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CLUSTERING OF AEROMONAS HYDROPHILA SEPTICAEMIA
1232 CLUSTERING OF AEROMONAS HYDROPHILA SEPTICAEMIA
SIR,-Further to Dr Ampel and Or Peter’s interesting account ofa of bacteraemia with Aeromonas hydrophilo (Oct. would like to report a cluster of four cases of 31, p. 987), due its isolation on hospital wards, and to this organism, septicaemia the use of biotyping to explore the epidemiology. The cases occurred in a 16 day period and will be reported in detail elsewhere. The patients had not sustained any aquatically related wounds in the preceding weeks and there was no history of contact with water through sport or occupation. All were debilitated before their episodes of septicaemia; two were severely neutropenic (total neutrophils <10/i.), being on cytotoxic therapy for acute myelomonocytic leukaemia and lymphosarcoma. None had any water acquired case we
Pedigree showing lymphocytes. Asterisks indicate different cultures.
the percentage
means
fra(X) (q27)
of two analyses of 100
or more
sites in
50-120 ,
lymphocytes from
The proband is moderately retarded and attends a special school. All three sibs of the proband are having difficulty with normal schooling, particuarly mathematics, as did their mother. The grandfather of the proband attended normal school, earned his living as a factory worker and fought as a soldier in the 1939-45 war. He has an unusual personality and this has been attributed to war neurosis. This pedigree confirms the expectation of transmission of the fra(X) (q27) site from an affected male and suggests the need for inclusion of apparently normal males in family studies. GRAHAM C. WEBB JOHN G. ROGERS DAVID B. PITT Birth Defects Research Institute, HALLIDAY JANE Children’s Royal Hospital, THERESA THEOBALD Parkville, Victoria 3052, Australia HAEMOLYTIC DISEASE OF THE NEWBORN CAUSED BY ANTI-U
SiR,-Anti-U antibody, a rarity, was first described by Wiener et al.in 1953, in a patient who had had a fatal haemolytic transfusion reaction. About 1% of American Blacks are U-negative subjects, the prevalence being higher in African Blacks. No White U-negative subjects have been reported. We have seen a case of haemolytic disease of the newborn caused by anti-U. The affected infant was the product of the seventh pregnancy, no previous infant having been recorded as being affected. Both parents are Nigerian. The mother is 0, Rh +, U -, and the father is 0, Rh+, U+. The mother had never been transfused, and there were no previous obstetric difficulties. The infant weighed 5.3 3kg at birth, and was delivered per vaginam, with some difficulty. The cord haemoglobin was 20 -22 g/dl. The direct Coombs test on the cord cells was strongly positive (IgG coating). The maternal antibody reacted strongly with all cells in a standard commercial cell panel. The specificity anti-U was confirmed at the regional transfusion centre, and subsequently anti-U was eluted from the infant’s cells. Maternal antibody titre by antiglobulin technique was 1:512. 3 h post-delivery, the infant’s bilirubin was 110 mol/1. The child underwent phototherapy, but despite this the bilirubin level rose to 336 mol/1, and the haemoglobin fell to 16-00 g/dl over the next 4 days. Exchange transfusion was then done with two units of compatible group 0, Rh+, U- blood, obtained from a family of donors found after an extensive search by the South London Transfusion Service, and stored in the Brentwood frozen blood bank. After exchange transfusion and continued phototherapy, the bilirubin level fell quickly over the next 5 days, and the haemoglobin remained stable at 16’00 g/dl.
hepatic dysfunction. All were attended by different doctors and nurses, were on different wards, and had been in hospital for more than a week. Three had received blood products and intravenous fluids, but in only one case was this shortly before his septicaemia and no A.hydrophila could be detected from his blood packs. A.hydrophila was isolated from all blood cultures in all cases within 24 h of their collection. Only one patient had diarrhoea but A. hydrophila was not isolated from sputa, skin, intravenous lines, or multiple faecal samples from any of these patients. Two of these patients responded rapidly to cefoxitin and another to gentamicin therapy. The fourth case, with neutropenia, died despite gentamicin therapy, to which the isolate was sensitive. No isolates of A.hydrophila in blood cultures in our hospital group had previously been encountered, and we can find no published report ofa similar cluster of cases. A. hydrophila was isolated from a soap dish in one ward and a sink in another; both isolates were recovered a week after the cases of septicaemia on the respective wards. These isolates were all biotyped 1,2 and shown to be distinct from one another and the four clinical isolates (see table). We cannot be certain that the Aeromonas was not acquired from the patients’ own faeces, despite multiple specimens being examined, because of possible intermittent excretion and in addition a selective medium was not used to pick up small numbers of the organisms. Moreover, since many biotypes can occur in the same water sample, a common source cannot be eliminated. This incident, however, does demonstrate that A.hydrophila can be isolated on hospital wards and, in the absence of other typing methods, biotyping may be useful in investigating possible outbreaks of cross-infection due to this organism. Department of Medical Microbiology, London Hospital, B. D. COOKSON E. C. HOUANG J. V. LEE
London E1 Maidstone Public Health
Laboratory
JV, Shread P, Furniss AL, Bryant TN. Taxonomy and description of Vibrto fluvialis sp nov (synonym group F vibrious, group EF6). J Appl Bacteriol 1981;50:
1. Lee
73-94. 2.
Ljungh A, Popoff M, Wadstrom T. Aeromonas hydrophila in acute diarrhoeal disease’ Detection of enterotoxin and biotyping of strains J Clin Microbiol 1977; 6: 96-100. BIOTYPING OF A. HYDROPHILA STRAINS I
-.--
N. DHANDSA M. WILLIAMS
Westminster Hospital, London SW1P 2AP
V. JOSS J. PATTEN D. JAMES L. SINCLAIR
1. Wiener AS, Unger LJ, Gordon EB. Fatal hemolytic transfusion reaction caused sensitisation to a new blood factor U. JAMA 1953; 153: 1444-46.
by
All isolates were sensitive to gentamicin, cefoxitin, and tobramycin and resistant to carbemcillin, except for case 4 which was sensitive to cefoxmn alone. VP Voges-Proskauer. =
SIR,-Further to Dr Ampel and Or Peter’s interesting account ofa of bacteraemia with Aeromonas hydrophilo (Oct. would like to report a cluster of four cases of 31, p. 987), due its isolation on hospital wards, and to this organism, septicaemia the use of biotyping to explore the epidemiology. The cases occurred in a 16 day period and will be reported in detail elsewhere. The patients had not sustained any aquatically related wounds in the preceding weeks and there was no history of contact with water through sport or occupation. All were debilitated before their episodes of septicaemia; two were severely neutropenic (total neutrophils <10/i.), being on cytotoxic therapy for acute myelomonocytic leukaemia and lymphosarcoma. None had any water acquired case we
Pedigree showing lymphocytes. Asterisks indicate different cultures.
the percentage
means
fra(X) (q27)
of two analyses of 100
or more
sites in
50-120 ,
lymphocytes from
The proband is moderately retarded and attends a special school. All three sibs of the proband are having difficulty with normal schooling, particuarly mathematics, as did their mother. The grandfather of the proband attended normal school, earned his living as a factory worker and fought as a soldier in the 1939-45 war. He has an unusual personality and this has been attributed to war neurosis. This pedigree confirms the expectation of transmission of the fra(X) (q27) site from an affected male and suggests the need for inclusion of apparently normal males in family studies. GRAHAM C. WEBB JOHN G. ROGERS DAVID B. PITT Birth Defects Research Institute, HALLIDAY JANE Children’s Royal Hospital, THERESA THEOBALD Parkville, Victoria 3052, Australia HAEMOLYTIC DISEASE OF THE NEWBORN CAUSED BY ANTI-U
SiR,-Anti-U antibody, a rarity, was first described by Wiener et al.in 1953, in a patient who had had a fatal haemolytic transfusion reaction. About 1% of American Blacks are U-negative subjects, the prevalence being higher in African Blacks. No White U-negative subjects have been reported. We have seen a case of haemolytic disease of the newborn caused by anti-U. The affected infant was the product of the seventh pregnancy, no previous infant having been recorded as being affected. Both parents are Nigerian. The mother is 0, Rh +, U -, and the father is 0, Rh+, U+. The mother had never been transfused, and there were no previous obstetric difficulties. The infant weighed 5.3 3kg at birth, and was delivered per vaginam, with some difficulty. The cord haemoglobin was 20 -22 g/dl. The direct Coombs test on the cord cells was strongly positive (IgG coating). The maternal antibody reacted strongly with all cells in a standard commercial cell panel. The specificity anti-U was confirmed at the regional transfusion centre, and subsequently anti-U was eluted from the infant’s cells. Maternal antibody titre by antiglobulin technique was 1:512. 3 h post-delivery, the infant’s bilirubin was 110 mol/1. The child underwent phototherapy, but despite this the bilirubin level rose to 336 mol/1, and the haemoglobin fell to 16-00 g/dl over the next 4 days. Exchange transfusion was then done with two units of compatible group 0, Rh+, U- blood, obtained from a family of donors found after an extensive search by the South London Transfusion Service, and stored in the Brentwood frozen blood bank. After exchange transfusion and continued phototherapy, the bilirubin level fell quickly over the next 5 days, and the haemoglobin remained stable at 16’00 g/dl.
hepatic dysfunction. All were attended by different doctors and nurses, were on different wards, and had been in hospital for more than a week. Three had received blood products and intravenous fluids, but in only one case was this shortly before his septicaemia and no A.hydrophila could be detected from his blood packs. A.hydrophila was isolated from all blood cultures in all cases within 24 h of their collection. Only one patient had diarrhoea but A. hydrophila was not isolated from sputa, skin, intravenous lines, or multiple faecal samples from any of these patients. Two of these patients responded rapidly to cefoxitin and another to gentamicin therapy. The fourth case, with neutropenia, died despite gentamicin therapy, to which the isolate was sensitive. No isolates of A.hydrophila in blood cultures in our hospital group had previously been encountered, and we can find no published report ofa similar cluster of cases. A. hydrophila was isolated from a soap dish in one ward and a sink in another; both isolates were recovered a week after the cases of septicaemia on the respective wards. These isolates were all biotyped 1,2 and shown to be distinct from one another and the four clinical isolates (see table). We cannot be certain that the Aeromonas was not acquired from the patients’ own faeces, despite multiple specimens being examined, because of possible intermittent excretion and in addition a selective medium was not used to pick up small numbers of the organisms. Moreover, since many biotypes can occur in the same water sample, a common source cannot be eliminated. This incident, however, does demonstrate that A.hydrophila can be isolated on hospital wards and, in the absence of other typing methods, biotyping may be useful in investigating possible outbreaks of cross-infection due to this organism. Department of Medical Microbiology, London Hospital, B. D. COOKSON E. C. HOUANG J. V. LEE
London E1 Maidstone Public Health
Laboratory
JV, Shread P, Furniss AL, Bryant TN. Taxonomy and description of Vibrto fluvialis sp nov (synonym group F vibrious, group EF6). J Appl Bacteriol 1981;50:
1. Lee
73-94. 2.
Ljungh A, Popoff M, Wadstrom T. Aeromonas hydrophila in acute diarrhoeal disease’ Detection of enterotoxin and biotyping of strains J Clin Microbiol 1977; 6: 96-100. BIOTYPING OF A. HYDROPHILA STRAINS I
-.--
N. DHANDSA M. WILLIAMS
Westminster Hospital, London SW1P 2AP
V. JOSS J. PATTEN D. JAMES L. SINCLAIR
1. Wiener AS, Unger LJ, Gordon EB. Fatal hemolytic transfusion reaction caused sensitisation to a new blood factor U. JAMA 1953; 153: 1444-46.
by
All isolates were sensitive to gentamicin, cefoxitin, and tobramycin and resistant to carbemcillin, except for case 4 which was sensitive to cefoxmn alone. VP Voges-Proskauer. =