Giardia Lamblia

Author: michele barbera
Date: 11/12/2009



Giardia lamblia was first discovered in 1681 by Antonie van Leeuwenhoek, who found the parasite in his own stools.

For many years, G. lamblia was considered to be of doubtful pathogenicity. Increased awareness of this parasite and appreciation for its clinical significance surfaced in the early 1970s with its recognition in a large percentage of visitors to the Soviet Union who returned with symptomatic giardiasis.
Giardiasis caused by G. lamblia is now recognized as a disease of travelers worldwide, particularly in the developing world.
In the United States, G. lamblia causes intestinal disease in persons drinking contaminated water, in children in day-care centers, and in homosexual males.
G. lamblia is currently the most frequently identified pathogen in all waterborne outbreaks in the United States.
This organism is endemic throughout the world, with the highest prevalence occurring in the tropics and subtropics.



The cysts are non-motile and egg-shaped. They measure 8–14 μm by 7–10 μm. The cysts are encased by a smooth and colorless, thick and refractile wall. Immediately after encystations, newly formed cysts contain two genetically identical nuclei. However, each organelle duplicates so that in permanently stained mature cysts, four prominent nuclei and four median bodies are observed. Compared to trophozoites, cysts also have twice the number of intracytoplasmic flagellar structures. The cysts are the infective form of the parasite and each cyst gives rise to two trophozoites.


Trophozoites are motile and non-infectious because they cannot survive long outside the host body. The trophozoites are pear shaped with a broad anterior end and a narrow posterior end. It is 9–21 μm long and 5–15 μm wide. The parasite is bilaterally symmetrical and dorsoventrally flattened. A large sucking disk, which allows the parasite to attach to the surface of the intestinal mucosa of the host, takes up most of the ventral surface of the parasite. Behind the sucking disks, two rods known as median bodies are seen. Four pairs of flagella are located anterior, lateral, ventral, and posterior on the body of the organism. The pair of anterior flagella, known as axome, is straight, closely approximated and parallel to each other, dividing the body of the organism into two halves longitudinally. Motility brought by the four pairs of flagella is essential for virulence of the parasite. The two spherical or ovoid nuclei, containing a large, central karyosome, can be found on each side of the axonemes. The parasite does not have peripheral chromatin.


Step 1
The life cycle of Giardia alternates between the cyst and the trophozoite forms, and both forms are found in feces. Cysts are more often found in non-diarrheal feces, and they are the infectious stage of the parasite. The cysts are hardy and resistant to standard concentrations of chlorine used in water treatment and they can persist for several months in cold, moist environment.

Step 2
Infection begins when a new host ingests cysts in contaminated food, water, fomites or fecal-orally. Mature cysts are able to survive the acidic environment of the stomach and migrate to the small intestine of the host.

Step 3
Exposure to stomach acid triggers a process called excystation, during which trophozoites are released from cysts. Each quadrinuclear cyst gives rise to two binuclear trophozoites.

Step 4
The trophozoites multiply asexually by binary fission in the small intestine, either as free floating bodies or attached to the intestinal epithelium. Trophozoites are the disease causing stage of the parasite and they colonize the small intestine by attaching to the intestinal mucosa using the ventral sucking disks. Trophozoites are largely noninvasive and do not invade other organs; however, at times they might penetrate down into the secretary tubules of the mucosa and be found in gallbladder and the biliary drainage.

Step 5
As trophozoites migrate toward the large intestine, they retreat into the cyst form in a process called encystation. Bile salts and intestinal mucous were found to enhance trophozoite multiplication and encystations. Trophozoites, if excreted in feces, cannot survive long in the environment and are therefore noninfectious. The cysts in excrements will quickly become infectious and will begin a new cycle of infection if ingested by a naïve host.


G. lamblia is a flagellate within the order Retortomonadida.
The dorsal surface apparently provides an area for diffusion of nutrients. Attachment of the sucking disk to the mucosal surface is
thought to be from negative pressure which develops in the concavity, in association with beating of the flagella. The trophozoites exhibit an erratic tumbling motion described as "falling leaf motility." Trophozoites divide by longitudinal binary fission, and cysts develop as liquid feces gradually dehydrate in transiting the large bowel.
The cysts can survive if kept cool and damp and have been shown to survive in water for up to 3
months. The cysts are ingested with contaminated food or water or are acquired from unwashed hands and pass through the stomach unharmed. Excystation occurs in the duodenum,
and the two trophozoites from each mature cyst establish themselves among the intestinal villi.
G. lamblia inhabits the duodenum and upper jejunum, where the alkaline pH is favorable for growth. Trophozoites firmly attach to the intestinal microvillus surface with their sucking disks or move about free in the lumen; actual invasion of the mucosa and submucosa has been documented
The trophozoites are most often found in liquid or soft stools and the more resistant, infective
cysts are seen in more formed stools.
Giardia trophozoites have been classified into three groups on the basis of morphologic criteria: G. agilis, G. muris, and G. duodenalis. Different strains of G. duodenalis (including G. lamblia) have been typed by using isoenzyme analysis, endonuclease restriction analysis of DNA, and response to in vitro excystation and culture techniques.
These studies suggest that intraspecific variation occurs within this morphologic group. Recognition of isolate differences may also be important in delineating the pathogenesis of infection. Recently, it has been found that human source Giardia isolates produce different patterns
of clinical disease and immune response in their gerbil hosts. In another study using isoelectric focusing of trophozoite protein from 10 human and animal source Giardia isolates, the authors report differences in banding patterns, thus confirming the heterogeneity of this morphological
group of Giardia spp.. Total protein studies have also shown that predictable banding patterns are not seen when strains from human and animal hosts residing in a
limited geographical area are examined.
Comparison of defined trophozoite proteins rather than total cell proteins may be more informative because of the complex banding patterns demonstrated by the latter.


Symptomatology differs from person to person, depending on such factors as inoculum size, duration of infection, and individual host and perhaps parasite factors. The incubation
period generally varies from 9 to 15 days. The acute stage usually begins with a feeling of intestinal uneasiness, followed by nausea and anorexia. Low-grade fever and chills
may also be early symptoms. Subsequent symptoms may include explosive, watery, foul-smelling diarrhea; marked abdominal gurgling and distention associated with the passage of foul gas; and perhaps belching, with a foul taste.
Upper or mid-epigastric cramps may also occur.
Blood and mucus in the stool are rare. The acute stage, which lasts 3 or 4 days, can resemble other causes of traveler's diarrhea and is often not recognized as being due to giardiasis. While most patients experience diarrhea during this time, some of the other symptoms occur less frequently.
Although some acute infection may clear spontaneously, a long-standing subacute or chronic infection may develop.
This phase may involve 2 or more years of intermittent diarrhea. In individuals returning from endemic areas, the acute stage may not be remembered, and these patients can
present with persistent or recurrent mild to moderate symptoms.
During this chronic phase, lassitude, headache, and myalgia may occur with continued weight loss, anorexia, and malabsorption. Chronic infection in children may present as failure to thrive. Urticaria, cholecystitis, and pancreatitis have been reported with Giardia infections. Uncommon associated symptoms including arthritis and retinal arteritis and iridocyclitis have responded to specific anti-Giardia treatment.
As stated by an experienced worker in the field, "the symptomatology of giardiasis is rich and unpredictable; individual variability and the intermittent nature and changing of the symptoms
are characteristic".
Many infections disappear after variable periods of time, and about 13% of infected adults and up to 50% of infected young children remain asymptomatic. The duration of the asymptomatic cyst-passing state has not been determined.
In patients with giardiasis, the hemogram is usually normal and eosinophilia is rare. Malabsorption of fat, glucose, lactose, xylose, vitamin A, and vitamin B12 has been shown in some patients.
Lactose intolerance, frequently present during infection, may persist for variable periods following apparent eradication of giardiasis with specific treatment. Because this symptom often occurs in individuals from ethnic groups who are predisposed to lactose intolerance, the need for further
anti-Giardia treatment must be carefully considered, especially in those with negative post-treatment specimens who have persistent typical giardiasis symptoms.


Giardia lamblia infection in humans is frequently misdiagnosed. Accurate diagnosis requires an antigen test or, if that is unavailable, an ova and parasite examination of stool. Multiple stool examinations are recommended, since the cysts and trophozoites are not shed consistently. Given the difficult nature of testing to find the infection, including many false negatives, some patients should be treated on the basis of empirical evidence; treating based on symptoms.
Human infection is conventionally treated with metronidazole , tinidazole or nitazoxanide.

Although Metronidazole is the current first-line therapy, it is mutagenic in bacteria and carcinogenic in mice, so should be avoided during pregnancy. It has not directly been linked to causing cancer in humans, only in other mammals, therefore appears safe. One of the most common alternative treatments is berberine sulfate (found in Oregon grape root, goldenseal, yellowroot, and various other plants). Berberine has been shown to have an antimicrobial and an antipyretic effect. Berberine compounds cause uterine stimulation, and so should be avoided in pregnancy. Continuously high dosing of berberine may lead to bradycardia and hypotension in some individuals.


Conventional water treatment plants that use coagulationsedimentation- filtration methods are needed to prevent waterborne giardiasis outbreaks. According to a Centers for Disease Control surveillance report on waterborne disease in the United States between 1986 and 1988, Giardia spp. were identified as the causative agent in 9 of 50 outbreaks, the largest of which affected more than 500 people.
Eight outbreaks were associated with deficiencies in community water systems, and six were associated with unfiltered surface water systems in which chlorination was the only treatment. While chlorination alone is often effective in killing most enteric organisms, Giardia cysts may require higher concentrations of chlorine and longer contact times to be inactivated, particularly in cold water.
For individual protection, bringing water to a rolling boil for 1 min destroys Giardia cysts. If boiling is not possible, 2 to 4 drops of household bleach or 0.5 ml of 2% tincture of iodine can be
added to each liter of water and the water can be held for 60 min before drinking. A longer treatment time (overnight) is recommended if the water is cold. Eating hot, cooked
foods helps to prevent ingestion of viable cysts from foods contaminated by infected water or fingers.
Presently, no drugs are available to use for Giardia prophylaxis. Considering the many sources from which giardiasis may be acquired, prophylactic therapy may not be of much value except for travel in highly endemic areas.

In other words, be carefull of what you drink!

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