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Giardia lamblia is the most frequently identified protozoan cause of intestinal infection. Over 200 million people are estimated to have acute or chronic giardiasis, with infection rates approaching 90% in areas where Giardia is endemic. Despite its significance in global health, the mechanisms of pathogenesis associated with giardiasis remain unclear, as the parasite neither produces a known toxin nor induces a robust inflammatory response. Giardia colonization and proliferation in the small intestine of the host may, however, disrupt the ecological homeostasis of gastrointestinal commensal microbes and contribute to diarrheal disease associated with giardiasis. To evaluate the impact of Giardia infection on the host microbiota, we used culture-independent methods to quantify shifts in the diversity of commensal microbes throughout the gastrointestinal tract in mice infected with Giardia. We discovered that Giardia's colonization of the small intestine causes a systemic dysbiosis of aerobic and anaerobic commensal bacteria. Specifically, Giardia colonization is typified by both expansions in aerobic Proteobacteria and decreases in anaerobic Firmicutes and Melainabacteria in the murine foregut and hindgut. Based on these shifts, we created a quantitative index of murine Giardia-induced microbial dysbiosis. This index increased at all gut regions during the duration of infection, including both the proximal small intestine and the colon. Giardiasis could be an ecological disease, and the observed dysbiosis may be mediated directly via the parasite's unique anaerobic fermentative metabolism or indirectly via parasite induction of gut inflammation. This systemic alteration of murine gut commensal diversity may be the cause or the consequence of inflammatory and metabolic changes throughout the gut. Shifts in the commensal microbiota may explain observed variations in giardiasis between hosts with respect to host pathology, degree of parasite colonization, infection initiation, and eventual clearance.KEYWORDS Giardia, microbiome, parasite, pathogenesis G iardia lamblia is a microaerophilic protozoan parasite of humans and animals that causes significant morbidity and diarrheal disease worldwide (1, 2). Giardiasis is a zoonotic disease with diverse animal reservoirs. Parasites infect and complete their life cycle in mammalian hosts, and infected animals shed Giardia cysts into water supplies. Over 200 million people are estimated to have acute or chronic giardiasis, and rates of giardiasis approach 90% in areas where it is endemic (3, 4). When prevalent, giardiasis has been implicated as a primary cause of growth restriction for children, resulting in long-term consequences, such as stunting, failure to thrive, malnutrition, and cognitive disabilities (1, 2, 5). In addition, Giardia has been associated with substantial postclearance irritable bowel symptoms in both children and adults (1, 6-8). The significant and adverse impact of giardiasis on global human health contrasts with a considerable lack of resea...

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Blastocystis is a gastrointestinal protist frequently reported in humans and animals worldwide. Wildlife populations, including deer, may serve as reservoirs of parasitic diseases for both humans and domestic animals, either through direct contact or through contamination of food or water resources. However, no studies of the occurrence and subtype distribution of Blastocystis in wildlife populations have been conducted in the United States. PCR and next generation amplicon sequencing were used to determine the occurrence and subtypes of Blastocystis in white-tailed deer (Odocoileus virginianus). Blastocystis was common, with 88.8% (71/80) of samples found to be positive. Twelve subtypes were identified, ten previously reported (ST1, ST3, ST4, ST10, ST14, ST21, and ST23–ST26) and two novel subtypes (ST30 and ST31). To confirm the validity of ST30 and ST31, MinION sequencing was used to obtain full-length SSU rRNA gene sequences, and phylogenetic and pairwise distance analyses were performed. ST10, ST14, and ST24 were the most commonly observed subtypes. Potentially zoonotic subtypes ST1, ST3, or ST4 were present in 8.5% of Blastocystis-positives. Mixed subtype infections were common (90.1% of Blastocystis-positives). This study is the first to subtype Blastocystis in white-tailed deer. White-tailed deer were found to be commonly infected/colonized with a wide diversity of subtypes, including two novel subtypes, zoonotic subtypes, and subtypes frequently reported in domestic animals. More studies in wildlife are needed to better understand their role in the transmission of Blastocystis.

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Little information is currently available on the epidemiology of parasitic and commensal protist species in captive non-human primates (NHP) and their zoonotic potential. This study investigates the occurrence, molecular diversity, and potential transmission dynamics of parasitic and commensal protist species in a zoological garden in southern Spain. The prevalence and genotypes of the main enteric protist species were investigated in faecal samples from NHP (n = 51), zookeepers (n = 19) and free-living rats (n = 64) by molecular (PCR and sequencing) methods between 2018 and 2019. The presence of Leishmania spp. was also investigated in tissues from sympatric rats using PCR. Blastocystis sp. (45.1%), Entamoeba dispar (27.5%), Giardia duodenalis (21.6%), Balantioides coli (3.9%), and Enterocytozoon bieneusi (2.0%) (but not Troglodytella spp.) were detected in NHP. Giardia duodenalis (10.5%) and Blastocystis sp. (10.5%) were identified in zookeepers, while Cryptosporidium spp. (45.3%), G. duodenalis (14.1%), and Blastocystis sp. (6.25%) (but not Leishmania spp.) were detected in rats. Blastocystis ST1, ST3, and ST8 and G. duodenalis sub-assemblage AII were identified in NHP, and Blastocystis ST1 in zookeepers. Giardia duodenalis isolates failed to be genotyped in human samples. In rats, four Cryptosporidium (C. muris, C. ratti, and rat genotypes IV and V), one G. duodenalis (assemblage G), and three Blastocystis (ST4) genetic variants were detected. Our results indicate high exposure of NHP to zoonotic protist species. Zoonotic transmission of Blastocysts ST1 was highly suspected between captive NHP and zookeepers.

Giardia duodenalis is a noninvasive luminal pathogen that impairs digestive function in its host in part by reducing intestinal disaccharidase activity. This enzyme deficiency has been shown in mice to require CD8 ؉ T cells. We recently showed that both host immune responses and parasite strain affected disaccharidase levels during murine giardiasis. However, high doses of antibiotics were used to facilitate infections in that study, and we therefore decided to systematically examine the effects of antibiotic use on pathogenesis and immune responses in the mouse model of giardiasis. We found that antibiotic treatment did not overtly increase the parasite burden but significantly limited the disaccharidase deficiency observed in infected mice. Moreover, while infected mice had more activated CD8 ؉ ␣␤ T cells in the small intestinal lamina propria, this increase was absent in antibiotictreated mice. Infection also led to increased numbers of CD4 ؉ ␣␤ T cells in the lamina propria and activation of T cell receptor ␥␦-expressing intraepithelial lymphocytes (IEL), but these changes were not affected by antibiotics. Finally, we show that activated CD8؉ T cells express gamma interferon (IFN-␥) and granzymes but that granzymes are not required for sucrase deficiency. We conclude that CD8؉ T cells become activated in giardiasis through an antibiotic-sensitive process and contribute to reduced sucrase activity. These are the first data directly demonstrating activation of CD8؉ T cells and ␥␦ T cells during Giardia infections. These data also demonstrate that disruption of the intestinal microbiota by antibiotic treatment prevents pathological CD8 ؉ T cell activation in giardiasis.T he protozoan Giardia duodenalis is a major cause of parasitic diarrheal disease worldwide. Infection with G. duodenalis provides an interesting model for studying mucosal immunity, as some of the immunopathology observed in human patients and infected animals resembles that of common noninfectious intestinal disorders. The reduction of intestinal disaccharidase enzymes, for example, is a pathological hallmark of giardiasis and is also commonly observed in gastroenteritis, celiac disease, ulcerative colitis, and Crohn's disease patients (1-4). Therefore, there are likely overlapping mechanisms involved. The reduction of disaccharidase enzymes in giardiasis results from a shortening of the intestinal epithelial microvilli structures and reflects a general impairment of digestion and nutrient absorption (5-7). We have demonstrated that wild-type mice exhibit reduced disaccharidase activity following infection with G. duodenalis but that CD4Another study has demonstrated that the adoptive transfer of purified CD8 ϩ T cells, but not CD4 ϩ T cells, from Giardia muris-infected mice into athymic naive recipients is sufficient to recapitulate shortening of microvilli and intestinal disaccharidase reduction (7). Collectively, these data suggest that CD8 ϩ T cells are involved in the pathological reduction of intestinal disaccharidases following infection...