728
association between the corrected pressure and the random zero was examined for each site. The simple linear regression coefficients
were 0.02 (95 % confidence interval - 0.05 to 0.10), - 0.08 ( - 0.18 toO.02),and -0-16(-0-25to -0-06) in the arm and right and left ankles, respectively. We obtained closely similar results in another study of systolic pressures in 600 patients with intermittent claudication. The association with the random zero was much weaker than that reported by Kronmal and colleagues, who showed a regression coefficient of - 0-869 for systolic blood pressure. We have found the random zero sphygmomanometer satisfactory to use but the slow-release valve and random zero wheel are prone to sticking so that frequent maintenance is required. We can confirm, however, that observer bias is negligible.1 Wolfson Unit for Prevention of Peripheral Vascular Diseases. Department of Community Medicine, Edinburgh University Medical School, Edinburgh EH8 9AG, UK
C. C. A. MACINTYRE F. G. R. FOWKES
Macintyre CCA, Prescott RJ, Ruckley CV. Variability of systolic pressures in the measurement of atherosclerotic peripheral arterial disease. J Epidemiol Community Health 1988; 42: 128-33.
1. Fowkes FGR, Housley E,
ankle and brachial
Helicobacter gastritis and intestinal metaplasia in a gastric cancer family SiR,—Familial clustering of carcinoma of the gastrointestinal tract is well known. In some families the cancer forms part of the spectrum of the cancer family syndrome, which in Warthin’s original account1 contained a large number of stomach neoplasms, though large bowel cancers are more frequent, accounting for about 50% of cancers in these families.2 We have investigated a family, in which two of four siblings presented at an early age (under 40 years) with gastric cancer. A third had antrectomy for gastric dysplasia, and the fourth sibling has extensive chronic atrophic gastritis and intestinal metaplasia at age 36. We investigated their eight children by endoscopy and biopsy. The following biopsy specimens were taken from each child-one from the duodenum, two from the gastric antrum, and four from the fundus. Specimens were examined histologically for the presence of chronic gastritis, intestinal metaplasia, and Helicobacter pylori, with a modified giemsa technique. Of the eight children, five (63%) have H pylori-positive, chronic atrophic gastritis (age at diagnosis 10-26 years) and in three of the five (60%) intestinal metaplasia developed, at 21, 23, and 34 years of age, respectively (see figure). In all three intestinal metaplasia was found in the gastric antrum but not in the body. H pylori infection and intestinal metaplasia are unusual before age 30. Seropositivity was shown in less than 20% of a random population of blood donors aged under 30 with an ELISA technique3 and in a recent combined serological and histological study of 113 symptom-free volunteers H pylori infection was documented in 10% (histological) to 20% (serological) of the 18-29 year age group."* Intestinal metaplasia was present in only 4% of an unselected rural population in Sweden.s In Leeds, we have found
this condition in one of sixty-one dyspeptic patients under age 30 with Hpylori-associated gastritis (unpublished data), and in a large multicentre study6 in which a mean of 37 biopsy specimens were examined per case intestinal metaplasia was found in only 4% of individuals aged under 30. The early occurrence of gastritis and intestinal metaplasia in members of our family may reflect a genetic predisposition to the metaplasia/dysplasia/carcinoma sequence described by û>rrea.1 More specifically, intestinal metaplasia arising in three out of five H pylori infected offspring would be consistent with a dominant pattern of inheritance for a gene concerned with the development of intestinal metaplasia. We postulate that H pylori acts as a promoter in the progression from normal to metaplastic epithelium, possibly by inducing a hyperproliferative state in the inflamed gastric mucosa. Eradication of the organism under these circumstances may remove a potential promoter and thus reduce the risk of gastric cancer.
Susceptibilty to cancer and gastritis in relatives of gastric cancer patients has been well documented. In most cases, however, increased risk has been confined to tumours classified as "diffuse" by Lauren’s histological criteria.8 Both tumours in the present study were of the "intestinal" type. This is in keeping with the carcinogenic sequence we propose and may reflect neoplastic development on a genetic basis different from that in diffuse type carcinomas. Departments of Pathology, Surgery, and Gastroenterology, Leeds General Infirmary, Leeds LS2 9JT, UK; ICRF Genetic Epidemiology Unit, University of Leeds; and Department of Pathology, St James’ Hospital
N. SCOTT M. LANSDOWN R. DIAMENT B. RATHBONE V. MURDAY J. I. WYATT M. MCMAHON M. F. DIXON P. QUIRKE
1. Warthin AS. Heredity with reference to carcinoma. Arch Intern Med 1913; 12: 546-55. 2. Lynch HT, Lynch PM, Albano WA, Lynch JF. The cancer syndrome: a status report.
Dis Col Rect 1981; 24: 311-22. 3.
Wyatt JI, Rathbone BJ. The role of serology in the diagnosis of Campylobacter pylori infection. Scand J Gastroenterol 1989; 24 (suppl 160): 27-34. 4. Dooley CP, Cohen H, Fitzgibbons PL, et al. Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons. N Engl J Med 1989; 23: 1562-66. 5. Siurala M, Isokoski M, Varis K, Kekki M. Prevalence of gastritis in a rural population Scand J Gastroentrol 1968; 3: 211-23. 6. Filipe MI, Potet F, Bogomoletz WV, et al. Incomplete sulphomucin-secreting intestinal metaplasia for gastric cancer: preliminary data from a prospective study from three centres. Gut 1985; 26: 1319-26. 7. Correa P. A human model of gastric carcinogenesis. Cancer Res 1988; 48: 3554-60. 8. Lauren P. The two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma. Acta Path Microbiol Scand 1965; 64: 31-49.
Helicobacter pylori, mucus, and ulcer
gastric
SIR,—Dr Sidebotham and Dr Baron (Jan 27, p 193) propose that Helicobacter pylori promotes gastric ulcer formation by means of its deleterious effect on gastric mucus. Their hypothesis closely resembles my suggestion that the microorganism alters the quality of mucus by means of urease production and that impaired mucus secretion may play a part in ulcer recurrence.1 Experiments support the view that H pylori does include changes in the structure of mucus, degrading both mucus glycoprotein2 and gastric mucosal lipids,3with a consequent reduction in the viscosity of the mucus
layer 2
Pedigree. [-]=Male,
0=female, 0’=deceased, C=heHcobacter gastritis,
(3= gastric carcinoma, (gastric dysplasia, C’ltestinai metaplasia, -
=
biopsy material available.
We should concede, however, that the observations on mucus permeability to H + ions under the effect of H pylori are somewhat conflicting2,4 and that the sequence of events can take place in reverse. I certainly concur that in gastric ulcer patients gastric mucus is qualitatively altered,5 but whether this is secondary to H pylori infection rather than a primary occurrence remains uncertain. In fact, my experience is that the quality of mucus in chronic non-erosive gastritis-a disorder closely associated with H pylori infection-is normal. It is possible that in gastric ulcer a primary defect in mucus structure allows colonisation of the mucosa by H pylori, which in turn can further alter mucus characteristics and lead to yet more damage to gastric mucosa."* This would
729
ABDOMINAL PARACENTESIS IN NEWBORN INFANTS WITH SUSPECTED NEC
with gastric ulcer in whom H pylori is not detectable and where a primary impairment of the mucus/ bicarbonate barrier can be sufficient to promote mucosal damage independently from colonisation by the microorganism. Both hypotheses are plausible, and for the time being we are free to speculate about either one.
account for those patients
Institute of Internal Medicine, University of Milan,
M. GUSLANDI
Milan, Italy
1. Guslandi M.
Antisecretory
treatment
and
Campylobacter pylori. Gastroenterol Clin
Biol 1989, 13: 641-42. 2 Sarosiek J, Slomiany A, Slomiany BL. Evidence for a weakening of gastric mucus integrity by Campylobacter pylori. Scand J Gastroenterol 1988; 23: 585-90. 3 Slomiany BL, Kasinathan C, Slomiany A. Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol). Am J Gastroenterol 1989; 84: 1273-77. 4 Thomsen L, Tasman-Jones C, Morris A, Wiggins P, Lee S, Forlong C. Ammonia produced by Campylobacter pylori neutralizes H moving through gastric mucus. Scand J Gastroenterol 1989; 24: 761-68. 5. Guslandi M, Ballarin E. Assessment of the mucus-bicarbonate barrier in the stomach of patients with chronic gastric disorders Clin Chim Acta 1984; 144: 133-36. 6. Fauchere JL, Rosenau A, Bonneville F. Virulence factors of Campylobacter pylori. Gastroenterol Clin Biol 1989; 13: 59-64B.
contained bacteria on smear indicated intestinal gangrene. Since 1977 we have applied this technique 46 times in forty infants with suspected or definite NEC stage I or 11.5 A retrospective analysis revealed that 40 samples had been evaluated according to Kosloske’s criteria. The white cells had been differentiated in 35 specimens. In all twelve infants showing more than 40% neutrophil granulocytes on smear purulent peritonitis and NEC were confirmed at laparotomy (ten infants) or the diagnosis of NEC was based on the triad of radiological pneumatosis, left shift, and very high C-reactive protein. However, intestinal gangrene/peritonitis was diagnosed incorrectly four times on Kosloske’s colour criterion, and purulent peritonitis/ intestinal gangrene was found at laparotomy after paracentesis in seven patients for whom Kosloske’s criteria had been falsely
negative.
Neutrophil ratio, ascites, surgery in infants with
and
timing of necrotising
enterocolitis SIR,-The indications for surgery in infants with necrotising enterocolitis (NEC) remain controversial; pneumoperitoneum is the only widely accepted criterion, but this sign usually occurs in advanced disease and is associated with an increased case fatality rate.’ Operation at an earlier stage of purulent peritonitis would be desirable but clinical signs of peritonitis are often lacking in babies bom preterm. Kosloske and colleagues introduced abnormal paracentesis to identify infants with intestinal gangrene before intestinal perforation, so permitting early surgical intervention.2-4 A paracentesis sample of 0-5 ml or more that was brown and/or
We have found a neutrophil count (as a percentage of total white cell count) of more than 40% on a smear of abdominal fluid to be a more reliable and earlier sign of purulent peritonitis than brown colour of ascites or bacteria on smear in newborn babies with suspcted NEC (figure, table). Abdominal paracentesis is a simple, safe, and reliable tool for identifying infants with purulent peritonitis. Differentiation of white cells on smears and serial punctures allow the intestinal disease to be followed up so that peritonitis can be detected early on, leading to better timed surgery.
Universitatskinderklinik, D-7900 Ulm/Donau, West Germany
F. POHLANDT P. BARTMANN L. GORTNER
AM, Papile LA, Burstein J. Indications for operation in acute necrotizing enterocolitis of the neonate. Surgery 1980; 87: 502-08. Kosloske AM, Lilly JR. Paracentesis and lavage for diagnosis of intestinal gangrene in neonatal necrotizing enterocolitis. J Pediatr Surg 1978; 13: 315. Kosloske AM, Goldthorn JF. Paracentesis as an aid to the diagnosis of intestinal gangrene. Arch Surg 1982; 117: 571-75. Ricketts RR. The role of paracentesis in the management of infants with necrotizing enterocolitis. Am Surg 1986; 52: 61-65. Bell MJ, Temberg JL, Feigin RD, et al. Neonatal necrotizing enterocolitis: therapeutic decisions based upon clinical staging. Ann Surg 1978; 187: 1. Mathers NJ, Pohlandt F. Diagnostic audit of C-reactive protein in neonatal infection. Eur J Pediatr 1987; 146: 147-51.
1. Kosloske 2. 3. 4. 5.
6.
More in
spider venom than venom?
SIR,-Mr Oppenheim and Dr Taggart (Jan 27, p 228) describe an interesting case of bacterial infection which, by inference, they attribute to the bite of an Austalian spider in a London hotel frequented by students. The facts as presented do not seem
Neutrophil (granulocyte) ratio infants with suspected NEC.
on smears
of ascitic fluid from
Diagnosis of NEC confirmed at laparotomy or based on triad of radiological pneumatosis, left shift, and increased C-reactive protein.’6
sufficient for this conclusion to be drawn. If the possibility is discounted that some visiting Australian student decided to counter the Kylie-and-Jason image by bringing along an unusual pet, an Australian spider in London must have stowed away. In general, species that produce substantial local tissue reactions do not live indoors and therefore are unlikely candidates for stowaway travel-even if the soft body had allowed survival of a long air trip. On the other hand in London, as in most other places, the notion of student accommodation allows for various other candidates for nocturnal assaults. If no identifiably antipodean spider was found at the scene, it seems most probable that the bite was inflicted by a local resident. Department of Physiology, University of Melbourne, Victoria 3052, Australia
CHRISTOPHER BELL
association between the corrected pressure and the random zero was examined for each site. The simple linear regression coefficients
were 0.02 (95 % confidence interval - 0.05 to 0.10), - 0.08 ( - 0.18 toO.02),and -0-16(-0-25to -0-06) in the arm and right and left ankles, respectively. We obtained closely similar results in another study of systolic pressures in 600 patients with intermittent claudication. The association with the random zero was much weaker than that reported by Kronmal and colleagues, who showed a regression coefficient of - 0-869 for systolic blood pressure. We have found the random zero sphygmomanometer satisfactory to use but the slow-release valve and random zero wheel are prone to sticking so that frequent maintenance is required. We can confirm, however, that observer bias is negligible.1 Wolfson Unit for Prevention of Peripheral Vascular Diseases. Department of Community Medicine, Edinburgh University Medical School, Edinburgh EH8 9AG, UK
C. C. A. MACINTYRE F. G. R. FOWKES
Macintyre CCA, Prescott RJ, Ruckley CV. Variability of systolic pressures in the measurement of atherosclerotic peripheral arterial disease. J Epidemiol Community Health 1988; 42: 128-33.
1. Fowkes FGR, Housley E,
ankle and brachial
Helicobacter gastritis and intestinal metaplasia in a gastric cancer family SiR,—Familial clustering of carcinoma of the gastrointestinal tract is well known. In some families the cancer forms part of the spectrum of the cancer family syndrome, which in Warthin’s original account1 contained a large number of stomach neoplasms, though large bowel cancers are more frequent, accounting for about 50% of cancers in these families.2 We have investigated a family, in which two of four siblings presented at an early age (under 40 years) with gastric cancer. A third had antrectomy for gastric dysplasia, and the fourth sibling has extensive chronic atrophic gastritis and intestinal metaplasia at age 36. We investigated their eight children by endoscopy and biopsy. The following biopsy specimens were taken from each child-one from the duodenum, two from the gastric antrum, and four from the fundus. Specimens were examined histologically for the presence of chronic gastritis, intestinal metaplasia, and Helicobacter pylori, with a modified giemsa technique. Of the eight children, five (63%) have H pylori-positive, chronic atrophic gastritis (age at diagnosis 10-26 years) and in three of the five (60%) intestinal metaplasia developed, at 21, 23, and 34 years of age, respectively (see figure). In all three intestinal metaplasia was found in the gastric antrum but not in the body. H pylori infection and intestinal metaplasia are unusual before age 30. Seropositivity was shown in less than 20% of a random population of blood donors aged under 30 with an ELISA technique3 and in a recent combined serological and histological study of 113 symptom-free volunteers H pylori infection was documented in 10% (histological) to 20% (serological) of the 18-29 year age group."* Intestinal metaplasia was present in only 4% of an unselected rural population in Sweden.s In Leeds, we have found
this condition in one of sixty-one dyspeptic patients under age 30 with Hpylori-associated gastritis (unpublished data), and in a large multicentre study6 in which a mean of 37 biopsy specimens were examined per case intestinal metaplasia was found in only 4% of individuals aged under 30. The early occurrence of gastritis and intestinal metaplasia in members of our family may reflect a genetic predisposition to the metaplasia/dysplasia/carcinoma sequence described by û>rrea.1 More specifically, intestinal metaplasia arising in three out of five H pylori infected offspring would be consistent with a dominant pattern of inheritance for a gene concerned with the development of intestinal metaplasia. We postulate that H pylori acts as a promoter in the progression from normal to metaplastic epithelium, possibly by inducing a hyperproliferative state in the inflamed gastric mucosa. Eradication of the organism under these circumstances may remove a potential promoter and thus reduce the risk of gastric cancer.
Susceptibilty to cancer and gastritis in relatives of gastric cancer patients has been well documented. In most cases, however, increased risk has been confined to tumours classified as "diffuse" by Lauren’s histological criteria.8 Both tumours in the present study were of the "intestinal" type. This is in keeping with the carcinogenic sequence we propose and may reflect neoplastic development on a genetic basis different from that in diffuse type carcinomas. Departments of Pathology, Surgery, and Gastroenterology, Leeds General Infirmary, Leeds LS2 9JT, UK; ICRF Genetic Epidemiology Unit, University of Leeds; and Department of Pathology, St James’ Hospital
N. SCOTT M. LANSDOWN R. DIAMENT B. RATHBONE V. MURDAY J. I. WYATT M. MCMAHON M. F. DIXON P. QUIRKE
1. Warthin AS. Heredity with reference to carcinoma. Arch Intern Med 1913; 12: 546-55. 2. Lynch HT, Lynch PM, Albano WA, Lynch JF. The cancer syndrome: a status report.
Dis Col Rect 1981; 24: 311-22. 3.
Wyatt JI, Rathbone BJ. The role of serology in the diagnosis of Campylobacter pylori infection. Scand J Gastroenterol 1989; 24 (suppl 160): 27-34. 4. Dooley CP, Cohen H, Fitzgibbons PL, et al. Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons. N Engl J Med 1989; 23: 1562-66. 5. Siurala M, Isokoski M, Varis K, Kekki M. Prevalence of gastritis in a rural population Scand J Gastroentrol 1968; 3: 211-23. 6. Filipe MI, Potet F, Bogomoletz WV, et al. Incomplete sulphomucin-secreting intestinal metaplasia for gastric cancer: preliminary data from a prospective study from three centres. Gut 1985; 26: 1319-26. 7. Correa P. A human model of gastric carcinogenesis. Cancer Res 1988; 48: 3554-60. 8. Lauren P. The two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma. Acta Path Microbiol Scand 1965; 64: 31-49.
Helicobacter pylori, mucus, and ulcer
gastric
SIR,—Dr Sidebotham and Dr Baron (Jan 27, p 193) propose that Helicobacter pylori promotes gastric ulcer formation by means of its deleterious effect on gastric mucus. Their hypothesis closely resembles my suggestion that the microorganism alters the quality of mucus by means of urease production and that impaired mucus secretion may play a part in ulcer recurrence.1 Experiments support the view that H pylori does include changes in the structure of mucus, degrading both mucus glycoprotein2 and gastric mucosal lipids,3with a consequent reduction in the viscosity of the mucus
layer 2
Pedigree. [-]=Male,
0=female, 0’=deceased, C=heHcobacter gastritis,
(3= gastric carcinoma, (gastric dysplasia, C’ltestinai metaplasia, -
=
biopsy material available.
We should concede, however, that the observations on mucus permeability to H + ions under the effect of H pylori are somewhat conflicting2,4 and that the sequence of events can take place in reverse. I certainly concur that in gastric ulcer patients gastric mucus is qualitatively altered,5 but whether this is secondary to H pylori infection rather than a primary occurrence remains uncertain. In fact, my experience is that the quality of mucus in chronic non-erosive gastritis-a disorder closely associated with H pylori infection-is normal. It is possible that in gastric ulcer a primary defect in mucus structure allows colonisation of the mucosa by H pylori, which in turn can further alter mucus characteristics and lead to yet more damage to gastric mucosa."* This would
729
ABDOMINAL PARACENTESIS IN NEWBORN INFANTS WITH SUSPECTED NEC
with gastric ulcer in whom H pylori is not detectable and where a primary impairment of the mucus/ bicarbonate barrier can be sufficient to promote mucosal damage independently from colonisation by the microorganism. Both hypotheses are plausible, and for the time being we are free to speculate about either one.
account for those patients
Institute of Internal Medicine, University of Milan,
M. GUSLANDI
Milan, Italy
1. Guslandi M.
Antisecretory
treatment
and
Campylobacter pylori. Gastroenterol Clin
Biol 1989, 13: 641-42. 2 Sarosiek J, Slomiany A, Slomiany BL. Evidence for a weakening of gastric mucus integrity by Campylobacter pylori. Scand J Gastroenterol 1988; 23: 585-90. 3 Slomiany BL, Kasinathan C, Slomiany A. Lipolytic activity of Campylobacter pylori: effect of colloidal bismuth subcitrate (De-Nol). Am J Gastroenterol 1989; 84: 1273-77. 4 Thomsen L, Tasman-Jones C, Morris A, Wiggins P, Lee S, Forlong C. Ammonia produced by Campylobacter pylori neutralizes H moving through gastric mucus. Scand J Gastroenterol 1989; 24: 761-68. 5. Guslandi M, Ballarin E. Assessment of the mucus-bicarbonate barrier in the stomach of patients with chronic gastric disorders Clin Chim Acta 1984; 144: 133-36. 6. Fauchere JL, Rosenau A, Bonneville F. Virulence factors of Campylobacter pylori. Gastroenterol Clin Biol 1989; 13: 59-64B.
contained bacteria on smear indicated intestinal gangrene. Since 1977 we have applied this technique 46 times in forty infants with suspected or definite NEC stage I or 11.5 A retrospective analysis revealed that 40 samples had been evaluated according to Kosloske’s criteria. The white cells had been differentiated in 35 specimens. In all twelve infants showing more than 40% neutrophil granulocytes on smear purulent peritonitis and NEC were confirmed at laparotomy (ten infants) or the diagnosis of NEC was based on the triad of radiological pneumatosis, left shift, and very high C-reactive protein. However, intestinal gangrene/peritonitis was diagnosed incorrectly four times on Kosloske’s colour criterion, and purulent peritonitis/ intestinal gangrene was found at laparotomy after paracentesis in seven patients for whom Kosloske’s criteria had been falsely
negative.
Neutrophil ratio, ascites, surgery in infants with
and
timing of necrotising
enterocolitis SIR,-The indications for surgery in infants with necrotising enterocolitis (NEC) remain controversial; pneumoperitoneum is the only widely accepted criterion, but this sign usually occurs in advanced disease and is associated with an increased case fatality rate.’ Operation at an earlier stage of purulent peritonitis would be desirable but clinical signs of peritonitis are often lacking in babies bom preterm. Kosloske and colleagues introduced abnormal paracentesis to identify infants with intestinal gangrene before intestinal perforation, so permitting early surgical intervention.2-4 A paracentesis sample of 0-5 ml or more that was brown and/or
We have found a neutrophil count (as a percentage of total white cell count) of more than 40% on a smear of abdominal fluid to be a more reliable and earlier sign of purulent peritonitis than brown colour of ascites or bacteria on smear in newborn babies with suspcted NEC (figure, table). Abdominal paracentesis is a simple, safe, and reliable tool for identifying infants with purulent peritonitis. Differentiation of white cells on smears and serial punctures allow the intestinal disease to be followed up so that peritonitis can be detected early on, leading to better timed surgery.
Universitatskinderklinik, D-7900 Ulm/Donau, West Germany
F. POHLANDT P. BARTMANN L. GORTNER
AM, Papile LA, Burstein J. Indications for operation in acute necrotizing enterocolitis of the neonate. Surgery 1980; 87: 502-08. Kosloske AM, Lilly JR. Paracentesis and lavage for diagnosis of intestinal gangrene in neonatal necrotizing enterocolitis. J Pediatr Surg 1978; 13: 315. Kosloske AM, Goldthorn JF. Paracentesis as an aid to the diagnosis of intestinal gangrene. Arch Surg 1982; 117: 571-75. Ricketts RR. The role of paracentesis in the management of infants with necrotizing enterocolitis. Am Surg 1986; 52: 61-65. Bell MJ, Temberg JL, Feigin RD, et al. Neonatal necrotizing enterocolitis: therapeutic decisions based upon clinical staging. Ann Surg 1978; 187: 1. Mathers NJ, Pohlandt F. Diagnostic audit of C-reactive protein in neonatal infection. Eur J Pediatr 1987; 146: 147-51.
1. Kosloske 2. 3. 4. 5.
6.
More in
spider venom than venom?
SIR,-Mr Oppenheim and Dr Taggart (Jan 27, p 228) describe an interesting case of bacterial infection which, by inference, they attribute to the bite of an Austalian spider in a London hotel frequented by students. The facts as presented do not seem
Neutrophil (granulocyte) ratio infants with suspected NEC.
on smears
of ascitic fluid from
Diagnosis of NEC confirmed at laparotomy or based on triad of radiological pneumatosis, left shift, and increased C-reactive protein.’6
sufficient for this conclusion to be drawn. If the possibility is discounted that some visiting Australian student decided to counter the Kylie-and-Jason image by bringing along an unusual pet, an Australian spider in London must have stowed away. In general, species that produce substantial local tissue reactions do not live indoors and therefore are unlikely candidates for stowaway travel-even if the soft body had allowed survival of a long air trip. On the other hand in London, as in most other places, the notion of student accommodation allows for various other candidates for nocturnal assaults. If no identifiably antipodean spider was found at the scene, it seems most probable that the bite was inflicted by a local resident. Department of Physiology, University of Melbourne, Victoria 3052, Australia
CHRISTOPHER BELL
