symptoms and what they thought it would be sensible to do about it. I copied these seemingly simple questions into my own history taking several years ago. The first question is usually met with considerable surprise, followed by detailed comments on the assumed pathogenesis, ranging from the scientifically sound to the bizarre. The second question provokes a blank facial expressionbefore the patient willingly goes on to say what he or she thinks appropriate. While the patient’s answers are heavily contaminated by expectations and previous experience with the medical system they always give away information about the conceptual framework of a patient’s illness and about his or her internal attitude and

approach, and the questions are welcomed. This information, gathered by simple listening, will be irrelevant to diagnostic or therapeutic decisions but to disregard it while explaining what has why, and how, always turns out to be a mistake, in terms of compliance or additional time spent. We do not treat people. We try to form alliances with them to alleviate conditions they cannot cope with on their own: if they could they would not have called us. to be done,

University Neurology Clinic, D-4300 Essen, Germany


1. Levi-Strauss C. Anthropologie structurale. Pans: Librairie Plon, 1958. 2. von Weizsacker V Falle und Probleme. Anthropologische Vorlesungen in der Medizinischen Klinik (1947): gesammelte Schriften Bd 9, Stuttgart: Suhrkamp, 1988.

SIR,- The "death without weeping" of 3-year-old girl Mercea, described by Scheper-Hughes (May 11, p 1144), vividly illustrates the dilemmas surrounding technical fixes for child survival such as oral rehydration (ORT) and the expanded programme on immunisation (EPI) in communities which are in the closing stage of the "demographic trap",1,2 assuming that hers is trapped, which seems probable. Whose welfare is to be chosen? That of the present child, that child in future condemned to malnutrition and an early death (Mercea), or that of the community in which child survival increases population pressure and therefore the threat of starvation? UNICEF argues that lowering the child death rate lowers the birth rate, and as evidence for this stresses the synergism between ORT (and EPI) and family planning. Unfortunately, there can be no synergism if there is no family planning-or if it is inappropriate or is severely discouraged, as by the Catholic Church. Dr M. Hellberg, of the international child health unit, Uppsala University, has argued that "for a long time it has been totally irresponsible to provide forms of health care and medical services without family planning". For communities deep in the demographic trap technical fixes for child survival do not necessarily have to be applied on a public health scale just because they are possible, especially without adequate family planning, because they increase demographic pressure and add to the person-years of human misery. Mercea is a case in point. Department of Public Health Medicine, University of Leeds, Leeds LS2 9LN, UK 1. 2.


King M. Health is a sustainable state. Lancet 1990; 336: 664-67. King M. Overpopulation and death in childhood. Lancet 1990; 336:



(very important disease) syndrome

SIR,- The VIP (very important patient) syndrome is well described. Most commonly recognised when the patient is a physician, the VIP, by virtue of his or her power, prestige, or fame, alters the treatment setting.1,2 Doctors must be alert to the special needs of the VIP without compromising too greatly generally accepted standards of medical practice. Recently we encountered a variant, the VID or very important disease syndrome. A patient came under our psychiatric care who had an enigmatic physical disease. He had been told at another hospital that his disease was unique and that there was no treatment for it. On the patient’s admission here, for a depression related to this chronic disabling illness, the physician who had done the work-up at the other hospital was contacted. This physician was clearly irritated that the patient had been admitted to another academic centre and

hesitated to discuss details of the investigation because the case had not yet been reported. In our hospital much of the work-up was repeated. Because of the unusual nature of his disease he was seen by a variety of specialists who proposed different lines of investigation. Because of the

patient’s despair about his disease,

his desperate wish to find out anything he could about it despite any discomfort, and the obvious seniority and prestige of the consultants who saw him, it was often difficult for the patient to say no to a procedure. When we assumed the role of the "primary" physicians we at once became aware of impulses in ourselves to find a "doctor" or tests that could make sense of the disease to overcome our own ignorance and helplessness; to avoid working with the patient on the immense helplessness he was experiencing; and to explore the possibility of collaborating in the description of his hitherto unreported disease. These three impluses could be viewed as a response to our own helplessness in the face of the patient’s primary medical illness and

his psychological response to it. Concentrating on the puzzle of an unclear medical illness can provide an easy and adaptive diversion from a difficult clinical situation: the desire to characterise and describe a patient’s disease can represent both a scientific ideal and a wish to avoid the discomfort of attending a patient who reveals our helplessness. The result can be a patient who feels rejected by physicians who have "finished with the tests". The VID should prompt careful consideration of the motives for investigative zeal and of the impact of such zeal on the patient who has the illness. Department of Psychiatry, University Medical College, Payne Whitney Clinic and New York Hospital,


New York, NY 10021, USA


1. Stoudemire A, Rhoads JM. When the doctor needs a doctor: special considerations for the physician-patient Ann Intern Med 1983; 98: 654-59. 2. Munich R. The VIP as patient: syndrome, dynamic, and treatment. In. Tasman A, Hales R, Frances A, eds. Review of psychiatry. Alexandria, Virginia: American Psychiatric Press, 1989: 580-93.

Antimicrobial prophylaxis for dental extractions after splenectomy SIR,-Patients who have undergone splenectomy are known to an increased risk of overwhelming infection, with an overall mortality of 2.5%.1 The risk of less severe infection in these patients has not been so extensively studiedThe spleen may also have a role in clearance of non-encapsulated organisms with benign transient have

bacteraemias. A 51-year-old white male presented with a 3-week history of low-grade fever. Seven years previously he had undergone splenectomy. Ten days before admission he was found to have an odontogenic abscess; a dental extraction was completed but antibiotic prophylaxis was not given. Physical examination revealed tender hepatomegaly. Laboratory studies showed a white cell count of 15-5 x 109/1 (80% neutrophils) aspartate aminotransferase 32 IU/1, alkaline phosphatase 435 IU/1, and gammaglutamyltranspeptidase 330 IU/1. Abdominal ultrasound and computed tomography (CT) found three hepatic abscesses. CTguided fine-needle aspiration into the largest abscess (9 cm) obtained 60 ml pus. That sample and two blood cultures grew Streptococcus intermedius. Despite intravenous high-dose penicillin (24 million IU/day), the largest abscess continued to increase in size. At laparotomy, a large lobulated liver abscess was drained (220 ml of pus). Postoperative recovery was uneventful. Antimicrobial prophylaxis after splenectomy has been thought to be cost-effective only in young children or high-risk adults during the first three years after surgery.Although risk of sepsis is greatest within two years of splenectomy, up to 30% of infections appear after 10 years.’ However, long-term prophylaxis may lead to bacterial resistance. Our case suggests that standard prophylaxis with a penicillin or another &bgr;-Iactam antibiotic does not protect against transient streptococcal bacteremia in patients who have undergone a splenectomy. The epidemiology of streptococcal infection suggests that the incidence of some invasive forms is increasing.5 Periodontal

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,


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


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









lansoprazole against Hpylori-


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


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

Antimicrobial prophylaxis for dental extractions after splenectomy.

1485 symptoms and what they thought it would be sensible to do about it. I copied these seemingly simple questions into my own history taking several...
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