33

it was ; indeed, RAMMELKAMP 10 suggests that theproportion of streptococcal infections that lead to

rheumatism remains relatively constant between

2% and 4%. As for the frequency of streptococcalinfections, the only figures readily available are thosefor the incidence and mortality of scarlet fever :HITCHENS drew attention to the close, although per-haps fortuitous, connection between the decline ofrheumatic fever and that of scarlet fever, which hasbecome steadily less common and less menacing from1935 onwards. From their study of Sheffield, Bristol,Grimsby, and Lincoln, and the administrative countyof Lincolnshire, HEWITT and STEWART 6 decidedthat poor housing and economic conditions per se

played little part. HITCHENS came to the same

conclusion, pointing out that the change took placein Cardiff before economic conditions improved.The incidence of rheumatic fever increases when the

haemolytic streptococcus has more opportunitiesto start infections, as it has among people living inovercrowded conditions-a point well brought outby a number of investigations in the American ArmedForces.1o HEWITT and STEWART found that childrenof unskilled workers suffered from rheumatism farmore commonly than did the children of professionaland skilled workers, and they believed that differentrisks of infection were the most likely cause for thesocial gradient. RAMMELKAMP concluded that latitude,altitude, crowding, dampness, economic circum-

stances, and age all had their bearing on rheumaticfever simply because of their influence on strepto-coccal infections in general. HITCHENS, however,made an important point in discussing the searchfor the cause of rheumatic fever’s decline : the changeshould not be considered on its own, but in relationto the comparable decrease in the incidence and

mortality in all infectious diseases, quite apart fromany recent advances in treatment. It seems unlikelythat this general improvement can be attributed

simply to alterations in the host-parasite relationshipof a number of different organisms ; and consequentlythere must be some associated economic factor stillto be considered. HzTCHEr7s suggested that the declinewas likely to be related more closely to such things as" an improving quality of maternal care rather thanto a straightforward economic or physical factor " ;and that the increased use of antibiotics did not playa big part in the decrease in rheumatic fever, whichhad already began before antibiotics were introduced.Though this is undoubtedly true, ROBINSON 3 reportsthat the recurrence-rate in San Francisco remainedrelatively high despite fewer initial attacks ; butafter a preventive campaign and the provision of

prophylactic drugs (either a small daily dose ofsulphadiazine or penicillin or the monthly injectionof a long-acting penicillin) the number of recurrencesfell from a yearly average of 22 for 1949-53 to 5 for1954-55.

Though the fundamental reason for the decline inrheumatic fever remains obscure, there seems no

doubt of the importance of reducing the number andspread of haemolytic streptococcal infections byimproving social conditions and providing prophylaxisin suitable circumstances.l

10. Rammelkamp, C. H., Denny, F. W., Wannamaker, L. W.In Rheumatic Fever. Minnesota, 1952.

11. See annotation, Lancet, 1955, i, 805.

Annotations

NEW YEAR HONOURS

THE long list of honours announced last Tuesdaycontains relatively few medical names. Dr. Janet

Vaughan was eminent in haematology before she becameprincipal of Somerville in 1945, and she has done finework for the Nuffield Trust as well as for Oxford

hospitals : her new title must often have been used

prematurely by her acquaintance, because it is so clearlyfitting. Sir Arthur Porritt is created K.C.v.o. for hisservices to the Sovereign, and General Drummond,director-general of Army Medical Services, becomesK.B.E. The knighthood conferred on Prof. G. L. Brown,of University College, London, coincides with his electionas a vice-president of the Royal Society : he has beena member of the Medical Research Council since 1951and is chairman of its Royal Naval Personnel ResearchCommittee. Finally, we note with pleasure the knight-hood for Mr. Charles Read, director of the Institute ofObstetrics and Gynaecology, whose helpful work as

president of, the Royal College of Obstetricians and

Gynaecologists has been appreciated by colleaguesboth inside and outside his specialty. These names andothers which are similarly respected will be found onp. 40.

1. Koprowski, H., Norton, T. W., Hummeler, K., Stokes, J., Hunt,A. D., Flack, A., Jervis, G. A. J. Amer. med. Ass. 1956,162, 1281.

2. Koprowski, H., Norton, T. W., Jervis, G. A., Nelson, T. L.,Chadwick, D. L., Nelsen, D. J., Meyer, K. F. Ibid, 1956,160, 954.

POLIOMYELITIS VIRUSES BY MOUTH

RESEARCH on immunisation with live attenuated

poliomyelitis viruses continues, and a new report 1describes how infants of under 6 months were fed withlive virus. It was known from earlier work thatimmune serum-globulin given to children intramuscularlyat the same time as live poliomyelitis virus was given bymouth did not prevent intestinal carriage of the virus orthe development of an immune response. Obviously,therefore, infection with attenuated poliomyelitis virusesshould be carried out in the presence of a serum-antibody" umbrella," which would probably reduce the chancesof producing paralytic poliomyelitis without decreasingthe immunising effect of the virus. Koprowski et al.11have infected a number of infants, most of whom hadmaternal antibody in their serum-that is, a naturalumbrella. With the consent of their parents, the infantswere fed between 1000 and 100,000 infective doses ofattenuated poliomyelitis viruses of types 1 and 2 in theirbottles, the virus-formula mixture being given just beforea regular feed. After they had had the viruses theinfants were isolated in hospital and everything whichwas removed from the contaminated areas was dis-infected.

Alimentary infection followed the virus feed, and viruswas excreted in the stools for from 55 to 108 days.Antibody responses were satisfactory in ten infants aged1-4 months, but of six infants less than a month old onlythree showed a satisfactory rise in antibody. The remain-

ing three, who had high titres of antibody at birth, showedeither a drop in antibody or stationary titres, andfurther investigation of these infants will be needed to seewhether the present antibody titres persist. So far,antibody titres have remained high in five infants testedup to 7 months after feeding.While it is useful to have this knowledge, its practical

application will have to wait until the problem ofvirus excretion is solved. It might be possible to trainchildren to such rigid habits of hygiene that they wouldnot spread poliomyelitis viruses with which they were

34

infected subclinically. But the difficulties of controlling,outside hospital, infants who are excreting virus for 3 or4 months seem insuperable at the moment, and it maybe wisest to concentrate on older children.

1. Erasmus, L. D. Quart. J. Med. 1956, 25, 507.2. Amberson, J. B. Bull. Johns Hopk. Hosp. 1954, 94, 227.3. Brock, R. C., Hodgkiss, F., Jones, H. O. Guy’s Hosp. Rep.

1942, 91, 131.4. Goadby, K. Diseases of the Gums and Oral Mucous Membrane.

London, 1923 ; pp. 112, 339.5. Bloomfield, A. L. Amer. Rev. Tuberc. 1921, 4, 847.6. Nichols, D. R., Herrell, W. E. J. Amer. med. Ass. 1946, 132, 200.7. Bishop, L. A., Rasmussen, R. F. Ibid, 1946, 131, 821.8. National Research Council. Ibid, 1946, 132, 470.9. Finland, M., Murray, R., Harris, H. W., Kilham, L., Meads, M.

Ibid, p. 16.10. Learner, N., Minnich, W. R. Ann. intern. Med. 1946, 25, 516.11. Harris, H. W., Murray, R., Paine, T. F., Finland, M. New

Engl. J. Med. 1947, 236, 611.12. Rosenthal, F. D. Lancet, 1949, ii, 743.13. Gill, R. J. Amer. J. med. Sci. 1951, 221, 5.14. Wasserman, E., Pomerantz, H. Z. Med. Ann. Distr. Columbia,

1951, 20, 435.15. Steinberg, H., Towbin, M. N. Dis. Chest, 1952, 21, 455.16. Weiss, W., Eisenberg, G. M., Alexander, J. D., Flippin, H. F.

Amer. J. med. Sci. 1954, 228, 148.17. Feinstone, W. H., Williams, R. D., Wolff, R. T., Huntington, E.,

Crossley, M. L. Bull. Johns Hopk. Hosp. 1940, 67, 427.18. Hyde, L., Hyde, B. Amer. J. med. Sci. 1943, 205, 660.19. Welford, N. T. Illinois med. J. 1946, 90, 185.

FRIEDLÄNDER’S PNEUMONIAPNEUMONIA caused by Friedlander’s bacillus usually

presents as an acute illness, but it often passes into achronic phase characterised by suppuration and cavityformation. Sometimes the disease is chronic from thestart, and, as the upper lobe is often involved and

penicillin is ineffective, tuberculosis or neoplasm may besuspected. It is important to give appropriate treatment’before the lung has been extensively destroyed, and itis widely believed that a characteristic, gelatinous,reddish-brown sputum is an early pointer to the diagnosis.It is disconcerting to learn, therefore, that this type ofsputum was seen in only 2 out of 17 cases of Friedlander’spneumonia recently reported by Erasmus 1 ; and thesewere the only 2 in which the diagnosis was made onclinical grounds. In 14 of these cases Erasmus regardedthe Friedlander bacillus as the primary invader of thelung, since it was isolated from the sputum in pure cultureor as the predominant organism on at least two suc-cessive days ; and it was thought to be a secondaryinvader in the other 3 cases in which it was recoveredfrom the sputum in association with other organisms onat least two successive days. Erasmus emphasises thata Friedlander infection is especially likely to be overlookedwhen it is superimposed on existing pulmonary disease.Amberson 2 suggested that Friedlander’s pneumonia is

caused by the aspiration of infected secretions from theupper respiratory passages into the lung, and Erasmusfound evidence that both the primary and the secondaryinvaders reached the lungs in this way. Compared withnon-suppurative pneumonia, the disease showed a pre-dilection for the posterior part of the upper lobe and forthe apex of the lower lobe-sites favoured by non-specificsuppurative aspiration pneumonia.3 In most cases therewas either gross dental sepsis, with which the Friedlanderbacillus is commonly associated,4 4 or other upper-respiratory-tract infection. Moreover, the Friedlanderbacillus is present in the mouth or upper respiratorytract in 1-5% of normal individuals.5 In some older

persons there was multifocal disease in the lower lobes,and this was attributed to the failure of a feeble coughto get rid of infected secretions.

There is evidence that streptomycin, 6-13 chloram-phenicol,14-16 and sulphadiazine 13 17-19 are effective inthis condition. In-vitro sensitivity tests in Erasmus’sseries showed that the organisms were sensitive in all 15cases tested to streptomycin, in all but 1 to chloram-

phenicol, and in two-thirds to sulphadiazine. All the

organisms were resistant to penicillin and erythromycin,and more than half were resistant to chlortetracycline

(aureomycin) and oxytetracycline (terramycin). Most ofthe patients were successfully treated with a combinationof streptomycin and sulphadiazine, but Erasmus recom-mends that chloramphenicol should be substituted forthese drugs after a few days since resistance to strepto-mycin may rapidly develop.11 In his experience withthese patients, the disease, though serious, did not sustainits formidable reputation : none of the patients died andin only 2 was the lung damage severe enough to requiresurgical resection. The fact that effective treatment isnow available makes early diagnosis all the more

important, and Erasmus’s experience suggests that thisis more likely to be achieved by the bacteriologist thanby the clinician.

20. Campbell, J. S. New Engl. J. Med. 1956, 254, 56.21. Howard, J. M., Rawson, A. G., hoop, C. E., Horn, R. C., Royster,

H. P. Surg. Gynec. Obstet. 1950, 90. 307.22. Glaser, K., Mehn, W. H., Schultz, L. W. J. Pediat. 1946, 28, 729.23. McFarland, J. H. Arch. Path. 1930, 9, 820.24. Wawro, N. W., Fredrichson, R. W., Tennant, R. Cancer, 1955,

8, 595.25. Lister, W. A. Lancet, 1938, i, 1429.26. Rhonchese, F. Amer. J. Surg. 1953 86, 376.

CONGENITAL ANGIOMA OF THE PAROTID GLAND

THE technique of operations on the parotid gland hasimproved in recent years. Wide exposure through anincision that is cosmetically acceptable, and preliminaryidentification of the facial nerve, have enabled adequateexcisions to be confidently though not lightly undertaken.The conditions for which these methods can be appliedinclude the parotid angiomas, which, though uncommon,are by no means so rare as to be merely a medicalcuriosity ; and Campbell 20 has lately reported 3 suchcases treated by subtotal parotidectomy. He states thatangioma is the most likely cause of chronic- unilateralparotid swelling in the first year of life (in a series of 21parotid tumours in children, Howard et a1.21 found 5

angiomas).The angioma is usually noticed in the first weeks or

months of life as a pre-auricular swelling of the consis-tence of rubber. A clue to the diagnosis may be given bya bluish colour of the skin or by an overlying cutaneousangioma ; but no case has yet been recorded in which aparotid angioma was associated with the more serious

congenital vascular abnormalities, such as intracranialcirsoid aneurysm. The lesion has no capsule and mayspread beyond the confines of the gland. It grows rapidlyduring the first months of life but there is no evidence oftrue malignant change. The gross appearance, Campbellremarks, " resembled nothing quite so much as an

enlarged, coarsely lobated and cyanosed parotid gland" "

-a point of some importance in exploration of thelesion.

Excision is usually advised. In the 46 recordedcases treated by surgery there were 2 deaths. Radio-

therapy has also been used with some success, but it maybe a dangerous weapon in the treatment of a benigncondition in this situation in a growing infant. Glaseret all describe a uniformly disastrous course if the condi-tion is not treated, leading to death in weeks or monthsdue to invasion and compression of the vital organs ofthe neck. But Campbell makes the pertinent commentthat only two references to such death, with post-mortemevidence, appeared in the literature he reviewed.23 Thereseems to be some doubt about the true natural historyof the untreated lesion. Wawro et a1.24 noted greatermitotic activity in the younger children and a tendencyto quiescence in the older patients. A parallel might bedrawn with the behaviour of cutaneous angiomas, andit may be that parotid angiomas would later regress, asmost of the cutaneous ones do.25 26 There certainly seemsto be a case for deferring operation for lesions which arenot enlarging rapidly when first seen ; but it would be

helpful to have more facts. Surgery has been successfuland there have been very few recorded recurrences; but