Intraepithelial Giardia Intestinalis

Martínez-Gordillo, Mario Noé; González-Maciel, Angélica; Reynoso-Robles, Rafael; Montijo-Barrios, Ericka; Ponce-Macotela, Martha

doi:10.1097/md.0000000000000277

Cited by 20 publications

(8 citation statements)

References 38 publications

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“…Infection with Giardia occurs after ingestion of the environmental cyst stage of the parasite, which upon gastric passage excysts to release two trophozoites into the less acidic and bile-enriched environment of the upper small bowel. Trophozoites adhere to epithelial cells and replicate but typically do not invade the intestinal mucosa or cause ulceration [ 6 , 66 ]. If symptoms develop, onset typically begins after a 6- to 15-day incubation period that oftentimes precedes detection of parasites in stool [ 5 ].…”

Section: Determining How Giardia Causes Diseasementioning

confidence: 99%

Advances in understanding Giardia: determinants and mechanisms of chronic sequelae

Bartelt¹,

Sartor²

2015

F1000Prime Rep

124

129

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Giardia lamblia is a flagellated protozoan that is the most common cause of intestinal parasitic infection in children living in resource-limited settings. The pathogenicity of Giardia has been debated since the parasite was first identified, and clinical outcomes vary across studies. Among recent perplexing findings are diametrically opposed associations between Giardia and acute versus persistent diarrhea and a poorly understood potential for long-term sequelae, including impaired child growth and cognitive development. The mechanisms driving these protean clinical outcomes remain elusive, but recent advances suggest that variability in Giardia strains, host nutritional status, the composition of microbiota, co-infecting enteropathogens, host genetically determined mucosal immune responses, and immune modulation by Giardia are all relevant factors influencing disease manifestations after Giardia infection.

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Section: Determining How Giardia Causes Diseasementioning

confidence: 99%

Advances in understanding Giardia: determinants and mechanisms of chronic sequelae

Bartelt¹,

Sartor²

2015

F1000Prime Rep

124

129

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“…It is also effective against Trichomonas spp., Entamoeba histolytica , Clostridium difficile , Clostridium perfringens , Helicobacter pylori , and Campylobacter jejuni [ 19 ]. It has been shown that NTZ has a similar efficacy for eliminating Giardia when compared to metronidazole, but has fewer adverse effects [ 20 – 23 ]. To the best of our knowledge, there are no formal studies on the effect of NTZ against clinical infections of Giardia in dogs.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of nitazoxanide to treat natural Giardia infections in dogs

et al. 2017

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Background Giardia parasites cause gastrointestinal disease in humans, dogs, and many other animals worldwide. The treatment of dogs for giardiasis requires further investigation to ascertain levels of drug efficacy and the possibility of adverse side effects. Nitazoxanide (NTZ) has shown good clinical anti-Giardia activity in humans, yet it has not been evaluated for the treatment of giardiasis in dogs.MethodsThirty-five dogs, naturally infected with Giardia were divided into five groups (n = 7): dogs in group NTZ1, NTZ2, and NTZ3 were treated with a single oral dose of 37.5 mg/kg, 75 mg/kg, and 150 mg/kg, respectively, of NTZ on days 0 and 14. The fourth group was treated with a commercially available regimen that includes a combination of pyrantel, praziquantel, and febantel (FEB) administered orally for three consecutive days. Additionally, an untreated control group was established. Giardia cysts from the stool of each dog were quantified on days -3, 0, 5, 7, 9, 11, 14, 18, 25, and 28. Biochemical parameters were evaluated in all dogs, before the first treatment and after concluding the experiment.ResultsShedding of Giardia cysts was reduced in all treated groups when compared to untreated controls (P < 0.01). However, NTZ2, NTZ3, and FEB had a lower risk during the study. Furthermore, NTZ was also effective against another protozoan, Cryptosporidium spp. at doses of 75 mg/kg and 150 mg/kg, in contrast to the combination of febantel + pyrantel + praziquantel. Biochemical parameters of treated animals, namely, aspartate transaminase and alanine transaminase enzymes, remained within physiological ranges.ConclusionsBased on these results, the implementation of NTZ as a treatment for giardiasis in dogs is proposed. The administration of a single dose is an important advantage of NTZ because it reduces workload, particularly in animals placed in shelters and kennels, where handling of large numbers of animals is required, and personnel is frequently scarce.

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“…The colonization of the gut is followed by alterations in the gut milieu in favor of the parasite. To do so, the protozoon uses different mechanisms [ 37 ]. Non-specific mechanisms involve adhesion to host enteric epithelial cells by mechanical suction force via the ventral suction or adhesive disk and alterations in the zonula occludens tight junctions [ 37 , 38 ].…”

Section: Parasite–host Interactionmentioning

confidence: 99%

“…To do so, the protozoon uses different mechanisms [ 37 ]. Non-specific mechanisms involve adhesion to host enteric epithelial cells by mechanical suction force via the ventral suction or adhesive disk and alterations in the zonula occludens tight junctions [ 37 , 38 ]. The ventral suction disk of Giardia lamblia is a means of attachment to the small intestine to protect the trophozoite from being carried away by enteric peristalsis and gut contents [ 39 ].…”

Section: Parasite–host Interactionmentioning

confidence: 99%

Gut Microbiota Crosstalk with Resident Macrophages and Their Role in Invasive Amebic Colitis and Giardiasis—Review

2023

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The innate immune response is highly dependent on the action of macrophages. They are abundant in the intestine subepithelial lamina propria of the mucosa, where they deploy multiple tasks and play a critical role. The balance between the gut microbiota and M2 macrophages is critical for gut health and homeostasis. Gut microbiota has the power to change macrophage phenotype and replenish the resident macrophage niche during and post infection. As far as the extracellular enteric parasitic infections invasive amebic colitis and giardiasis are concerned, a change of macrophages phenotype to a pro-inflammatory state is dependent on direct contact of the protozoan parasites with host cells. Macrophages induce strong pro-inflammatory response by inflammasome activation and secretion of interleukin IL-1β. Inflammasomes play a key role in the response to cellular stress and microbe attacks. The balance between gut mucosal homeostasis and infection is dependent on the crosstalk between microbiota and resident macrophages. Parasitic infections involve NLRP1 and NLRP3 inflammasome activation. For Entamoeba histolytica and Giardia duodenalis infections, inflammasome NLRP3 activation is crucial to promote the host defenses. More studies are needed to further elucidate possible therapeutic and protective strategies against these protozoan enteric parasites’ invasive infections in humans.

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Intraepithelial Giardia Intestinalis

Cited by 20 publications

References 38 publications

Advances in understanding Giardia: determinants and mechanisms of chronic sequelae

Advances in understanding Giardia: determinants and mechanisms of chronic sequelae

Efficacy of nitazoxanide to treat natural Giardia infections in dogs

Gut Microbiota Crosstalk with Resident Macrophages and Their Role in Invasive Amebic Colitis and Giardiasis—Review

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