1486 surgery has been associated with high rates (60-70%) of positive blood cultures that frequently include anaerobic streptococci.6 However, we have not found other reports of hepatic abscesses caused by S milleri in patients who have had a splenectomy. Although this pathogen causes hepatic abscesses, even in patients with an intact spleenreports of minor infections in patients without a spleen are urgently needed. Should patients who have a splenectomy receive a short course of antimicrobial prophylaxis before undergoing a procedure, such as dental extraction, which may lead to transient bacteraemia. J. M. LLIBRE Department of Internal Medicine, J. CUCURULL Hospital Sant Jaume, 08370 Calella,

A. ALOY J. A. HERNANDEZ

Barcelona, Spain

1. Shaw JHF, Print CG. Postsplenectomy sepsis. Br J Surg 1989; 76: 1074-81. 2. Hibberd PL, Rubin RH. Approach to immunization of the immunosuppressed host. Infect Dis Clin North Am 1990; 4: 123-42. 3. Gaston MH, Verter JI, Woods G, et al. Prophylaxis with oral penicillin in children with sickle cell anemia. N Engl J Med 1986; 314: 1593-99. 4. Gopal V, Bisno AL. Fulminant pneumococcal infection in "normal" asplenic hosts. Arch Intern Med 1977; 137: 1526-30. 5. Schwartz B, Facklam RR, Breiman RF. Changing epidemiology of group A streptococcal infection in the USA. Lancet 1990; 336: 1167-71. 6. Lucas Tomas M. Odontogenic septicaemia. Inf Ter Sist Nac Salud 1990; 14: 293-97. 7. Chua D, Reinhart HH, Sobel JD. Liver abscess caused by Streptococcus milleri. Rev Infect Dis 1989; 11: 197-202.

Activity of lansoprazole against Helicobacter pylori

counted by plating dilutions of suspension in triplicate on agar and enumeratory colonies after 5 days. A bactericidal effect (99 9%) was observed after 24 h with long/1 lansoprazole (figure). With as little as 1 mg/l, there was a decrease in viable bacteria. In other experiments, 100 mg/1 produced a 4 log reduction in viable count. Transmission electronmicroscopy of thin sections6 revealed a significant change in the morphology of H pylori. Coccoidal forms, known to be degenerating organisms, appeared after 6 h of contact and affected most bacteria present after 24 h. The main feature was vesicle formation due to a separation between the inner and outer membranes of the bacterial cell wall. This action was not observed after 1 h. We do not know how lansoprazole exerts its action on H pylori but its selectivity for this bacterium is striking. The clinical relevance has yet to be determined. Benzimidazoles have a specific localisation in the gastric mucosa7 but we do not know what the concentration of these protein pump inhibitors is in the mucus layer where H pylori is found. If this concentration proves to be in sufficient to eradicate H pylori-and eradication is the goal if ulcer relapse is to be avoided8-it could be responsible for the clearance observed in some studies and for improved eradication rates when associated with an antimicrobial therapy such as amoxycillin or amoxycillin plus metronidazole. were

Hôpital des Enfants, 33000 Bordeaux, France, and Hôpital St André, Bordeaux

1.

SIR,-Proton pump inhibitors have emerged as potent drugs in the treatment of peptic ulcers and oesophagitis. However, their action against Helicobacter pylori remains controversial. Mainguet et all and Biasco et alz have reported clearance of H pylori after omeprazole alone. Omeprazole in combination therapy led to eradication of H pylori at a higher rate than did amoxycillin alone.3 It is not clear if omeprazole acts only by increasing the pH (thereby improving the action of the antimicrobial agents’) or if it itself has an antimicrobial action, or both. We have done susceptibility tests in vitro using omeprazole (Astra) and lansoprazole (Houde), a novel proton pump inhibitor. Minimum inhibitory concentrations (MIC) of 40 H pylori strains

by a standard agar dilution technique with control drug and Campylobacter jejuni and Escherichia coli as control microorganisms. A bacteriostatic effect was found against H pylori for omeprazole and for lansoprazole but not against Cjejuni or E coli. The MI Cso was lower for lansoprazole than for omeprazole (16 versus 64 mgl). Subsequently, H pylori strain CIP 101260 was used to determine the killing curve of lansoprazole in an in-vitro model with epithelial cells (HEp2) in 25 cm2 tissue culture flasks.S The medium was MEM containing 10% fetal calf serum and 0, 1, 5, and 10 mg/1 of lansoprazole at neutral pH, with incubation at 37°C in a microaerobic atmosphere. At times 0, 1, 6, and 24 h, viable bacteria

were

evaluated

amoxycillin

as

CFU/ftask

Killing

curves

of

lansoprazole against Hpylori-

FRANCIS MEGRAUD LUDMILA BOYANOVA HERVE LAMOULIATTE

Mainguet P, Delmée M, Debongnie JC. Omeprazole, Campylobacter pylori,

and duodenal ulcer. Lancet 1989; ii: 389-90. 2. Biasco G, Miglioli M, Barbara L, et al. Omeprazole, Helicobacter pylori, gastntis, and duodenal ulcer. Lancet 1989; ii: 1403. 3. Unge P, Gad A, Gnarpe H, Olsson J. Does omeprazole improve antimicrobial therapy directed towards gastric Campylobacter pylori in patients with antral gastritis. Scand J Gastroenterol 1989; 24 (suppl 167) 49-54. 4. McNulty CAM, Dent JC, Ford GA, et al. Inhibitory antimicrobial concentrations against Campylobacter pylon m gastric mucosa. J Antimicrob Chemother 1988; 22: 729-38. 5. Mégraud F, Trimoulet P, Lamouliatte H, Boyanova L. Bacterial effect of amoxycillin on Helicobacter pylori in an in vitro model using epithelial cells. Antimicrob Agents Chemother (in press). 6. Néman-Simha V, Mégraud F. In vitro model to study Campylobacter pylori adherence properties. Infect Immun 1988; 56: 3329-33. 7. Helander HF, Ramsay CH, Regardh CG. Localization of omeprazole and metabolites in the mouse. Scand J Gastroenterol 1985; 20 (suppl 108): 95-104. 8. Rauws EAJ, Tytgat GNJ. Cure of duodenal ulcer associated with eradication of Helicobacter pylori. Lancet 1990; 335: 1233-35.

Campylobacter upsaliensis enteritis associated with canine infections SIR,-Animals may be implicated in the spread of Campylobacter in particular dogs have been cited as a probable cause of

jejuni;

infection.1 C upsaliensis may be an unrecognised and frequent cause of diarrhoea in man.2 However, there are no data on the sources of human infection of these organisms. Sandstedt et aP isolated C upsaliensis in faeces from 63 dogs; the organism was found in dogs with diarrhoea as well as in healthy animals. We report C upsaliensis enteritis possibly associated with canine infection. On March 28, 1991, a previously healthy 53-year-old male physician had a temperature of 38’6°C, lower abdominal cramps, nausea, and diarrhoea. Stools were bloody and C upsaliensis was isolated by the filter method.4 Oral amoxycillin and clavulanic acid was started immediately; after 24 h the patient improved and stools became negative for C upsaliensis. A serological response against the isolated strain was shown by western blotting. The only possible factor contributing to infection was exposure to the patient’s 3-year-old healthy dog, and C upsaliensis was isolated from the dog’s stools. Phenotypic characterisation, antibiotic susceptibility, plasmid analysis, protein profiles,4 and immunotyping,s showed that strains isolated from the patient and the dog might be identical. We also investigated the presence of this organism in 42 dogs with diarrhoea; 13 (31 %) proved positive only for C upsaliensis. Thus C upsaliensis may be a frequent cause of diarrhoea in dogs. Doctors should be aware of the prevalence of C upsaliensis and its possible association with diarrhoea, especially in children,2 and that