eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Giardiasis

Author: Murat Hökelek, MD, PhD, Technical Consultant of Parasitology Laboratory, Associate Professor, Department of Clinical Microbiology, Ondokuz Mayis University Medical School, Turkey
Coauthor(s): Michael D Nissen, MBBS, BMedSc, FRACP, FRCPA, Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital
Contributor Information and Disclosures

Updated: Dec 17, 2008

Introduction

Background

Giardia intestinalis (formerly Giardia lamblia) was described in 1681 by Van Leeuwenhoek from own stool. It is a widespread GI protozoon that may be identified in individuals with asymptomatic colonization or acute or chronic diarrheal illness. Infection is more common in children than in adults.^1,2

Giardiasis is a zoonotic infection. A few species include G intestinalis in humans, primates, dogs, beavers; Giardia muris in rodents; Giardia agilis in amphibians; Giardia psittaci and Giardia ardeae in birds; and Giardia microti in voles and muskrats.^3,4,5
 
Giardia species are endemic in areas of the world that have poor sanitation. In developing countries, the disease is an important cause of morbidity, and water-borne and food-borne outbreaks are common. Because of only 10 cysts of organisms may be enough to cause infection, giardiasis is common in daycare center attendees and institutionalized patients in developed countries. G intestinalis is a particularly significant pathogen for people with malnutrition, immunodeficiencies, or cystic fibrosis. Beavers may be an important reservoir host for G intestinalis.^6,7,8

G intestinalis is genetically heterogeneous, with two major genotypes (A and B) are found in both humans and animals. Another 5 genotypes (C–G) are host-specific. Some strains appear more biologically suitable than other strains. This feature is potentially important in giardiasis pathogenesis.^9,10

High-risk groups for giardiasis include travelers to highly endemic areas, immunocompromised individuals, and certain sexually active homosexual men. Cyst passage rates as high as 20% have been reported among certain groups of sexually active homosexual men. These individuals were frequently symptomatic.^11,6

Pathophysiology

The mechanisms by which G intestinalis causes diarrhea and intestinal malabsorption are probably multifactorial and not yet fully elucidated. Although the parasite appears to alter epithelial structure and function, leading to malabsorption, diarrhea can occur in individuals in the absence of obvious light microscopic changes in small intestinal structure. Also, marked or moderate partial villous atrophy in the jejunum can be observed in histologic sections from asymptomatic individuals who are infected. In addition to disrupting the mucosal epithelium, effects in the luminal may contribute to malabsorption and the production of diarrhea.^12,1

G intestinalis trophozoites attach to the epithelium and distort microvilli at the site of attachment. The trophozoite has a convex dorsal surface and a flat ventral surface containing a disk, which is often referred to as the sucking or adhesive disk. The parasite has powerful adhesion, catching, and holding abilities with its disk. In the murine model of giardiasis, the ventral disk adhesion imprints are marked but less impressive than in the human small intestine. However, this direct injury is an unlikely cause of the more extensive reduction in microvillus surface area, the reduction in disaccharidase activities, and the more pronounced abnormalities of villous architecture.^13,14

Varying degrees of malabsorption of sugars (eg, xylose, disaccharides), fats, and fat-soluble vitamins (eg, vitamins A and E) may contribute to substantial weight loss. The histopathologic response to giardiasis varies and imperfectly correlates with the clinical symptoms.^15,7

G intestinalis may release cytopathic substances that damage the intestinal epithelium. Giardia species contain thiol-dependent and thiol-independent proteinases, which may find substrates in the microvillus membrane. In addition, the surface mannose-binding lectin of G intestinalis may contribute to epithelial damage. Whatever the mechanism by which G intestinalis damages villous epithelial cells, the result consistently appears to be an increase in crypt length and crypt cell proliferation.¹⁶

Enterocytic injury is mediated by activated host T lymphocytes. Pathophysiological activation of lymphocytes is secondary to Giardia -induced disruption of epithelial tight junctions, which, in turn, increases intestinal permeability. Loss of epithelial barrier function is a result of Giardia -induced enterocyte apoptosis.^12,17,18

Epithelial barrier dysfunction in cases with chronic giardiasis is associated with increased rates of enterocyte apoptosis. Consistent with these observations, recent findings from microarray analyses on the effects of G intestinalis on human CaCo2 cells found that the parasite–host interactions lead to a pronounced up-regulation of genes implicated in the apoptotic cascade and the formation of reactive oxygen species. Giardia can also prevent the formation of nitric oxide, a compound known to inhibit giardial growth, by consuming local arginine, which effectively removes the substrate needed by enterocytes to produce nitric oxide. This mechanism may contribute to Giardia -induced enterocyte apoptosis because arginine starvation in these cells is known to cause programmed cell death.^13,19

Genotypically diverse isolates of Giardia species may vary in their ability to produce morphologic changes in the small intestine epithelium and to impair fluid, electrolyte, and solute transport.

Frequency

United States

G intestinalis is the parasite most commonly identified in stool specimens. The age-specific prevalence of giardiasis is highest in childhood and adolescence and begins to decline thereafter. Overall, the asymptomatic carriage rate of G intestinalis is estimated to be 3-7%. The asymptomatic carriage rate in children may be as high as 20% in southern regions and in children younger than 36 months who attend daycare centers. Asymptomatic carriage may persist for several months. Many children with giardiasis are symptomatic, have been shown to spread the disease within their homes, and may contribute to high endemic rates in their communities.¹¹

The incidence is high among individuals who camp and backpack in mountainous Western states. Incidences of 30-40% have been reported in Europeans and North Americans traveling to certain parts of the former Soviet Union (1974). In the 46 states reporting giardiasis, the mean number of cases per 100,000 population varies by state, with a range of 0.1-23.5 cases. Most cases are reported between June and October and are associated with the summer recreational water season and camping.²⁰

International

Giardiasis occurs in temperate and tropical regions worldwide and continues to be the most frequently identified human protozoal enteropathogen. In the industrialized world, overall prevalence rates are 2-5%. In the developing world, G intestinalis infects infants early in life. Prevalence rates of 15-20% in children younger than 10 years are common.^9,21

• New Zealand reports more than 30 cases of giardiasis per 100,000 population every year, which is one of the highest among the industrialized countries.²²
• Prevalence rates of 0.94-4.66% and 2.41-10.99% have been reported in Italy.²³
• The highest prevalence of G intestinalis reached 73.4% in Western Nepal.
• In Bangladesh, a disparity between health prevention and health spending is observed. The Dhaka study performed within the urban areas had identified G intestinalis in 11% of diarrheal stool specimens.²⁴

Mortality/Morbidity

Most infected individuals are asymptomatic, and most infections are self-limited. However, chronic infections marked by chronic diarrhea or steatorrhea and malabsorption can occur and may last from weeks to months.^20,25

Death is rare and usually occurs in malnourished children. Giardiasis is not associated with mortality except in cases of extreme dehydration, primarily in infants. Morbidity is moderate and involves primary GI symptoms. G intestinalis has been implicated as the chief cause of growth retardation in infected children, even after other diarrhea-causing agents are controlled.^17,11

Race

No racial predilection is observed.

Sex

Giardiasis is slightly more common in males than in females.²⁶

Age

All ages are affected. Infants and young children have an increased susceptibility to giardiasis, although infection is rare during the first 6 months of life in breastfed infants. Age-specific prevalence of giardiasis continues to rise through infancy and childhood and begins to decline only in adolescence.^25,11

Clinical

History

Most individuals with Giardia intestinalis are probably asymptomatic. Giardiasis produces symptoms more often in children than in adults.²⁰

• The incubation period from the time of ingestion of G intestinalis cysts until the onset of symptoms is 1-2 weeks (average, 8 d).
• Symptoms develop in an estimated 40-80% of infected children.
• Clinical signs and symptoms include the following:^1,2,11
  • Diarrhea
  • Malaise, weakness
  • Abdominal distention
  • Flatulence
  • Abdominal cramps
  • Nausea
  • Malodorous, greasy stools
  • Anorexia
  • Weight loss
  • Vomiting
  • Low-grade fever (infrequent)
  • Various neurologic symptoms (eg, irritability, sleep disorder, mental depression, neuroasthenia)
  • Urticaria

Physical

Physical examination reveals no specific findings, although general abdominal tenderness may be present in children (see History).

Causes

Giardiasis is caused by G intestinalis infection acquired by means of fecal-oral transmission; contaminated water ingestion; or, less commonly, contaminated food ingestion.^27,28

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