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CAMPYLOBACTERS IN OTTAWA
135 been devised. Supratrigonal denervation of the bladder by transection is still popular,16 and cystolysis produces good early results but late follow-up is disappointing. 17,189 Although the final resort may be a urinary diversion,9 bladder augmentation (such as ileocystoplasty2O and caecocystoplastylb) can be highly effective in relieving the pain and increasing the bladder volume at the same time as removing the unhealthy part of the bladder above the trigone.
CAMPYLOBACTERS IN OTTAWA INTEREST in campylobacters received a notable boost-if it needed boosting-with the Australian discovery of the relation between a new campylobacter-like organism (Campylobacter pyloridis) and gastritis. "We believe that pyloric campylobacter is aetiologically related to chronic antral gastritis and, probably, to peptic ulceration also" was Marshall and Warren’s statement quoted by The Lancet, and "Bets are probably being taken" was the comment it drew.2 How much nearer the punters are to getting an answer was apparent at the Third International Workshop on Campylobacter Infections, held in Ottawa on July 7- 1,0 under the joint auspices of the Laboratory Centre for Disease Control (Health and Welfare Canada) and the Public Health Laboratory Service of England and Wales. Not surprisingly these gastric bacteria received a lot of attention. Researchers from around the world reported the detection of C pyloridis in 50% or more of patients attending gastroscopy clinics, and from Japan (a country with a particularly high incidence of gastric disorders) a figure of 84% was reported. All confirmed a close correlation between bacterial colonisation of the mucosa and clinical and histological gastritis. Correlation with peptic ulceration was not quite so close, and there was variation between countries. Evidence that C pyloridis causes the gastritis, and is not simply an opportunist harmlessly occupying a favourable ecological niche, can now be summarised as follows. Firstly, the bacteria colonise the surface of the gastric epithelium (protected by gastric mucus) in enormous numbers, and where there is colonisation the epithelium is thinned and polymorphonuclear leucocytes are present. Ultrastructural studies show that there are "pedestal" attachments between bacteria and epithelial cells, microvilli are flattened or absent, and bacteria can be found in phagosomes of epithelial cells and polymorphs. Secondly, when bacteria are eliminated by antibacterial therapy, the lesions disappear. It so happens that bismuth salts such as the subcitrate (’De-Nol’) and subsalicylate (’Pepto-Bismol’) are active against these bacteria and it is suggested that their ulcer healing effect is due to their antibacterial action. Thirdly, antibodies specific for Cpyloridis are found in the sera ofcolonised patients. And, fourthly, gastritis was produced in a volunteer (Dr Marshall himself) who swallowed a pure culture of C pyloridis. 3,4 ever
16. Turner-Warwick R, Ashken MH The functional result of partial, subtotal and total cystoplasty with special reference to ureterocaecocystoplasty, selective sphincterotomy and cystocystoplasty. Br J Urol 1967; 39: 3-12. 17. Worth PHL, Turner-Warwick R. The treatment of interstitial cystitis by cystolysis with observations on cystoplasty Br J Urol 1973, 45: 65-71. 18. Worth PHL The treatment of interstitial cystitis by cystolysis with observations on cystoplasty. A review after 7 years Br J Urol 1980; 52: 232 19 Freiha FS, Faysal MH, Stamey TA. The surgical treatment of intractable interstitial cystitis J Urol 1980, 123: 632-34 20 Yeates WK. A technique of ileocystoplasty Br J Urol 1956, 28: 410-13. 1 Warren JR, Marshall B Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983, 1: 1273-75. 2 Editorial. Spirals and ulcers. Lancet 1984, i: 1336-37 3 Marshall BJ, Armstrong JA, McGeckie DB, Glaucy RJ. Attempt to fulfill Koch’s postulates for pyloric camplybacter. Med J Aust 1985; 142: 436-39 4. Editorial Pyloric campylobacter finds a volunteer Lancet 1985; i: 1021-22.
Thus the accumulating evidence is tending to support rather than refute the Australian hypothesis: the odds are shortening. Yet more work needs to be done before we accept a concept that could radically change the management of dyspepsia and ulcer diseases. A prime need is for an animal model; none has been found so far. Trials of antibacterial agents without physiological action on the stomach would help to determine whether elimination of the bacteria alone can bring about ulcer healing. The source of these bacteria is completely unknown. Reports of failure to find them in saliva, gum crevices, or other sites in the alimentary tract may reflect the insensitive nature of current isolation methods rather than their absence from such sites. Ultrastructural studies cast some doubt on their credentials for membership of the genus Campylobacter, but equally one could say "If you know a better genus, go to it". They probably warrant a new genus. The more traditional campylobacters that cause acute diarrhoea (C jejuni and C coli) were by no means eclipsed, at the Ottawa meeting, by their gastric "cousins". Better methods for their isolation and detection were described and it is now clear that most strains produce at least one of two toxins, one of which is antigenically related to cholera and Escherichia coli (heat-labile) enterotoxins. On the epidemiological front there were some notable advances. It is known that raw cow’s milk, untreated water, and occasionally undercooked chicken have been sources of outbreaks of campylobacter enteritis, but the origins of most of the day-today sporadic infections have remained elusive. Hard evidence is now beginning to emerge from the results of case-control studies and more penetrating epidemiological studies, which have become feasible through the application of improved serotyping and biotyping methods. Not surprisingly, chickens, already known to be a major source of infection, have come out badly, particularly "New York dressed" (ungutted) birds. Inexperience on the part of the person preparing chicken meals was found to be a major risk factor through cross-contamination of other foods or the consumption of raw or undercooked meat. In a particularly interesting study in an American university, campylobacter isolations from students were ten times more common than salmonella isolations and it was calculated that 70% of infections were attributable to the eating of chicken. An unexpected finding was that the second-rank risk factor was contact with cats; cat contact emerged as a risk factor in a study in Peru. The sudden exposure to inexpertly prepared foods on entry to university was likened by the authors to a second period of weaning. It will be interesting to see whether attempts to instruct the students in elementary food hygiene will make any impact on infection rates. One experienced (veterinary) voice was sceptical that the culinary habits of the general public could be materially influenced even if those of the students could; he thought the best chances of control lay in attempts to reduce contamination at the slaughter and processing of poultry. Since the first of these campylobacter workshops in 1981, progress has been gratifyingly rapid; but a sense of perspective was wonderfully restored by Dr Kist of Freiburg who, in a historical review, surprised his audience with a paper by Escherich published in 1886 describing and illustrating what was indisputably campylobacter enteritis.5 As a delegate was heard to say "Scientists will keep inventing the wheel".
5 Escherich T
Beitráge zur Keuntriss der Darmbacterien. Munch
Med Wschr Nov 9, 1886
CAMPYLOBACTERS IN OTTAWA INTEREST in campylobacters received a notable boost-if it needed boosting-with the Australian discovery of the relation between a new campylobacter-like organism (Campylobacter pyloridis) and gastritis. "We believe that pyloric campylobacter is aetiologically related to chronic antral gastritis and, probably, to peptic ulceration also" was Marshall and Warren’s statement quoted by The Lancet, and "Bets are probably being taken" was the comment it drew.2 How much nearer the punters are to getting an answer was apparent at the Third International Workshop on Campylobacter Infections, held in Ottawa on July 7- 1,0 under the joint auspices of the Laboratory Centre for Disease Control (Health and Welfare Canada) and the Public Health Laboratory Service of England and Wales. Not surprisingly these gastric bacteria received a lot of attention. Researchers from around the world reported the detection of C pyloridis in 50% or more of patients attending gastroscopy clinics, and from Japan (a country with a particularly high incidence of gastric disorders) a figure of 84% was reported. All confirmed a close correlation between bacterial colonisation of the mucosa and clinical and histological gastritis. Correlation with peptic ulceration was not quite so close, and there was variation between countries. Evidence that C pyloridis causes the gastritis, and is not simply an opportunist harmlessly occupying a favourable ecological niche, can now be summarised as follows. Firstly, the bacteria colonise the surface of the gastric epithelium (protected by gastric mucus) in enormous numbers, and where there is colonisation the epithelium is thinned and polymorphonuclear leucocytes are present. Ultrastructural studies show that there are "pedestal" attachments between bacteria and epithelial cells, microvilli are flattened or absent, and bacteria can be found in phagosomes of epithelial cells and polymorphs. Secondly, when bacteria are eliminated by antibacterial therapy, the lesions disappear. It so happens that bismuth salts such as the subcitrate (’De-Nol’) and subsalicylate (’Pepto-Bismol’) are active against these bacteria and it is suggested that their ulcer healing effect is due to their antibacterial action. Thirdly, antibodies specific for Cpyloridis are found in the sera ofcolonised patients. And, fourthly, gastritis was produced in a volunteer (Dr Marshall himself) who swallowed a pure culture of C pyloridis. 3,4 ever
16. Turner-Warwick R, Ashken MH The functional result of partial, subtotal and total cystoplasty with special reference to ureterocaecocystoplasty, selective sphincterotomy and cystocystoplasty. Br J Urol 1967; 39: 3-12. 17. Worth PHL, Turner-Warwick R. The treatment of interstitial cystitis by cystolysis with observations on cystoplasty Br J Urol 1973, 45: 65-71. 18. Worth PHL The treatment of interstitial cystitis by cystolysis with observations on cystoplasty. A review after 7 years Br J Urol 1980; 52: 232 19 Freiha FS, Faysal MH, Stamey TA. The surgical treatment of intractable interstitial cystitis J Urol 1980, 123: 632-34 20 Yeates WK. A technique of ileocystoplasty Br J Urol 1956, 28: 410-13. 1 Warren JR, Marshall B Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983, 1: 1273-75. 2 Editorial. Spirals and ulcers. Lancet 1984, i: 1336-37 3 Marshall BJ, Armstrong JA, McGeckie DB, Glaucy RJ. Attempt to fulfill Koch’s postulates for pyloric camplybacter. Med J Aust 1985; 142: 436-39 4. Editorial Pyloric campylobacter finds a volunteer Lancet 1985; i: 1021-22.
Thus the accumulating evidence is tending to support rather than refute the Australian hypothesis: the odds are shortening. Yet more work needs to be done before we accept a concept that could radically change the management of dyspepsia and ulcer diseases. A prime need is for an animal model; none has been found so far. Trials of antibacterial agents without physiological action on the stomach would help to determine whether elimination of the bacteria alone can bring about ulcer healing. The source of these bacteria is completely unknown. Reports of failure to find them in saliva, gum crevices, or other sites in the alimentary tract may reflect the insensitive nature of current isolation methods rather than their absence from such sites. Ultrastructural studies cast some doubt on their credentials for membership of the genus Campylobacter, but equally one could say "If you know a better genus, go to it". They probably warrant a new genus. The more traditional campylobacters that cause acute diarrhoea (C jejuni and C coli) were by no means eclipsed, at the Ottawa meeting, by their gastric "cousins". Better methods for their isolation and detection were described and it is now clear that most strains produce at least one of two toxins, one of which is antigenically related to cholera and Escherichia coli (heat-labile) enterotoxins. On the epidemiological front there were some notable advances. It is known that raw cow’s milk, untreated water, and occasionally undercooked chicken have been sources of outbreaks of campylobacter enteritis, but the origins of most of the day-today sporadic infections have remained elusive. Hard evidence is now beginning to emerge from the results of case-control studies and more penetrating epidemiological studies, which have become feasible through the application of improved serotyping and biotyping methods. Not surprisingly, chickens, already known to be a major source of infection, have come out badly, particularly "New York dressed" (ungutted) birds. Inexperience on the part of the person preparing chicken meals was found to be a major risk factor through cross-contamination of other foods or the consumption of raw or undercooked meat. In a particularly interesting study in an American university, campylobacter isolations from students were ten times more common than salmonella isolations and it was calculated that 70% of infections were attributable to the eating of chicken. An unexpected finding was that the second-rank risk factor was contact with cats; cat contact emerged as a risk factor in a study in Peru. The sudden exposure to inexpertly prepared foods on entry to university was likened by the authors to a second period of weaning. It will be interesting to see whether attempts to instruct the students in elementary food hygiene will make any impact on infection rates. One experienced (veterinary) voice was sceptical that the culinary habits of the general public could be materially influenced even if those of the students could; he thought the best chances of control lay in attempts to reduce contamination at the slaughter and processing of poultry. Since the first of these campylobacter workshops in 1981, progress has been gratifyingly rapid; but a sense of perspective was wonderfully restored by Dr Kist of Freiburg who, in a historical review, surprised his audience with a paper by Escherich published in 1886 describing and illustrating what was indisputably campylobacter enteritis.5 As a delegate was heard to say "Scientists will keep inventing the wheel".
5 Escherich T
Beitráge zur Keuntriss der Darmbacterien. Munch
Med Wschr Nov 9, 1886