Giardiasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Giardiasis is a common enteric infectio caused by Giardia lamblia, a flagellated protozoan parasite. It is a worldwide infection that is common in settings of poor sanitation. Giardiasis may be classified based on the duration of clinical manifestations into either acute (2-4 weeks) or chronic (more than 4 weeks). Common risk factors in the development of giardiasis include recent history of hiking and camping, immunosuppression, young age (especially < 5 years of age), exposure to infected individuals, drinking unsafe water, recent sexual history with unprotected anal or oral-anal contact, and recent travel to developing countries. Giardia is usually transmitted via the fecal-oral route through personal contact and contaminated water and food. Following transmission of Giardia, patients may remain asymptomatic for 1-3 weeks. Early symptoms typically include acute, profuse, watery diarrhea, bloating, and abdominal cramping, which are usually self-limited. If left untreated, giardiasis may persist in a small proportion of patients and subsequently results in chronic giardiasis, which typically manifests with chronic diarrhea, anorexia, weight loss, malaise, and failure to thrive. Complications may be related to either severe dehydration (e.g. acute kidney injury), malabsorption (e.g. vitamin B12 deficiency), post-infectious diseases (e.g. reactive arthritis, chronic fatigue syndrome), or rarely, spread of Giardia to extraluminal sites (e.g. involvement of the gallbladder, pancreas, or eyes). The prognosis is generally excellent. Recurrence of the disease is particularly common among children even with optimal treatment. The diagnosis of giardiasis requires the detection of Giardia parasites in at least 1 out of 3 stool samples upon ova and parasite examination. Multiple stool collections (i.e., three stool specimens collected on separate days) should be performed for ova and parasite examination (O & P) to increase test sensitivity since Giardia cysts are excreted intermittently (detects approximately 80% of cases). Patients diagnosed with giardiasis require antimicrobial therapy. Medical therapy for giardiasis includes either metronidazole, albendazole or quinacrine. Furazolidone or nitazoxanide may be used in pediatric patients. Patients must be monitored for the persistence of symptoms following adequate therapy (suggestive of treatment failure) or the re-development of symptoms (recurrence). There is no vaccine against giardiasis. Prophylaxis against giardiasis is not recommended. Hygiene practices (such as hand washing, drinking safe water) may help reduce the risk of Giardia transmission.

The trophozoite form of Giardia was first observed in 1681 by Antoni van Leeuwenhoek in his own diarrheal stools. Giardia was initially named Cercomonas intestinalis by Lambl in 1859. It was then renamed Giardia lamblia by Stiles in 1915 in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague.^[1]

Giardiasis may be classified based on the duration of clinical manifestations into either acute (2-4 weeks) or chronic (more than 4 weeks).

Giardia is usually transmitted via the fecal-oral route through personal contact and contaminated water and food. Giardia is a zoonotic infection that may also transmitted from animals to humans. Major reservoir hosts include beavers, dogs, cats, horses, and cattle. Following transmission, Giardia colonizes the human intestine and attaches to the epithelium by a ventral adhesive disc. The mechanism of pathogenesis of Giardia is thought to include increased pro-apoptotic processes, subsequent loss of intestinal epithelial barrier, hypersecretion of electrolytes, and increased exposure to luminal antigens to subepithelial host immune cells. It is thought lymphocyte activation, particularly CD8+ T-cells, results in local inflammation, as well as diffuse shortening of microvilli (without villous atrophy). Dysfunctional microvilli are then unable to absorb luminal nutrients, resulting in the development and worsening of clinical manifestations of giardiasis.

Giardiasis is caused by Giardia lamblia (synonymous with Lamblia intestinalis and Giardia duodenalis), a flagellated protozoan parasite.

Giardiasis must be differentiated from other causes of abdominal pain, bloating, acute or chronic diarrhea, and weight loss, such as other infectious causes of gastroenteritis, including bacterial, viral, fungal, and parasitic pathogens, in addition to non-infectious causes, including acute pancreatitis, appendicitis, bowel obstruction, diverticulitis, drug reaction, hyperthyroidism, inflammatory bowel disease, celiac disease, lactose intolerance, Whipple disease, tropical sprue, and lymphoma.

Giardiasis is a worldwide infection. It is the most common cause of parasitic diarrhea with a prevalence that may be as high as 20% to 40% in settings of poor sanitation. In the USA, the incidence of giardiasis is thought to be decreasing from 20 to 25 cases per 100,000 individuals between 1990 and 1998 to approximately 4 to 5 cases per 100,000 individuals in 2012. Children, particularly < 5 years of age, are more frequently affected with giardiasis than adults. There is no gender or racial predilection for the development of giardiasis.

Risk factors in the development of giardiasis include recent history of hiking and camping, immunosuppression, young age (especially < 5 years of age), exposure to infected individuals, drinking unsafe water, recent sexual history with unprotected anal or oral-anal contact, and recent travel to developing countries.

Following transmission of Giardia, patients may remain asymptomatic for 1-3 weeks. Early symptoms typically include acute, watery diarrhea, bloating, and abdominal cramping, which are usually self-limited. If left untreated, giardiasis may persist in a small proportion of patients and subsequently results in chronic giardiasis. Complications may be related to either severe dehydration (e.g. acute kidney injury), malabsorption (e.g. vitamin B12 deficiency), post-infectious diseases (e.g. reactive arthritis, chronic fatigue syndrome), or spread of Giardia to extraluminal sites (e.g. involvement of the gallbladder, pancreas, or eyes). The prognosis is generally excellent. Recurrence of disease is common among children even with optimal treatment.

Symptoms of acute giardiasis include watery diarrhea, steatorrhea, bloating,abdominal pain, indigestion, flatulence, and vomiting. Symptoms of chronic giardiasis include anorexia, weight loss, malaise, and failure to thrive. Less common symptoms of giardiasis include low-grade, intermittent fever, symptoms of allergic reaction, and neurologic symptoms (neurasthenia, sleep disorder, depression).

Physical examination among patients with giardiasis is usually unremarkable. In the acute phase, patients with giardiasis often appear sick-looking. In the chronic phase, patients with giardiasis often appear malnourished with significant weight loss. Physical examination findings may include low-grade fever, dry mucus membranes (dehydration), and abdominal distention and tenderness.

The diagnosis of giardiasis requires the detection of Giardia in at least 1 out of 3 stool samples upon ova and parasite examination. Multiple stool collections (i.e., three stool specimens collected on separate days) should be performed for ova and parasite examination (O & P) to increase test sensitivity since Giardia cysts are excreted intermittently (detection of approximately 80% of cases). Blood samples are usually unremarkable. Fecal immunoassays may also be used for the diagnosis of Giardia if stool collections were negative and giardiasis is still suspected. Only molecular testing, such as polymerase chain reaction techniques, can be used to identify the subtypes of Giardia. Blood samples are usually unremarkable.

No other tests are required for the diagnosis of giardiasis. Other diagnostic studies may include the entero-test (string test), D-xylose absorption test for patients with giardiasis-related vitamin B12 deficiency, and esophagogastroduodenoscopy with small bowel biopsy for patients who are suspected to have giardiasis despite negative lab findings or patients who remain symptomatic after adequate therapy.

Patients diagnosed with giardiasis require antimicrobial therapy. Medical therapy for giardiasis includes either metronidazole, albendazole or quinacrine. Furazolidone or nitazoxanide may be used in pediatric patients. Patients must be monitored for the persistence of symptoms following adequate therapy (suggestive of treatment failure) or the re-development of symptoms (recurrence).

There is no vaccine against giardiasis. Prophylaxis against giardiasis is not recommended. Hygiene practices (such as hand washing, drinking safe water) may help reduce the risk of Giardia transmission.

Template:Protozoal diseases

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The trophozoite form of Giardia was first observed in 1681 by Antoni van Leeuwenhoek in his own diarrheal stools. Giardia was initially named Cercomonas intestinalis by Lambl in 1859. It was then renamed Giardia lamblia by Stiles in 1915 in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague.^[1]

• The trophozoite form of Giardia was first observed in 1681 by Antoni van Leeuwenhoek in his own diarrheal stools.
• Giardia was initially named Cercomonas intestinalis by Lambl in 1859.^[1]
• It was then renamed Giardia lamblia by Stiles in 1915 in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague.^[1]

Template:Protozoal diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Giardiasis may be classified based on the duration of clinical manifestations into either acute (2-4 weeks) or chronic (more than 4 weeks).

Giardiasis may be classified based on the duration of clinical manifestations into:

• Acute (less than 2-4 weeks of symptoms)
• Chronic (more than 4 weeks of symptoms)

Template:Protozoal diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Giardia is usually transmitted via the fecal-oral route through personal contact and contaminated water and food. Giardia is a zoonotic infection that may also transmitted from animals to humans. Major reservoir hosts include beavers, dogs, cats, horses, and cattle. Following transmission, Giardia colonizes the human intestine and attaches to the epithelium by a ventral adhesive disc. The mechanism of pathogenesis of Giardia is thought to include increased pro-apoptotic processes, subsequent loss of intestinal epithelial barrier, hypersecretion of electrolytes, and increased exposure to luminal antigens to subepithelial host immune cells. It is thought lymphocyte activation, particularly CD8+ T-cells, results in local inflammation, as well as diffuse shortening of microvilli (without villous atrophy). Dysfunctional microvilli are then unable to absorb luminal nutrients, resulting in the development and worsening of clinical manifestations of giardiasis.

• Giardia is usually transmitted via the fecal-oral route through personal contact and contaminated water and food.
• Giardia is also thought to be a zoonotic infection (unconfirmed association) that may also transmitted from animals to humans. Major reservoir hosts include beavers, dogs, cats, horses, and cattle.

• Following transmission, Giardia colonizes the human intestine.
• Giardia attaches to the epithelium by a ventral adhesive disc.

• It is thought that Giardia induces caspase-mediated enterocytic apopotosis and results in the impairment of cellular tight junction integrity.^[1][2][3]
• The following mechanisms are altered among patients with giardiasis:

• Increased concentration of reactive oxygen species
• Reduced concentration of nitric oxide, which normally inhibits growth of Giardia
• Down-regulation of anti-apoptotic proteins (e.g. Bcl-2)
• Up-regulation of pro-apoptotic proteins (e.g. Bax)

• Enterocyte apoptosis results in the loss of the intestinal epithelial barrier and subsequent increased permeability.^[4][5][6][3]
• Accordingly, subepithelial host immune cells are more likely to be activated by antigens located in the intestinal lumen.
• The increased susceptibility of subepithelial immune activation, particularly CD8+ T-cells, results in local inflammation and the retraction of the of the microvilli of the small intestine (shortening of the intestinal brush border).

• Despite the absence of villus atrophy, giardiasis-mediated immune cell activation results in intestinal malabsorption through the process of diffuse microvilli shortening, whereby microvilli are unable to absorb nutrients in the intestinal lumen.^{[6][7][8][9][3]}
• In addition, electrolytes are hypersecreted (e.g. chloride hypersecretion), resulting in fluid accumulation in the intestinal lumen and development of clinical manifestations (i.e. watery diarrhea).^[6][3]

Template:Protozoal diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Giardia lamblia (synonymous with Lamblia intestinalis and Giardia duodenalis) is a flagellated protozoan parasite that is responsible for the development of giardiasis.

Eukaryota, Diplomonadida group, Diplomonadida, Hexamitidae, Giardiinae, Giardia, G. lamblia

• Giardia affects humans and animals, such as cats, dogs, cows, beavers, deer, and sheep.

• Giardia lamblia is a flagellated, microaerophilic parasite.
• The trophozoite form of G. lamblia is pear-shaped and has a unique morphology that includes two identical nuclei, a ventral disc for adhesion to the host intestine, and flagella.

• G. lamblia genome consists of 1.2 million base pairs (average GC content: 46%).^[1]
• The genome pairs are distributed across five linear chromosomes.^[1]
• Similar to other eukaryotes, each chromosome is flanked by the telomere sequence (5’TAGGG3’).^[1]

Giardia belongs among the diplomonads.

• 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 feces.
• While the trophozoites may be found in the feces, 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.

• 
  SEM depicts the dorsal surface of a Giardia protozoan, isolated from a rat’s intestine. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts the mucosal surface of the small intestine of a gerbil infested with Giardia sp. protozoa. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts a Giardia lamblia protozoan in a late stage of cell division that was about to become two separate organisms, producing a heart-shaped form. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts the ventral surface of a Giardia muris trophozoite. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts dorsal surface of a Giardia protozoan, isolated from a rat’s intestine. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts some of the ultrastructural morphologic details of an oblong-shaped Giardia sp. protozoan cyst. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts the ventral surface of a Giardia muris trophozoite that had settled atop the mucosal surface of a rat’s intestine. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts a Giardia lamblia protozoan that was about to become two separate organisms, as it was caught in a late stage of cell division. From Public Health Image Library (PHIL). ^[2]
• 
  SEM depicts a Giardia muris protozoan adhering itself to the microvillous border of an intestinal epithelial cell. From Public Health Image Library (PHIL). ^[2]
• 
  This photomicrograph depicts Giardia lamblia parasites using indirect immunofluorescence test for giardiasis. From Public Health Image Library (PHIL). ^[2]

Giardia lamblia infection must be differentiated from other causes of viral, bacterial, and parasitic gastroentritis.

8Small bowel diarrhea: watery, voluminous with less than 5 WBC/high power field

Large bowel diarrhea: Mucousy and/or bloody with less volume and more than 10 WBC/high power field
† It could be as high as 1000 based on patient’s immunity system.

The table below summarizes the findings that differentiate inflammatory causes of chronic diarrhea^{[3][4][5][6][6]}

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Giardiasis must be differentiated from other causes of abdominal pain, bloating, acute or chronic diarrhea, and weight loss, such as other infectious causes of gastroenteritis, including bacterial, viral, fungal, and parasitic pathogens, in addition to non-infectious causes, including acute pancreatitis, appendicitis, bowel obstruction, diverticulitis, drug reaction, hyperthyroidism, inflammatory bowel disease, celiac disease, lactose intolerance, Whipple disease, tropical sprue, and lymphoma.

• Giardiasis must be differentiated from other causes of acute or chronic diarrhea, bloating, abdominal pain, and fever (less common).
• Differential diagnosis of giardiasis includes the following:

• Bacterial infections (e.g. E. coli infection, shigellosis, salmonellosis, C. jejuni infection)
• Viral infections (e.g. norovirus, rotavirus, astrovirus, HIV)
• Fungal infections (e.g. Candida spp.)
• Parasites (E. histolytica, Cryptosporidium spp., Cyclospora)

The following are the non-infectious differential diagnoses of E. coli enteritis:

• Acute pancreatitis
• Adrenal insufficiency and Waterhouse-Friedrichsen syndrome
• Allergy (e.g. insect bite allergy or anaphylaxis)
• Appendicitis
• Bowel obstruction
• Celiac disease
• Diverticulitis
• Drug reaction (e.g. antimicrobial agents, antihypertensive therapy, chemotherapy, anticonvulsants)
• Endometriosis
• Familial Mediterranean fever
• Gastrointestinal perforation
• Hyperthyroidism
• Ileus
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis)
• Intussusception
• Ischemic colitis
• Ketoacidosis
• Lactose intolerance
• Lymphoma
• Mesenteric ischemia
• Necrotizing enterocolitis
• Ogilvie syndrome
• Peritonitis
• Pneumonia
• Poisoning and toxicity (e.g. carbon monoxide poisoning, organophosphate poisoning, digitoxin toxicity)
• Ruptured abdominal aortic aneurysm
• Spider bite
• Tropical sprue
• Volvulus
• Urinary tract infection
• Whipple disease

To view a comprehensive list of abdominal pain differential diagnoses, click here.
To view a comprehensive list of diarrhea differential diagnoses, click here.

Giardiasis must be differentiated from other diseases that may cause chronic diarrhea, weight loss, and abdominal pain especially in immunocompromised patients.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Giardiasis is a worldwide infection. It is the most common cause of parasitic diarrhea with a prevalence that may be as high as 20% to 40% in settings of poor sanitation. In the USA, the incidence of giardiasis is thought to be decreasing from 20 to 25 cases per 100,000 individuals between 1990 and 1998 to approximately 4 to 5 cases per 100,000 individuals in 2012. Children, particularly < 5 years of age, are more frequently affected with giardiasis than adults. There is no gender or racial predilection for the development of giardiasis.

• Giardiasis is a worldwide infection. It is the most common cause of parasitic diarrhea.^[1]
• In the USA, the incidence of giardiasis is thought to be decreaesing. In 2012, the incidence of giardiasis was approximately 4 to 5 cases per 100,000 individuals in the USA, compared with 20 to 25 cases per 100,000 individuals between 1990 and 1998.^[2][3]
• The prevalence of giardiasis is highly variable. In settings with poor sanitation, the prevalence of giardiasis may be as high as 40%.^[1]

• Children, particularly < 5 years of age, are more frequently affected with giardiasis than adults.

• There is no gender predilection for the development of giardiasis.

• There is no racial predilection for the development of giardiasis.

• In developed countries, the incidence of giardiasis is decreasing.
• The decrease is attributed to improved sanitation and available resources.

• The majority of cases of giardiasis occur in developing countries, where the prevalence may be as high as 20% to 40% in settings of poor sanitation.^[1]

Template:Protozoal diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Yazan Daaboul, M.D.; Serge Korjian M.D.

Risk factors in the development of giardiasis include recent history of hiking and camping, immunosuppression, young age (especially < 5 years of age), exposure to infected individuals, drinking unsafe water, recent sexual history with unprotected anal or oral-anal contact, and recent travel to developing countries.

Risk factors in the development of giardiasis include the following:

• Recent history of hiking and camping
• Immunosuppression
• Young age (especially children < 5 years of age)
• Exposure to infected individuals
• Drinking contaminated or untreated water (.e.g lakes, wells, streams, ponds)
• Individuals with recent sexual history of unprotected anal or oral-anal contact
• Recent travel to developing countries

Template:Protozoal diseases

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Following transmission of Giardia, patients may remain asymptomatic for 1-3 weeks. Early symptoms typically include acute, watery diarrhea, bloating, and abdominal cramping, which are usually self-limited. If left untreated, giardiasis may persist in a small proportion of patients and subsequently results in chronic giardiasis. Complications may be related to either severe dehydration (e.g. acute kidney injury), malabsorption (e.g. vitamin B12 deficiency), post-infectious diseases (e.g. reactive arthritis, chronic fatigue syndrome), or spread of Giardia to extraluminal sites (e.g. involvement of the gallbladder, pancreas, or eyes). The prognosis is generally excellent. Recurrence of disease is common among children even with optimal treatment.

• Following transmission of Giardia, patients may remain asymptomatic for 1-3 weeks.
• The development of clinical manifestations is dependent on the parasite load, presence of virulence factors, and the host immune response (immunocompetent vs. immunocompromised).
• Early symptoms typically include watery diarrhea, bloating, and abdominal cramping.
• The majority of patients with giardiasis experience a self-limited acute infection.
• If left untreated, giardiasis may persist in a small proportion of patients and subsequently results in chronic giardiasis.
• Patients with chronic giardiasis typically report chronic watery diarrhea, steatorrhea, malaise, anorexia, malabsorption, weight loss, and failure to thrive.
• Giardiasis is generally a luminal infection (i.e. does not usually spread outside the lumen of the intestine). However, extraluminal manifestations have been reported (see Complications).

Complications of giardiasis have mostly been described in case-series. Reported complications included the following:

• Chronic fatigue syndrome
• Severe dehydration
• Acute kidney injury
• Lactase deficiency
• Vitamin B12 deficiency
• Allergic reaction (urticaria, elevated IgE)^[1]
• Erythema multiforme
• Reactive arthritis^[2]
• Ocular disease (usually in children)^[1]

• “Salt and pepper” retinal changes^[3]
• Retinal hemorrhage
• Iridocyclitis
• Choroiditis

• Hypokalemic myopathy^[4]
• Cognitive impairment
• Post-infectious irritable bowel syndrome^[1]
• Malignancy (unconfirmed association)

• Pancreatic cancer^[5]
• Gallbladder cancer^[6]

• The majority of patients with giardiasis experience a self-limited acute infection.
• Development of chronic infection generally depends on viral infectivity and host factors.
• With adequate treatment, the prognosis of giardiasis is excellent.
• Recurrence of disease is common among children even with optimal treatment.

Template:Protozoal diseases