Giardiasis
Giardia cell, SEM
Giardiasis — popularly known as beaver fever — is a disease caused by the flagellate protozoan Giardia lamblia (also sometimes called Giardia intestinalis and Giardia duodenalis). The giardia organism inhabits the digestive tract of a wide variety of domestic and wild animal species, as well as humans. It is a common cause of gastroenteritis in humans, infecting approximately 200 million people worldwide.
Signs and symptoms
Symptoms include loss of appetite, diarrhea, hematuria (blood in urine), loose or watery stool, stomach cramps, upset stomach, projectile vomiting (uncommon), bloating, flatulence, and burping (often sulphurous). Symptoms typically begin one to two weeks after infection and may wane and reappear cyclically. Symptoms are caused by Giardia organisms coating the inside of the small intestine and blocking nutrient absorption. Most people are asymptomatic; only about a third of infected people exhibit symptoms. Untreated, symptoms may last for six weeks or longer.
Symptomatic infections are well recognised as causing lactose intolerance, which, while usually temporary, may become permanent. Although hydrogen breath tests indicate poorer rates of carbohydrate absorption in those asymptomatically infected, such tests are not diagnostic of infection. It has been suggested that these observations are explained by symptomatic giardia infection allowing for the overgrowth of other bacteria.
Some studies have shown giardiasis should be considered as a cause of vitamin B12 Deficiency as a result of the problems caused within the intestinal absorption system.
Transmission
Giardiasis is passed via the fecal-oral route. Primary routes are personal contact and contaminated consumables. The more susceptible are institutional or day-care workers, travelers, those eating improperly treated food or drink, and people who have contact with individuals already infected.
It is a particular danger to people hiking or backpacking in wilderness areas worldwide, especially if they have no immediate access to medical supplies. Giardia is also suspected to be zoonotic—communicable between humans and other animals. Major reservoir hosts include beavers, dogs, cats, horses, humans, cattle and birds.
Pathophysiology
Although the mechanisms by which Giardia causes injury have not been fully elucidated yet, the research points to a multifaceted attack. Those putative attack sites include endothelial brush border damage, enterotoxin production, immunological reaction, and alternation of gut motility.
The attachment of trophozoites, of which Giardia lamblia is one, causes loss of brush border surface area, villus flattening, and inhibition of dissachardidase activities. Ultimately, the enteric microbiota of the intestine overgrow and may be the cause of further symptoms. This idea has not been fully investigated. The alteration of the brush border and villi leads to an inability for nutrient and water absorption from the intestine. This results in diarrhea, one of the predominant symptoms. In the case of asymptomatic giardiasis, there can be malabsorption with or without histological changes to the small intestine. The degree to which malabsorption occurs in symptomatic and asymptomatic cases is highly varied.
Interestingly, the species Giardia intestinalis has proteinases that attack the villi of the brush border and appear to increase crypt cell proliferation and crypt length. Crypt cells existing on the sides of the villi.
On an immunological level, activated host T-lymphocytes attack endothelial cells that have been injured in order to remove the cell. This occurs after the disruption of the tight junctions between endothelial cells that make up the brush border. The result is heavily increased intestinal permeability.
There appears to be a further increase in apoptosis by Giardia intestinalis which further damages the intestinal barrier to permeability. There is siginificant up-regulation of the apoptotic cascade by the parasite. Furthermore, substantial down regulation of the anti-apoptotic proteins Bcl-2 and upregulation of the proapoptotic protein Bax. These connections suggest a role of caspase-dependent apoptosis in the pathogenesis of giardiasis.
Giardia protects its own growth by reducing the formation of nitric oxide by consuming all local arginine which is the necessary substrate for the production of nitric oxide. Arginine starvation is known to be a cause of programmed cell death and local removal is a strong apoptotic agent.
Diagnosis
Treatment
Drugs used to treat adults include metronidazole, albendazole and quinacrine. Furazolidone and nitazoxanide may be used in children. Treatment is not always necessary, as the body can defeat the infection by itself.
The drug tinidazole can treat giardiasis in a single treatment of 2000 mg, instead of the longer treatment of the other medications listed. The shorter duration of treatment may also cause patient less distress. Tinidazole is now approved by the FDA and available to US patients.
Signs and symptoms
Symptoms include loss of appetite, diarrhea, hematuria (blood in urine), loose or watery stool, stomach cramps, upset stomach, projectile vomiting (uncommon), bloating, flatulence, and burping (often sulphurous). Symptoms typically begin one to two weeks after infection and may wane and reappear cyclically. Symptoms are caused by Giardia organisms coating the inside of the small intestine and blocking nutrient absorption. Most people are asymptomatic; only about a third of infected people exhibit symptoms. Untreated, symptoms may last for six weeks or longer.
Symptomatic infections are well recognised as causing lactose intolerance, which, while usually temporary, may become permanent. Although hydrogen breath tests indicate poorer rates of carbohydrate absorption in those asymptomatically infected, such tests are not diagnostic of infection. It has been suggested that these observations are explained by symptomatic giardia infection allowing for the overgrowth of other bacteria.
Some studies have shown giardiasis should be considered as a cause of vitamin B12 Deficiency as a result of the problems caused within the intestinal absorption system.
Transmission
Giardiasis is passed via the fecal-oral route. Primary routes are personal contact and contaminated consumables. The more susceptible are institutional or day-care workers, travelers, those eating improperly treated food or drink, and people who have contact with individuals already infected.
It is a particular danger to people hiking or backpacking in wilderness areas worldwide, especially if they have no immediate access to medical supplies. Giardia is also suspected to be zoonotic—communicable between humans and other animals. Major reservoir hosts include beavers, dogs, cats, horses, humans, cattle and birds.
Pathophysiology
Although the mechanisms by which Giardia causes injury have not been fully elucidated yet, the research points to a multifaceted attack. Those putative attack sites include endothelial brush border damage, enterotoxin production, immunological reaction, and alternation of gut motility.
The attachment of trophozoites, of which Giardia lamblia is one, causes loss of brush border surface area, villus flattening, and inhibition of dissachardidase activities. Ultimately, the enteric microbiota of the intestine overgrow and may be the cause of further symptoms. This idea has not been fully investigated. The alteration of the brush border and villi leads to an inability for nutrient and water absorption from the intestine. This results in diarrhea, one of the predominant symptoms. In the case of asymptomatic giardiasis, there can be malabsorption with or without histological changes to the small intestine. The degree to which malabsorption occurs in symptomatic and asymptomatic cases is highly varied.
Interestingly, the species Giardia intestinalis has proteinases that attack the villi of the brush border and appear to increase crypt cell proliferation and crypt length. Crypt cells existing on the sides of the villi.
On an immunological level, activated host T-lymphocytes attack endothelial cells that have been injured in order to remove the cell. This occurs after the disruption of the tight junctions between endothelial cells that make up the brush border. The result is heavily increased intestinal permeability.
There appears to be a further increase in apoptosis by Giardia intestinalis which further damages the intestinal barrier to permeability. There is siginificant up-regulation of the apoptotic cascade by the parasite. Furthermore, substantial down regulation of the anti-apoptotic proteins Bcl-2 and upregulation of the proapoptotic protein Bax. These connections suggest a role of caspase-dependent apoptosis in the pathogenesis of giardiasis.
Giardia protects its own growth by reducing the formation of nitric oxide by consuming all local arginine which is the necessary substrate for the production of nitric oxide. Arginine starvation is known to be a cause of programmed cell death and local removal is a strong apoptotic agent.
Diagnosis
- The mainstay of diagnosis of giardiasis is stool microscopy. This can be for motile trophozoites or for the distinctive oval G.lambliacysts.
- The entero-test uses a gelatin capsule with an attached thread. One end is attached to the inner aspect of the patient's cheek, and the capsule is swallowed. Later, the thread is withdrawn and shaken in saline to release trophozoites which can be detected microscopically.
- A new immunologic test, enzyme-linked immunosorbent assay (ELISA), is now available. These tests are capable of a 90% detection rate or more.
- Because Giardia lamblia is difficult to detect, often leading to misdiagnoses, several tests should be conducted over a one-week period.
Treatment
Drugs used to treat adults include metronidazole, albendazole and quinacrine. Furazolidone and nitazoxanide may be used in children. Treatment is not always necessary, as the body can defeat the infection by itself.
The drug tinidazole can treat giardiasis in a single treatment of 2000 mg, instead of the longer treatment of the other medications listed. The shorter duration of treatment may also cause patient less distress. Tinidazole is now approved by the FDA and available to US patients.