- Email: [email protected]
SODIUM AND WATER DEPLETION IN ILEOSTOMY PATIENTS
625
physician to try to relieve unpleasant
symptoms
as
promptly and
effectively as possible. Some of the clinical manifestations of the British patients appear those described in Jamaica. However, there are today 5000 patients with sickle cell disease living in Britain3 and the British experience in the management of this severe hereditary condition must be heeded. to be different from
Department of Haematology, Central Middlesex Hospital, London NW10 7NS
MILICA BROZOVIC SALLY C. DAVIES ANNE YARDUMIAN
King’s College Hospital, London SE5
A. BELLINGHAM
North Middlesex Hospital, London N18
G. MARSH
St Bartholomew’s Hospital, London EC1
A. D. STEPHENS
1. Sickle Cell Society. A handbook on sickle cell disease: a guide for families. London: Sickle Cell Society, 1982. 2. Baughton ASJ, ed. Pain in sickle cell disease. London: Sickle Cell Society, 1983. 3. Prashew U, Anionwu E, Brozovic M. Sickle cell anaemia: Who cares? London: Runnymede Trust, 1985.
INTACT SMALLPOX VIRUS PARTICLES IN AN ITALIAN MUMMY OF SIXTEENTH CENTURY
SIR,-A year or so ago there was a debate in The Lancet’s correspondence columns about the capacity of smallpox virus to survive in its victims post mortem and hence about the risk to those who might disturb their remains.1-3 The mummy of a 2-year-old boy, who died in Naples around the middle of the XVIth century,4 revealed a widespread vesiculopustular exanthema type eruption (fig 1). The macroscopic aspects and the regional distribution suggested smallpox.5 Light microscopy, on samples of skin with vesicles rehydrated according to Sandison6 confirmed this possibility. We decided to look for the virus in the skin lesions of this well-preserved mummy. Myxoviruslike particles were detected in a Peruvian mummy from around 950 AD,’but the only attempt to identify smallpox viruses in the mummy of Ramses V failed.8 Electron microscopy revealed, among the residual bands of collagen fibres, elastic tissue, pyknotic nuclei, and membrane
Fig 2-Ultrathin section of skin incubated with anti-vaccinia-virus antiserum followed by protein-A/gold. (a) dense particle completely covered by protein-A/gold. (b) partly labelled particle. Only a very few gold grains are scattered over the skin tissue. Scale bar =03 pm.
remains with rare desmosomes, many egg-shaped, dense virus-like particles (250 nm x 150 nm), composed of a central dense region surrounded by a zone of lower density. After incubation with human anti-vaccinia-virus antiserum, followed by protein-A/gold complex inununostaining,9-11 the particles were completely covered by protein-A/gold (fig 2). The controls were uniformly negative. This Neapolitan child, who died some four centuries ago, had a severe form of smallpox. This is the first time that a virus has been identified, by this method, on mummified ancient tissues. We cannot yet comment on the biological activity of the virus in this mummy. The antigenic structure of the viral particles is well preserved. Cultivation of the virus will be attempted. Institute of Pathological and Histology, Medical School, University of Pisa, 56100 Pisa, Italy
Anatomy
GINO FORNACIARI ANTONIO MARCHETTI
1. Zuckerman AJ. Palaeontology of smallpox. Lancet 1984; ii: 1454. 2. Hopkins DR. Smallpox entombed. Lancet 1985; ii: 175. 3. Meers PD. Smallpox still entombed? Lancet 1985; ii: 1103. 4. Fornaciari G. The mummies of the Abbey of Saint Domenico Maggiore in Naples: a plan of research. Paleopath Newsl 1984; 45: 9-10. 5. Fornaciari G. The mummies of the Abbey of Saint Domenico Maggiore in Naples: a preliminary report. Arch Antrop Etnol 1985; 115; 215-26. 6. Sandison AT. The histological examination of mummified material. Stain Technol 1955; 30: 277-83. 7. Dalton HP, Allison MJ, Pezzia A. The documentation of communicable diseases in Peruvian mummies. Med Coll Virg Quart 1976; 12: 43-48. 8. Hopkins DR. Princes and peasants: Smallpox in history. Chicago: University of Chicago Press, 1983: 15. 9. Roth J, Bendayan M, Orci L. Ultrastructural localization of intracellular antigens by the use of protein-A/gold complex. Histochem Cytochem 1978; 26: 1074-81. J 10. Horisberger M. Evaluation of colloidal gold as a cytochemical marker for transmission and scanning electron microscopy. Biol Cellul 1979; 36: 253-58. 11. Bendayan M, Zollinger M. Ultrastructural localization of intracellular antigen by the use of protein-A/gold complex. J Histochem Cytochem 1983; 31: 101-09.
SODIUM AND WATER DEPLETION IN ILEOSTOMY PATIENTS
SIR,—The risk of sodium and water depletion in patients with an is not always appreciated by clinicians, although it was described almost 30 years ago.! We have lately seen two elderly patients with longstanding ileostomies who presented as emergencies with hypotension and prerenal uraemia, precipitated, in one case at least, by a mild attack of diarrhoea. Two factors are responsible for this tendency to serious sodium and water depletion. One is the unavoidable loss of sodium in the ileal effluent (130
ileostomy
mmol/1) and consequent, but often asymptomatic, chronic salt and water deficiency; the other is "low-salt diuresis", first described by Fig 1--Child’s face, showing diffuse vesiculopustular exanthema.
Kramer2 20 years ago. The following table shows the striking increase in urine volume that accompanied a change from 250 mmol
626 to 30 mmol per day in dietary sodium in an ileostomy patient who had presented with severe dehydration, hyponatraemia (110 mmol/1), and uraemia (30 mmol/1) due to excessive ileal losses:
*30 mmol sodium per day.
While studying this diuretic response to sodium restriction in eight otherwise healthy volunteers with ileostomies, we were impressed by the variation in basal sodium status before any dietary manipulation, as indicated by the 24 hour urinary sodium excretion and mean daily salivary aldosterone concentration (normal range 8-150 pmol/1); we have previously reported that the mean of five 4-hourly daytime estimates of salivary aldosterone is a reliable measure of daily aldosterone secretion.3 As might be expected, there was a significant inverse correlation between these measurements (Kendall’s tau - 0-714; two tail p < 0-05). Few of the patients could remember being given advice about regular sodium supplementation; two discovered the need for this themselves (muscle cramps and lethargy in hot weather), but one had stopped this because of the adverse publicity surrounding dietary salt. The patient with the highest salivary aldosterone (1933 pmol/1) and 24 h urinary sodium excretion of less than 3 mmol admitted on closer questioning to tiredness and lethargy. We suggest that failure to consider latent sodium and water depletion in ileostomy patients is an important cause of morbidity, and that mean daily salivary aldosterone is a more sensitive and useful index of chronic salt and water depletion than 24 hour sodium excretion alone. Medical Unit and Department of Chemical St Mary’s Hospital, London W2 1PG
Pathology,
DAVID CARMICHAEL JOHN FEW STANLEY PEART ROBERT UNWIN
Gallagher ND, Harrison DD, Skyring AP. Fluid and electrolyte disturbances in patients with long-established ileostomies. Gut 1962; 3: 219-23. 2. Kramer P. The effect of varying sodium loads on the ileal excreta of human ileostomized subjects. J Clin Invest 1966; 45: 1710-18. 3. Carmichael DJS, Few J, Unwin RJ. Changes in salivary aldosterone (SA) concentration m two healthy males. J Physiol 1986; 377: 71P.
consequence of somatostatin and as a cause of the dilatation is probably not well founded since the hormone’s property of reducing the secretion volume seems to predominate, if the dose is correct.S,7-9 A more probable reason for the aspiration is postoperative gastrointestinal obstruction; a necropsy study would end speculation about this. Fistulas caused by chronic diseases such as Crohn’s disease or ulcerative colitis are not suitable for this treatment. Provided the dose and period of treatment are correct, somatostatin is a reasonable conservative treatment, complementary to TPN, for enterocutaneous fistulas.
P. HILD J. DOBROSCHKE K. HENNEKING B. RIECK
Department of Surgery, Justus Liebig University, D-6300 Giessen, West Germany
1.
Kingsnorth AN, Moss JG, Small WP. Failure of somatostatin to accelerate closure of enterocutaneous fistulas in patients receiving total parenteral nutrition. Lancet 1986; i:
1271.
2. Dobroschke J, Hild P. Somatostatin in der Behandlung von Dunndarmfistein. Klinikarzt 1981; 10: 947-54. 3. Hild P, Dobroschke J, Kahle M, Aigner K. Somatostatin bei Dünndarmfisteln. Chirurg 1980; 51: 155-57. 4. Hild P, Stoyanov M, Dobroschke J, Aigner K. La somatostatine dans le traitement médical des fistulas du pancréas et de l’intestin grêle. Ann Chir 1982; 36: 193-96. 5. Hild P, Henneking K, Schwall G, Dobroschke J. The inhibitory effect of somatostatin on the secretion from enterocutaneous duodenal fistulas. Langenbecks Arch Chir 1983; (suppl): 13-17. 6. Hild P, Dobroschke J, Henneking K. Treatment of enterocutaneous fistulas by somatostatin. Klinikarzt 1986; 15: 24-29. 7. Arnold R, Creuzfeldt W. Hemmung der pentagastrin—induzierten Säuresekretion des Magens beim Menschen durch Somatostatin. Dtsch Med Wschr 1975; 100: 1014-16. 8. Konturek SJ. Somatostatin and gastrointestinal secretion and motility. Adv Exp Med Biol 1978; 106: 227-34. 9. Konturek SJ. Somatostatin and the gastrointestinal secretions. Scand J Gastroenterol 1976; 11: 1-4.
1.
TREATMENT OF ENTEROCUTANEOUS FISTULAS WITH SOMATOSTATIN
SiR,—Kingsnorth et all have reported that somatostatin failed to accelerate the closure of enterocutaneous fistulas in patients on total parenteral nutrition (TPN). Since 1979 we have been using somatostatin for enterocutaneous fistulas2-6 and have devised a successful scheme that differs in several ways from that described by Kingsnorth et al. Somatostatin is only indicated if surgical fistula closure is not advisable, if fistulas persist chronically despite TPN, or if the loss of intestinal secretion is life-threatening. We have treated more than fifty patients in this way, starting somatostatin on the 18th postoperative day on average 6 In our experience hormone infusion for 4 days is seldom successful, and the mean treatment time in our cases has been 13 days. After an average of 11 days fistula occlusion was achieved in 80% cases.6 To avoid a rebound effect somatostatin ought to be given for 2 days after the fistula has closed, and the dose should be reduced step by step.2,5 In gastrointestinal bleeding, in the treatment of pancreatitis, and in the management of enterocutaneous fistulas, the dose should be a continuous infusion of 3-0 or 3-5 Ilgfkgfh (6 mg in 24 hours) over the whole treatment period. In our experience the regimen used by Kingsnorth et al was bound to be unsuccessful. In no case have we seen aspiration as a consequence of acute stomach dilatation: for somatostatin infusion, as for fistula treatment by TPN alone, continuous drainage of the gastric secretion by a gastric tube is indispensable. Kingsnorth and colleagues’ speculation about reduced gastrointestinal motility as a
CAMPYLOBACTER PYLORIDIS, UREASE, AND GASTRIC ULCERS
SIR,-Discussing our hypothesis on the role of urease in gastric ulcer formation (July 5, p 15) Dr Rathbone and colleagues (Aug 16, p 400), referring to an animal (ferret) model, stated "that there is no evidence of mucosal inflammation is against Hazell and Lee’s hypothesis". We made no claim, explicit or implied, that the urease activity of Campylobacter pyloridis was responsible for "mucosal inflammation". Rather, some preliminary studies we have conducted would indicate that C pyloridis, acting on complement, releases substances chemotactic to leucocytes and that this process may contribute to C pyloridis induced gastritis. animals are colonised by urease-producing bacteria, both in the stomach and in the intestinal tract. All of these organisms will have unique features fitting them to their particular niche. Our hypothesis proposed that because of the peculiar colonisation pattern of C pyloridis and its high urease activity, the organism would induce back-diffusion of hydrogen ions and that this, in conjunction with factors such as reduced cytoprotection, would result in gastric ulcer formation. The ferret model of gastric colonisationl,2 referred to by Rathbone et al does have the potential to aid in the development of our understanding of how C pyloridis produces disease. However, animal models per se may give only a limited picture of the primary disease processes in man, and any extrapolation of results from such models must be tempered by an appreciation of these limitations.
Many
School of Microbiology,
University of New South Wales, Kensington, New South Wales 2033,
S. L. HAZELL A. LEE
Australia
JG, Edrise BM, Cabot EB, Beaucage C, Murphy JC, Prostak KS. Campylobacter-like organisms isolated from gastric mucosa of ferrets. Am J Vet
1. Fox
Res 1986; 47: 236-39. 2. Cave
DR, Taylor N, Tuczynski C, Fox JR. Campylobacter-like organisms (CLO)
from
man
and ferret: Towards
Gastroenterology 1986; 90: 1368.
an
animal model of CLO induced disease.
physician to try to relieve unpleasant
symptoms
as
promptly and
effectively as possible. Some of the clinical manifestations of the British patients appear those described in Jamaica. However, there are today 5000 patients with sickle cell disease living in Britain3 and the British experience in the management of this severe hereditary condition must be heeded. to be different from
Department of Haematology, Central Middlesex Hospital, London NW10 7NS
MILICA BROZOVIC SALLY C. DAVIES ANNE YARDUMIAN
King’s College Hospital, London SE5
A. BELLINGHAM
North Middlesex Hospital, London N18
G. MARSH
St Bartholomew’s Hospital, London EC1
A. D. STEPHENS
1. Sickle Cell Society. A handbook on sickle cell disease: a guide for families. London: Sickle Cell Society, 1982. 2. Baughton ASJ, ed. Pain in sickle cell disease. London: Sickle Cell Society, 1983. 3. Prashew U, Anionwu E, Brozovic M. Sickle cell anaemia: Who cares? London: Runnymede Trust, 1985.
INTACT SMALLPOX VIRUS PARTICLES IN AN ITALIAN MUMMY OF SIXTEENTH CENTURY
SIR,-A year or so ago there was a debate in The Lancet’s correspondence columns about the capacity of smallpox virus to survive in its victims post mortem and hence about the risk to those who might disturb their remains.1-3 The mummy of a 2-year-old boy, who died in Naples around the middle of the XVIth century,4 revealed a widespread vesiculopustular exanthema type eruption (fig 1). The macroscopic aspects and the regional distribution suggested smallpox.5 Light microscopy, on samples of skin with vesicles rehydrated according to Sandison6 confirmed this possibility. We decided to look for the virus in the skin lesions of this well-preserved mummy. Myxoviruslike particles were detected in a Peruvian mummy from around 950 AD,’but the only attempt to identify smallpox viruses in the mummy of Ramses V failed.8 Electron microscopy revealed, among the residual bands of collagen fibres, elastic tissue, pyknotic nuclei, and membrane
Fig 2-Ultrathin section of skin incubated with anti-vaccinia-virus antiserum followed by protein-A/gold. (a) dense particle completely covered by protein-A/gold. (b) partly labelled particle. Only a very few gold grains are scattered over the skin tissue. Scale bar =03 pm.
remains with rare desmosomes, many egg-shaped, dense virus-like particles (250 nm x 150 nm), composed of a central dense region surrounded by a zone of lower density. After incubation with human anti-vaccinia-virus antiserum, followed by protein-A/gold complex inununostaining,9-11 the particles were completely covered by protein-A/gold (fig 2). The controls were uniformly negative. This Neapolitan child, who died some four centuries ago, had a severe form of smallpox. This is the first time that a virus has been identified, by this method, on mummified ancient tissues. We cannot yet comment on the biological activity of the virus in this mummy. The antigenic structure of the viral particles is well preserved. Cultivation of the virus will be attempted. Institute of Pathological and Histology, Medical School, University of Pisa, 56100 Pisa, Italy
Anatomy
GINO FORNACIARI ANTONIO MARCHETTI
1. Zuckerman AJ. Palaeontology of smallpox. Lancet 1984; ii: 1454. 2. Hopkins DR. Smallpox entombed. Lancet 1985; ii: 175. 3. Meers PD. Smallpox still entombed? Lancet 1985; ii: 1103. 4. Fornaciari G. The mummies of the Abbey of Saint Domenico Maggiore in Naples: a plan of research. Paleopath Newsl 1984; 45: 9-10. 5. Fornaciari G. The mummies of the Abbey of Saint Domenico Maggiore in Naples: a preliminary report. Arch Antrop Etnol 1985; 115; 215-26. 6. Sandison AT. The histological examination of mummified material. Stain Technol 1955; 30: 277-83. 7. Dalton HP, Allison MJ, Pezzia A. The documentation of communicable diseases in Peruvian mummies. Med Coll Virg Quart 1976; 12: 43-48. 8. Hopkins DR. Princes and peasants: Smallpox in history. Chicago: University of Chicago Press, 1983: 15. 9. Roth J, Bendayan M, Orci L. Ultrastructural localization of intracellular antigens by the use of protein-A/gold complex. Histochem Cytochem 1978; 26: 1074-81. J 10. Horisberger M. Evaluation of colloidal gold as a cytochemical marker for transmission and scanning electron microscopy. Biol Cellul 1979; 36: 253-58. 11. Bendayan M, Zollinger M. Ultrastructural localization of intracellular antigen by the use of protein-A/gold complex. J Histochem Cytochem 1983; 31: 101-09.
SODIUM AND WATER DEPLETION IN ILEOSTOMY PATIENTS
SIR,—The risk of sodium and water depletion in patients with an is not always appreciated by clinicians, although it was described almost 30 years ago.! We have lately seen two elderly patients with longstanding ileostomies who presented as emergencies with hypotension and prerenal uraemia, precipitated, in one case at least, by a mild attack of diarrhoea. Two factors are responsible for this tendency to serious sodium and water depletion. One is the unavoidable loss of sodium in the ileal effluent (130
ileostomy
mmol/1) and consequent, but often asymptomatic, chronic salt and water deficiency; the other is "low-salt diuresis", first described by Fig 1--Child’s face, showing diffuse vesiculopustular exanthema.
Kramer2 20 years ago. The following table shows the striking increase in urine volume that accompanied a change from 250 mmol
626 to 30 mmol per day in dietary sodium in an ileostomy patient who had presented with severe dehydration, hyponatraemia (110 mmol/1), and uraemia (30 mmol/1) due to excessive ileal losses:
*30 mmol sodium per day.
While studying this diuretic response to sodium restriction in eight otherwise healthy volunteers with ileostomies, we were impressed by the variation in basal sodium status before any dietary manipulation, as indicated by the 24 hour urinary sodium excretion and mean daily salivary aldosterone concentration (normal range 8-150 pmol/1); we have previously reported that the mean of five 4-hourly daytime estimates of salivary aldosterone is a reliable measure of daily aldosterone secretion.3 As might be expected, there was a significant inverse correlation between these measurements (Kendall’s tau - 0-714; two tail p < 0-05). Few of the patients could remember being given advice about regular sodium supplementation; two discovered the need for this themselves (muscle cramps and lethargy in hot weather), but one had stopped this because of the adverse publicity surrounding dietary salt. The patient with the highest salivary aldosterone (1933 pmol/1) and 24 h urinary sodium excretion of less than 3 mmol admitted on closer questioning to tiredness and lethargy. We suggest that failure to consider latent sodium and water depletion in ileostomy patients is an important cause of morbidity, and that mean daily salivary aldosterone is a more sensitive and useful index of chronic salt and water depletion than 24 hour sodium excretion alone. Medical Unit and Department of Chemical St Mary’s Hospital, London W2 1PG
Pathology,
DAVID CARMICHAEL JOHN FEW STANLEY PEART ROBERT UNWIN
Gallagher ND, Harrison DD, Skyring AP. Fluid and electrolyte disturbances in patients with long-established ileostomies. Gut 1962; 3: 219-23. 2. Kramer P. The effect of varying sodium loads on the ileal excreta of human ileostomized subjects. J Clin Invest 1966; 45: 1710-18. 3. Carmichael DJS, Few J, Unwin RJ. Changes in salivary aldosterone (SA) concentration m two healthy males. J Physiol 1986; 377: 71P.
consequence of somatostatin and as a cause of the dilatation is probably not well founded since the hormone’s property of reducing the secretion volume seems to predominate, if the dose is correct.S,7-9 A more probable reason for the aspiration is postoperative gastrointestinal obstruction; a necropsy study would end speculation about this. Fistulas caused by chronic diseases such as Crohn’s disease or ulcerative colitis are not suitable for this treatment. Provided the dose and period of treatment are correct, somatostatin is a reasonable conservative treatment, complementary to TPN, for enterocutaneous fistulas.
P. HILD J. DOBROSCHKE K. HENNEKING B. RIECK
Department of Surgery, Justus Liebig University, D-6300 Giessen, West Germany
1.
Kingsnorth AN, Moss JG, Small WP. Failure of somatostatin to accelerate closure of enterocutaneous fistulas in patients receiving total parenteral nutrition. Lancet 1986; i:
1271.
2. Dobroschke J, Hild P. Somatostatin in der Behandlung von Dunndarmfistein. Klinikarzt 1981; 10: 947-54. 3. Hild P, Dobroschke J, Kahle M, Aigner K. Somatostatin bei Dünndarmfisteln. Chirurg 1980; 51: 155-57. 4. Hild P, Stoyanov M, Dobroschke J, Aigner K. La somatostatine dans le traitement médical des fistulas du pancréas et de l’intestin grêle. Ann Chir 1982; 36: 193-96. 5. Hild P, Henneking K, Schwall G, Dobroschke J. The inhibitory effect of somatostatin on the secretion from enterocutaneous duodenal fistulas. Langenbecks Arch Chir 1983; (suppl): 13-17. 6. Hild P, Dobroschke J, Henneking K. Treatment of enterocutaneous fistulas by somatostatin. Klinikarzt 1986; 15: 24-29. 7. Arnold R, Creuzfeldt W. Hemmung der pentagastrin—induzierten Säuresekretion des Magens beim Menschen durch Somatostatin. Dtsch Med Wschr 1975; 100: 1014-16. 8. Konturek SJ. Somatostatin and gastrointestinal secretion and motility. Adv Exp Med Biol 1978; 106: 227-34. 9. Konturek SJ. Somatostatin and the gastrointestinal secretions. Scand J Gastroenterol 1976; 11: 1-4.
1.
TREATMENT OF ENTEROCUTANEOUS FISTULAS WITH SOMATOSTATIN
SiR,—Kingsnorth et all have reported that somatostatin failed to accelerate the closure of enterocutaneous fistulas in patients on total parenteral nutrition (TPN). Since 1979 we have been using somatostatin for enterocutaneous fistulas2-6 and have devised a successful scheme that differs in several ways from that described by Kingsnorth et al. Somatostatin is only indicated if surgical fistula closure is not advisable, if fistulas persist chronically despite TPN, or if the loss of intestinal secretion is life-threatening. We have treated more than fifty patients in this way, starting somatostatin on the 18th postoperative day on average 6 In our experience hormone infusion for 4 days is seldom successful, and the mean treatment time in our cases has been 13 days. After an average of 11 days fistula occlusion was achieved in 80% cases.6 To avoid a rebound effect somatostatin ought to be given for 2 days after the fistula has closed, and the dose should be reduced step by step.2,5 In gastrointestinal bleeding, in the treatment of pancreatitis, and in the management of enterocutaneous fistulas, the dose should be a continuous infusion of 3-0 or 3-5 Ilgfkgfh (6 mg in 24 hours) over the whole treatment period. In our experience the regimen used by Kingsnorth et al was bound to be unsuccessful. In no case have we seen aspiration as a consequence of acute stomach dilatation: for somatostatin infusion, as for fistula treatment by TPN alone, continuous drainage of the gastric secretion by a gastric tube is indispensable. Kingsnorth and colleagues’ speculation about reduced gastrointestinal motility as a
CAMPYLOBACTER PYLORIDIS, UREASE, AND GASTRIC ULCERS
SIR,-Discussing our hypothesis on the role of urease in gastric ulcer formation (July 5, p 15) Dr Rathbone and colleagues (Aug 16, p 400), referring to an animal (ferret) model, stated "that there is no evidence of mucosal inflammation is against Hazell and Lee’s hypothesis". We made no claim, explicit or implied, that the urease activity of Campylobacter pyloridis was responsible for "mucosal inflammation". Rather, some preliminary studies we have conducted would indicate that C pyloridis, acting on complement, releases substances chemotactic to leucocytes and that this process may contribute to C pyloridis induced gastritis. animals are colonised by urease-producing bacteria, both in the stomach and in the intestinal tract. All of these organisms will have unique features fitting them to their particular niche. Our hypothesis proposed that because of the peculiar colonisation pattern of C pyloridis and its high urease activity, the organism would induce back-diffusion of hydrogen ions and that this, in conjunction with factors such as reduced cytoprotection, would result in gastric ulcer formation. The ferret model of gastric colonisationl,2 referred to by Rathbone et al does have the potential to aid in the development of our understanding of how C pyloridis produces disease. However, animal models per se may give only a limited picture of the primary disease processes in man, and any extrapolation of results from such models must be tempered by an appreciation of these limitations.
Many
School of Microbiology,
University of New South Wales, Kensington, New South Wales 2033,
S. L. HAZELL A. LEE
Australia
JG, Edrise BM, Cabot EB, Beaucage C, Murphy JC, Prostak KS. Campylobacter-like organisms isolated from gastric mucosa of ferrets. Am J Vet
1. Fox
Res 1986; 47: 236-39. 2. Cave
DR, Taylor N, Tuczynski C, Fox JR. Campylobacter-like organisms (CLO)
from
man
and ferret: Towards
Gastroenterology 1986; 90: 1368.
an
animal model of CLO induced disease.