In view of the observations made of late years on the action of red light in variola, it was thought that it might be of interest to ascertain, if possible, whether the red, or other rays of daylight, exerted any influence in cases of vaccinia; that is to say, with a disease the specific virus of which differs from that of variola probably only in that its pathogenic capabilities are modified, while vaccinia presents clinically many points of resemblance to variola.

The action of air containing nitrogen peroxide upon flour, in quantities up to 300 c.c. of nitrogen peroxide to one kilogramme of flour, may be summarised as follows:—

I. The golden-yellow tint of the flour is destroyed. Immediately after bleaching no difference in tint due to excess of the bleaching agent could be observed with Lovibond's tintometer, but on keeping for several days the more highly bleached samples became decidedly yellow, while those treated with 30 to 100 c.c. of nitrogen peroxide per kilogramme became still whiter, the maximum of bleaching effect being attained within these limits.

II. The amount of nitrous acid or nitrites present in a freshly bleached flour is approximately proportional to the amount of nitrogen peroxide employed, and corresponds to about 30% of the total nitrogen absorbed, rising to 40% in the more highly bleached samples. After the lapse of several days, the proportion of nitrites present decreases considerably in the higher concentrations, but remains very nearly the same in the more slightly bleached samples.

III. Approximately 60% of the total nitrogen introduced as nitrogen peroxide into the flour during bleaching can be recovered as ammonia a short time after bleaching by reducing the aqueous extract of the flour with a copper-zinc couple, and may be assumed to be present in the flour as nitric and nitrous acids or as nitrates and nitrites. After keeping the bleached flour for some days the amount of nitric acid extracted with cold water decreases. Experiments with pure glutenin and gliadin indicated that in certain circumstances nitric acid may be withdrawn from solution or “adsorbed” by these proteins.

IV. In highly bleached flour a considerable increase in the amounts of soluble proteins and soluble carbohydrates takes place. If one kilogramme of flour is bleached with 300 c.c. of nitrogen peroxide, the amount of soluble nitrogen is doubled. This appears to be due almost entirely to the solubility of gliadin in nitric acid of certain concentrations. The simultaneous increase of soluble carbohydrates would seem to point to an intimate relationship between the gliadin and certain carbohydrates in flour.

V. If highly bleached flour is allowed to stand for some time after bleaching, the oil undergoes very considerable alteration and acquires the characteristics of an oxidised oil. About 6 to 7% of the nitrogen introduced as nitrogen peroxide during bleaching is absorbed by the oil.

VI. The absorption of nitrogen peroxide by flour does not appear to be accompanied by the production of free nitrogen, nor was any evidence obtained of the formation of diazo-compounds.

VII. Sodium nitrite was found to exert no inhibitory action on the digestion of soluble starch by saliva, but the rate of digestion was greatly retarded if the starch had been previously treated with nitrogen peroxide gas. Bleaching was found to exercise an inhibitory effect on the salivary digestion of flour.

We examined the association between contact with children and the clinical course of COVID-19 among COVID-19-positive adult patients. Participants completed a survey to assess demographics, medical information related to their COVID-19 diagnosis, contact with children at home and at the workplace. Patients were aged 45.68 ± 14.38 years, mostly female (72.1%), 842 were not hospitalized and 167 were hospitalized. At home, there were no differences between groups for the number of child contact hours or total child hours (hours × number of children) per week (Ps > 0.05). The number of children at home was greater among patients not hospitalized (P < 0.05), however this was no longer significant after controlling for covariates (P > 0.05). At the workplace, there were no differences between groups (all Ps > 0.05). Sub-group analysis found the proportion of patients that were treated in the intensive care unit (ICU) was greater among patients with no child contact (P < 0.05). A secondary analysis found that patients with no child contact had an increased likelihood of thromboembolism (P < 0.05) and a trend towards more overall COVID-19-related complications (P = 0.076). Overall, an association between contact with children and hospitalization was not found when adjusting for covariates. Sub-group analysis indicated a possible protective effect for more severe disease; however, these findings need further study.

Diphtheria toxoid lozenges were given to eighty-eight children aged 10–12 years who had previously been immunized by parenteral injection, and the antitoxin titres before and after administration were compared with those in a similar group of forty-six children who received formol toxoid by injection.

The results showed that a course of two lozenges at an interval of 1 week was a satisfactory means of reinforcing immunity in the children. The antitoxin response was less than that after injection, but a substantial response occurred in the children with low initial titres.

It is suggested that the lozenges might replace an injection as a means of reinforcing immunity in children aged 10–12 years and that they might be a valuable means of rapidly reinforcing the immunity of a large number of children in an epidemic.

The lozenges must be given under supervision to ensure that the children allow them to dissolve slowly in their mouths.

We should like to thank Dr J. D. Abbott of the Public Health Laboratory, Manchester, for separating the sera.

In the present paper an attempt has been made to devise a method of determining mortality rates at ages from causes of death associated with childbearing. The sources of possible fallacy in this procedure have been discussed, and it is probable that the results found will represent fairly accurately the true course of mortality in this country.

From all causes of death in childbearing, mortality follows this course: beginning with a high value in the age group 15–20, the rate drops to a minimum in the second quinquennium of reproductive life and thereafter gradually increases with age.

The main components of the death rate exhibit a similar age distribution, but other less important causes of death show an uninterrupted increase with age from the commencement of the reproductive period.

Eclampsia is much more common in young women, but this may be entirely due to the greater proportion of primiparae at these young ages. Estimated in terms of first births the death rate increases rapidly and steadily with age, subject to a small exception in the first quinquennium which may possibly be a consequence of unfavourable marital selection at that age.

The high puerperal mortality of young mothers cannot wholly be accounted for by the excessive dangers of primiparity. Evidence has, however, been submitted that these young women are, on the average, a less healthy sample of the total female population at that age and that, apart from primiparity and adverse selection, the death rate from childbed causes probably follows the same law of mortality as of women in general from all other causes of death.

There has been within recent years a decline of nearly 50 per cent, in the puerperal mortality in young mothers of 15–20 and a smaller decrease in the second quinquennium of reproductive life; but there is no evidence of any improvement at later ages. These phenomena have been brought into relation with the change which has taken place in the death rate from all other causes in married women at these ages. The youngest group of married women, relative to unmarried of the same age, were in the more recent period studied in a much more favourable position with regard to their mortality from causes other than those connected with childbearing than they had been formerly. No corresponding improvement has taken place in the relative mortalities from all other causes in older women within the childbearing ages.

These results suggest that the general health of the mother is a factor of great importance in determining the height of the mortality rate in pregnancy.

During the experimental comparison of different types of hot-water heating systems in a school at Easter 1934 about a thousand kata readings were taken. These were taken mostly in pairs, one immediately after the other, and a third reading was taken only when the first two differed by more than about 10 per cent.

1. None of forty-eight strans of Brucella abortus, ten of Br. melitensis and seven or Br.suis were shown to be lysogenic.

2. It was not possible to ‘adapt’ bacteriophages that were active upon other species of bacteria to lyse brucellas.

3. Thirty samples of faeces, mainly from cows, four sewage samples, twelve specimens of uterine fluid from cows that had aborted, and twenty samples of bulk milk failed to yield bacteriophages active upon brucellas.

As mentioned in Chapter 1, the Brown Institution was staffed by a remarkable series of Superintendents, seven out of eight of whom were, or became, Fellows of the Royal Society. Much of the research work they undertook has already been referred to in preceding chapters, but it seems only fitting that something should be said about their personalities and careers. In preparing the short accounts that follow, I am greatly indebted to obituary notices in the various scientific journals, especially those in the Proceedings of the Royal Society; to the pen sketches given by Professor Sharpey-Schafer (1927) in his History of the Physiological Society;and to the Memoirs in book form of Sir John Burdon-Sanderson by his wife (1911)and of Sir Victor Horsley by Sir Stephen Paget (1919).

The germicidal efficiencies of hot water (140–150° F.) under pressure (method 1), hot water + 2% (w/v) detergent solution (method 2) and hot water + detergent + 200 p.p.m. solution of available chlorine (method 3) were compared at six sites in a bacon factory. Results indicated that sites 1 and 2 (tiled walls) were satisfactorily cleaned by each method. It was therefore considered more economical to clean such surfaces routinely by method 1. However, this method was much less efficient (31 % survival of micro-organisms) on site 3 (wooden surface) than methods 2 (7% survival) and 3 (1% survival). Likewise the remaining sites (debarring machine, black scraper and table) were least efficiently cleaned by method 1. The most satisfactory results were obtained when these surfaces were treated by method 3.

Pig carcasses were shown to be contaminated by an improperly cleaned black scraper. Repeated cleaning and sterilizing (method 3) of this equipment reduced the contamination on carcasses from about 70 % to less than 10 %.

The bed-bug finds an almost ideal environment in a prison, which is centrally heated in winter, and in which it has good harbourage in the wooden cell furniture and an easily available food supply at night. Under such favourable conditions, bugs increase about seventy-fold in a year. It is therefore no mean achievement to obliterate bugs from an infested prison while the prison is still occupied, and is, I think, worth putting on record.

The primary object of these papers is to attempt to give a brief review of the present state of opinion regarding the many questions involved in the subject of immunity,—a review intended chiefly for those whose work is concerned with other fields of hygienic research. The carrying out of this aim has necessitated the re-statement of many facts familiar to bacteriologists, in order that the continuity of the discussion might be maintained. Wherever it has been considered advisable the details of the data which have formed the basis of theory have been given, but as a rule the leading results have been alone dealt with, partly because details might obscure the general principles it was intended to emphasise, partly because considerations of space have made an exhaustive treatment of the subject impossible.

Fluorescent antibody techniques were used for detection of plague antigens in infected mouse carcasses stored at 4°–5° C., 20°–25° C. (room temperature) and 370° C. for periods as long as 340 days in certain cases. Tissues of two guinea-pigs infected with Pasteurella pestis were examined after 7 years storage at room temperature. The efficacy of the fluorescent antibody test was compared with blood agar plate culture and animal inoculation during periods in which viable plague bacilli were presumed to be present, and compared with Larson's modified Ascoli test for the presence of soluble plague antigens during periods in which plague bacteria were presumed to be non-viable.

Fluorescent antibody tests were superior to animal inoculation or cultural methods in detection of P. pestis antigens in mouse carcasses stored for 4 days or longer at 37° C., for 8 days or longer at 20°–25° C. (room temperature), and for 34 days or longer at 4°–5° C. Upon examination of specimens presumed to lack viable plague organisms the fluorescent antibody test and precipitin tests were approximately equal in efficiency for detection of plague antigens in carcasses stored for 16–82 days at 37° C. and for 16–82 days at 20°–25° C. Ten of 21 mice stored for longer periods (140 and 340 days) at 4°–5° C. were negative by precipitin tests, whereas 19 of the same 21 rodents were positive by fluorescent antibody tests. In addition, after 7 years storage at room temperature tissues of two plague-infected guinea-pigs were negative by Larson's modified Ascoli test but positive by the fluorescent antibody test.

The predominant causative organism of whooping cough in Australia is of a serotype which has normally been associated overseas with unvaccinated communities. Australian DTP vaccines pass the statutory mouse test for Bordetella pertussis potency but this test is now believed to be relatively insensitive to certain factors, especially the major type-specific agglutinogens, which are presumably also important in the human host-parasite relationship. Because endemic B. bronchiseptica infections make some laboratory animals unsatisfactory for testing B. pertussis agglutinin responses, we have developed a test in which young farm sheep were immunized with vaccines. Type-specific agglutinins in their sera were assayed after absorption of non-specific agglutinins by suspensions of selected bordetella strains. Three well-reputed European DTP vaccines and two recent batches of Australian DTP vaccine were tested and compared thus. All evoked significant agglutinin responses to the main agglutinogens.

Pre- and post-vaccination serum samples from 278 volunteers, who were given live influenza vaccines, were tested by haemagglutination inhibition (HI) and single radial immunodiffusion tests (SRDT) for antibody to influenza A/Hong Kong/1/68 (H3N2) virus envelope antigens. Those with high antibody titres detected in both tests were less frequently infected, and 85% of the 159 infected showed rises by HI and 70% by SRDT. Similarly, 69 pairs were tested for antibody to Hong Kong (N2) neuraminidase by neuraminidase inhibition test (NI) and by SRD tests. Those with high titres in both tests resisted infection and those who were infected showed a rise in antibody detected both by NI and SRD tests. In general, SRDT was less sensitive than HI and NI in detecting antibody and antibody rises, but in some volunteers it did detect antibody rises which were not detected by conventional tests. Because of its simplicity and speed it appeared to be of use in evaluating such vaccines.

Two units, within a mouse-breeding colony, with different breeding systems, have been compared from the point of view of general healthiness of the breeding stock. In one unit the monogamous-pair system, involving post-partum oestrus mating, was employed and in the other the harem system, with isolation of the pregnant females for each litter-down until after the post-partum oestrus. The two units were housed separately and had different staffs. The monogamous-pair unit was accommodated in four small rooms not directly connected; the harem unit in two larger connecting rooms. The methods of cageing, bedding, feeding, watering, care, culling and subsequent procedures were identical for both units and the same system of recording individual detailed information relating to health and breeding was followed for the two units. The size of the two populations studied was 1198 and 1024, respectively, the larger number belonging to the harem unit in which the mice were retained for a significantly longer period. These mice were moved more frequently and handled much more often.

Apart from a small outbreak of Tyzzer's disease (in the harem-bred unit) and sporadic cases in both units spread over the whole period of the survey—some 3–4 years—the general health of the two units was good. There were no cases of salmonella infection, mousepox, pasteurellosis or other serious infections. Throughout the period both units maintained a high standard of productivity and there was no evidence that the mating of the monogamous pairs at the post-partum oestrus led to any weakness or ill health. As would be expected, however, the losses from death and culling were greater among the females in both units.

The health record of the monogamous-pair bred unit was consistently higher than that of the harem-bred unit. There were more cases of Tyzzer's disease in the harem-bred mice and more evidence generally of ill health in this unit. Infertility was three times greater with the harem-bred mice as compared with those in the monogamous-pair unit.

Details of the two systems are discussed and although the records maintained for the two may not be strictly comparable it is concluded that, under the conditions obtaining, the monogamous-pair breeding system yielded a healthier colony of mice than the harem breeding system.

I should like to thank Dr J. S. Patterson and Mr R. Cook for placing many of their records at my disposal, Mr S. Peto and his staff for carrying out much of the tedious compilation of data, and Dr D. W. Henderson, F.R.S., for affording me facilities for this work. To these I am especially grateful for their interest, advice and assistance.

The following conclusions appear to us to be justified as a result of the experiments cited above:—

(1) Close contact of plague-infected animals with healthy animals, if fleas are excluded, does not give rise to an epizootic among the latter. As the go-downs were never cleaned out, close contact includes contact with faeces and urine of infected animals, and contact with, and eating of food contaminated with, faeces and urine of infected animals, as well as with pus from open plague ulcers. This conclusion is justified from Experiments I and II and especially from Experiment VI, in which close contact with infected animals was maintained for nearly a month. In Experiment I the animals were inoculated cutaneously, and in many cases had developed ulcers at the site of inoculation.

(2) Close contact of young, even when suckled by plague-infected mothers, did not give the disease to the former.

(3) If fleas are present, then the epizootic, once started, spreads from animal to animal, the rate of progress being in direct proportion to the number of fleas present. Thus, in the experiments during the months of December, January and February, the epizootic was very rapid in those go-downs, namely, Nos. 1 and 2, Experiments IV and V, in which the flea population was abundant and was kept up by a natural supply from the roof: it was much slower in Experiment VII, go-down No. 5, in which the flea supply was kept up artificially; and, finally, it was slowest of all in go-down No. 6, Experiment VI, in which there was no definite natural supply of fleas, and from which the fleas were daily removed for a period of six days, after which removal only a comparatively small number could be caught.

(4) An epizootic of plague may start without direct contact of healthy animal and infected animal. Thus, in the case of Experiment V in go-down No. 1 the healthy guinea-pigs were not put in until the last inoculated guinea-pig had died and been removed.

(5) We have in Part II shown by direct experiment that the rat flea can convey plague from rat to rat. Further experiments (Experiments VI, VII and XI) of a similar nature with the fleas removed from infected go-downs are now recorded.

(6) Infection can take place without any contact with contaminated soil. Thus in go-downs Nos. 1 and 2 (Experiments VIII, IX), guinea-pigs placed in wire cages two inches above the ground developed plague; also the monkey in go-down No. 2 (Experiment XIII) was never in contact with the ground.

(7) Aerial infection is excluded. Thus, guinea-pigs suspended in a cage two feet above the ground did not contract the disease, while in the same go-down those animals allowed to run about and those placed two inches above the floor became infected. Further, the monkey surrounded by tangle-foot was exposed as much to aerial infection as the control animal which contracted the disease.

1. The red blood corpuscles of different species have definite and distinct mean lytic points.

2. The apparent tonicity of sheep serum has no relation to the mean lytic point of the red corpuscles of that individual.

3. The apparent tonicity of sheep serum is not due to its proteins but to its lipoids.

4. The residue of sheep serum, after removal of proteins and lipoids, is sufficiently alkaline to cause lysis.