*Gas permeable


PMMA hard



daily wear or extended wear soft contact


reflect two disorders with different risks. Furthermore, failure to isolate an organism does not rule out a microbial cause. The high frequency of minor microbial keratitis in lens wearers may be due in part to increased awareness of the problem in those who use contact lenses (resulting in earlier attendance for treatment) and in part to a difference in the pathogenesis of microbial keratitis in CL users and non-CL-users. The diagnosis itself has a substantial impact in terms of investigations, treatment, and hospital visits. Your correspondents’ second area of concern reflects a statistical misunderstanding. Although the confidence intervals for dailywear SCL and GPHCL users overlap, the trend was highly significant, implying a real difference between lens types. We published only our most conservative estimates, based on our group B controls. Had we used the 507 Bl controls, who had no lens-related disease, the difference would have been much larger (4-2,95% CI 1 - 1-16-0). The review referred to is not yet available to us but it may include studies by Macrae et al2 and Hamano et al.3 Data in the first come from premarketing studies in the USA; patients take part after giving informed consent and are debarred if they do not attend frequent follow-up visits. Such patients are not typical of contact lens wearers and would be expected to show reduced rates of complications. The second study was an uncontrolled retrospective review of case-notes from 66 218 wearers; ascertainment of diagnosis, indication for lens wear, and type of lens were poor. Guillon and Benjamin imply that patients using extended-wear SCL are not compliant if lenses are worn for more than 6 days. When our data were collected, this US Food and Drug Administration recommendation had not been issued and many of our patients had been advised that lenses could be worn safely for much longer, a month or more in some cases. In the UK there is little control over the advice contact lens practitioners give to patients. The guidelines cited by Guillon and Benjamin are based on the results of studies such as ours, before which longer periods of extended wear were recommended. The risk in extended-wear SCL users increases by 5% for each additional night of overnight wear.4 Your correspondents misunderstand the risk factor of 4-5, which compares risks within the extended-wear SCL group (not with the GPHCL group); the risk is 4-5 x higher for extended-wear SCL users who use their lenses continuously for more than 13 days, than in those who use them for 6 days or less. Their point about misuse of lenses disregards the fact that the 5 cases were extended-wear SCL only, not a mixed group. The figures we gathered for the control group of 86 users showed that misuse amongst controls was similar and unlikely to lead to bias. Misuse occurred in 20% of both cases and controls who reported overnight wear. This, we agree, is very relevant to contact lens practitioners.

J. K. G. DART Moorfields Eye Hospital, London EC1V 2PD, UK


1. Bates AK, Morris RJ, Stapleton F, Minassian DC, Dart JKG. "Sterile" corneal infiltrates in contact lens wearers Eye 1989; 3: 803-10. 2.Macrae S, Herman C, Stulting D, et al. Corneal ulcer and adverse reaction rates in

premarket contact lens studies. Am JOphthalmol 1990; 111: 457-65. 3. Hamano H, Kitano J, Mitsunaga S, Kojima S, Kissling GE. Adverse effects of contact lens wear in a large Japanese population. Contact Lens Assoc Ophthalmologists 1985; 11: 141-47. 4.Schein OD, Glynn RJ, Poggio EC, Seddon JC, Kenyon KR. The relative risk of ulcerative keratitis among users of daily wear and extended wear soft contact lenses. N Engl J Med 1989; 321: 773-78.

Endoscopic closure of recurrent tracheo-oesophageal fistula SiR,—The frequency of recurrent tracheo-oesophageal fistula after surgical repair for this condition and oesophageal atresia varies between 5 and 15 %.1 Operation on the fistula is associated with high mortality-in one series this was as high as 50%.2 We report a 13-year-old girl with recurrent tracheo-oesophageal fistula, which was related to an oesophageal atresia. She had had five surgical repairs in the past. When she was referred to our unit, she had had typical symptoms of tracheo-oesophageal fistula for at least a year. At endoscopy, the fistula was about 0-6 mm in diameter and about 2-0 cm long, and was in direct communication with the middle part of the right lung. Surgical repair was not recommended because of other congenital thoracic malformations, but mainly because of very poor pulmonary function. The fistula was treated several times with a combination of n-butyl-z-cyanoacrylfate (’Histoacryle’) and polidocanol (’Aetoxysclerol’), and closure was complete after the fourth application. The combination of these products to close a recurrent tracheooesophageal fistula has, as far as we are aware, been described only once, in a newborn baby (2-3 kg) with a very small fistula.3 Only 0-5 ml of n-butyl-z-cyanoacrylfate was needed in this infant; we had to inject 8 ml before closure was obtained. The last injection was given more than 3 months ago and the girl remains symptom-free. Endoscopic closure is a non-invasive intervention. Even if the closure is temporary this procedure could be repeated twice or three times in a year, which would be preferable to surgical repair. But the main advantage is that good pulmonary function is restored, and that surgical intervention would be no longer life threatening because of lung disease. Academic Children’s Hospital, Free University of Brussels, 1090 Brussels, Belgium


Oesophageal atresia and tracheo-esophageal fistula. In: Richman PP, Irving IM, eds. Neonatal surgery. London: Butterworth, 1978: 200-01. 2. Wayson EF, Granjobst W, Chandler JJ. Esophageal atresia with tracheo-oesophageal fistula. Am J Surg 1965; 110: 162-67. 3. Al-Samarai AYI, Jessen K, Haque K. Endoscopic obliteration of a recurrent tracheo-oesophageal fistula. J Pediatr Surg 1987; 993: 22. 1. Cudmore RF.

Lister J,

Primary prevention of Streptococcus suis meningitis SIR,-We report a fatal case of Streptococcus suis meningitis that feel resulted from preventable occupational infection. A 59-year-old meat porter presented with a 5-day history of headache, vomiting, diarrhoea, confusion, and deafness. He was drowsy but


rousable and disoriented in time and place. His pulse was 100 beats per min and regular, blood pressure was 150/100 mm Hg, and temperature was 37’9°C. Neurological examination was normal apart from neck rigidity and apparent bilateral deafness. He had 12-6 x 109/1 (neutrophils 88%), thrombocytopenia 95 x 109/1, and serum sodium of 125 mmol/1, which proved to be due to the secretion of inappropriate antidiuretic hormone (SIADH). Cerebrospinal fluid was turbid, with 1035/ul white cells (neutrophils), a protein concentration of 2 g/l, and gram-positive diplococci on staining. Culture yielded a pure growth of S suis type II that was sensitive to penicillin and chloramphenicol; blood cultures were also positive for this organism. Despite appropriate antibiotics he remained confused, febrile, and deaf. Contrast-enhanced brain computed tomography on three occasions revealed no evidence of intracranial abscess formation. Repeat lumbar puncture after 10 days of treatment showed resolution of the inflammatory changes in the meninges with a protein of 06 g/1 and a white cell count of 34/1. A week after admission he had catastrophic gastrointestinal haemorrhage and an actively bleeding arteriovenous malformation on the greater curve of the stomach was repaired at laparotomy. Massive intragastric haematoma formation had torn the short gastric veins, with further intraperitoneal haemorrhage. Post-operative hepatorenal failure followed and he died two weeks after admission. Necropsy showed changes of bronchopneumonia, pulmonary embolism with infarction, bilateral deep calf thrombosis of the



calves, and prostatic plexus, and

a resolved pyogenic meningitis. The eighth cranial nerves were grossly intact and there was no intracerebral abscess formation. S suis type II is a porcine zoonosis caused by a group R streptococcus that is responsible for septicaemia, meningitis, and arthritis in young pigs and meningitis in man.1 Case reports’have documented the importance of exposure to, or close contact with, pigs or unprocessed pork. Presentation with bilateral perceptive nerve deafness is characteristic of this disease.’,4 Young pigs are probably infected via the nasopharynx,s but the portal of entry in man is uncertain. Arends and Zanen’ reported 19 of 30 patients infected with probable occupational wounds, and skin injury was documented in 13 of 44 cases recorded in Europe.3 Lacerations of the skin of the hands and arms could well increase the risk of transmission from infected meat. Our patient’s wife reported a recent laceration of his left forearm ten days before admission, the result of trauma from the sharp rib-end of a carcass. Similar injuries of the hand are common in abattoir workers.6 Although S suis meningitis is rare (3 per 100 000), the rate of this disease in abattoir workers in the Netherlands in 1968-84 was 1500 times that for other workers.’ We feel that people in daily contact with pigs or pork should be advised to use protective handwear, and work practices in the meat processing industry should be revised to keep such trauma to a minimum.

Departments of Medicine North Middlesex Hospital, London N18 1QX, UK




1. Arends

JP, Zanen HC. Meningitis caused by Streptococcus suis in humans. Rev Infect Dis 1988; 10: 131-37. 2. Zanen HC, Engel HWB. Porcine streptococci causing meningitis and septicaemia in man. Lancet 1975; i: 1286-88. 3. Lutticken R, Temmen N, Hahn G, Bartelheimer EW Meningitis caused by Streptococcus suis: case report and review of the literature. Infection 1986; 14: 181-85. 4. Shneerson JM, Chattopadhyay B, Murphy MFG, Fawcett IW. Permanent perceptive

deafness due to Streptococcus suis type II Infection. J Laryngol Otol 1980; 94: 425-27. 5. Elliott SD, Alexander TJL, Thomas H. Streptococcal infection in young pigs. II. Epidemiology and experimental production of the disease J Hyg (Camb) 1966, 64: 213-20. 6. Fraser CAM, Ball LC, Moms CA, Noah ND. Serological characterization of group A streptococci associated with skin sepsis in meat handlers. J Hyg (Camb) 1977; 78: 283-96.

Hypoplastic left heart syndrome: some clues to its aetiology SIR,-Hypoplastic left-heart syndrome (HLHS) is exhibited by between 1 in 5000 and 1 in 10 000 newborn babies. Without surgery it is fatal.! Between 1985 and 1991 HLHS was the reason for about 40% of heart transplants on infants done at Loma Linda University Medical Center, California. The cause is probably multifactorial but we hypothesised that defective growth-factor production could contribute. We report here immunocytochemical studies on sections of heart removed from 15 infants with HLHS who had heart transplants at age 4 to 90 days. Staining was assessed relative to that seen in normal hearts of roughly the same age, which showed only mild immunoreactivity for all growth factors. Staining (scored as negative-to-mild, moderate, strong, or intense) was strong or intense in 11 cases for platelet-derived growth factor (PDGF)-BB, 7 cases for PDGF-AA, 7 cases for transforming growth factor (TFG )-et, and 2 cases for TGF-&bgr;3 (figure). Where growth factors were overexpressed staining was seen in both ventricles. TGF-&bgr;3’ while implicated in valve formationwas not inappropriately expressed among the hypoplastic left heart tissues we examined. PDGF-BB stimulates growth and inhibits differentiation of L6 myoblastswhich are comparable to cardiac myocytes.4 Thus, the high levels of this peptide found here within neonatal myocytes may be significant to the aetiology of some forms of congenital heart disease such as HLHS. The role ofTFG-ot in cardiogenesis is unknown but EGF (which has the same biological activity) is a powerful chronotropic and inotropic agent for cardiac

Immunocytochemical detection of growth factors. Sections of heart stained by standard immunocytochemical techniques and avidin-biotin complex (Dako) Top left: normal heart (14 weeks), showing lack of staining for PDGF-AA Top nght: strong staining for TG F:x in hypoplastic left ventricle. Bottom strong staining m hypoplastic left ventricle for PDG F-AA (left) and PDGF-BB (right).

cells.While overexpression of TFG-x may contribute to abnormal development of the heart it is also possible that it modulates some aspect of cardiovascular physiology in HLHS. We found overexpression of PDGF and TGF-rx in myocytes associated with HLHS in both ventricles. If these factors are associated with the aetiology of HLHS why is it only the left side of the heart that fails to develop? One explanation is that they are expressed globally in an attempt to rectify the deformity. We thank Prof C.-H. Heldin (Uppsala, Sweden) for the gift of PDGF antisera. This work was supported in part by the Research Endowment Trust of St Thomas’ Hospital, London. We thank Norwich Eaton Ltd for their support. UMDS,

Guy’s Hospital, London SE1, UK

Department of Pathology, Immunology Center, and Department of Surgery, Loma Linda, University Medical Centre,

P. B.


Loma, Linda, California


Oncogene Science Inc, Uniondale, NY


Department of Surgery, Division of Cardiothoracic Surgery, Loma Linda University Medical Center, Loma Linda, California 92354, USA



Bailey LL, Nehlsen-Cannarella SL, Doroshow RW, et al. Cardiac allotransplantation in new-boms as therapy for hypoplastic left-heart syndrome. N Engl J Med 1986; 315: 949-51.

JD, Dagle JM, Walder JA, Weeks DL, Runyan RB. Epithelial mesenchymal embryonic cardiac endothelial cells is inhibited by a modified antisence oligodeoxynucleotide to transforming growth factor &bgr;3. Proc Natl Acad

2. Potts

transformation of

Sci USA 1991, 88: 1516-20. Jin P, Sejersen T, Ringerts NR. Recombinant platelet-denved growth factor BB stimulates growth and inhibits differentiation of rat L6 myoblasts. J Biol Chem 1991, 266: 1245-49 4. Schneider MD, Parker TG. Cardiac myocytes as targets for the action of peptide growth factors. Circulation 1990; 81: 1443-56. 5. Nair BG, Rashed HM, Patel TB. Epidermal growth factor stimulated rat cardiac adenylate cyclase through a GTP-binding regulatory protein. Biochem J 1989, 264: 3.


Primary prevention of Streptococcus suis meningitis.

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