- Email: [email protected]
STREPTOCOCCUS BOVIS BACTERAEMIA AND ITS ASSOCIATION WITH ALIMENTARY-TRACT NEOPLASM
163
patients 51%)".
said they were upset by some of what they read (43, or Stein concluded that "the benefits seem to outweigh the
costs".
Sergeant states that 26 % of staff knew of at least one patient who had been harmed. But he does not acknowledge that Stein suggests they may all have been referring to the same one or two patients; that 70% of staff believed access "helped the treatment of most patients"; and that none thought that access was generally harmful. He cites McFarlane’s study2 in which psychiatric patients with major psychoses saw their records and says of it only that there were "no differences between those granted access to their current hospital records and those who were not". McFarlane found no difference on matters such as refusal of medication, but reported that those who saw their records were "more likely to have correct information about their condition and treatment" and that viewing the record had sometimes proved helpful by "allaying suspicions, developing trust and even in achieving consent for a specific treatment". McFarlane concluded that access was not detrimental and could be used as a therapeutic tool. Most of those who argue for a right of access accept the need for some limitation in a minority of cases, perhaps to allow access to be deferred until after a period of acute disturbance. But the published evidence suggests that the crucial safeguard is the presence of staff to explain what is seen in the record and that, given this, access is not generally harmful—on the contrary, it may be of great value. ,
Campaign for Freedom of Information, 3 Endsleigh Street, London WC1H ODD
MAURICE FRANKEL
1 Stein EJ, Furedy RL, Simonton MJ, Neuffer CH. Patient access to medical records on a psychiatric inpatient unit. Am J Psychiatry 1979; 136: 327-29. 2 McFarlane WJG, Bowman RG, MacInnes M. Patient access to hospital records. Can J Psychiatry 1980; 25: 497-502
LEGAL INTERFERENCE AND CLINICAL FREEDOM
SIR,-I have the dilemma of sharing the views of both Dr Lunn (Jan 3, p 45) and Dr Tomlin (Dec 6, p 1337) about the safety of patients when anaesthetised. The presence of a vigilant anaesthetist may appear to be a first requirement of minimal monitoring of the anaesthetised patient. This does not solve Tomlin’s logistic difficulty of caring for his anaesthetised patient in the operating room and also his patients in the recovery area. Nor does it address the circumstances where patients are, for practical purposes, anaesthetised for hours or days in the intensive care unit and are receiving intravenous opioids, hypnotics, and muscle relaxants administered intermittently or by infusion (by nurses). It is not my experience that an anaesthetist is physically present at all times at the bedside of patients anaesthetised in this way. There surely must be a middle course somewhere between the views expressed by Tomlin and Lunn. Whether anaesthetists have assistants who are paramedics, nurse anaesthetists, or (as now) nurses trained or training in intensive care, I would hope that the law could recognise that delegation of responsibility in anaesthesia (and other medical specialties is a fact of life. Shackleton Department of Anaesthetics, Southampton General Hospital, Southampton SO9 4XY
FATTY ACID
J. M. MANNERS
&bgr;-OXIDATION DEFECTS AND SUDDEN INFANT DEATH
SIR,-Dr Bennett and colleagues (Dec 20/27, p 1470) state that our population of sudden infant death (SIDS) related cases in which we found inherited disorders of fat oxidation1 was highly selected. There may have been selection in the sense that our interest in fatty acid-p-oxidation defects was known but there has not been a true selection on our part. However, we are not claiming that 60% of SIDS
fat oxidation defect. Within eleven cases, near-miss SIDS cases and their siblings, and infants reacting abnormally to immunisation) 13 had a fat-oxidation defect. These 13 infants had an abnormal odour. The perception of such an odour (sweaty feet odour in the room or an acrid, fatty smell on the breath or skin) is the starting point for our biochemical investigations. These disorders cases are
related
to a
months, among 39 children (siblings of SIDS
are
thought to be rare in the general population but our clinical and
biochemical investigations in infants without
a
SIDS-related
problem allowed us to recognise 37 cases of multiple acyl-CoA dehydrogenase deficiency, ethylmalonic-adipicaciduria, or medium-chain acyl-CoA dehydrogenase deficiency. These potentially severe disorders may not be so infrequent, and it is not surprising that they may be encountered in families with SIDS antecedents. It seems too early to try to determine the exact frequency of such disorders in the general population of infants or in SIDS families. In every pioneering study, the typical cases appear first, those without problems of diagnosis. Later on, with more detailed and more sensitive methods, problems of interpretation arise. For example, in mid-November, we introduced a rapid screening method for medium-chain acyl-CoA dehydrogenase deficiency, measuring octanoic acid in plasma and urine before and after alkaline hydrolysis. Normally, there is no detectable octanoic acid in plasma, and urinary concentrations are 1-3 umol/mmol creatinine. Among 15 siblings of SIDS cases, near-miss SIDS cases, or infants with abnormal reactions after an immunisation, selected on the perception of an acrid, fatty smell on their skin, and studied under normal conditions, we have found 8 infants with plasma octanoic values between 9 and 45 Nmol/I (mean 20). In 7 patients whose urine was studied, the level of free octanoic acid was above 3 /lffiol/mmol before alkaline hydrolysis and increased sharply afterwards. Are these infants homozygous or heterozygous for mediumchain acyl-CoA dehydrogenase deficiency? Should we wait for a metabolic crisis to confirm the diagnosis and begin treatment? Study of octanoate oxidation by leucocytes will help us to confirm the diagnosis in some cases. However, it seems that the octanoate oxidation rate has no predictive value for disease severity. With the same residual octanoate oxidation rate, some patients have expressed the disease clinically. Others have not: are they "time bombs" or will they never express the disease? This is a new challenge-whether to treat or not to treat such infants, who may be at risk for SIDS. Paediatric Clinic, Hôpital de la Salpêtrière, 75651 Pans, France
JEAN-PAUL HARPEY
Biochemistry Laboratory, CHU Necker-Enfants Malades, Paris
CHRISTIANE CHARPENTIER
INSERM U 134, Hôpital de la Salpêtrière
MARION PATURNEAU-JOUAS
1.
2
Harpey J-P, Charpentier C, Coudé M, Divry P, Patumeau-Jouas M. Sudden infant death syndrome (SIDS) and multiple acyl-CoA dehydrogenase deficiency (MADD), ethylmalonic-adipic (EMA-AD) aciduria or systemic carnitine deficiency (SCD). 24th annual symposium of Society for the Study of Inborn Errors of Metabolism (Amersfoort, Netherlands, September, 1986) abstr 56. Duran M, Hofkamp M, Rhead WJ, et al. Sudden child death and "healthy" affected family members with medium-chain acyl-coenzyme A dehydrogenase deficiency. Pediatrics 1986, 78: 1052-57.
STREPTOCOCCUS BOVIS BACTERAEMIA AND ITS ASSOCIATION WITH ALIMENTARY-TRACT NEOPLASM
SiR,—Following Klein and colleagues’1 description in 1977 of two patients with Streptococcus bovis endocarditis and adenocarcinoma of the colon several publications have reported Strep bovis endocarditis coincident with cancer of the However, there is still no proof of a causal gastrointestinal connection between these observations. Most reports have been anecdotal and there have been few series; such series, numbering 29-36 patients with Strep bovis bacteraemia, have revealed a frequency of gastrointestinal neoplasm, polyposis, or other gastrointestinal disorder of between 17 and 55%. Another difficulty is the identification of Strep bovis in clinical laboratories.’ Furthermore, the interval between bacteraemia and recognition of the neoplasm has not been established. Since colonic cancer has an estimate doubling time of 626 days clinical recognition of a bacteraemia
or
tract.
up to 7 years,S Finally, we need to know the natural incidence of the gastrointestinal neoplasm in this
malignant disease could take population.
We have analysed 90 cases of Strep bovis bacteraemia (table). The strains were collected in the period 1951-80 and identified in the
164 STREP BOVIS BACTERAEMIA IN
90 PATIENTS CORRELATED WITH
DEVELOPMENT OF GASTROINTESTINAL NEOPLASMS
*From bacteraemia to neoplasm. The initial diagnosis at first admission was endocarditis in 4 cases, bacteraemia m 9, and colonic neoplasm (with pyrexia of unknown origin or 2. tgastrointesdnal neoplasm suspected or diagnosed in first 2 weeks of primary admission. Adenocarcmomas unless otherwise specified.
endocarditis)
’
reference’ laboratory of Statens Seruminstitut, Information on neoplastic disease obtained by surgery, at necropsy, or on death certificates are recorded in the Danish Cancer Registry. We identified 15 (17%) patients with gastrointestinal cancer in this case material. The results seem to confirm a high incidence of neoplasms in patients with a history of Strep bovis septicaemia, particularly in patients with endocarditis, even several years after the episode- of bacteraemia. Further statistical analysis, taking into account the natural incidence of gastrointestinal neoplasms in this population is in progress.
streptococcal Copenhagen.
Rigshospitalet, Copenhagen
Section of Parasite Growth and Differentiation, Laboratory of Parasitic Diseases,
NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Diagnostic Bacteriology, Statens Seruminstitut, DK-2300 Copenhagen, Denmark; and Department of Clinical Microbiology,
his co-workers for their studies on the isoenzymes of Entamoeba.1; This medium requires erythromycin at all times to control the growth of the Escherichia coli and must be added afresh at each subculture of the amoebae. Let us not forget the battering from antibiotics and other antibacterial compounds E histolytica must face from the moment it excysts and takes up an abode in the gut of human beings of today. For where is there a person, except possibly in the hinterlands of the poorest of the developing countries, who has not taken these drugs, not once but many times? And how many of these individuals took them when they were unknowingly infected with the amoeba? The prevalence of the infection throughout the world is such that the number must be enormous. Any collection of cultures made as part of a survey today must contain several E histolytica isolates obtained from such patients. Thus E histolytica is constantly being assaulted by potent antibacterial compounds whether in the in-vivo environment of the gut of the host or in vitro. For the present, we must recognise this situation as one of the uncontrollable factors in the study of amoebiasis. The three culture systems used in the cultivation of E histolytica (xenic, monoxenic, and axenic) provide us with a means of studying and manipulating under a different set of conditions one of nature’s most adaptable and intriguing protozoan parasites. No one system is more valuable than the other two.
PER Z. HØNBERG ERNÖ GUTSCHIK
RS, Recco RA, Catalano MT, Edberg SC, Casey YI, Steigbigel NH. Association of Streptococcus bovis with carcinoma of the colon. N Engl J Med 1977; 297: 800-02 2. Murray HW, Roberts RB. Streptococcus bovis bacteremia and underlying gastrointestinal disease. Arch Intern Med 1978, 138: 1097-99. 3. Klein RS, Catalano MT, Edberg SC, Casey JL, Steigbigel NH. Streptococcus bovis septicemia and carcinoma of the colon. Ann Intern Med 1979; 91: 560-62. 4. Ravreby WD, Bottone EY, Keusch GT. Group D streptococcal bacteremia with emphasis on the incidence and presentation of infection due to Streptococcus bovis. N Engl J Med 1973; 289: 1400-03. 5. Moyer CA, Rhoads JE. Neoplastic disease—general considerations. In. Moyer CA, Rhoads JE, Allen JG, Harkins HN, eds. Surgery. principles and practice, 3rd ed. Philadelphia: J B Lippincott, 1965: 204-11. 1. Klein
AMOEBIC RESEARCH
SIR,-Your Nov 15 editorial suggests that some of the failings of axenic cultures of Entamoeba histolytica can be ascribed to "the battering by antibiotics required for axenisation". Why single out axenic cultures when the same applies to their ultimate source, the xenic cultures (in the sense of Dougherty,t a xenic culture is one in which there are present an unknown number of associated organisms)? The amoebae in xenic cultures suffer the same battering with antibacterial compounds, including antibiotics, to maintain them in vitro. The first to use such substances was no less an authority on the xenic cultivation of entozoic amoebae than Clifford Dobell .2 He introduced acriflavine to control and eliminate, if possible, bacteria which fermented starch, an essential ingredient of all media used for cultivating E histolytica with a mixed bacterial flora. Dobell used the drug knowing full well that its addition "often modifies the accompanying bacterial flora profoundly, and not always in the desired direction". Ralph A. Nea1/ one of today’s most knowledgeable students of xenic cultures, states: "The establishment of amoebae in vitro demands skill and experience, since it is vital to establish a bacterial flora which is favourable to the growth of the amoebae and to eliminate those bacteria which are deleterious." This is most readily achieved, says Neal, by incorporating into the medium an antibacterial compound such as acriflavine, penicillin, or streptomycin. "When growth of the amoebae becomes profuse and regular, the antibacterial agents can be omitted from the medium." Such is the practice followed in my laboratory. This cannot be done with the much-touted Robinson’s medium used by Sargeaunt and
LOUIS S. DIAMOND
Introduction to axenic cultures of invertebrate metazoa: a goal. Ann NY Acad Sci 1959; 77: 27-54. 2. Dobell C, Laidlaw PP. On the cultivation of Entamoeba histolytica and some other entozoic amoebae. Parasitol 1926; 18: 283-318. 3. Neal RA. In vitro cultivation of Entamoeba. In: Taylor AER, ed. Problems of in vitro culture (5th Symposium of the British Society for Parasitology). Oxford: Blackwell Scientific Publications, 1967: 9-26. 4. Sargeaunt PG, Williams JE. Electrophoretic isoenzyme patterns of Entamoeba histolytica and Entamoeba coli. Trans R Soc Trop Med Hyg 1978; 72: 164-66. 1.
Dougherty EC.
WATER-BORNE OUTBREAK OF CAMPYLOBACTER LARIDIS-ASSOCIATED GASTROENTERITIS
SIR,-Campylobacter laridis (previously called nalidixic-acidresistant thermophilic campylobacter) has been isolated from a variety of birds and mammals, but most frequently from wild seagulls of the genus Larus.1 Before 1984, only 4 human isolations of C laridis had been reported and none of these was clearly associated with disease,l.2 In 1984, Nachamkin et aP described a fatal case of C laridis bacteraemia in an immunocompromised patient, the first indication of this organism’s potential pathogenicity for man. Tauxe et al4 have since reported the isolation of C laridis from 5 sporadic cases of enteric infection. We now report the isolation of C laridis associated with a water-borne outbreak of gastroenteritis in March, 1985. A power station’s municipally treated drinking water supply was accidentally contaminated by a faulty plumbing connection with surface water from Lake Ontario. 162 symptomatic cases were reported, mostly in construction workers. Virtually all affected individuals had drunk contaminated water. The illness was characterised by diarrhoea (86-9%), abdominal pain (70-0%), vomiting (50-6%), nausea (50-0%), malaise (256%), fever (20-0%), headache (16-9%), and dizziness (7-5%), and lasted an average of 4 days (range 1-10 days). Only 1 individual reported bloody stools. Water samples were collected during the time the population at risk was exposed (10 days) and yielded high levels of faecal coliforms (more than 60/dl). Stool specimens were collected 3-20 days (mean 11 days) after the onset of symptoms from 125 patients. Most specimens (87 %) were transported to the laboratory in dry containers. The specimens were analysed for Salmonella, Shigella, Yersinia, Campylobacter, and Aeromonas spp. Skirrow’s selective medium was used for the isolation of campylobacters. C laridis was isolated from 7 patients, 1 of whom was also positive for Cjejuni. 3 other cases were positive, one each of C jejuni, S haardt, and S hadar. The Campylobacter spp were identified by methods previously described.1,2 Serotyping and
patients 51%)".
said they were upset by some of what they read (43, or Stein concluded that "the benefits seem to outweigh the
costs".
Sergeant states that 26 % of staff knew of at least one patient who had been harmed. But he does not acknowledge that Stein suggests they may all have been referring to the same one or two patients; that 70% of staff believed access "helped the treatment of most patients"; and that none thought that access was generally harmful. He cites McFarlane’s study2 in which psychiatric patients with major psychoses saw their records and says of it only that there were "no differences between those granted access to their current hospital records and those who were not". McFarlane found no difference on matters such as refusal of medication, but reported that those who saw their records were "more likely to have correct information about their condition and treatment" and that viewing the record had sometimes proved helpful by "allaying suspicions, developing trust and even in achieving consent for a specific treatment". McFarlane concluded that access was not detrimental and could be used as a therapeutic tool. Most of those who argue for a right of access accept the need for some limitation in a minority of cases, perhaps to allow access to be deferred until after a period of acute disturbance. But the published evidence suggests that the crucial safeguard is the presence of staff to explain what is seen in the record and that, given this, access is not generally harmful—on the contrary, it may be of great value. ,
Campaign for Freedom of Information, 3 Endsleigh Street, London WC1H ODD
MAURICE FRANKEL
1 Stein EJ, Furedy RL, Simonton MJ, Neuffer CH. Patient access to medical records on a psychiatric inpatient unit. Am J Psychiatry 1979; 136: 327-29. 2 McFarlane WJG, Bowman RG, MacInnes M. Patient access to hospital records. Can J Psychiatry 1980; 25: 497-502
LEGAL INTERFERENCE AND CLINICAL FREEDOM
SIR,-I have the dilemma of sharing the views of both Dr Lunn (Jan 3, p 45) and Dr Tomlin (Dec 6, p 1337) about the safety of patients when anaesthetised. The presence of a vigilant anaesthetist may appear to be a first requirement of minimal monitoring of the anaesthetised patient. This does not solve Tomlin’s logistic difficulty of caring for his anaesthetised patient in the operating room and also his patients in the recovery area. Nor does it address the circumstances where patients are, for practical purposes, anaesthetised for hours or days in the intensive care unit and are receiving intravenous opioids, hypnotics, and muscle relaxants administered intermittently or by infusion (by nurses). It is not my experience that an anaesthetist is physically present at all times at the bedside of patients anaesthetised in this way. There surely must be a middle course somewhere between the views expressed by Tomlin and Lunn. Whether anaesthetists have assistants who are paramedics, nurse anaesthetists, or (as now) nurses trained or training in intensive care, I would hope that the law could recognise that delegation of responsibility in anaesthesia (and other medical specialties is a fact of life. Shackleton Department of Anaesthetics, Southampton General Hospital, Southampton SO9 4XY
FATTY ACID
J. M. MANNERS
&bgr;-OXIDATION DEFECTS AND SUDDEN INFANT DEATH
SIR,-Dr Bennett and colleagues (Dec 20/27, p 1470) state that our population of sudden infant death (SIDS) related cases in which we found inherited disorders of fat oxidation1 was highly selected. There may have been selection in the sense that our interest in fatty acid-p-oxidation defects was known but there has not been a true selection on our part. However, we are not claiming that 60% of SIDS
fat oxidation defect. Within eleven cases, near-miss SIDS cases and their siblings, and infants reacting abnormally to immunisation) 13 had a fat-oxidation defect. These 13 infants had an abnormal odour. The perception of such an odour (sweaty feet odour in the room or an acrid, fatty smell on the breath or skin) is the starting point for our biochemical investigations. These disorders cases are
related
to a
months, among 39 children (siblings of SIDS
are
thought to be rare in the general population but our clinical and
biochemical investigations in infants without
a
SIDS-related
problem allowed us to recognise 37 cases of multiple acyl-CoA dehydrogenase deficiency, ethylmalonic-adipicaciduria, or medium-chain acyl-CoA dehydrogenase deficiency. These potentially severe disorders may not be so infrequent, and it is not surprising that they may be encountered in families with SIDS antecedents. It seems too early to try to determine the exact frequency of such disorders in the general population of infants or in SIDS families. In every pioneering study, the typical cases appear first, those without problems of diagnosis. Later on, with more detailed and more sensitive methods, problems of interpretation arise. For example, in mid-November, we introduced a rapid screening method for medium-chain acyl-CoA dehydrogenase deficiency, measuring octanoic acid in plasma and urine before and after alkaline hydrolysis. Normally, there is no detectable octanoic acid in plasma, and urinary concentrations are 1-3 umol/mmol creatinine. Among 15 siblings of SIDS cases, near-miss SIDS cases, or infants with abnormal reactions after an immunisation, selected on the perception of an acrid, fatty smell on their skin, and studied under normal conditions, we have found 8 infants with plasma octanoic values between 9 and 45 Nmol/I (mean 20). In 7 patients whose urine was studied, the level of free octanoic acid was above 3 /lffiol/mmol before alkaline hydrolysis and increased sharply afterwards. Are these infants homozygous or heterozygous for mediumchain acyl-CoA dehydrogenase deficiency? Should we wait for a metabolic crisis to confirm the diagnosis and begin treatment? Study of octanoate oxidation by leucocytes will help us to confirm the diagnosis in some cases. However, it seems that the octanoate oxidation rate has no predictive value for disease severity. With the same residual octanoate oxidation rate, some patients have expressed the disease clinically. Others have not: are they "time bombs" or will they never express the disease? This is a new challenge-whether to treat or not to treat such infants, who may be at risk for SIDS. Paediatric Clinic, Hôpital de la Salpêtrière, 75651 Pans, France
JEAN-PAUL HARPEY
Biochemistry Laboratory, CHU Necker-Enfants Malades, Paris
CHRISTIANE CHARPENTIER
INSERM U 134, Hôpital de la Salpêtrière
MARION PATURNEAU-JOUAS
1.
2
Harpey J-P, Charpentier C, Coudé M, Divry P, Patumeau-Jouas M. Sudden infant death syndrome (SIDS) and multiple acyl-CoA dehydrogenase deficiency (MADD), ethylmalonic-adipic (EMA-AD) aciduria or systemic carnitine deficiency (SCD). 24th annual symposium of Society for the Study of Inborn Errors of Metabolism (Amersfoort, Netherlands, September, 1986) abstr 56. Duran M, Hofkamp M, Rhead WJ, et al. Sudden child death and "healthy" affected family members with medium-chain acyl-coenzyme A dehydrogenase deficiency. Pediatrics 1986, 78: 1052-57.
STREPTOCOCCUS BOVIS BACTERAEMIA AND ITS ASSOCIATION WITH ALIMENTARY-TRACT NEOPLASM
SiR,—Following Klein and colleagues’1 description in 1977 of two patients with Streptococcus bovis endocarditis and adenocarcinoma of the colon several publications have reported Strep bovis endocarditis coincident with cancer of the However, there is still no proof of a causal gastrointestinal connection between these observations. Most reports have been anecdotal and there have been few series; such series, numbering 29-36 patients with Strep bovis bacteraemia, have revealed a frequency of gastrointestinal neoplasm, polyposis, or other gastrointestinal disorder of between 17 and 55%. Another difficulty is the identification of Strep bovis in clinical laboratories.’ Furthermore, the interval between bacteraemia and recognition of the neoplasm has not been established. Since colonic cancer has an estimate doubling time of 626 days clinical recognition of a bacteraemia
or
tract.
up to 7 years,S Finally, we need to know the natural incidence of the gastrointestinal neoplasm in this
malignant disease could take population.
We have analysed 90 cases of Strep bovis bacteraemia (table). The strains were collected in the period 1951-80 and identified in the
164 STREP BOVIS BACTERAEMIA IN
90 PATIENTS CORRELATED WITH
DEVELOPMENT OF GASTROINTESTINAL NEOPLASMS
*From bacteraemia to neoplasm. The initial diagnosis at first admission was endocarditis in 4 cases, bacteraemia m 9, and colonic neoplasm (with pyrexia of unknown origin or 2. tgastrointesdnal neoplasm suspected or diagnosed in first 2 weeks of primary admission. Adenocarcmomas unless otherwise specified.
endocarditis)
’
reference’ laboratory of Statens Seruminstitut, Information on neoplastic disease obtained by surgery, at necropsy, or on death certificates are recorded in the Danish Cancer Registry. We identified 15 (17%) patients with gastrointestinal cancer in this case material. The results seem to confirm a high incidence of neoplasms in patients with a history of Strep bovis septicaemia, particularly in patients with endocarditis, even several years after the episode- of bacteraemia. Further statistical analysis, taking into account the natural incidence of gastrointestinal neoplasms in this population is in progress.
streptococcal Copenhagen.
Rigshospitalet, Copenhagen
Section of Parasite Growth and Differentiation, Laboratory of Parasitic Diseases,
NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Diagnostic Bacteriology, Statens Seruminstitut, DK-2300 Copenhagen, Denmark; and Department of Clinical Microbiology,
his co-workers for their studies on the isoenzymes of Entamoeba.1; This medium requires erythromycin at all times to control the growth of the Escherichia coli and must be added afresh at each subculture of the amoebae. Let us not forget the battering from antibiotics and other antibacterial compounds E histolytica must face from the moment it excysts and takes up an abode in the gut of human beings of today. For where is there a person, except possibly in the hinterlands of the poorest of the developing countries, who has not taken these drugs, not once but many times? And how many of these individuals took them when they were unknowingly infected with the amoeba? The prevalence of the infection throughout the world is such that the number must be enormous. Any collection of cultures made as part of a survey today must contain several E histolytica isolates obtained from such patients. Thus E histolytica is constantly being assaulted by potent antibacterial compounds whether in the in-vivo environment of the gut of the host or in vitro. For the present, we must recognise this situation as one of the uncontrollable factors in the study of amoebiasis. The three culture systems used in the cultivation of E histolytica (xenic, monoxenic, and axenic) provide us with a means of studying and manipulating under a different set of conditions one of nature’s most adaptable and intriguing protozoan parasites. No one system is more valuable than the other two.
PER Z. HØNBERG ERNÖ GUTSCHIK
RS, Recco RA, Catalano MT, Edberg SC, Casey YI, Steigbigel NH. Association of Streptococcus bovis with carcinoma of the colon. N Engl J Med 1977; 297: 800-02 2. Murray HW, Roberts RB. Streptococcus bovis bacteremia and underlying gastrointestinal disease. Arch Intern Med 1978, 138: 1097-99. 3. Klein RS, Catalano MT, Edberg SC, Casey JL, Steigbigel NH. Streptococcus bovis septicemia and carcinoma of the colon. Ann Intern Med 1979; 91: 560-62. 4. Ravreby WD, Bottone EY, Keusch GT. Group D streptococcal bacteremia with emphasis on the incidence and presentation of infection due to Streptococcus bovis. N Engl J Med 1973; 289: 1400-03. 5. Moyer CA, Rhoads JE. Neoplastic disease—general considerations. In. Moyer CA, Rhoads JE, Allen JG, Harkins HN, eds. Surgery. principles and practice, 3rd ed. Philadelphia: J B Lippincott, 1965: 204-11. 1. Klein
AMOEBIC RESEARCH
SIR,-Your Nov 15 editorial suggests that some of the failings of axenic cultures of Entamoeba histolytica can be ascribed to "the battering by antibiotics required for axenisation". Why single out axenic cultures when the same applies to their ultimate source, the xenic cultures (in the sense of Dougherty,t a xenic culture is one in which there are present an unknown number of associated organisms)? The amoebae in xenic cultures suffer the same battering with antibacterial compounds, including antibiotics, to maintain them in vitro. The first to use such substances was no less an authority on the xenic cultivation of entozoic amoebae than Clifford Dobell .2 He introduced acriflavine to control and eliminate, if possible, bacteria which fermented starch, an essential ingredient of all media used for cultivating E histolytica with a mixed bacterial flora. Dobell used the drug knowing full well that its addition "often modifies the accompanying bacterial flora profoundly, and not always in the desired direction". Ralph A. Nea1/ one of today’s most knowledgeable students of xenic cultures, states: "The establishment of amoebae in vitro demands skill and experience, since it is vital to establish a bacterial flora which is favourable to the growth of the amoebae and to eliminate those bacteria which are deleterious." This is most readily achieved, says Neal, by incorporating into the medium an antibacterial compound such as acriflavine, penicillin, or streptomycin. "When growth of the amoebae becomes profuse and regular, the antibacterial agents can be omitted from the medium." Such is the practice followed in my laboratory. This cannot be done with the much-touted Robinson’s medium used by Sargeaunt and
LOUIS S. DIAMOND
Introduction to axenic cultures of invertebrate metazoa: a goal. Ann NY Acad Sci 1959; 77: 27-54. 2. Dobell C, Laidlaw PP. On the cultivation of Entamoeba histolytica and some other entozoic amoebae. Parasitol 1926; 18: 283-318. 3. Neal RA. In vitro cultivation of Entamoeba. In: Taylor AER, ed. Problems of in vitro culture (5th Symposium of the British Society for Parasitology). Oxford: Blackwell Scientific Publications, 1967: 9-26. 4. Sargeaunt PG, Williams JE. Electrophoretic isoenzyme patterns of Entamoeba histolytica and Entamoeba coli. Trans R Soc Trop Med Hyg 1978; 72: 164-66. 1.
Dougherty EC.
WATER-BORNE OUTBREAK OF CAMPYLOBACTER LARIDIS-ASSOCIATED GASTROENTERITIS
SIR,-Campylobacter laridis (previously called nalidixic-acidresistant thermophilic campylobacter) has been isolated from a variety of birds and mammals, but most frequently from wild seagulls of the genus Larus.1 Before 1984, only 4 human isolations of C laridis had been reported and none of these was clearly associated with disease,l.2 In 1984, Nachamkin et aP described a fatal case of C laridis bacteraemia in an immunocompromised patient, the first indication of this organism’s potential pathogenicity for man. Tauxe et al4 have since reported the isolation of C laridis from 5 sporadic cases of enteric infection. We now report the isolation of C laridis associated with a water-borne outbreak of gastroenteritis in March, 1985. A power station’s municipally treated drinking water supply was accidentally contaminated by a faulty plumbing connection with surface water from Lake Ontario. 162 symptomatic cases were reported, mostly in construction workers. Virtually all affected individuals had drunk contaminated water. The illness was characterised by diarrhoea (86-9%), abdominal pain (70-0%), vomiting (50-6%), nausea (50-0%), malaise (256%), fever (20-0%), headache (16-9%), and dizziness (7-5%), and lasted an average of 4 days (range 1-10 days). Only 1 individual reported bloody stools. Water samples were collected during the time the population at risk was exposed (10 days) and yielded high levels of faecal coliforms (more than 60/dl). Stool specimens were collected 3-20 days (mean 11 days) after the onset of symptoms from 125 patients. Most specimens (87 %) were transported to the laboratory in dry containers. The specimens were analysed for Salmonella, Shigella, Yersinia, Campylobacter, and Aeromonas spp. Skirrow’s selective medium was used for the isolation of campylobacters. C laridis was isolated from 7 patients, 1 of whom was also positive for Cjejuni. 3 other cases were positive, one each of C jejuni, S haardt, and S hadar. The Campylobacter spp were identified by methods previously described.1,2 Serotyping and