731

but slow and the relapse-rate about 12%. Systemicreactions were met with after only 0-5% of injections,and the compound appears to have been well toleratedby sufferers from late syphilitic affections, particularlycardiovascular lesions, which showed some encourag-ing improvement. Among the 823 patients therewere 5 examples of arsphenamine dermatitis and 5 ofpurpura hsemorrhagica. There were no deaths, andno examples of hepatitis or jaundice, though this

complication has been reported occasionally by othersusing bismarsen. The long-term results are of specialinterest. Of 71 patients treated for early syphilis andobserved for periods ranging from six months to four-teen years, serological relapse occurred alone in 4 andin conjunction with the reappearance of infectioussurface lesions in 4 others. One or more examinationsof the cerebrospinal fluid were made during the periodof observation in 48 of these 71, and only 6 showedany abnormality ; about half of the patients withfixed serological reactions showed a later reversal toa negative. Although healing of the tertiary osseousand cutaneous lesions in middle-aged and elderlypatients takes place more slowly, it seems that bis-marsen may be used with advantage in these patientsespecially when they do not tolerate other organicarsenical compounds well.

Postarsphenamine jaundice, under the title of

Salvarsan ’ jaundice, was a formidable interrupterof treatment and a cause of ill health and some deathsduring the last war, and there has lately been a recur-rence of the unsatisfying discussions on the roleplayed by suspected factors other than arsphenaminein its production.2 The old ground of alcohol, diet,vitamins, intercurrent infection and so on has beenexplored again without bringing to light any veryilluminating facts, but although instances of jaundicefollowing bismuth treatment alone are occasionallyencountered the possibility of bismuth being a factorseems to have been neglected. KULCHAR andREYNOLDS report that of the 1032 male prisoners inthe United States prison at San Quentin receivingtreatment for syphilis between 1936 and 1942, 144(13-9%) became jaundiced, and in 121 (10-3%) ofthese jaundice appeared while bismuth was beinggiven. The treatment system consisted of neoarsphen-amine or ’Mapharsen’ in courses of ten weeklyinjections in alternation with courses of twentyweekly injections of sodium iodobismuthite. Therewas no epidemic of catarrhal jaundice among theprisoners during the period of this study and theendemic rate was low-0.1% in 1941. Among the121 cases of jaundice during bismuth treatment, 4became jaundiced during the first course of bismuth,and previous arsenical therapy could be excluded.The remaining 117 received arsenicals in some formbefore the course of bismuth during which the hepatitisoccurred. Jaundice began within four weeks of thelast injection of an arsenical in 34 cases and in thesethe arsenic is considered as a possible factor. Jaundicewas not evident until the fourth to the eighth week ofbismuth therapy in 83 cases and in the ninth week orlater in 56 cases. It was thought that the time inter-vening since the last injection of an arsenical in thesecases made it unlikely that the jaundice was entirelydue to previous arsenical therapy. Many syphilolo-2. See Lancet, 1942, ii, 287.3. Kulchar, G. V. and Reynolds, W. J. J. Amer. med. Ass. 1942, 120,

343.

gists, however, would not accept this short time limitas permitting the exclusion of arsenic as a possiblefactor, for examples of postarsphenamine jaundicemay be met with up to four or five months after thelast arsenical injection. Although the evidence pre-sented by KULCHAR and REYNOLDS for ascribing amajor role to bismuth in these cases is not unequivocal,their report serves as a reminder that bismuth puts anadditional load on the liver, and might, like arsenic,prepare the ground for virus infection.

Annotations

ALLERGY IN CHILDHOOD

Sir Arthur Hurst, speaking at the section of disease inchildren of the Royal Society of Medicine on Nov. 2.7,glanced at fashions in asthma cures during the pastcentury : the nasal cauterisation of Francis, the earlyskin tests of Chandler Walker of Boston, the allergen-freechambers of Van Leeuwen, and modern methods ofdesensitisation. The most potent cause of an attack,he finds, is expectation ; and he thinks it better to injecta small dose of adrenaline to abort an attack in its earlystages rather than to keep a patient on an abnormal dietand in a special environment. Despite this discouragingpicture, Dr. George Bray believes in having a try.Attacks of asthma in early childhood, he considers, allhave an allergic basis, but as the attacks recur they beginto be precipitated by non-allergic factors such as excite-ment, emotion, exertion, and fatigue. He recognisesthree types : a hereditary type with a family history ofallergy ; a variant of this which he calls the eczema-prurigo-asthma type; and a tissue-damage type,associated with severe colds, bronchitis and pneumonia.In a third of the hereditary cases there is a history ofinfantile facial eczema, and in three-quarters of them theasthma sets in before the third year. The breast-fedchild often becomes sensitive to such things as milk andgruel, eggs and egg concentrates, egg milk chocolate, milkdrinks containing eggs, and cotton-seed which is a com-ponent of ’Lactagol.’ Allergic mothers should avoidsuch foods during pregnancy and lactation, he suggests.On weaning the child may become allergic to cow’s milkor some cereal such as wheat, oats or barley. If cow’smilk is responsible it should be boiled for 5 minutes andafter the scum has been removed should be acidified.These processes have already been carried out on

’Allergilao’ ; other substitutes for fresh cow’s milk areevaporated or condensed milk, goat’s milk or syntheticmilk made from soya bean flour. The eczema-prurigo-asthma syndrome commonly appears during the firstsix months of life with itching, vesicular and papulareruptions and lichenification from scratching, the flexuresbeing particularly affected ; in the second or third yearbronchitis, asthmatic and hay-fever attacks may beadded to the picture, and all are persistent up to puberty.The skin is ichthyotic in a fifth of the children. Sensi-

tising agents vary with the age of the child ; in infantileeczema up to the age of 9 months for each 20 foodreactions (usually to egg, milk or wheat) there is only1 inhalant ; between 9 months and 2 years the propor-tions are 20 food reactions to 8 inhalants ; over 2, incases of flexural eczema, the proportions are 20 foodreactions (usually fish, pig, nuts or vegetables) to 24inhalant reactions (usually to animal hairs, pollen, orfeathers), and in cases of asthma, vasomotor rhinitis andhay-fever, for 20 food there are 100 inhalant reactions.It is among this last group that some of the largestreactions are seen to pollens and horsehair. In the

tissue-damage type of allergy, asthmatic attacks are oftenrestricted to the winter months and a respiratory infec-tion sometimes associated with measles or whooping-cough provokes the first attack. In this type of allergy,

732

fibrotic changes may be seen in radiograms of the lungs,but in the other two types they are rare. Sensitivity isusually to inhalants-feathers or down, among which thechild spends his time when ill. He may occasionally alsobecome sensitive to foods such as milk, gruel, barley andalbumin water. Dr. Bray believes in restricting the dietof the allergic child and suggested a basic diet whichexcludes cow’s milk in its natural state, pig and pigproducts, shellfish, nuts, chocolate, strawberries, apples,bananas, beans, peas, tomatoes, potatoes, cabbage, andcelery. The child’s bedroom should be airy and freefrom dust, without hair or feathers in the bedding. Herecommends only two medicines : min. 10-20 of hydro-chloric acid in water before meals if there is hypochlor-hydria ; and ephedrine linctus at bedtime every night forseveral months. If the child is sensitive to dust or

pollen, desensitising injections often give good results.In’ the light of long experience Mr. James Crooks

suggested that while nasal surgery was not curative ofallergic conditions any septic focus should be dealt withon general lines ; and Dr F. A. Knott remarked thatsensitisation with bacteria had never been demonstratedin any cases he had seen.

NINE LIVES OF STATUS LYMPHATICUS

AFTER a careful pathological and statistical analysisof 600-odd cases of either sudden death in apparentlyhealthy people or death in people of 15 years or over whohad an apparently glandular thymus, Young and Turn-

bull 1 in 1931 reported that they found no evidence thatso-called status thymo-lymphaticus had any existenceas a pathological entity, and a leader in our own columns 2seemed justified in announcing, without sorrow, the endof the status. A few years later Cohen 3 agreed that " theterm status lymphaticus used in the coroner’s court is ameaningless expression." Yet three years ago Taylor 4reported on 14 cases in which the only explanation ofdeath was in his view a general excess of lymphoid tissue,making it clear that it was this general excess ratherthan enlargement of the thymus which should be lookedupon as predisposing to death from trivial causes. Andnow Millar and Ross 5 have satisfied themselves that oneof the other characteristics of the lymphatic state-aortic hypoplasia-is significantly associated with acci-dental death. In a series of autopsies in which theymeasured the aortic circumference at a fixed level theyfirst eliminated aortas with well-marked atheroma, andthose from obese, emaciated or oedematous patients,leaving 300 measurements for analysis, 26 being from

patients dying as a result of accident. By applyingmultiple regression corrections, variations for height, age,weight and sex were eliminated, and it then appearedthat the mean aortic circumference in the accident caseswas 1.48 mm. less than in non-accident cases. Fromthis Millar and Ross argue that aortic hypoplasia is con-nected, probably indirectly, with liability to accident,and even imply a connexion with " accident-proneness."The argument is fallacious. We are told no details of theaccidents, whether they were in air-raid, factory or onthe road. The existence of accident-proneness is wellestablished from close observation of the precise natureof industrial accidents ; without detailed study of cir-cumstances it would not be right to connect 26 accidentaldeaths with accident-proneness as Newbold 6 understandsit. Technical improvement in post-mortem work is, dayby day, finding causes for deaths which only 10 years agowould have been regarded as mysterious, and in theheyday of status lymphaticus would have been assignedthereto. Careful interpretations of data have elucidateddeaths from functional causes like vagal inhibition,carotid and reflex,’ and careful technique has established1. Young, M. and Turnbull, H. M. J. Path. Bact. 1931, 34, 213.2. Lancet, 1931, i, 593. 3. Cohen, H. Practitioner, 1936, 136, 252.4. Taylor, J. R. Proc. R. Soc. Med. 1939, 33, 119.5. Millar, W. G. and Ross, T. F. J. Path. Bact. 1942, 54, 455.6. Newbold, E. M. J. R. statist. Soc. 1927, 90, 487.7. Gardner, E. Med.-leg. Rev. 1942, 10, 120.

the unsuspected frequency of air embolism, amnioticembolism,9 allergic death 10 and the like, all missed withease. There may well exist, as Campbell 11 puts it, " acondition of such lowered resistance and hypersuscepti-bility that the patient so affected is in danger of suddendeath from trivial causes " ; one feature of this conditionmay be a type of aorta with narrowing and hypoplasiaof its wall, but the connexion between the two has yetto be convincingly established. And there is alwaysa cause of death awaiting detection.THE BRITISH STANDARD HÆMOGLOBINOMETERTHE British Standards Institution, which has already

done good work in drawing up standard specifications forthe various pipettes used in haematology, has nowtackled the hæmoglobinometer itself. British standard1079 : 1942 gives the specifications for constructing astandard Haldane hæmoglobinometer.12 Both the tubeinto which the blood is put for dilution and that contain-ing the standard solution of carboxyhæmoglobin are

described and the colour of this standard solution isdefined. The standard solution is so prepared that, asbefore, 100 per cent. corresponds to 13’8 g. haemoglobinper 100 c.cm. blood. A regular source of annoyance inthe,,past has been that hsemoglobinometer tubes were notinterchangeable-even if from the same manufacturer ;the blood tube had to be carefully checked against thecomparator tube to ensure that the distance between the20% and 100% marks corresponded ; only too often itdid not. Adoption of the standard will stop this commonsource of error. Since the manufacturers are representedon this organisation, it should follow that all haemoglobin -ometers will now conform to standard. It is up to thepurchasers to insist that their hæmoglobinometertubes should be marked " B.S. 1079," and to refuse allothers. This will help to make haemoglobin estimationstruly comparable. The next task for the institution isto define standards for the next most popular hæmo-

globinometer-the Sahli.STAPHYLOCOCCAL SCARLET FEVER

SINCE the early twenties, when the ætiological relation-ship of the hæmolytic streptococcus to scarlet fever wasestablished by the Dicks and Dochez, it has been acommon experience among clinicians who use thethroat-swab as an adjunct to diagnosis to find that asmall proportion of clinically typical cases fail to yieldStreptococcus pyogenes from nose, throat or open infectedlesion. There are several possible explanations for thisapparent anomaly-the swabs may have been inexpertlytaken (but repeat swabbings have proved negative), theinfection may be deep-seated and inaccessible, the

infecting strain of streptococcus may be a non-hæmolyticvariant such as Colebrook and his co-workers 13 recoveredfrom septic wounds, or the streptococcus may fail togrow or fail to produce haemolysis under aerobic con-ditions. ’ Now that anaerobic culture is more widelypractised it is not uncommon to find strains of Strep.pyogenes which grow only, or much more profusely,anaerobically than aerobically on primary culture, andthere is point in the practice adopted in some laboratoriesof inoculating the swab as a " pour-plate " which ensuresgrowth in the medium as well as on it and encouragesboth the growth and haemolysin production of strainswhich are aerobically shy. With these obstaclesovercome, it is probably a fair estimate to say that 98%of scarlet fever is due to an erythrogenic streptococcus.From time to time, however, evidence is adduced infavour of the staphylococcus as setiological agent, andthis evidence is reviewed by Aranow and Wood 14 along8. Simpson, K. Lancet, 1942, i, 697.9. Ibid, 1942, ii, 490. 10. Ibid, 1941, ii, 319.

11. Campbell, E. H. Penn. med. J. 1937, 41, 407.12. B.S.I. Publications Dept., 28, Victoria Street, London, S.W.1.

2s. 3d. post free.13. Colebrook, L., Elliott, S. D., Maxted, W. R., Morley, C. W. and

Mortell, M. Lancet, 1942, ii, 30.14. Aranow, H. and Wood, W. B. J. Amer. med. Ass. 1942, 119, 1491.