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with the report of a case of staphylococcal scarlet fever.This was. a girl, aged 13, who developed a scarlatinalsyndrome as a complication of acute osteomyelitis withsepticaemia (54 colonies of Staphylococcus aureus per c.cm.of blood). The rash was typical in character and distri-bution and was followed by general desquamation; therewas a "raspberry " tongue, and the fever and toxaemiaapparently responded dramatically to scarlatinal anti-toxin. A high antistreptolysin titre was found inconvalescence. A filtrate of the infecting staphylococcusgrown in broth gave positive Dick tests in a dilution of100 ; that is, the organism was poorly toxigenic com-pared with the scarlatinal streptococci, but its toxin wasspecifically neutralised by streptococcus antitoxin, andits activity was destroyed by heat at 61° C. for one hourOther workers have isolated erythrogenic staphylococcifrom the throat or other sites in cases of non-streptococcalscarlet fever, and Satake 15 reproduced the scarlatinalsyndrome by injection of such a staphylococcal filtrate.The erythrogenic toxin is apparently unrelated to themore common staphylococcal hsemolysin and leucocidin.This evidence in favour of the staphylococcus as a rarecause of scarlet fever is perhaps in line with the broaden-ing concept regarding erythrogenic toxins. Instead of a

single streptococcus and a single toxin, antigenicallyidentical whatever its source, we now know that manydifferent serological types (and possibly Lancefield

groups other than A) of the haemolytic streptococcus canproduce erythrogenic toxin, and that streptococcaltoxins of differing antigenicity are capable of producingscarlet fever.

SEEING IS BELIEVING

THE pathologist is not always right even if, speakingbroadly, he has a good pull over the clinician. One ofthe happiest hours in the Swiss medical student’s weekwas the Saturday midday when that brilliant pathologistErnst Hedinger put the dead " meat " on the tableand challenged physicians and surgeons to justify theirin-vivo impressions. The pathologist however does notoften get the chance of checking up a long series of clinicaldiagnoses with the post-mortem findings. For nearly20 years it has been the custom at the Royal AdelaideHospital for the house-surgeon to fill in a request cardwhen he obtains permission for autopsy. On this cardis written the clinical diagnosis which it is presumedwould have been placed on the death certificate had therebeen no autopsy. Prof. J. B. Cleland has analysed 162500 of these entries and finds that the clinical diagnosiswas right (or reasonably so) in 67-8%, partly right in12-4%, wrong in 14.6%, whilst in the remaining 5-2%no diagnosis was made or the nature of the lesionremained obscure even after autopsy. It should beborne in mind, he says, that in a large general hospitalmany patients are admitted in extremis, or die before aproper examination can be made. In 89 cases at leastof the 362 in which the clinical diagnosis proved wrongdeath had occurred on the day of admission to hospitalor on the following day. Some of the larger groups ofdiseases are analysed in detail. Thus it was noted thatin malignant disease the number of cases missed wasnearly but not quite counterbalanced by those in whichit was suspected but not present. In cardiac infarctiona correct diagnosis was made in 80% ; the instances inwhich this condition was present but’ not diagnosed werecounterbalanced by those in which it was diagnosed butnot present. Cerebral haemorrhage and cerebral soften-ing were usually correctly diagnosed, but more cases ofsoftening were diagnosed as hsemorrhage than the otherway round. Of wrong diagnoses, failure to recognisepneumococcal peritonitis stands out in the list as most

15. Satake, T. J. orient. Med. 1927, 6, 17 (quoted by Aranow andWood).

16. Med. J. Aust. 1942, i 579.

important ; most pathologists would agree that this isoften missed. Of the rest, general peritonitis due toperforation, bronchopneumonia as a cause of coma,chronic fibrosing pulmonary tuberculosis with pleuraleffusion simulating heart disease, are diagnostic snareswhich routine autopsy is apt to reveal.. On the wholeProfessor Cleland’s figures bear out the adage that thecommon things are commonest.

NORTHERN ROSES

HIP-COLLECTING has become a scientific pursuit.In an address to the Pharmaceutical Society on Dec. 10,Mr. R. Melville, PhD, botanist to the Royal BotanicGardens, Kew, recalled that we learned of the vitamin-Ccontent of hips mainly through Russian researches.In a survey of British roses made last year withPyke 1 the found that the vitamin-C values of the hips ofdifferent species ranged from 1260 mg. per 100 g. inRosa mollis to 80 mg. in R. arvensis. In addition toB. mollis, the species with the highest content wereR. sherardi, R. coriifolia and R. afzeliana, and thesefour only form an appreciable part of the rose popula-tion north of the Lake District, which explains whyScottish hips have given a much better yield of thevitamin than those gathered in the south. These speciesalso happen to be among the earliest to ripen, but thereis no true correlation between vitamin-C content of thehips and early ripening, since some of those species whichripen first have a poor content of the vitamin. Thereal correlation is probably with the length of day in theperiod just before ripening, for this fits in with the, latitu-dinal correlation noted by both English and Russianworkers. To avoid loss of vitamin the hips should be pro-cessed with as little delay as possible, but if they mustbe stored the temperature should be well below freezingpoint. Melville has found that cool storage at tempera-tures round about freezing point is not satisfactory;there are appreciable losses of vitamin during the firstthreeweeks, and though a fairly steady level is maintainedduring the second month the content drops again rapidlyin the third month. The initial losses were greatestin over-ripe hips, and it is thus important, he pointedout, to stop the collection of hips before they begin toshow signs of softening. To travel well and withstanddelays they should be full red but quite hard.

HISTORIAN OF THE I M S’ Colonel D. G. Crawford, who died at Ealing on Dec. 9at the age of 85, has left his own memorial. Born atChinsura in 1857, his father being a member of theBengal civil service, he qualified at Edinburgh in 1881and entered the IMS the same year. He retired in

1911, rejoining for five further years on hospital shipsduring the late war. His History of the Indian MedicalService (1600-1913), published in 1914, throws manycurious sidelights on old-time Anglo-Indian life, but itsmain purpose was to record the evolution of a homo-

geneous service from the small beginnings of the 17thcentury. True to British precedent, early mistakeswere made good and utilised to achieve order andsuccess. In Emerson’s words, which Crawford was wontto quote, they builded better than they knew. Craw-ford’s history ranks with the best of the many regimentalhistories of the British Army, and in 1930 he completed "

his Roll of the Indian Medical Service. How he foundtime in the short human span to collect his knowledge

. and compile these rolls is easy to ask but can only beanswered by those aware of the self sacrificing devotionentailed ; and Crawford found time also to be generous,for he contributed many notes about the Army MedicalService which have yet to- see the light in an addition toJohnston’s roll.

1. Pyke, M. and Melville, R. Biochem J. 1942, 36, 336.