PSITTACOSIS

1120 of the Poor Law Act as it affected children. The labours of that committee led to a complete change in poor-law education and a central ophthalmic isolation hospital school came at last to be built when the Metropolitan Asylums Board was charged with the responsibility of looking after the physically defective children in poor-law schools. The central hospital school, White Oak Hospital, Swanley, was opened in 1903, and a year later the sister institution, Highwood Hospital at Brentwood. Trachoma quickly ceased to be a problem of importance: as against 292 cases admitted in 1903, 10 were admitted last year, despite the fact that the hospital draws nowadays not only on what is left of the poor-law school services, but also on the whole of the elementary schools under the London County Council. Indeed, trachoma was stamped out with surprising ease once the proper machinery was established, and White Oak Hospital is no longer a school devoted exclusively or mainly to trachoma, but has become a highly specialised institute for dealing with chronic eye diseases in children. The lesson that Mr. Arnold Sorsby emphasises in his review of the origin and development of White Oak Hospita1,1 which he serves as visiting ophthalmologist, is the one to which the Board of Education drew attention in 1929-namely, that there is still a dead weight of external eye conditions in children all over the country. It must be admitted that London, with its rate of 4-9 per 1000 as against 14.7 for the country as a whole, has reason to be satisfied with the achievement of its hospital school institution, and it is regrettable that there is only one such institution in the whole of the country. The change in the character of White Oak Hospital leaves one wondering not so much that the problem which the hospital has solved was ever allowed to arise, but that the road to its eradication should have been so full of difficulties and obstruction. Like most successful public health measures, the history of the hospital illustrates not so much the " inevitability of gradualness" as the desperate gradualness of the

working

inevitable. ABNORMALITIES OF SWEATING

.

ABNORMALITIES of sweating may be the result of interference in the nervous supply, of alteration in the sweat glands themselves, or, as in the case recently quoted by Berkman and Horton, at a staff meeting of the Mayo Clinic,2 of hysteria. Several cases have been quoted by Wilson 3 and another by Uprus, Gaylor, and Carmichael, in which excessive sweating has occurred on certain parts of the face in association with salivation, when the normal sympathetic nervous supply has been interfered with as a result of previous trauma. Cases of auriculo-temporal syndrome and " crocodile tears " show phenomena of a similar type. Wilson suggests that the condition is caused by a hyperactive state of the sweat glands, as the result of removal of inhibition resulting from the degeneration of their sympathetic nerve-supply. In the case presented by Mogens Fog5 the lesion was one of the glands. His patient, following a attack of prolonged paratyphoid fever, was unable to sweat when exposed to great heat, or after prolonged muscular exercise, such as would produce profuse sweating in a normal individual. He complained of intense discomfort, palpitation, and burn1 Ann. Rep. London County Council for 1935. London, Vol. IV. Part III. Pp. 69. 1937. 2 B. and T. J. Proc. Clin. Horton, (1937) Mayo Berkman, 3 M., 12,4 161. Wilson, W. C. (1936) Clinical Science, 2, 273.

Uprus, V., Gaylor, J. B., and Carmichael, E. A. (1934) Brain, 57, 443. 5 Fog, M. (1936) Amer. J. med. Ass. 107, 2040.

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ng and flushing of his skin, particularly of his face. Microscopic examination of his skin showed considerable destruction of his sweat glands. Mogens Fog suggests that these phenomena are the result of the body’s attempt to promote heat loss by radiation by extreme dilatation of the skin vessels, in the absence of the usual elimination by sweat formation and evaporation. The most interesting feature of Berkman and Horton’s case of hysteria associated with absence of sweating is the unconscious resistance on the part of the patient to any muscular effort which might cause a rise in body temperature and so promote sweating; when the nature of her disorder was explained to the patient and this resistance was overcome normal sweating resulted. Uprus, Gaylor, and Carmichael were of the opinion that the immersion method of warming the subject was a more certain and satisfactory method of raising the blood temperature and promoting sweating than the dry air-bath method used by Berkman and Horton. The latter point out that their patient, although showing, in their opinion, signs of sympathetic dysfunction, did not present the usual features of heat allergy, such as the urticaria usually complained of, and they do not mention any history of intense flushing or of dry scaly skin, which were both such marked features in Mogens Fog’s case. It is unfortunate that they were not able to test any of the other systems under sympathetic nervous control. PSITTACOSIS

IN 1929 the Minister of Health issued a memorandum

calling attention to the existence of psittacosis in England both in birds and in man, and asking that material from suspected cases should be sent to the laboratory of the Ministry for investigation. A new report has now been issued1 in which the methods for the laboratory diagnosis of the disease are described in such detail that with its aid it ought to be possible to investigate cases of psittacosis in any properly equipped bacteriological department. The Ministry obviously now consider that diagnostic methods have reached a state, when they can be relied on for routine use. The new report describes the precautions necessary in handling infectious material and stresses the risks of infection from experimental material. The morbid anatomy of the disease in infected birds is described. Findings suggestive of psittacosis are: (1) fibrinous pericardial effusion; (2) greatly enlarged spleen, sometimes with necrotic nodules; and (3) a pale or yellow liver with necrotic or hoamorrhagic spots. It is recommended that direct smears should be made from obviously affected organs and from the lungs and heart blood. The smears are stained with Giemsa or by Bedson and Bland’s or Lepine’s modification of Castenada’s method. If the smears are clearly positive for virus bodies no further procedures are necessary in routine diagnosis. If they are negative or doubtful the ground-up tissues are injected intraperitoneally into mice. Mice injected with virulent material usually die in 5 to 30 days. The post-mortem appearances vary somewhat according to the time taken by the mice to die. If death takes place three or more days after injection the peritoneal exudate is thick and fibrinous and virus bodies can generally be demonstrated in the macrophage cells of the exudate. In man the sputum, blood, and pleural exudate from the living patient, particularly during the early stages of the disease, or such post-mortem material 1 Laboratory Diagnosis of Psittacosis. Rep. publ. Hlth med. Subj. Lond., No. 80. London : H.M. Stationery Office. 1937. Pp. 11. 6d.

1121 should be examined the spleen, affected lung, &c., both directly and after passage through mice. In all psittacosis infection, whether of birds, rodents, or man, the essential change iR the invasion and destruction of the reticulo-endothelial cells, and special attention should therefore be given to these cells in the search for virus bodies. A good coloured plate shows the characteristic appearances of these bodies. The concluding paragraphs of the report discuss the special problem of psittacosis in budgerigars (love-birds). The disease in these birds is less severe than in ordinary parrots and parakeets, and instead of dying they may survive to become carriers of the virus. Further investigation is required as to the extent of infection among the budgerigar flocks of this country and the Ministry asks pathologists to endeavour to obtain more information on the matter. as

SERUM TREATMENT OF PNEUMONIA THE treatment of lobar pneumonia with specific antibacterial sera began in America soon after the discovery of the serological types of the pneumococcus in 1913, and later it received a decided fillip from Felton’s discovery of a practical process for the refinement and concentration of antisera to Types I and II pneumococci. Following the good reports of Cole, Park, Bullowa, Cecil, Finland, and others, several of the United States, notably Massachusetts and New York, have begun a " pneumonia service " to encourage the serum treatment of lobar pneumonia in smaller urban and rural districts-a plan which may be recommended especially to the industrial areas in the midlands and north of England and to Scotland where pneumonia is more common than it is in the south. Meanwhile the pioneers forge ahead. The division of the heterogeneous Group IV pneumococci into some 29 specific types by Cooper and her co-workers has enabled the clinician to find out the relative incidences of these types as causal organisms of lobar pneumonia and the serologist to prepare antisera to the more common of °them. In particular, the treatment of lobar pneumonia due to Types V, VII, VIII, and XIV pneumococci has been under investigation. For example, Bullowa and Wilcox have collected 249 cases of Type V lobar pneumonia (or 7.5 per cent. of the total pneumonias) at the Harlem Hospital, New York, in the past seven years : in comparison with a mortality-rate of 20-8 per cent. in an untreated series of 163, there were only 5 deaths (7-5 per cent.) among 67 treated with serum. Similarly Finland and co-workers,2 at the City Hospital, Boston, isolated Type VII pneumococcus from 195 patients in seven years, representing 5-5 per cent. of all the cases from which specifically typed pneumococci were obtained during this period. Of these, 160 were suffering from pneumonia and it is significant that whereas Type I and II infections are almost constantly lobar in type, about one-fifth of the Type VII cases were classified as bronchopneumonia. In a series of 30 cases of Type VII lobar pneumonia, rapid and permanent clinical improvement followed treatment with concentrated3 type-specific antiserum. Finland and Tilghman have reported similar results in a small series of Type V lobar pneumonia. Nor, in the pursuit of new types, has Type I been forgotten, as may be seen from the paper4 Cecil read to the International Micro-

1 Bullowa, J. G. M., and Wilcox, C. (1936) J. clin. Invest. 2 Finland, M., Ruegsegger, J. M., Dowling, H. F., and Tilghman, R. C. (1937) Amer. J. med. Sci. 193, 48, 59. 3 Finland, M., and Tilghman, R. C. (1936) New Engl. J. med. 15, 711.

215,

1211.

4 Cecil, R.

L.

(1937) J. Amer. med. Ass. 108,

689.

biological Congress last summer. The illness, he says, from being a serious exhausting infection of 7-8 days’ duration can be reduced by early serum treatment almost to the status of an influenzal attack ; in other words, it is dramatically aborted. Spread of infection is prevented, bacteriaemia is checked, complications are inhibited, and the death-rate is cut to approximately one-sixth of the standard mortality for Type I pneumonia. Meanwhile, despite the truth of Cecil’s remark that reports on serotherapy of lobar pneumonia have been without exception favourable, little enthusiasm for this new line of treatment is being shown in this country. We were glad, therefore, to be able to publish a few weeks ago the observations made by Drs. Langley, Mackay, and Stent ó on Types I and II pneumococcal pneumonias treated with specific sera at the Hope Hospital, Salford. Though some of their conclusions are open to argument, it is clear that the work they are doing is of real value. THE SEX HORMONES IN ECLAMPSIA

THE work of 0. W. Smith and G. Van S. Smith the secretion of sex hormones in eclampsia and has already been annotated in these pre-eclampsia columns.6 These authors reported that the blood, urine, and placentas of eclamptic subjects contained excessive amounts of a gonadotropic hormone, and, less constantly, a paucity of cestrogenic hormones. Their experimental results indicated that the extra gonadotropic hormone was the same luteinising type (prolan B) that is found in normal pregnancy; and that it was derived from the placenta. The methods at present available for the assay of sex hormones are far from satisfactory, but if the above observations are correct it becomes important to find out whether over-secretion of prolan B is responsible, partly or wholly, for eclampsia, or whether it is merely a secondary response to some other dislocation of endocrine balance-analogous, for instance, to the excessive output of prolan A which is seen at the menopause. With an equation involving so many inter-related variables as the reproductive cycle it is no easy task to distinguish between cause and effect. The fact that toxaemia is especially common in multiple pregnancy and in cases of hydatidiform mole suggests that increased secretion of prolan B may be of primary rather than secondary import. But the inference is not conclusive and it is more to the point to ask whether, when eclampsia complicates an otherwise normal pregnancy, hypersecretion of prolan precedes or merely accompanies the clinical symptoms. Preliminary observations by Smith and Smith suggested that over-secretion may antedate symptoms by several weeks, and they nowbring forward further evidence that bears out this suggestion. They have collected serial samples of blood and urine throughout pregnancy in a series of 27 pregnant women, and estimated the prolan and oestrin content of the samples. Their series includes 11 diabetic subjects, who were selected because the incidence of toxemia is high in diabetes. Of their 27 patients, 6 developed pre-eclampsia, 4 of these being diabetics ; 17, including 5 diabetics, remained free from symptoms ; while the remaining 4 pregnancies were neither normal nor frankly toxsemic. In the toxaemic patients high prolan and low cestrin figures were observed, and it seems clear that the rise in serum on

5 Langley, G. F., Mackay, W., and Stent, L., Lancet, April 3rd, 1937, p. 795. 6 Lancet, 1935, 2, 564. Amer. J. Obstet. Gynec. 1937, 33, 365.