Medical microbiology is a rapidly growing and changing subject: new organisms are constantly being identified and our understanding of the pathogenic potential of recognised pathogens is being expanded. In addition, the taxonomists keep changing the names of familiar organisms.

Procalcitonin (PCT) is a newly recognised marker of bacterial infections. PCT is the prohormone of calcitonin. It was discovered by chance that PCT increases during infection. This discovery has led to the use of PCT as a marker of bacterial infection. A prospective study showed that PCT was high only in bacterial infections, and that initially high PCT values decreased in patients treated with antibiotics, whereas PCT remained constantly low in patients infected with viruses or suffering from inflammatory diseases (Gendel & Bohoun, 2000). Unlike other markers such as ESR and C-reactive protein (CRP), PCT remains low during episodes of known inflammatory diseases such as lupus, connective tissue diseases, in inflammatory rheumatism and digestive tract inflammatory diseases. In one recent study of patients suffering from lupus and vasculitis, PCT increased only in cases of bacterial super infections making it possible to distinguish between inflammatory flare-up and super infection, which was not possible with CRP. Inflammatory phenomena are extensive in immunologic attacks, particularly in transplant patients in the rejection phase.

A study by Hammer et al (1998) concerned a total of 78 patients who had undergone heart or lung transplant. Acute rejection in each case lead to increase in PCR, whereas PCT remained low, as in viral infection. Generalised bacterial infections led to increases of PCT, making it possible in all cases to distinguish such infections from rejection. Procalcitonin remains low during viral infections, as in inflammatory diseases, in the absence of bacterial super infection. This is one of the principal advantages of PCT and differentiates it completely from other markers. Thus procalcitonin is a promising marker because of its sensitivity and its high specificity. In most cases it distinguishes infection and inflammation that acute phase proteins such as CRP cannot do. In addition to PCT and CRP, Interleukin-6 (IL-6) is also used as a marker for bacterial infections (Toikka, 2000). The semi quantitative method of determination used at the patients bedside is based on immunochromatography. A test kit using this method is available commercially with Brams Diagnostica, Berlin, Germany (Assicot, 1993).

KEYWORDS: Procalcitonin, Bacterial infections, CRP, ESR, Interleukin-6

Gendel D, Bohoun C (2000), Procalcitonin as a marker of bacterial infections. Pediatr Infect Dis J 19:679-688

Hammer S et al (1998), Procalcitonin: a new marker for diagnosis of acute rejection and bacterial infection in patients after heart and lung transplantation. Transplant Immunol 6:235-241

Assicot M et al (1993), High serum procalcitonin concentrations in patients with sepsis and infection. Lancet 34:515-518

Toikka P et al (2000), Serum procalcitonin, C-reactive protein and interleukin-6 for distinguishing bacterial and viral pneumonia in children. Pediatr Infect Dis J 19:593-602

During the last 15 years, the role of Helicobacter pylori (H.pylori) infection in the pathogenesis of gastritis and peptic ulcer disease has been elucidated. Therapy of H.pylori infection heals peptic ulcer disease. Furthermore, H.pylori infection is involved in the pathogenesis of gastric adenocarcinoma and lymphoma. H.pylori infection can be diagnosed by culture of gastric biopsy tissue on non-selective media (e.g. chocolate agar) or selective media (e.g. Skirrow). Organisms usually can be visualised on histologic section with Warthin-Starry silver, Giemsa, Steiner or Genta staining. Infection with H.pylori can be diagnosed but not excluded on the basis of H & E stains. Because of production of urea by the organisms, urea testing of gastric specimen can give a rapid and specific microbiologic diagnosis. Each of these tests requires endoscopy and biopsy. Available non-invasive tests include the urea breath test, which detects labelled carbon dioxide in expired air after oral administration of isotopically labelled urea and serology for presence of immunoglobulin IgG to H.pylori. Each of these diagnostic tests has a sensitivity and specificity of 95% or more. With increased insight into the pathogenesity of H.pylori the demand for a non-invasive reliable diagnostic test for H.pylori has emerged.

What this study adds:

Because many studies support the hypothesis of a faecal-oral route of infection and because H.pylori has been detected in stool, increased interest has been focused on the diagnostic detection of H.pylori antigens in stool samples. A newly developed H.pylori antigen test in stool (faecal) specimens (HpSA) detects bacterial material in faeces. The new non-invasive, low cost H.pylori antigen test in the faeces can replace C-urea breath test for the detection of H.pylori infection. In a multinational European study 501 patients had the stool test, gastric endoscopy and biopsy, and urea breath test. Two hundred and seventy-two patients had H.pylori infection shown on biopsy and of these, 256 had a positive stool antigen test. Two hundred and nineteen patients did not have H.pylori infection and the stool test was positive in 18 of them. The stool antigen test was therefore 94% sensitive and 92% specific. In the various centres the stool antigen test was 84-100% sensitive. Four weeks after treatment for H.pylori infection the sensitivities and specificities for persisting infection were : HpSA 90% and 95%, urea breath test 90% and 99%. A new test for H.pylori antigen in the stool is accurate and convenient in the diagnosis of H.pylori gastritis.

Braden B et al (2000), Comparison of new faecal antigen test with C-urea breath test for detecting Helicobacter pylori infection and monitoring eradication of treatment: prospective clinical evaluation. BMJ 320: 148

Vaira D et al (1999), Diagnosis of Helicobacter pylori infection with a new non-invasive antigen-based assay. Lancet 354:30