# Food and Drinking Water as Sources of Pathogenic Protozoans: An Update
## 8 Blastocystis hominis
hominis_ infection were observed with type 2 diabetes, bacterial co-infection, and immunosuppressive treatments, except corticosteroid treatment [23]. _B. hominis_ infection was associated with cutaneous manifestations such as urtic, rash, and itching and these symptoms ceased when the infection was treated [27] as in a recent case of urticatic complicated by arthritis andenosmovitis that did not improve with antihistamine treatment in an 18-year-old woman. The patient was found to be infected with _B. hominis_ and completely recovered after administration of metronidazoleae, naproxen, and prednisolone [226]. _B. hominis_ infection was found to be associated with the development of irritable bowel syndrome (IBS), inflammatory bowel disease (IBD) [27; 30; 225; 227], and autoimmune disorders [33]. In a case-control study that included patients with different autoimmune diseases divided into a group with gastrointestinal problems (cases) and a group without gastrointestinal symptoms (controls), _B. hominis_ was significantly more frequent in cases(16.6%) [33]. _B. hominis_ infection can exacerbate symptoms of the autoimmune disease [PERSON]'s thyroiditis (HT) by increasing serum levels of interleukin (IL-17) which has a relevant role in pathogenesis. HT patients improved after treatment of _B. hominis_ infection which led to lower levels of IL-17, thyroid-stimulating hormone (TSH), and thyroid peroxidase antibodies (anti-TPO) [228]. Some studies found an association between _B. hominis_ and CRC, suggesting that its presence was favored by immunosuppression. It was also suggested that the _B. hominis_ antigen induces the proliferation of HCT116 colon carcinoma cells through the downregulation of p53 and proapoptotic genes and upregulation of IL-6 [34]. However, a case-control study in Egypt showed that patients with CRC did not have a higher prevalence of _B. hominis_ infection but a significantly higher frequency of urtic. Moreover, _B. hominis_ infection rates increased with CRC stage advancement [32]. A recent study demonstrated the alteration of the gut microbiota in the presence of _B. hominis_. In particular, individuals positive for _B. hominis_ showed higher abundances of Prevotellaceae and Ruminococcaceae, while _B. hominis_-negative subjects showed a higher abundance of _Akkermansia_ spp., _Bacteroides_ spp., Verrucomicrobiota, and Firmicutes. In the presence of bacterial suspension from symptomatic individuals, a _B. hominis_ isolate obtained from asymptomatic individual showed an increased cysteine protease activity. In addition, antigens of _B. hominis_ isolated from asymptomatic individuals which were co-cultured with bacteria from symptomatic individuals showed an increased capacity to induce colon cell proliferation. Protease expression in _B. hominis_ is considered a virulence factor for causing the degradation of secretory immunoglobulin A and activation of IL-8 expression. Therefore, it was proposed that the gut microbiota influences the pathogenic potential of _B. hominis_[229]. A study on discovery and validation cohorts highlighted that _B. hominis_ STs 1, 2, 3 and--to a lesser extent--ST4 negatively affected executive functions. Significant differences in the gut bacterial microbiota composition were revealed for all STs with negative associations of these with the actinomycetes _Bifidobacterium; Actinomyces_ and _Collinsella_; Lachospiraceae _Blautia_; _Roseburia_ and _Faecalibacterium_, which are short-chain fatty acid (SCFA)-producers; and _Lactobacillus_ species. Microbiome functionality analysis showed that _B. hominis_ STs 1-3 were positively correlated with aromatic amino acid, folate-mediated pyrimidine, and one-carbon microbial metabolism. Analysis of the circulating metabolome in the presence of _B. hominis_ STs 1-3 revealed the activation of pathways with important roles in central nervous system (CNS) function, including neurotransmitter metabolism, synaptic vesicle cycle, and transmission across chemical synapses. A fecal microbiota transplantation experiment in mice showed that _B.