obstruction, embryotomy, and pelvic damage,
completely avoided and maternal survival was guaranteed. We then compared perinatal mortality at various birthweights in booked women who remained free of medical and obstetric complications throughout pregnancy but not necessarily in labour; booked women in whom complications developed during pregnancy; and unbooked emergencies. The latter were those who had no intention of receiving institutional care; they arrived late for treatment when life-threatening complications developed, usually during labour. At birthweight 3,0-3,5 kg, which is associated with the best fetal outcomes, perinatal mortality per 1000 singleton births was 10 in the booked-healthy group, 34 in the booked-antenatal complications group, and 170 in the unbooked emergencies. For very-low-birthweight babies ( 1000 g) the chances of survival were very poor. Neither good maternal health nor the acceptance of hospital antenatal care changed this outlook. Obviously, only the additional effect of appropriate western technology can do so. Thus data accord with Pearce and Chamberlain’s views in respect of fetal outlook but not necessarily in relation to maternal survival. Dr Campbell and colleagues (May 4, p 1095), commenting on a report by two of us (March 2, p 553), were puzzled about why, among hospital booked patients, the differential in maternal health rates between the less educated and better educated was more striking in Port Harcourt than in Zaria. One of the reasons was socioeconomic. Conditions surrounding hospital treatment, including back-up services and the provision of essential supplies and consumable items, were good in the 1970s when the Zaria data were collected. At that time, with a buoyant economy countrywide, hospital treatment, including surgery, was free of charge. Compliance was therefore satisfactory, and booked hospital patients needing surgery received it without too much delay. All that changed in the 1980s, when the country had a major economic decline coinciding with data collection in Port Harcourt. Fees were charged for hospital treatment, and those needing surgery had to purchase their own consumable items. Compliance deteriorated and delay in treatment became inevitable. The hardship, though widespread, affected the less educated much more than the better educated.
Office of the Vice-Chancellor, and Departments of Obstetrics and Gynaecology, and Paediatrics and Child Health, Choba, Port Harcourt, Nigeria
K. A. HARRISON N. D. BRIGGS R. S. ORUAMABO
1. Harrison KA. Child-bearing, health and social priorities: a survey of 22 774 consecutive hospital births in Zaria, Northern Nigeria. Br J Obstet Gynaecol 1985; (suppl 5): 3-22, 61-71, 100-16. 2. Anon. Maternal health in sub-Saharan Africa. Lancet 1987; i: 255-57.
Yeasts susceptibility testing StR,—The British Society for Antimicrobial Chemotherapy Working Party (June 29, p 1577) refers to high minimum inhibitory concentrations (MICs) of fluconazole for Candida glabrata correlating with clinical resistant infections.!
patients, the resistant strains were isolated during relapsing episodes but for patient C, the candidosis persisted for 5 months despite increasing doses of fluconazole (50,100, and 150 mg daily). In this patient, primary resistance was suspected. In our retrospective study, the serum concentrations of fluconazole were not assayed but the drug is usually well absorbed. These clinical observations are similar to those for experimental infections in which the most resistant isolates in vitro were the least susceptible to fluconazole treatment.3 We believe that a standardised method should be used to test the susceptibility of C albicans isolated from patients with AIDS, to allow rapid administration of an appropriate antifungal agent. Department of Parasitology- Mycology, CHU Cochin-Port Royal, 75014 Paris, France
JEAN DUPOUY-CAMET ANDRÉ PAUGAM
1. Warnock DW, Burke J, Cope NJ, Johnson EM, Von Fraunhofer NA, Williams EW. Fluconazole resistance in Candida glabrata. Lancet 1988; ii: 1310. 2. Guinet R, Nerson D, De Closet F, et al. Collaborative evaluation in seven laboratories of a standardised micromethod for yeast susceptibility testing. J Clin Microbiol 3.
1988; 26: 2307-12. Galgiani JN. Susceptibility of Candida albicans and other yeasts to fluconazole: relation between in vitro and in vivo studies. Rev Infect Dis 1990; 12 (suppl 3P): S272-75.
Laparoscopic surgery in the treatment of varicocele SIR,-We report laparoscopic testicular vein division for the treatment
of varicocele. Until
have done testicular vein
using an extraperitoneal approach. During laparoscopic cholecystectomy we have seen the testicular veins and noted that the anatomy of the internal inguinal ring is easily visible through the peritoneum. We have therefore pursued the idea of dividing the testicular vein laparoscopically. We have now done this novel procedure on three occasions, using two 11 mm cannulae and one 5 mm cannula, inserted via the umbilicus and lower abdomen. On each occasion the testicular vein was readily exposed, separated from the testicular artery, quadruple clipped, and divided, resecting a short segment. Operating time was under thirty minutes in each case. One patient spent the night in hospital, the other two were day cases. Subsequent recovery was rapid, with disappearance of the varicocele. We feel that this further application of the minimally invasive surgical approach is a useful improvement over other procedures, and we are not aware of any previous report of its use.
J. BLACK Department of Surgery, Worcester Royal Infirmary, Worcester WR5 1HN, UK
R. O. BECK N. C. HICKEY C. W. O. WINDSOR
Intrinsic factor antibodies and pernicious anaemia
We also observed such a correlation, but with strains of C albicans, when we tested the MICs of fluconazole for 50 C albicans strains isolated from inpatients. For this test, we adapted the standardised ’Mycototal’ micromethod to fluconazole (HoechstBehring)Four strains which required MICs of 50 mg/1 or more were regarded as resistant in vitro. These strains had been isolated from patients with AIDS who, according to clinical records, had been treated for several months with usual doses of fluconazole and had had resistant episodes of oropharyngeal candidosis (table). In 3
SIR,-Intrinsic factor (IF) is a protein that is produced by gastric parietal cells and binds to and facilitates the absorption of vitamin B,2.’ Antibodies to IF are found in the serum of 55-57% of patients with pernicious anaemia, many of whom have such antibodies in gastric secretion.1,2 The role of IF antibodies in the development of pernicious anaemia is unclear. Although they prevent IF-mediated vitamin B,2 absorption3 and are almost exclusively confined to patients with pernicious anaemia,1,4 nearly half such patients do not have IF antibodies in either serum or gastric juice,l and there are no
DATA FOR AIDS PATIENTS WITH FLUCONAZOLE-RESISTANT CANDIDA ALBlCANS
antibodies.5,6 Rarely, IF antibodies are found in patients without pernicious anaemia1,4 and it has been suggested that such cases represent a pre-disease state.4 Short-term follow-up7 of 11 patients did not show evidence to support this hypothesis, but no long-term data are available. We report a patient who has had IF antibodies for 27 years without pernicious anaemia developing. This woman proved to have high-titre IF and parietal-cell antibodies in serum at age 44 while receiving treatment for myxoedema. Her haemoglobin was 15 g/dl and serum vitamin B12 350 pg/ml (normal 200-400). She had normoblastic erythropoiesis
apparent differences between those with and those without IF
in bone marrow and a 24-hour urinary 57CO-B12 excretion (Schilling test) of 20-5% (normal > 10%).IF antibodies were not detectable in gastric juice. Normal amounts of free acid and IF were present in an augmented histamine test and gastric biopsy revealed mild superficial gastritis only. Follow-up at 3 years7 showed no substantial change in these results, and 12 years later her serum vitamin B12 and Schilling test remained normal (350 pg/ml and
15 1 %, respectively). At age 71 she was referred with signs of early dementia and a vitamin B12 of 159 pg/ml. There was no evidence of peripheral neuropathy. Her haemoglobin was 15 g/dl, mean corpuscular volume 92 fl, white blood cell count 8-8 x 109/1 (normal differential), and platelet count 287 000/)il. Red-cell folate was 284 ng/ml (normal 200-800 ng/ml) and repeat serum vitamin B12 was 150 pg/ml. IF and parietal-cell antibodies were still present in serum. Bone-marrow and deoxyuridine suppression test were normal, and 24-hour urinary 57CO-B12 excretion was 13-2%. Serum immunoglobulins and circulating CD4 and CD8 lymphocyte counts were normal. Gastric biopsy revealed slight superficial gastritis. The cause of this patient’s low vitamin B12 level is uncertain, but she may have had a mild dietary deficiency. However, pernicious anaemia has not developed despite the presence of IF antibodies in serum for over 27 years. This case supports the view that serum IF antibody in itself is not important in the pathogenesis of this disease. It is noteworthy that patients with IF antibodies but normal vitamin B12 absorption usually have no demonstrable IF antibody in gastric juice.4 The final precipitating factor lacking in these patients might be IgA IF antibody produced by lymphoid cells in the stomach wall, or cell-mediated immunity may also be necessary for the complete destruction of the gastric mucosa.7 serum
Edgware General Hospital, Edgware, Middlesex HA8 0AD,
DAVID CUMMINS SIMON ARDEMAN
1. Chanarin I. The megaloblastic anaemias, 3rd ed. Oxford: Blackwell Scientific Publications, 1990. 2. Ardeman S, Chanarin I. Method for assay of human gastric intrinsic factor and for detection and titration of antibodies against intrinsic factor. Lancet 1963; ii: 1350. 3. Taylor KB. Inhibition of intrinsic factor by pernicious anaemia sera. Lancet 1959; ii: 4. 5. 6. 7. 8.
106. Ardeman S, Chanarin I, Krafchik B, Singer W. Addisonian pernicious anaemia and intrinsic factor antibodies in thyroid disorders. QJ Med 1966; 35: 421-31. Ardeman S, Chanarin I. Steroids and Addisonian pernicious anemia. N Engl J Med 1965; 273: 1352-58. Chanarin I, Ardeman S. Consequences of intrinsic factor antibodies. Proc R Soc Med 1966; 59: 690-91. Rose MS, Doniach D, Chanarin I, Brostoff J, Ardeman S. Intrinsic factor antibodies in absence of pernicious anaemia. 3-7 year follow-up. Lancet 1970; ii: 9-13. Herbert V, Streiff RR, Sullivan LW. Notes on vitamin B12 absorption; autoimmunity and childhood pernicious anaemia; relation of intrinsic factor to blood group substance. Medicine (Baltimore) 1964; 43: 679-87.
identification was confirmed at the NCTC with fastidious anaerobe agar (’Lab M’) incubated anaerobically at 37°C to grow the organism, and API ZYM3.4 and rapid carbohydrate tests to confinn the identification. In April, 1991, an 80-year-old woman was admitted having collapsed at home for no apparent reason. She was usually fairly active but had become very tired and had lost her appetite. On admission she was pyrexial and there was no obvious cause for her collapse. At first a urinary tract infection was suspected and she was started on amoxycillin. Urine culture proved negative, but blood culture on admission grew a gram-negative tapering rod. This was sent to the NCTC for identification. Since the organism was sensitive to amoxycillin and the patient was clinically improving this treatment was continued. The patient was discharged home well after 9 days. After the organism had been identified as C canirrwrsus the patient was asked whether she had any contacts with dogs. She denied any history of a dog-bite but clearly recalled having been scratched by a dog, with blood being drawn, 4 days before admission. It should be remembered that infection may be acquired from cat bites as well as from dogs.s Westwell et al6 found that 28 of 158 healthy cats had these organisms in their gingival crevicesThese cases underline the importance of obtaining a clear clinical history with respect to contact with animals and being aware of the range of fastidious organisms that can cause serious infection so that effective treatment can be started even if isolation of the causative organism proves difficult. National Collection of Type Cultures, Central Public Health Laboratory, London NW9 5HT, UK
Department of Microbiology, Harold Wood Hospital, Harold Wood
Z. N. ADHAMI
Department of Microbiology, Dryburn Hospital, Durham
AK, Hartley RB, Maddocks AC. Waterhouse-Friderichsen syndrome caused by a DF-2 bacterium in a splenectomised patient. J Clin Pathol 1981; 34: 172-73. Zumla A, Lipscomb G, Corbett M, McCarthy M. Dysgonic fermenter-type 2: an emerging zoonosis: report of two cases and review. Q J Med 1988; 68: 741-52. Kristiansen JE, Bremmelgaard A, Busk HE, Heltberg O, Frederiksen W, Justesen T. Rapid Identification of Capnocytophaga isolated from septicemic patients. Eur J Clin Microbiol 1984; 3: 236-40. Heltberg O, Busk HE, Bremmelgaard A, Kristiansen JE, Frederiksen W. The cultivation and rapid enzyme identification of DF-2. Eur J Clin Microbiol 1984; 3: 241-43. Carpenter PD, Heppner BT, Gnann JW. DF-2 bacteremia following cat bites. Report of two cases. Am J Med 1987; 82: 621-23. Westwell AJ, Spencer MB, Kerr KG, Hutchinson DN. DF-2 bacteremia following cat bites. Am J Med 1987; 83: 1170.
Isolation and identification of
Capnocytophaga canimorsus (DF-2) from blood culture SIR,-Dr Gallen and Dr Ispahani (Feb 2, p 308) and Dr Kristensen and colleagues (April 6, p 849) describe patients infected with Capnocytophaga canirnorsus (formerly dysgenic fermenter 2) following dog bites. In both patients it was known that they had had a dog bite, and C canimorsus infection was suspected and appropriate antibiotic treatment initiated. Since the first DF-2 was reported in the UK in 1979123 clinical isolates of C canimorsus have been referred to the National Collection of Type Cultures (NCTC) for identification and confirmation. Several of these strains have been isolated from blood cultures of patients whose possible contact with dogs was investigated only after the organism was identified. The 2 cases well publicised by Zumla et all are examples of the difficulties of isolation and identification of these organisms. The first case was initially diagnosed as hepatitis, possibly viral, and the second as meningococcal meningitis. In both patients the history of contacts with dogs was revealed by the consultant microbiologist, after the isolation of slender gram-negative rods from blood culture (BACTEC system) which failed to grow on subculture after 24-48 h incubation. The NCTC was contacted and it was suggested that the organism might be C canimorsus. 24 h later the
Fulminant Eubacterium plautii infection following dog bite in asplenic man SIR,-Increased rates of septic complications after splenectomy have been reported in the past decade.1 Among microorganisms that tend to cause severe late infection,2 Capnocytophaga caninwrsus (formerly dysgonic fermenter 2) has been widely described after bites or close contact with dogs and, occasionally, cats. 3,4 We report such a late infection due to another slow growing bacillus, Eubacterium plautii, which has not been described previously as far as we are aware.
A 35-year-old man underwent splenectomy after a car accident when he was 11. He was bitten by his dog on the right hand. He was admitted 24 h later, and was drowsy but alert. Diffuse petechial and deeply violaceous lesions were seen on the arms and legs. His temperature was 39’2°C, blood pressure 80-60 mm Hg, and pulse rate 140 beats/min. The cerebrospinal fluid (CSF) showed a leucocyte count of 8/1, glucose was 5-1 mmol/1, and proteins 0-72 g/1. Gram staining was negative. Laboratory studies revealed evidence of disseminated intravascular coagulation and renal failure (creatinine 450 pmol/1). The presumptive diagnosis was C canimorsus septicaemia and the patient was treated with benzylpenicillin and plasma volume expansion. He improved slowly and was discharged