Mepacrine may also be used for refractory cases.Probiotics, when given in combination with the standard treatment, has been shown to assist with clearance of Giardia.During pregnancy, paromomycin is the preferred treatment drug because of its poor intestinal absorption, resulting in less exposure to the fetus. Alternatively, metronidazole can be used after the first trimester as there has been wide experience in its use for trichomonas in pregnancy. Prognosis
In people with a properly functioning immune system, infection may resolve without medication. A small portion, however, develop a chronic infection. People with an impaired immune system are at higher risk of chronic infection. Medication is an effective cure for nearly all people although there is growing drug-resistance.Children with chronic giardiasis are at risk for failure to thrive as well as more long-lasting sequelae such as growth stunting. Up to half of infected people develop a temporary lactose intolerance leading symptoms that may mimic a chronic infection. Some people experience post-infectious irritable bowel syndrome after the infection has cleared. Giardiasis has also been implicated in the development of food allergies. This is thought to be due to its effect on intestinal permeability. Epidemiology
In some developing countries Giardia is present in 30% of the population. In the United States it is estimated that it is present in 3–7% of the population.The number of reported cases in the United States in 2018 was 15,584. All states that classify giardiasis as a notifiable disease had cases of giardiasis.
The degree to which malabsorption occurs in symptomatic and asymptomatic cases is highly varied.The species Giardia intestinalis uses enzymes that break down proteins to attack the villi of the brush border and appears to increase crypt cell proliferation and crypt length of 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 proteins that connect brush border endothelial cells to one another. The result is increased intestinal permeability.There appears to be a further increase in programmed enterocyte cell death by Giardia intestinalis, which further damages the intestinal barrier and increases permeability. There is significant upregulation of the programmed cell death cascade by the parasite, and, furthermore, substantial downregulation of the anti-apoptotic protein 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 the gas nitric oxide by consuming all local arginine, which is the amino acid necessary to make nitric oxide. Arginine starvation is known to be a cause of programmed cell death, and local removal is a strong apoptotic agent. Host defense
Host defense against Giardia consists of natural barriers, production of nitric oxide, and activation of the innate and adaptive immune systems. Natural barriers
Natural barriers defend against parasite entering the hosts body. Natural barriers consist of mucus layers, bile salt, proteases, and lipases.