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Dysbiosis (also called dysbacteriosis) is a term for a microbial imbalance or maladaptation on or inside the body,[1][2] such as an impaired microbiota. For example, a part of the human microbiota, such as the skin flora, gut flora, or vaginal flora, can become deranged, with normally dominating species underrepresented and normally outcompeted or contained species increasing to fill the void. Dysbiosis is most commonly reported as a condition in the gastrointestinal tract,[2] particularly during small intestinal bacterial overgrowth (SIBO) or small intestinal fungal overgrowth (SIFO).[3][4]

Typical microbial colonies found on or in the body are normally benign or beneficial. These beneficial and appropriately sized microbial colonies carry out a series of helpful and necessary functions, such as aiding in digestion.[5] They also help protect the body from the penetration of pathogenic microbes. These beneficial microbial colonies compete with each other for space and resources.[6]

Contents

CausesEdit

Dysbiosis may be caused by such diverse things as repeated and inappropriate antibiotic exposure,[7][unreliable medical source?] alcohol misuse,[8][9] or inappropriate diet.[10][unreliable medical source?]

EffectsEdit

When this balance is disturbed, these colonies exhibit a decreased ability to check each other's growth, which can then lead to overgrowth of one or more of the disturbed colonies which may further damage some of the other smaller beneficial ones in a vicious cycle. As more beneficial colonies are damaged, making the imbalance more pronounced, more overgrowth issues occur because the damaged colonies are less able to check the growth of the overgrowing ones. If this goes unchecked long enough, a pervasive and chronic imbalance between colonies will set in, which ultimately minimizes the beneficial nature of these colonies as a whole.

Microbial colonies also excrete many different types of waste byproducts.[11] Using different waste removal mechanisms, under normal circumstances the body effectively manages these byproducts with little or no trouble. Unfortunately, oversized and inappropriately large colonies, due to their increased numbers, excrete increased amounts of these byproducts. As the amount of microbial byproducts increases, the higher waste byproducts levels can overburden the body's waste removal mechanisms.

It is the combination of these two negative outcomes that causes many of the negative health symptoms observed when dysbiosis is present.

Associated IllnessesEdit

Disruptions in the microbiome can allow outside factors or even pathogenic members of the microbiome to take hold in the gut environment. Dysbiosis has been reported to be associated with illnesses, such as periodontal disease,[12] inflammatory bowel disease,[13][14] chronic fatigue syndrome,[15] obesity,[16][17] cancer,[18][19] bacterial vaginosis,[20] and colitis.[21]

CancerEdit

Sustained periods of dysbiosis lead to extended amounts of stress and inflammation in the gut microbiome, which can in turn promote the production of carcinogenic metabolites.[22]

Clostridium DifficileEdit

C. difficile is an opportunistic bacteria that commonly infects patients following a disruption in the microbiome, such as treatment with antibiotics.[23][24] Infection can lead to several different symptoms including watery diarrhea, fever, loss of appetite, nausea, and abdominal pain.[25] Severe or chronic infections of C. difficile can lead to inflammation of the colon, a condition known as colitis.[26]

PeriodontitisEdit

Periodontitis is an oral infection that can damage the bones supporting teeth and lead to tooth loss.[27] One of the major risk factors for periodontitis is the disruption of the oral microbiome such that there is an accumulation of pathogenic bacteria.[12]

TreatmentsEdit

AntibioticsEdit

Because of the complex interactions in the microbiome, not much data exists on the efficacy of using antibiotics to treat dysbiosis. However, a broad-spectrum antibiotic that has low impact on the intestinal gut microbiome called rifixin, has been shown to be effective in improving several of the ailments associated with dysbiosis, including Irritable Bowel Syndrome,[28] Ulcerative Coilitis[29] and Crohn's Disease.[30]

Fecal Microbiota Transplant (FMT)Edit

FMTs use the same line of reasoning as probiotics; to recreate a healthy balance of microbiota in the microbiome by inserting beneficial microbes into the environment. FMT accomplishes this by taking a donation of fecal matter from a healthy individual, diluted, strained and introduced to a diseased patient.[31] FMTs are currently used to treat patients with Clostridium Difficile infections, who have proved resistant to other therapies.[32] Because the process is not sterile and contaminations can pass from donor to patient, there is a push to isolate key microbiota and culture them independently.[33]

ProbioticsEdit

The World Health Organization defines probiotics as "live microorganisms, which when administered in adequate amounts, confer a health benefit on the host."[34] The benefit of using probiotics to treat dysbiosis related diseases lies in its ability to treat the underlying cause of said diseases. Some benefits include their ability to suppress inflammation in the microbiome[35][36] and disrupt colonization by pathogens.[37]

See alsoEdit

Notes and referencesEdit

  1. ^ Tamboli CP, Neut C, Desreumaux P, Colombel JF (January 2004). "Dysbiosis in inflammatory bowel disease". Gut. 53 (1): 1–4. doi:10.1136/gut.53.1.1. PMC 1773911. PMID 14684564.
  2. ^ a b Moos WH, Faller DV, Harpp DN, Kanara I, Pernokas J, Powers WR, Steliou K (2016). "Microbiota and Neurological Disorders: A Gut Feeling". BioResearch Open Access. 5 (1): 137–45. doi:10.1089/biores.2016.0010. PMC 4892191. PMID 27274912. As reviewed in this report, synthetic biology shows potential in developing microorganisms for correcting pathogenic dysbiosis (gut microbiota-host maladaptation), although this has yet to be proven.
  3. ^ Fujimori S (June 2015). "What are the effects of proton pump inhibitors on the small intestine?". World Journal of Gastroenterology. 21 (22): 6817–9. doi:10.3748/wjg.v21.i22.6817. PMC 4462721. PMID 26078557. Several meta-analyses and systematic reviews have reported that patients treated with PPIs, as well as post-gastrectomy patients, have a higher frequency of small intestinal bacterial overgrowth (SIBO) compared to patients who lack the aforementioned conditions. Furthermore, there is insufficient evidence that these conditions induce Clostridium difficile infection. At this time, PPI-induced dysbiosis is considered a type of SIBO.
  4. ^ Erdogan A, Rao SS (April 2015). "Small intestinal fungal overgrowth". Current Gastroenterology Reports. 17 (4): 16. doi:10.1007/s11894-015-0436-2. PMID 25786900. Small intestinal fungal overgrowth (SIFO) is characterized by the presence of excessive number of fungal organisms in the small intestine associated with gastrointestinal (GI) symptoms. Candidiasis is known to cause GI symptoms particularly in immunocompromised patients or those receiving steroids or antibiotics. However, only recently, there is emerging literature that an overgrowth of fungus in the small intestine of non-immunocompromised subjects may cause unexplained GI symptoms. Two recent studies showed that 26 % (24/94) and 25.3 % (38/150) of a series of patients with unexplained GI symptoms had SIFO. The most common symptoms observed in these patients were belching, bloating, indigestion, nausea, diarrhea, and gas. The underlying mechanism(s) that predisposes to SIFO is unclear but small intestinal dysmotility and use of proton pump inhibitors has been implicated. However, further studies are needed; both to confirm these observations and to examine the clinical relevance of fungal overgrowth, both in healthy subjects and in patients with otherwise unexplained GI symptoms.
  5. ^ Kau AL, Ahern PP, Griffin NW, Goodman AL, Gordon JI (June 2011). "Human nutrition, the gut microbiome and the immune system". Nature. 474 (7351): 327–36. doi:10.1038/nature10213. PMC 3298082. PMID 21677749.
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  8. ^ Yan AW, Fouts DE, Brandl J, Stärkel P, Torralba M, Schott E, Tsukamoto H, Nelson KE, Brenner DA, Schnabl B (January 2011). "Enteric dysbiosis associated with a mouse model of alcoholic liver disease". Hepatology. 53 (1): 96–105. doi:10.1002/hep.24018. PMC 3059122. PMID 21254165.
  9. ^ Mutlu E, Keshavarzian A, Engen P, Forsyth CB, Sikaroodi M, Gillevet P (October 2009). "Intestinal dysbiosis: a possible mechanism of alcohol-induced endotoxemia and alcoholic steatohepatitis in rats". Alcoholism, Clinical and Experimental Research. 33 (10): 1836–46. doi:10.1111/j.1530-0277.2009.01022.x. PMC 3684271. PMID 19645728.
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  11. ^ Carding S, Verbeke K, Vipond DT, Corfe BM, Owen LJ (2015-02-02). "Dysbiosis of the gut microbiota in disease". Microbial Ecology in Health and Disease. 26: 26191. doi:10.3402/mehd.v26.26191. PMC 4315779. PMID 25651997.
  12. ^ a b Nath SG, Raveendran R (July 2013). "Microbial dysbiosis in periodontitis". Journal of Indian Society of Periodontology. 17 (4): 543–5. doi:10.4103/0972-124X.118334. PMC 3800425. PMID 24174742.
  13. ^ Marteau P (2009). "Bacterial flora in inflammatory bowel disease". Digestive Diseases. 27 Suppl 1: 99–103. doi:10.1159/000268128. PMID 20203504.
  14. ^ Lepage P, Leclerc MC, Joossens M, Mondot S, Blottière HM, Raes J, Ehrlich D, Doré J (January 2013). "A metagenomic insight into our gut's microbiome". Gut. 62 (1): 146–58. doi:10.1136/gutjnl-2011-301805. PMID 22525886.
  15. ^ Lakhan SE, Kirchgessner A (October 2010). "Gut inflammation in chronic fatigue syndrome". Nutrition & Metabolism. 7: 79. doi:10.1186/1743-7075-7-79. PMC 2964729. PMID 20939923.
  16. ^ Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI (December 2006). "An obesity-associated gut microbiome with increased capacity for energy harvest". Nature. 444 (7122): 1027–31. doi:10.1038/nature05414. PMID 17183312.
  17. ^ Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI (January 2009). "A core gut microbiome in obese and lean twins". Nature. 457 (7228): 480–4. doi:10.1038/nature07540. PMC 2677729. PMID 19043404.
  18. ^ Castellarin M, Warren RL, Freeman JD, Dreolini L, Krzywinski M, Strauss J, Barnes R, Watson P, Allen-Vercoe E, Moore RA, Holt RA (February 2012). "Fusobacterium nucleatum infection is prevalent in human colorectal carcinoma". Genome Research. 22 (2): 299–306. doi:10.1101/gr.126516.111. PMC 3266037. PMID 22009989.
  19. ^ Kostic AD, Gevers D, Pedamallu CS, Michaud M, Duke F, Earl AM, Ojesina AI, Jung J, Bass AJ, Tabernero J, Baselga J, Liu C, Shivdasani RA, Ogino S, Birren BW, Huttenhower C, Garrett WS, Meyerson M (February 2012). "Genomic analysis identifies association of Fusobacterium with colorectal carcinoma". Genome Research. 22 (2): 292–8. doi:10.1101/gr.126573.111. PMC 3266036. PMID 22009990.
  20. ^ Africa CW, Nel J, Stemmet M (July 2014). "Anaerobes and bacterial vaginosis in pregnancy: virulence factors contributing to vaginal colonisation". International Journal of Environmental Research and Public Health. 11 (7): 6979–7000. doi:10.3390/ijerph110706979. PMC 4113856. PMID 25014248.
  21. ^ Mazmanian SK (April 2008). "Capsular polysaccharides of symbiotic bacteria modulate immune responses during experimental colitis". Journal of Pediatric Gastroenterology and Nutrition. 46 Suppl 1: E11–2. doi:10.1097/01.mpg.0000313824.70971.a7. PMID 18354314.
  22. ^ Sheflin AM, Whitney AK, Weir TL (October 2014). "Cancer-promoting effects of microbial dysbiosis". Current Oncology Reports. 16 (10): 406. doi:10.1007/s11912-014-0406-0. PMC 4180221. PMID 25123079.
  23. ^ Knoop FC, Owens M, Crocker IC (July 1993). "Clostridium difficile: clinical disease and diagnosis". Clinical Microbiology Reviews. 6 (3): 251–65. PMC 358285. PMID 8358706.
  24. ^ Surawicz CM, Brandt LJ, Binion DG, Ananthakrishnan AN, Curry SR, Gilligan PH, McFarland LV, Mellow M, Zuckerbraun BS (April 2013). "Guidelines for diagnosis, treatment, and prevention of Clostridium difficile infections". The American Journal of Gastroenterology. 108 (4): 478–98, quiz 499. doi:10.1038/ajg.2013.4. PMID 23439232.
  25. ^ "Clostridium difficile Infection Information for Patients". Centers for Disease Control. Retrieved 2018-06-27.
  26. ^ Surawicz CM, McFarland LV, Elmer G, Chinn J (October 1989). "Treatment of recurrent Clostridium difficile colitis with vancomycin and Saccharomyces boulardii". The American Journal of Gastroenterology. 84 (10): 1285–7. PMID 2679049.
  27. ^ "Periodontitis - Symptoms and causes". Mayo Clinic. Retrieved 2018-06-27.
  28. ^ Sharara AI, Aoun E, Abdul-Baki H, Mounzer R, Sidani S, Elhajj I (February 2006). "A randomized double-blind placebo-controlled trial of rifaximin in patients with abdominal bloating and flatulence". The American Journal of Gastroenterology. 101 (2): 326–33. doi:10.1111/j.1572-0241.2006.00458.x. PMID 16454838.
  29. ^ Guslandi M, Petrone MC, Testoni PA (April 2006). "Rifaximin for active ulcerative colitis". Inflammatory Bowel Diseases. 12 (4): 335. doi:10.1097/01.MIB.0000215092.85116.6c. PMID 16633057.
  30. ^ Shafran I, Johnson LK (August 2005). "An open-label evaluation of rifaximin in the treatment of active Crohn's disease". Current Medical Research and Opinion. 21 (8): 1165–9. doi:10.1185/030079905X53252. PMID 16083525.
  31. ^ "What is FMT? – The Fecal Transplant Foundation". thefecaltransplantfoundation.org. Retrieved 2018-06-27.
  32. ^ Smith MB, Kelly C, Alm EJ (February 2014). "Policy: How to regulate faecal transplants". Nature. 506 (7488): 290–1. doi:10.1038/506290a. PMID 24558658.
  33. ^ Dupont HL (October 2013). "Diagnosis and management of Clostridium difficile infection". Clinical Gastroenterology and Hepatology. 11 (10): 1216–23, quiz e73. doi:10.1016/j.cgh.2013.03.016. PMID 23542332.
  34. ^ Food and Agriculture Organization of the United Nations; World Health Organization. Health and Nutritional Properties of Probiotics in Food Including Powder Milk with Live Lactic Acid Bacteria.Córdoba, Argentina: Food and Agriculture Organization of the United Nations, World Health Organization; 2001.
  35. ^ Drakes M, Blanchard T, Czinn S (June 2004). "Bacterial probiotic modulation of dendritic cells". Infection and Immunity. 72 (6): 3299–309. doi:10.1128/IAI.72.6.3299-3309.2004. PMID 15155633.
  36. ^ Kim SO, Sheikh HI, Ha SD, Martins A, Reid G (December 2006). "G-CSF-mediated inhibition of JNK is a key mechanism for Lactobacillus rhamnosus-induced suppression of TNF production in macrophages". Cellular Microbiology. 8 (12): 1958–71. doi:10.1111/j.1462-5822.2006.00763.x. PMID 16889627.
  37. ^ Kendall MM, Sperandio V (January 2007). "Quorum sensing by enteric pathogens". Current Opinion in Gastroenterology. 23 (1): 10–5. doi:10.1097/MOG.0b013e3280118289. PMID 17133078.

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