Updated: Nov 18, 2009
Giardia lamblia was originally identified by von Leeuwenhoek in the 1600s and was first recognized in human stool by Vilem Dusan Lambl (1824-1895) in 1859 and by Alfred Giard (1846-1908) after whom it is named. Although it 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. (See images below and Images 1-2.)
Giardia has one of the simplest life cycles of all human parasites. The life cycle is composed of 2 stages, as follows: (1) the trophozoite (see Image 2), 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 Image 1) 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.
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 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.7 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.
The mechanism of epithelial injury remains unclear.8 However, a study by 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, suggesting a possible role for caspase-dependent apoptosis in the pathogenesis of giardiasis.9
This organism remains the most commonly identified intestinal parasite. From 1964-1984, G lamblia caused at least 90 water-borne outbreaks of diarrhea, affecting more than 23,000 people. Groups most at risk for infection include travelers, children, homosexual men, and individuals with immunoglobulin deficiency states (inherited or acquired). A study by Yoder et al reported that, although giardiasis occurs throughout the United States, the incidence is greatest in northern states with a peak onset from early summer through early fall.10 However, this may be related to the differences in individual state surveillance systems and may not necessarily reflect a true increased incidence in northern states.10
This organism has a worldwide distribution and is a major cause of epidemic childhood diarrhea in developing countries. Prevalence rates vary from 4-42%. It is the most common gut parasite in the United Kingdom, and infection rates are especially high in Eastern Europe.
Physical examination does not contribute to the diagnosis of giardiasis. Some evidence of weight loss may be present, but no known unique physical findings are attributable to giardiasis.
| Amebiasis | Lactose Intolerance |
| Bacterial Overgrowth Syndrome | Sprue, Tropical |
| Cryptosporidiosis | |
| Gastroenteritis, Viral | |
| Irritable Bowel Syndrome |
Bacterial enteritis
Viral enteritis
No classic universal histologic abnormalities result from infection with G lamblia. Patients with giardiasis who undergo EGD 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.
Surgical therapy is not indicated for giardiasis.
Antibiotic therapy is standard in the treatment of giardiasis.12,18
The therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.19
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. Most commonly prescribed antibiotic for giardiasis.
250 mg PO tid for 5 d
5 mg/kg PO tid for 10 d
Cimetidine may increase toxicity; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy
Decreases ATP production in worm, causing energy depletion, immobilization, and, finally, death. To avoid inflammatory response in CNS, patient also must be started on anticonvulsants and high-dose glucocorticoids.
400 mg PO qd for 3 d
15 mg/kg PO qd for 3 d
Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue use if LFTs increase significantly (resume when levels decrease to pretest values)
Nitrofuran with antiprotozoal activity. Alternative drug for children because of availability in liquid suspension. Most common adverse effects are GI upset and brown discoloration of urine.
100 mg PO qid for 7 d
25-50 mg PO qid for 7 d
Increases levodopa blood concentrations and, thus, potential for toxicity; causes disulfiram reactions when taken with alcohol; toxicity of meperidine, paroxetine, fluoxetine, sertraline, trazodone, MAOIs, sympathomimetic amines, and tricyclic antidepressants increases when taken with furazolidone
Documented hypersensitivity; infants <1 mo; prior sensitivity to nitrofurans
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in G-6-PD deficiency when administering prolonged treatments; medication inhibits enzyme monoamine oxidase
Inhibits growth of C parvum sporozoites and oocysts and G lamblia trophozoites. Elicits antiprotozoal activity by interfering with pyruvate-ferredoxin oxidoreductase (PFOR) enzyme-dependent electron transfer reaction, which is essential to anaerobic energy metabolism. Available as a 20-mg/mL oral susp.
500 mg PO bid for 3 d
<1 year: Not established
1-4 years: 100 mg (5 mL) PO q12h for 3 d with food
4-11 years: 200 mg (10 mL) PO q12h for 3 d with food
>11 years: Administer as in adults
Tizoxanide (nitazoxanide metabolite) is >99.9% bound to plasma protein and may displace other highly plasma protein–bound drugs, resulting in increased toxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause abdominal pain, diarrhea, vomiting, or headache; administer with food; caution when coadministered with other highly plasma protein–bound drugs with narrow therapeutic indices
Nitroimidazole antiprotozoal agent. The mechanism by which tinidazole exhibits activity against Giardia and Entamoeba species is not known.
2 g PO once with food
<3 years: Not established
>3 years: 50 mg/kg PO once with food; not to exceed 2 g/dose
Limited data exist; interaction information based on experience with other nitroimidazole derivatives (ie, metronidazole); may prolong PT when coadministered with warfarin; avoid alcoholic beverages and preparations containing ethanol or propylene glycol during and 3 d following administration (may cause disulfiramlike reaction); may increase serum levels of lithium, phenytoin, cyclosporine, tacrolimus, and fluorouracil; CYP450 inducers (eg, phenobarbital, rifampin, phenytoin) may increase elimination; CYP450 inhibitors (eg, cimetidine, ketoconazole) may decrease elimination; concurrent administration with cholestyramine may decrease oral bioavailability; oxytetracycline may antagonize effect
Documented hypersensitivity; first trimester of pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Carcinogenicity has been observed in mice and rats treated with long-term administration of metronidazole (another nitroimidazole), although not observed with tinidazole, use cautiously; seizures and peripheral neuropathy have been reported; caution with history of blood dyscrasia; may cause metallic/bitter taste, nausea, anorexia, vomiting, weakness, fatigue, dizziness, or headache; if administered on day of hemodialysis, administer additional dose equivalent to half of recommended dose following dialysis
Daly ER, Roy SJ, Blaney DD, Manning JS, Hill VR, Xiao L, et al. Outbreak of giardiasis associated with a community drinking-water source. Epidemiol Infect. Sep 15 2009;1-10. [Medline].
Robertson L, Gjerde B, Hansen EF, Stachurska-Hagen T. A water contamination incident in Oslo, Norway during October 2007; a basis for discussion of boil-water notices and the potential for post-treatment contamination of drinking water supplies. J Water Health. Mar 2009;7(1):55-66. [Medline].
Eisenstein L, Bodager D, Ginzl D. Outbreak of giardiasis and cryptosporidiosis associated with a neighborhood interactive water fountain--Florida, 2006. J Environ Health. Oct 2008;71(3):18-22; quiz 49-50. [Medline].
Nishi L, Baesso ML, Santana RG, Fregadolli P, Falavigna DL, Falavigna-Guilherme AL. Investigation of Cryptosporidium spp. and Giardia spp. in a public water-treatment system. Zoonoses Public Health. Jun 2009;56(5):221-8. [Medline].
Robertson LJ, Forberg T, Gjerde BK. Giardia cysts in sewage influent in Bergen, Norway 15-23 months after an extensive waterborne outbreak of giardiasis. J Appl Microbiol. Apr 2008;104(4):1147-52. [Medline].
Ryu H, Alum A, Mena KD, Abbaszadegan M. Assessment of the risk of infection by Cryptosporidium and Giardia in non-potable reclaimed water. Water Sci Technol. 2007;55(1-2):283-90. [Medline].
Hanevik K, Hausken T, Morken MH, Strand EA, Morch K, Coll P, et al. Persisting symptoms and duodenal inflammation related to Giardia duodenalis infection. J Infect. Dec 2007;55(6):524-30. [Medline].
Buret AG. Mechanisms of epithelial dysfunction in giardiasis. Gut. Mar 2007;56(3):316-7. [Medline].
Panaro MA, Cianciulli A, Mitolo V, Mitolo CI, Acquafredda A, Brandonisio O, et al. Caspase-dependent apoptosis of the HCT-8 epithelial cell line induced by the parasite Giardia intestinalis. FEMS Immunol Med Microbiol. Nov 2007;51(2):302-9. [Medline].
Yoder JS, Beach MJ. Giardiasis surveillance--United States, 2003-2005. MMWR Surveill Summ. Sep 7 2007;56(7):11-8. [Medline].
Escobedo AA, Almirall P, Alfonso M, Cimerman S, Rey S, Terry SL. Treatment of intestinal protozoan infections in children. Arch Dis Child. Jun 2009;94(6):478-82. [Medline].
Jiménez JC, Pinon A, Dive D, Capron M, Dei-Cas E, Convit J. Antibody response in children infected with Giardia intestinalis before and after treatment with Secnidazole. Am J Trop Med Hyg. Jan 2009;80(1):11-5. [Medline].
Abdul-Wahid A, Faubert G. Characterization of the local immune response to cyst antigens during the acute and elimination phases of primary murine giardiasis. Int J Parasitol. May 2008;38(6):691-703. [Medline].
Nagaty IM, Hegazi MM. Dot-ELISA copro-antigen and direct stool examination in diagnosis of giardiasis patients. J Egypt Soc Parasitol. Aug 2007;37(2):641-8. [Medline].
Morken MH, Nysaeter G, Strand EA, Hausken T, Berstad A. Lactulose breath test results in patients with persistent abdominal symptoms following Giardia lamblia infection. Scand J Gastroenterol. 2008;43(2):141-5. [Medline].
Busatti HG, Vieira AE, Viana JC, Silva HE, Souza-Fagundes EM, Martins-Filho OA, et al. Effect of metronidazole analogues on Giardia lamblia cultures. Parasitol Res. Dec 2007;102(1):145-9. [Medline].
Monajemzadeh SM, Monajemzadeh M. Comparison of iron and hematological indices in Giardia lamblia infection before and after treatment in 102 children in Ahwaz, Iran. Med Sci Monit. Jan 2008;14(1):CR19-23. [Medline].
Busatti HG, Santos JF, Gomes MA. The old and new therapeutic approaches to the treatment of giardiasis: Where are we?. Biologics. 2009;3:273-87. [Medline]. [Full Text].
Escobedo AA, Cimerman S. Giardiasis: a pharmacotherapy review. Expert Opin Pharmacother. Aug 2007;8(12):1885-902. [Medline].
Dizdar V, Gilja OH, Hausken T. Increased visceral sensitivity in Giardia-induced postinfectious irritable bowel syndrome and functional dyspepsia. Effect of the 5HT3-antagonist ondansetron. Neurogastroenterol Motil. Dec 2007;19(12):977-82. [Medline].
Penrose AS, Wells EV, Aiello AE. Infectious causation of chronic disease: examining the relationship between Giardia lamblia infection and irritable bowel syndrome. World J Gastroenterol. Sep 14 2007;13(34):4574-8. [Medline].
Hanevik K, Dizdar V, Langeland N, Hausken T. Development of functional gastrointestinal disorders after Giardia lamblia infection. BMC Gastroenterol. Apr 21 2009;9:27. [Medline]. [Full Text].
Abdel-Fattah NS, Nada OH. Effect of propolis versus metronidazole and their combined use in treatment of acute experimental giardiasis. J Egypt Soc Parasitol. Aug 2007;37(2 Suppl):691-710. [Medline].
Alizadeh A, Ranjbar M, Kashani KM, Taheri MM, Bodaghi M. Albendazole versus metronidazole in the treatment of patients with giardiasis in the Islamic Republic of Iran. East Mediterr Health J. Sep 2006;12(5):548-54. [Medline].
Goka AK, Rolston DD, Mathan VI, Farthing MJ. The relative merits of faecal and duodenal juice microscopy in the diagnosis of giardiasis. Trans R Soc Trop Med Hyg. Jan-Feb 1990;84(1):66-7. [Medline].
Hlavsa MC, Watson JC, Beach MJ. Giardiasis surveillance--United States, 1998-2002. MMWR Surveill Summ. Jan 28 2005;54(1):9-16. [Medline].
LeChevallier MW, Norton WD, Lee RG. Giardia and Cryptosporidium spp. in filtered drinking water supplies. Appl Environ Microbiol. Sep 1991;57(9):2617-21. [Medline].
LeChevallier MW, Norton WD, Lee RG. Occurrence of Giardia and Cryptosporidium spp. in surface water supplies. Appl Environ Microbiol. Sep 1991;57(9):2610-6. [Medline].
Oberhuber G, Stolte M. Giardiasis: analysis of histological changes in biopsy specimens of 80 patients. J Clin Pathol. Aug 1990;43(8):641-3. [Medline].
Petersen H. Giardiasis (lambliasis). Scand J Gastroenterol Suppl. 1972;14:1-44. [Medline].
Petri WA. Treatment of Giardiasis. Curr Treat Options Gastroenterol. Feb 2005;8(1):13-17. [Medline].
Pickering LK, Woodward WE, DuPont HL, Sullivan P. Occurrence of Giardia lamblia in children in day care centers. J Pediatr. Apr 1984;104(4):522-6. [Medline].
Sahagún J, Clavel A, Goni P, Seral C, Llorente MT, Castillo FJ, et al. Correlation between the presence of symptoms and the Giardia duodenalis genotype. Eur J Clin Microbiol Infect Dis. Jan 2008;27(1):81-3. [Medline].
Schultz MG. Editorial: Giardiasis. JAMA. Sep 29 1975;233(13):13833-4. [Medline].
Schuurman T, Lankamp P, van Belkum A, Kooistra-Smid M, van Zwet A. Comparison of microscopy, real-time PCR and a rapid immunoassay for the detection of Giardia lamblia in human stool specimens. Clin Microbiol Infect. Dec 2007;13(12):1186-91. [Medline].
Sterk M, Muller J, Hemphill A, Muller N. Characterization of a Giardia lamblia WB C6 clone resistant to the isoflavone formononetin. Microbiology. Dec 2007;153:4150-8. [Medline].
Strickland GT. Giardiasis. In: Hunter GE, Strickland GT, eds. Hunter's Tropical Medicine. 7th ed. Philadelphia, Pa: WB Saunders; 1991.
Thompson RC, Monis PT. Variation in Giardia: implications for taxonomy and epidemiology. Adv Parasitol. 2004;58:69-137. [Medline].
Wahnschaffe U, Ignatius R, Loddenkemper C, Liesenfeld O, Muehlen M, Jelinek T, et al. Diagnostic value of endoscopy for the diagnosis of giardiasis and other intestinal diseases in patients with persistent diarrhea from tropical or subtropical areas. Scand J Gastroenterol. Mar 2007;42(3):391-6. [Medline].
Zhou P, Li E, Shea-Donohue T, Singer SM. Tumour necrosis factor alpha contributes to protection against Giardia lamblia infection in mice. Parasite Immunol. Jul 2007;29(7):367-74. [Medline].
giardiasis, lambliasis, , , , intestinal parasite, , treatment, giardiasis symptoms, giardiasis treatment, protozoan parasites, endemic diarrheal illness, epidemic diarrheal illness, intestinal parasites, gut parasites, protozoal infection
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: 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.
Manoop S Bhutani, MD, FACG, FACP, Professor, Department of Medicine, Division of Gastroenterology, Director, Center for Endoscopic Ultrasound, Co-Director, Center for Endoscopic Research, Training and Innovation, University of Texas Medical Branch at Galveston
Manoop S Bhutani, MD, FACG, FACP 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.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Brooks D Cash, MD, FACP, to the development and writing of this article.
Further ReadingClinical guidelines
WGO practice guideline: acute diarrhea.
World Gastroenterology Organisation - Medical Specialty Society. 2008 Mar. 28 pages. NGC:006567
Parasitic infections. In: Guidelines for prevention and treatment of opportunistic infections among HIV-exposed and HIV-infected children.
Centers for Disease Control and Prevention - Federal Government Agency [U.S.]. 2004 Dec 3 (revised 2008 Jun 20). 17 pages. NGC:007350
Clinical trials
Efficacy of BIO-K+ CL1285® Prophylaxis in the Prevention of Traveler's Diarrhea in Adults
Parasitic Infections of the Gastrointestinal Tract
Related eMedicine topics
Giardiasis (Emergency Medicine)
Giardiasis (Pediatrics: General Medicine)
Intestinal Protozoal Diseases
Malabsorption
Malabsorption Syndromes
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)