1174

years, this patient had renewed chronic wheezing in association with a serologically documented reinfection with C pneumoniae. In Finland, increasing prevalence of C pneumoniae infection since the 1970s3 correlates with striking increases in adult asthma 4 Since

C TRACHOMATIS IN FAMILIES OF SEVEN POSITIVE "ASTHMATIC" CHILDREN (A-G)

C pneumoniae is a recognised cause of bronchitis, we should also increase in acute bronchitis in adults that correlates with a rise in adult asthma between 1970 and 1981 in England and Wales.s There is also a temporal relation between the appearance of C pneumoniae infection6 and adult asthmain Denmark. I agree with Crane et al that appropriate use of bronchodilator medication is important to keep to a minimum the adverse effects on asthma. I would urge asthma researchers also to consider the possibility that C pneumoniae infection could be one of the underlying (and potentially treatable) causes of a disease whose management has so far been only palliative.

note an

Arcand Park Clinic, 3434 East Washington Ave, Madison WI 53704, USA

DAVID L. HAHN

1. Bone RC.

Chlamydial pneumonia and asthma: a potentially important relationship. JAMA 1991; 266: 265. 2. Hahn DL, Dodge R, Golubjatnikov R. Association of Chlamydia pneumomae (strain TWAR) infection with wheezing, asthmatic bronchitis and adult-onset asthma. JAMA 1991; 266: 225-30. 3. Puolakkainen M, Ukkonen P, Saikku P. The seroepidemiology of Chlamydiae in Finland over the period 1971 to 1987. Epidem Infect 1989; 102: 287-95. 4. Klaukka T, Peura S, Martikainen J. Why has the utilization of antiasthmatics increased in Finland? J Clin Epidermiol 1991; 44: 859-63. 5. Fleming DM, Crombie DL. Prevalence of asthma and hayfever in England and Wales. Br Med J 1987; 294: 279-83. 6. Grayston JT. TWAR. A newly discovered Chlamydia organism that causes acute respiratory tract infections. Infect Med 1988; 5: 215-48. 7. Pedersen P, Weeke ER. Epidemiology of asthma in Denmark. Chest 1987; 91: 107-14S.

Chlamydia trachomatis infection in children with wheezing simulating asthma SIR,-Ghlamydia trachomatis, according to WHO estimates is, after Trichomonas vaginalis, the most frequent sexually acquired pathogen in adults, carrying the possibility of contamination at birth of babies bom to infected mothers. It is difficult to establish how older children become infected with this organism, sexual abuse apart, but serological evidence of C trachomatis is found in an increasing proportion of the population with time. The rate varies not just with age but also with socioeconomic and environmental factors; in prepubertal age groups, rates of 26-7% and 47 2% have been reported.1,2 We have looked for C trachomatis infection in 20 wheezing children (13 boys, 7 girls; aged 6 months to 10 years, mean 32 months). They were negative on allergic evaluation and did not respond to bronchodilator agents. Pharyngeal and conjunctival swabs, for culture on McCoy cells and for a direct immunofluorescent test with monoclonal antibodies, were collected. In an attempt to trace the route of transmission we also examined the families of positive children. C trachomatis was identified by culture in 7 (35%) children in the pharynx, with concordance of results by both methods in only 1 case. In these 7 children, the organism was identified in the conjunctiva in 6; 4 of these had eye symptoms, present at the time of examination in 2. Treatment with erythromycin ethylsuccinate (50 mg/kg daily) for 2 weeks was successful in 6 of the 7 cases. In the other child, a further course of the same antibiotic eradicated the infection. C trachomatis was demonstrated by culture of at least one site in several parents of positive children (table). In one family, where the parents were both negative, we found on further inquiry that other relatives living in the same apartment were positive. Doxycycline 200 mg twice a day for 21 days was given to the adult relatives and the cousin was treated with erythromycin for 2 weeks. Control swabs after completion of this therapy were all negative. The asthmatic symptoms remitted in all 7 C trachomatis infected children, and the ocular symptoms also stopped. At 1-year follow-up these 7 children remained negative for C trachomatis on culture and had had no further asthma attacks. C pneumoniae strain TWAR can be excluded as the explanation in these 7 wheezing children because this agent grows only on HeLa

*Results for culture, immunofluorescence t- irrelevant or not done

(direct)

=

229 cells and

not on

the

McCoy

cells

we

used for

our

isolation

procedures. In these

children, C trachomatis infection could have arisen

through family contacts, the trigger being a primary infection in one adult.3 The findings in the family living in an overcrowded apartment suggest the possibility of C trachomatis spreading to children from adults directly by close daily contact with secretions (eg, saliva, tears) and/or hands or indirectly through fomites, toys, towels, and bedlinen, for example. Our data indicate that wheezing may be another clinical expression of C trachoma tis infection and that this organism should be sought as a routine in children who wheeze but have no demonstrable allergy and do not respond to the usual anti-asthmatic medications.

Supported by grant 9103613 from CNR P.F. FATMA. Institute of Paediatrics, La Sapienza University, and CNR Institute of Experimental Medicine, 00161 Rome, Italy

MARIA BAVASTRELLI MARIO MIDULLA DANIELA ROSSI MARCO SALZANO

1. Black SB, Grossman M, Cles L, Schachter J. Serologic evidence of infection in children. Pediatr 1981; 98: 65-67. J 2. San Joaquin VH, Rettig PJ, Newton JY, Marks MI. Prevalence of antibodies in children. Am J Dis Child 1982; 136: 425-27. 3. Medici A, Sollecito D, Rossi D, Midulla M. Family outbreak of trachomatis. Lancet 1988; ii: 682.

chlamydial chlamydial

Chlamydia

Reversal by ceftriaxone of dilated cardiomyopathy Borrelia burgdorferi infection SIR,-Dilated cardiomyopathy is a life-threatening disorder, which, when progressive, leads to chronic heart failure. It has been suggested that, in several cases, Borrelia burgdorferi could be associated with chronic myocarditis and dilated cardiomyopathy. Thus B

burgdorferi could be isolated and cultured from a myocardial biopsy specimen in a patient with dilated cardiomyopathy.1 However, data about B burgdorferi in dilated cardiomyopathy and its treatment are scant, especially with respect to reversibility of changes in myocardial functions We report a prospective study in which we examined specifically for B burgdorferi infection, serum for IgG and IgM (ELISA), and the history in 42 patients with dilated cardiomyopathy (mean left-ventricular ejection fraction [LVEF] 30% [SEM 12%] assessed by cardiac catheterisation). 9 (21 %) patients with a mean LVEF of 34% (2-2%) were seropositive for B burgdorferi, and 7 of those had a typical history of tick bite and erythema chronicum

1175

HAEMODYNAMIC AND TREATMENT DATA

9 patients have been treated with intravenous ceftriaxone 2 g twice daily for 14 daYS.6.7 6 patients with dilated cardiomyopathy recovered completely and showed a normal EF after 6 months, 2 had enhanced left ventricular function, and 1 did not improve at all. Our results indicate that B burgdorferi infection could play a decisive part in the development of dilated cardiomyopathy, especially in an area such as Graz, where B burgdorferi is endemic. Furthermore, we conclude that in a striking number of patients seropositive for B burgdorferi, dilated cardiomyopathy can be reversed and LVEF improved with adequate antibiotic treatment.

migrans. These

R. GASSER

J. DUSLEAG Borreliosis Study Group, Division of Cardiology, Department of Medicine, University of Graz, A8036 Graz, Austria, Department of Medicine,

E. REISINGER R. STAUBER B. FEIGL S. PONGRATZ W. KLEIN C. FURIAN K. PIERER

LKH-Hartberg; and Hygiene Institute, University of Graz

*In donor A= theatre, B=1 1 post hormone package, C=70min CPS, D=170min CPS; in recipients 1 h post-transplant AoP=aortic pressure, CVP=central venous pressure, PA=pulmonary artery pressure, PCWP=pulmonary capillary wedge pressure, CO=cardiac output, CI=cardiac mdex, SVR=systemic vascular resistance, LVSWI=left ventricular stroke work mdex, ADH=antidiuretic hormone. Values for inotropes in frg

kg-lmin-1 1. Stanek

G, Klein W, Bittner R, et al. Isolation of Borrelia burgdorferi from the myocardium of a patient with longstanding cardiomyopathy. N Engl JMed 1990;

322: 249-52. 2. Wunderlich E, GrafA, Thess G, et al. Dilated myocardial disease as sequela of chronic Lyme-carditis. Z Kardiol 1990; 79: 599-600. 3. Slavik Z, Janousek J, Tax P, et al. Heart involvement in Lyme borreliosis. Cesk Pediatr 1990; 45: 276-78. 4. Steere AC, Batsford WP, Weinberg M, et al. Lyme-carditis: cardiac abnormalities of Lyme-disease. Ann Inter Med 1980; 93: 8-16 5. Marcus LC, Steere AC, Duray PH, et al. Fatal pancarditis in a patient with coexistent Lyme-disease and babesiosis. demonstration of spirochaetes in the myocardium. Ann Intern Med 1985; 103: 374-76. 6. Kristoferitsch W, Baumhackl U, Zeiler K, et al. Ceftriaxone therapy in meningopolyneuritis Garin-Bujadoux-Banwarth. In: Stanek, ed. Lyme borreliosis II. Zbl Bakt (suppl 18). Stuttgart, Gustav Fischer, 1989: 269-75. 7. Dattwyler RJ, Halpern JJ, Volkman DJ, et al. Treatment of late Lyme borreliosis: randomised comparison of ceftriaxone and penicillin. Lancet 1988; i: 1191-94.

Haemodynamic correction in multiorgan donation SIR,-About 30% of donor referrals for cardiac transplantation refused on grounds of "medical unsuitability", predominantly because of apparently haemodynamic function, poor notwithstanding inotropic support. Following pilot studies on methods of reversing the adverse metabolic consequences of brain death, over the past 14 months we are

have been able to restore normal haemodynamics in 14 of 61 brain-dead candidate donors who had unsatisfactory cardiorespiratory function on initial evaluation (cardiac index < 2 -0

1/min per m2, pulmonary capillary wedge pressure > 12 mm Hg, inotropes > 5 /lg/kg per min against an afterload of 800-1200 dyne.s/cm5). A hormone package (triiodothyronine, antidiuretic hormone, and insulin) is given as a continuous infusion during the 2-3 h that organ retrieval takes. These 14 pharmacologically "resuscitated" hearts showed a mean increase in left-ventricular stroke work index of 173% compared with 75% in untreated donors. We felt that where pharmacological correction has not succeeded haemodynamic restoration might be achieved by a form of cardiopulmonary bypass (CPS) that is increasingly used in the USA for cardiorespiratory support of both high-risk angioplasty patients and patients not responding to conventional cardiopulmonary resuscitation. CPS allows the downward spiral of hypoxia, hypothermia, and cardiac decompensation to be broken whilst providing stability during the splanchnic dissection. Bypass has been used by transplant teams (heart-lung retrieval) for total body cooling and it was used by Barnard to support the first clinical heart donor. We report the use of CPS to restore haemodynamics in a brain-dead man whose family had given permission for multiorgan

donation. In a road traffic accident, a 21-year-old man sustained a subdural haematoma leading to diffuse cerebral oedema and brainstem death 7 days later. He had been given large volumes of crystalloid and colloid, leading to a positive fluid balance of 2litres on day 7; a

falling urine output and blood pressure required increasing inotropic support. Relatives gave permission for multiorgan donation. The ethical aspects of using advanced methods for improving the quality of donor organs has been discussed with our ethics committee. Since some active donor management is required in most instances, additional consent from the relatives for CPS was not thought to be appropriate. On transfer to theatre this donor was in cardiogenic shock despite substantial inotropic support (table), and he had been anuric for 6 h. Splanchnic dissection revealed ischaemic bowel with a blue, congested liver. The heart was distended, and poorly contracting. The hormone package led to striking haemodynamic improvement after 1 h but function was still unacceptable. We decided to try CPS. A Medtronic CPS circuit, comprising a hollow-fibre membrane oxygenator with integral heat exchanger and centrifugal blood pump, was primed with 800 ml of Plasmalyte A and connected to the donor via a single right atrial cannula and high aortic cannulation. The blood flow was adjusted to unload the heart whilst still providing pulsatile arterial pressure. There was a rapid improvement in cardiac contractility and blood flow in the splanchnic vascular bed, together with a resumption in urine output after 20 min of CPS. After 70 min, CPS

was

withdrawn but

haemodynamic function, though it had improved (table), was still deemed insufficient and it was decided to continue CPS for a further 2 h. During this period dobutamine support could be withdrawn, laboratory findings became normal, normal urine output was restored, and the heart was unloaded. Final haemodynamic assessment demonstrated very acceptable cardiac function. The liver was not used, though biopsy post-CPS was normal. Both kidneys functioned very well after transplantation and post-transplant cardiac function was normal. D. R. W. is

supported by the British Heart Foundation.

Transplant Unit, Papworth Hospital, Cambridge CB3 8RE, UK

D. R. WHEELDON C. D. O. POTTER J. DUNNING S. GRAY A. ODURO

J. WALLWORK S. R. LARGE

Uveitis and antineutrophil cytoplasmic antibody in immunoglobulin batches SIR,-Dr Ayliffe and colleagues (Feb 29, p 558) reported a case of uveitis associated with immunoglobulin replacement therapy. A boy with X-linked agammaglobulinaemia presented with a granulomatous uveitis, which was attributed to a localised vasculitis. Neutrophil cytoplasmic antibody (ANCA) activity was detected in intravenous immunoglobulin (IVIG) batches and was