Jing Liu

Stephanie Nevins

ParaSites Project Final

Winter 2009

 

 

Giardiasis

 

Introduction

 

Giardiasis in humans is called by the infection of the small bowel by a single-celled organism called Giardia lamblia.  Giardiasis occurs worldwide with a prevalence of 20-30% in developing countries.  Additionally, Giardia  has a wide range of human and other mammalian hosts, thus making it very difficult to eliminate.  The CDC reports that Giardia has an infection rate of over 2.5 million annually. 

 

Agent

The disease causing agent of giardiasis in humans is the enteric protozoan parasite Giardia Lamblia.

 

Fig. 1. Giardia trophozoites.

Source: http://www.pathobio.sdu.edu.cn/sdjsc/webteaching/Course/webteach/Protozoan/Giardia-20lamblia/GiardiaTroph(1).jpg

 

Cross Referencing and Synonyms: G. intestinalis, G. duodenalis, Giardiasis, Giardia enteritis, Lambliasis, lamblia intestinalis, "beaver fever”.[1]

 

Taxonomy and Classification of G. lamblia:

Kingdom: Protista

Subkingdom: Protozoa

Phylum: Sarcomastigophora

Subphylum: Mastigophora

Class: Zommastigophora

Order: Diplomonadida

Family: Hexamitidae

Genus: Giardia

Species: lamblia[2]

 

The phylogeny of Giardia is unclear. Because the organisms have simple intracellular structures, they might represent an early branching of eukaryotic lineage that diverges before the acquisition of mitochondria. Elucidating the taxonomy of giardia would significantly aid the understanding of eukaryotic evolution.[3] In addition to G. lamblia, which is the only species found in humans,[5] other species of giardia have been identified. Distinction of giardia on the species level is controversial and difficult because of limited knowledge. Based on morphological difference, six species are named: G. lamblia (affecting a wide range of mammals such as humans and livestock), G. agilis (affect amphibians), G. muris (affect rodents), G. ardeae and G. psittaci (affect birds), and G. microti (affect muskrats and voles). However, forty-one species can be named if species classification is based on host origins.[4] Recently, advances in molecular biology tools such as PCR have helped elucidate the genetic relationships among morphological identical “strains” of Giardia.[5]

 

Discovery History

Antony van Leeuwenhoek of Delft, Netherlands, known as the “father of microbiology”, was the first person to discover G. lamblia in 1681. Leeuwenhoek observed the trophozoite stage parasites in his own watery diarrheal stool under a single-lensed microscope and was able to provide a description of the parasite. In his letter, Leeuwenhoek detailed what he observed in the stool: “I have sometimes also seen tiny creatures moving very prettily; some of them a bit bigger, others a bit less, than a blood-globule but all of one and the same make. Their bodies were somewhat longer than broad, and their belly, which was flattish, furnished with sundry little paws, wherewith they made such a stir in the clear medium and among the globules, that you might even fancy you saw a woodlouse running up against a wall; and albeit they made a quick motion with their paws, yet for all that they made but slow progress.”[6]

 

 

 

 


Fig. 2. Leeuwenhoek’s letter describing G. lamblia trophozoites in his own stool. [6]

 

Fig. 3. Portrait of Leeuwenhoek.

Source: http://timothyministries.org/images/Antoni_van_Leeuwenhoek.png

 

       

Fig. 4. Original drawing by Leeuwenhoek of G. lamblia organisms.

Source: http://www.euronet.nl/users/warnar/bacter.jpg

 

Fig. 5. Leeuwenhoek’s microscope.

Source: http://www.jic.ac.uk/microscopy/images/Leeuwenhoek_microscope.jpg

 

Although Leeuwenhoek was the first person to discover G. lamblia, he was not able to provide an informative illustration of the parasite. Further studies and better illustrations of the morphology of the organism in their intestinal environments were made in 1859 by Vilem Lambl, a Czech physician.[7][8] He also named the organism as Cercomonas intestinalais.[8] Despite his significant contribution, Lambl did not link the diarrheal disease with the giardia parasite, but rather erroneously assumed that the organism is part of the normal, harmless flora of the intestines.[9]

Fig. 6. Portrait of Vilem Lambl.

Source: http://www.stanford.edu/group/parasites/ParaSites2006/Giardiasis/images/lambl.jpg

        

In 1888, Raphael Anatole Emile Blanchard named the parasite Lamblia intestinalis. In 1915, Charles Wardell Stiles, an American Parasitologist, gave the parasite its current name, Giardia lambli, to commemorate the work on giardia by Professor A. Giard in Paris and Dr. Lambl in Praguee.[6]  Charles Wardell Stiles also suspected a link between giardia and diarrhea for the first time. The pathogenicity of giardia was further studied during the First World War, when a large number of soldiers developed diarrhea. Giardia cysts were isolated from their feces and found to cause diarrheal symptoms in laboratory animals.[7] In 1926, a physician in London named Reginald Miller found that giardia causes malabsorption in some children but not in others.[7] The causal link between giardia and the disease was finally and conclusively established in 1954 by Dr. Robert Rendroff of the United States.[7] To elucidate the natural history of giardia, such as the incubation period and the minimal number of cysts needed for infection, Rendroff fed capsules containing known numbers of giardia cysts to prisoner volunteers. The incubation period was shown to be 6 to 15 days, and that as few as 10 to 25 cysts were competent to produce infection. Furthermore, Rendroff observed that some patients were cured of giardia spontaneously without treatment intervention.[10]

 

Today, Giardia continues to affect large populations of people world wide. In developed nations, Giardia infects 2-5% of the population.  In developing countries with poor sanitation and contaminated food or water sources, Giardia may affect up to 20-30% of the population.[11] It is also the most commonly diagnosed enteric parasite in the United States and Canada.

 

Clinical Presentation in Humans

 

A range of clinical syndromes may occur, with gastrointestinal syndromes being the most prevalent. 

 

Gastrointestinal:

A small number of infected individuals experience an abrupt onset of abdominal cramps, explosive, watery diarrhea, vomiting, foul flatus and fever which may last for 3-4 days before proceeding into a more subacute phase.  The majority of infected persons develop gradual symptoms that become recurrent or resistant. [26]

In both the acute and insidious onsets of symptoms, stools become greasy and malodorous but do not contain blood or pus because giardiasis does not involve dysenteric symptoms.  Watery diarrhea may cycle with soft stools and constipation.  Upper GI symptoms including nausea, early satiety, bloating, substernal burning and acid indigestion may be exacerbated by eating and are generally present in the absence of soft stools.  [26]

 

Constitutional:

            The most common constitutional symptoms are anorexia, malaise, and fatigue.  Weight loss affects more than 50% of patients.  Adults with long lasting malabsorption syndrome and children with failure to thrive may experience chronic illness. [26]

 

Additional syndromes may include lactose intolerance and allergic manifestations such as erythema multiforme, bronchospasm, biliary tract disease and urticaria. 

 

Physical:

 

            Abdominal examination may expose nonspecific tenderness even there is no sign of peritoneal irritation.  Rectal examination should expose heme-negative stools and in severe cases, there may be evidence of dehydration. [26]

 

Transmission:

           

            Giardiasis is caused by the ingestion of infective cysts. There are multiple modes of transmission including person-to-person, water-borne, and venereal.  Person-to-person transmission accounts for a majority of Giardia infections and is usually associated with poor hygiene and sanitation.  Water-borne transmission is common in United States Giardia epidemics, which are often associated with the ingestion of unfiltered water (contaminated).  Venereal transmission happens through fecal-oral contamination.  Additionally, diaper changing and inadequate hand washing are risk factors for transmission from infected children.  Lastly, food-borne epidemics of Giardia have developed through the contamination of food by infected food-handlers.  [26]

 

Vector: No vector

 

Reservoir

Giardia affects a wide range of human and mammalian reservoir hosts. Small aquatic or semi-aquatic wild mammals, such as beavers, muskrats, and small rodents harbor water-born cysts of giardia and serve as important reservoir hosts.[12]

Fig. 7. Beavers are important zoonotic reservoir of giardia.

Source: http://animals.nationalgeographic.com/staticfiles/NGS/Shared/StaticFiles/animals/images/primary/beaver.jpg

 

Larger wild animals such as coyotes, grizzly bears, and wolves also harbor the organism.[12] Domestic animals are also important reservoirs for giardia. The parasite was isolated in 22 species of household stocks, ranging from sheep, cows, goats, to ducks.[13] It is also a parasite that commonly affects cats and dogs.

 


Fig. 8. Livestock such as sheep are important reservoirs for giardia.

Source: http://www.nineoaksfarm.net/images/links_sheep.jpg

 

Furthermore, a variety of birds may also serve as reservoirs of giardia.[12] Contaminated water supplies, such as water in rivers and lakes and improperly treated water in developing countries, are also reservoirs of the waterborne cysts.[11] Often, contamination of surface water is caused by rain and wind carrying cysts from fields containing or fertilized by manures of infected humans, livestock, or wild animals to nearby rivers and streams. Giardia cysts can remain viable in surface water for approximately two months.[12] As a result, it is more dangerous for hikers to consume water from rivers and lakes during and immediately after raining seasons as contamination tend to be most severe during these periods. Finally, the organism can often be found in soil, food, and surfaces contaminated with feces containing infectious cysts.[14]

 

Fig. 9. Rivers and lakes often harbor hardy giardia cysts.

Source: http://mongabay.org/images/thai/rocky_creek_02.jpg

 

Incubation Period:

 

Symptoms usually begin 1 to 2 weeks (average 7 days) after an individual becomes infected.  In otherwise healthy individuals, symptoms may last 2 to 6 weeks.  Though symptoms may last longer, medications can help decrease the duration of symptoms. [26]

 

Morphology

Fig. 11. Illustration of giardia trophozoite and cysts.

Source: http://www.stanford.edu/group/parasites/ParaSites2006/Giardiasis/images/giardia%20drawing.jpg

 

Cysts

The cysts are non-motile and egg-shaped. They measure 8-14 mm by 7-10 mm.[18] The cysts are encased by a smooth and colorless, thick and refractile wall.[17] [18] Immediately after encystations, newly formed cysts contain two genetically identical nuclei.[17] However, each organelle duplicates so that in permanently stained mature cysts, four prominent nuclei and four median bodies are observed.[18] Compared to trophozoites, cysts also have twice the number of intracytoplasmic flagellar structures.[18]  The cysts are the infective form of the parasite and each cyst gives rise to two trophozoites.

File written by Adobe Photoshop® 5.2

Fig. 12. Microscopic view of stained cyst. Genetic materials can be clearly seen.

http://www.umanitoba.ca/faculties/science/zoology/faculty/dick/z346/images/giard6.jpg

 

File written by Adobe Photoshop® 5.0

Fig. 13. A group of cysts under microscope.

http://www.vet.uga.edu/VPP/IVM/ENG/Modes/Images/gldic2s.jpg

 

 

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.[18] It is 9-21 mm long and 5-15 mm wide.[18] The parasite is bilaterally symmetrical and dorsoventrally flattened.[18] 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.[17] Behind the sucking disks, two rods known as median bodies are seen.[18] 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.[18] 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.[17][18] The parasite does not have peripheral chromatin.[18]

 

Software: Microsoft Office

Fig. 14. Giardia trophozoite.

Source: http://www.stanford.edu/group/parasites/ParaSites2003/Giardia/GIARDIA2_files/image006.jpg

 

 

Fig. 15. Giardia trophozoite. Intracellular organelles can be seen clearly.

Source: http://www.umanitoba.ca/faculties/science/zoology/faculty/dick/z346/images/giard3.jpg

 

Life Cycle of Giardia[15]

Fig. 10. Life cycle of G. lamblia.

Source: http://www.dpd.cdc.gov/dpdx/HTML/Giardiasis.htm

 

Step 1 in life cycle

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.[15][16]

 

Step 2 in life cycle

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 in life cycle

Exposure to stomach acid triggers a process called excystation, during which trophozoites are released from cysts.[16] Each quadrinuclear cyst gives rise to two binuclear trophozoites.[17]

 

Step 4 in life cycle

The cysts 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.[18]

 

Step 5 in life cycle

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.[16] 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 naēve host.

 

Diagnostic Tests:

 

 

Giardia cysts in a stained fecal preparation

Source: http://pcwww.liv.ac.uk/testapet/Giardia%20ident_7.htm

 

 

 

 

Giardia-Cel IF test: in vitro immunofluorescent test for the detection of Giardia cysts in fecal and environmental samples.

Source: http://www.tcsbiosciences.co.uk/giardia-cel.php

 

 

 

 

Š      String Test:

o   String test (entero-test) involves a gelatin capsule connected to a weighted nylon string.

o   The patient tapes one end of the string to his cheek and then swallows the capsule

o   After the gelatin is dissolved in the stomach, the weight carries the string into the duodenum.

o   The string is left there for 4-6 hours or overnight while the patient fasts.

o   After removal, the string is examined for bilious staining, which identifies successful passage into the duodenum.

o   The mucus from the string is examined for trophozoites in iodine or saline. 

 

 

Giardia lamblia cysts

8-19 Ķm long by 7-10 Ķm wide

Source: http://www.cmpt.ca/images/parasites/giardia_cysts.jpg

 

[26] “Diagnostic Tests” section source

 

Management Therapy

First-line Treatment

Metronidazole (Flagyl)

Adult dosage: 250 mg three times a day for 5 days[19]

Pediatric dosage: 15 mg per kilogram of body weight per dose, 3 times per day, for 5 days[19]

Side effects: Found in 7.1% of cases.[20]  Include unpleasant metallic taste which might cause noncompliance in patients, GI discomfort such as vomiting, nausea, diarrhea, abdominal cramps, pancreatitis, vertigo, headache, CNS toxicity, transient leukemia, dizziness, drowsiness, lassitude, paraethesias, urticaria, and pruritis.[20] It causes mutation in salmonella and induces tumor in rodents,[20] but mutagenicity has never been observed in humans.[21]

Contraindication: Avoid alcohol while taking metronidazole. Metronidazole causes severe vomiting, headache, and GI discomfort by inhibiting aldehyde dehydrogenase, which breaks down alcohol..[21]

Additional drug facts: Metronidazole is a member of the family of nitroimidazoles, commercially known as Flagyl.[20] The tablets are quickly and completely absorbed by the small intestine[21] and found to have antigiardial effects on the trophozoites both in vivo and in vitro.[20] However, it is ineffective against cysts.[20] The drug is able to penetrate body tissues and could be found in saliva, breast milk, semen, and vaginal fluid.[21] It is metabolized in liver and secreted in urine.[21] Metronidazole targets trophozoites by forming active metabolites, which selectively inhibit DNA segregation in anaerobic protozoa such as giardia by DNA breakage and cross-linking.[20] It has minimal effects on host cells lining the intestinal lumen. Resistance is induced in laboratory and is correlated with decreased activity of parasite pyruvate.[21][22]

 

Fig. 16. Molecular structure of metronidazole.[20]

 

Tinidazole (Fasigyn)

Adult dosage: 2 g once[19]

Pediatric dosage: 50 mg per kilogram of body weight once (max. 2 g)[19]

Side effects: Side effects similar to metronidazole[20] but appears to be better tolerated and just as effective.[19] Common side effects include better taste, vertigo, and GI discomfort.[21] The drug should be taken with food to minimize side effects.[19]

Additional drug facts: Tinidazole was FDA approved. It is another member of the nitro-imidazole family. Health care providers recommend travelers (especially those traveling to Asia countries) buy the drug at the country of their destination and take it in an event of giardia infection.[21] The drug tablets can also be crushed and mixed with cherry syrup (Humco and others) for children. The syrup suspension can be kept at room temperature for 7 days and should be shaken before use.[19]

 

Fig. 17. Molecular structure of tinidazole.[20]

 

Nitaxonzanide

Adult dosage: 500 mg two times a day for 3 days

Pediatric dosage: 1-3 yrs: 100 mg every 12 hours for 3 days[19]; 4-11 yrs: 200 mg every 12 hours for 3 days[19]

Side effects: A variety of side effects were reported but they occurred infrequently in all studies.[23] Studies failed to provide sufficiently similar results for a comprehensive analysis of the side effects of nitaxonzanide.[23] Some probable adverse effects include abdominal pain, dyspepsia, constipation, yellow discoloration of urine, dysuria and dry mouth, and dizziness.[23] The drug should be taken with food to minimize adverse effects.[19]

Additional drug facts: Nitazonxanide is FDA-approved as an oral suspension for treatment of giardiasis. It can be purchased in 500-mg tablets and in oral suspension.[19]

Fig. 18. ZimdaX-DT, containing nitazoxanide tablets.

Source: http://www.usvindia.com/i/zim.jpg

 

Alternative Treatment

Paromomycin (Humatin)

Adult dosage: 25-35 mg per kilogram of body weight per dose, 3 doses per day for 7 days[19]

Pediatric dosage: 25-35 mg per kilogram of body weight per dose, 3 doses per day for 7 days[19]

Side effects: ototoxicity and nephrotoxicity with systemic administration[21]

Contraindication: Patients with impaired kidney function should use paramomycin with caution[21]

Additional drug facts: Paramomycin is a member of the aminoglycoside family.[20] It inhibits giardia protein synthesis by targeting the 50S and 30S ribosomal subunits.[21] Its activity in vitro is lower than nitroimidazoles; however, because it is poorly absorbed by small intestine, a higher concentration of the drug remains in the lumen to combat giadia organisms.[21] It is also the choice of drug to treat G. lamblia in resistant infection and during pregnancy.[21]

 

Fig. 19. Molecular structure of paramomycin.[20]

 

Furazolidone (Furoxone)

Adult dosage: 100 mg four times a day for 7-10 days[19]

Pediatric dosage: 6 mg per kilogram of body weight per dose, 4 doses per day for 7-10 days[19]

Side effects: Gastrointestinal symptoms (nausea, vomiting, diarrhea) are observed in 10% of patients. Other side effects include brown discoloration of urine, and hemolysis in G6PDH-deficinet patients.[21]

Additional drug facts: it is a member of the nitrofuran family[20] penetrate body tissues and could be found in saliva, breast milk, semen and vaginal fluid.[21] Not recommended to treating pregnant patients because it has been shown to cause mammary tumor in rats and mutations in bacteria.[21]

 

Fig. 20. Molecular structure of furazolidone.[20]

 

Quinacrine

Adult dosage: 100 mg three times a day for 5 days[19]

Pediatric dosage: 2 mg per kilogram of body weight, three times per day for 5 days (max. 300 mg/d)[19]

Side effects: bitter taste and vomiting observed in 28% of study participants; yellow/orange discoloration of the skin, sclerae, and urine. Other common side effects include nausea, vomiting, headache, dizziness and fever. Drug induced psychosis has been observed but is very rare. Dermatitis and drug-induced retinopathy are also uncommon.[21] The drug also acts with lower efficacy in children because the drug has bitter taste and children are less compliant.[21]

Contraindication: Pregnant patients should avoid taking the drug because quinacrine can cross placenta and it might cause spina bifida and renal agenesis in the infant.[21]

Additional drug facts: The drug, unlike metronidazole, also target _____cysts_________.

This drug cannot be purchased commercially, but as a service can be made by Panorama Compounding Pharmacy, 6744 Balboa Blvd, Van Nuys, CA  91406 (800-247-9767) or Medical Center Pharmacy, New Haven, CT (203-688-6816).    

Albendazole (Albenza)

Adult dosage: 400 mg once a day for 5 days[21]

Pediatric dosage: 15 mg per kilogram of body weight per day for 5 to 7 days (max. 400 mg)[21]

Mebendazole (Vermox)

Adult dosage: 200-400 mg per day for 5 to 10 days[21]

Side effects for Albendazole and Mebendazole: common side effects include anorexia and constipation. Rare side effects include reversible neutropenia and elevated liver function tests.  Whether they are terotogenic is unclear[21]

Contraindication of Albendazole and Mebendazole: Albendazole should be taken with caution for pregnant patients because there is a possibility that it might induce tumors. However, animal studies did not reveal increased incidences of cancer.[21]

Additional drug facts: Albendazole and Mebendazole are members of the benzimidazole family.  They target G. lamblia by binding to b-tubulin and stopping cytoskeletal formation.  It also interferes with glucose uptake of the organism.[21]

 

Fig. 21. Molecular structures of (a) Mebendazole and (b) Albendazole.[20]

 

Special Circumstances in Management Therapy

 

A. Drug Use During Pregnancy and Lactation:

Pregnant patients who are infected but asymptomatic are advised not to receive treatment for giardia because there are underlying risks in current therapies.[21] For instance, metronidazole is rapidly absorbed and easily enters fetal circulation. Studies have shown mixed results regarding the adverse effects of metronidazole on the development of the fetus. One retrospective study involving 1469 women who took Metronidazole during the first trimester of pregnancy showed no adverse effects on the fetus.[24] However, in the Collaborative Perinatal Project with over 50,000 mother-child pairs, the infants of 31 mothers who took metronidazole during the first trimester of pregnancy were found to developed drug-associated malformation.[25]

 

Paramomycin is the choice of drug for treating pregnant women infected with giardia because it is poorly absorbed by the mother and excreted almost 100% in feces; hardly any of the drugs would reach the fetus.[21]

 

Treating Asymptomatic Infections

Management of asymptomatic infections is at the center of debate. In endemic areas, treating asymptomatic patients might not be efficient because they are likely to become quickly re-infected. However, treatment might be desirable for children who experienced growth retardation to allow for catch up growth.[21] However, asymptomatic infections in people with small chances of being re-infected (such as returning travelers) and who have high chances of transmitting the disease to naēve hosts (such as food handlers) should be treated[21] to stop spread of disease in the population.

 

Treating Drug Resistant Patients

Giardia parasites have developed resistance to all of the common anti-giardial drugs, such as metronidazole, quinacrine, and albendazole.[21] Additionally, according to Dr. Upi Singh, a physician and Giardia specialist at Stanford Medical Center, drug resistance in lab isolates have been developed and used for studies. Fortunately, clinical drug resistance is minimal.[22] Often times, diarrhea due to post-giardial lactose intolerance can be confused with treatment failure due to drug resistance. In such cases, physicians must examine the stool of the patients to rule out the presence of giardia organisms.[21] Treatment for truly resistant strains consists of three options: 1) treating with the original drug for a longer period of time or at higher doses; 2) using a drug from a different class to treat the resistant infection—the most efficacious approach, avoiding potential cross-resistance; and 3) using a combination of different classes of drugs, such as metronidazole-albendazole and metronidazole-quinacrine.[21]

 

Epidemiology:

 

            Prevalence rates for giardiasis range from 20-30% in most developing countries and 2-7% in developed countries. The CDC estimates that there are more than 2.5 million cases of giardiasis annually.  Giardiasis occurs worldwide with increased prevalence in areas with poor water treatment facilities and unsanitary conditions. The area of highest prevalence is the tropics and subtropics.  Despite this, giardiasis does affect a large number of individuals living in highly developed nations with strong infrastructure and water systems.  In the United States, giardiasis is the most commonly reported pathogenic protozoan disease. [27]

            High infection rates occur in hikers and backpackers in the United States.  Giardiasis is a common infection in active outdoors population because of their exposure to areas inhabited by infected wild animals and ingestion of free flowing water which may contain cysts.  Furthermore, giardiasis is common in tourists and business travelers to developing countries, especially Mexico, Southeast Asia, western South America and the Soviet Union. [28]  An increased prevalence of giardiasis among homosexual men has been reported by a number of studies. [29]  Lastly, because infection may be caused by poor hygiene, giardiasis has high infection rates in daycare centers and nursing homes, though the groups most at risk for infection are overseas travelers and hikers. [30]

 

In the United States, many of the reported cases of Giardia occur in the summer months.  Why is this? According to virologist and epidemiologist Dr. Donald Francis, first, this is the time when hikers and backpackers are avid because of the ideal climate during these months.  Also, this may be due to the use of community swimming areas by young diaper-aged children during the summer. 

 

 

                                    Giardia Incidence, 2002 [32]

 

 

 

 

 

Public Health and Prevention Strategies/Vaccines:

 

            Currently, there is no vaccine to protect humans from acquiring giardiasis.  Thus, various public health and prevention strategies should be taken to decrease risk of infection.

First and foremost, avoid contaminated water.  Hikers and overseas travelers to developing countries should consider all water sources contaminated and thus boil, filter, or treat all water with halogenated tablets or solutions. 

Second, avoid foods washed in contaminated water or that cannot be cooked or peeled, which is especially important for travelers to developing countries.  Using only bottled water and avoiding raw fruits and vegetables decreases risk of infection dramatically. [33]

            Third, wash hands frequently, especially before eating and after using the bathroom, with soap and water for at least 15 seconds.   Similarly, wash children with soap and water after diaper changes and before getting back into water (pool, lake, etc.) 

            Fourth, avoid swallowing water in swimming pools and spas.  Since public pools are not always adequately treated, they act as a potential source of Giardia contamination.  [34]

            Ultimately, practice good hygiene including avoiding contact with the feces of an infected person.  Being aware of this helps to prevent spread of the infection.

 

 

Useful Web Links:

 

eMedicine Health- Giardiasis

http://www.emedicinehealth.com/giardiasis/article_em.htm

 

Giardiasis

http://www.giardiasis.org/Index.aspx

 

http://www.bbc.co.uk/health/conditions/giardiasis1.shtml

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Works Cited

 

 

1.             Giardia lamblia - Material Safety Data Sheets (MSDS). http://www.phac-aspc.gc.ca/msds-ftss/msds71e-eng.php Retrieved on 2009-02-24.

 

2.             Taxonomical Classification. https://www.msu.edu/course/zol/316/glamtax.htm Retrieved on 2009-02-24.

 

3.             Thompson, R.C.A. and Monis, P.T. (2004). Variation in Giardia: Implications for Taxonomy and Epidemiology. Adv. Parasitol. 58: 69-137. doi:10.1016/S0065-308X(04)58002-8.

 

4.             Triosephosphate Isomerase Gene Characterization and Potential Zoonotic Transmission of Giardia duodenalis. http://www.cdc.gov/ncidod/EID/vol9no11/03-0084.htm Retrieved on 2009-02-24.

 

5.             Thompson, R.C.A. (2008). Giardiasis: Modern Concepts in Control and Management. Ann Nestlé 66: 23-29. doi:10.1159/000113306.

 

6.             Ford, B.J. (2005). The Discovery of Giardia. Microscope 53(4): 147-153.

 

7.             Cox, F.E.G. (2002). History of Human Parasitology. Clin. Microbiol. Rev. 15(4): 595-612. doi:10.1128/CMR.15.4.595-612.2002.

 

8.             Smith, H.V. and Paget, T. (2007). “11. Giardia.” Infectious Disease: Foodborne Diseases. Humana Press Inc. doi:10.1007/978-1-59745-501-5_11.

 

9.             Giardiasis. http://www.bbc.co.uk/health/conditions/giardiasis1.shtml Retrieved on 2009-02-24.

 

10.          Rendtorff, R.C. (1954). The experimental transmission of human intestinal protozoan parasites. II. Giardia lamblia cysts given in capsules. Am. J. Hyg. 59(2): 209-220.

 

11.          Giardiasis. http://www.emedicinehealth.com/giardiasis/article_em.htm Retrieved on 2009-02-24.

 

12.          Baker, J.R. (2007). Advances in Parasitology. Elsevier Science & Technology Books. p. 131.

 

13.          Sullivan, P.S., DuPont, H.L., Arafat, R.R., Thornton, S.A., Selwyn B.J., El Alamy, M.A., Zaki. A.M. (1988). Illness and reservoirs associated with Giardia lamblia infection in rural Egypt: The case against treatment in developing world environment of high endemicity. Am. J. Epidemiol. 127(6): 1272-1281.

 

14.          Giardiasis. http://diseases.emedtv.com/giardiasis/giardiasis.html Retrieved on 2009-02-24.

 

15.          Giardiasis. http://www.dpd.cdc.gov/dpdx/HTML/Giardiasis.htm Retrieved on 2009-02-24.

 

16.          Giardiasis (Giardia) Fact Sheet. http://www.missionpharmacal.com/Press/Fact_Sheets/Fact-TIN-Giardiasis.aspx Retrieved on 2009-02-24.

 

17.          Intestinal Giardiasis. http://www.addl.purdue.edu/newsletters/2002/summer/igiardiasis.shtml Retrieved on 2009-02-24.

 

18.          John, D.T. and Petri, W.A. (2006). Markell and Voge’s Medical Parasitology (9 ed.). Philadelphia: W. B. Saunders. p. 49.

 

19.          “Drugs for Parasitic Infection” (PDF). http://www.medletter.com/freedocs/parasitic.pdf The Medical Letter, 2004.

 

20.          Harris, J.C., Plummer, S., Lloyd, D. (2001). Antigiardial drugs. Appl. Microbiol. Biotechnol. 57: 614-619. doi:10.1007/s00230100720.

 

21.          Gardner, T.B. and Hill, D.R. (2001). Treatment of Giardiasis. Clin. Microbiol. Rev. 14(1): 114-128. doi:10.1128/CMR.14.1.114-128.2001.

 

22.          Singh, Upi. “Insert title here.” Email from the author. # Feb 2009.

 

23.          Abubakar, I., Aliyu, S.H., Arumugam, C., Usman, N.K., Hunter, P.R. (2007). Treatment of cryptosporidiosis in immunocompromised individuals: systematic review and meta-analysis. Br. J. Clin. Pharmacol. 63(4): 387-393. doi:10.1111/j.1365-2125.2007.02873.x.

 

24.          Berget, A. and Weber, T. (1972). Metronidazole and pregnancy. Ugeskr Laeger. 134(40): 2085-2089.

 

25.          Heinonen, O. P., Slone, D., Shapiro, S. (1977). “Birth Defects and Drugs in Pregnancy”. Littleton: Publishing Sciences Group. pp. 296-302.

 

26. Pennardt, MD, Andre. "Giardiasis." EMedicine. 4 Feb. 2004. 20 Feb. 2009 <http://www.emedicine.com/EMERG/topic215.htm>.

 

27. "Giardiasis." Giardiasis.org. <http://www.giardiasis.org/Prevalence.aspx>.

 

28. Brodsky RE, Spencer HC Jr, Schultz MG. Giardiasis in American travelers to the Soviet Union. J Infect Dis. 1974 Sep;130(3):319-23.

 

29. Peters CS, Sable R, Janda WM, Chittom AL, Kocka FE. Prevalence of enteric parasites in homosexual patients attending an outpatient clinic. J Clin Microbiol. 1986 Oct;24(4):684-5.

 

30. Schrader, MD, Betsy. "Giardiasis." EMedicine Health. 10 Aug. 2005. 26 Feb. 2009 <http://www.emedicinehealth.com/giardiasis/article_em.htm>.

 

31. Schrader, MD, Betsy. "Giardiasis Prevention." EMedicine Health. 10 Aug. 2005. 26 Feb. 2009 <http://www.emedicinehealth.com/giardiasis/page9_em.htm#Prevention>.

 

32. Hlavsa MC, Watson JC, Beach MJ. Giardiasis surveillance--United States, 1998-2002. MMWR Surveill Summ. 2005 Jan 28;54(1):9-16.

                                                                                                                              

33. Schrader, MD, Betsy. "Giardiasis Prevention." EMedicine Health. 10 Aug. 2005. 26 Feb. 2009 <http://www.emedicinehealth.com/giardiasis/page9_em.htm#Prevention>.

 

34. "Giardiasis." Giardiasis.org. <http://www.giardiasis.org/Prevention.aspx>.