Biomedical subjects
Publications and source records attributed to C A McNulty.
Radon and thoron gas emanation from tableware with ceramic glazes containing elevated uranium levels was determined using alpha-scintillation cells. Though gamma spectroscopy noted significant uranium concentrations in the glazed, no radioactive gas emanation was observed, contradicting a previous report.
BACKGROUND: The Cortecs Diagnostics Helisal Assay test is a quantitative immunoassay for salivary IgG antibodies against Helicobacter pylori. Saliva can be obtained simply with the kit in the general practitioners surgery. AIMS: To compare the new saliva serological test for H pylori with 'gold standard' evidence of H pylori infection (antral biopsy specimens for histology, culture, and urease test) and a new serum serological test. PATIENTS: Eighty six unselected dyspeptic patients undergoing endoscopy. METHODS: Each patient provided saliva and serum before endoscopy for H pylori serology, which was compared against 'gold standard' evidence of infection. RESULTS: Thirty two patients were H pylori positive by the 'gold standard' tests. At a cut off value of 0.15 EU/ml the saliva test had a sensitivity of 88% and a specificity of 71%, with a negative predictive value of 90%. If patients who were taking omeprazole or had recent antibiotics are excluded, the sensitivity is unchanged but the specificity increases to 79%. The serum test had a similar sensitivity of 85% but better specificity of 78%. CONCLUSION: Serum testing remains the best serological test for H pylori in the hospital setting. Saliva testing may have a role in epidemiological studies and in screening dyspeptic patients in general practice, especially in children in whom venesection is more difficult.
METHODS: Forty-three patients positive for Helicobacter pylori by histology and culture of antral biopsies (n = 40) or histology alone (n = 3) were investigated. They received either regimen 1--tripotassium dicitrato bismuthate 120 mg q.d.s. and tetracycline 250 mg q.d.s. for 4 weeks, with metronidazole 200 mg q.d.s. for the first 2 weeks, or regimen 2--omeprazole 20 mg b.d., amoxycillin 500 mg t.d.s., tetracycline 500 mg q.d.s. each for 3 weeks. Gastric antral biopsies were scored (0-3) histologically for mucus depletion, polymorphonuclear and mononuclear cell infiltrate. H. pylori eradication was assessed by biopsy and culture 1 month after the cessation of treatment. RESULTS: With regimen 1, pre-treatment mucus depletion was significantly higher where eradication was successful (median score 2) compared to where it was not (median score 1, P < 0.01); there were no differences in the scores for polymorphonuclear or mononuclear cell infiltrates. In patients receiving regimen 2, there were no differences in either mucus depletion or polymorphonuclear or mononuclear cell infiltrate, between those where eradication was successful and those where it was not. Metronidazole minimum inhibitory concentrations rose when eradication with regimen 1 was unsuccessful (median before 0.19 mg/L, median after treatment 16 mg/L; P = 0.04). CONCLUSION: Pre-treatment mucus depletion is identified as a factor affecting H. pylori eradication. Preservation of mucus may facilitate acquisition of metronidazole resistance.
A hundred elderly dyspeptic patients were studied to assess the prevalence of Helicobacter pylori infection and the correlation between histological and serological findings. Eighty-one per cent of the patients with gastritis and 63% with gastric ulcer were H. pylori positive. All patients who had H. pylori negative gastritis and gastric ulcers were on nonsteroidal anti-inflammatory drugs (NSAIDs). There were 24 patients who had evidence of H. pylori infection and were on NSAIDs. H. pylori positive patients had more dyspeptic symptoms in comparison with those who were H. pylori negative. In patients who were taking NSAIDs, the presence of severe active gastritis seemed to correlate with the presence of H. pylori but not with the use of NSAIDs. Serology had a sensitivity of 90% and a specificity of 93% with a negative predictive value of 86%. There was a significant correlation between IgG titre and the degree of inflammation and H. pylori infection. We conclude that H. pylori gastritis is the commonest histopathological finding in elderly dyspeptic patients. H. pylori infection may be an important risk factor in elderly patients who take NSAIDs, increasing their risk of gastric ulcer. H. pylori serology in elderly people has a high sensitivity and specificity comparable with those in young age groups.
Fifteen elderly patients with type B gastritis caused by Helicobacter pylori infection were treated with triple therapy consisting of colloidal bismuth subcitrate, amoxycillin and metronidazole. All were followed up every 6 weeks for 3 months. After triple therapy, eradication of the infection was confirmed in 12 patients (85%) by histology and bacteriology. In this group, a significant reduction in IgG antibody levels against H. pylori was detected (p < 0.001). In a control group of 15 patients with type B gastritis who received no antibacterial treatment, the specific IgG antibody titre remained unchanged during 3 months of follow-up. We conclude that this simple and noninvasive serological test would be suitable for follow-up after treatment of H. pylori infection in elderly patients.
Variation amongst strains of Helicobacter pylori was examined by 35S-methionine-labelled protein SDS-PAGE (Radio-PAGE), immunoblot and DNA fingerprinting techniques. These methods allowed discrimination amongst isolates and showed total correlation. Pig and baboon gastric Helicobacter pylori-like organisms were found to be very similar to Helicobacter pylori by both Radio-PAGE and immunoblotting, whereas a Helicobacter mustelae isolate was markedly different. The HindIII restriction endonuclease digest patterns of Helicobacter pylori DNA illustrated the considerable genomic variation of this organism. The Radio-PAGE and immunoblot typing methods both gave precise identification of Helicobacter pylori strains, but Radio-PAGE was found to give higher resolution and represents a standardised universally applicable fingerprinting method for Helicobacter pylori.
The presence of C pylori infection was determined in 1445 patients undergoing upper gastrointestinal endoscopy over a 12 month period. The presence of C pylori was detected in gastric mucosal biopsy specimens by the biopsy urease test, microscopy (Gram stained smears and histology) and culture. Two media were used for the biopsy urease test: Christensen's urea broth (for the first 600 patients) and the Christensen's urea broth modified by increasing the concentration of phenol red and omitting the nutrients, glucose and peptone (for the remaining patients). Both the Christensen's urea broth and modified urea broth were almost 100% specific when compared with detection of C pylori by Gram, culture and histopathology. The modified broth was more sensitive (96% sensitivity compared with culture) than the Christensen's broth (92% sensitivity) but this difference was not statistically significant. The modified broth gave significantly more positive results (58%) in less than 30 minutes than the Christensen's broth (48%). Seventy four per cent of positive results were available in less than two hours. Specimens from patients with extensive C pylori infection gave more rapid results: 86% of specimens that yielded a profuse growth of C pylori and 76% that contained numerous organisms on histological sections had a positive urease test in less than one hour. There was no significant difference between the specificity and sensitivity of our modified urea broth and the other modified broths described in the literature. This test is a cheap and rapid alternative to the diagnosis of C pylori by Gram stained smears or culture.
A new spiral bacterium, distinct from Campylobacter pylori, was found in the gastric mucosa of six patients with gastrointestinal symptoms. All patients had chronic active type B gastritis and four had oesophagitis. Culture and microscopy for C pylori infection was negative. These unculturable spiral organisms were probably an incidental finding in patients presenting for upper gastrointestinal endoscopy, but it is not possible to say from this small series whether these organisms cause chronic active gastritis. The organism is helical, 3.5-7.5 microns long and 0.9 micron in diameter with truncated ends flattened at the tips, and up to 12 sheathed flagella 28 nm in diameter at each pole. It is proposed that this spiral bacterium should be called "Gastrospirillum hominis Gen.nov., Sp.nov."
There is now much worldwide evidence that Campylobacter pylori plays a pathogenic role in the aetiology of gastritis rather than colonizing an already inflamed gastric mucosa. 1) There is a very close association between the presence of C. pylori on the gastric mucosa and histologically confirmed Type B chronic active gastritis. Ninety percent of patients with C. pylori infection have gastritis whereas less than 5% of patients with normal mucosa are colonized. 2) C. pylori only colonizes gastric type mucosa; it is not found colonizing intestinal type mucosa in the stomach. 3) Two volunteer studies have confirmed Koch's third and fourth postulates. Ingestion of C. pylori led to the development of histologically proven gastritis. 4) Outbreaks of hypochlorhydric C. pylori gastritis have occurred. In one such epidemic 17 of 37 volunteers developed C. pylori hypochlorhydric gastritis after acid secretion studies were undertaken with an unsterilized pH electrode. 5) Susceptible animal models (gnotobiotic piglets and the macacus monkey) inoculated with a suspension of C. pylori have developed histologically proven gastritis. 6) Clearance of C. pylori with antimicrobial agents (amoxicillin or nitrofurantoin) or bismuth salts (colloidal bismuth subcitrate or bismuth salicylate), alone or in combination, leads to rapid resolution of the histologically confirmed gastritis. If relapse occurs the gastritis returns.
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Contaminating bacteria from the oropharynx and bacteria that colonise the stomachs of patients with a high gastric pH impede the isolation of Campylobacter pylori from gastric biopsy specimens. Commercially available selective supplements are inhibitory to this organism and therefore a specific selective medium is needed for isolation. Potential selective agents were evaluated for their activity against 97 strains of Campylobacter pylori. A modification of Skirrow's medium was developed; cefsulodin (5 mg/l) was substituted for polymyxin, and amphotericin B (5 mg/l) was added to inhibit Candida spp., a common contaminant of the stomach. No strains of Campylobacter pylori were inhibited by the Campylobacter pylori selective medium and it supported the growth of all strains compared with the biopsy urease test and Gram stained smear. Colonies were slightly larger and more easily recognised on the new medium compared with those grown on chocolate blood agar. This medium greatly improves the isolation of Campylobacter pylori and could be used alone, without a non-selective medium.
The MICs of 21 antimicrobial agents were determined for 97 clinical isolates of Campylobacter pylori. The beta-lactams (penicillin, ampicillin, cefoxitin and cephalexin), macrolides (erythromycin and azithromycin), quinolones (ciprofloxacin and ofloxacin), nitrofurans, gentamicin and tetracycline all had MIC90 values of less than or equal to 0.5 mg/l. Aztreonam, flucloxacillin, amifloxacin and rifampicin had moderate activity. All isolates were resistant to vancomycin, cefsulodin and amphotericin B. Five percent of the strains were inhibited by 8 mg/l of polymyxin. Of the oral agents tested, the nitrofurans and ampicillin are probably the most appropriate antimicrobial agents. Azithromycin and the oral form of cefuroxime are promising alternatives. Cefsulodin, vancomycin and amphotericin B would be suitable constituents of selective media for isolation of Campylobacter pylori.
Gastric mucosal concentrations of erythromycin, amoxycillin, ampicillin and ciprofloxacin were determined in patients at upper gastrointestinal endoscopy 38-480 min after a 500 mg dose of erythromycin ethyl succinate, erythromycin stearate, amoxycillin, pivampicillin or ciprofloxacin. All the agents attained concentrations greater than the MIC 90 for Campylobacter pylori. The macrolides attained the lowest concentrations. There was no significant difference between concentrations attained with erythromycin ethyl succinate and stearate. High concentrations were attained by amoxycillin (range 14.6-322 mg/kg) and pivampicillin (range 47.5-209 mg/kg). Ciprofloxacin attained very high concentrations (range 35-1762 mg/kg); inhibitory concentrations 35 mg/kg) were still present at 6 h after the dose. Ciprofloxacin and erythromycin are ineffective in vivo despite these high gastric mucosal concentrations. Penetration into the gastric mucus and crypts where C. pylori is found will be determined by physicochemical properties of the antimicrobials, such as pKa, stability, activity over a wide range of pH, and lipid solubility.
One hundred and fifty isolates of Campylobacter pylori were divided into nine groups by immunoblot fingerprinting. All isolates were typable and reproducibility between immunoblots was good provided both antigen and antibody preparation were standardised. Discrimination was a problem as Groups 1 and 2 accounted for 66% of isolates. Recurrence after bismuth treatment was due to indistinguishable strains in five patients and different strains in three patients.
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