Any description of the outbreaks of venereal disease is of necessity bound up with the migration of races, or parts of races, with wars and the consequent dislocation of the social system resulting from them. There are many inferences available from current writers showing how this contagious disease was spread and there is a good deal of reason to believe that some, at least, of the numerous cases of “leprosy” for which provision was made on frequent trade routes in past times were really cases of venereal disease.

1. During the pre-epidemic stage of the spread of bacterial infection among mice, single deaths, or small groups of deaths, due to the specific infection being studied, are found to occur at considerable intervals before the rise of the main epidemic wave, and to afford a warning that such a wave is at hand.

2. In many cases there may be observed, during the same period, an increase in the daily mortality from all causes.

I should wish to express my thanks to Dr Major Greenwood for the interest he has shown in this investigation, and for much useful information with regard to epidemiological records. I am again greatly mdebted to my co-workers, Dr H. B. Weir and Dr G. S. Wilson, for their assistance in these experiments.

1. If a mouse-population, which has been exposed to the risk of infection, be dispersed into several small groups during the pre-epidemic stage, the total mortality will be far less than if the animals be retained as a single large group. The specific mortality will be reduced to a still greater extent.

2. During the period of dispersal, the mice forming the small groups will, in most cases, have passed through an extended pre-epidemic phase of the spread of infection. In so doing they will have acquired an appreciable degree of immunity.

3. If the small groups be later re-combined into a single aggregate, further deaths will occur; but the total mortality among a group of mice, which has been dispersed and then re-accumulated, will always be less than among a similar group, which has been retained from the commencement as a single unit of population. The specific mortality will generally show a still greater reduction.

It remains for me again to express my thanks to my colleagues, Dr H. B. Weir and Dr G. S. Wilson, for their assistance in this investigation.

The following paper contains a discussion of the results of the bacteriological examinations of samples of Grade “A” milk from two farms numbered 5 and 6.

1. No entamoebae, cysts, or other parasites were found.

2. Streptococci were present in the stools of all babies more than three weeks old, but only three haemolytic strains were isolated, which appears to be a lower proportion than occurs in adult stools.

3. Colon bacilli were present in the stools of all babies more than two weeks old, and haemolytic strains occurred in 12 per cent, of the specimens examined, that is in the same proportion as in adult stools.

4. Staphylococcus albus was much more commonly found than in adult stools and in greater abundance.

5. There was no bacteriological difference between the stools of the 78 breast-fed babies and those of the 13 artificially-fed infants, except that the haemolytic strains of B. coli occurred relatively more frequently in the case of the artificially-fed infants but owing to the small number of haemolytic strains isolated it would be unwise to lay too much stress on these figures.

In conclusion I wish to offer my sincere thanks to Dr Jewesbury, Physician to the Children's Department of St Thomas's Hospital, for supplying me with the necessary material and for information as to methods of feeding, and I am also greatly indebted to Professor Dudgeon and Dr Wordley for their constant help and advice.

While research on the immediate cause of cancer is being pursued with tireless zeal by many earnest investigators it seems that there is still some work to be done on the nature of what may be termed the secondary or accessory causes, those external or envioronmental factors or conditions which predispose to, or favour the onset of the disease in the presence of the determining cause, whether this be chronic irritation of some kind superadded to an inborn tendency and special suceptibility in the patient or the activity of some micro-organism.

1. Pneumonic Plague epidemics arise as a secondary manifestation of Bubonic Plague.

2. The prevalence of purely septicaemic cases towards the end of the epidemic is significant as a probable explanation of its decline and termination.

3. Subacute or chronic plague may exist among tarabagans (Arctomys bobac) in Mongolia and Siberia, giving rise to periodical outbreaks of bubonic plague in man, as a result of direct infection from injury due to skinning by trappers or marmot eaters.

4. The tarabagan is easily susceptible to pneumonic plague produced by inhalation of B. pestis in spray form.

5. The existence of Pneumonic Plague carriers has been proved in the 1921 Manchurian epidemic.

6. Rooms where patients have died of pneumonic Plague are not particularly dangerous. In all four instances recorded, sick patients travelling in railway carriages have not infected their fellow passengers.

7. Disinfectants and antiseptics, even in strengths above those usually employed, have very little effect upon plague sputum. Alcohol is the surest means of sterilising the hands and gloves in plague work.

8. We have cultivated B. pestis from seemingly dry sputum of partients.

9. The mask is the principal means of personal protection against Pneumonic Plague.

10. The problem of successful vaccination against Pneumonic Plague still awaits solution.

1. In the foregoing experiments evidence is adduced to show that bacteria in spleen broth or neutral Ringer's solution carry a negative charge and move to the anode in an electric field. The addition of a slight trace of a positive trivalent ion such as La or Ce or Yb to the solutions containing the bacteria immediately lessens or neutralises this negative charge, and if the concerntration of these ions is further increased completely abolishes it, and the bacteria undergo flocculation or agglutination. Living bacteria seem much more sensitive to the action of these ions than non-living colloidal particles. The addition of negative trivalent ions to bacterial cultures is without any effect on their movement in an electric field; the negative charge on the bacteria is not increased.

2. Some inconclusive evidence has been brought forward in support of Girard and Audubert's work regarding the influence of the double electric layer of the bacterial cell wall in controlling their biological properties.

1. The experimental derivation of a mucoid form of B. paratyphosus B is described.

2. This form, though at one stage non-motile, agreed closely with the “capsulated mucoid forms” of paratyphoid B, isolated by W. Fletcher from two chronic “carrier” cases.

3. The mucoid paratyphoid B was highly dys-agglutinable, and it would not on serological examination be identified as a paratyphoid B.

4. Its colonies were also entirely unlike colonies of paratyphoid B, being large, slimy, and usually dome-shaped, though at other stages of their metamorphosis they presented either an umbilication, or a nipple-like elevation in the centre.

5. The mucoid bacillus possessed the distinctive sugar reactions of paratyphoid B.

6. On suitable manipulation it reverted to the ordinary form.

1. For the particular toxin tested, the intravenous m.l.d. for mice was 60 times and the intramuscular m.l.d. for mice 100 times, the guinea-pig sub cutaneous m.l.d.

2. Antitoxin has the same neutralising power for toxin in mice as in guinea-pigs.

(1) An animal may be in a state of active immunity before any circulating antitoxin can be detected and, further

(2) The condition of active immunity continues after the disappearance of all circulating antitoxin produced by the animal in response to a previous stimulus.

The injection of the small amount of diphtheria toxin used in the Schick test may act as a secondary stimulus.

A Schick test may therefore cause a great and rapid increase in the immunity of the animals tested.

Examples are quoted of six rabbits and twelve guinea-pigs in Tables II to VII.

2. A fraction of a Schick dose may act as a secondary stimulus. Rabbit G 23 quoted in Table IV, injected with 1/10 of a Schick dose, showed an immunity response, the antitoxic content of its blood rising from 1/50 to nearly 1/10 unit per c.c. in six days.

3. The action of a Schick dose as a secondary stimulus may cause an animal to give a negative reaction when tested seven days or more after the first positive reaction.

This is illustrated by rabbits G 7 in Table III, G 31 in Table II, G 32 and G 34 in Table V and four guinea-pigs in Table VI.

4. The antigenic value of a Schick dose of toxin as a secondary stimulus may be as high as that of a reasonable dose of a toxin-antitoxin mixture suitable for human immunisation. Examples are given comparing the results of the injection of a Schick dose of toxin and of a toxin-antitoxin mixture in the same rabbit in Table III, in different rabbits, G 20 and G 22 in Table IV and reference is made to the companion rabbits to those quoted in Table V.

5. The antigenic value of a Schick dose as a secondary stimulus can be demonstrated:

A. In animals which have not produced a detectable quantity of antitoxin (that is less than 1/2000 of a unit per c.c.) as the result of a primary stimulus.

See both rabbits in Table II, rabbit G 20 in Table IV, both rabbits in Table V, and guinea-pig FF 19. v in Table VII. The four guinea-pigs in Table VI probably come under the same heading.

B. In animals whose actively produced antitoxin has fallen below a de tectable level.

See rabbit G 7 in Table III.

(These results add further confirmation to the phenomenon reported in the paper “Active immunity to diphtheria in the absence of detectable antitoxin” (Glenny and Allen, 1922).

6. A Schick dose of toxin which gives a positive reaction may, by acting as a secondary stimulus, produce a rapid increase in the antitoxic value of animals already containing some actively produced antitoxin.

See guinea-pig LL 17. vi in Table VII.

7. A Schick dose of toxin which causes no reaction may, by acting as a secondary stimulus, produce a rapid increase in the antitoxic value of animals already containing some actively produced antitoxin.

See guinea-pigs in Table VII.

8. A Schick dose of toxin may fail as a secondary stimulus if the antitoxic content at the time of injection is comparatively high.

See rabbit G 21 in Table IV.