328 1970-77
REGISTRY DATA FOR NEW YORK STATE EXCLUSIVE OF
NEW YORK CITY
(WHITE WOMEN)
groups
are
required before it
tion screening,
as
can be recommended for Moncada et al. claim.
popula-
Department of Dermatology, Bristol Royal Infirmary,
J. L. BURTON
Bristol BS2 8HW
PHAGE TYPING OF GROUP B STREPTOCOCCI
*
Excludes breast cancer and carcinoma M=married.
(in situ) of cervix.
S=single.
prognosis than those whose first child was a In studying young breast-cancer patients (<45 years of age at the time of diagnosis) we found the opposite to be true (unpublished). Patients whose first child was male had a poorer prognosis than those whose first child was a female. I think this is further evidence of a reversal or biphasic effect of
had
a
better
daughter.
pregnancy on subsequent breast-cancer experience. The reversal and its specific relationship to the sex of the offspring may provide a clue to the biology and etiology of these tumours. The following hypothesis is based on three premises: first, that a greater or different type of maternal immune tolerance is required during pregnancy with a male compared to a female child; second, that some portion of the fetal antigens are similar to antigens on breast cancer cells; and third, that actively growing cancer cells can permanently be destroyed by a fully competent immune system, but latent cancer cells cannot. I propose that some latent breast tumours are stimulated to active growth when the immune system is suppressed during pregnancy, and that many of these tumours are subsequently destroyed when the immune system returns to normal after pregnancy. This produces the eventual protective effect of pregnancy. A few tumours, perhaps those which grew most aggressively during the period of immune suppression when the child was in utero, could have established themselves beyond the stage where they could be destroyed by the unsuppressed immune system. This would produce the adverse effect seen in the higher rate of breast cancer in married women between 25 and 40 years of age. It can be shown that this would also explain why there is a noticeably increased risk of breast cancer among women who have their first child at a late
age.3 Cancer Control Bureau, New York State Department of Albany, N.Y. 12237, U.S.A.
Health, DWIGHT T.
JANERICH
EAR-LOBE CREASE
SIR,—Dr Moncada and his colleagues (Jan. 27, p. 220) showed that in Mexico a diagonal ear-lobe crease is associated with an increased risk of cardiac ischaemia. Before ear-lobe inspection becomes a mandatory prelude to life-assurance I should like to mention some conflicting data. An American studyl of 211 patients undergoing coronary arteriography showed no significant association between such creases and coronary-artery disease. A British study2 showed that bilateral ear-lobe creases were present in 52% of 48 males with myocardial infarction and in 58% of 48 age-matched controls. This conflict may relate to differences in methodology, but further studies of the significance of this sign in homogeneous ethnic
SIR,—There is little doubt that early-onset neonatal infection due to group-B streptococci is the result of maternal carriage of the organism. However, the source of infection in lateonset sepsis is obscure because it is seldom the mother, and babies of mothers not carrying the organism often acquire it.’1 To study this, it is essential to monitor carriage and spread of the organism. Unfortunately the serological typing technique used for this purpose recognises only five major types and is therefore insufficiently discriminating. We have developed a bacteriophage typing system which greatly improves this position. Group B streptococcal bacteriophages were obtained by cross-spotting and mitomycin-C-induction techniques,2and thirty-one phages, each used at a predetermined titre, now form the routine typing set. Of the group-B streptococci sent to this laboratory for serotyping, 77% were lysed strongly by one or more bacteriophages and were therefore considered typable. The reproducibility of the method has been assessed using sets of related group-B streptococci isolated from the same or multiple sites on the same individual, within 14 days. Fewer than 2% of these strains differed from their index strain by one or more strong lytic reactions. We conclude therefore that a difference of one or more strong bacteriophage reactions constitutes reliable grounds for discrimination between strains.3It is clear that all members of a single serotype are not identical, numerous distinct lytic patterns can be recognised within each serotype, but none of the patterns is specific for any one. Serological typing alone yields serotypes la, ib, 11, and III all at frequencies of 20-27% in any population. The frequency of the types determined by combined serological and bacteriophage typing rarely exceed 3%, thus greatly increasing the ability to distinguish between strains. With this typing system, studies of long-term and multiplesite carriage have confirmed that the same strain of group-B streptococcus can be carried by a patient for many months.4 In investigations of the spread of group-B infection in hospitals, bacteriophage typing has confirmed that the members of the serotypes involved are usually indistinguishable, but this is not always so. In a nursery where there were hospital-acquired infections with serological type III, two mothers were found to be carrying that type. Phage-typing showed that the two strains were not identical and only one of the women was responsible for spread within the nursery. The same strain also colonised babies in a parallel unit where none of the mothers were carriers of group-B streptococci, the only common factor here being the staff.5 We feel that bacteriophage typing applied to group-B streptococci is a useful additional technique for the subdivision of strains within a serological type. This laboratory is prepared to investigate strains of this organism that have caused serious disease, and groups of organisms apparently related epidemiologically in clinically important situations. ,
Cross-Infection Reference Laboratory, Central Public Health Laboratory, London NW9 5HT
1. Paredes, A.,
Wong, P., Mason, E. O., Taber, L. H., Barrett, F. F. Pediatrics, 1977, 59, 679. 2. Wannamaker, L. W., Skjold, S., Maxted, W. R. J. infect. Dis. 1970, 121, 407.
3.
W. R. in Pathogenic and animals (edited by M. T.
Streptococci: streptococcal disParker). London (in the press). 4. Sanderson, P. J., Ross, J., Anderson, H., Stringer, J. ibid. 5. Anthony, B. F., Okada, D. M., Hobel, C. J. Unpublished. Stringer, J., Maxted, ease m man
1. Mehta, J., Hamby, R. I. New Engl. J. Med. 1974, 291, 260. 2. Ben Halim, M. M. M.D. thesis, Bristol University 1976.
JACQUELINE STRINGER W. R. MAXTED