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Giardiasis
Article Last Updated: Apr 9, 2008
AUTHOR AND EDITOR INFORMATION
Section 1 of 12  
Author: 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 is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Coauthor(s):
Mark H Johnston, MD, Associate Professor of Medicine, Uniformed Services University of Health Sciences; Consulting Staff, Lancaster Gastroenterology Inc
Editors: 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; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group; Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine; 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
Author and Editor Disclosure
Synonyms and related keywords:
lambliasis, Giardia lamblia, G lamblia, protozoan parasites, endemic diarrheal illness, epidemic diarrheal illness, diarrhea, acute watery diarrhea, chronic diarrhea, water-borne intestinal pathogens, intestinal parasites, gut parasites, protozoal infection, encystation-specific secretory vesicles, ESVs, malabsorption, steatorrhea, abdominal cramping, bloating, flatulence
Background
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. Giardiasis is the most prevalent protozoal infection of the human intestine. G lamblia is one of the most common causative agents of epidemic and endemic diarrheal illness throughout the world. It continues to be the most frequently identified water-borne intestinal pathogen in the United States and has been responsible for at least 34 reported community outbreaks over the last 20 years. G lamblia has been found in as many as 80% of raw water supplies from lakes, streams, and ponds and in as many as 15% of filtered water samples.
Pathophysiology
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 Media file 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 Media file 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. 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. However, a recent 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.1
Frequency
United States
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 recent 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.2 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.2
International
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.
Mortality/Morbidity
- Most infected subjects are asymptomatic, and most infections are self-limited. However, chronic infections, marked by chronic diarrhea/steatorrhea and malabsorption, can occur and can last from weeks to months.
- Death is rare and usually occurs in malnourished children.
- G lamblia has been implicated as the chief cause of growth retardation in infected children, even after control of other agents that cause diarrhea.
Race
- No racial predilection exists for infection.
Sex
- Infection occurs equally in both sexes.
Age
- Children are particularly at risk for infection through exposure at day-care centers. Many of the epidemics documented over the last 2 decades have originated in day-care centers.
- Estimates of the prevalence of infection, defined by the presence of cyst passage, have been as high as 20-25% in children younger than 3 years.
History
- Approximately 15% of cases of giardiasis are asymptomatic, with cyst passage only.
- Approximately 50% of patients infected with Giardia may present with a variety of symptoms, including acute watery diarrhea, chronic diarrhea with malabsorption and weight loss, and abdominal cramping.
- Acute diarrhea is the most common symptom of Giardia infection, occurring in 90% of symptomatic subjects.
- Abdominal cramping, bloating, and flatulence occur in 70-75% of symptomatic patients.
- The pathogenesis of diarrhea in giardiasis is unknown. Proposed mechanisms include occlusion of the mucosa by large numbers of the organisms, competition with the host for nutrients, epithelial damage, immune-mediated absorptive changes such as transient lactase deficiency, altered mucus secretion, and alterations in motility.
- The parasite is known to invade the colonic epithelium, but the significance of invasion is not known. The most important result of invasion by the parasite is subsequent activation of host immune processes.
- Steatorrhea, vitamin B-12, vitamin A, protein, and D-xylose malabsorption all have been documented in patients with chronic infection.
- Symptoms of chronic infection include chronic diarrhea, malaise, nausea, and anorexia.
- Weight loss, as extensive as 10-15 pounds in an adult, occurs in approximately 66% of symptomatic patients.
- Chronic sporadic diarrhea may continue for months.
- Postinfection lactose deficiency also is a common finding, occurring in 2-40% of cases.
- Extraintestinal manifestations are rare.
- Symptoms such as urticaria and reactive arthritis have been reported.
- The etiology of such extraintestinal symptoms is likely a result of host immune system activation and cross-reactivity/molecular mimicry.
Physical
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.
Causes
- Subjects become infected through ingestion of infectious G lamblia cysts, either in contaminated water or food or via direct person-to-person contact.
- The infectious load required to produce disease may be as low as 10 cysts.
- The protozoan is known to have multiple strains with varying abilities to cause disease, and several different strains may be found in one host during infection.
Amebiasis
Bacterial Overgrowth Syndrome
Cryptosporidiosis
Gastroenteritis, Viral
Irritable Bowel Syndrome
Lactose Intolerance
Sprue, Tropical
Other Problems to be Considered
Bacterial enteritis
Viral enteritis
Lab Studies
- The traditional basis of diagnosis is identification of G lamblia trophozoites or cysts in the stool of infected patients via a stool ova and parasite (O&P) examination.
- Stool examination may be performed on fresh specimens or after preservation with polyvinyl alcohol or 10% formalin (with appropriate staining).
- Ideally, 3 specimens from different days should be examined because of potential variations in fecal excretion of cysts.
- Stool O&P testing remains the diagnostic method with which other tests are compared.
- Aspiration of duodenal contents and demonstration of trophozoites also have been used for diagnosis but this is more invasive than stool examination and, in direct comparison studies to stool microscopy, may have a lower diagnostic yield.
- Stool antigen enzyme-linked immunosorbent assays also are available.
- These tests are similar to the stool O&P test in terms of cost and have a sensitivity of 88-98% and a specificity of 87-100%.
- These tests are best used as a screening test for high-incidence settings such as day-care centers or for identification of subjects during an epidemic, but they should not take the place of stool microscopy or other possible diagnoses may be overlooked.
- Routine laboratory tests (CBC count, electrolyte levels) usually are normal; eosinophilia is an uncommon feature of infection.
- In summary, stool O&P tests aid in the diagnosis of giardiasis in 80-85% of patients. If the results from the 3 O&P tests are negative and the disease is still suspected, stool antigen enzyme-linked immunosorbent assay (ELISA) may be helpful. If both of these methods result in negative findings but the patient has symptoms consistent with small bowel diarrhea/malabsorption, upper endoscopy with biopsies and duodenal aspirate is a reasonable alternative.
Imaging Studies
- No imaging studies are required in the workup of giardiasis.
- Small bowel plain films may show nonspecific thickening of the duodenal and jejunal folds.
- Barium radiography should always follow stool examination because barium can obscure identification of parasites for as long as 10 days.
Other Tests
- Fecal fat quantification or a qualitative fecal fat analysis with Sudan stain may confirm steatorrhea. Serum carotene, folate, and vitamin B-12 levels may be variably depressed as a result of malabsorption. The findings from D-xylose absorption tests may be abnormal.
- Disaccharidase deficiency is common during and after treatment and can be diagnosed with the aid of a lactose tolerance breath test.
- Serum electrophoresis can help diagnose immunoglobulin A, immunoglobulin M, and, occasionally, immunoglobulin G deficiency states.
- Serologic studies are being investigated.
Procedures
- Esophagogastroduodenoscopy (EGD) may be employed to assess the small bowel architecture and obtain biopsy specimens from patients in whom the diagnosis is suspected but unproven after stool microscopy and ELISA. This also may be used for patients who continue to manifest symptoms of malabsorption after adequate therapy.
Histologic Findings
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.
Medical Care
- Evaluation usually can be conducted in an outpatient setting.
- Inpatient studies rarely are necessary.
- Standard medical therapy consists of antibiotic therapy. Metronidazole is the most commonly prescribed antibiotic for this condition.
Surgical Care
Surgical therapy is not indicated for giardiasis.
Consultations
- No specific consultations are required for the diagnosis and management of giardiasis.
- In difficult cases, consulting a gastroenterologist and infectious disease specialist may be useful.
Diet
- No special diet is required.
- A significant portion of patients have symptoms of lactose intolerance (cramping, bloating, diarrhea), and maintenance on a lactose-free diet for several months may be helpful.
Activity
- Activity restrictions are not indicated.
- Infected subjects who are at risk of spreading the infection should be isolated and treated.
Antibiotic therapy is standard in the treatment of giardiasis.
Drug Category: Antibiotics
The therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
| Drug Name | Metronidazole (Flagyl) |
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| Description | 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. |
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| Adult Dose | 250 mg PO tid for 5 d |
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| Pediatric Dose | 5 mg/kg PO tid for 10 d |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Cimetidine may increase toxicity; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy |
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| Drug Name | Albendazole (Albenza) |
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| Description | 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. |
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| Adult Dose | 400 mg PO qd for 3 d |
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| Pediatric Dose | 15 mg/kg PO qd for 3 d |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity |
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| 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
|
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| Precautions | Discontinue use if LFTs increase significantly (resume when levels decrease to pretest values) |
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| Drug Name | Furazolidone (Furoxone) |
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| Description | 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. |
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| Adult Dose | 100 mg PO qid for 7 d |
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| Pediatric Dose | 25-50 mg PO qid for 7 d |
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| Contraindications | Documented hypersensitivity; infants <1 mo; prior sensitivity to nitrofurans |
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| Interactions | 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 |
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| 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
|
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| Precautions | Caution in G-6-PD deficiency when administering prolonged treatments; medication inhibits enzyme monoamine oxidase |
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| Drug Name | Nitazoxanide (Alinia) |
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| Description | 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. |
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| Adult Dose | 500 mg PO bid for 3 d |
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| Pediatric Dose | <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 |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Tizoxanide (nitazoxanide metabolite) is >99.9% bound to plasma protein and may displace other highly plasma protein–bound drugs, resulting in increased toxicity |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | 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 |
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| Drug Name | Tinidazole (Tindamax) |
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| Description | Nitroimidazole antiprotozoal agent. The mechanism by which tinidazole exhibits activity against Giardia and Entamoeba species is not known. |
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| Adult Dose | 2 g PO once with food |
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| Pediatric Dose | <3 years: Not established
>3 years: 50 mg/kg PO once with food; not to exceed 2 g/dose |
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| Contraindications | Documented hypersensitivity; first trimester of pregnancy |
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| Interactions | 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 |
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| 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
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| Precautions | 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 |
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Further Inpatient Care
- The patient should be admitted if evidence of severe dehydration or a malnourished state is present.
Further Outpatient Care
- Carefully monitor the patient's response to medications, and note any adverse effects.
Complications
- Weight loss, disaccharidase deficiency, malabsorption, and growth retardation are possible complications.
Prognosis
- Giardiasis usually is responsive to therapy, although reinfection is possible and some resistance has been observed.
Patient Education
- Patients and at-risk individuals should be instructed regarding appropriate hygiene methods and signs/symptoms of infection. Travelers, in particular, should be educated.
- For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article, Giardiasis.
Medical/Legal Pitfalls
- Failure to recognize other enteric infections such as amoebiasis or cryptosporidiosis
Special Concerns
- This is a common cause of chronic diarrhea and growth retardation in children in developing countries.
- Antimicrobial resistance has been reported.
- Furazolidone is the antibiotic of choice in pregnant women. No clinical reports have indicated teratogenicity in the fetus or newborn infant.
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.
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Giardiasis excerpt Article Last Updated: Apr 9, 2008
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