1. The influence of temperature on the germicidal power of selected disinfectants has been studied, and it has been found that germicides may be classified broadly into three main groups, viz.

Germicidal power (a) unaffected by rise in temperature: chiefly chemical substances, possessing reducing properties;

(b) approximately doubled by rise in temperature from 20 to 37°C.—phenol, alcohol;

(c) increased as much as 10 or 20-fold by the same temperature rise: oxidising agents.

2. The effect of temperature on bactericidal action is different for B. coli and B. fluorescens, thus causing very complex changes in selective action, which are discussed in this paper.

3. The temperature coefficient for the process of protein-precipitation by phenol is 2·2 per 10°C. rise in temperature, and thus similar in magnitude to the coefficient for disinfection by phenol. This supports the view that the germicidal action of phenol is associated with its denaturating effect on the cell-proteins.

4. Previous experimental work had suggested that the bactericidal action of the quinones was due to their chemical reactivity with the simple cell-constituents, e.g. the amino-acids, rather than with the complex colloids. The temperature coefficient of the reaction between benzoquinone and glycine is, however, the normal one, viz. 2 for 10° C. rise, for chemical action, although the germicidal action of the quinones may be actually 20 times more effective at 37° than at 20° C. The presence of certain inorganic cell-constituents accelerates the velocity of reaction between quinone and glycine, but does not increase the temperature coefficient.

5. The bactericidal power of picric acid and potassium permanganate, as well as the quinones, is greatly increased by rise in temperature: and there would appear to be some other factor common to all these disinfectants associated with their high temperature coefficient.

In the present study an attempt has been made to determine the relative importance of several factors on the mortality rates of infancy. In view of the differences in the rates at the several ages under one year and of the differential decline in these rates within recent years, it has been suggested that for any complete consideration of the death rates in infancy, some subdivision of the rate, either of a biological or temporal character, must be effected, and each of these subdivisions examined separately. The infant mortality rate has been treated in three broad categories, namely, the antenatal, neo-natal and post-natal death rates; and it has been shown that each of these depends on different factors.

Considered as death rates per unit of time the neo-natal rate is much higher than at any other period of life. The ante-natal death rate is much lower than this, and the post-natal rate lowest of all.

In relation to these rates, the influence of three, presumably important, factors have been measured. These are:

1. The provision of skilled attendance to mothers in childbed.

2. The health of the mothers.

3. Environmental and social conditions.

The indices used as measures of these three variables and their limitations have been pointed out. The author feels only too conscious of these limitations and, with such vital statistical data as the only indices available of the factors the influence of which on the mortalities of infancy it is desired to measure, it is probable that any conclusions drawn from such an analysis should be accepted with some degree of caution and reserve. Nevertheless. I am firmly convinced that even these (to the clinician and administrator) rather crude results are immeasurably superior to expressions of opinion, unsupported by facts, so frequently found forming the basis of much of the medical literature on the subject. That we have so relatively little exact quantitative knowledge of the influential factors concerned in the growth, nutrition and mortality of infants is surely not for lack of opportunity of collecting the requisite data. An admirable machinery for such a purpose—the various maternity and child welfare centres—is in extensive operation throughout this country; and if the medical officers in charge of these centres could only be persuaded to collect and analyse (or have analysed) periodically the data contained in suitably framed and completed questionnaires, many questions of scientific importance as well as of the efficacy of administrative efforts would soon cease to be subjects of controversy.

Our results show that, of these factors, only the provision of skilled medical assistance to mothers in childbed is of importance in connection with antenatal mortality. The general health of the mother and external environmental conditions have no direct influence on the death rate at this period of life. The magnitude of the correlation leads to the further conclusion that a great part of the still-birth rate is not to be controlled by improvements in even all of these factors.

The neo-natal death rate is related both to variations in external environment and in the obstetrical assistance available for mothers in childbed. At this state of life, again, the health of the mother has no substantial influence on the death rate. External surroundings and the quality of the obstetrical assistance afforded to the mother are of approximately equal importance in determining these rates; but here again the conclusion is advanced that the greater part of the death rate at this stage of life is beyond human efforts of control.

The post-natal death rate seems to offer the greatest scope for administrative measures. In this case the health of the mother would appear to come first in order of importance, environment also is of some importance, whereas the effects of variations in obstetrical services have now ceased to be reflected on the mortality of infancy.

In isolated rural communities there is a part of the post-natal death rate which could be eliminated by the speedy arrival of skilled medical assistance.

Foreign statistics have been collected and analysed to enquire into the causation of still-births. An obvious defect in these was pointed out, namely, the large proportion of deaths due to unknown causes. A comparison of these figures with those collected from several maternity hospitals has shown that hospital figures give a biassed view of the problem. The proportion of deaths due to causes in which the life of the mother as well as that of the foetus is endangered is greatly magnified, and consequently will produce a too optimistic estimate of the amount of amelioration which will result from increased attention to pregnant and parturient women. The statistics which have been given in this section show that in a really random sample of the population only a small proportion of still-births is the result of causes which can be controlled by this method, and that the chief causes of ante-natal death are developmental defects of the foetus and prematurity.

A short study has been made of certain statistico-anatomical features of the foetus and infant. From this it has been inferred that the foetus is physically in a state of extreme instability, that the conditions which kill in utero are rapidly fatal to the foetus, and that this instability is a somewhat more prominent feature in the male than in the female. As infancy advances, visceral variability decreases steadily, so that it would seem probable that some time is necessary for the foetus to adapt itself to its new mode of existence after birth. This state of unstable equilibrium in early life may provide some reason for the higher mortalities at these ages.

1. No evidence was found of the presence of furunculosis in trout farms. Over 100 trout from four farms in S. England were examined with entirely negative results.

2. Of eighteen live trout taken from the Kennet, three were carrying the B. salmonicida in their blood. All three were in poor condition but alive and active, and two of them were so-called “black fish”.

3. Bacteriological analyses of Kennet water at eleven selected points were carried out in the month of August. They revealed no serious pollution nor any definite relationship between high bacterial content and the disease.

4. Laboratory experiments to test pathogenicity of B. salmonicida appear to show:

(a) That the bacillus is lethal to goldfish when injected into the muscle but not necessarily so when rubbed into a skin wound.

(b) That in the case of gobies infection from water polluted with pure broth cultures of B. salmonicida is possible and may cause death in about fifteen days after the introduction of the culture.

(c) That fish (gobies) which had survived the last experiment for a period of six weeks were capable of infecting healthy “contacts”, when kept with them in fresh running water.

5. A few laboratory experiments on the behaviour of B. salmonicida in sewage appeared to indicate that the bacillus persists longer in tap and distilled water than in crude sewage and sewage effluent.

6. Specimens of fish (salmon and trout) infected with furunculosis were also received during the summer from the Rivers Lledr (Wales), Lyon (Scotland) and a private hatchery on the Test at Whitchurch. The conditions in the two latter cases suggested that the outbreak was mainly due to carriers.

7. Measures suggested in the case of infected streams are: avoidance of over-stocking, bacteriological scrutiny of source of fresh stocks, removal of sick and ill-conditioned fish, and sewage control.

A given strain of Bact. aertrycke Mutton has been tested repeatedly for its virulence to mice, and on some of these occasions the virulence of 10 single colony cultures taken from this strain has likewise been tested. Between these single colony cultures such marked differences in virulence have been found as to constitute definite discontinuous variations. Side by side in the same culture there have been found virulent and avirulent organisms. Daily subculture in broth under certain atmospheric conditions resulted in the fall in virulence of the whole culture; this was accompanied by a replacement of the virulent organisms by organisms that were either completely avirulent or were only weakly virulent. The evidence suggests that the fall in virulence of the whole culture is not due to a simultaneous fall in the virulence of each of its constituent organisms, but to a replacement of the highly virulent organisms by organisms of a lower degree of virulence. During the process of replacement two or three different variants, showing discontinuous variations in virulence, may be demonstrated together in the same culture. The conclusions to be drawn from these findings, and their bearing on the interpretation of the results of experimental epidemiology, are discussed.

In January 1923, after the publication of The Epidemiology of Botulism by Dr K. F. Meyer and his colleagues in America, and after the publication of the official report to the Scottish Board of Health on the Loch Maree tragedy, it seemed obvious that an accurate knowledge of the distribution of the Bacillus botulinus in Scotland was very desirable. Dr Meyer had shown that this was an organism which lived in the soil, and he had already published the results of the bacteriological examination of a great number of soils in America and other countries. None of them, however, came from Scotland. I therefore suggested to the Scottish Board of Health that they should ask the Medical Research Council to undertake such an examination, and offered my own services for the purpose of collecting soils from all the Scottish counties. The Board at once agreed, and the Medical Research Council on having the request put to them also at once agreed and appointed Professor Basil Buxton, F.R.C.V.S., to undertake the bacteriological investigation. Prof. Buxton and myself arranged exactly the kind of samples which should be taken, and the method of taking them, and he supplied me from time to time with a number of sterilised containers into which samples of soil were put and forwarded to him for examination.

(1) The review of the published data furnishes additional evidence in support of the view that no technique whatsoever, Dreyer's technique included, based on the quantitative method of the agglutination reaction hitherto used, is capable of affording a differentiation between inoculation and infection agglutinins.

(2) These techniques are concerned always exclusively in the demonstration of the labilotropic H agglutinins of B. typhosus and B. paratyphosus A. and B. and it is the behaviour of these agglutinins that is the responsible factor in producing the phenomena.

(3) In various febrile conditions in inoculated individuals these H agglutinins undergo a re-stimulation resulting in a curve of agglutination which is indistinguishable from that due to specific stimulation. The re-stimulation of the labilotropic inoculation agglutinins is of the same nonspecific character (i.e. heterologous) in the course of enteric infections as in the course of other febrile diseases.

(4) The observation of this non-specific re-stimulation is independent of the technique used; living bacilli and suspensions preserved with phenol or formalin (Dreyer's technique included) do not in this respect behave differently.

(5) The proposed qualitative method for the Widal test depends, in inoculated individuals, exclusively upon the behaviour of the stabilotropic O agglutinins. In their presence it is capable of affording the certain diagnosis of an enteric infection; in their absence the negative result of the test is not conclusive; if T.A.B. vaccine has been used it is only possible to diagnose enteric group without being able to differentiate typhoid from paratyphoid A. or B.; if T. vaccine has been used then A. or B. infection can be differentiated but not T.

(1) The conclusions previously arrived at by means of the qualitative method of the Widal test were fully confirmed. By eliminating the labilotropic H agglutinins from any consideration—in the case of previously sensibilised individuals—agglutination due to the specific stimulation in active enteric infection can be distinguished definitely from that due to the nonspecific re-stimulation by various febrile diseases.

(2) Normal and immune O agglutinins for B. typhosus and B. paratyphosus A. and B., as well as those for B. proteus X 19, are not liable to non-specific stimulation in the course of various febrile diseases.

(3) One more of the supposed differences in nature between the Widal test and the Weil-Felix test is thereby eliminated.

(4) The difference in the response to non-specific stimulation shown to exist in stabilotropic and labilotropic agglutination seems more likely to be one of degree than one in nature and needs further investigation.

No information from official or non-official sources is available on the prevalence of enteric fevers in Palestine in pre-war days. Since the establishment of the British Administration (1919) the Annual Reports of the Government Department of Health invariably emphasise the high incidence of enteric fevers. Several papers dealing with the epidemiology of the disease appeared in the Hebrew periodicals Briuth Haam and Harefuah and in 1926 an elaborate Report was submitted to the Department of Health by a Committee of Enquiry appointed by the Department to consider and advise on the situation as regards enteric fever in the country. The data thus accumulated, although very valuable for the local health authorities, did not reveal any peculiar features of more than local interest. Their publication abroad seemed, therefore, superfluous.

1. When a solution of commercial peptone is substituted for antigen in a complement-fixation test with the unheated normal serum of certain species (man, ox, sheep, horse, rabbit, white rat), a definite fixation reaction occurs both at 37° C. and at 0° C. In the ox, sheep, horse and rabbit this property of serum is partially stable at 55° C., but normal human serum and the serum of the white rat are inactive after heating at this temperature. The property is resident mainly in the carbonic-acid-insoluble globulins of the serum.

2. The same results are obtained when ethyl alcohol diluted with several volumes of normal saline solution is substituted for antigen in a complement-fixation test with normal serum.

3. Analysis of these reactions shows a close correspondence with complement-fixation by the sera of normal animals plus the Wassermann “antigen”—the Wassermann reaction of normal animals.

4. Marked complement-fixation effects are also obtained with heated normal serum of the rabbit, ox, sheep, horse plus cholesterol suspension, and particularly cholesterolised-peptone, these effects occurring in parallel with those produced by serum plus alcohol-saline, peptone solutions and the Wassermann “antigen.” The heated normal serum of the pig, white rat and guinea-pig do not exhibit these reactions, and the same applies to heated normal human serum. Unheated pig serum fails to react. Such results also elicit a close relationship between these non-specific reactions and the Wassermann reactions of normal animals.

5. The reacting property is absent from the serum (heated and unheated) of young rabbits during the first 2 to 3 weeks of life, but appears soon after this (e.g. by the 37th day) and is progressive in development. Its development in early life runs parallel to that of the natural haemolytic property of the serum for sheep's blood (due to a natural antibody-like substance). The two properties are, however, independent as illustrated by absorption tests.

6. Besides the agents referred to above as capable of fixing complement along with normal sera, other substances possess a similar property, e.g. certain alcohols, sodium oleate, tissue proteins, certain amino-acids and sodium nucleate. Commercial peptone purified by precipitation with alcohol is equally active with the original material. Cholesterolisation of these agents may yield a product whose activity is greater than that due to summation of effects.

7. Wassermann-positive and -negative human sera have been tested in the complement-fixation reaction with certain of these “pseudo-antigens,” viz. alcohol-saline, peptone, cholesterol, and cholesterolised-peptone, but a uniform parallelism has not been demonstrated between the reactions with these agents and the Wassermann effect. Some Wassermann-positive sera react also with alcohol-saline, peptone, cholesterol and cholesterolised-peptone, while sera from selected normal persons are quite inactive. A considerable proportion of Wassermann-positive sera yields definite complement-fixation with cholesterol and cholesterolised-peptone; a small proportion of Wassermann-negative sera reacts with these agents.

8. The thermolability of the serum principles acting with various “pseudoantigens” has been studied by testing unheated serum and serum heated at temperatures ranging from 46° to 60° C. Two types of thermolability curve have been demonstrated with different specimens of rabbit serum: (1) a more or less progressive weakening of the various reactions with inactivation at 60° C.; (2) inactivation of the effects with Wassermann “antigen,” alcoholsaline and cholesterol at 50–52° C., activation of the effects with the Wassermann “antigen” and cholesterol at 54–56°C. and inactivation again above 60° C.; in this case the curves for peptone and cholesterolised-peptone do not show such double inactivation. Unheated normal human serum yields reactions with the various agents (including the Wassermann “antigen”) but inactivation occurs at 50° to 54° C. whereas certain syphilitic sera yield thermolability curves somewhat similar to type (1) of rabbit serum, with inactivation at 60° C. or over.

The results of this investigation show that tuberculosis in captive wild mammals may be caused by any one of the three types of tubercle bacilli—human, bovine or avian.

In the Primates, which under experimental conditions are susceptible in an equal degree to bovine and human tubercle bacilli, natural tuberculosis may result from infection with either type. The human tubercle bacillus is however found more frequently than the bovine bacillus. Taking the condition of the regionary lymphatic glands of the body as an indication of the probable portal of entry of the infecting bacilli, e.g. greater enlargement and more advanced caseation of the thoracic than of the abdominal lymphatic glands as denoting respiratory infection, it would appear that the monkey may become infected with bovine tubercle bacilli, as well as with human tubercle bacilli, not only through the alimentary tract but also by inhalation.

Cultures of acid-fast bacilli were obtained from four caymans, one frog and one snake, which died in the Zoological Society's Gardens.

The strains from the four caymans were identical and indistinguishable from Aronson's Mycobacterium marinum.

The snake strain closely resembled the fish tubercle bacillus of Bataillon, Dubard and Terre.

The frog strain could not be identified with any of the cold-blooded strains of tubercle bacilli mentioned above.

Skin tests made with the toxin obtained from Tunnicliff's strain of green producing streptococcus on normal individuals, and on cases prior to and after an attack of measles did not give any definite positive evidence of the etiological relationship of this organism to measles. Further, an attack of measles did not produce any apparent increase in the antitoxic content of a patient's serum for this toxin.

In a previous paper (Williams and Hoy, 1927) it was shown that living and virulent tubercle bacilli could be demonstrated in the faeces of six apparently healthy cows from among a total of 391 which were examined. All these cows were living the normal life of the herds in which they were discovered, and three of them were brought to the Institute in order that a study might be made of the frequency with which tubercle bacilli could be found in their faeces.

We hope that this summary of our researches will be sufficient to make clear the nature of the danger spoken of at the beginning of this article. We see that certain bodies, not poisons in themselves in the usual sense of the word, can provoke physiological disorders and organic lesions, the etiology of which remains generally unnoticed, when they are absorbed daily for months and years. Such products are most certainly responsible for many illnesses, the frequence of which augments with the alimentary conditions imposed upon us by modern civilisation in a manner inexplicable beforehand.

Our object will have been attained if we succeed in attracting the attention of physicians and hygienists to certain problems, the study of which is perhaps not very attractive but the solution of which is of considerable practical interest.