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exchange, partially stopped by immunosuppressive drugs.25)Nevertheless, some contrary evidence suggests that furthersynthesis of antibody depends on the presence of antigen,26and autoantibodies in man may not behave the same asantibodies in animals immunised with foreign antigens.Certainly a major hazard would be removed if immuno-suppression proved unnecessary after all.

If there are some doubts about the place of plasma exchangein treating severe anti-GBM nephritis there is completeuncertainty about the use of the treatment in severe immunecomplex nephritis. A few patients with acute SLE26-28 andidiopathic immune complex nephritis and polyarteritis"l 27-30have been treated by plasma exchange and immuno-suppression, with similar problems of infection, particularlyin older patients. Some dramatic improvements in renalfunction coincided with the treatment. Though concentrationsof circulating immune complexes undoubtedly can be depletedin these patients the treatment may be no better than immuno-suppression alone2-4 or immunosuppression combined withanticoagulation.3' Probably the results in severe disease arecomparable, particularly in SLE, and there is no dramaticbenefit from plasma exchange apparently shown by patientswith severe nephritis associated with anti-GBM antibody.Both the recent reviews11 14 are understandably cautious aboutthe treatment in immune complex nephritis. One of theproblems in examining the few data available is the hetero-geneity of these patients, whose only common features areuraemia, severe nephritis, and extensive crescents. This.heterogeneity makes a controlled trial equally difficult; andthe failure of the MRC working party on glomerulonephritisto gain enough patients for collaborative trials of immuno-suppressive and anticoagulant treatment suggests that itwould be no easier to mount such a trial for plasmapheresis.The outlook is little better for controlled trials of plasma

exchange in anti-GBM nephritis. The disease is rare, and itsincidence varies throughout the world: it is commoner in theUSA than in Europe, and one part of the North Island ofNew Zealand,26 with one-hundredth the population ofBritain, seems to have as many patients. Many doctors seeingthese patients would be unhappy to withhold plasmapheresis,especially in those with pulmonary haemorrhage, and patientswould have to be carefully matched for the degree of renalimpairment.

1 British Medical 7ournal, 1978, 1, 1011.2 Sonsino, E, et al, Advances in Nephrology, 1972, 2, 121.3 Spargo, B G, Ordonez, N G, and Ringus, J C, Human Pathology, 1977,

8, 187.4 Morrin, P A F, et al, American journal of Medicine, 1978, 65, 446.5 Wilson, C I, and Dixon, F J, Kidney International, 1973, 3, 74.6 Peters, D K, in Progress on Glomerulonephritis, ed P Kincaid-Smith,

A F D'Apice, and R C Atkins. New York, John Wilev, in press.7 Loughlin, G M, et al,JYournal of Pediatrics, 1978, 93, 181.8 Mintz, G, et al,_journal of Rheumatology, 1978, 5, 39.9 Modzelewska, I, and Korobowicz, E, Acta Paediatrica Academiae

Scientiaruim Hungaricae, 1974, 15, 233.10 Swainson, C P, et al, Clinical and Experimental Immunology, 1978, 32, 233.1 Pinching, A J, British_journal of Hospital Medicine, 1978, 20, 552.12 Ewan, P, et al, New England journal of Medicine, 1977, 295, 1391.13 Lockwood, C M, et al, Lancet, 1976, 1, 711.14 Kincaid-Smith, P, and D'Apice, A J F, Anmerican j'ournal of Medicine,

1978, 65, 564.15 Walker, R G, et al, Medical3journal of Australia, 1977, 1, 875.16 Proskey, A J, et al, American journal of Medicine, 1970, 48, 162.17 Munro, J E, Geddes, A M, and Lamb, W L, British Medical jrournal,

1967, 4, 95.18 Cohen, L H, Wilson, C B, and Freeman, R M, Archives of Internal

Medicine, 1976, 136, 835.19 Dahlerg, P J, et al, Mayo Clinic Proceedings, 1978, 53, 533.20 Depner, T A, et al, Kidney International, 1975, 8, 409.21 Lang, C H, et al, Archives of Internal Medicine, 1977, 137, 1076.22 Johnson, J P, et al, American journal of Medicine, 1978, 64, 354.

23 McLeish, K R, et al, Clinical Nephrology, 1978, 10, 71.24 Rees, A J, Lockwood, C M, and Peters, D K, British Medical Journal,

1977, 2, 723.25 Branda, R F, et al, Transfusion, 1975, 15, 570.26 Teague, C A, et al, Kidney International, 1978, 13, 492.27 Jones, J V, et al, Lancet, 1976, 1, 709.28 Moran, C J, et al, British MedicalJournal, 1977, 1, 1573.29 Pussell, B A, et al, Lancet, 1978, 2, 359.30 Becker, G J, et al, Medical_Journal of Australia, 1977, 2, 693.31 Cameron, J S, in Proceedings of the Seventh International Congress of

Nephrology, p 419. Basle, Karger, in press.

Visceral larva migrans againThe most common cause of visceral larva migrans in man isinfection with the dog roundworm Toxocara canis. Interest inthe infection was stimulated in 1950 by Wilder's report offinding nematode larvae in eyes removed from childrenthought to have retinoblastoma and the almost simultaneousreport of nematode larvae in the liver of a child with fever andeosinophilia.2 Both the indentification of the parasite and therecognition of the connection between the different syndromeswere due to work by Beaver and his colleagues.3 4T canis is a roundworm parasite of dogs. Puppies become

infected in utero by transplacental passage ofthe larvae, thoughmilk-borne infection is another possibility.5 The pups shed theinfection at the age of about 6 months, as they acquireimmunity. When a bitch becomes pregnant she loses herimmunity and reacquires infection-probably owing to thewidespread contamination of the environment with eggs, butpossibly also to the reanimation of dormant larvae in her body.Man becomes infected from swallowing the eggs passed by

infected dogs-mostly puppies-and the infection is mostoften seen in its florid form in young children with young dogsas pets and in those such as kennel maids in working contactwith dogs. Two clinical syndromes have been recognised: theocular form, in which a larva in the eye of a child presents witha granulomatous pseudotumour ofthe retina; and a generalisedform, in which the presence ofnumerous larvae in the liver andother organs gives fever and eosinophilia. A recent reviewarticle6 pointed to the curiosity that ocular lesions are seldomfound in the generalised form of the disease. This is a paradox,for the chances of a larva finding its way into the retina mightseem to be much greater if the presence of numerous larvae inthe body is manifest. There may be a clue in the observationthat the ocular form of the disease is seen almost exclusivelyin young children, whereas the generalised disease is seen atall ages. In patients with generalised infection there is oftengood circumstantial evidence of recent exposure to massiveinfection, such as pica, whereas such a history is rare in patientswith ocular lesions.There is no fundamental reason why humans should not be

infected in utero, just as puppies are. If this did occur theocular lesions of toxocara infection could then be late mani-festations of congenital infection, just as in the case of toxo-plasma choroidoretinitis. This hypothesis would be supportedby a finding of toxocara antibodies in the blood of a dispro-portionately large number of the mothers of children withocular toxocariasis.The numerical importance of toxocara infection in causing

disease in Britain is probably small, though the results ofserological tests suggest that asymptomatic infections arewidespread. Rare though it may be, the symptomatic infectionis serious to the child who loses an eye or to the patient with

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a debilitating febrile illness lasting a year or more. Treatmentremains unsatisfactory, so that every attempt should be madeto prevent infection. This must depend on a reduction ofcontacts between dog faeces and people, especially children.Those who keep dogs and children in the same house shouldat least ensure that the dogs are regularly-and frequently-wormed.

1 Wilder, H C, Transactions of the American Academy of Ophthalmology,1950, 55, (Nov-Dec) 99.

2 Mercer, R, et al, American3ournal of Diseases of Children, 1950, 80, 46.3 Beaver, P C, et al, Pediatrics, 1952, 9, 7.4Beaver, P C, Experimental Parasitology, 1956, 5, 587.5 Stone, W, and Smith, F W, Experimental Parasitology, 1973, 34, 306.6 Zinkham, W H, American Journal of Diseases of Children, 1978, 132, 627.

Bundle branch blockTiny deviations from the normal pattern on a strip of papermay be fraught with importance: an abnormal electrocardio-gram (ECG) alone may ruin a man's career.' 2 The telltaledeformities of the QRS complex called bundle branch blockare the only evidence we have that depolarisation of theventricles is pursuing an abnormal course and that one daythe electrical union between atria and ventricles may besevered. A prolonged PR interval may be observed too, butin most cases of bundle branch block this is in the normalrange of less than 0-22 seconds. Bundle branch block is rare:in a population of over 28 000 attending a screening centre inBelgium the incidence of left bundle branch block was0.6% in men and 0 88°', in women. Right bundle branchblock was found in 131% of men and 0-64%/ of women.3Among 42 000 patients having ECGs in hospital 0-7700 hadbundle branch block,4 though the incidence was many timesless in large surveys of United States Air Force personnel.57Our understanding of heart block and bundle branch block

was greatly advanced about ten years ago by the developmentof His bundle recording.8 This exquisite example of appliedelectrophysiology has resulted in an explosion of researchinterest. When the electrode catheter is carefully positionedacross the tricuspid valve and the electrical potentials aresuitably amplified three deflections are seen: A, whichcorresponds to the P wave of the surface electrocardiogramand coincides with depolarisation of the lower portion of theright atrium; H, a small deflection, caused by depolarisationof the bundle of His; and V, which reflects depolarisation ofthe ventricles and corresponds to the QRS complex of thesurface ECG. Measurement of the intervals A-H and H-Vand of the duration of the His deflection itself providesinformation on the level of delayed or blocked conduction,which may be supra-, intra- or infra-His. The first typeusually represents delayed conduction in the atrioventricularnode, and the third delayed conduction in the bundle branchesor Purkinje network.At about the time that His bundle recording became

fashionable Rosenbaum9 10 popularised the concept ofventricular activation by three channels or fascicles: theright bundle branch, and the anterior and posterior divisionsof the left bundle branch. The ECG interpretation of rightand left bundle branch block stood as before, but the newconcepts of left anterior and left posterior hemiblock wereintroduced and approved," and with them the terms single,bifascicular, and trifascicular block. The ECG manifestationof left anterior hemiblock is left axis deviation, and of right

posterior hemiblock right axis deviation, though the definitionof the precise degree of axis shift is arbitrary. Histologists'2 13point out that the left bundle seldom if ever shows tworecognisable divisions but is a fan-shaped structure; theelectrophysiologists agree that this may be so but that theconcept is functionally useful; and clinicians all over theworld have adopted the terminology.To the practising cardiologist the potential importance of

His bundle recording lies in its ability to predict-if it can-which of his patients with fascicular block, though free fromsymptoms at present, are most at risk from heart block andStokes-Adams attacks in the future-and might thereforestand to benefit from a pacemaker. For example, if twofascicles are blocked prolongation of the H-V interval in theremaining conducting channel might imply a special riskfrom syncope or sudden death. Such notions have promptedmany His bundle studies,14-'8 but unfortunately their con-clusions have not been uniform. McAnulty and colleagues'9have now reported a prospective study, with an averagefollow-up of 25 months, of 257 patients with high risk bundlebranch block (bifascicular or trifascicular) all of whom hadHis bundle studies and none of whom had a documentedbradyarrhythmia or implanted pacemaker at the time ofevaluation. These patients formed a selected group culledfrom a survey of 125 000 ECGs, of which 1211 showedbifascicular or trifascicular block (an incidence of 0.960 0).Though 50 patients died in the follow-up period, death wassudden in only 27 and in 17 of these was not due to brady-arrthythmia. Those with a prolonged PR or HV interval, andeven those with a history of syncope, failed to emerge as agroup especially prone to sudden death. These resultsemphasise that the poor prognosis usually attributed tobundle branch block in statements of the overall mortalityrate'9 20 is not necessarily due to failure of atrioventricularconduction but frequently to other consequences of cardiacdisease.We should therefore avoid hasty decisions in the manage-

ment of asymptomatic bundle branch block. If the subject'slivelihood is at stake investigation by His bundle recording orcoronary angiography may be justified: aircrew in the UnitedStates Air Force have even been permitted to fly after suchevaluation.7 As to general anaesthesia for surgery, the risk ofprovoking complications from heart block appears to besmall,21 and protection by a temporary pacemaker is seldomindicated. Permanent pacing is still best reserved for patientsin whom atrioventricular block has been found together with ahistory of syncope or other symptoms related to bradycardia;prophylactic pacing in asymptomatic patients with bifascicularor trifascicular block appears unjustified-at least until furtherconduction studies have identified a group particularly atrisk.'9

I Medical Aspects of Fitness to Drive, 3rd ed, Medical Commission onAccident Prevention. London, 1976.

2 Working Party of the Cardiology Committee, Royal College of Physiciansof London, British Heart3Journal, 1978, 40, 335.

3 Kulbertus, H E, et al, American3Journal of Cardiology, 1978, 41, 385.4 McAnulty, J H, et al, Archives of Internal Medicine, 1978, 138, 30.5 Lamb, L E, Kable, K D, and Averill, K H, AmericanJrournal ofCardiology,

1960, 6, 130.6 Johnson, R L, Averill, K H, and Lamb, L E, American J3ournal of

Cardiology, 1960, 6, 143.7 Rotman, M, and Triebwasser, J H, Circulation, 1975, 51, 477.8 Scherlag, B J, et al, Circulation, 1969, 39, 13.9 Rosenbaum, M B, et al, American Heart Journal, 1969, 78, 450.

10 Rosenbaum, M B, Modern Concepts of Cardiovascular Disease, 1970,39, 141.

1 Trevino, A J, and Beller, B M, American Journal of Medicine, 1971, 51,362, 374.

12 Massing, G K, and James, T N, Circulation, 1976, 53, 609.

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