Pathophysiology of enteric infections with Giardia duodenalis (original) (raw)
Related papers
Pathophysiology of enteric infections withGiardia duodenalis
Parasite, 2008
Giardia is the most prevalent human intestinal parasitic protist in the world, and one of the most common parasite of companion animals and young livestock. Giardia is a major cause of diarrhea in children and in travelers. The host-microbial interactions that govern the outcome of infection remain incompletely understood. Findings available to date indicate that the infection causes diarrhea via a combination of intestinal malabsorption and hypersecretion. Malabsorption and maldigestion mainly result from a diffuse shortening of epithelial microvilli. This enterocytic injury is mediated by activated host T lymphocytes. Pathophysiological activation of lymphocytes is secondary to Giardia-induced disruption of epithelial tight junctions, which in turn increases intestinal permeability. Loss of epithelial barrier function is a result of Giardia-induced enterocyte apoptosis. Recent findings suggest that these effects may facilitate the development of chronic enteric disorders, including inflammatory bowel disease, irritable bowel syndrome, and allergies, via mechanisms that remain poorly understood. A newly discovered SGLT-1 glucose uptake-mediated host cytoprotective mechanism may represent an effective modulator of the epithelial apoptosis induced by this parasite, and, possibly, by other enteropathogens. A better understanding of the pathogenesis of giardiasis will shed light on new potential therapeutic targets.
Current Tropical Medicine Reports, 2015
Giardia duodenalis is a very common, ubiquitous, intestinal protozoan parasite infecting animals and humans. Of the eight distinct genetic assemblages known to date, assemblages A and B are infectious to humans. Giardia is the most commonly recognized cause of traveller's diarrhea. Giardiasis impairs weight gain and is responsible for a variety of extraintestinal and post-infectious complications, including postinfectious irritable bowel syndrome, chronic fatigue, failure to thrive, and cognitive impairment. Giardiasis occurs in the absence of invasion of the intestinal tissues by the trophozoites and in the absence of any overt inflammatory cell infiltration, with the exception of a modest increase in intraepithelial lymphocytes and mast cells. In endemic parts of the World where the infection is often concurrent with bacterial enteritis causing inflammation-driven diarrheal disease, giardiasis appears to be protective against diarrhea. Recent observations have demonstrated that this effect may be due to a direct immuno-modulating effect of the parasite via its cathepsin B cysteine protease which cleaves pro-inflammatory CXCL8. No known toxin has yet been directly implicated in the pathophysiology of giardiasis. Diarrhea in giardiasis is mostly malabsorptive in nature, rather than hypersecretory. Findings from ongoing research indicate that the post-infectious effects of giardiasis may be due to microbiota dysbiosis induced by the parasite during the acute phase of infection.
Extra-intestinal and long term consequences of Giardia duodenalis infections
World Journal of Gastroenterology, 2013
Giardiasis is the most common waterborne parasitic infection of the human intestine worldwide. The etiological agent, Giardia duodenalis (syn. G. intestinalis , G. lamblia ), is a flagellated, binucleated protozoan parasite which infects a wide array of mammalian hosts. Human giardiasis is a true cosmopolitan pathogen, with highest prevalence in developing countries. Giardiasis can present with a broad range of clinical manifestations from asymptomatic, to acute or chronic diarrheal disease associated with abdominal pain and nausea. Most infections are self-limiting, although re-infection and chronic infection can occur. Recent evidence indicating that Giardia may cause chronic post-infectious gastrointestinal complications have made it a topic of intense research. The causes of the post-infectious clinical manifestations due to Giardia , even after complete elimination of the parasite, remain obscure. This review offers a state-of-the-art discussion on the long-term consequences of Giardia infections, from extra-intestinal manifestations, growth and cognitive deficiencies, to post-infectious irritable bowel syndrome. The discussion also sheds light on some of the novel mechanisms recently implicated in the production of these postinfectious manifestations.
Giardia duodenalis (syn. G. intestinalis, or G. lamblia) is a leading cause of waterborne diarrheal disease that infects hundreds of millions of people annually. Research on Giardia has greatly expanded within the last few years, and our understanding of the pathophysiology and immunology on this parasite is ever increasing. At peak infection, Giardia trophozoites induce pathophysiological responses that culminate in the development of diarrheal disease. However, human data has suggested that the intestinal mucosa of Giardia-infected individuals is devoid of signs of overt intestinal inflammation, an observation that is reproduced in animal models. Thus, our understanding of host inflammatory responses to the parasite remain incompletely understood and human studies and experimental data have produced conflicting results. It is now also apparent that certain Giardia infections contain mechanisms capable of modulating their host’s immune responses. As the oral route of Giardia infection is shared with many other gastrointestinal (GI) pathogens, co-infections may often occur, especially in places with poor sanitation and/or improper treatment of drinking water. Moreover, Giardia infections may modulate host immune responses and have been found to protect against the development of diarrheal disease in developing countries. The following review summarizes our current understanding of the immunomodulatory mechanisms of Giardia infections and their consequences for the host, and highlights areas for future research. Potential implications of these immunomodulatory effects during GI co-infection are also discussed.
Persisting symptoms and duodenal inflammation related to Giardia duodenalis infection
Journal of Infection, 2007
Objectives: After a large waterborne outbreak of Giardia infection in Bergen, some patients experienced persisting abdominal symptoms despite metronidazole treatment. This study aimed at investigating possible causes for their symptoms. Methods: Over a 15 months period, 124 referred patients were evaluated in a prospective cohort analysis with a standardised investigation including duodenal biopsies and aspirate, blood tests and faecal parasite and calprotectin tests. Recovered subjects were recruited for symptom analysis. Results: Persisting Giardia duodenalis infection was found in 40 patients (32.3%). Duodenal biopsies showed signs of inflammation in 57 patients (47.1%). Microscopic duodenal inflammation was present in 34 (87.2%) of the Giardia positive and 23 (28.0%) of the Giardia negative patients. There were significant associations between persistent Giardia positivity, microscopic duodenal inflammation and a positive calprotectin test. Duodenal aspirate and duodenal biopsies performed poorly in diagnosis of persistent giardiasis. Conclusions: In patients with persisting symptoms after metronidazole treated Giardia infection we commonly found chronic Giardia infection and microscopic duodenal inflammation, especially in illness duration less than 7 months. Both these findings subsided over time. Increasingly, investigations could not determine a definite cause for the persistent symptoms. The very long-term post-giardiasis diarrhoea, bloating, nausea and abdominal pain documented here need further study.
Study of Nonoutbreak Giardiasis: Novel Findings and Implications for Research
American Journal of Medicine
The burden of nonoutbreak-related Giardia infections in the US is poorly understood, with little information on its impact on people's lives and on unusual manifestations of infection. This study was designed with the objectives of better defining the impact of infection, examining the occurrence of extraintestinal manifestations, and determining risk factors for delayed treatment of infection. METHODS: Foodborne Diseases Active Surveillance Network surveillance was used to identify persons with nonoutbreak-related, laboratory-confirmed Giardia infection. People were enrolled into the Risk Factor arm and the Delayed Enrollment arm. Detailed questionnaires collected information on clinical manifestations, impact on activities of daily living, health care utilization, and treatment.
Giardia duodenalis pathogenicity on immunosuppressed animal model
Tropical Biomedicine, 2020
Giardiasis is the major water-borne diarrheal disease present worldwide caused by the common intestinal parasite, Giardia duodenalis. This work aims to investigate the effect of G. duodenalis infection pathogenicity in immunosuppressed animals through histopathological examination. A total of 45 BALB/c mice were divided into four groups; G1 (negative control), G2 (healthy animals exposed to Giardia); G3 (immunosuppressed animals exposed to Giardia), and G4 (non-exposed immunosuppressed animals). Our study revealed that G3 was the most affected group with an infection rate of 100%. The animals showed general weakness, soft stool, and high death rate with severe histopathological changes in the duodenum and mild degenerative changes in hepatic tissues. In G2, the maximal lesions in both duodenum and liver were on the 11 th day. We spotted damage in the villi, edema in the central core, and submucosa, in addition to increased cellular infiltration with inflammation in lamina propria. The presence of the parasites within the villi and the lumen was clear. Most of the hepatocytes revealed hydropic and fatty changes, also dilated congested central veins and edema were observed. G3 changes were more intense than G2 with massive Giardia trophozoites between the intestinal villi, lumen, and extensive fatty liver degeneration. Immune suppression plays a significant role in the severity of injury with the Giardia parasites in duodenum and liver cells.
Giardiasis in Man: Review and Updates
مجلة جامعة الملك عبدالعزيز-العلوم الطبية, 2014
Giardia lamblia (known as G. duodenalis or G. intestinalis) is a microscopic flagellated organism. This protozoan parasite was described for the first time by van Leeuwenhoek in 1681 followed by Lambl in 1859. Giardia is one of the most common causes of diarrhea, with 280 million cases per year. It is included in the ''Neglected Tropical Diseases'' of the World Health Organization. The organism has two life forms; motile flagellated trophozoite, and a non-motile cyst. The mode of transmission is through ingestion of viable cysts from water, food and by faecal-oral route from person-to-person. Giardia infection may result in clinical aspects that range from the asymptomatic cyst passer state to acute or chronic diarrhea, malabsorption and failure to thrive. The reference method for giardiasis diagnosis is by microscopic detection of the diagnostic stages in faecal samples. Detection of coproantigen of Giardia by enzyme-linked immunosorbent assay or direct immunofluorescence may be helpful. Additionally, molecular techniques are able to detect and identify the parasite in stool. Duodenal biopsy and aspirate could be a useful tool in diagnosis. Human Giardia infections are unlikely to be ever eradicated, and thus, chemotherapy and other methods of control of the disease will always be required.
American journal of physiology. Gastrointestinal and liver physiology, 2016
Irritable Bowel Syndrome (IBS) is the most frequent functional gastrointestinal disorder. It is characterized by abdominal hypersensitivity leading to discomfort and pain, as well as altered bowel habits. While it is common for IBS to develop following the resolution of infectious gastroenteritis (then termed Post-Infectious-IBS), the mechanisms remain incompletely understood. G. duodenalis is a cosmopolitan waterborne enteropathogen that causes intestinal malabsorption, diarrhea, and post-infectious complications. Cause-to-effect studies using a human enteropathogen are sorely lacking to help investigate the mechanisms of PI-IBS. In an attempt to establish causality between giardiasis and post-infectious visceral hypersensitivity, this study describes a new model of PI-IBS in neonatal rats infected with Giardia duodenalis. Fifty days post-infection with Giardia (Assemblage A or B), long after the parasite was cleared, rats developed visceral hypersensitivity to luminal balloon dist...