Gastrointestinal Assay Kit

CoproELISA H Pylori Assay Kit

$430.00

The CoproELISA H Pylori Assay Kit is an Enzyme-Linked Immunosorbent Assay (ELISA) for use as a screening and detection test of Helicobacter pylori in human stool of suspected patient. The Eagle Biosciences CoproELISA H. pylori Assay Kit is for Research Use Only and is not intended for diagnostic or therapeutic purposes.

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CoproELISA H Pylori Assay Kit

The CoproELISA H Pylori Assay Kit is For Research Use Only

Size: 1×96 wells
Sensitivity: Cut-Off Control
Incubation Time: < 2 hours
Sample Type: Stool
Sample Size: 0.1 to 0.3 g
Alternative Name: Heliobacter pylori

Assay Background

H. pylori (previously known as Campylobacter pyloridis) is a type of bacteria that infects the stomach and is a common cause of peptic ulcers. H. pylori bacteria can be passed from person to person through direct contact with saliva, vomit or fecal matter. H. pylori can also be spread through contaminated food or water. The infection is normally acquired during childhood. H. pylori usually goes undiagnosed until symptoms of a peptic ulcer occur. H. pylori infection is quite common and is present in about half the people in the world.

Assay Principle

Break-apart microwells are coated with monoclonal anti- H. pylori capture antibodies. Patient samples are diluted in H. pylori Stool Diluent and added to the microwells. A monoclonal antibody conjugated to horseradish peroxidase (HRP) is added to the microwells and incubated for 60 minutes at room-temperature. Unbound conjugate is removed by washing. TMB-substrate is added; the substrate is hydrolyzed by the peroxidase and yields a blue solution of the reduced substrate. Upon the addition of the stop solution, the blue color turns yellow and should be read by an ELISA reader at a wavelength of 450/620 nm.

Related Products

CoproELISA Blastocystis Assay Kit
CoproELISA C. difficile GDH Assay Kit

Additional Information

Assay Background

Helicobacter pylori (H. pylori) is a Gram-negative, micro-aerophilic  bacterium restricted to the stomach and the duodenum. It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren, who found that it was present in patients with chronic gastritis and gastric ulcers, conditions that were not previously believed to have a microbial cause. H. pylori has also been associated as an etiologic agent in the development of duodenal ulcers and stomach cancer. More than fifty percent of the world’s population harbor H. pylori in their upper gastrointestinal tract. However, over 80 percent of individuals infected with this bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology. H. pylori is a contagious bacterium, although the exact route of transmission is not known. Person-to-person transmission by either the oral-oral or fecal-oral route is most frequent. Consistent with these transmission routes, the bacteria have been isolated from feces, saliva and dental plaques of some infected patients. Transmission occurs mainly within families in developed nations, yet can also be acquired from the community in developing countries.

Cross Reaction

The CoproELISA Entamoeba test was evaluated using stool specimens defined as positive for various gastrointestinal pathogens. No cross-reactivity of interference by mixed infection with any of the pathogens listed: Blastocystis,  C. difficile, Cryptosporidium, E. coli, E. nana, D. fragilis, G. lamblia, Salmonella spp.

References

  1. Blaser M. J. (2006). “Who are we? Indigenous microbes and the ecology of human diseases”. EMBO Reports 7(10): 956-60.
  2. Mégraud F. (1995). “Transmission of Helicobacter pylori: faecal–oral versus oral–oral route”. Aliment Pharmacol Ther 9(2):85-91.
  3. Cave D. R. (1996). “Transmission and epidemiology of Helicobacter pylori”. Am J Med 100(5A):12–17; discussion 17-18.
  4. Delport W. van der Merwe S. W. (2007). “The transmission of Helicobacter pylori: the effects of analysis method and study population on inference”. Best Pract Res Clin Gastroenterol 21(2):215-36.
  5. Bytzer P. Dahlerup J. F. Eriksen J. R. Jarbøl D. E. Rosenstock S. Wildt S. (2011). “Diagnosis and treatment of Helicobacter pylori infection”. Dan Med Bull 58(4): C4271.
  6. Butcher, Graham P. (2003). Gastroenterology: An Illustrated Colour Text. Elsevier Health Sciences. p. 5-25.
  7. Ryan K. (2010). Sherris Medical Microbiology. McGraw-Hill. pp.573, 576.
  8. Stenström B. Mendis A. Marshall B. (2008). “Helicobacter pylori- The latest in diagnosis and treatment”. Aust Fam Physician 37(8):608-12.
  9. Malfertheiner P. Megraud F. Morain O. (2002). “Current concepts in the management of Helicobacter pylori infection” – The Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther 16:167-80.

Manual

Product Manual