Giardia lamblia

Giardia lamblia (synonymous with Lamblia intestinalis and Giardia duodenalis) is a flagellated protozoan parasite that colonises and reproduces in the small intestine, causing giardiasis. The giardia parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission[1]. Giardiasis does not spread via the bloodstream, nor does it spread to other parts of the gastro-intestinal tract, but remains confined to the lumen of the small intestine[2]. Giardia trophozoites absorb their nutrients from the lumen of the small intestine, and are anaerobes.


Giardia affects humans, but is also one of the most common parasites infecting cats, dogs and birds . Mammalian hosts also include cows, beavers, deer, and sheep.

Life cycle

Giardia infection can occur through ingestion of dormant cysts in contaminated water, or by the fecal-oral route (through poor hygiene practices). The Giardia cyst can survive for weeks to months in cold water[3], and therefore can be present in contaminated wells and water systems, and even clean-looking mountain streams, as well as city reservoirs, as the Giardia cysts are resistant to conventional water treatment methods, such as chlorination and ozonolysis.[3] Zoonotic transmission is also possible, and therefore Giardia infection is a concern for people camping in the wilderness or swimming in contaminated streams or lakes, especially the artificial lakes formed by beaver dams (hence the popular name for giardiasis, “Beaver Fever”).

As well as water-borne sources, fecal-oral transmission can also occur, for example in day care centres, where children may have poorer hygiene practices. Those who work with children are also at risk of being infected, as are family members of infected individuals. Not all Giardia infections are symptomatic, so some people can unknowingly serve as carriers of the parasite.

The life cycle begins with a noninfective cyst being excreted with faeces of an infected individual. Once out in the environment, the cyst becomes infective. A distinguishing characteristic of the cyst is 4 nuclei and a retracted cytoplasm. Once ingested by a host, the trophozoite emerges to an active state of feeding and motility. After the feeding stage, the trophozoite undergoes asexual replication through longitudinal binary fission. The resulting trophozoites and cysts then pass through the digestive system in the faeces. While the trophozoites may be found in the faeces, only the cysts are capable of surviving outside of the host.

Distinguishing features of the trophozoites are large karyosomes and lack of peripheral chromatin, giving the two nuclei a halo appearance. Cysts are distinguished by a retracted cytoplasm. This protozoa lacks mitochondria, although the discovery of the presence of mitochodrial remnant organelles in one recent study “indicate that Giardia is not primitively amitochondrial and that it has retained a functional organelle derived from the original mitochondrial endosymbiont”[4]

Manifestation of infection

Nomenclature for Giardia species are difficult, as humans and other animals appear to have morphologically identical parasites.

Colonisation of the gut results in inflammation and villous atrophy, reducing the gut’s absorptive capability. In humans, infection is symptomatic only about 50% of the time, and protocol for treating asymptomatic individuals is controversial.[3] Symptoms of infection include (in order of frequency) diarrhea, malaise, excessive gas (often flatulence or a foul or sulphuric-tasting belch, which has been known to be so nauseating in taste that it can cause the infected person to vomit), steatorrhoea (pale, foul smelling, greasy stools), epigastric pain, bloating, nausea, diminished interest in food, possible (but rare) vomiting which is often violent, and weight loss.[3] Pus, mucus and blood are not commonly present in the stool. In healthy individuals, the condition is usually self-limiting, although the infection can be prolonged in patients who are immunocompromised, or who have decreased gastric acid secretion.[3] People with recurring Giardia infections, particularly those with a lack of IgA, may develop chronic disease. Lactase deficiency may develop in an infection with Giardia, however this usually does not persist for more than a few weeks, and a full recovery is the norm[citation needed].

Cats can be cured easily, lambs usually simply lose weight, but in calves the parasites can be fatal and often are not responsive to antibiotics or electrolytes. Carriers among calves can also be asymptomatic. Dogs have a high infection rate, as 30% of the population under one year old are known to be infected in kennels. The infection is more prevalent in puppies than in adult dogs. This parasite is deadly for chinchillas, so extra care must be taken by providing them with safe water. Infected dogs can be isolated and treated, or the entire pack at a kennel can be treated together regardless. Kennels should also be then cleaned with bleach or other cleaning disinfectants. The grass areas used for exercise should be considered contaminated for at least one month after dogs show signs of infection, as cysts can survive in the environment for long periods of time. Prevention can be achieved by quarantine of infected dogs for at least 20 days and careful management and maintenance of a clean water supply.

Prevention and Treatment

Treatment of drinking water for Giardiais not ordinarily indicated in wilderness regions, including much of the Sierra Nevada and other similar locations in North America.

In many other areas frequented by hikers and campers, as well as places where many residents rely on untreated surface water, reliable prevention may involve filtration and/or chemical disinfection of available surface water, such as chlorination or ozonation.

Normal concentrations of chlorine and ozone used in mass water treatment for most urban areas of the United States may not be adequate to kill all cysts. Giardia cysts are generally present in very small numbers in many such urban water supplies in the United States.

Yet typically these very common and very low concentrations in public water supplies are not a realistic health concern.

Scooping water from the top of a stream or river is not an effective way to avoid Giardia. Filtering (<1µm pore) or boiling is recommended for purification of drinking water from suspect sources.

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.

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.[3] One of the most common alternative treatments is berberine sulfate (found in Oregon grape root, goldenseal, yellowroot, and various other plants).[citation needed] Berberine has been shown to have an antimicrobial and an antipyretic effect.[citation needed] Berberine compounds cause uterine stimulation, and so should be avoided in pregnancy.[citation needed] High doses of berberine can cause bradycardia and hypotension. [5]

Drug Treatment duration Possible Side Effects
Metronidazole 5-7 days Metallic taste; nausea; vomiting; dizziness; headache; disulfiram-like effect; neutropenia
Tinidazole Single dose Metallic taste; nausea; vomiting; belching; dizziness; headache; disulfiram-like effect
Nitazoxanide 3 days Abdominal pain; diarrhea; vomiting; headache; yellow-green discolouration of urine

Table adapted from Huang, White..[3]


Under a normal compound light microscope, Giardia often looks like a “clown face,” with two nuclei outlined by adhesive discs above dark median bodies that form the “mouth.” Cysts are oval, have four nuclei, and have clearly visible axostyles.


Giardia alternates between two different forms — a hardy, dormant cyst that contaminates water or food and an active, disease-causing form that emerges after the parasite is ingested. National Institute of General Medical Sciences grantee Dr. Frances Gillin of the University of California, San Diego and her colleagues cultivated the entire life cycle of this parasite in the laboratory, and identified biochemical cues in the host’s digestive system which trigger Giardia’s life cycle transformations.[6][7] They also uncovered several ways in which the parasite evades the defences of the infected organism. One of these is by altering the proteins on its surface, which confounds the ability of the infected animal’s immune system to detect and combat the parasite (called antigenic variation). Gillin’s work reveals why Giardia infections are extremely persistent and prone to recur. In addition, these insights into Giardias biology and survival techniques may enable scientists to develop better strategies to understand, prevent, and treat giardia infections.


The trophozoite form of Giardia was first observed in 1681 by Antonie van Leeuwenhoek in his own diarrhea stools. In 1915, the parasite was named in honour of Professor A. Giard of Paris. His observations were recreated, using a single lensed microscope of the kind used by Leeuwenhoek, by British microbiologist Brian J. Ford who showed how clearly one could view Giardia through a primitive microscope.[8]

In 1998, a highly publicised Giardia and Cryptosporidium outbreak was reported in Sydney, Australia, but it was found to be due to mis-measurement of the concentrations of microbes in the water supply. A 2004 outbreak in Bergen (Norway) hastened work on adding UV treatment to the water facilities. In October 2007, Giardia was found in the water supply for parts of Oslo, prompting authorities to advise the public to boil drinking water; but subsequent test showed levels of contamination too low to pose a threat, so this advice has since been cancelled.

See also

List of parasites (human)


  1. ^ Oxford textbook of Medicine, Fourth Edition, Volume 1. Oxford University Press pp759-760
  2. ^ Harrison’s Internal Medicine, Harrison’s Online Chapter 199 Protozoal intestinal infections and trochomoniasis
  3. ^ a b c d e f g Huang DB, White AC (2006). “An updated review on Cryptosporidium and Giardia”. Gastroenterol. Clin. North Am. 35 (2): 291-314, viii. doi:10.1016/j.gtc.2006.03.006. PMID 16880067.
  4. ^ Tovar J, León-Avila G, Sánchez LB, et al (2003). “Mitochondrial remnant organelles of Giardia function in iron-sulphur protein maturation”. Nature 426 (6963): 172-6. doi:10.1038/nature01945. PMID 14614504.
  5. ^ UpToDate (Lexi-Comp, Inc.) retrieved 28 August 2007
  6. ^ Hetsko ML, McCaffery JM, Svärd SG, Meng TC, Que X, Gillin FD (1998). “Cellular and transcriptional changes during excystation of Giardia lamblia in vitro“. Exp. Parasitol. 88 (3): 172-83. doi:10.1006/expr.1998.4246. PMID 9562420.
  7. ^ Svärd SG, Meng TC, Hetsko ML, McCaffery JM, Gillin FD (1998). “Differentiation-associated surface antigen variation in the ancient eukaryote Giardia lamblia”. Mol. Microbiol. 30 (5): 979-89. doi:10.1046/j.1365-2958.1998.01125.x. PMID 9988475.
  8. ^ Ford, BJ The discovery of Giardia The Microscope 2005;53(4):148-153.


One response to “Giardia lamblia

  1. makasih ya boz

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