proven to be an enigmatic and interesting organism [2]. Although giardiasis is currently recognized as one of the main causes of diarrheal disease and a leading cause of death and illness among children under 5 years old in developing countries [3], the long-term impact of pediatric giardiasis remains unclear. Recent cohort studies have confirmed a high prevalence of persistent, subclinical giardiasis and its association with growth shortfalls [4], but such evidence has not been consistently reported in the literature.

Commonly, giardiasis prevalence among poor populations is reported as very high, and when the infection became chronic, it has been associated also with malnutrition and cognitive deficits [5]. In developed countries, giardiasis represents the leading cause of traveler’s diarrhea and is frequently reported among citizens that traveled to developing countries and expose themselves to untreated water from lakes, streams, and swimming pools [68]. These and other epidemiologic characteristics of giardiasis will be discussed in detail in this chapter based on the classical and latest literature.


2. Etiologic agent

G. lamblia is a parasitic protozoan of the order Retortomonadida that alternates between trophozoites and cysts forms within its life cycle, stages responsible for the clinical illness, and the transmission of the disease, respectively. Under the light microscope, trophozoites appear actively swimming and with its characteristically teardrop (viewed dorsoventrally) or spoon (viewed from the side) shaped, measuring 10–20 μm by 5–15 μm by 2–4 μm, containing four pairs of flagella, two identical nuclei, with a convex dorsum and a ventral disc that acts as a suction cup to facilitate attachment of the organism to the small bowel villi (Figure 1A). On high-quality slides, the parasite movement shows “falling leave mobility” and resembles a human face because of the positions of the median bodies, nuclei, and axonemes. Uncharacteristically Giardia trophozoites lack definable Golgi, peroxisomes, and true mitochondria, but have a menant mitosome. Trophozoites divide by binary fission, and cyst develops as feces dehydrated in transiting to the large bowel.

Figure 1.

Giardia lamblia. Stained trophozoite (A) with its characteristic teardrop shape, binucleate structure, and four pairs of flagella clearly visible. Stained (B) and unstained (C) cysts with its characteristic median (parabasal) bodies and four nuclei. Images are some of the best public-domain light micrographs of Giardia, published by the National Institute of Infectious Diseases of Tokyo, Japan. Images were originally published at

Microscopically, Giardia cysts look oval shaped, measures about 11–14 by 7–10 μm, contains four nuclei (mature cyst)—usually situated at one end—and curved median bodies and linear axonemes (Figure 1B and C). During the process of encystment, which can be observed under the microscope, trophozoites initially become inactive, rounded, and increasingly refractile as encystment begins. Then, nuclear division (but not cytoplasmic) occurs to produce the quadrinucleate infectious cyst. Giardia cysts have a thick hyaline wall that protects them from environmental stressors such as the alkaline environment that characterize the small intestinal, water chlorination, high-altitude, or extreme temperatures such as in boiling water. Also, such strong protection allows cysts to survive in water up to 3 months [9]. Upon excystation in the small bowel, each cyst releases two trophozoites, which continue the life cycle.

Giardia species are currently classified in six species, which are distinguished based on its morphology and hosts: Gracilinanus agilis (amphibians), G. lamblia (mammals), Giardia muris (rodents), Giardia psittaci, and Giardia ardeae (both mainly in birds) (Table 1) [2]. Previously, many more species of Giardia were listed based only on microscopic and epidemiological criteria as well, but using molecular tests such as polymerase chain reaction (PCR), the list was shortened. Later on, genotyping studies confirmed that the species of Giardia could be classified in eight genetic groups (A–H): Groups A and B, which are found in humans and many domestic animals and wildlife [10], and the host-specific groups C–H. Among the latest ones, groups C and D infect dogs, cats, coyotes, and wolves [11]; group E infects cattle, sheep, goats, pigs, water buffaloes, and mouflons [12]; group F infects cats [12]; group G infects rats [12]; and group H infects marine animals [13]. This classification could be of great clinical value given that in addition to many genetic differences found, these genotypes exhibit several relevant biologic differences also. In example, genotype B seems to be more pathogenic than genotype A in humans, although they appear to grow slower [14]. Contradictory, the genetics of parasites of the genus Giardia is still poorly understood. Furthermore, recent evidence has cast doubt the classical view of an asexually replicating organism in favor of the occurrence of meiosis and genetic exchange. Such game breaker discovery demanded that the whole population genetics of Giardia should be reevaluated to take into account the effect of recombination on G. lamblia species [14].

Species Hosts Morphology
G. agilis Amphibians Longer and slender than G. lamblia, with a teardrop-shaped median body
G. ardeae Herons and other birds Similar to G. lamblia
G. lamblia Mammals including humans, dogs, and some wild species Teardrop shaped with claw-shaped median bodies
G. microti Rodents, voles, and muskrats Similar to G. lamblia
G. muris Rodents Shorter and rounder than G. lamblia, with small rounded median body
G. psittaci Psittacine birds Similar to G. lamblia

Table 1.

Giardia species.

Adapted from Adam [2] and Caccio and Ryan [14].


3. Life cycle

Life cycle begins with the infection by the ingestion of the cyst. Then the excystation continues, which starts at the stomach triggered by the exposure of the cyst to the gastric acid, the presence of bile and trypsin in the duodenum and/or the alkaline, protease-rich milieu, duodenum [2]. Excystation ends at the proximal small intestine where the emerging parasites (excyzoites) quickly transform into trophozoites that attach to the intestinal epithelial cells using the adhesive disc. The adhesive disc is essential for attachment and appears to play a major role in the virulence of Giardia [15]. Several disc-associated proteins have been identified using proteomics [16], and it is clear that the disc is an advanced cytoskeletal structure [17]. At the jejunum, the trophozoites start to encyst forming the wall that enables the parasite to survive outside the host for several weeks in cold water. This process is triggered by a particular composition of biliary secretions, possibly by a deprivation of cholesterol [18]. Regulatory factors are encystation-specific transcription factors, chromatin remodeling enzymes, and posttranslational modifications, which vary their expression in correlation with the variation of antigens on the parasite surface [19]. Finally, trophozoites and cysts are released with the stool, with cysts continuing the transmission of the disease when ingested by another host.

Reservoir hosts include humans, as well as a variety of animals, including cats, dogs, dairy cattle, beavers, and other farm, wild, and domesticated animals such as horses, pigs, cows, chinchillas, alpacas, lemurs, sheep, guinea pigs, monkeys, goats, and rats [20]. However, among all these animal hosts, only beavers, dogs, and humans have been implicated as a source of infection in different waterborne epidemics and outbreaks of giardiasis in humans. Additionally, it is important to highlight the key role of “reverse zoonotic transmission” (zooanthroponotic) in the epidemiology of Giardia infections, which means that humans have been identified as the source of infection for beavers, muskrats, and coyotes in the Unites States and Canada [2123], muskoxen in the Canadian arctic [24], nonhuman primates (gorillas) and painted dogs in Africa [25], marsupials in Australia, house mice in remote islands [26], and marine mammals (seals) in various parts of the world [27].

Even in developed countries such as the United States, it is common to isolate Giardia cysts in the water reservoirs and unfiltered water supplies of major cities, the water supply that is not filtrated [28].


4. Incidence and burden of disease

G. lamblia has been consistently reported as one of the most common pathogens worldwide [29]. Due to high endemicity among humans, and domestic and wildlife animals, it is considered of public health and veterinary health importance [12]. Symptomatic infections have been reported by millions in Asia, Africa, and Latin America by the World Health Organization, which have estimated that it causes 183 million (confidence interval of 95%, 130–262 million) cases of giardiasis [30].

Worldwide, the incidence of Giardiasis has been estimated in 2.8 × 108 cases per year [31]. However, several epidemiological studies have reported that such rates could be significantly underestimated, with giardiasis prevalence rates ranging from 10 to 20% of the general population [32], from 10 to 50% in developing countries [33, 34], and from 2 to 5% in developed countries [35, 36]. This could be explained by the large fraction of asymptomatic carriers, which regardless of the absence of symptoms also contribute to the transmission of the diseases.

Giardiasis is a ubiquitous disease so it occurred across broad epidemiological contexts and with a broad range of distributions. On one side, in most developed countries such as the United Kingdom [37] and Germany [8], Giardia is mostly reported as a rare disease affecting travelers. Furthermore, in the countries such as the Unites States, where Giardia is continually under surveillance, Giardia has higher incidences (incidence rate ratios, 1.2–1.5) in counties with higher private well reliance compared to counties with lower well reliance [38]. On the other side, in most developing countries, Giardia has been associated with poor health hygiene, poor toilet training, overcrowding, and low socioeconomic status [39]. Furthermore, due to the high prevalence of Giardia among children, and its higher exposure to dogs in poor setting, it is believed that Giardia has developed zoonotic transmission. This possibility has been reported concordantly by genotyping and molecular studies from Mexico [40], Jamaica [41], and Cambodia [42].

The high prevalence of Giardia among children raised a major concern about their long-term impacts, which currently have been well documented and reported as more worrisome due to the association between persistent Giardia and children’s growth [43]. Giardia infections can be detected repetitively in over 40% of children suggesting that persistent infections are common and associated with a damage of the intestinal permeability, which—independently of diarrhea—can lead to stunted growth. In fact, according to the results from the MAL-ED birth cohort study, the persistence of Giardia before 6 months of age was associated with a −0.29 (95% CI, −0.53 to −0.05) deficit in weight-for-age z score and −0.29 (95% CI, −0.64 to 0.07) deficit in length-for-age z score at 2 years [44].


5. Giardiasis epidemiology

The Giardia cysts are overall highly infectious, and as few as 10 cysts can cause an infection in an individual. Giardiasis prevalence rates have been reported consistently as high among young children from developing countries, with high rates of repeated infection even within the first year of life. However, many developed countries have many regions with endemic giardiasis or regular outbreaks. At these countries giardiasis outbreaks are particularly common during the summer months (likely due to recreational swimming exposure) or throughout the year around day-cares and nurseries, infecting children under 5 years old—and their caregivers—the most [45]. In fact, an investigation of 242 outbreaks, affecting 41,000 persons, reported that most outbreaks resulted from waterborne (74.8%), foodborne (15.7%), person-to-person (2.5%), and animal contact (1.2%) transmission, with waterborne outbreaks been that largest ones in terms of number of cases per outbreak [46].

Surveillance data cases have shown that giardiasis infects populations with a bimodal age distribution, peaking at ages 0–9 years and 45–49 years, without gender preferences [35], and within areas that are endemic, giardiasis commonly shows a seasonal pattern, with most cases occurring in the summer months due to a recent history of drinking untreated surface water and a history of swimming in a lake or pond or swimming in any natural body of fresh water [47]. Other risk factors that have been reported as associated to giardiasis in endemic areas include living in areas that use at-risk tap water (i.e., filtered or unfiltered surface water [48, 49] or unfiltered shallow well water [48]) or in rural areas [49].

One of the most common mechanisms of transmission of Giardia infections is a waterborne transmission but also can be transmitted by fecal-oral transmission with contaminated food or direct fecal-oral contact among family members, person-to-person contact, and sexual transmission (oral-anal contact). Although it is unclear which ones are clinically the most important, there is a common understanding about the populations at high risk of giardiasis, which include:

  • diaper-age children who attend day-care centers [50, 51];

  • adults that work in child-care organizations or day-care centers [52];

  • institutionalized individuals [53];

  • men who have sex with men [54];

  • immunocompromised individuals (chronic variable immunodeficiency, hypogammaglobulinemia, HIV, immunosuppressed individuals, cystic fibrosis, and others) [55, 56]; and

  • international travelers or any subject (hikers, campers, sportsman’s adventures, and others) exposed to drinking untreated water from lakes, streams, and swimming pools [57].

Waterborne transmission is recognized as the most common transmission, with numerously documented outbreaks throughout the world [46, 58]. This includes the consumption of contaminated water from pools, rivers, or lakes, as well as from contaminated drinking water, either unpurified or inadequately purified. There have been multiple documented cases of cysts in the municipal water supply here in the United States, although such scenarios do not account for the vast majority of infections [35].

Foodborne transmission of G. lamblia is much less common than waterborne transmission, but there are many ways food can be fecally contaminated. For example, street food and any food prepared with the unclean hands of an infected subject could easily transmit giardiasis given a few cysts necessary to transmit the disease. Ingestion of 100 or more cysts is required to ensure infection in humans, but as few as 10 cysts have proven to be enough to infect a volunteer [59].

Fecal-oral transmission is also a significant mechanism of transmission and is the one responsible for the outbreaks in day-cares and nurseries. These outbreaks reflect the close contact between young children, who are significantly more likely to pass the parasite fecal-orally at day-cares than at home. For example, in the Netherlands, where around half of preschool children are cared for in day-care centers, a mean of 2.5 days a week, children at day-care centers are twice as likely to test positive to G. lamblia as their home-care counterparts [45], infecting around 4.2% of them [60].

Sexual transmission of Giardia is now a very well described form of oral-anal transmission and fecal-oral transmission among men who have sex with men. Currently, there exist a large body of publications that have led to improving our understanding of giardiasis as a sexually transmitted infection. According to these studies, prevalence rates of giardiasis among men who have sex with men range from 2 to 30% [61]. Although giardiasis is not a major cause of AIDS-associated diarrhea, the prevalence of giardiasis, as well as the chronicity of symptoms, is greater in patients with AIDS, especially in developing countries [62]. Overall, every immunocompromised group, like AIDS patients, is recognized as more susceptible to the development of chronic giardiasis [63].

To sum up, it is really important that healthcare providers consider Giardia as a differential diagnosis among high-risk populations that match giardiasis epidemiology, and if patients tested positive, it is really important that they provide patients with appropriate therapy and follow-up, as well as proper counseling to increase treatment compliance rate. And in the case of men who have sex with men, also encourage partner notification, and teach them strategies for preventing the transmission of this disease, including the discussion of the risk of enteric infections after oral-anal sexual contact.


  1. 1. Ford BJ. The discovery of giardia. Microscope. 2005;53:147-153
  2. 2. Adam RD. Biology of Giardia lamblia. Clinical Microbiology Review. 2001;14:447-475
  3. 3. Kotloff KL, Nataro JP, Blackwelder WC, Nasrin D, Farag TH, Panchalingam S, Wu Y, Sow SO, Sur D, Breiman RF, Faruque AS, Zaidi AK, Saha D, Alonso PL, Tamboura B, Sanogo D, Onwuchekwa U, Manna B, Ramamurthy T, Kanungo S, Ochieng JB, Omore R, Oundo JO, Hossain A, Das SK, Ahmed S, Qureshi S, Quadri F, Adegbola RA, Antonio M, Hossain MJ, Akinsola A, Mandomando I, Nhampossa T, Acacio S, Biswas K, O'Reilly CE, Mintz ED, Berkeley LY, Muhsen K, Sommerfelt H, Robins-Browne RM, Levine MM. 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;382:209-222
  4. 4. Bartelt LA, Platts-Mills JA. Giardia: A pathogen or commensal for children in high-prevalence settings? Current Opinion in Infectious Disease. 2016;29:502-507
  5. 5. Fraser D, Bilenko N, Deckelbaum RJ, Dagan R, El-On J, Naggan L. Giardia lamblia carriage in Israeli Bedouin infants: Risk factors and consequences. Clinical Infectious Disease. 2000;30:419-424
  6. 6. Brodsky RE, Spencer HC Jr., Schultz MG. Giardiasis in American travelers to the Soviet Union. Journal of Infectious Disease. 1974;130:319-323
  7. 7. Lopez CE, Juranek DD, Sinclair SP, Schultz MG. Giardiasis in American travelers to Madeira Island, Portugal. American Journal of Tropical Medicine and Hygiene. 1978;27:1128-1132
  8. 8. Jelinek T, Loscher T. Epidemiology of giardiasis in German travelers. Journal of Travel Medicine. 2000;7:70-73
  9. 9. Wolfe MS. Giardiasis. Clinical Microbiology Review. 1992;5:93-100
  10. 10. Monis PT, Caccio SM, Thompson RC. Variation in giardia: Towards a taxonomic revision of the genus. Trends in Parasitology. 2009;25:93-100
  11. 11. Caccio SM, Thompson RC, McLauchlin J, Smith HV. Unravelling Cryptosporidium and giardia epidemiology. Trends in Parasitology. 2005;21:430-437
  12. 12. Feng Y, Xiao L. Zoonotic potential and molecular epidemiology of Giardia species and giardiasis. Clinical Microbiology Review. 2011;24:110-140
  13. 13. Lasek-Nesselquist E, Welch DM, Sogin ML. The identification of a new Giardia duodenalis assemblage in marine vertebrates and a preliminary analysis of G. duodenalis population biology in marine systems. Int Journal of Parasitology. 2010;40:1063-1074
  14. 14. Caccio SM, Ryan U. Molecular epidemiology of giardiasis. Molecular and Biochemical Parasitology. 2008;160:75-80
  15. 15. Dawson SC. An insider's guide to the microtubule cytoskeleton of giardia. Cellular Microbiology. 2010;12:588-598
  16. 16. Hagen KD, Hirakawa MP, House SA, Schwartz CL, Pham JK, Cipriano MJ, De La Torre MJ, Sek AC, Du G, Forsythe BM, Dawson SC. Novel structural components of the ventral disc and lateral crest in Giardia intestinalis. PLoS Neglected Tropical Disease. 2011;5:e1442
  17. 17. Brown JR, Schwartz CL, Heumann JM, Dawson SC, Hoenger A. A detailed look at the cytoskeletal architecture of the Giardia lamblia ventral disc. Journal of Structural Biology. 2016;194:38-48
  18. 18. Lujan HD, Mowatt MR, Byrd LG, Nash TE. Cholesterol starvation induces differentiation of the intestinal parasite Giardia lamblia. Proceedings of National Academy Science United States of America. 1996;93:7628-7633
  19. 19. Einarsson E, Troell K, Hoeppner MP, Grabherr M, Ribacke U, Svard SG. Coordinated changes in gene expression throughout encystation of Giardia intestinalis. PLoS Neglected Tropical Disease. 2016;10:e0004571
  20. 20. Gilman RH, Brown KH, Visvesvara GS, Mondal G, Greenberg B, Sack RB, Brandt F, Khan MU. Epidemiology and serology of Giardia lamblia in a developing country: Bangladesh. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1985;79:469-473
  21. 21. Trout JM, Santin M, Fayer R. Giardia and Cryptosporidium species and genotypes in coyotes (Canis latrans). Journal of Zoo and Wildlife Medicine. 2006;37:141-144
  22. 22. Thompson RC, Colwell DD, Shury T, Appelbee AJ, Read C, Njiru Z, Olson ME. The molecular epidemiology of Cryptosporidium and Giardia infections in coyotes from Alberta, Canada, and observations on some cohabiting parasites. Veterinary Parasitology. 2009;159:167-170
  23. 23. Fayer R, Santin M, Trout JM, DeStefano S, Koenen K, Kaur T. Prevalence of Microsporidia, Cryptosporidium spp., and Giardia spp. in beavers (Castor canadensis) in Massachusetts. Journal of Zoo and Wildlife Medicine. 2006;37:492-497
  24. 24. Kutz SJ, Thompson RA, Polley L, Kandola K, Nagy J, Wielinga CM, Elkin BT. Giardia assemblage A: Human genotype in muskoxen in the Canadian Arctic. Parasit Vectors. 2008;1:32
  25. 25. Graczyk TK, Bosco-Nizeyi J, Ssebide B, Thompson RC, Read C, Cranfield MR. Anthropozoonotic Giardia duodenalis genotype (assemblage) a infections in habitats of free-ranging human-habituated gorillas, Uganda. Journal of Parasitology. 2002;88:905-909
  26. 26. Moro D, Lawson MA, Hobbs RP, Thompson RC. Pathogens of house mice on arid Boullanger Island and subantarctic Macquarie Island, Australia. Journal of Wildlife Disease. 2003;39:762-771
  27. 27. Appelbee AJ, Thompson RC, Olson ME. Giardia and Cryptosporidium in mammalian wildlife—current status and future needs. Trends in Parasitology. 2005;21:370-376
  28. 28. Beer KD, Gargano JW, Roberts VA, Hill VR, Garrison LE, Kutty PK, Hilborn ED, Wade TJ, Fullerton KE, Yoder JS. Surveillance for waterborne disease outbreaks associated with drinking water—United States, 2011-2012. MMWR Morbidity and Mortality Weekly Report. 2015;64:842-848
  29. 29. Pires SM, Fischer-Walker CL, Lanata CF, Devleesschauwer B, Hall AJ, Kirk MD, Duarte AS, Black RE, Angulo FJ. Aetiology-specific estimates of the global and regional incidence and mortality of diarrhoeal diseases commonly transmitted through food. PLoS One. 2015;10:e0142927
  30. 30. Torgerson PR, Devleesschauwer B, Praet N, Speybroeck N, Willingham AL, Kasuga F, Rokni MB, Zhou XN, Fevre EM, Sripa B, Gargouri N, Furst T, Budke CM, Carabin H, Kirk MD, Angulo FJ, Havelaar A, de Silva N. World Health Organization estimates of the global and regional disease burden of 11 foodborne parasitic diseases, 2010: A data synthesis. PLoS Medicine. 2015;12:e1001920
  31. 31. Lane S, Lloyd D. Current trends in research into the waterborne parasite Giardia. Critical Reviews in Microbiology. 2002;28:123-147
  32. 32. Gbakima AA. Intestinal parasitic infections and swamp development in Sierra Leone. African Journal of Health Sciences. 1994;1:175-178
  33. 33. Savioli L, Smith H, Thompson A. Giardia and Cryptosporidium join the 'neglected diseases initiative'. Trends in Parasitology. 2006;22:203-208
  34. 34. Daly ER, Roy SJ, Blaney DD, Manning JS, Hill VR, Xiao L, Stull JW. Outbreak of giardiasis associated with a community drinking-water source. Epidemiology and Infection. 2010;138:491-500
  35. 35. Painter JE, Gargano JW, Collier SA, Yoder JS. Centers for Disease C, Prevention. Giardiasis surveillance—United States, 2011-2012. MMWR. 2015;64(3):15-25
  36. 36. Yoder JS, Gargano JW, Wallace RM, Beach MJ, Centers for Disease C, Prevention. Giardiasis surveillance--United States, 2009-2010. MMWR Surveillance Summary. 2012;61:13-23
  37. 37. Takaoka K, Gourtsoyannis Y, Hart JD, Armstrong M, Daniel A, Mewse E, Phillips D, Bailey RL. Incidence rate and risk factors for giardiasis and strongyloidiasis in returning UK travellers. Journal of Travel Medicine. 2016;23(5):1-6
  38. 38. Schnell K, Collier S, Derado G, Yoder J, Gargano JW. Giardiasis in the United States—an epidemiologic and geospatial analysis of county-level drinking water and sanitation data, 1993-2010. Journal of Water and Health. 2016;14:267-279
  39. 39. Rodriguez-Morales AJ, Granados-Alvarez S, Escudero-Quintero H, Vera-Polania F, Mondragon-Cardona A, Diaz-Quijano FA, Sosa-Valencia L, Lozada-Riascos CO, Escobedo AA, Liseth O, Haque U. Estimating and mapping the incidence of giardiasis in Colombia, 2009-2013. International Journal of Infectious Disease. 2016;49:204-209
  40. 40. Garcia-Cervantes PC, Baez-Flores ME, Delgado-Vargas F, Ponce-Macotela M, Nawa Y, De-la-Cruz-Otero MD, Martinez-Gordillo MN, Diaz-Camacho SP. Giardia duodenalis genotypes among schoolchildren and their families and pets in urban and rural areas of Sinaloa, Mexico. Journal of Infection in Developing Countries. 2017;11:180-187
  41. 41. Lee MF, Cadogan P, Eytle S, Copeland S, Walochnik J, Lindo JF. Molecular epidemiology and multilocus sequence analysis of potentially zoonotic Giardia spp. from humans and dogs in Jamaica. Parasitology Research. 2017;116:409-414
  42. 42. Moore CE, Elwin K, Phot N, Seng C, Mao S, Suy K, Kumar V, Nader J, Bousfield R, Perera S, Bailey JW, Beeching NJ, Day NP, Parry CM, Chalmers RM. Molecular characterization of Cryptosporidium Species and Giardia duodenalis from symptomatic Cambodian children. PLoS Neglected Tropical Diseases. 2016;10:e0004822
  43. 43. Kosek MN, Investigators M-EN. Causal pathways from enteropathogens to environmental enteropathy: Findings from the MAL-ED birth cohort study. EBioMedicine. 2017;18:109-117
  44. 44. Rogawski ET, Bartelt LA, Platts-Mills JA, Seidman JC, Samie A, Havt A, Babji S, Trigoso DR, Qureshi S, Shakoor S, Haque R, Mduma E, Bajracharya S, Gaffar SMA, Lima AAM, Kang G, Kosek MN, Ahmed T, Svensen E, Mason C, Bhutta ZA, Lang DR, Gottlieb M, Guerrant RL, Houpt ER, Bessong PO. Determinants and impact of Giardia infection in the first 2 years of life in the MAL-ED birth cohort. Journal of the Pediatric Infectious Diseases Society. 2017;6:153-160
  45. 45. Pijnacker R, Mughini-Gras L, Heusinkveld M, Roelfsema J, van Pelt W, Kortbeek T. Different risk factors for infection with Giardia lamblia assemblages A and B in children attending day-care centres. European Journal of Clinical Microbiology and Infectious Disease. 2016;35:2005-2013
  46. 46. Adam EA, Yoder JS, Gould LH, Hlavsa MC, Gargano JW. Giardiasis outbreaks in the United States, 1971-2011. Epidemiology and Infection. 2016;144:2790-2801
  47. 47. Dennis DT, Smith RP, Welch JJ, Chute CG, Anderson B, Herndon JL, von Reyn CF. Endemic giardiasis in New Hampshire: A case-control study of environmental risks. Journal of Infectious Disease. 1993;167:1391-1395
  48. 48. Gagnon F, Duchesne JF, Levesque B, Gingras S, Chartrand J. Risk of giardiasis associated with water supply in an endemic context. International Journal of Environmental Health Research. 2006;16:349-359
  49. 49. Odoi A, Martin SW, Michel P, Holt J, Middleton D, Wilson J. Determinants of the geographical distribution of endemic giardiasis in Ontario, Canada: A spatial modelling approach. Epidemiology and Infection. 2004;132:967-976
  50. 50. Duffy TL, Montenegro-Bethancourt G, Solomons NW, Belosevic M, Clandinin MT. Prevalence of giardiasis in children attending semi-urban daycare centres in Guatemala and comparison of 3 giardia detection tests. Journal of Health, Population and Nutrition. 2013;31:290-293
  51. 51. Nunez FA, Hernandez M, Finlay CM. Longitudinal study of giardiasis in three day care centres of Havana City. Acta Tropica. 1999;73:237-242
  52. 52. Boreham PF, Shepherd RW. Giardiasis in child-care centres. Medical Journal of Australia. 1984;141:263
  53. 53. Mascarini LM, Donalisio MR. Giardiasis and cryptosporidiosis in children institutionalized at daycare centers in the state of Sao Paulo. Revista da Sociedade Brasileira de Medicina Tropical. 2006;39:577-579
  54. 54. Beltrami JF, Shouse RL, Blake PA. Trends in infectious diseases and the male to female ratio: Possible clues to changes in behavior among men who have sex with men. AIDS Education and Prevention. 2005;17:49-59
  55. 55. Abaza SM, Makhlouf LM, el-Shewy KA, el-Moamly AA. Intestinal opportunistic parasites among different groups of immunocompromised hosts. Journal of the Egyptian Society of Parasitology. 1995;25:713-727
  56. 56. Cruz I, Ricardo JL, Nunes JF, Serras AC, Porto MT, Lopes JM, Veloso FT, Freitas J. Giardia and immune deficiency. American Journal of Gastroenterology. 1991;86:1554-1555
  57. 57. Holtan NR. Giardiasis. A crimp in the life-style of campers, travelers, and others. Postgraduate Medicine Journal. 1988;83:54-6, 59-61
  58. 58. Guzman-Herrador B, Carlander A, Ethelberg S, Freiesleben de Blasio B, Kuusi M, Lund V, Lofdahl M, MacDonald E, Nichols G, Schonning C, Sudre B, Tronnberg L, Vold L, Semenza JC, Nygard K. Waterborne outbreaks in the Nordic countries, 1998 to 2012. EuroSurveillance. 2015;20
  59. 59. Rendtorff RC, Holt CJ. The experimental transmission of human intestinal protozoan parasites. IV. Attempts to transmit Entamoeba coli and Giardia lamblia cysts by water. American Journal of Hygiene. 1954;60(3):327-338
  60. 60. Enserink R, Scholts R, Bruijning-Verhagen P, Duizer E, Vennema H, de Boer R, Kortbeek T, Roelfsema J, Smit H, Kooistra-Smid M, van Pelt W. High detection rates of enteropathogens in asymptomatic children attending day care. PLoS One. 2014;9:e89496
  61. 61. Escobedo AA, Almirall P, Alfonso M, Cimerman S, Chacin-Bonilla L. Sexual transmission of giardiasis: A neglected route of spread? Acta Tropica. 2014;132:106-111
  62. 62. Manatsathit S, Tansupasawasdikul S, Wanachiwanawin D, Setawarin S, Suwanagool P, Prakasvejakit S, Leelakusolwong S, Eampokalap B, Kachintorn U. Causes of chronic diarrhea in patients with AIDS in Thailand: A prospective clinical and microbiological study. Journal of Gastroenterology. 1996;31:533-537
  63. 63. Espelage W, an der Heiden M, Stark K, Alpers K. Characteristics and risk factors for symptomatic Giardia lamblia infections in Germany. BMC Public Health. 2010;10:41

Written By

Antonio Marty Quispe Gutiérrez

Submitted: October 13th, 2016 Reviewed: July 7th, 2017 Published: December 13th, 2017