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OXOID PYLORI TEST

Code: DR0130

Oxoid Pylori Test is a rapid latex agglutination test for the qualitative detection of Helicobacter pylori total antibodies in serum as an aid in the diagnosis of infection by Helicobacter pylori. The product is intended for use to test patients with symptoms of gastro-intestinal disorders.

Introduction
In 1983, Marshall and Warren cultured a new pathogen from patients with gastritis¹. These findings stimulated research into the relationship between Helicobacter pylori and gastric disease. Studies have established that Helicobacter pylori (formerly Campylobacter pylori) can cause chronic gastritis², and an increasing amount of evidence indicates that there is an association between Helicobacter pylori infection and peptic ulcers^3,4,5. Recently Helicobacter pylori has also been identified as a risk factor for gastric cancer^6,7. Nearly 100% of patients with duodenal ulcers^8,9, 70 % of those with gastric ulcer^2,10,11 and more than 80% of patients with gastric cancer^6,12 have Helicobacter pylori infection.
Once infection caused by Helicobacter pylori has been diagnosed, the patient can be treated with antimicrobial drugs. Successful eradication of Helicobacter pylori leads to disappearance of gastric inflammation¹³. Among duodenal ulcer patients, eradication of Helicobacter pylori has been followed by healing of the ulcer and by reduced rate of ulcer relapse^14,15. Several techniques, both invasive and non-invasive, are now available for diagnosing Helicobacter pylori infection. The invasive methods include culture, histological examination and urease testing of biopsy specimens. They require the collection of multiple pinch biopsy samples taken during upper gastro-intestinal endoscopy. Although commonly used, the invasive methods are rather tedious and time consuming, and require a sampling procedure that may cause patient discomfort. In addition, Helicobacter pylori is a delicate organism, and is therefore easily destroyed if transported.
The non-invasive methods available include the urea breath test requiring patient ingestion of carbon isotope derivatives of urea^16,17,18 and serological detection of serum antibodies to Helicobacter pylori^19,20.21. Helicobacter pylori elicits a specific serological response in the infected person and detection of antibodies to Helicobacter pylori in the patient’s serum is a reliable indicator of Helicobacter pylori infection²² . Serology has also proven to be a useful tool for monitoring efficacy of antimicrobial treatment ²² .

Principle of the test
Oxoid Pylori Test Latex Reagent containing latex particles sensitised with partially purified Helicobacter pylori antigens, is dried on the test card as dry spots. Helicobacter pylori antibodies present in serum specimens will react with the sensitised latex particles, resulting in visually detectable agglutination. Sera containing antibodies reactive to Helicobacter pylori, and sera free of antibodies to Helicobacter pylori, are included in the kit as positive and negative controls respectively.

Components of the Kit
Test Cards DR0131
Four card packages, each containing two test cards with three reaction circles. Latex reagent sensitised with partially purified Helicobacter pylori antigens, and containing <1% sodium azide, is dried on the reaction circles.
Positive Control DR0133
One vial (0.5 ml) of diluted rabbit serum having antibodies reactive to Helicobacter pylori, and containing <0.1% sodium azide as a preservative. This reagent is supplied ready for use. Allow the reagent to warm to 18–25°C prior to conducting an assay.
Negative Control DR0134
One vial (0.5 ml) of diluted newborn calf serum, non-reactive to Helicobacter pylori, and containing <0.1% sodium azide as a preservative. This reagent is supplied ready for use. Allow the reagent to warm to 18–25°C prior to conducting an assay.
Dilution Buffer DR0132
One bottle (30 ml) of phosphate buffered saline, pH 7.2 ± 0.1 containing <0.1% sodium azide as a preservative. The buffer is supplied ready for use, but should be allowed to warm to 18–25°C prior to use.
Mixing Sticks
Thirty double ended mixing sticks for mixing latex and diluted serum.
Plastic storage pouch
One plastic pouch for storage of the opened test card package containing unused test cards.
Materials required but not provided
Micropipette
Micropipettes capable of delivering volumes of 40 µl, 50 µl and 150 µl (see Procedure, Dilution Method A), or 10 µl and 30 µl (see Procedure, Dilution Method B) are needed.
Test Tubes
Plastic or glass tubes for diluting patient serum samples prior to testing, if using Dilution Method A.
For full proceedure please see produt insert.

Precautions
The dried latex reagent on the cards contain as preservative <1% sodium azide which is harmful when inhaled, swallowed, on in contact with skin. The dissolved latex reagent contains <0.1% sodium azide which is not considered to be a harmful concentration. The other reagents in the kit contain <0.1% sodium azide, as preservative. The copper and lead used in some plumbing systems can react with azides to form explosive salts. The quantities of azide used in this kit are small; nevertheless when disposing of azide-containing materials, they should be flushed away with a large volume of water.
Although the reagents do not contain Helicobacter pylori infectious agents, they are prepared from biological materials and should be handled and discarded as a potential biohazard.

References.
1. Warren JD, and Marshall BJ (1983). Lancet, i:1273–1275.
2. Marshall BJ and Warren JR (1984). Lancet, i:131 I–1314
3. Johnston BJ et al. (1986). Gut, 27: 1132–1137.
4. Goodwin CS (1988). Lancet. ii: 1467–1469.
5. Rathbone BJ et al. (1986). Gut, 27: 635–641.
6. Parsonnet J et al.(1991). N. EngI. J. Med., 325:1127–1131.
7. Forman D et al. (1990). Int. J. Cancer, 46:608–611.
8. Graham DY (1989). Scand. J. Gastroenterol., 24 (suppl. 160): 46–52.
9. Vaira D et al.(1988). J. Clin. Pathol., 41: 355– 356
10. Price AB (1988). Scand. J. Gastroenterol., 23 (suppl. 142): 21–24
11. Dooly CP and Cohen H (1988). Ann. Intern. Med., 108: 70–79.
12. Nomura A et al. (1991). N. Engl. J. Med., 325: 1132–1136
13. Valle J et al. (1991). Scand. J. Gastroenterol., 26:1057–1066
14. Marshall BJ et al. (1988). Lancet, ii: 1437–1441.
15. Seppälä KM et al. (1992). Scand. J.Gastro-enterol., 27:973–976.
16. Graham DY, Klein PD, Evans DL (1987). Lancet, i: 1174–1177.
17. Marshall BJ, Surveyor l (1988). J. Nucl. Med., 219:11–16.
18. Rauws EAJ, Van Royen EA, Langenberg W (1989). Gut, 30(6): 798–803.
19. Evans DJ; Evans DG, Graham DY, Klein PD (1989). Gastroenterol., 96: 1004–1008.
20. Newell DG, Rathbone BJ (1989). Serodiag. and Immunother. Infect. Dis., 3: 1–6.
21. Evans DJ, Evans DG, Smith KE, Graham DY (1989). Infect. Immun., 57(3): 664–667.
22. Kosunen TU et al (1992). Lancet, 339: 893–895.
23. Siurala M, Isokoski M, Varis K, Kekki M (1968). Scand. J. Gastroenterol., 3:211–223.
24. Kekki M, Villako M, Tamre A, Siurala M (1977). Scand. J. Gastroenterol., 12: 321–324.
25. Pettross CW, et al. (1988). Dig. Dis. Sci., 33: 649–653.
26. Rauws EA, Langenberg W, Houthoff HJ, Zanen HC, Tytgat GN (1988). Gastroenterol., 94:3340.
27. Barthel JS, Westblom TU, Jauy AD, Gonzalez F, Everett ED(1988). Arch. Intern. Med., 148:1149–1151.
28. Jones DM, Eldridge J, Fox AJ, Sethi P, Whenwell PJ (1986). J. Med. Microbiol., 22: 57–62.
29. Dooley, CP, et. al.(1989). NewEng. J. Med.,321: 1562–1566.
30. Data on file, Oxoid Ltd