Parasites can be made of one cell, as in the case of Giardia , or many cells, as with parasitic worms. In developing countries unicellular parasites, such as Plasomdium , the cause of malaria, are a major sources of disease. Waterborne parasites, such as Giardia and Cryptosporidium are the most common causes of parasitic disease in the United States. Eurofins CRL does not currently offer testing against parasites. Fungi are diverse in terms of their shape, size and means of infecting humans.
Fungi are eukaryotes, meaning that like parasites, their cells have a true nucleus and complex internal structures. They are most commonly found as environmentally resistant spores and molds, but can cause disease in humans in the form of yeasts. Fungi most often cause skin infections and pneumonia. Introduction to Bacteria, Viruses, Fungi, and Parasites.
Viruses With the exception of prions, viruses are the smallest known agents of infectious disease. Bacteria Bacteria are generally ten to times larger than viruses. Parasites Parasites are part of a large group of organisms called eukaryotes.
Fungi Fungi are diverse in terms of their shape, size and means of infecting humans. About Parasites. Minus Related Pages. An adult Ascaris lumbriocoides worm. They can range from 15 to 35 cm. An adult louse. Acutal size is about as big as a sesame seed. To receive email updates about this page, enter your email address: Email Address.
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Cancel Continue. These results suggested that Blastocystis colonization may be associated with expansion of members of the intestinal microbiota generally associated with a healthy gut microbiota, rather than with expansion of bacteria associated with gut dysbiosis.
Trichomonas vaginalis , the causative agent of trichomoniasis and an extracellular parasite of the human urogenital tract, is the most common nonviral sexually transmitted infection globally Women are disproportionally impacted by trichomoniasis, with symptomatic infection primarily impacting the vaginal mucosa. Variation in clinical presentation of disease may be impacted by the composition of the vaginal microbiota.
In a study of the vaginal microbiota of T. In summary, the referenced human studies suggest that there is a strong link between the composition of the intestinal bacterial microbiota and mucosa-associated enteric protozoa Table 1. Future studies are needed to understand the nature of the connection and how it can be utilized for disease prevention.
However, the distribution of clinical malaria is highly heterogeneous. In studies in Kenya and Senegal, the number of clinical episodes of disease ranged from 0 to 40 per child over a 5-year period in the same community 56 , Clinical variation has been attributed to genetic differences. For example, heterozygous carriers of the hemoglobin variant HbS, associated with sickle cell disease, are healthy and are protected from severe forms of malaria, including cerebral malaria Variation in exposure and variance in immune response are also implicated.
However, these factors may not completely explain such a large clinical variation 55 , The intestinal bacterial microbiota might represent an environmental factor that may contribute to this variability.
In a recent study, stool samples were collected from a cohort of Malian children and adults just before the P. The compositions of gut bacterial communities in these individuals were determined and compared to the risks of acquiring P. A significant association was found between microbiota composition and the prospective risk of P.
The intestinal microbiota of subjects who did not become infected had a significantly higher proportion of Bifidobacterium and Streptococcus species than subjects who became infected with P. However, no relationship was observed between microbiota composition and the risk of developing febrile malaria once P. The authors note that this is possibly due to a lack of statistical power. The preliminary finding of an association between gut microbiota composition and P. Gut bacteria might influence extraintestinal disease via many pathways, such as by alteration of adaptive immunity and augmentation of the magnitudes of T cells and B cell-mediated responses and perhaps by enhancement of innate immune pathways via trained immunity Mechanisms underlying these extraintestinal effects are poorly understood.
Metabolic products, such as short-chain fatty acids 61 , 62 , or host-derived factors, such as damage-associated molecular pattern molecules induced by the microbiota 63 , 64 , might be partially responsible for these effects. The metabolite pools present in animal models with differential, microbiota-dependent susceptibility to Plasmodium infection varied significantly in one study, with decreases in nucleotides, amino acids, and the substrates involved in the biosynthesis of these compounds in resistant mice, along with more-robust T and B cell responses 20 , The gut microbiota has also been shown to have a systemic influence on serum metabolites in both animal models and humans 66 , Blood-stage parasites have been shown to be highly susceptible to metabolic dysregulation induced by antimalarials 68 and might also be influenced by changes induced by the microbiota.
Therefore, the intestinal microbiota may influence the clinical outcome of a Plasmodium infection via alteration of the metabolome and modulation of innate or adaptive immunity.
Patient cohorts and future microbiome epidemiological studies will establish a more complete understanding of variation in clinical presentations of infection with parasitic protozoa. However, population-based studies do not allow us to test the effects of the microbiota on parasite survival and proliferation. Therefore, in vitro and in vivo disease models provide a useful tool to understand how the intestinal bacterial microbiota may influence severity and progression of infection and what mechanisms might underlie that progression.
In vitro culture models allow interactions between infecting agents and individual components of the microbiota to be analyzed. A study of the in vitro effects of six Lactobacillus acidophilus strains and Lactobacillus johnsonii La1 on Giardia duodenalis survival, for example, demonstrated that L.
The potential protective role of L. In another in vitro study, common human commensal bacteria were cocultured with E. A previous study demonstrated a link between decreased Lactobacillus and amebiasis in Indian patients 72 , further supporting a potential link between these bacteria and resistance to ameba infection. As mentioned previously, lactobacilli may impact susceptibility to T. Mechanisms underlying this effect are still being studied; however, inhibition of adhesion of the parasite might help explain protection.
In one study, adhesion assays were carried out by incubating vaginal epithelial cells VECs with T. Studies such as these may lay the foundation for utilizing individual components of the microbiota to provide cost-effective prophylactic treatment for parasite infection without the overuse of antimicrobial agents Table 1 Unfortunately, current coculture experiments do not allow us to explore the influence of the host immune system.
Although differences exist between the murine and human gut microbiotas, murine models provide a powerful tool to explore host-microbiota-pathogen interactions in the context of an active immune system The development of murine models of parasitic protozoan infections has allowed for more-detailed immunophenotyping of the mammalian host response to changes in the microbiota and its influence on infectious disease 1 , Murine models have also offered unexpected advancements in our understanding of interactions between the microbiota and the host due to variation in the communities of bacteria present in commercial animal vendors facilities, notably segmented filamentous bacteria SFB 44 , 45 , Alteration of the intestinal microbiome in model systems and careful observation of variation between models in different environments therefore allow for a better understanding of immune factors that may help explain clinical variation in parasitic disease.
Variation in the microbiota in commercial animal facilities can result in significant changes in the progression of inflammatory and infectious diseases 76 , A salient example of this is colonization with a single murine commensal Clostridium SFB 78 , This suggested that a difference in the microbiotas of mice between these two vendors might underlie the difference in cytokine induction.
Ivanov et al. Research in murine models has also shown that the immune response induced by SFB alters the severity of extraintestinal autoimmune encephalomyelitis 77 , 80 , — Recently, with a murine model of E. In exploring the responsiveness of immune cells in these mice, it was discovered that bone marrow-derived dendritic cells BMDCs from SFB-colonized mice produced significantly higher levels of IL- There was also an increase in neutrophils in the intestine, which resulted only after ameba infection IL is a cytokine 29 linked to induction of ILA and neutrophils, which in turn have been shown to be important in immunity to the ameba 30 , This work suggested that a gut-associated commensal might alter the responsiveness of bone marrow-derived cells to subsequent inflammatory challenges Fig.
Model of SFB-mediated protection against E. SFB segmented filamentous bacteria colonization of the intestine may induce soluble mediators, including SAA, which may increase intestinal immune responses against ameba as well as trigger systemic epigenetic changes in bone marrow that support more-robust granulopoiesis and protection against intestinal E. Republished with modifications from mBio [ 83 ]. In this model of amebiasis, a host damage-associated molecular pattern molecule, serum amyloid A SAA 84 was also increased in the sera of SFB-colonized mice compared to the level in the sera of mice lacking the commensal.
Transient gut colonization with SFB or SAA administration alone increased the H3K27 histone demethylase Jmjd3 in the bone marrow and persistently increased bone marrow Csf2ra expression as well as granulocyte monocyte precursors GMPs , and protected from ameba infection.
Protection was associated with increased intestinal neutrophils These results indicate that alteration of the microbiota and systemic exposure to host SAA can influence granulopoiesis and susceptibility to amebiasis, potentially via epigenetic mechanisms. Gut microbiota-marrow communication is a previously unrecognized mechanism of innate protection from ameba infection 63 , 83 Fig. The intestinal microbiota likely has significant extraintestinal effects on the host immune response to parasites.
These changes may be relatively long term, perhaps via induction of immune memory pathways, such as trained innate immunity 60 , or via influences on adaptive immunity that are yet to be fully understood. Antibiotic treatment which disrupts the commensal microbiota is often utilized to establish infection with pathogens in model systems.
Observation of differences between the immune response in antibiotic-treated mice and untreated mice may therefore lead to insights into the role of the microbiota in the host response. In a model of Giardia duodenalis infection, for example, antibiotic alteration of the microbiome was shown to prevent CD8 T cell activation by Giardia 6.
One potential mechanism is that during infection, the parasite promotes breakdown of the intestinal barrier. Giardia duodenalis infections can have a long-term impact on human heath, and the reduction of host disaccharidases associated with Giardia infections may play an important role.
Disaccharidases are required for the complete assimilation of nearly all carbohydrates present in food and drinks. The deficiency in disaccharidases has been thought to result from epithelial damage and shortening of the intestinal epithelial microvilli.
This study suggests that differences in antibiotic usage and their effects on the human microbiome might be important factors to consider when evaluating the clinical outcome of a Giardia infection. Following infection, significant differences in parasitemia were observed between the genetically identical mice from different vendors, with mice from Jackson Laboratory and Taconic Farms being resistant to the parasite.
Resistant mice exhibited increased abundances of Lactobacillus and Bifidobacterium compared to those in susceptible mice. Additionally, susceptible mice treated with antibiotics followed by probiotics made from these bacterial genera displayed a decreased parasite burden.
Therefore, the composition of the gut microbiota may be an unidentified risk factor for severe malaria and alteration of the intestinal microbiota might augment the host response to extraintestinal parasites. The primary focus of this review has been parasitic protozoa and influences of the bacterial microbiota on host immunity to these protozoa.
However, it is important to note that an emerging body of work suggests that protozoa may also alter host immunity to subsequent exposures Fecal-oral ingestion of Giardia cysts leads to varied clinical syndromes ranging from acute or chronic diarrhea to long-term asymptomatic colonization A recent study of children in Bangladesh showed that early-life Giardia exposure neither increased nor decreased the odds of acute diarrhea from any cause.
However, Giardia infection was a risk factor for stunting but not poor weight gain It has also been noted that patients that have been infected with Giardia often have gut dysfunction well after their infection is cleared 86 , Giardia infection has been associated with protection from diarrhea in other cases 17 , 88 , Mechanisms underlying these disparate outcomes in Giardia infection in humans are not presently well understood. However, recent work in murine models provides a demonstration of how protozoan infection might provide protection from infection while exacerbating colitis.
Tritrichomonas musculis is a common murine commensal found in wild mice and some animal colonies. It has recently been shown to cause expansion of tuft cells, a unique epithelial cell subtype important in the generation of type 2 immune responses This work suggests that commensal protozoa may be important in establishing the basic structure of the mammalian intestine.
The protozoon has also just been shown to lead to expansion of adaptive Th1 cells and Th17 effector cells in the colonic mucosa. This expansion was dependent on distinct, migratory DC subsets but also required the production of IL by epithelial cells. Interestingly, T. However, colonization with T. This effect of T. Combined, these studies revealed novel host-protozoan interactions that led to increased mucosal host defenses while also increasing the risk of inflammatory disease.
Recent studies have highlighted the potential contribution of the intestinal microbiome to clinical variation in parasitic protozoan infections. The microbiome and parasites may interact in various ways, which may include i alteration of parasite virulence, ii induction of dysbiosis or perhaps even beneficial shifts in the microbiota that increase competition for the niche of the lumen of the gut, and finally, iii modulation of host immunity to the parasite.
The courses of both mucosal and systemic parasite infection may also be shaped by specific members of the microbiota, and in turn parasite infection may alter the microbiota in such a way that the unique signature can be diagnostic of the presence of the parasite.
The exact mechanisms underlying microbiota modulation of host immunity are not yet fully understood; however, it is becoming increasingly apparent that components of the microbiota can alter both innate and adaptive immune cell populations so that a more robust response is mounted following subsequent challenge with infectious agents, including parasitic protozoa. Mechanisms underlying this shift might include the recently described concept of trained innate immunity, in which epigenetic changes enable innate immune cells to more effectively clear unrelated pathogens, and by enhancement of adaptive immunity.
Ultimately, further exploration of interactions between the gut microbiome and parasitic protozoans will provide additional tools and approaches that will help in the diagnosis and treatment of infectious and inflammatory diseases. Study of protozoan interactions with the host immune system and the microbiota also help us to better understand fundamental mechanisms of mammalian immunology.
National Center for Biotechnology Information , U. Journal List Infect Immun v. Infect Immun. Published online Jul Prepublished online Jun 5. Stacey L. Burgess , Carol A. Gilchrist , Tucker C. Lynn , and William A. Petri, Jr. Anthony T. Maurelli, Editor Anthony T. Maurelli, University of Florida;. Author information Copyright and License information Disclaimer. Corresponding author. Address correspondence to William A. Parasitic protozoa and interactions with the host intestinal microbiota.
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