1. The kinds of bacteria that are isolated by the gelatin plate method from certain river waters freshly polluted with sewage are different from those found in the same water collected a long distance below the point of pollution.

2. In the freshly polluted river water non-chromogenic Staphylococci were found much more abundantly than in the purer waters.

3. In the freshly polluted water the fluorescent bacteria and a group of non-gas-producing, non-liquefying bacteria (Group XI.) were less abundant than in the purer waters.

4. A larger proportion of organisms belonging to the Proteus group were isolated from gelatin plates than from fermentation tubes. The reverse is true of the B. coli and B. lactis aerogenes types. A certain selective influence even upon gas-producing organisms would seem from this to be exerted by the conditions within the fermentation tube.

5. The study of a rather large number of separately isolated cultures belonging to the class of fluorescent microorganisms shows that the differences between the ‘liquefying’ and ‘non-liquefying’ varieties are more constant than is sometimes assumed. The action of these forms upon milk is just as diagnostic as their action upon gelatin. All the strains of fluorescent bacteria that were encountered (58) proved to be motile.

6. Considering as a whole the various physiological tests applied to the several groups of microorganisms, it is found that within almost every group as constituted in the accompanying tables divergence is shown by closely allied organisms in respect to indol formation and reduction of nitrates. The formation of a surface pellicle on broth is also a phenomenon that presents no apparent correlation with more s alient physiological characteristics.

(1) The graphic method is more easy of application and requires less mathematical knowledge than the extended analytical method.

(2) In our experience it produces smooth curves of px and Ex.

(3) The analytical in the selection of the best process of interpolation appeals to the graphic method.

(4) While either the analytical or graphic process may in unskilful or careless hands give erroneous results, owing to errors in working out, the analytical process, unlike the graphic, presents a wide choice of methods, which although accurately worked out, give incomparable results.

(5) The facts given in the table on page 321 and in Fig. 1 A and B and table on page 317 show that almost identical results are obtained by the graphic method and by the improved extended analytical method. We regard this as important testimony to the accuracy of each of these methods, and at the same time as indicating the inaccuracy of the analytical methods giving different results.

(6) As the results obtained by the modified short analytical method and by the combined analytical and graphic method approximate so closely to those obtained by the detailed graphic method, either of them may safely be adopted by those who cannot spare time for working out a detailed Life Table by the graphic method.

(7) Every published Life Table should give exact details of the method of its construction, in order that the comparability of data and results may be tested. Much confusion has arisen, and important errors in comparison between different Life Tables have been produced, by the use of different methods of construction and the non-publication of details of methods.

In South Africa one finds quite a number of ailments occurring in the domesticated animals, and while the onset, symptoms, and morbid anatomy of those affected show the ailments to be peculiar to Africa, the names given to the maladies are unknown in any other country.

1. Compressed air above 5 atm. lessens the CO2 output, and lowers the body temperature in mice, rats, and young rabbits.

2. Oxygen at and above 1 atm. has the same effect. It is a sign of oxygen poisoning.

3. Compressed air at 10 atm. is more damaging–at least to small animals—than oxygen at 2 atm.

4. Compressed air increases the loss of body heat both because it is a better conductor, and because it is saturated with moisture.

5. The saturation of the air with moisture in caissons does not prevent evaporation from the body because the skin temperature is above that of the air. The wet air by damping fur or clothes increases loss of heat.

6. Highly compressed air may possibly interfere with the diffusion of CO2 from the alveolar air, and may, owing to increased friction, hinder the passage of air in and out of the air-tubes.

7. The nitrogen output in dogs is not altered in any noteworthy degree by exposure for six hours to 8 atm. air.

8. Inflammation and consolidation of the lungs is produced by exposure to 8 atm. air for over 24 hours. 1½ atm. of pure oxygen has a similar effect. The higher the oxygen tension the more rapidly does the inflammation ensure, e.g. 6 atm. O2 produces marked congestion in 2 hours.

9. It does not seem likely that inflammation of the lungs should be produced in the pressures and times of exposure usual in caissons.

10. Excised frog's hearts, muscles, and nerves are not rapidly poisoned by even 50 atm. O2. A heart will beat more than an hour exposed to this pressure. The vagus nerve endings appear to be paralysed by such exposure, while inhibition can be obtained by stimulating the crescent. The thin sartorius muscle is much more easily affected than the gastrocnemius, and soon gives a curve like a fatigue curve.

11. All animals investigated, vertebrates and invertebrates, are instantly convulsed and killed by exposure to 50 atm. O2.

12. Convulsions are frequently produced in vertebrates by exposure to 4—5 atm. O2, while exposure to 6—25 atm. O2 produces dyspnoea and coma, and the convulsive stage does not usually appear. Cleaning movements, salivation, gaping, jerky deep respiration, are symptoms which precede the convulsions, and coma soon follows them.

13. We have not observed convulsions with air pressures up to 12 atm. Salivation, dyspnoea, and coma are the symptoms.

14. The blood-gases increase in compressed air or oxygen according to Dalton's law, but the process of complete saturation of blood and tissues takes some time.

15. The circulation is unaffected mechanically by compressed air.

16. The cause of caisson-sickness is the escape of gas bubbles in the blood vessels and tissue fluids on decompression. An animal exposed for 4 hours to 8 atm. air and quickly decompressed is like an opened bottle of soda-water. The fluids of the body generally effervesce.

17. The effervescence can be studied in the circulation of the frog's web or bat's wing, the animals being enclosed in a suitable chamber. It takes a little time for the bubbles to grow to an appreciable size.

18. Recompression causes the bubbles to go into solution, and if applied quickly enough the circulation recommences.

19. The bubbles after rapid decompression can be seen post-mortem in the blood vessels, in the heart, retinae, aqueous humour, connective tissue spaces, etc. The alimentary canal is blown out with gas. The bubbles produce cyst-like cavities in solid organs, e.g. in the central nervous system, the liver. The cells are compressed round these cysts.

20. In the case of oxygen an animal may recover after an extraordinary amount of this gas has been set free by rapid decompression. The nerve cells are not killed by the oxygen bubbles, and the animals are convulsed and exhibit hyper-reflex-excitability.

21. The varying symptoms of caisson-sickness are due to the varying seat of the air emboli.

22. Young men escape caisson-sickness owing to the elasticity of their tissues, and greater facility for collateral pathways of circulation.

23. Animals can be safely exposed to 8 atm. of air for 4 hours if 2 hours be spent in gradual decompression. Such exposure can be safely repeated three times a week.

24. By the choice of suitable men, and proper regulation of the period of compression and decompression, caisson and diver's sickness can be avoided.

During the past four years it has been part of our routine work to examine samples of ground waters from wells and springs in various portions of Ohio, and, in so doing, organisms have been obtained from time to time conforming to the tests usually given as differentiating faecal bacteria.

The task with which I have been honoured—of reporting upon the action of English Public Health Authorities in regard to tuberculosis—can, I believe, be best fulfilled (a) by a review of the history of the mortality from tuberculosis in England since 1837, when vital statistics first became available, (b) by a statement of the factors which have been instrumental in causing the reduction in the mortality from tuberculosis shown in these statistics, and an attempt at weighing their relative importance, (c) by a description of the more direct measures taken in England to diminish the prevalence of tuberculosis, and (d) by a forecast of the lines on which preventive measures against this disease are likely to be extended.

It has long been known that individuals who suffer from such chronic diseases as nephritis and cirrhosis of the liver are very liable to develop an acute infection during the last stages of their illness. These patients rarely die of their chronic ailment. Often in the very last days, or perhaps hours, of the disease pneumonia, a dysentery, an acute endocarditis, or a streptococcus infection sets in, which quickly terminates fatally and must be regarded as the immediate cause of death. So familiar is this course of events that such pneumonias or dysenteries are now known as a fairly definite group of infections, namely, terminal infections. Often they are not recognized before death, but at autopsy their frequency and varying characters have been well shown by Flexner in his statistical and experimental study upon the subject; and though in some cases of terminal septicaemia the portal of entry was not easily found, yet it is important to note how frequently such local infections as leg ulcer or tonsilitis served as a starting point for the general invasion of bacteria. Of still more importance are his observations upon the bactericidal action of the blood of patients who have chronic diseases. The serum from six out of nine such patients showed a distinct decrease in its destructive power toward the Staphylococcus aureus and two of three patients whose serum did not show a diminished bactericidal action left the hospital improved.

The various problems of infantile mortality are not only supremely interesting to the medical officer of health, but, with the continued decline in the birth rate, are calculated to assume even greater practical importance in the birth rate, are calculated to assume even greater practical importace in the near future. Of these problems none is more in need of solution than the exact etiology of infantile diarrhoea.

That blood or serum and other body fluids, such as the natural or artificially excited exudations, possess bacteriolytic power is a familiar observation.

Of all British colonies New Zealand is the one that most closely resembles Great Britain in size, in situation, and in climate. And the inhabitants of the two countries are of practically the same race. The vital statistics of New Zealand are therefore eminently suitable for comparison with those of Great Britain. In the present paper comparison has been restricted to the birth-rates and death-rates, and in this limited survey several points of interest present themselves.

The prominence given to the intravascular use of antiseptics has hardly been in accord with the results achieved by this method.

The injection of formalin in various amounts and strengths has been given an extended trial in the treatment of pulmonary tuberculosis, and is claimed to have produced beneficial results. Similarly Baccelli has injected corrosive sublimate intravenously in the treatment of syphilis, cerebro-spinal meningitis, and acute rheumatism in man. In animals he has used intravenous injections of corrosive sublimate in the treatment of aphtha epizootica. In this disease he claims that the intravenous injections of corrosive sublimate are of undoubted use in terminating an attack of the disease.

When the publication of the series of Reports for each separate County, dealing with the facts ascertained at the Census of 1901, was completed last March, it was possible for anyone, who would take the trouble, to arrive at the facts relating to the whole of England and Wales, that is, to ascertain not only the finally corrected total population number, but the numbers classified into age and sex groups.

The alimentary canal of Anopheles consists of the following parts:— 1. Mouth, 2. Buccal cavity, 3. Pharynx or Pumping-Organ, 4. Oesophagus, with which are connected, 5. Three food reservoirs (two situated dorsally and one ventrally), 6. Oesophageal Valve, 7. Mid-gut, 8. Ileum, 9. Colon, 10. Rectum, 11. Anus. (See Plate VI, Fig. 1.)

The Select Committee of the House of Commons which was first appointed on April 16th, 1902, and subsequently re-appointed with certain changes in its constitution, for the purpose of inquiring into the Ventilation of the House, instructed the author to make for their information a number of analyses of the air in the Debating Chamber and many other parts of the House. In this communication only the methods used and the results obtained in the case of the Debating Chamber will be referred to. The Committee reported to the House on the 28th July last, and its report, which is published by H.M.'s Stationary Office (No. 283), should be consulted for particulars of its conclusions and recommendations in regard to the ventilation of the House.

1. Powerful anti-sera may be produced by the intravenous injection of smaller quantities of serum than have hitherto generally been used (p. 260).

2. Nuttall's quantitative method affords a simple and fairly accurate means of determining the quantity of precipitum formed. By its means quantitative differences can be appreciated which are scarcely, or not at all, apparent in the tubes on inspection (p. 263).

3. Normal saline solution is the best diluent for normal sera, and 1—21 has been found to be a convenient dilution. Increase of salt has very little effect on the production of precipitum (p. 266).

4. The quantity of precipitum formed is not influenced by the temperature at which the experiment is conducted (i.e. between the temperature of the ice-chest and 37° C.) (p. 268).

5. In the case of dried bloods time per se does not destroy their capacity for reacting with their homologous anti-sera. Fluid sera appear to deteriorate slightly by keeping (pp. 269—274).

6. Putrefaction of the serum, or anti-serum, does not affect the production of a specific precipitum (p. 274).

7. Although the intimate mixture of lime and blood completely destroys the latter, the former is not present in sufficient quantity in ordinary earths to affect blood mixed with earth. The presence of small quantities of lime, however, gives rise to a clouding in solution, which can be got rid of by the passage of CO2, and subsequent filtration (pp. 276—281).

8. The presence of even small quantities of acids, or alkalis, rapidly reduces the quantity of precipitum formed (pp. 281—284).

9. In diseased conditions a marked alteration may occur in the quantity of precipitum (pp. 265 and 285).

10. The volatile antiseptics produce little effect on sera, even after long contact, but formalin, corrosive sublimate, lysol, lysoform, the sulphates of copper and iron, and nitrate of silver, especially in strong solutions, exert a very deleterious action (pp. 287 and 358).

11. Blood dried on fabrics, and materials in common use (with the exception of certain leathers) may with adequate precautions be readily diagnosed (p. 290).

12. After an undiluted anti-serum has been raised to a temperature beyond 60° C. the capacity for producing precipitum is diminished, and it is destroyed completely after exposure to 68° C. These effects seem to be produced at lower temperatures in normal undiluted sera (pp. 354–55).

13. The precipitum-producing power of normal sera is reduced by filtration through a Chamberland filter, but not by passage through a Berkefeld filter (as far as the experiment was conducted) (p. 357).

It is almost impossible to avoid some confusion when one has to deal with diseases which it is difficult to define clearly either by means of symptoms and lesions, or by means of some causal agent capable of demonstration in the majority of cases.

The investigations described in the present paper were undertaken during the summer of 1902, at the request of the Select Committee on the Ventilation of the House of Commons.

In the first place cultures of the nitroso-bacterium were developed in inorganic solutions. These carried to a 5th dilution exhibited practically a pure culture of this species.

Secondly, cultures of the nitroso-bacterium were inoculated into solutions containing small quantities of organic matter. In these they were able to oxidise the ammonia present. It was found that a culture developing in the presence of small quantities of organic matter was better able to oxidise the ammonia in higher percentages of organic matter than a culture taken directly from an inorganic solution.

In growing this species on plates silica jelly has the disadvantage of being difficult to prepare. It was 18 months before I obtained a satisfactory plate. This jelly grows the nitroso-bacterium well, but other species can also develop colonies on it. Ammonia agar also grows the species, as shown by the oxidation of the ammonia, and the colonies assume a characteristic form.

As to beef broth agar and gelatine, these media grew colonies of a micro-organism similiar to the nitroso-bacterium from oxidised ammonia cultures. Pieces of these plates containing such colonies in pure culture frequently oxidised ammonia in solutions. On the other hand pieces of such plates showing no colonies never produced any oxidations of the ammonia. Furthermore the single colonies from silica and ammonia agar plates, which oxidised the ammonia in the media into which they were sub-cultured, grew well on beef broth agar and gelatine.

From the above results I have come to the following conclusions:

(1) That the nitroso-bacterium grows well on any ordinary medium.

(2) That the supposed parallel organism is no other than the nitroso-bacterium itself.

(3) That in the presence of large percentages of organic matter the nitroso-bacterium, although growing very profusely, loses for a time the power of converting ammonia into a nitrite.

1. Diphtheria bacilli have been found in a considerable proportion of persons who have come into contact with cases of diphtheria or with other infected persons.

2. Such persons have been shown to be a grave danger to public health, especially when frequenting schools or institutions, and to constitute the usual channel by which the disease is spread.

3. Very satisfactory results have followed on the isolation of convalescents from the disease and of infected “contacts,” where two or more consecutive negative examinations have been required before release.

4. Carefully conducted investigations amongst healthy persons, who have not at a recent date been in contact with diphtheria cases or infected “contacts,” have shown that virulent diphtheria bacilli are very seldom (3 examples amongst 1511 persons) present in the mouths of the normal population. This fact renders the discovery and isolation of infected persons a practicable possibility and offers a fair prospect of discovering and isolating the majority of them in any outbreak.

5. Diphtheria bacilli are usually distinguishable on morphological and cultural grounds, but whenever possible it is desirable that their virulence should be tested.

6. The bacillus of Hofmann is innocuous to man, and is a very common organism in the mouths of the poorer classes. The distribution of this bacillus points to the conclusion that it is carried from mouth to mouth in the same way as the diphtheria bacillus, and therefore its widespread prevalence in schools attended by poorer children is significant, as showing how widely spread and uncontrollable an outbreak of diphtheria may become unless measures are early taken to deal with infected contacts.

The outbreak which is the subject of the present paper was discovered in the course of an enquiry which is at present being made on the request of the Home Secretary by Mr J. S. Martin, Inspector of Mines, and one of us, into the ventilation of Cornish mines. A number of cases of anaemia had occurred among the miners employed at Dolcoath Mine, Cornwall; and as the anaemia was generally attributed to some defect in the ventilation, this mine, was among the first visited. On examination into the state of the mine, the symptoms of the affected men, and the history of the outbreak, it appeared that the anaemia was almost certainly caused by ankylostomiasis. A more detailed enquiry, in which we have both been engaged, established beyond all doubt the nature of the disease, and has furnished the opportunity of investigating a number of points bearing on the nature and method of spread of ankylostomiasis. A short report on the outbreak has already appeared. We are indebted to Dr S. G. Scott, who has also been engaged in the Home Office Enquiry, for a number of valuable notes as to blood-examinations, and many other details.